178 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
78. Happ M, Tuite P, Dobbin K, DiVirgilio-Thomas D, Kitutu J. Communication 112. Bredemeyer S, Reid S, Poverinom J, Wacadlo C. Implementation and evalu-
ability, method, and content among nonspeaking nonsurviving patients ation of an individualized developmental care program in a neonatal inten-
treated with mechanical ventilation in the Intensive Care Unit. Am J Crit sive care unit. J Spec Ped Nurs 2008; 13: 281–91.
Care 2004; 13(3): 210–18. 113. Suhonen R, Valimaki M, Leino-Kilpi A. Individualized care, quality of life
79. Travaline JM. Communication in the ICU: an essential component of patient and satisfaction with nursing care. J Adv Nurs 2005; 50: 283–92.
care. J Crit Illness 2002; 17(11): 451–6. 114. Karkkainen O, Bondas T, Eriksson K. Documentation of individualized
80. Alasad J, Ahmad M. Communication with critically ill patients. J Adv Nurs patient care: A qualitative metasynthesis. Nurs Ethics 2005; 12: 123–32.
2005; 50(4): 356–62. 115. Campinha-Bacote J. The process of cultural competence in the delivery
81. Lawrence M. The unconscious experience. Am J Crit Care 1995; 4: 227–32. of healthcare services. 2002 [cited December 2010]. Available from:
82. Green A. An explanatory study of patients’ memory recall of their stay in an www.transculturalcare.net/Cultural_Competence_Model.
adult intensive therapy unit. Intens Crit Care Nurs 1996; 12: 131–37. 116. Ka’ai T, Higgins R. Te ao Māori: Māori worldview. In: Ka’ai TM, Moorfield
83. Benner P, Shobe T. Seeing the person beyond the disease. Am J Crit Care JC, Reilly MPJ, Mosley S, eds. Ki te whaiao: an introduction to Māori culture
2004; 13(1): 75–8. and society. Auckland: Pearson Education; 2004. p. 13–25.
84. Hupcey JE. Feeling safe: the psychosocial needs of ICU patients. J Nurs 117. Wilson DL. The Treaty of Waitangi, nurses and their practice. NZ Nurs Rev
Scholar 2000; 32(4): 361–7. 2002; 3(4): 18.
85. Happ MB, Roesch TK, Garrett K. Electronic voice-output communication 118. Reilly MPJ. Whanaungatanga – kinship. In: Ka’ai TM, Moorfield JC, Reilly
aids for temporarily nonspeaking patients in a medical intensive care unit: MPJ, Mosley S, eds. Ki te whaiao: an introduction to Māori culture and society.
a feasibility study. Heart Lung 2004; 33: 92–101. Auckland: Pearson Education; 2004. p. 61–72.
86. Narayanasamy A, Clissett P, Parumal L, Thompson D, Annasamy S, Edge R. 119. Royal Commission on Social Policy. Volume 2, Part Two: Future directions,
Response to the spiritual needs of older people. J Adv Nurs 2004; 48(1): associated papers. Wellington, NZ: Royal Commission on Social Policy, April
6–16. 1988.
87. Wepa D. Cultural safety in Aotearoa. Auckland, NZ: Pearson Education; 2004. 120. King A, Turia T. He Korowai Oranga: Māori health strategy. Wellington, NZ:
88. Farrell M. Smeltzer & Bare’s textbook of medical–surgical nursing. Sydney: Ministry of Health; 2002.
Lippincott, Williams & Wilkins; 2005. 121. Reilly MPJ. Te timatanga mai o nga atua. In: Ka’ai TM, Moorfield JC, Reilly
89. Leninger MM. Cultural care diversity and universality: a theory of nursing. New MPJ, Mosley S, eds. Ki te whaiao: an introduction to Māori culture and society.
York: National League for Nursing Press; 2001. Auckland: Pearson Education; 2004. p. 1–12.
90. Giger JN, Davidhizar RE. Transcultural nursing: assessment and intervention, 3rd 122. Stenhouse J, Paterson L. Nga poropiti me nga Hatu – prophets and the
edn. St Louis: Mosby; 1999. churches. In: Ka’ai TM, Moorfield JC, Reilly MPJ, Mosley S, eds. Ki te whaiao:
91. Charon JM. Symbolic interactionism: an introduction, an interpretation, an inte- an introduction to Māori culture and society. Auckland, NZ: Pearson Education;
gration, 6th edn. Upper Saddle River: Prentice Hall; 1998. 2004. p. 163–70.
92. Miles R. Racism. London: Routledge; 1989. 123. Durie M. Whaiora: Māori health development, 2nd edn. Auckland, NZ: Oxford
93. Ryan A, Carryer J, Patterson L. Healthy concerns: sociology for New Zealand University Press; 1998.
nursing and midwifery students. Auckland, NZ: Pearson Education; 2003. 124. Australian Bureau of Statistics. 4713.0 Population characteristics, Aboriginal
94. Wilson D. The nurse’s role in improving indigenous health. Contemp Nurse and Torres Strait Islander Australians, 2006. Indigenous population. [Cited
2003; 15(3): 232–40. January 2011]. Available from: http://www.abs.gov.au/AUSSTATS/[email protected]/
95. Mosley S, ed. Ki te whaiao: an introduction to Māori culture and society. Auck- Lookup/82742A1B597A338CCA257718002A6FCE?
land, NZ: Pearson Education; 2004: 61–72. 125. Australian Bureau of Statistics. 4704.0 The Health and Welfare of Australia’s
96. Jackson D, Brady W, Stein I. Toward (re)conciliation: (re)constructing Aboriginal and Torres Strait Islander Peoples, Oct 2010. [Cited February
relationships between indigenous health workers and nurses. J Adv Nurs 2011]. Available from: http://www.abs.gov.au/AUSSTATS/[email protected]/lookup
1999; 29(1): 97–103. /4704.0Chapter700Oct+2010.
97. Coyle J. Understanding dissatisfied users: developing a framework for 126. Eckerman A, Dowd T, Chong E, Nixon L, Gray R, Johnson S. Binan Goonj:
comprehending criticisms of health care work. J Adv Nurs 1999; 30(3): bridging cultures in Aboriginal health, 2nd edn. Sydney: Churchill Livingstone;
723–31. 2006.
98. Ramsden I. Kawa Whakaruruhau: cultural safety in nursing education. 127. National Aboriginal Health Strategy Working Party. A national Aboriginal
Wellington, NZ: Ministry of Health; 1990. health strategy. Canberra: Department of Aboriginal Affairs; 1989.
99. Ramsden IM. Cultural safety and nursing education in Aotearoa and Te 128. Commonwealth Department of Health and Ageing & Office for Aboriginal
Pounamu. Unpublished doctoral thesis, 2002: Victoria University of and Torres Strait Islander Health. ‘Gettin em n keeping em.’ Report of the
Wellington, New Zealand. [Cited January 2011]. Available from: http:// Indigenous Nursing Education Working Group; 2002.
culturalsafety.massey.ac.nz/thesis.htm. 129. Latour JM, Fullbrook P, Albarron JW. EfCCNa survey: European intensive
100. Wood PJ, Schwass M. Cultural safety: a framework for changing attitudes. care nurses’ attitudes and beliefs towards end-of-life care. Nurs Crit Care
Nurs Prax NZ 1993; 8(1): 4–15. 2009; 14: 110–21.
101. Rosenjack Burchum JL. Cultural competence: an evolutionary perspective. 130. Halligan P. Caring for patients of Islamic denomination: Critical care nurses’
Nurs Forum 2002; 37(4): 5–15. experiences in Saudi Arabia. J Clin Nurs 2006; 15: 1565–73.
102. Geron SM. Cultural competency: How is it measured? Does it make a 131. Kongsuwan H. Promoting peaceful death in the intensive care unit in Thai-
difference? Generations 2002; 26(3): 39–45. land. Int Nurs Rev 2009; 56: 106–12.
103. Wilson D. The significance of culturally appropriate health service for indig- 132. Blockley C. Meeting patients’ religious needs. Kai Tiaki Nursing New Zealand
enous Māori women. Contemp Nurs 2008; 28: 173–88. 2001/2002; 7(11): 15–17.
104. Durie M. Cultural competence and medical practice in New Zealand. Paper 133. Bagshaw SM, Webb SAR, Delany A et al. Very old patients admitted to inten-
presented to the Australian and New Zealand Boards and Council Con- sive care in Australia and New Zealand: a multi centre cohort analysis. Crit
ference, Wellington, NZ; 2001. Care 2009; 13(2): R45.
105. Wilson D, Roberts M. Māori health initiatives. In: Wepa D, ed. Cultural safety 134. Warren N. Critical care family members’ satisfaction with bereavement
in Aotearoa/New Zealand. Auckland, NZ: Pearson Education; 2004. experiences. Crit Care Nurs Q 2002; 25(2): 54–60.
106. Chambers-Evans J, Stelling J, Godin M. Learning to listen: serendipitous 135. Puri VK. Death in the ICU: feelings of those left behind. Chest 2003; 124(1):
outcomes of a research training experience. J Adv Nurs 1999; 29(1): 11–13.
79–87. 136. Gries CJ, Curtis JR, Wall RJ, Engelberg RA. Family member satisfaction with
107. Funnell MM. Patient empowerment. Crit Care Nurs Q 2004; 27(2): 201–4. end-of-life decision making in the ICU. Chest 2008; 133: 704–12.
108. Conning AM, Rowland LA. Staff attitudes and the provision of individualised 137. Gaeta S, Price KJ, End-of-life issues in critically ill, cancer patients. Crit Care
care: What determines what we do for people with long-term psychiatric Clin 2010; 26: 219–27.
disabilities? J Ment Health 1992; 1(1): 71–80. 138. Rocker GM, Heyland DK, Cook DJ, Dodek PM, Kutsogiannis DJ. Most
109. Proctor S. Whose evidence? Agenda setting in multi-professional research: critically ill patients are perceived to die in comfort during withdrawal
observations from a case study. Health, Risk Soc 2002; 4(1): 45–99. of life support: a Canadian multicentre study. Can J Anesth 2004; 51(6):
110. Waters KR, Easton N. Individualized care: is it possible to plan and carry 623–30.
out? J Adv Nurs 1999; 29(1): 79–87. 139. Kuschner WG, David A, Gruenewald DA, Clum N, Beal A, Ezeji-Okoye SC.
111. Christensen JC. Nursing partnership: a model for nursing practice – Hauora Implementation of ICU palliative care guidelines and procedures: a quality
takirua: he tauira mo nga kaupapa hauora. Wellington, NZ: Daphne Brasell improvement initiative following an investigation of alleged euthanasia.
Associates Press; 1995. Chest 2009; 135: 26–32.
Family and Cultural Care of the Critically Ill Patient 179
140. Mularski RA, Puntillo K, Varkey B, Erstad BL, Grap MJ et al. Pain manage- 152. Fauri D, Ettner B, Kovacs P. Bereavement services in acute care settings. Death
ment within the palliative and end-of-life care experience in the ICU. Chest Stud 2000; 24: 51–64.
2009; 135: 1360–69. 153. Golden A-MJ, Dalgleish T. Is prolonged grief distinct from bereavement-
141. Puntillo KA, Benner P, Drought T, Drew B, Stotts N et al. End-of-life issues related posttraumatic stress? Psychiatry Res 2010; 178: 336–41.
in intensive care units: a national random survey of nurses’ knowledge and 154. Casarett D, Kutner J, Abrahm J. Life after death: a practical approach to grief
beliefs. Am J Crit Care 2001; 10(4): 216–29. and bereavement. Ann Intern Med 2001; 134(3): 208–15.
142. O’Mahony S, McHugh M, Zallman L, Selwyn P. Ventilator withdrawal: 155. Fauri D, Oliver R, Sturtevant J, Scheetz J, Fallat M. Beneficial effects of a
procedures and outcomes. Report of a collaboration between a critical care hospital bereavement intervention program after traumatic childhood death.
division and a palliative care service. J Pain Symptom Manage 2003; 26(4): J Trauma 2001; 50(3): 440–48.
954–61. 156. Williams R, Harris S, Randall L, Nichols R, Brown S. A bereavement after-care
143. Enes SPD. An exploration of dignity in palliative care. Palliat Med 2003; 17: service for intensive care relatives and staff: the story so far. Nurs Crit Care
263–9. 2003; 8(3): 109–15.
144. Schaefer KG, Block SD. Physician communication with families in the ICU: 157. Valks K, Mitchell ML, Inglis-Simmons C, Limpus A. Dealing with death: an
evidence-based strategies for improvement. Curr Opin Crit Care 2009; 15: audit of family bereavement programs in Australian intensive care units. Aust
569–77. Crit Care 2005; 18(3): 257–68.
145. Cook D, Rocker DM, Heyland D. Dying in the ICU: strategies that may 158. Brosche TA. Death, dying, and the ICU nurse. Dimens Crit Care Nurs 2003;
improve end-of-life care. Can J Anesth 2004; 51(3): 266–72. 22(4): 173–9.
146. Johnson N, Cook D, Giacomini M, Willms D. Towards a ‘good’ death: 159. Main J. Management of relatives of patients who are dying. J Clin Nurs 2002;
end-of-life narratives constructed in an intensive care unit. Cult Med Psychia- 11: 794–801.
try 2000; 24: 275–95. 160. Rogers S, Babgi A, Gomez C. Educational Interventions in End-of-Life Care:
147. Mosenthal AC, Murphy PA, Barker LK, Lavery R, Retano A, Livingston DH. Part I. Adv Neonatal Care 2008; 8(1): 56–65.
Changing the culture around end-of-life care in the trauma intensive care 161. Rees E, Hardy J. Novel consent process for research in dying patients unable
unit. J Trauma 2008; 64(6): 1587–93. to give consent. BMJ 2003; 327: 198–202.
148. Clarke EB, Curtis R, Luce JM, Levy M, Danis M et al. Quality indicators for 162. Kutash M, Northrop, L. Family members’ experiences of the intensive care
end-of-life care in the intensive care unit. Crit Care Med 2003; 31(9): unit waiting room. J Adv Nurs 2007; 60(4): 384–8.
2255–62. 163. Roberti SM, Fitzpatrick JJ. Assessing family satisfaction with care of
149. Krueger G. Meaning-making in the aftermath of sudden infant death critically ill patients: a pilot study. Crit Care Nurs 2010; 30(6):
syndrome. Nurs Inq 2006; 13(3): 163–71. 18–26.
150. Campbell M, Thill M. Bereavement follow up to families after death in the 164. Damghi N, Khoudri I, Oualili L, Abidi K, Madani N et al. Measuring the
intensive care unit. Crit Care Med 2000; 28(4): 1252–3. satisfaction of intensive care unit patient families in Morocco: A regression
151. Nelson JE, Angus DC, Weissfeld LA, Puntillo KA, Danis M et al. End-of-life tree analysis. Crit Care Med 2008; 36(7): 2084–91.
care for the critically ill: A national intensive care unit survey. Crit Care Med 165. Silvestri LA. Saunders comprehensive review for the NCLEX-RN(R) examination,
2006; 34(10): 2547–53. 3rd edn. St Louis: Elsevier Saunders; 2005.
Cardiovascular Assessment
9 and Monitoring
Thomas Buckley
Frances Lin
RELATED ANATOMY
Learning objectives AND PHYSIOLOGY
After reading this chapter, you should be able to: The cardiovascular system is essentially a transport system
● describe the normal blood flow through the cardiovascular for distributing metabolic requirements to, and collecting
system byproducts from, cells throughout the body. The heart
● define each stage of the cardiac action potential pumps blood continuously through two separate circula-
● describe the determinants of cardiac output tory systems: both to the lungs, and all other parts of the
● describe the reasons for the assessment and monitoring of body (see Figure 9.1). Structures on the right side of the
critically ill patients heart pump blood through the lungs (the pulmonary
● summarise the key principles underpinning cardiac circulation) to be oxygenated. The left side of the heart
pumps oxygenated blood throughout the remainder of
assessment and monitoring the body (the systemic circulation). The two systems
1,2
● identify the recommended anatomical landmarks for are connected, so the output of one becomes the input
cardiac auscultation and identify normal and common of the other.
abnormal heart sounds
● describe the physiological bases and reasons for different
types of haemodynamic monitoring CARDIAC MACROSTRUCTURE
The heart is cone-shaped and lies diagonally in the medi-
astinum towards the left side of the chest. The point of
the cone is called the apex and rests just above the dia-
phragm; the base of the cone lies just behind the medi-
astinum. The adult heart is about the size of that
Key words individual’s fist, weighs around 300 g, and is composed
of chambers and valves that form the two separate pumps.
cardiovascular macrostructure The upper chambers, the atria, collect blood and act as a
coronary perfusion primer to the main pumping chambers, the ventricles. As
cardiovascular electrophysiology the atria are low-pressure chambers, they have relatively
cardiovascular assessment thin walls and are relatively compliant. As the ventricle
heart sounds propels blood against either pulmonary or systemic pres-
electrocardiography sure, they are much thicker and more muscular walls than
the atria. As pressure is higher in the systemic circulation,
haemodynamic monitoring the left ventricle is much thicker than the right ventricle.
chest X-ray Dense fibrous connective tissue rings provide a firm
diagnostic imaging anchorage for attachments of atrial and ventricular muscle
and valvular tissue. 1,4
One-way blood flow in the system is facilitated by valves.
Valves between the atria and ventricles are composed of
INTRODUCTION cusps or leaflets sitting in a ring of fibrous tissue and col-
lagen. The cusps are anchored to the papillary muscles by
This chapter reviews the support of cardiovascular func- chordae tendinae so that the cusps are pulled together
tion in the face of many compromises to the system. It is and downwards at the onset of ventricular contraction.
essential that the reader has a thorough knowledge of The atrioventricular valves are termed the tricuspid valve
both electrical and mechanical functions of the cardiac in the right side of the heart and the mitral or bicuspid
system. Methodology for assessment of cardiovascular valve in the left side of the heart. Semilunar valves prevent
elements are discussed, along with best practice ideas and backflow from the pulmonary artery (pulmonic valve)
180 diagnostic techniques. and aorta (aortic valve) into the right and left ventricles
Cardiovascular Assessment and Monitoring 181
Capillary beds of
lungs where gas
exchange occurs
Pulmonary Pulmonary
arteries veins
Pulmonary circuit
Superior vena cava
Aorta and
Inferior vena cava Left branches
atrium
Right
atrium Left
ventricle Oxygenated blood from
Deoxygenated blood Right the lungs to the whole body
returned to the lungs ventricle
Systemic circuit
Capillary beds of all
body tissues where
gas exchange occurs
FIGURE 9.1 The systemic and pulmonic circulations. 3
correspondingly. The muscles in the ventricles follow a The pericardium provides physical protection for the
distinct spiral path so that during contraction, blood is heart against mechanical force and forms a barrier to
propelled into the respective outflow tracts of the pulmo- infection and inflammation from the lungs and pleural
nary artery and aorta. The aortic valve sits in a tubular space. Branches of the vagus nerve, the phrenic nerves and
area of mostly non-contractile collagenous tissue, which the sympathetic trunk enervate the pericardium.
contains the opening of the coronary arteries. The coro-
nary arteries run through deep grooves that separate the The myocardium forms the bulk of the heart and is com-
atria and ventricles. The two sides of the heart are divided posed primarily of myocytes. Myocytes are the con tractile
by a septum, which ensures that two separate but inte- cells, and autorhythmic cells, which create a conduction
grated circulations are maintained. 1,4 pathway for electrical impulses. Myocytes (see Figure 9.2)
are cylindrical in shape and able to branch to intercon-
The heart wall has three distinct layers: the outer protec- nect with each other. The junctions between myocytes are
tive pericardium, a medial muscular layer or myocar- termed intercalated discs and contain desmosomes and
6
dium, and an inner layer or endocardium that lines the gap junctions. Desmosomes act as anchors to prevent
heart. The pericardium is a double-walled, firm fibrous the myocytes from separating during contraction. Gap
sac that encloses the heart. The two layers of the pericar- junctions contain connexons, which allow ions to move
dium are separated by a fluid-filled cavity, enabling the from one myocyte to the next. The movement of ions
layers to slide over each other smoothly as the heart beats. from cell to cell ensures that the whole myocardium acts
182 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
Red cell in
A band capillary
Capillary
I band endothelium
Invagination of Connective
sarcolemma by tissue
transverse tubule
Transverse tubule Intercalated
disk
Mitochondria
M line in Gap junction
H zone
Sarcolemma
Z line
Sarcomere Sarcoplasmic
reticulum
FIGURE 9.2 Diagram of an electron micrograph of cardiac muscle showing mitochondria, intercalculated discs, tubules and sarcoplasmic reticulum. 5
as one unit, termed a functional syncytium. When isch- ultimately branch into a dense network of capillaries to
aemia occurs, the gap junctions may uncouple, so ions support cardiac myocytes. Anastomoses between branches
do not move as freely. Uncoupling may also contribute of the coronary arteries often occur in mature individuals
to the poor conduction evidenced on ECG during when myocardial hypoxia has been present. These anas-
ischaemia. 5 tomoses are termed collateral arteries, but the contribu-
tion to normal cardiac perfusion during occlusion of
The endocardium is composed primarily of squamous coronary arteries is unclear. 1
epithelium, which forms a continuous sheet with the
endothelium that lines all arteries, veins and capillaries. The cardiac veins collect venous blood from the heart.
The vascular endothelium is the source of many chemical Cardiac venous flow is collected into the great coronary
mediators, including nitric oxide and the endothelin vein and coronary sinus and ultimately flows into the
involved in vessel regulation. It has been theorised that right atrium. Lymph drainage of the heart follows
the endocardium may also have this function. 1,4 the conduction tissue and flows into nodes and into the
superior vena cava.
Coronary Perfusion
The heart is perfused by the right and left coronary arter- PHYSIOLOGICAL PRINCIPLES
ies that arise from openings in the aorta called the coro-
nary ostia (see Figure 9.3). The right coronary artery Mechanical Events of Contraction
(RCA) branches supply the atrioventricular node, right Energy is produced in the myocytes by a large number
atrium and right ventricle, and the posterior descending of mitochondria contained within the cell. The mito-
branch supplies the lower aspect of the left ventricle. The chondria produce adenosine triphosphate (ATP), a
left coronary artery divides into the left anterior descend- molecule that is able to store and release chemical energy.
ing artery (LAD) and the circumflex artery (CX) shortly Other organelles in the myocyte, called sarcoplasmic
after its origin. The LAD supplies the interventricular reticulum, are used to store calcium ions. The myocyte
septum and anterior surface of the left ventricle. The CX cell membrane (sarcolemma) extends down into the cell
supplies the lateral and posterior aspects of the left ven- to form a set of transverse tubules (T tubules), which
tricle. This is the most common distribution of the coro- rapidly transmit external electrical stimuli into the cell.
nary arteries, but it is not uncommon for the right Cross-striated muscle fibrils, which contain contractile
coronary artery to be small and the CX to supply the units, fill up the myocyte. These fibrils are termed
inferior wall of the left ventricle. The coronary arteries sarcomeres.
Cardiovascular Assessment and Monitoring 183
Left main coronary artery Pulmonary veins
Superior
vena cava
Superior
vena cava
Left circumflex
Right Inferior vena
coronary cava
artery
Right
coronary
artery (RCA)
Left anterior Posterior
descending (LAD) descending artery (PDA)
ANTERIOR POSTERIOR
FIGURE 9.3 Location of the coronary arteries. 5
Electrical events of Depolarisation, Resting
Potential and Action Potential
Myosin
filament Automaticity and rhythmicity are intrinsic properties of
all myocardial cells. However, specialised autorhythmic
cells in the myocardium generate and conduct impulses
in a specific order to create a conduction pathway. This
Cross-
Hinge bridge pathway ensures that contraction is coordinated and
rhythmical, so that the heart pumps efficiently and con-
tinuously. Electrical impulses termed action potentials
Actin filament Z line are transmitted along this pathway and trigger contrac-
tion in myocytes. Action potentials represent the inward
and outward flow of negative and positive charged ions
across the cell membrane (see Figure 9.5).
Cell membrane pumps create concentration gradients
across the cell membrane during diastole to create a
resting electrical potential of −80 mV. Individual fibres
are separated by membranes but depolarisation spreads
rapidly because of the presence of gap junctions. There
are five key phases to the cardiac action potential:
FIGURE 9.4 Actin and myosin filaments and other cross-bridges respon- 0. depolarisation
sible for cell contraction. 5 1. early rapid repolarisation
2. plateau phase
3. final rapid repolarisation
4. resting membrane phase. 8
The sarcomere contains two types of protein myofila-
ments, one thick (myosin) and one thin (actin, tropo- The contractile response begins just after the start of
myosin and troponin) (see Figure 9.4). The myosin depolarisation and lasts about 1.5 times as long as the
molecules of the thick filaments contain active sites that depolarisation and repolarisation (see Figure 9.6).
form bridges with sites of the actin molecules on the thin The action potential is created by ion exchange triggered
filaments. These filaments are arranged so that during by an intracellular and extracellular fluid trans-membrane
contraction, bridges form and the thin filaments are imbalance. There are three ions involved: sodium, potas-
pulled into the lattice of the thick filaments. As the fila- sium and calcium. Normally, extracellular fluid contains
ments are pulled towards the centre of the sarcomere, the approximately 140 mmol/L sodium and 4 mmol/L
degree of contraction is limited by the length of the sar- potassium. In intracellular fluid these concentrations are
comere. Starling’s law states that, within physiological reversed. The following is a summary of physiological
limits, the greater the degree of stretch, the greater the events during a normal action potential:
force of contraction. The length of the sarcomere is the
physiological limit because too great a stretch will discon- ● at rest cell membranes are more permeable to potas-
nect the myosin–actin bridges. sium and consequently;
184 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
● potassium moves slowly and passively from intracel- ● the final resting phase occurs when slow potassium
lular to extracellular fluid; leakage allows the cell to increase its negative charge
● rapid ion movement caused by sodium flowing into to ensure that it is more negative than surrounding
the cell alters the charge from −90 mV to +30 mV; fluid, before the next depolarisation occurs and the
● there follows a brief influx of calcium via the fast cycle repeats. 6
channel and then more via the slower channel to
create a plateau, the time of which determines stroke Cardiac muscle is generally slow to respond to stimuli
volume due to its influence on the contractile strength and has relatively low ATPase activity. Its fibres are depen-
of muscle fibres; dent on oxidative metabolism and require a continuous
● the third phase occurs when the potassium channel supply of oxygen. The length of fibres and the strength of
opens, allowing potassium to leave the cell, to restore contraction are determined by the degree of diastolic
the negative charge, causing rapid repolarisation. filling in the heart. The force of contraction is enhanced
by catecholamines. 2
Depolarisation is initiated in the sino-atrial (SA) node
and spreads rapidly through the atria, then converges
40 on the atrio-ventricular (AV) node; atrial depolarisation
2
0 normally takes 0.1 second. There is a short delay at the
AV node (0.1 sec) before excitation spreads to the ven-
-40 Resting tricles. This delay is shortened by sympathetic activity
potential 3 and lengthened by vagal stimulation. Ventricular depo-
-80 4 4 larisation takes 0.08–0.1 sec, and the last parts of the
heart to be depolarised are the posteriobasal portion of
the left ventricle, the pulmonary conus and the upper
septum. 8
The electrical activity of the heart can be detected on the
A ARP RRP body surface because body fluids are good conductors;
the fluctuations in potential that represent the algebraic
sum of the action potential of myocardial fibres can be
recorded on an electrocardiogram (see later in chapter).
0 3
4 Threshold Cardiac Macrostructure and Conduction
4
B The electrical and mechanical processes of the heart
differ but are connected. The autorhythmic cells of the
FIGURE 9.5 (A) Action potential in a ‘fast response’, non-pacemaker cardiac conduction pathway ensure that large portions
myocyte: phases 0–4, resting membrane potential −80 mV, absolute refrac- of the heart receive an action potential rapidly and
tory period (ARP) and relative refractory period (RRP). (B) Action potential
in a ‘slow response’, pacemaker myocyte. The upward slope of phase 4, on simultaneously. This ensures that the pumping action
reaching threshold potential, results in an action potential. of the heart is maximised. The conduction pathway is
7
Phase 1
20 mV
Phase 2
Mechanical
Phase 3
contraction
Phase 0
ACTION
POTENTIAL 90 mV Phase 4 90 mV
QRS
T
ECG
Depolarisation Repolarisation
FIGURE 9.6 Action potential. 5
Cardiovascular Assessment and Monitoring 185
Sinus node
LBB
(anterior fascicle)
AV node LBB
(posterior fascicle)
Bundle of His
RBB
LBB
(septal fibres)
FIGURE 9.7 Cardiac conduction system: AV, atrioventricular; RBB, right bundle branch; LBB, left bundle branch. 5
composed of the sinoatrial (SA) node, the atrioventricular CARDIAC OUTPUT
(AV) node, the bundle of His, right and left bundle
branches and Purkinje fibres (see Figure 9.7). The cells Determinants of Cardiac Output
contained in the pathway conduct action potentials Cardiac performance is altered by numerous homeostatic
extremely rapidly, 3–7 times faster than general myo- mechanisms. Cardiac output is regulated in response to
cardial tissue. Pacemaker cells of the sinus and stress or disease, and changes in any of the factors that
atrioventricular nodes differ, in that they are more per- determine cardiac output will result in changes to cardiac
meable to potassium, so that potassium easily ‘leaks’ output (see Figure 9.8). Cardiac output is the product of
back out of the cells triggering influx of sodium and heart rate and stroke volume; alteration in either of these
calcium back into cells. This permits the spontaneous will increase or decrease cardiac output, as will alteration
automaticity of pacemaker cells. in preload, afterload or contractility. In the healthy indi-
vidual, the most immediate change in cardiac output is
At the myocyte, the action potential is transmitted to the
myofibrils by calcium from the interstitial fluid via seen when heart rate rises. However, in the critically ill,
channels. During repolarisation (after contraction), the the ability to raise the heart rate in response to changing
calcium ions are pumped out of the cell into the intersti- circumstances is limited, and a rising heart rate may have
tial space and into the sarcoplasmic reticulum and stored. negative effects on homeostasis, due to decreased dia-
Troponin releases its bound calcium, enabling the tropo- stolic filling and increased myocardial oxygen demand.
myosin complex to block the active sites on actin, and Preload is the load imposed by the initial fibre length of
the muscle relaxes. the cardiac muscle before contraction (i.e. at the end of
diastole). The primary determinant of preload is the
The cardiac conduction system and the mechanical effi- amount of blood filling the ventricle during diastole, and
ciency of the heart as a pump are directly connected. as indicated in Figure 9.8, it is important in determining
Disruption to conduction may not prevent myocardial stroke volume. Preload influences the contractility of the
contraction but may result in poor coordination and ventricles (the strength of contraction) because of the
lower pump efficiency. Interruption to flow through the relationship between myocardial fibre length and stretch.
coronary arteries may alter depolarisation. Disrupted However, a threshold is reached when fibres become
conduction from the SA to the AV node may allow another overstretched, and force of contraction and resultant
area in the conduction system to become the new domi- stroke volume will fall.
nant pacemaker and alter cardiac output. Although the
autonomic nervous system influences cardiac function, Preload reduces as a result of large-volume loss (e.g.
the heart is able to function without neural control. haemorrhage), venous dilation (e.g. due to hyperthermia
Rhythmical myocardial contraction will continue because or drugs), tachycardias (e.g. rapid atrial fibrillation or
automaticity and rhythmicity are intrinsic to the supraventricular tachycardias), raised intrathoracic pres-
myocardium. sures (a complication of IPPV), and raised intracardiac
186 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
Ventricular chamber
pressure
Preload Contractility Afterload
Ventricular chamber
dimension/wall thickness
Stroke volume Heart rate
Systemic vascular
resistance
Arterial
oxygen Cardiac output
content
Oxygen Mean arterial
delivery (DO ) pressure
2
Oxygen
utilisation
(oxygen
consumption, VO )
2
Deoxygenated
venous return
FIGURE 9.8 Determinants of cardiac function and oxygen delivery. 9
pressures (e.g. cardiac tamponade). Some drugs such as It is measured during systole, and is inversely related to
vasodilators can cause a decrease in venous tone and a stroke volume and therefore cardiac output, but it is not
resulting decrease in preload. Preload increases with fluid synonymous with systemic vascular resistance (SVR), as
overload, hypothermia or other causes of venous con- this is just one factor determining left ventricular after-
striction, and ventricular failure. Body position will also load. Factors that increase afterload include:
affect preload, through its effect on venous return.
● increased ventricular radius
The volume of blood filling the ventricles is also affected ● raised intracavity pressure
by atrial contraction: a reduction in atrial contraction ● increased aortic impedance
ability, as can occur during atrial fibrillation, will result ● negative intrathoracic pressure
in a reduction in ventricular volume, and a corresponding ● increased SVR.
fall in stroke volume and cardiac output.
As afterload rises, the speed of muscle fibre shortening
Preload of the left side of the heart, assessed at the end and external work performed falls, which can cause a
of filling of the left ventricle from the left atrium using decrease in cardiac output in critically ill patients. After-
the pulmonary capillary wedge pressure (PCWP), is load of the right side of the heart is assessed during the
assumed for clinical purposes to reflect left ventricular ejection of blood from the right ventricle into the pulmo-
end-diastolic volume (LVEDV). Due to the non-linear nary artery. This volume is indirectly assessed by calculat-
relationship between volume and pressure, caution ing pulmonary vascular resistance. Ventricular afterload
10
must, however, be taken when interpreting these values, can be altered to clinically affect cardiac performance.
as rises in LVEDP may indicate pathology other than Reducing afterload will increase the stroke volume and
increased preload. Preload of the right side of the heart cardiac output, while also reducing myocardial oxygen
is indirectly assessed at the end of filling of the right demand. However, reductions in afterload are associated
ventricle from the right atrium through central venous with lower blood pressure, and this limits the extent to
pressure (CVP) monitoring. which afterload can be manipulated.
Afterload is the load imposed on the muscle during con- Contractility is the force of ventricular ejection, or the
traction, and translates to systolic myocardial wall tension. inherent ability of the ventricle to perform external work,
Cardiovascular Assessment and Monitoring 187
AP of a
Electrical activity of the heart cell
ventricular
myocardial
ECG Repolarisation
Depolarisation
Mitral Aortic Aortic Mitral
valve valve valve valve
closes opens closes opens
Heart status
Isovolumic contraction Isovolumic relaxation
Slow Atrial Rapid Reduced Rapid Slow
filling systole ejection ejection filling filling
120
Aortic pressure
100
Pressure (mmHg) 80 Left ventricular
pressure
60
Left atrial
40
20 pressure
0
a c v
wave wave wave
FIGURE 9.9 The cardiac cycle. 5
independent of afterload or preload. It is difficult to normally 50–100 mL/beat, and equal amounts are ejected
measure clinically. It is increased by catecholamines, from the right and left ventricle.
calcium, relief of ischaemia and digoxin. It is decreased
by hypoxia, ischaemia, and certain drugs such as thiopen- Cardiac output is dependent on a series of mechanical
tone, β-adrenergic blockers, calcium channel blockers or events in the cardiac cycle (see Figure 9.9). As normal
sedatives. Such changes affect cardiac performance, with average heart rate is maintained at approximately 70
increases in contractility causing increased stroke volume beats/min the average phases of the cardiac cycle are
and cardiac output. Increasing contractility will increase completed in less than a second (0.8 sec). Electrical stim-
myocardial oxygen demand, which could have a detri- ulation of myocardial contraction ensures that the four
mental effect on patients with limited perfusion. Stroke chambers of the heart contract in sequence. This allows
volume is the amount of blood ejected from each ven- the atria to act as primer pumps for the ventricles, while
tricle with each heartbeat. For an adult, the volume is the ventricles are the major pumps that provide the
188 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
impetus for blood through the pulmonary and systemic
vascular systems. The phases of the cardiac cycle are char- Increased
acterised by pressure changes within each of the heart contractility
chambers, resulting in blood flow from areas of high 125
pressure to areas of lower pressure.
During late ventricular diastole (rest), pressures are lowest 100 Normal
contractility
in the heart and blood returns passively to fill the atria.
This flow also moves into the ventricle through the open Ventricular stroke work (mmHg) 75
AV valves, producing 70–80% of ventricular filling. The Decreased
pulmonic and aortic valves are closed, preventing back- 50 contractility
flow from the pulmonary and systemic systems into the
ventricles. Depolarisation of the atria then occurs, some-
times referred to as atrial kick, stimulating atrial contrac- 25
tion and completing the remaining 20–30% of ventricular
filling.
During ventricular systole (contraction), the atria relax 0 4 8 12 16
while the ventricles depolarise, resulting in ventricular Left ventricular end-diastolic filling pressure (LVEDP)
contraction. Pressure rises in the ventricles, resulting in FIGURE 9.10 The Frank-Starling curve. As left ventricular end-diastolic
the AV valves closing. When this occurs, all four cardiac pressure increases, so does ventricular stroke work. 5
valves are closed, blood volume is constant and contrac-
tion occurs (isovolumetric contraction). When the pres-
sure in the ventricles exceeds the pressure in the major According to this mechanism, within limits, the more
vessels the semilunar valves open. This occurs when pres- stretch on the cardiac muscle fibre before contraction, the
sure in the left ventricle reaches approximately 80 mmHg greater the strength of contraction. The ability to increase
and in the right ventricle approximately 27–30 mmHg. strength of contraction in response to increased stretch is
During the peak ejection phase, pressure in the left ven- because there is an optimal range of cross-bridges that
tricle and aorta reaches approximately 120 mmHg and in can be created between actin and myosin in the myocyte.
the right ventricle and pulmonary artery approximately Under this range, when venous return is poor, fewer
25–28 mmHg.
cross-bridges can be created. Above this range, when heart
During early ventricular diastole, the ventricles repolarise failure is present, the cross-bridges can become partially
and ventricular relaxation occurs. The pressure in the ven- disengaged, contraction is poor, and higher filling pres-
tricles falls until the pressures in the aorta and pulmonary sures are needed to achieve adequate contractile force.
artery are higher and blood pushes back against the semi- Ventricular contraction is also intrinsically influenced by
lunar valves. Shutting of these valves prevents backflow the size of the ventricle and the thickness of the ventricle
into the ventricles, and pressure in the ventricles declines wall. This mechanism is described by Laplace’s law, which
further. During ventricular contraction, the atria have states that the amount of tension generated in the wall
been filling passively, so the pressure in the atria rises to of the ventricle required to produce intraventricular pres-
higher than that in the ventricles and the AV valves open, sure depends on the size (radius and wall thickness) of
allowing blood flow to the ventricles. Any rise in heart the ventricle. As a result, in heart failure, when ventricu-
1
rate will shorten the resting period, which may impair lar thinning and dilation is present, more tension or
filling time and coronary artery flow as these arteries fill contractile force is required to create intraventricular pres-
during diastole. 1
sure and therefore cardiac output.
Regulation of Cardiac Output The heart’s ability to pump effectively is also influenced
The heart is a very effective pump and is able to adapt to by the pressure that is required to generate above end
meet the metabolic needs of the body. The activities of diastolic pressure to eject blood during systole. This addi-
the heart are regulated by two responsive systems: intrin- tional pressure is usually determined by how much resis-
sic regulation of contraction, and the autonomic nervous tance is present in the pulmonary artery and aorta, and
system. is in turn influenced by the peripheral vasculature. This
systemic vascular resistance, causing resistance to flow
Intrinsic regulation of contraction responds to the rate of
blood flow into the chambers. Blood flow into the heart known and measured as afterload, is in relation to the
depends on venous return from systemic and pulmonic left ventricle and is influenced by vascular tone and
veins and varies according to tissue metabolism, total disease.
blood volume and vasodilation. Venous return contrib-
utes to end-diastolic volume (preload) and pressure, Autonomic nervous system control and
which are both directly related to the force of contraction regulation of heart rate
in the next ventricular systole. The intrinsic capacity of Although the pacemaker cells of the heart are capable of
the heart to respond to changes in end-diastolic pressure intrinsic rhythm generation (automaticity), inputs from
can be represented by a number of length–tension curves the autonomic nervous system regulate heart rate changes
and the Frank-Starling mechanism (see Figure 9.10). in accordance with body needs by stimulating or
Cardiovascular Assessment and Monitoring 189
depressing these pacemaker cells. Cardiac innervation Capillary Capillary
includes sympathetic fibres from branches of T1–T5, and Endothelial cells network
10
parasympathetic input via the vagus nerve. The heart
rate at any moment is a product of the respective inputs
of sympathetic stimuli (which accelerate) and parasym-
pathetic stimuli (which depress) on heart rate. Rises in
heart rate can thus be achieved by an increase in sympa-
thetic tone or by a reduction in parasympathetic tone
(vagal inhibition). Conversely, slowing of the heart rate
can be achieved by decreasing sympathetic or increasing
parasympathetic activity. 4
Hormonal, biochemical and pharmacological inputs also
exert heart rate influences by their effect on autonomic Lumen
neural receptors or directly on pacemaker cells. In Valve
mimicking the effects of direct nervous inputs, these Tunica intima:
influences may be described as sympathomimetic or Endothelium
parasympathomimetic. Sympathomimetic stimulation Subendothelial layer
(e.g. through the use of isoprenaline) achieves the same Internal elastic lamina
cardiac endpoints as direct sympathetic activity, increas- Artery Vein
ing the heart rate, while sympathetic antagonism (e.g. Tunica media
beta-blockade therapy) slows the heart through receptor Tunica adventitia
inhibition. By contrast, parasympathomimetic agonist 3
activity slows the heart rate, while parasympathetic anta- FIGURE 9.11 The structure of arteries, veins and capillaries.
gonism (e.g. via administration of atropine sulphate)
raises the heart rate by causing parasympathetic receptor
blockade. 4
veins are numerous and have thinner, less muscular walls,
THE VASCULAR SYSTEM which can dilate to store extra blood (up to 64% of total
The vascular system is specialised according to the differ- blood volume at any time). Some veins, particularly in
ent tissue it supplies, but the general functions and char- the lower limbs, contain valves to prevent backflow and
acteristics are similar. All vessels in the circulatory system ensure one-way flow to the heart. Venous return is pro-
are lined by endothelium, including the heart. The endo- moted during standing and moving by the muscles of the
thelium creates a smooth surface, which reduces friction legs compressing the deep veins, promoting blood flow
and also secretes substances that promote contraction towards the heart. 1,4
and relaxation of the vascular smooth muscle. Arteries
function to transport blood under high pressure and are Blood Pressure
characterised by strong elastic walls that allow stretch Blood flow is maintained by pulsatile ejection of blood
during systole and high flow. During diastole, the artery from the heart and pressure differences between the
walls recoil so that an adequate perfusion pressure is blood vessels. Traditionally, blood pressure is measured
maintained. Arterioles are the final small branches of the from the arteries in the general circulation at the
arterial system prior to capillaries, and have strong mus- maximum value during systole and the minimum value
cular walls that can contract (vasoconstrict) to the point occurring during diastole. The cardiovascular system must
of closure and relax (vasodilate) to change the artery supply blood according to varying demands and in a
lumen rapidly in response to tissue needs. The lumen range of circumstances, with at least a minimal blood
created by the arterioles is the most important source of flow to be maintained to all organs. At a local level this
resistance to blood flow in the systemic circulation (just is achieved by autoregulation of individual arteries, such
under 50%).
as the coronary arteries, in response to the metabolic
Capillaries function to allow exchange of fluid, nutrients, needs of the specific tissue or organ. The exact mecha-
electrolytes, hormones and other substances through nism is unknown, but it has been proposed that increased
highly permeable walls between the blood plasma and vascular muscle stretch and/or metabolites and decreased
interstitial fluid (see Figure 9.11). Just before the capillary oxygen levels are detected and cells release substances
beds are precapillary sphincters, bands of smooth muscle such as adenosine. These substances result in rapid
4
that adjust flow in the capillaries. Venules collect blood vasodilation and increased perfusion. The vascular endo-
from the capillaries to veins. Excess tissue fluid is col- thelium actively secretes prostacyclin and endothelial-
lected by the lymphatic system. Lymphatic veins have a derived relaxing factor (nitric oxide), both vasoactive
similar structure to the cardiovascular system veins agents.
described below, with lymph returning to this system at
the right side of the heart. There are three main regulatory mechanisms of blood
pressure control: (a) short-term autonomic control; (b)
Veins collect and transport blood back to the heart at low medium-term hormonal control; and (c) long-term renal
pressure and serve as a reservoir for blood. Therefore, system control.
190 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
Autonomic control It is important to create a health history, if not already
The cardiovascular control centre connects with the hypo- obtained. This history should aim to elicit a description
thalamus to control temperature, the cerebral cortex and of the present illness and chief complaint. A useful guide
the autonomic system to control cardiac activity and in taking a specific cardiac history is to use directed ques-
peripheral vascular tone. Information about blood pres- tions to seek information regarding symptom onset,
sure and resistance is sensed by neural receptors (barore- course, duration, location, precipitating and alleviating
ceptors) in the aortic arch and the carotid sinuses, which factors. Some common cardiovascular disease related
detect changes in blood supply to the body and the brain. symptoms to be observant for include: chest discomfort
Impulses from these receptors initiate a blood-pressure or pain, palpitations, syncope, generalised fatigue, dys-
regulating reflex in the cardiovascular centre, which acti- pnoea, cough, weight gain or dependent oedema. Chest
vates the parasympathetic system and sympathetic system pain, discomfort or tightness should be initially consid-
to alter cardiac activity and dilation or constriction of ered indicative of cardiac ischaemia until proven other-
arterioles and veins to lower or raise blood pressure. The wise by further examination and diagnostic assessment.
cardiovascular system also maintains a constant resting Additionally, a health history should be inclusive of
tone of intermediate tension in the arteries. known cardiovascular risk factors, such as hyperlipidae-
mia or hypertension, and any medications the patient
Hormonal control may be taking including over the counter medications.
Changes in blood pressure are also detected by the Prior to inspecting or palpating the patient, the nurse
adrenal medulla, which secretes catecholamines as cardiac should take note of the patient’s general appearance
output declines. The two main catecholamines, norepi- noting whether the patient is restless, able to lie flat, in
nephrine (noradrenaline) and epinephrine (adrenaline), pain or distress, is pale or has decreased level of con-
mimic the action of the sympathetic system. Noradrena- sciousness. Patients with compromised cardiac output
line directly stimulates the alpha-adrenergic receptors of will likely have decreased cerebral perfusion and may
the autonomic system, causing vasoconstriction and have mental confusion, memory loss or slowed verbal
raising blood pressure, while adrenaline has a wider responses. Additionally, assessment of any pain should
range of effects, including stimulating β 1 -adrenergic be noted.
receptors, resulting in increased cardiac contractility and
heart rate and thereby also raising blood pressure. Specific physical assessment in relation to cardiovascular
function should be inclusive of:
Renal control ● vital signs
Renal control of blood pressure in the long-term occurs ● respiratory assessment for signs of pulmonary oedema
via control of blood volume. Generally, as blood pressure (shortness of breath or basal crepitations)
or volume rises, the kidneys produce more urine; con- ● assessment of neck vein distension for signs of right
versely, as blood pressure or volume falls, the kidneys sided venous congestion
produce less urine. ● assessment for signs of peripheral oedema
● capillary refill time with >3 sec return indicative of
In addition to longer term fluid regulation, during acute
illness or time of acute hypotension, the renin-angiotensin- sluggish capillary return
aldesterone system (RAAS) plays an important role in ● 12-lead ECG for signs of ischaemia or cardiac
maintaining blood pressure. This negative feedback pathology
system results in both reabsorption of intravascular fluid ● appearance and temperature of the skin for signs of
and increases peripheral resistance, in an effort to increase peripheral constriction or dehydration
blood pressure. Further details on the RAAS system can ● core body temperature measurement
be found in Chapter 18. ● urine output with <0.5 mL/kg/hour a potential indi-
cator of decreased renal perfusion. 12
ASSESSMENT ASSESSMENT OF PULSE
It is essential that the critical care nurse conducts a com- In the critical care environment, the heart rate can be
prehensive cardiac assessment on a critically ill patient. observed from a cardiac monitor; however, this does not
The nursing assessment aims to both define patient car- give qualitative information about the arterial pulse. Rou-
diovascular status as well as to inform implementation of tinely performed as part of most patient assessments,
an appropriate clinical management plan. The focus of information gathered from pulse assessment can give
the cardiovascular assessment varies according to the useful cues and direct further assessments. Although the
setting, clinical presentation and treatments commenced, radial pulse is distant from the central arteries, it is useful
if any. However, the main priority should be to determine for gathering information on rate, rhythm and strength.
whether the patient is haemodynamically stable or requir- Heart rate below 60 beats per minute is defined as ‘bra-
ing initiation or adjustment of supportive treatments.
dycardia’ (‘brady’ is Greek for slow, and ‘kardia’ means
A thorough cardiac assessment requires the critical care heart). A heart rate greater than 100 beats per minute is
nurse to be competent in a wide range of interpersonal, called ‘tachycardia’ (’tachy’ in Greek meaning swift). An
observational, and technical skills. A cardiac assessment important aspect of pulse assessment involves assessment
should be performed as part of a comprehensive patient for regularity. Detection of an irregular pulse should
assessment and should consider the following elements. trigger further investigation and prompt ECG assessment
Cardiovascular Assessment and Monitoring 191
for atrial fibrillation, a condition in which atrial contrac-
tion becomes lost due to chaotic electrical activity with TABLE 9.1 Guide to placement of stethoscope when
variable ventricular response. In addition to rate and listening to heart sounds
rhythm, assessment of pulse, especially if palpated in the
carotid or femoral artery, can reveal a bounding pulse, Auditable region
that may be indicative of hyperdynamic state or aortic Stethescope placement of heart
regurgitation. An alternating strong and weak pulse,
known as pulsus alternans, may be observed in advanced 2nd intercostal space right of sternum aortic valve
heart failure. 2nd intercostal space left of sternum pulmonary valve
4th intercostal space left side of sternum tricuspid valve
AUSCULTATION OF HEART SOUNDS
5th intercostal space midclavicular line mitral valve
Auscultation of the heart involves listening to heart
sounds over the pericardial area using a stethoscope.
While challenging to achieve competence in, cardiac aus- In assessment of the critically ill patient, extra heart
cultation is an important part of cardiac physical exami- sounds, labelled S3 and S4, may be heard during times
nation and relies on sound understanding of cardiac of extra ventricular filling or fluid overload. Often referred
anatomy, cardiac cycle and physiologically associated to as ‘gallops’, these extra heart sounds are accentuated
sounds. For accurate auscultation, experience in assess- during episodes of tachycardia. S3, ventricular gallop,
ment of normal sounds is critical and can only be occurs during diastole in the presence of fluid overload.
obtained through constant practice. When auscultating Considered physiological in children or young people,
heart sounds, normally two sounds are easily audible due to rapid diastolic filling, S3 may be considered patho-
known as the first (S1) and second (S2) sounds. A useful logical when due to reduced ventricular compliance and
technique when listening to heart sounds is to feel the associated increased atrial pressures. As S3 occurs early
carotid pulse at the same time as auscultation which will in diastole, it will be heard and associated more closely
help identify the heart sound that corresponds with ven- with S2.
tricular systole.
S4 is a late diastolic sound and may be heard shortly
before S1. S4 occurs when ventricular compliance is
reduced secondary to aortic or pulmonary stenosis, mitral
Practice tip regurgitation, systemic hypertension, advanced age or
ischaemic heart disease. Patients with severe ventricular
When learning to interpret heart sounds, feel the carotid pulse dysfunction may have both S3 and S4 audible, although
at the same time as auscultation which will help identify the when coupled with tachycardia, these may be difficult to
heart sound that corresponds with ventricular systole (S1). differentiate and will require specialist assessment.
The critical care nurse auscultating the heart should also
listen for a potential pericardial rub. This ‘rubbing’ or
The first heart sound (S1) occurs at the beginning of ‘scratching’ sound is secondary to pericardial inflamma-
ventricular systole, following closure of the intra-cardiac tion and/or fluid accumulation in the pericardial space.
valves (mitral and tricuspid valves). This heart sound is To differentiate pericardiac rub from pulmonary rub, if
best heard with the diaphragm of the stethoscope and possible the patient should be instructed to hold their
loudest directly over the corresponding valves (4th inter- breath for a short duration as pericardial rub will con-
costal space [ICS] left of sternum for triscupid and 5th tinue to be audible in the absence of breathing, heard
ICS left of the midclavicular line for mitral valve). Fol- over the 3rd ICS to the left of the mid sternum. Detection
lowing closure of these two valves, ventricular contraction of pericardial rub warrants further investigation by
and ejection occurs and a carotid pulse may be palpated ultrasound.
at the same time that S1 is audible.
The second heart sound (S2) occurs at the beginning of
diastole, following closure of the aortic and pulmonary Practice tip
valves and can be best heard over these valves (2nd ICS
to the right and left of the sternum respectively). It is To differentiate pericardial rub from pulmonary rub, ask the
important to remember that both S1 and S2 result from patient to hold their breath for a short duration as pericardial
events occurring in both left and right sides of the heart. rub will continue to be audible in the absence of breathing and
While normally left sided heart sounds are loudest and pleural rub will not be audible while the patient is not
occur slightly before right sided events, careful listening breathing.
during inspiration and expiration may result in left and
right events being heard separately. This is known as
physiological splitting of heart sounds, a normal physio-
logical event. In addition to pericardial rub, murmurs may also be
audible. Murmurs are generally classified and character-
A guide to placement of stethoscope when listening to ised by location with the most common murmurs associ-
heart sounds is presented in Table 9.1. ated with the mitral or aortic valves due to either stenosis
192 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
TABLE 9.2 Classification of heart murmurs using
the Levine scale 12
Grade 1 low intensity and difficult to hear
Grade 2 low intensity, but audible with a RA I
stethoscope but no palpable thrill LA
Grade 3 medium intensity and easily heard with a
stethoscope aV R aV L
Grade 4 loud and audible and with palpable thrill
Grade 5 very loud but cannot be heard outside the II III
praecordium and with palpable thrill
aV F
Grade 6 audible with the stethoscope away from
the chest
LL
or regurgitation at these locations. Murmurs are best
thought of as turbulent flow or vibrations associated with
the corresponding valve and can be of variable pitch.
17
Specialist cardiac referral is indicated upon detection of FIGURE 9.12 Einthoven triangle formed by standard limb leads.
cardiac murmurs to differentiate pathological murmurs
as seen during valvular dysfunction or myocardial infarc-
tion from innocent systolic ‘high flow’ murmurs detected When the primary purpose of monitoring is to detect
in children or adolescents as a result of vigorous ventricu- ischaemic changes leads III and V3 usually present the
lar contraction. Murmurs may be classified using the optimal combination. 14
12
Levine scale, seen in Table 9.2.
The skin must be carefully prepared before electrodes are
CONTINUOUS CARDIAC MONITORING attached, as contact is required with the body surface and
In the case of the critically ill patient, there are two main poor contact will lead to inaccurate or unreadable record-
forms of cardiac monitoring, both of which are used to ings, causing interference or noise. Patients who are
generate essential data: continuous cardiac monitoring, sweaty need particular attention, and it may be necessary
and the 12-lead ECG. to shave the areas where the electrodes are to be placed
in very hairy people.
Internationally, a minimum standard for an ICU requires
availability of facilities for cardiovascular monitoring. 12-LEAD ECG
13
Continuous cardiac monitoring allows for rapid assess- The Dutch physiologist Einthoven was one of the first to
ment and constant evaluation with, when required, the
instantaneous production of paper recordings for more represent heart electrical conduction as two charged elec-
16
trodes, one positive and one negative. The body can be
detailed assessment or documentation into patient
records. In addition, practice standards for electrocardio- likened to a triangle, with the heart at its centre, and this
has been called Einthoven’s triangle. Cardiac electrical
graphic monitoring in hospital settings have been
established. 14 activity can be captured by placing electrodes on both
arms and on the left leg. When these electrodes are
It is now common practice for five leads to be used for connected to a common terminal with an indifferent
5
continuous cardiac monitoring, as this allows a choice electrode that stays near zero, an electrical potential is
of seven views. The five electrodes are placed as follows: 15 obtained. Depolarisation moving towards an active elec-
trode produces positive deflection.
● right and left arm electrodes: placed on each
shoulder; The 12-lead ECG consists of six limb leads and six chest
● right and left leg electrodes: placed on the hips or level leads. The limb leads examine electrical activity along a
with the lowest ribs on the chest; vertical plane. The standard bipolar limb leads (I, II, III)
● V-lead views can be monitored: for V1 place the elec- record differences in potential between two limbs by
trode at the 4th ICS, right of the sternum; for V6 place using two limb electrodes as positive and negative poles
the electrode at the 5th ICS, left mid-axillary line. (see Figure 9.12): Leads I, II, and III all produce positive
17
deflections on the ECG because the electrical current
The monitoring lead of choice is determined by the flows from left to the right and from upwards to down-
15
patient’s clinical situation. Generally, two views are wards. Placement should be:
better than one. V1 lead is best to view ventricular activity
and differentiate right and left bundle branch blocks; ● I = negative electrode in right arm and positive elec-
therefore, one of the channels on the bedside monitor trode in left arm
should display a V lead, preferably V1, and the other ● II = negative electrode in right arm and positive elec-
display lead II or III for optimal detection of arrhythmias. trode in left leg
Cardiovascular Assessment and Monitoring 193
● III = negative electrode in left arm and positive elec- ● V4 = 5th ICS on the midclavicular line
trodes in left leg ● V5 = 5th ICS, anterior axillary line
● V6 = 5th ICS on the midaxilla line
The three unipolar limb leads (aVR, aVL, aVF) record
activity of the heart’s frontal plane. Each of these unipolar Amplitude (voltage) in the ECG is measured by a series
leads have only one positive electrode (the limb electrode of horizontal lines on the ECG (see Figure 9.14). Each
such as left arm, right arm and left leg), with the centre line is 1 mm apart and represents 0.1 mV. Amplitude
of the Einthoven’s triangle acting as the negative elec- reflects the wave’s electrical force and has no relation to
trode. The waveforms of these leads are usually very small
therefore they are augmented by the ECG machine to
increase the size of the potentials on the ECG strip.
17
These three leads views the heart at different angles: Anterior
view
● Lead aVR produces a negative reflection because the
electrical activity moves away from the lead. Lead aVR Angle of Louis
does not provide a specific view of the heart.
● Lead aVL produces a positive deflection because the
electrical activity moves towards the lead. Lead aVL
views the electrical activity from the lateral wall.
● Lead aVF also produces a positive deflection on the
ECG because the electrical activity flows toward V 1 V 2
this lead. It views the electrical activity from the V 3 V 5 V 6
inferior wall. V 4
The six unipolar chest leads (precordial leads) are desig-
nated V1–6 and examine electrical activity along a hori-
zontal plane from the right ventricle, septum, left ventricle
and the left atrium. They are positioned in the following
way (see Figure 9.13):
● V1 = 4th ICS, to the right of the patient’s sternum R L
● V2 = 4th ICS, to the left of the patient’s sternum
● V3 = equidistant between V2 and V4 FIGURE 9.13 Position of chest leads.
17
3 sec
0.20 sec
10 mm
0.04 sec
5 mm
1 mm
0.20 sec
17
FIGURE 9.14 ECG graph paper.
194 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
8
the muscle strength of ventricular contraction. Duration plus >25% of R wave height) may indicate a previous
of activity within the ECG is measured by a series of verti- myocardial infarction, however, not every myocardial
18
cal lines also 1 mm apart (see Figure 9.14). The time infarction will result in a pathological Q wave and
interval between each line is 0.04 sec. Every 5th line is some abnormal Q waves, in combination of other
printed in bold, producing large squares. Each represents ECG changes and patient symtoms, may indicate a
19
0.5 mV (vertically) and 0.2 sec (horizontally). current myocardial infarction. Pathological Q waves
could also be seen in non-ischaemic conditions such
Key Components of the ECG as Wolff–Parkinson–White syndrome (WPW). 20
Key components of the cardiac electrical activity are ● The Q–T interval is the time taken from ventricular
termed PQRST (see Figure 9.15): stimulation to recovery. It is measured from the begin-
ning of the QRS to the end of the T wave. Normally,
● The P wave represents electrical activity caused by this ranges from 0.35 to 0.45 sec, but shortens as heart
spread of impulses from the SA node across the atria rate increases. It should be less than 50% of the pre-
and appears upright in lead II. Inverted P waves indi- ceding cycle length.
cate atrial depolarisation from a site other than the SA ● The T wave reflects repolarisation of the ventricles. A
node. Normal P wave duration is considered less than peaked T wave indicates hyperkalaemia, myocardial
0.12 sec. infarction (MI) or ischaemia, while a flattened T wave
● The P–R interval reflects the total time taken for the usually indicates hypokalaemia. An inverted T wave
atrial impulse to travel through the atria and AV node. occurs following an MI, or ventricular hypertrophy.
It is measured from the start of the P wave to the Normal T wave is 0.16 sec. The height of the T wave
beginning of the QRS complex, but is lengthened by should be less than 5 mm in all limb leads, and less
AV block or some drugs. Normal P–R interval is than 10 mm in the praecordial leads. 17
0.12–0.2 sec. ● The ST segment is measured from the J point (junction
● The QRS complex is measured from the start of the Q of the S wave and ST segment) to the start of the T
wave to the end of the S wave and represents the time wave. It is usually isoelectric in nature, and elevation
taken for ventricular depolarisation. Normal QRS or depression indicates some abnormality in the onset
duration is 0.08–0.12 sec. Anything longer than of recovery of the ventricular muscle, usually due to
0.12 sec is abnormal and may indicate conduction myocardial injury.
disorders such as bundle branch block. The deflec- ● The U wave is a small positive wave sometimes seen
tions seen in relation to this complex will vary in size, following the T wave. Its cause is still unknown but it
depending on the lead being viewed. However, small
QRS complexes occur when the heart is insulated, as
in the presence of a pericardial effusion. Conversely,
an exaggerated QRS complex is suggestive of ventricu-
lar hypertrophy. Normal, non-pathological Q waves Practice tip
are often seen in leads I, aVL, V5, V6 from septal The 6-second measurement for heart rate calculation is particu-
depolarisation which are less than 25% of the R larly useful when the patient’s heart rate is irregular.
height, and 0.04 sec. A ‘pathological’ Q wave (>0.04 sec
Atrial Ventricular Ventricular
depolarisation depolarisation depolarisation
R
Atrial Ventricular
systole systole
T
P
Q S
PR ST
interval QRS segment
QT interval
FIGURE 9.15 Normal ECG.
17
Cardiovascular Assessment and Monitoring 195
is exaggerated in hypokalaemia. Inverted U waves may
be seen and often associated with coronary heart Practice tip
disease (CHD), and these may appear transiently
during exercise testing. 18 Think of the leads I, II, III, aVR, aVL, aVF, V1-V6 as the ‘eyes’ that
are looking at the heart’s electrical activity from different angles
ECG Interpretation and view the heart’s different areas.
Interpretation of a 12-lead ECG is an experiential skill,
requiring consistent exposure and practice. Some steps to
aid interpretation are noted below. HAEMODYNAMIC MONITORING
● Calculate heart rate: The blood’s dynamic movement in the cardiovascular
● There are many ways to calculate the heart rate. system is referred to as haemodynamics. Haemodynamic
One way is to count the R waves on a 6 sec strip monitoring is performed to provide the clinician with a
and multiply by 10 to calculate the rate (the top greater understanding of the pathophysiology of the
of the ECG paper is usually marked at 3 sec problem being treated than would be possible with clini-
intervals). cal assessment alone. Knowledge of the evidence that
● Use an ECG ruler if one is available. underpins the technology and the processes for interpre-
● Check R-R intervals (rhythm): tation is therefore essential to facilitate optimal usage and
● Are the rhythms regular? evidence-based decisions. 22
● To assess regularity: mark the duration of two
neighbouring R waves (R-R interval) on a plain This section explores the principles related to haemody-
piece of paper, move this paper to check other R-R namic monitoring and the different types of monitoring
intervals on the ECG strip. R-R intervals should be available, and introduces the most recent and appropriate
uniform in a normal ECG which means the patient evidence related to haemodynamic monitoring. The
has a regular ECG rhythm. reasons for haemodynamic monitoring are generally
● Locate P waves (check atrial activity): threefold:
● Observe for the presence or absence of P waves. 1. to establish a precise health-related diagnosis
● Check regularity and shape. 2. to determine appropriate therapy
● Is the P wave positive? 3. to monitor the response to that therapy.
● The relationship between P waves and QRS com-
plexes: is there a P wave preceding every QRS Haemodynamic monitoring can be non-invasive or inva-
complex? sive, and may be required on a continuous or intermittent
23
● What is the duration of the P wave? basis depending on the needs of the patient. In both
● Measure P-R interval (check AV node activity): cases, signals are processed from a variety of physiological
● What is the duration of the P-R interval? variables, and these are then clinically interpreted within
● Measure QRS duration (check ventricular activity): the individual patient’s context.
● Is the ventricular electrical activity normal? Non-invasive monitoring does not require any device to
● Is the QRS complex too wide or narrow? be inserted into the body and therefore does not breach
● Check the presence of Q wave. If present, is it the skin. Directly measured non-invasive variables include
normal or pathological? body temperature, heart rate, blood pressure, respiratory
● Note other clues: rate and urine output, while other processed forms can
● Observe whether the isoelectric line is present be generated by the ECG, arterial and venous Dopplers,
between the S and T waves. transcutaneous pulse oximetry (using an external probe
● Examine the T wave to see whether it is positive, on a digit such as the finger or on the ear), and expired
negative, or flat. Is it less than 0.16 sec? carbon monoxide monitors.
● Examine the duration of the Q-T interval: is it too
long? Invasive monitoring requires the vascular system to be
● Observe for any extra complexes and note their rate cannulated and pressure or flow within the circulation
and shape, and whether they have the same or dif- interpreted. Invasive haemodynamic monitoring tech-
ferent morphology. nology includes:
● systemic arterial pressure monitoring
● central venous pressure
● pulmonary artery pressure
Practice tip ● cardiac output (thermodilution).
The presence of Q waves does not always indicate past myocar- Invasive monitoring has also facilitated greater use of
dial infarct. Other patient clinical information is needed to inter- blood component analyses, such as arterial and venous
pret the significance of Q waves. blood gases.
ECG interpretation should always take a patient’s clinical infor- The invasive nature of this monitoring allows the pres-
mation (patient symptoms, complaints, other haemodynamic sures that are sensed at the distal ends of the catheters to
information) into account. be transduced, and to continuously display and monitor
the corresponding waveforms. The extent of monitoring
196 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
should reflect how much information is required to opti- monitor should display zero (0 mmHg), as this equates
mise the patient’s condition, and how precisely the data to current atmospheric pressure (760 mmHg at sea level).
are to be recorded. As Pinsky argues, a great deal of infor- With the improved quality of transducers, repeated
mation is generated by this form of monitoring, and yet zeroing is not necessary, as once zeroed, the drift from
24
29
little of this is actually used clinically. Consequently, the baseline is minimal. Some critical care units,
monitors are not substitutes for careful examination and however, continue to recalibrate transducer(s) at the
do not replace the clinician. The accuracy of the values beginning of each clinical shift.
obtained and a nurse’s ability to interpret the data and Fast-flush square wave testing, or dynamic response mea-
choose an appropriate intervention directly affect the surement, is a way of checking the dynamic response of
29
patient’s condition and outcome. 25
the monitor to signals from the blood vessel. It is also a
PRINCIPLES OF HAEMODYNAMIC check on the accuracy of the subsequent haemodynamic
pressure values. The fast-flush device within the system,
MONITORING when triggered and released, exposes the transducer to
A number of key principles need to be understood in the amount of pressure in the flush solution bag (usually
relation to invasive haemodynamic monitoring of the 300 mmHg). The pressure waveform on the monitor will
critically ill patients. These include haemodynamic accu- show a rapid rise in pressure, which then squares
racy, the ability to trend data and the maintenance of off before the pressure drops back to the baseline (see
minimum standards. These are reviewed below. Figure 9.17).
Haemodynamic Accuracy Interpretation of the square wave testing is essential; the
clinician must observe the speed with which the wave
Accuracy of the value obtained from haemodynamic returns to the baseline as well as the pattern produced.
monitoring is essential, as it directly affects the patient’s One to three rapid oscillations should occur immediately
condition. 26,27 Electronic equipment for this purpose has after the square wave, before the monitored waveform
four components (see Figure 9.16): resumes. The distance between these rapid oscillations
29
1. an invasive catheter attached to high-pressure should not exceed 1 mm or 0.04 sec. Absence, or a
tubing reduction, of these rapid oscillations, or a ‘square wave’
2. a transducer to detect physiological activity with rounded corners, indicates that the pressure moni-
3. a flush system toring system is overdamped; in other words its respon-
4. a recording device, incorporating an amplifier to siveness to monitored pressures and waveforms is reduced
increase the size of the signal, to display (see Figure 9.18). An underdamped monitoring system
information. will produce more rapid oscillations after the square wave
than usual.
High-pressure (non-distensible) tubing reduces distor-
tion of the signal produced between the intravascular Data Trends
device and the transducer; the pressure is then converted The ability to trend data via a monitor or a clinical infor-
into electrical energy (a waveform). Fluid (0.9% sodium mation system is essential for critical care practice. Current
chloride) is routinely used to maintain line patency using monitoring systems used in Australia and New Zealand
a continuous pressure system; the pressure of the flush can retain data for a period of time, produce trend graphs,
system fluid bag should be maintained at 300 mmHg, and link to other devices to allow review of data from
which normally delivers a continual flow of 3 mL/h.
locations other than the immediate bedside. The data
Accuracy is dependent on levelling the transducer to the trends can be used to assess the progression of a patient’s
appropriate level (and altering this level with changes in clinical condition and monitor the patient’s response to
patient position as appropriate), then zeroing the trans- treatment.
ducer in the pressure monitoring system to atmospheric
pressure (called calibration) as well as evaluating the Haemodynamic Monitoring Standards
response of the system by fast-flush wave testing. There are stated minimum standards for critical care units
The transducer must be levelled to the reference point of in Australia and New Zealand. 30,31 The standards require
the phlebostatic axis, at the intersection of the 4th inter- that patient monitoring include circulation, respiration
costal space and the midthoracic anterior-posterior diam- and oxygenation, with the following essential equipment
27
eter (not the midaxillary line). Error in measurement available for every patient: an ECG that facilitates con-
can occur if the transducer is placed above or below the tinual cardiac monitoring; a mechanical ventilator, pulse
phlebostatic axis. 26,27 Measurements taken when the oximeter; and other equipment available where necessary
patient is in the lateral position are not considered as to measure intra-arterial and pulmonary pressures, cardiac
accurate as those taken when the patient is lying supine output, inspiratory pressure and airway flow, intracranial
or semirecumbent up to an angle of approximately 60 pressures and expired carbon dioxide. 30
degrees. 28
BLOOD PRESSURE MONITORING
Zeroing the transducer system to atmospheric pressure
(calibration of the system) is achieved by turning the Indirect and direct means of monitoring blood pressure
3-way stopcock nearest to the transducer open to the air, are widely used in critical care units. These are outlined
and closing it to the patient and the flush system. The in more detail below.
Cardiovascular Assessment and Monitoring 197
Bedside monitor
Normal saline and
pressure bag
Macrodrip
chamber
Electrical
cable
High-
pressure Fluid-
tubing filled
tubing
for flush
Invasive
45° catheter
Roller
clamp
30°
Electrical
connection
3-way
stopcock
Disposable (air reference)
transducer
Phlebostatic
axis Manual
flush
0°
Patient with invasive catheter
FIGURE 9.16 Haemodynamic monitoring system. 5
● a low, muffled noise that is continuous in nature and
Non-invasive Blood Pressure Monitoring is heard when the diastolic pressure is reached;
Non-invasive blood pressure (NIBP) monitoring requires as the cuff pressure diminishes further, the sound
the use of a manual or electronic sphygmomanometer. disappears.
Oscillation in the pressure generated by alterations
in arterial flow is captured either through auscultation For critically ill patients, this method of blood pressure
or automatic sensing. On auscultation, a number of monitoring has limitations and is often used when inva-
33
Korotkoff sounds can be heard as the cuff pressure is sive methods cannot be utilised. It is a less accurate
released: 32 alternative, as results vary with the size of cuff used,
equipment malfunction, and incorrect placement of the
● a sharp thud that is heard when the patient’s systolic sphygmomanometer (this must be placed at heart level).
pressure is reached In addition, the pressures generated by the inflating cuff,
● a soft tapping, intermittent in nature particularly those generated by automatic machines, can
● a loud tapping, intermittent in nature be high and frequent measurements of blood pressure in
198 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
120 Systole
Pressure (mmHg) 110 Dicrotic notch
100
90
80 Diastole
Time
58
FIGURE 9.19 Arterial pressure waveform.
● accidental disconnection (the insertion sites should
be always visible)
● accidental drug administration through the arterial
catheter; all arterial lines and connections should be
clearly identified as such (e.g. marked with red stickers
FIGURE 9.17 Normal dynamic response test. or have red bungs).
Blood pressure is the same at all sites along a vertical level
but when the vertical level is varied, pressure will change.
Consequently, referencing is required to correct for
changes in hydrostatic pressure in vessels above and
below the heart; if not, the blood pressure will appear to
rise when this is not really the case. It is important to zero
the monitoring system at the left atrial level. 27
Arterial waveform
A steep upstroke (corresponding to ventricular systole) is
followed by brief, sustained pressure (anacrotic shoul-
der). At the end of systole pressure falls in the aorta and
left ventricle, causing a downward deflection (see Figure
9.19). A dicrotic notch can be seen in the downward
FIGURE 9.18 Over-damped dynamic response test. deflection which represents the closure of the aortic valve.
The systolic pressure corresponds to the peak of the wave-
form. The arterial pressure waveform changes its contours
when recorded at different sites. It can become sharper in
this method may become uncomfortable for the patient. distal locations.
It is therefore important that skin integrity be checked
regularly to prevent ischaemia and that the frequency of Disease process has an effect on waveforms: for example,
automated inflations be minimised. 33 atherosclerosis causes an increase in systolic waveform, as
well as a decrease in the size of the diastolic wave and
Invasive Intra-arterial Pressure Monitoring dicrotic notch due to changes in elasticity. Cardiomyopa-
Arterial pressure recording is indicated when precise and thy causes reduced stroke volume and mean arterial pres-
continuous monitoring is required, especially in periods sure, and there is a late secondary systolic peak seen on
of fluid volume, cardiac output and blood pressure insta- the waveform.
34
bility. An arterial catheter is commonly placed in the
radial artery, although other sites can be accessed, includ- Invasive arterial pressure versus cuff pressure
ing the brachial, femoral, dorsalis pedis and axillary arter- At times the accuracy of the invasive arterial pressure
ies. Arterial catheter insertion is performed aseptically, reading may be checked by comparing the reading against
and it is important that collateral circulation, patient that generated by a non-invasive device using an inflating
comfort and risk of infection be assessed before insertion cuff. However, there is no basis for comparing these
is attempted. The radial artery is the most common site, values. Invasive blood pressure values are a measure of
as the ulnar artery provides additional supply to extremi- the actual pressure within the artery whereas those from
ties if the radial artery becomes compromised. the cuff depend on flow-induced oscillations in the arte-
35
rial wall. Pressure does not equal flow, as resistance does
Complications of arterial pressure monitoring include:
not remain constant. In addition, radial arterial pressure
● infection is normally higher than that obtained by brachial non-
● arterial thrombosis invasive pressure monitoring because the smaller vessel
● distal ischaemia size exerts greater resistance to flow, and therefore gener-
● air embolism ates a high pressure reading. 27,35
Cardiovascular Assessment and Monitoring 199
INVASIVE CARDIOVASCULAR MONITORING
For many critically ill patients, haemodynamic instability TABLE 9.3 Haemodynamic pressures
is a potentially life-threatening condition that necessi-
tates urgent action. Accurate assessment of the patient’s Parameter Resting values
intracardiac status is therefore essential. A number of Central venous pressure 0 to +8 mmHg (mean)
values can be calculated, and Tables 9.3 and 9.4 list the
measurements commonly made. Right ventricular pressure +15 to +30 mmHg systolic
0 to +8 mmHg diastolic
Preload Pulmonary artery wedge +5 to +15 mmHg (mean)
pressure
As noted earlier, preload is the filling pressure in the
ventricles at the end of diastole. Preload in the right ven- Left atrial pressure +4 to +12 mmHg (mean)
tricle is generally measured as CVP, although this may be Left ventricular pressure 90 to 140 mmHg systolic
an unreliable predictor because CVP is affected by intra- +4 to +12 mmHg diastolic
thoracic pressure, vascular tone and obstruction. Left Aortic pressure 90 to 140 mmHg systolic
37
ventricular preload can be measured as the pulmonary 60 to 90 mmHg diastolic
capillary wedge pressure (PCWP), but again, due to 70 to 105 mmHg (mean)
unreliability, this parameter provides an estimate rather
than a true reflection of volume. 38,39 In view of this,
TABLE 9.4 Normal haemodynamic values 10,36
Parameter Description Normal values
Stroke volume (SV) Volume of blood ejected from left ventricle/beat 50–100 mL/beat
SV = CO/HR
Stroke volume index (SVI) Volume of blood ejected/beat indexed to BSA 25–45 mL/beat
Cardiac output (CO) Volume of blood ejected from left ventricle/min 4–8 L/min
CO = HR × SV
Cardiac index (CI) A derived value reflecting the volume of blood ejected 2.5–4.2 L/min/m (normal
2
from left ventricle/min indexed to BSA assumes an average
CI = CO/BSA weight of 70 kg)
Flow time corrected (FTc) Systolic flow time corrected for heart rate 330–360 msec
Systemic vascular resistance (SVR) Resistance left heart pumps against 900–1300 dynes/sec/cm −5
SVR = [(MAP − RAP) × 79.9]/CO
Systemic vascular resistance index (SVRI) Resistance left heart pumps against indexed to body 1700–2400 dynes/sec/cm /
5
surface area m 2
SVRI = [(MAP − RAP) × 79.9]/CI
Pulmonary vascular resistance (PVR) Resistance right heart pumps against 20–120 dynes/sec/cm −5
PVR = [(mPAP − LVEDP) × 79.9]/CO
5
Pulmonary vascular resistance index (PVRI) Resistance right heart pumps against indexed to body 255–285 dynes/sec/cm /m 2
surface area
PVRI = [(mPAP − LVEDP) × 79.9]/CI
Mixed venous saturation (SvO 2 ) Shows the balance between arterial O 2 supply and 70%
oxygen demand at the tissue level
Left ventricular stroke work index (LVSWI) Amount of work performed by LV with each heartbeat 50–62 g-m/m 2
(MAP – LVEDP) × SVI × 0.0136
Right ventricular stroke work index (RVSWI) Amount of work performed by RV with each heartbeat 7.9–9.7 g-m/m 2
(mPAP – RAP) × SVI × 0.0136
Right ventricular end-systolic volume (RVESV) 50–100 mL/beat
The volume of blood remaining in the ventricle at the
Right ventricular end-systolic volume index end of the ejection phase of the heartbeat 30–60 mL/m 2
(RVESVI)
Right ventricular end-diastolic volume (RVEDV) 100–160 mL/beat
The amount of blood in the ventricle immediately
Right ventricular end-diastolic volume index before a cardiac contraction begins 60–100 mL/m 2
(RVEDVI)
BSA = Body surface area
200 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
other modalities are now being explored, including right problems and the need for repeated dressing changes.
ventricular end-diastolic volume evaluation via fast- These include beard growth, diaphoresis and poor control
response pulmonary artery catheters, left ventricular of oral secretions.
end-diastolic area measured by echocardiography and The subclavian approach is used often, perhaps because
intrathoracic blood volume measured by transpulmonary of a reported lower risk of catheter-related bloodstream
thermodilution. 40
infection. 46,47 Coagulopathy is a significant contraindica-
Central venous pressure monitoring tion for this approach, as puncture of the subclavian
artery is a known complication. There is also a risk of
Central venous catheters are inserted to facilitate the pneumothorax, which rises if the patient is receiving
monitoring of central venous pressure; facilitating the intermittent positive pressure ventilation (IPPV).
47
administration of large amounts of IV fluid or blood; Complications of any central venous access catheters
providing long-term access for fluids, drugs, specimen include air embolism, pneumothorax, hydrothorax and
collection; and/or parenteral feeding. CVP monitoring haemorrhage. 44
has been used for many years to evaluate circulating
blood volume, despite discussion as to its validity to do Pulmonary artery pressure (PAP) monitoring
so. 41-43 However, it is a common monitoring practice and Pulmonary artery pressure monitoring began in the
continues to be used. Therefore clinicians need to be 1970s, led by Drs Swan, Ganz and colleagues, and was
48
aware of possible limitations to this form of measure- subsequently adopted in ICUs worldwide. Pulmonary
ment and interpret the data accordingly. CVP monitoring artery catherisation facilitates assessment of filling pres-
can produce erroneous results: a low CVP does not always sure of the left ventricle through the pulmonary artery
mean low volume and it may reflect other pathology, wedge (occlusion) pressure (see Figure 9.20). 45,49 By using
including peripheral dilation due to sepsis. Hypovolae- a thermodilution pulmonary artery catheter (PAC),
mic patients may have normal CVP due to sympathetic cardiac output and other haemodynamic measurements
nervous system activity increasing vascular tone. An can also be calculated. PAP monitoring is a diagnostic
increase in CVP can also be seen in patients on mechani- tool that can assist in determination of the nature of a
cal ventilation with application of PEEP. 41-43
haemodynamic problem and improve diagnostic accu-
Central venous catheters used for haemodynamic moni- racy. In addition to measuring PA pressures, PAC may also
toring are classed as short-term percutaneous (non- be used for accessing blood for assessment of mixed-
tunnelled) devices. Short-term percutaneous catheters are venous oxygenation levels (see Chapter 13).
inserted through the skin, directly into a central vein, and
usually remain in situ for only a few days or for a The beneficial claims of PAP monitoring have, however,
50
maximum of 2–3 weeks. They are easily removed and been questioned, with some proposing a moratorium.
37
changed, and are manufactured as single- or multi-lumen In response, two consensus conferences were held in the
types. However, they can be easily dislodged, are throm- USA to make recommendations for future practice. It was
bogenic due to their material, and are associated with a concluded that there was no basis for a moratorium on
high risk of infection. 37,44 the use of PACs; instead, education and knowledge about
the use of this technology must be standardised and
A number of locations can be used for central venous monitored. Further research was indicated, particularly
access. The two commonly used sites in critically ill focusing on the use of PACs. 51,52 More recently, an obser-
patients are the subclavian and the internal jugular veins. vational cohort study of 7310 patients found that PAC use
Other less common sites are the antecubital fossa (gener- was not associated with an overall higher mortality,
ally avoided but may be used when the patient cannot be although the authors concluded that severity of illness
positioned supine), the femoral vein (associated with should be examined when considering the use of this
53
high infection risk), and the external jugular vein measurement tool. The PAC-Man study, a randomised
(although the high incidence of anomalous anatomy and controlled clinical trial, suggested that the use of PAC did
54
the severe angle with the subclavian vein make this an not improve the critically ill patients’ outcome. A sys-
55
unpopular choice). 44 tematic review on PAC use by Harvey et al. by the
Cochrane Collaboration suggested that more empirical
Internal jugular cannulation has a high success rate for
insertion; however, complications related to insertion via studies are needed to identify the appropriate patient
this route include carotid artery puncture and laceration groups that could benefit from the use of PAC and the
of local neck structures arising from needle probing. 44,45 protocols for their use. In the meantime, proponents for
There are a number of key structures adjacent to the vein, continuing clinical use of the PAC argue that it provides
including the vagus nerve (located posteriorly to the a physiological rationale for diagnosis and assists in the
internal jugular vein); the sympathetic trunk (located titration of therapies such as inotropes, which would
29,49,51
behind the vagus nerve); and the phrenic nerve (located otherwise be potentially dangerous.
laterally to the internal jugular). Damage can also occur Since the benefit of use of PAC is still arguable, the indica-
46
to the sympathetic chain, which leads to Horner’s syn- tions of PAP monitoring are largely based on clinical
drome (constricted pupil, ptosis, and absence of sweat experience. PAP monitoring may be indicated for adults
gland activity on that side of the face). Central venous in severe hypovolaemic or cardiogenic shock, where there
catheters inserted in the internal jugular vein pose a may be diagnostic uncertainty, or where the patient is
number of nursing challenges which can cause fixation unresponsive to initial therapy. The PAP is used to guide
Cardiovascular Assessment and Monitoring 201
A
B
C
FIGURE 9.20 Pulmonary artery catheter. 5
administration of fluids, inotropes and vasopressors. PAP A number of measurements can be taken via the PAC,
monitoring may also be utilised in other cases of haemo- either by direct measurement, for example using pulmo-
dynamic instability when diagnosis is unclear. It may be nary capillary wedge pressure (PCWP), which is an esti-
helpful when clinicians want to differentiate hypovolae- mate of left ventricular preload (LVEDV) or through
mia from cardiogenic shock or, in cases of pulmonary calculation of derived parameters, such as cardiac output
34
oedema, to differentiate cardiogenic from non-cardiogenic (CO) and cardiac index (CI) (see Table 9.4 for descrip-
origins. It has been used to guide haemodynamic tors and normal values).
56
support in a number of disease states such as shock, and
to assist in assessing the effects of fluid management Pulmonary capillary wedge pressure
therapy. 34,49 (PCWP) monitoring
Complications do arise from PACs, as these catheters PCWP, or pulmonary artery occlusion pressure (PAOP),
share all the complications of central lines and are addi- is measured when the pulmonary artery catheter balloon
tionally associated with a higher incidence of arrhythmia, is inflated with no more than 1–1.5 mL air. The inflated
valve damage, pulmonary vascular occlusion, emboli/ balloon isolates the distal measuring lumen from the
infarction (reported incidence of 0.1–5.6%) and, very pulmonary arterial pressures, and measures pressures in
rarely, knotting of the catheter. 44 the capillaries of the pulmonary venous system, and
202 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
Flow-directed
catheter
Pressure Right atrium Right ventricle Pulmonary artery Pulmonary artery wedge (PAOP)
30
mmHg
20
mmHg
10
mmHg
0
mmHg
FIGURE 9.21 Pulmonary artery pressure and wedge waveforms. 5
indirectly the left atrial pressure. The PAP waveform looks development enables the patients to self monitor LAP
similar to that of the arterial waveform, with the tracing under their doctors’ guidance, which was found to be a
showing a systolic peak, dicrotic notch and a diastolic dip valuable tool to improve the management of patients
(see Figure 9.21). When the balloon is inflated, the wave- with advanced heart failure. Other modes of monitor-
60
form changes shape and becomes much flatter in appear- ing can also be used to achieve comprehensive left atrial
ance, providing a similar waveform to the CVP. There are assessment, such as Doppler echocardiography. 61
two positive waves on the tracing: the first reflects atrial
contraction, and the second reflects pressure changes Afterload
from blood flow when the mitral valve closes and the As previously noted, afterload is the pressure that the
ventricles contract. The PCWP should be read once the ventricle produces to overcome the resistance to ejection
57
‘wedge’ trace stops falling at the end-expiratory phase of generated in the systematic or pulmonary circulation by
the respiratory cycle (see Figure 9.21). the arteries and arterioles. It is calculated by cardiac
If balloon occlusion occurs with <1 mL air, then the output studies: left heart afterload is reflected as systemic
balloon is wedged in a small capillary and consequently vascular resistance (SVR), and right heart afterload is
will not accurately reflect LA pressure. Conversely, if reflected as pulmonary vascular resistance (PVR) (see
1.5 mL air does not cause occlusion, the balloon may Table 9.4).
have burst (which can result in an air embolus) or it may
be floating in a larger vessel. If balloon rupture is sus- Systemic and pulmonary vascular resistance
pected, no further attempts to inflate the balloon should Systemic vascular resistance (SVR) is a measure of resis-
be made, and interventions to minimise the risk of air tance or impediment of the systemic vascular bed to
embolism should be initiated. 7,58 Note: it is essential that blood flow. An elevated SVR can be caused by vasocon-
the balloon be deflated as soon as the wedge has been strictors, hypovolaemia or late septic shock. A lowered
recorded, as continued occlusion will cause distal pulmo- SVR can be caused by early septic shock, vasodilators,
nary vasculature ischaemia and infarction. 59 morphine, nitrates or hypercarbia. Afterload is a major
determinant of blood pressure, and gross vasodilation
Left atrial pressure monitoring causes peripheral pooling and hypotension, reducing
SVR. The precise estimation of SVR enables safer use of
Left atrial pressure (LAP) monitoring directly estimates therapies such as vasodilators (e.g. sodium nitroprusside)
left heart preload. It used to require an open thorax to and vasoconstrictors (e.g. noradrenaline). 62
enable direct cannulation of the atrium. It was used only
in the postoperative cardiac surgical setting, although Pulmonary vascular resistance (PVR) is a measure of resis-
such use was infrequent since the widespread use of PAC. tance or the impediment of the pulmonary vascular
Recent advancement in cardiac implantable devices bed to blood flow. An elevated PVR (‘pulmonary
Cardiovascular Assessment and Monitoring 203
hypertension’) is caused by pulmonary vascular disease, as the indicator substance, the calculation of cardiac
pulmonary embolism, pulmonary vasculitis or hypoxia. output is as follows:
A lowered PVR is caused by medications such as calcium
(
channel blockers, aminophylline or isoproterenol, or by CO = VO / CaO − CvO 2 )
2
2
the delivery of O 2 . 62,63
where VO 2 is oxygen consumption, CaO 2 is arterial
Contractility oxygen concentration, and CvO 2 is venous oxygen
Contractility reflects the force of myocardial contraction, concentration.
and is related to the extent of myocardial fibre stretch
(preload, see above) and wall tension (afterload, see Thermodilution methods
above). It is important because it influences myocardial Thermodilution methods calculate cardiac output by
oxygen consumption. Contractility of the left side of the using temperature change as the indicator in Fick’s
heart is measured by calculating the left ventricular stroke method. Cardiac output and associated pressures such as
40
work index (LVSWI), although the clinical use of this global end-diastolic volume can be calculated using a
value is not widespread. thermodilution PA catheter. Cardiac output can be moni-
tored intermittently or continuously using the PA cathe-
Right ventricular stroke work index (RVSWI) can be simi- ter. Intermittent measurements obtained every few hours
larly calculated. Contractility can decrease as a result of produce a snapshot of the cardiovascular state over that
excessive preload or afterload, drugs such as negative ino- time. By injecting a bolus of 5–10 mL of crystalloid solu-
tropes, myocardial damage such as that occurring after tion, and measuring the resulting temperature changes,
MI, and changes in the cellular environment arising from an estimation of stroke volume is calculated. Cold injec-
acidosis, hypoxia or electrolyte imbalances. Increases tate (run through ice) was initially recommended, but
in contractility arise from drugs such as positive studies now support the use of room temperature injec-
inotropes. 64
tate, providing there is a difference of 12° Celsius between
67
Cardiac Output injectate and blood temperature. Three readings are
taken at the same part of the respiratory cycle (normally
As discussed earlier in the chapter, the cardiac output end expiration), and any measurements that differ by
(CO) refers to the blood volume ejected by the heart in more than 10% should be disregarded (see Table 9.4 for
one minute. Stroke volume (SV) is the blood ejected by normal values). Since the 1990s, the value of having con-
the heart in one beat. Therefore cardiac output can be tinuous measurement of cardiac output has been recog-
49
calculated as the heart rate multiplied by stroke volume. nised and this has led to the development of devices
Stroke volume is determined by the heart’s preload, after- which permit the transference of pulses of thermal energy
load and the contractility. to pulmonary artery blood – the pulse-induced contour
method. 61
The variety of cardiac output measurement techniques
65
has grown over the past decade since the development Pulse-induced contour cardiac output
of thermodilution pulmonary artery catheters, pulse-
induced contour devices and less invasive techniques Pulse-induced contour cardiac output (PiCCO) provides
such as Doppler. As many critically ill patients require continuous assessment of CO, and requires a central
mechanical ventilation support, the associated rises in venous line and an arterial line with a thermistor (not a
68
intrathoracic pressure, as well as changing ventricular PAC). A known volume of thermal indicator (usually
compliance, make accurate haemodynamic assessment room temperature saline) is injected into the central vein.
difficult with the older technologies. Therefore, volumet- The injectate disperses both volumetrically and thermally
ric measurements of preload, such as right ventricular within the cardiac and pulmonary blood. When the
end-systolic volume (RVESV), right ventricular end- thermal signal is detected by the arterial thermistor, the
diastolic volume (RVEDV) and index (RVESVI/RVEDVI) temperature difference is calculated and a dissipation
69
as well as measurements of right ventricular ejection frac- curve generated. From these data, the cardiac output can
tion (RVEF) are now being used to more accurately deter- be calculated. These continuous cardiac output measure-
mine cardiac output. The parameters RVEF, CO and/or ments have been well researched over the past 10 years
CI, and stroke volume (SV) are generated using thermo- and appear to be equal in accuracy to intermittent injec-
dilution technology, and from these the parameters of tions required for the earlier catheters. 65,70,71 The para-
68
RVEDV/RVEDVI and RVESV/RVESVI can be calculated meters measured by PiCCO include:
10
(see Table 9.4 for normal values). The availability of ● Pulse-induced contour cardiac output: derived normal
continuous modes of assessment has further improved a value for cardiac index 2.5–4.2 L/min/m .
2
clinician’s ability to effectively treat these patients. 10 ● Global end-diastolic volume (GEDV): the volume of
blood contained in the four chambers of the heart;
The Fick principle assists in the calculation of intrathoracic blood
Several cardiac output measurement methods use the volume. Derived normal value for global end-diastolic
Fick principle. In 1870, Fick proposed that ‘in an organ, blood volume index 680–800 mL/m .
2
the uptake or release of an indicator substance is the ● Intrathoracic blood volume (ITBV): the volume of
product of the arterial-venous concentration of this sub- the four chambers of the heart plus the blood volume
66
stance and the blood flow to the organ’. Using oxygen in the pulmonary vessels; more accurately reflects
204 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
circulating blood volumes, particularly when a patient from the end of diastole to the end of the ejection phase
is artificially ventilated. Derived normal value for is measured and combined with an individual calibration
2
intrathoracic blood volume index 850–1000 mL/m . factor. The algorithm is capable of computing each single
● Extravascular lung water (EVLW): the amount of water stroke volume after being calibrated by an initial trans-
content in the lungs; allows quantification of the pulmonary thermodilution.
degree of pulmonary oedema (not evident with X-ray PiCCO preload indicators of intrathoracic blood volume
or blood gases). Derived normal value for extravascu- (ITBV) and global end-diastolic volume (GEDV) are more
lar lung water index is 3–7 mL/kg. EVLW has been sensitive and specific to cardiac preload than the standard
shown to be useful as a guide for fluid management cardiac filling pressures of CVP and PCWP, as well as right
67
in critically ill patients. An elevated EVLW may be an ventricular end-diastolic volume. One advantage of
40
effective indicator of severity of illness, particularly ITBV and GEDV is that they are not affected by mechani-
after acute lung injury or in ARDS, when EVLW is cal ventilation and therefore give correct information on
72
elevated due to alterations in hydrostatic pressures. the preload status under almost any condition. Extravas-
Other patients at risk of high EVLW are those with left cular lung water correlates moderately well with severity
heart failure, severe pneumonia, and burns. There may of ARDS, length of ventilation days, ICU stay and mortal-
be an association between a high EVLW and increased ity, and appears to be of greater accuracy than the
74
mortality, the need for mechanical ventilation and a traditional assessment of lung oedema by chest X-ray.
72
higher risk of nosocomial infection. A decision tree Disadvantages of PiCCO include its potential unreliabil-
outlining processes of care guided by information pro- ity when heart rate, blood pressure and total vascular
vided by PiCCO is provided in Figure 9.22.
resistance change substantially. 10,68
PiCCO removes the impact of factors that can cause vari-
ability in the standard approach of cardiac output mea- Doppler ultrasound methods
surement, such as injectate volume and temperature, and
73
timing of the injection within the respiratory cycle. The Oesophageal Doppler monitoring enables calculation of
additional fluid volume injected with the standard tech- cardiac output from assessment of stroke volume and
nique is significant in some patients; with the continuous heart rate, but uses a less invasive technique than those
75
technology this is eliminated. A further advantage is that outlined previously. Stroke volume is assessed by mea-
virtually real-time responses to treatment can be obtained, suring the flow velocity and the area through which the
removing the time delay that was a potential problem forward flow travels. Flow velocity is the distance one red
with standard thermodilution techniques. 61 blood cell travels forward in one cardiac cycle, and the
measurement provides a time velocity interval (TVI). The
An arterial catheter is widely used in critical care to enable area of flow is calculated by measuring the cross-sectional
frequent blood sampling and blood pressure monitoring, area of the blood vessel or heart chamber at the site of
76
and is used to measure beat-by-beat cardiac output, the flow velocity management. Oesophageal Doppler
obtained from the shape of the arterial pressure wave. The monitoring can be performed at the level of the pulmo-
area under the systolic portion of the arterial pulse wave nary artery, mitral valve or aortic valve.
2
CI (L/min/m ) <3.0 >3.0
Results
GEDI (mL/m 2 ) <700 >700 <700 >700
2
or ITBI (mL/m ) <850 >850 <850 >850
ELWI (mL/kg) <10 >10 <10 >10 <10 >10 <10 >10
Therapy
V+ V+! Cat Cat V+ V+! V–
Cat V–
Target
1.GEDI (mL/m 2 ) >700 700–800 >700 700–800 >700 700–800 700–800
or ITBI (mL/m ) >850 850–1000 >850 850–1000 >850 850–1000 850–1000
2
2.Optimise SVV (%)* <10 <10 <10 <10 <10 <10 <10 <10
GEF (%) >25 >30 >25 >30
or CFI (1/min) >4.5 >5.5 >4.5 >5.5 OK!
ELWI (mL/kg) ≤10 ≤10 ≤10 ≤10
(slowly responding)
V+ = volume loading (! = cautiously) V- = volume contraction Cat = catecholamine / cardiovascular agents
*SVV only applicable in ventilated patients without cardiac arrhythmia
Without guarantee
FIGURE 9.22 PiCCO decision tree (Courtesy Pulsion Medical Systems).
Cardiovascular Assessment and Monitoring 205
Decreased preload Increased preload or perforation, severe bleeding problems, or with patients
on an intra-aortic balloon pump. 77
Fluids The Doppler probe that sits in the oesophagus is approxi-
mately the size of a nasogastric tube, is semirigid and is
77
inserted using a similar technique. The patient is usually
82
sedated but it has been used in awake patients. In such
cases, however, the limitation is that the probe is more
likely to require more frequent repositioning. 76
A The waveform that is displayed on the monitor is trian-
gular in shape (see Figure 9.23) and captures the systolic
Poor contractility Increased contractility portion of the cardiac cycle – an upstroke at the begin-
ning of systole, the peak reflecting maximum systole, and
Inotropes the downward slope of the ending of systole. The wave-
form captures real-time changes in blood flow and
can therefore be seen as an indirect reflection of left
83
ventricular function. Changes to haemodynamic status
will be reflected in alterations in the triangular shape (see
Figure 9.23).
B
Ultrasonic cardiac output monitor
Introduced in 2001 in Australia, the Ultrasonic cardiac
High afterload (high SVR) Decreased afterload
output monitor (USCOM) monitors CO non-invasively
using continuous doppler ultrasound wave by placing a
Vasodilators ultrasound transducer probe supra- or parasternally. The
principles of CO calculation in this method is the same
as Oesophageal Doppler monitoring. Empirical study
suggests that the use of non-invasive USCOM provided
adequate clinical data in patients in different shock cat-
egories and it was safe and cost effective. 84
C
Impedance cardiography
FIGURE 9.23 Oesophageal doppler waveforms.
Transthoracic bioimpedance (impedance cardiography)
is another form of non-invasive monitoring used to esti-
mate cardiac output, and was first introduced by Kubicek
85
Doppler principles are that the movement of blood pro- in 1966. It measures the amount of electrical resistance
duces a waveform that reflects blood flow velocity, in this generated by the thorax to high-frequency, very-low-
case in the descending thoracic aorta, by capturing the magnitude currents. This measure is inversely propor-
change in frequency of an ultrasound beam as it reflects tional to the content of fluid in the thorax: if the amount
23
off a moving object (see Figure 9.23). This measure- of thoracic fluid increases, then transthoracic bioimped-
ment is combined with an estimate of the aorta’s cross- ance falls. Changes in cardiac output can be reflected as
23
sectional area for the stroke volume, cardiac output and a change in overall bioimpedance. The technique requires
cardiac index to be calculated, using the patient’s age, six electrodes to be positioned on the patient: two in the
height and weight. 77 upper thorax/neck area, and four in the lower thorax.
These electrodes also monitor electrical signals from
Oesophageal Doppler monitoring provides an alternative
77
for patients who would not benefit from PAC insertion, the heart.
and can be used to provide continuous measurements Overall, transthoracic bioimpedance is determined by:
under certain conditions: the estimate of cross-sectional (a) changes in tissue fluid volume; (b) volumetric changes
area must be accurate; the ultrasound beam must be in pulmonary and venous blood caused by respiration;
directed parallel to the flow of blood; and there should and (c) volumetric changes in aortic blood flow produced
be minimal variation in movement of the beam between by myocardial contractility. Accurate measurements of
86
measurements. There is some debate at present among changes in aortic blood flow are dependent on the ability
clinicians about the accuracy of Oesophageal Doppler to measure the third determinant, while filtering out any
monitoring when compared with thermodilution tech- interference produced by the first two determinants. Any
nique for calculating cardiac output. 78-80 However, Austra- changes to position or to electrode contact will cause
lian research purports that this technology has become, alterations to the measurements obtained, and recordings
and will continue to be, an invaluable tool in critical should therefore be undertaken with the electrodes posi-
81
care. This form of monitoring can be used periopera- tioned in the same location as previous readings. Caution
tively and in the critical care unit, on a wide variety of is required for patients with high levels of perspiration
patients. It should not, however, be used in patients with (which reduces electrode contact), atrial fibrillation
aortic coarctation or dissection, oesophageal malignancy (irregular R–R intervals makes estimation of the
206 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
ventricular ejection time difficult), or pulmonary oedema, with a small amount of air, injected into the peripheral
pleural effusions or chest wall oedema (which alter vein to produce images of the heart functions. 66
bioimpedance readings irrespective of any changes in In the critical care setting, the preparation of critically ill
cardiac output). The use of transthoracic bioimpedance patients for this examination is important. The nurse
in critically ill patients is variable, due in part to limita- needs to help the sonographer to position the patient to
tions of its usefulness in patients who have pulmonary achieve best results. For TOE preparation, fasting time
oedema. 87,88
must be followed to avoid complications such as respira-
tory aspiration. The nurse will also need to assist the
anaesthetist and the TOE operator, and continue to
monitor the patient’s clinical conditions during the
Practice tip procedure.
Current evidence-based literature suggests that haemody- BLOOD TESTS
namic measurements such as CVP, PAWP and PAP can be accu-
rately measured with the patient’s position of supine to head A number of blood tests are often conducted to assist the
– up to 60 degrees. 28 clinical assessment of the critically ill patients in the criti-
cal care setting.
Full Blood Count
DIAGNOSTICS The full blood count (FBC) assesses the status of three
major cells that are formed in the bone marrow: red
Apart from the haemodynamic monitoring methods to blood cells (RBC), white blood cells (WBC) and platelets.
facilitate cardiac assessment of patients’ clinical condi- Although normal values have been given (see Appendix
tion, a variety of diagnostic tests are often used. Echocar- C), for critically ill patients changes will occur in certain
diography and blood tests are the most commonly used conditions. For example, Hb is reduced in the presence
in critical care. Other tests such as Computerised Tomo- of haemorrhage and also in acute fluid overload causing
graphy (CT) and Nuclear medicine cardiac examination haemodilution.
are also used when indicated. Exercise stress tests and
cardiac angiography are also used and are reviewed in Haemoconcentration can occur during acute dehydra-
Chapter 10. tion, which would show as a high Hb. Similar conditions
will also affect the haematocrit. WBC levels will be ele-
ECHOCARDIOGRAPHY vated during episodes of infection, tissue damage and
inflammation. When infections are severe, the full blood
Echocardiography (shortened to ECHO) is often used in count will show a dramatic rise in the number of imma-
critical care to assess patients’ cardiovascular conditions ture neutrophils. Platelets are easily lost during haemor-
such as heart failure, hypertensive heart disease, valve rhage, and spontaneous bleeding is a danger when the
disease, and pericardial disease in critically ill patients. It count falls to below 20 × 10 /L. 91,92
9
adopts a technique of detecting the echoes produced by
a heart from a beam of very high frequency sound – the Electrolytes
ultrasound. Two dimensional, three dimensional and
contrast ECHO images can be obtained using non- The assessment of electrolyte levels in critically ill patients
invasive transthoracic technique or the invasive trans- is important in diagnosing the patient’s condition. Elec-
oesophageal technique (TOE). The transthoracic ECHO trolyte imbalances, such as potassium and calcium level
uses a transducer probe externally to the heart to obtain changes, can cause cardiovascular abnormalities such as
images (same as a normal ultrasound technique). This arrhythmias. Electrolyte levels are often checked regularly
method is painless and does not require sedation. The in critically ill patients.
TOE technique involves placing a transducer probe into The functions of electrolytes and their cardiac implica-
the oesophageal cavity to assess the function and struc- tions are listed in Table 9.5.
ture of the heart. This method produces better images of
66
the heart than the normal ECHO. However this method Cardiac Enzymes
requires sedation during the procedure and the patient
needs to fast for a few hours prior to the examination. Recent studies have revealed that cardiac troponin levels
are elevated in critically ill septic patients who do not
Two-dimensional ECHO images are valuable resources have evidence of MI. Further, mortality rates are higher
for assessment of the function and structure of the heart. in troponin-positive patients than in those who are
Three dimensional images offer more realistic visualisa- troponin-negative, suggesting that this may become an
tion of the heart’s structure and function. The contrast important enzyme to measure; however, more research is
ECHO provides enhanced images of left and right ven- still required to refine the testing. 93,94 For patients with
tricular definition to facilitate the diagnosis of complex suspected acute myocardial infarction, testing of the
cardiac conditions such as congenital heart defects, valve enzyme troponin T or I is now standard. But not all criti-
stenosis and regurgitation. 83,89,90 The contrast ECHO tech- cally ill patients with elevated cardiac troponin levels
nique uses gas air microbubbles, produced by hand- should be treated as having myocardial infarction unless
95
agitating a syringe containing 10 mL of normal saline there is support from other data. All injured cells release
Cardiovascular Assessment and Monitoring 207
TABLE 9.5 Electrolyte functions and pathophysiology 17,66,106
Electrolyte Functions Common imbalances and causes Signs and symptoms
Potassium Maintain normal functions Hyperkalaemia Muscle weakness, ECG changes in
of nerve and muscle cells Renal failure, dehydration, diabetes, diuretic cardiac toxicity, severe hyperkalaemia
Acid–base balance medications (Serum K between 6 and 6.5 mEq/L)
needs prompt attention because it
can cause life threatening arrhythmia.
Hypokalaemia Muscle weakness, respiratory failure,
Kidney disease, diarrhoea, vomiting, diuretic ECG changes
medications
Sodium Regulate body fluid Hypernatraemia Thirst, confusion, hyperreflexia, seizures
movement Renal failure, dehydration, diarrhoea, vomiting
Maintain cell functions
Acid–base balance Hyponatraemia Altered personality, confusion, seizures,
Acute renal failure, heart failure, pancreatitis, coma, death
peritonitis, burns
Calcium Bone metabolism Hypercalcaemia Polyuria, constipation, nausea, vomiting,
Blood coagulation Hyperparathyroidism, vitamin D toxicity, cancer muscle weakness, confusion, coma,
Muscle contraction ECG changes (shortened QT intervals
Nerve conduction
Hypocalcaemia Paraesthesias, tetany. In severe cases,
Hypoparathyroidism, vitamin D deficiency, renal seizures, encephalopathy, ECG
disease changes (prolonged ST and QT
intervals), heart failure
Magnesium Activate sodium-potassium Hypermagnesaemia Hypotension, respiratory depression, AV
pumps Renal failure conduction disturbances which can
Inactivate calcium channels lead to cardiac arrest (often in renal
Neuromuscular transmission failure patients)
Hypomagnesaemia Anorexia, nausea, vomiting, lethargy, It
Inadequate intake and absorption, or increased may contribute to hypokalaemia
excretion due to hypercalcaemia or diuretics development therefore cardiac
arrhythmias may be present.
Note: associated hypocalcaemia is
common in hypomagnesaemia
Phosphorus Intracellular energy Hyperphosphataemia Usually asymptomatic. However, when
production (ATP) and Kidney failure, metabolic and respiratory hypocalcaemia co-occur, symptoms
enzyme regulation acidosis of hypocalcaemia may be present
Tissue oxygen delivery
Bone metabolism Hypophosphataemia Usually asymptomatic. Severe cases
Burns, diuretic medications, respiratory may have muscle weakness, heart
alkalosis, acute alcoholism failure, coma
For Cardiac implications of electrolytes imbalances, see Chapter 10 and Chapter 11.
enzymes, and by measuring the levels of enzymes it is Cardiac Chest X-ray Interpretation
possible to determine which cells are damaged, thus
aiding diagnosis. See Table 9.6 for cardiac enzyme To interpret the chest X-ray for cardiac assessment, the
parameters and normal values. For abnormal cardiac following steps should be followed to ensure a thorough
enzymes in myocardial infarction, please refer to diagnosis:
Chapter 10. 1. First the heart size needs to be checked to see if the
size of the heart is appropriate. The cardiac silhou-
CHEST X-RAY ette should be no more than 50% of the diameter
Chest X-ray is the oldest non-invasive way to visualise the of the thorax, this is called the cardiothoracic
96
images of the heart and blood vessels, and is one of the ratio. The position of the heart should be 1 3 of
most commonly taken diagnostic procedures in critical heart shadow to the right of the vertebrae and 2 3
93
care. To interpret a chest X-ray for cardiac diagnosis, the of the shadow to the left of the vertebrae. The size
basic knowledge of the normal anatomical cardiac struc- of the heart can be determined in a matter of
ture is important to identify abnormality, and basic under- seconds even for the novice clinician, since this can
standing of the how chest X-ray works is essential. Please be simply determined by visualising the cardiotho-
review the basic concepts, such as what water, air and racic ratio.
bone show on X-ray, and the concepts of AP and PA films, 2. The shape of the heart should be inspected next on
in Chapter 13 before you move on to the next section. the film once the size of the heart was inspected.
208 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
TABLE 9.6 Cardiac enzymes – normal values 91
Enzyme Description Normal value
Troponin T Detected within 4–6 hours of infarction, peaking in 10–24 hours. not normally detected
Creatine kinase (CK) Levels of CK are raised in diseases affecting skeletal muscle. It can be used to Adult female: 30–180 U/L
detect carrier status for Duchenne muscular dystrophy, although not all Adult male: 60–220 U/L
carriers have increased levels.
CK-MB is the first of cardiac enzymes to rise, levels peaking in 24 hours but CK-MB: 0–5% of total CK
returning to normal within 2–3 days.
Aspartate aminotransferase Detection and monitoring of liver cell damage. No cardiac-specific <40 U/L
(AST) isoenzymes; today rarely used because it is released after renal, cerebral
and hepatic damage.
Lactate dehydrogenase (LDH) Of no value in the diagnosis of myocardial infarction. Occasionally useful in 110–230 U/L
the assessment of patients with liver disease or malignancy (especially
lymphoma, seminoma, hepatic metastases); anaemia when haemolysis or
ineffective erythropoiesis suspected. Although it may be elevated in
patients with skeletal muscle damage, it is not useful in this situation.
Post-AMI, cardiac-specific isoenzyme LDH peaks between 48 and 72 hours.
1
D-Dimer Presence indicates deep vein thrombosis, myocardial infarction, DIC <0.25 ng/L
DIC = disseminated intravascular coagulation.
The border of the heart on the X-ray film is deter- needed to thoroughly assess the patients for accurate
mined by the heart anatomy. The border is formed diagnosis. 98
by: the right atrial shadow as the right convex
cardiac border; the superior vena cava as the supe-
rior border; and the left ventricle as the left heart
border and cardiac apex. In the frontal chest X-ray, Practice tip
the right ventricle is not a border-forming structure Critical care nurses should take a systematic approach to inter-
because it is directly superimposed on the cardiac preting chest X-rays. The respiratory, cardiac structures, tubes,
silhouette. Similarly, the normal left atrium should wires and other devices should all be identified in the chest
not be visible on a posteroanterior (PA) film. The X-ray film.
border of the heart should be sharp. If the left
atrium becomes enlarged, it shows a convex supe-
rior left heart border. 96 A widened mediastinum and abnormal aortic contour
3. The next step should move to the superior border may indicate aortic dissection. Similar to heart failure,
to identify the aortic arch and the pulmonary further tests such as TOE, MRI or angiography are needed
arteries. The aortic arch is called the knob. The to confirm the diagnosis. Subtle abnormalities in the
pulmonary arteries and the branches radiate hilar region may indicate pulmonary hypertension (PAH).
outward from the hili (see Figure 9.24). The hilum A decrease in pulmonary vascular markings and promi-
in the mediasternal region is formed by the pul- nent main and hilar pulmonary arterial shadows in the
monary arteries and the main stem bronchi lung fields on the chest film are classic signs of pulmo-
shadows on the film. The focus of this step is to nary hypertension. However the sensitivity of this for
check for prominence of vessels in this region, as excluding PAH is lacking. In pericardial disease, the
99
this suggests vascular abnormalities. 97
chest X-ray often appears normal unless the accumulated
fluid in the pericardial space is over 250 mL. Note that
Chest X-ray in Diagnosing Cardiac Conditions accumulation of fluid is indicated in many cardiac condi-
For coronary heart disease assessment, an initial chest tions therefore other tests need to be carried out to
X-ray film is useful to exclude other causes of chest confirm the diagnosis. 100
pain, such as pneumonia, pneumothorax and aortic
aneurysm, and to assess whether heart failure and/or The position of a Pulmonary Artery Catheter, a Central
pulmonary congestion are present. Patients with chronic Venous Catheter, and pacing wires can be identified on
heart failure show cardiomegaly, Kerby B lines or pul- the chest X-ray. The position of these catheters need to be
monary oedema. Cardiomegaly is the enlarged heart on checked regularly to ensure the catheters and wires are in
the X-ray film. Kerby B lines on the X-ray film is the appropriate places. More details on how to identify the
result of pulmonary congestion and fluid accumulation catheters and pacing wires are in Chapter 13.
in the interstitium. Although cardiomegaly and pulmo- Due to the individual variations in shape, size and rota-
nary oedema indicate heart failure, the chest X-ray alone tion of the heart, and the complexity of cardiac signs,
cannot diagnose the condition. Other forms of tests are chest X-rays often play a minor role in cardiac diagnosis.
Cardiovascular Assessment and Monitoring 209
Aortic arch (knob)
Main and left pulmonary
arteries
Left atrial appendage
Left ventricle
FIGURE 9.24 Chest PA radiograph. The convex right cardiac border is formed by the right atrium (thin arrows) and the heavy arrows indicate the location
of the superior vena cava.
A patient’s clinical condition and other diagnostic test of a coronary artery lesion. In addition, the most appro-
results must be taken into account when diagnosing a priate radiation and contrast dose have not been
cardiac condition. 99,101 determined. 103
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) is a non-invasive
method that can provide cardiac-specific biochemical
Practice tip information such as tissue integrity, cardiac aneurysms,
ejection fraction, and cardiac output. These techniques
Comparison of earlier chest X-ray film(s) with current film is are sometimes considered superior to radiography and
important to diagnose a patient’s clinical condition progress, ultrasound examination methods because the MRI is not
response to treatment, and any movements of catheter affected by bone structure. The techniques include
positions. perfusion imaging, atherosclerosis imaging and coronary
104
artery imaging. MRI is considered an accurate method
to predict the presence of significant coronary artery
disease. However, MRI use in critically ill patients has
105
its limitations. Because of the magnetic field required for
X-RAY COMPUTED TOMOGRAPHY, MAGNETIC this method, the patient cannot be fitted with any pumps
RESONANCE IMAGING (MRI) AND NUCLEAR or machines that have metal parts in them. Organising
MEDICINE STUDIES OF THE HEART appropriate equipment for the critically ill patients who
Since 2000, more non-invasive imaging diagnostic tech- are undergoing this test can be a challenge.
niques are used to aid cardiac assessment. Some of these Nuclear Medicine Cardiac Studies
techniques have shown significant advantages, such as
lowered cost, but they also have their limitations. 66 There are several types of radionuclide imaging methods
available to assess a patient’s cardiac information, includ-
ing the radionuclide isotopes, thallium scan and stress
Cardiac Computed Tomography test radionuclide scan. The purpose of radionuclide
17
Cardiac computed tomography (cardiac CT) is a recent imaging is to assess the perfusion status of cardiac muscle.
development in diagnosing cardiac conditions such as When lowered perfusion in cardiac muscle is identified
suspected coronary heart disease, and in the evaluation this may indicate heart muscle damage. Radionuclide
of coronary artery bypass grafts. It provides a method imaging is often used in patients who have been diag-
to visualise the anatomical structure of the heart and nosed with a myocardial infarction and further investiga-
102
coronary arteries reliably and accurately in patients. tion is required to determine if interventions such as
However, limitations remain with this method including cardiac stent or coronary artery bypass surgery are likely
the inability to assess the haemodynamic relevance to benefit the patient.
210 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
Nursing Care of Patients Undergoing Cardiac urgent action. In the critical care environment two main
CT, MRI and Nuclear Medicine Studies forms of cardiac monitoring are commonly employed:
All the above methods have advantages and benefits in continuous cardiac monitoring, and the 12-lead ECG.
assessing patient cardiac condition. For the critical care Accurate assessment of the patient’s intracardiac status is
nurse, preparation of patients for these examinations is frequently employed and often considered essential to
important because the patients often need to be trans- guide management. The beneficial claims of invasive pul-
ported to the radiology or nuclear medicine departments. monary artery pressure monitoring have, however, been
Important considerations include: questioned in the literature. Consequently, as invasive
pulmonary artery monitoring is frequently utilised in
● Patient’s allergy profile in relation to imaging contrast practice, there is great need for continuing education
needs to be evaluated before the requests are made. about the use of this technology and a need to ensure
● These tests all require the patient to lie still for certain that patient safety is always considered. In day-to-day
periods of time, therefore sedation may be required management of critically ill patients, critical care nurses
during the procedure. must ensure they are skilled and educated in the tech-
● Appropriate equipment, such as non-metal equip- niques of non-invasive and invasive cardiovascular moni-
ment, needs to be organised beforehand if the patient toring techniques and technologies, and be able to
is having an MRI study. synthesise all data gathered and base their practice on the
best available evidence to date.
A strength of this study is the prospective observational
Practice tip design utilised allowing serial measurements to be
Hearing aids and partial dental plates with metal parts must be recorded. However, the findings need to be considered in
removed prior to MRI. Additionally, patients with implantable light of the small sample size and the potential for varia-
devices such as permanent pacemakers cannot have MRI. tion in vasoactive medications used that may have con-
founded results reported. While this study does not
definitively answer a well-debated issue regarding the
SUMMARY value of monitoring peripheral temperatures as a surro-
gate for invasive cardiac output and SVR the potential
The cardiovascular system is essentially a transport system value of simple noninvasive peripheral temperature and
for distributing metabolic requirements to, and collecting clinical assessment in monitoring trends in the intensive
byproducts from, cells throughout the body. A thorough care patient following cardiac surgery is highlighted.
understanding of anatomical structures and physiological
events are critical to inform a comprehensive assessment Of interest for the critical care nurse, subjective peripheral
of the critically ill patient. Findings from assessment assessment was recorded using a simple method that can
should define patient cardiovascular status as well as easily be applied in practice. Foot warmth was recorded
inform the implementation of a timely clinical manage- on a scale of 1–3, with a core of 1 equating to the whole
ment plan. A thorough cardiac assessment requires the foot being cool, a score of 2 equating warm feet but cool
critical care nurse to be competent in a wide range of toes and a score of 3 being equal to the whole foot being
interpersonal, observational and technical skills. warm, including the toes. Using this assessment method,
subjective skin assessment was significantly associated
Current minimum standards for critical care units in with both lactate levels and blood pressure while changes
Australia and New Zealand require that patient monitor- in peripheral skin assessment correlated to changes in
ing include circulation, respiration and oxygenation. For cardiac output and SVR. It has so often been said that
many critically ill patients, haemodynamic instability is there is no complete substitute for hands-on clinical
a potentially life-threatening condition that necessitates examination and this study reinforces this mantra.
Case study
Mr Ryan, a 47-year-old man, was admitted to the Intensive Care ● passing dark urine and pale stools frequently
Unit from the hospital medical ward. The following is a summary ● denied abdominal pain, jaundice, haematuria, prodromal or
of events prior to admission taken from the patient hospital presyncopal symptoms
records:
In the emergency department the patient observations were as
Relevant past medical history included: follows:
● hypercholesterolaemia ● BP 100/70 mmHg
● elevated blood sugar levels ● HR 126/min, Sinus tachycardia
● Body temp 37.9–38.1°C per axilla
Admitted to hospital 2 days ago following collapse: ● SaO 2 96% on room air
● with a 4-day history of fever, sweats and rigors ● jugular venous pressure noted as normal
● anorexic: only able to drink 5–6 glasses fluid per day ● tongue dry
● lethargic: able to carry out ADLs with effort
● heart sounds audable S1, S2 and considered normal
Cardiovascular Assessment and Monitoring 211
Case study, Continued
● bibasal creps ● a pulmonary artery catheter was inserted and the following
● hepatomegaly – (non-tender) 16 cm values noted:
● bowel sounds active – CVP 18 mmHg
● urinalysis showed protein +++ and large amount of blood – PA pressures 51/31 mmHg
● intravenous fluids were commenced and the patient was trans- – PAWP 22 mmHg
ferred to a medical ward – CI 1.9 l L/min/m 2
– SVRI 2956 dynes/sec/cm −5
Differential diagnosis: Acute infection, possible urinary tract infec-
tion, acute hepatitis, renal impairment secondary to dehydration – BP 90/57 mmHg
– A dobutamine infusion was commenced @ 5 mcg/kg/min
Key events during hospitalisation A transthoracic echocardiography (TOE) was performed with the
Day 1 following hospital admission: following findings:
● the patient remained febrile (temperature up to 39°C) ● moderate/severe global dysfunction
● at 2100 hr BP noted in charts to be 90/50 with HR 120 bpm ● LVEF 25–30%
● RV severe hypokinesis
Day 2 post admission: ● valves structurally normal
● 0935 hr ● PA pressures ∼40 mmHg (mean)
● SaO 2 97–99% with non-rebreathing mask at 10 L/min ● no pleural effusion visible
overnight
● Patient became disorientated and pulling off mask: SaO 2 Discussion
81% on room air This case study illustrates the complexities of critical illness in the
● patient pale, tachypnoea RR 40 per minute presence of several risk factors and comorbidities. Initial non-
● mottled appearance on legs and abdomen invasive assessments following admission focused on treatment
● audible crackles right base and management of an acute infection and restoration of intravas-
● ECG taken: new T wave changes noted in lead III cular fluid volumes. When the patient was unresponsive to initial
● indwelling urinary catheter inserted: dark urine minimal treatment strategies, following admission to the intensive care
amount drained unit, invasive monitoring was required to guide patient manage-
● awaiting ICU medical assessment and transfer ment. Continuous invasive arterial monitoring aided titration of
● 1130 hr vasoconstrictor therapy and insertion of a central venous line
● the patient became unresponsive and had increasingly aided with directing fluid therapy. It would have been easy to have
laboured respirations focused on treating the patient as a patient in septic shock at this
● an emergency team call was made by the RN point based on clinical trends but the value of invasive pulmonary
● patient was given a bolus of 2 L Hartmans and O 2 adminis- artery readings and a transthoracic echocardiography guided
tered via a non-rebreathing mask management direction with evidence of cardiogenic shock (as
● 1230 hr evident by low cardiac index, low left ventricular ejection fraction
● the patient was transferred to the ICU and elevated pulmonary pressures in the presence of ECG T wave
● hypotensive, unresponsive to fluids, hypoxic despite 100% changes) prompting the commencement of a dobutamine infu-
O 2 via non-rebreather mask (SaO 2 76%) sion directed at increasing cardiac contractility and decreasing
● temperature 39.3°C preload. For the critical care nurse at the bedside, this patient dem-
● arterial line and internal jugular venous line inserted onstrates the need to be able to synthesise all assessment findings,
● IV noradrenaline infusion commenced with the aim of main- invasive and non-invasive, and titrate prescribed therapies to
tain a MAP > 75 mmHg achieve optimal tissue perfusion while providing holistic nursing
● heart rate 140 bpm sinus care in a complex and changing environment. Without invasive
● chest X-ray showed bilateral pulmonary infiltrates monitoring, management of this patient would have been techni-
● the patient was sedated, intubated and ventilation therapy cally challenging and required a trial and error approach until a
commenced successful treatment plan was accomplished. This patient did ulti-
● urine output 52 mL since IDC inserted (3 hours) mately get discharged from ICU on day 6 to the medical ward
● peripheries cool and dark/mottled in appearance, cap return and was eventually discharged back home after five weeks
>5 secs hospitalisation.
212 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
Research vignette
Schey BM, Williams DY, Bucknall T. Skin temperature as a noninva- Results
sive marker of haemodynamic and perfusion status in adult cardiac Cardiac output was a significant predictor for objectively measured
surgical patients: an observational study. Intensive and Critical Care skin temperature and CPTG (P = 0.001 and P = 0.004, respectively).
Nursing 2009; 25(1): 31–7. Subjective assessment of skin temperature was significantly related
Abstract to cardiac output, systemic vascular resistance, and serum lactate
Objective (P < 0.001, respectively).
Foot temperature has long been advocated as a reliable noninva- Conclusions
sive measure of cardiac output despite equivocal evidence. The These results support the utilisation of skin temperature as a non-
aim of this pilot study was to investigate the relationship between invasive marker of cardiac output and perfusion. The use of CPTG
noninvasively measured skin temperature and the more invasive was shown to be unnecessary, given the parallels in results with
core-peripheral temperature gradients (CPTGs), against cardiac the less invasive skin temperature parameters. A larger study is
output, systemic vascular resistance, serum lactate and base however required to validate these findings.
deficit.
Critique
Research methodology This interesting pilot study brings attention to the potential value
The study was of a prospective, observational and correlational of simple non-continuous monitoring and subjective clinical
design. Seventy-six measurements were recorded on ten adults assessment in guiding management of patients following cardiac
post-cardiac surgery. Haemodynamic assessments were made via surgery. The use of noninvasive skin and core temperature gradi-
bolus thermodilution. Skin temperature was measured objec- ents as an indicator of systemic vascular resistance (SVR) and
tively via adhesive probes, and subjectively using a three-point cardiac output (CO) is far from a new technique, although prior
scale.
work, mostly dated, has demonstrated equivocal findings related
Setting to its value. Additionally, the value of subjective clinical assessment
The study was conducted within a tertiary level intensive care is often undervalued in today’s more invasive intensive care
unit. nursing and medical practices.
Learning activities
Learning activities 1–4 relate to the case study. of central line insertion and what strategies can you implement
1. Consider the case study and discuss why haemodynamic mon- to reduce the likelihood of those complications?
itoring is important for this patient’s management. Include 3. What are the key points to remember when interpreting hae-
consideration of the aspects of haemodynamic monitoring modynamic monitoring results in a patient receiving mechani-
that provide particular benefit in this specific case. cal ventilation?
2. Describe the rationale of inserting a central line when the 4. Consider the indications for PAP monitoring, and explain why
patient was first admitted to ICU. What are the complications PAP monitoring was beneficial for this patient’s management.
ONLINE RESOURCES 6. Campbell AM, Hulf JA. Aspects of myocardial physiology. Update in Anaes-
thesia [serial on the Internet]. 2004; 18(Article 14): Available from: http://
American Heart Foundation, www.americanheart.org www.nda.ox.ac.uk/wfsa/html/u18/u1814_01.htm.
Australian Institute of Health and Welfare, www.aihw.gov.au 7. Bersten AD, Soni N, Oh TE. Oh’s intensive care manual, 6th edn. Oxford:
National Heart Foundation of Australia, www.heartfoundation.org.au Butterworth-Heinemann; 2009.
Australian College of Critical Care Nurses, www.acccn.com.au 8. Johns CI, Gallagher R. Nursing management: arrhythmias. In: Brown D,
Australian and New Zealand Intensive Care Society, www.anzics.com.au Edwards H, eds. Lewis’ medical and surgical nursing. Sydney: Mosby/Elsevier;
British Association of Critical Care Nurses, www.baccn.org.uk 2005.
Critical Care Forum, www.ccforum.com/home 9. Elliott D. Shock. In: Romanini J, Daly J, eds. Critical care nursing: Australian
Intensive Care, www.intensivecare.com perspectives. Sydney: Harcourt Brace; 1994. p. 687.
World Federation of Critical Care Nurses, www.wfccn.org 10. Leeper B. Monitoring right ventricular volumes: a paradigm shift. AACN
Clinical Issues 2003; 14(2): 208–19.
REFERENCES 11. Sugerman RA. Structure and function of the neurological system. In:
McClance KL, Huether SE, Brasher VL, Rote NS, eds. Pathophysiology: the
1. McCance K, Brashers VL. Structure and function of the cardiovascular biological basis for disease in adults and children, 6th edn. Maryland Heights:
and lymphatic systems. In: Huether SE, McCance K, eds. Understanding patho- Mosby Elsevier; 2010.
physiology. St. Louis, Mo: Mosby; 2008. 12. Johnson K, Rawlings-Anderson K. Oxford handbook of cardiac nursing. New
2. Copstead L. Pathophysiology, 3rd edn. St. Louis, Mo.: Elsevier Saunders; 2005. York: Oxford University Press; 2007.
3. Novak B, Filer L, Hatchett R. The applied anatomy and physiology of the 13. Australian and New Zealand College of Intensive Care Medicine. Minimum
cardiovascular system. In: Hatchett R, Thompson D, eds. Cardiac nursing: a standards for intensive care units. [Cited Jan 2011.] Available from: http://
comprehensive guide. Philadelphia: Churchill Livingstone Elsevier; 2002. www.cicm.org.au/cmsfiles/IC-1%20Minimum%20Standards%20for%20
4. Guyton AC. Textbook of medical physiology, 11th edn. Philadelphia: Elsiever: Intensive%20Care%20Units.pdf.
Saunders; 2006. 14. Drew BJ, Califf RM, Funk M, Kaufman ES, Krucoff MW et al. Practice stan-
5. Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: diagnosis and dards for electrocardiographic monitoring in hospital settings: an American
management, 5th edn. St Louis: Mosby/Elsevier; 2006. Heart Association scientific statement from the Councils on Cardiovascular
Cardiovascular Assessment and Monitoring 213
Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: 45. Truwit JD. Technique and measurements: getting a line on the hemodynamic
Endorsed by the International Society of Computerized Electrocardiology undercurrent. J Crit Illness 2003; 18(1): 9–20.
and the American Association of Critical-Care Nurses. Circulation 2004; 46. Ruesch S, Walder B, Tramèr MR. Complications of central venous catheters:
110(17): 2721–6. internal jugular versus subclavian access – a systematic review. Crit Care Med
15. Jacobson C. Bedside cardiac monitoring. Critical Care Nurse 2003; 23(6): 2003; 30(2): 454–60.
71–3. 47. Rubinson L, Diette GB. Best practices for insertion of central venous catheters
16. Shoemaker WC. Routine clinical monitoring in acute illness. In: Shoemaker in intensive care units to prevent catheter-related bloodstream infections.
WC, Vehmohos GC, Demetridas D, eds. Procedure and monitoring for the criti- J Lab Clin Med 2004; 143(1): 5–13.
cally ill. Philadelphia: W.B. Saunders; 2002. p. 155–66. 48. Swanz HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D. Cath-
17. Urden L, Stacy KL, Lough ME, eds. Critical care nursing: diagnosis and manage- eterisation of the heart in man with use of flow-directed balloon-tipped
ment, 6th edn. St Louis: Mosby/Elsevier; 2010. catheter. N Eng J Med 1970; 283(9): 447–51.
18. Conover MB. Understanding electrocardiography, 8th edn. St Louis: Mosby; 49. Truwit JD. The pulmonary artery catheter in the ICU, part 2: clinical applica-
2003. tions; how to interpret the hemodynamic picture. J Crit Illness 2003; 18(2):
19. Morris F, Brady WJ. Clinical review: ABC of clinical electrocardiography. 63–71.
Acute myocardial infarction – Part I. BMJ 2002; 324: 831–4. 50. Dalen JE, Bone RC. Is it time to pull the pulmonary artery catheter? JAMA
20. Americal Heart Association. Myocardial ischemia, injury and infarction. 1996; 276(11): 916–18.
2008. Available from: http://www.americanheart.org/presenter.jhtml? 51. Prentice D, Ahrens T. Controversies in the use of the pulmonary artery
identifier=251. catheter. J Cardiovas Nurs 2001; 15(2): 1–5.
21. Raistin AM, Soars L. Nursing assessment: cardiovascular system. In: Brown 52. Society of Critical Care Medicine. Pulmonary Artery Catheter Consenus
D, Edwards H, eds. Lewis’ medical-surgical nursing. Sydney: Mosby/Elsevier; conference. Consensus statement. Crit Care Med 1997; 25(6):
2005. 910–25.
22. Aitken LM. Critical care nurses’ use of decision-making strategies. J Clin Nurs 53. Chittock DR, Dhingra VK, Ronco JJ, Russell JA, Forrest DM et al. Severity of
2003; 12(4): 476–83. illness and risk of death associated with pulmonary artery catheter use. Crit
23. Chaney JC, Derdak S. Minimally invasive haemodynamic monitoring for the Care Med 2004; 32(4): 911–15.
intensivist: current and emerging technology. Crit Care Med 2002; 30(10): 54. Harvey S, Harrison D, Singer M, Ashcroft J, Jones CM et al. Assessment of
2338–45. the clinical effectiveness of pulmonary artery catheters in management of
24. Pinsky MR. Rationale for cardiovascular monitoring. Curr Opin Crit Care patients in intensive care (PAC-Man): a randomized controlled trial. Lancet
2003; 9(3): 222–4. 2005; 366: 472–7.
25. Dietz B, Smith TT. Enhancing the accuracy of haemodynamic monitoring. 55. Harvey S, Young D, Brampton W, Cooper A, Doig GS et al. Pulmonary artery
J Nurs Care Qual 2002; 17(1): 27–34. catheters for adult patients in intensive care. Cochrane Database of Systematic
26. Rice WP, Fernandez EG, Jarog D, Jensen A. A comparison of hydrostatic level- Reviews 2006; (3).
ing methods in invasive pressure monitoring. Crit Care Nurse 2000; 20(6): 56. Cruz K, Franklin C. The pulmonary artery catheter: uses and controversies.
20–30. Crit Care Clinics 2001; 17(2): 271–91.
27. McGhee BH, Bridges MEJ. Monitoring aterial blood pressure: what you may 57. Bridges EJ. Pulmonary artery pressure monitoring: when, how, and what else
not know. Crit Care Nurse 2002; 22(2): 60–79. to use. AACN Adv Crit Care 2006;17(3): 286–303.
28. American Association of Critical Care Nurses (AACN). Pulmonary artery 58. Woodrow P. Intensive care nursing. London: Routledge; 2000.
pressure monitoring. 2004 [Cited July 2010]. Available from: www.aacn.org. 59. Bowdle TA. Complications of invasive monitoring. Anaesthesiology Clinics N
29. Quaal SJ. Improving the accuracy of pulmonary artery catheter measure- Am 2002; 20(3): 571–8.
ments. J Cardiovas Nurs 2001; 15(2): 71–82. 60. Ritzema J, Troughton R, Melton I, Crozier I, Doughty R et al. Physician-
30. Australian Council of Health Care Standards. Intensive Care Indicators directed patient self-management of left atrial pressure in advanced chronic
Version 3. 2006. [Cited Jan 2011]. Available at: http://www.achs.org.au/ heart failure. Circulation 2010; 121(9): 1086–95.
31. Intensive Care Clinical Advisory Group. Intensive care services in New Zealand: 61. Ott K, Johnson K, Ahrens T. New technologies in the assessment of hemo-
a report to the Deputy Director-General, Clinical Services. Wellington: Ministry dynamic parameters. J Cardiovascular Nurs 2001; 15(2): 41–55.
of Health; 2005. 62. Carelock J, Clark AP. Heart failure: pathophysiologic mechanisms. Am J Nurs
32. O’Sullivan J, Allen J, Murray A. The forgotten Korotkoff phases: how often 2001; 101(12): 26–33.
are phases II and III present and how often do they relate to the other 63. Rodgers JM, Reeder SJ. Current therapies in the management of systolic and
Korotkoff phases? Am J Hypertension 2002; 15(3): 264–8. diastolic dysfunction. Dimensions Crit Care Nurs 2001; 20(6): 2–10.
33. Dobbin KR. Non-invasive blood pressure monitoring. Crit Care Nurse 2002; 64. Lough ME. Cardiovascular assessment and diagnostic procedures. In: Urden
22(2): 123–4. L, Stacy KL, Lough ME, eds. Priorities in critical care nursing. St Louis: Mosby;
34. Hung DT, Lilly CM. Making the most of hemodynamic monitoring in the 2004.
ICU: observing and optimizing appropriate parameters. J Crit Illness 2003; 65. Gödje O, Höke K, Goetz AE, Felbinger TW, Reuter DA et al. Reliability of a
18(5): 198–208. new algorithm for continuous cardiac output determination by pulsecon-
35. Imperial-Perez F, McRae M. Arterial pressure monitoring. Crit Care Nurse tour analysis during hemodynamic instability. Crit Care Med 2002; 30(1):
2002; 22(1): 70–72. 52–8.
36. Chatfield D, Rees-Padlar S. Jugular venous oxygen saturation: is it relevant 66. Moser DK, Reigel B. Cardiac nursing: a companion to Brauwald’s heart disease.
to the nurse? Nurs Crit Care 2001; 6(4):187–91. St Louis: Elsevier; 2008.
37. Woodrow P. Central venous catheters and central venous pressure. Nurs 67. Faybik P, Hetz H, Baker A, Yankovskaya E, Krenn CG, Steltzer H. Iced versus
Stand 2002; 16(26): 45–51. room temperature injectate for assessment of cardiac output, intrathoracic
38. Bellomo R, Uchino S. Cardiovascular monitoring tools: use and misuse. Curr blood volume and extravascular lung water by single transpulmonary ther-
Opin Crit Care 2003; 9(3): 225–9. modilution. J Crit Care 2004; 19(2): 103–7.
39. Kumar A, Anel R, Bunnell E, Habet K, Zanotti S et al. Pulmonary artery 68. Cottis R, Magee N, Higgins DJ. Haemodynamic monitoring with pulse-
occlusion pressure and central venous pressure fail to predict ventricular induced contour cardiac output (PiCCO) in critical care. Intens Crit Care Nurs
filling volume, cardiac performance, or the response to volume infusion in 2003; 19(5): 301–7.
normal subjects. Crit Care Med 2004; 32(3): 691–9. 69. Salukhe TV, Wyncoll DL. Volumetric haemodynamic monitoring and con-
40. Michard F, Alaya S, Zarka V, Bahloul M, Richard C, Teboul JL. Global end- tinuous pulse contour analysis: an untapped resource for coronary and high
diastolic volume as an indicator of cardiac preload in patients with septic dependency care units? Brit J Cardiology (Acute and Interventional Cardiology)
shock. Chest 2003; 124(5): 1900–8. 2002; 9(1): 20–25.
41. Weyland A, Grune F. Cardiac preload and central venous pressure. Anaesthe- 70. Gödje O, Friedl R, Hannekum A. Accuracy of beat-to-beat cardiac output
tist 2009; 58(5): 506–12. monitoring by pulse contour analysis in hemodynamical unstable patients.
42. Pinsky MR. Functional hemodynamic monitoring. Intens Care Med 2002; Med Sci Monitor 2001; 7(6): 1344–50.
28(4): 392–8. 71. Hofer CK, Bulmann S, Jaeggi P, Genoni M, Zollinger A. Cardiac output
43. Schummer W. Central venous pressure. Validity, informative value and measurement after cardiac surgery: Thermodilution compared with two
correct measurement. Anaesthetist 2009; 58(5): 499–505. alternative methods. Euro J Anaesthesiol 2002; 19(Suppl. 27): 9–11.
44. McGee DC, Gould MK. Current concepts: preventing complications 72. Chung F-T, Lin S-M, Lin S-Y, Lin H-C. Impact of extravascular lung water
of central venous catheterization. N Eng J Med 2003; 348(12): index on outcomes of severe sepsis patients in a medical intensive care unit.
1123–33. Resp Med 2008; 102(7): 956–61.
214 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
73. Jansen JJ. The thermodilution method for the clinical assessment of cardiac with conventional echocardiography and cardiac catheterization. Portuguese
output. Intens Care Med 1995; 21(8): 691–7. J Cardiology 2002; 21(5): 555–72.
74. Martin GS, Eaton S, Mealer M, Moss M. Extravascular lung water in patients 90. Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A et al.
with severe sepsis: a prospective cohort study. Crit Care 2005;9(2):74–82. Echocardiographic assessment of valve stenosis: EAE/ASE Recommendations
75. King S, Lim T. The use of the oesophageal Doppler monitor in the intensive for clinical practice. Morrisville, NC: American Society of Echocardio graphy;
care unit. Crit Care Resusc 2004; 6(2): 113–22. 2010.
76. Hett A, Jonas MM. Non-invasive cardiac output monitoring. Intens Crit Care 91. Royal College of Pathoiogists Australasia. RCPA manual. Version 46. 2011.
Nurs 2004; 20(2): 103–8. [Cited March 2011]. Available at: http://www.rcpa.edu.au/Publications/
77. Turner MA. Doppler-based haemodynamic monitoring. AACN Clinical Issues RCPAManual.htm.
2003; 14(2): 220–31. 92. Pagana KD. Mosby’s diagnostic and laboratory test reference, 8th edn. St Louis:
78. Bein B, Renner J, Tonner PH. Transoesophageal echocardiography for the Mosby/Elsevier; 2007.
determination of cardiac output: beware of improper comparisons. Anaes- 93. Van Bockel EAP, Tulleken JE, Ligtenberg JJM, Zijlstra JG. Troponin in septic
thesia 2005; 60(5): 512–14. and critically ill patients. Chest 2005; 127(2): 687–8.
79. Engoren M, Barbee D. Comparison of cardiac output determined by bio- 94. Ammann P, Maggiorini M, Bertel O, Haenseler E, Joller-Jemelka HI et al.
impedance, thermodilution and the Fick method. Am J Crit Care 2005; Troponin as a risk factor for mortality in critically ill patients without acute
14(1): 40–45. coronary syndromes. J Am College Cardiol 2003; 41(11): 2004–9.
80. Bettex DA, Hinselmann V, Hellermann JP, Jenni R, Schmid ER. Transo- 95. Klein-Gunnewiek JMK, Van der hoeven JG. Cardiac troponin elevations
esophageal echocardiography is unreliable for cardiac output assessment among critically ill patients. Curr Opin Crit Care 2004; 10: 324–46.
after cardiac surgery compared with thermodilution. Anaesthesia 2004; 96. Erkonen WE, Wilbur LS. Radiology 101: the basics and fundamentals of imaging,
59(12): 1184–92. 3rd edn. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.
81. McLean AS. Transoesophageal echocardiography in the intensive care unit. 97. Lareau C, Wootton J. The ‘frequently’ normal chest x-ray. Canadian J Rural
Anaesthesia Intens Care 1998; 26(1): 22–5. Med 2004; 9(3): 183–6.
82. Atlas G, Mort T. Placement of the esophageal Doppler ultrasound probe in 98. Malcolm J, Arnold O. Heart Failure. The MERCK manual for healthcare profes-
awake patients. Chest 2001; 119(1): 319. sionals. 2009. Available from: http://www.merckmanuals.com/professional/
83. Miyagawa S, Masai T, Fukuda H, Yamauchi T, Iwakura K, Itoh H et al. Coro- sec07/ch074/ch074a.html
nary microcirculatory dysfunction in aortic stenosis: myocardial contrast 99. McGoon M, Gutterman D, Steen V, Barst R, McCrory DC et al. Screening,
echocardiography study. Annals Thoracic Surg 2009; 87: 715–19. early detection, and diagnosis of pulmonary arterial hypertension: ACCP
84. Haas LEM, Tjan DHT, van Wees J, van Zanten ARH, eds. Validation of evidence-based clinical practice guidelines. Chest 2004; 126(1 Suppl):
the USCOM-1A cardiac output monitor in hemodynamic unstable intensive S14–34.
care patients. Conference Paper: Annual Intensive Care Society Congress, 100. Parmet S, Lynm C, Glass RM. Pericarditis. JAMA 2003; 289(9): 1194.
Netherlands; 2006. 101. O’Brien T, Paul S. Chest x-ray and vascular studies. In: Taylor G, ed. Primary
85. Lasater M, VonRueden KT. Outpatient cardiovascular management care management of heart disease. St Louis: Mosby; 2000.
utilizing impedance cardiography. AACN Clinical Issues 2003; 14(2): 102. Wijesekera NT, Duncan MK, Padley SPG. X-ray computed tomography of the
240–50. heart. Brit Med Bull 2010; 93: 49–67.
86. Albert NM. Bioimpedance cardiography measurements of cardiac output 103. Ropers D. Multislice computer tomography for detection of coronary artery
and other cardiovascular parameters. Crit Care Nursing Clinics N Am 2006; disease. J Interventional Cardiol 2006; 19: 574–82.
18(2): 195–202. 104. Lima J, Desai M. Cardiovascular magnetic resonance imaging: current and
87. Sageman WS, Riffenburgh RH, Spiess BD. Equivalence of bioimpedance and emerging applications. J Am College Cardiol 2004; 44: 1164–71.
thermodilution in measuring cardiac index after cardiac surgery. J Cardiotho- 105. Paetsch I, Gebker R, Fleck E, Nagel E. Cardiac magnetic resonance imaging:
racic Vascular Anesthesia 2002; 16(1): 8–14. a noninvasive tool for functional and morphological assessment of coronary
88. Raaijmakers E, Faes TJ, Scholten RJ, Goovaerts HG, Heethaar RM. A meta- artery diease: current clinical applications and potential future concepts. J
analysis of three decades of validating thoracic impedance cardiography. Crit Interventional Cardiol 2003; 16: 457–63.
Care Med 1999; 27(6): 1203–13. 106. Lewis J. Fluid and electrolytes metabolism The MERCK manual for healthcare
89. Almeida AG, Sargento L, Gabriel HM, da Costa JM, Morais J et al. Evaluation professionals. 2009: Available from: http://www.merck.com/mmpe/sec12/
of aortic stenosis severity: role of contrast echocardiography in comparison ch156/ch156b.html.
Cardiovascular Alterations
and Management 10
Robyn Gallagher
Andrea Driscoll
Learning objectives Key words
After reading this chapter, you should be able to: arrhythmia
● explain the pathophysiology of coronary artery disease, acute coronary syndrome
clinical manifestations of acute coronary syndromes and myocardial infarction
management of events percutaneous coronary intervention
● discuss the collaborative care for a patient with chest pain acute heart failure
● list the diagnostic tests used to assess myocardial ischaemia left ventricular failure
● outline the actions and contraindications of thrombolytic right ventricular failure
drugs aortic aneurysm
● outline the clinical manifestations of right and left endocarditis
ventricular failure cardiomyopathy
● discuss the goals of heart failure treatment hypertensive emergencies
● discuss the pathophysiology of the four different types of ventricular aneurysm
cardiomyopathy and how it affects cardiac function
● outline the actions of angiotensin converting enzyme
inhibitors, beta-blockers, loop diuretics and spironolactone
and how they relate to the pathophysiology of heart failure CORONARY HEART DISEASE
Coronary heart disease (CHD) is the term used to describe
the effects of a reduction or complete obstruction of
blood flow through the coronary arteries due to narrow-
INTRODUCTION ing from atherosclerosis and/or thrombus. Although
some patients may be asymptomatic, the commonest
This chapter reviews the support of cardiovascular func- manifestations of CHD are chest pain due to angina,
tion in the face of many compromises to the system. It acute coronary syndrome (ACS, a term used to collec-
focuses on two of the most prevalent and fatal diseases tively describe acute myocardial infarction [AMI] and
affecting the heart: coronary heart disease and heart unstable angina) and sudden death. CHD may also cause
failure. These diseases are also a common co-morbidity arrhythmias and heart failure. 1
in elderly patients admitted to critical care units. The first
section on coronary heart disease reviews the pathophysio- CHD is the leading cause of death, premature death and
2,3
logical concepts of myocardial ischaemia and associated disability in Australia and New Zealand. In 2007, more
complications, with detailed consideration of the clinical than 22,000 people died of CHD in Australia, more than
2-4
implications, assessment and associated management. 5000 in New Zealand in 2004 and 7.2 million worldwide.
Heart failure is discussed in terms of the body’s compen- Death rates have fallen by about 76% since the 1960s,
satory mechanisms and the clinical sequelae and associ- primarily due to improvements in risk factors and health
ated clinical features of heart failure. Nursing and medical care for those at risk. However, the burden of CHD
management is outlined including the management of remains high, with 1.5% of Australians reporting CHD
2
acute exacerbations of heart failure. Finally, other cardio- symptoms. Furthermore, CHD is the single leading
vascular disorders commonly managed in critical care health problem worldwide because of a rising incidence
4
units are reviewed ranging from other forms of heart in developing countries.
failure to hypertensive emergencies and aortic aneurysms.
The case study presented at the end of the chapter high- MYOCARDIAL ISCHAEMIA
lights the key aspects of the management of coronary When coronary blood flow is insufficient to meet myo-
heart disease and heart failure in patients admitted to cardial tissue demand for oxygen, myocardial ischaemia
critical care units. occurs. Critical restriction to blood flow occurs when the 215
216 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
diameter of the lumen of the blood vessel is reduced by Platelet Distal platelet
more than half. Coronary blood flow is also determined white thrombus emboli
by perfusion pressure, which can be adversely affected by
abnormalities in blood flow (valvular disease), vessel
wall (coronary spasm) and the blood (anaemia, polycy-
5
thaemia). Myocardial oxygen demand is influenced by
heart rate, strength of myocardial contraction and left Blood flow
ventricular wall tension. As the myocardium receives
most of its blood supply during diastole, a rise in heart
rate will decrease the duration of diastole and therefore
coronary perfusion. Sympathetic stimulation increases
the force of contraction and therefore oxygen demand.
Lipid
Left ventricular wall tension increases with the changes Endothelium Ruptured Lipid
core
in preload associated with filling and afterload associated A plaque core
with systemic vascular resistance. During activity, pyrexia
and arrhythmias, these effects may compound due to
sympathetic stimulation, causing an increased oxygen Fibrin and RBCs
demand and reduced coronary perfusion. red thrombus
ANGINA
Angina is the commonest manifestation of CHD and is
the term used to describe the symptoms of discomfort
that occur during myocardial ischaemia. The classic Blood flow
angina pattern consists of retrosternal constricting pain/
discomfort, which may radiate to the arms, throat, jaw,
teeth, back or epigastrium. Associated symptoms often
include shortness of breath, nausea, vomiting, sweating,
palpitations and weakness.
White Vessel occlusion
A fixed coronary artery lesion, causing limitation of B thrombus
oxygen supply at times of increased demand, results in
stable angina. Therefore, symptoms arise during periods FIGURE 10.1 (A) Plaque rupture exposes thrombogenic lipid. A white
thrombus is formed by activated platelets adhering. This lesion is unstable
of physical and emotional stress and resolve within 2–10 and may lead to thrombin activation. (B) Thrombin activation leads to a
minutes of rest. Symptoms tend to be worse in the mesh of fibrin and red blood cells, leading to a ‘red thrombus’.
105
morning (coinciding with a peak in blood pressure), after
heavy meals and in cold weather. The severity of symp-
toms has little correlation with the progress of the disease.
However, a patient with a typical history of angina has a if the patient experiences more than 20 minutes of pain
high probability of CHD and a higher risk of AMI and at rest (pain at rest is associated with changes in ST
sudden death in the following year. 6 segment of 1 mm or more on a 12-lead ECG), if there
UNSTABLE ANGINA AND ACUTE was MI within the previous two weeks, or if pulmonary
7
oedema or mitral regurgitation is present.
MYOCARDIAL INFARCTION
Unstable angina and AMI form a continuum on the MYOCARDIAL INFARCTION
basis of reduction in coronary blood flow and subse- Myocardial infarction (MI) occurs when blood flow to
quent damage to myocardial cells. Unstable angina may the myocardium is severely impaired for more than 20
indicate transient ischaemia, whereas AMI indicates minutes as myocardial cell necrosis begins. Coronary
myocardial tissue death. The term ‘acute coronary syn- artery thrombus arising from an atherosclerotic plaque is
7
drome’ (ACS) is now used to represent this continuum. found in the majority of patients dying of AMI. Cellular
8
ACS results from the rupture or erosion of an atheroscle- death begins in the subendocardial layer and progresses
rotic plaque, leading to release of vasoconstrictor sub- through the full muscle thickness, so that by 2 hours with
stances and potentially triggering coagulation activity total occlusion a full ‘transmural’ infarction will result.
(see Figure 10.1). Formation of thrombi results in inter- However, the full extent of tissue death may occur as a
mittent and/or prolonged obstruction of the coronary single incident or evolve over several days, depending on
artery. Therefore, ACS typically presents as a recent the degree of obstruction to blood flow.
history of angina (within the past 4–6 weeks); a change
in symptoms including increased frequency, more easily The size and location of the infarction will influence the
provoked or occurring in the absence of physical or emo- clinical manifestations and risk of death and determine
tional stress, more severe or prolonged and/or less treatment. The size of the infarction is determined by the
responsive to nitrate therapy. ACS is a medical emer- extent, severity and duration of the ischaemic event, the
gency, with up to a third of ACS patients at risk of AMI amount of collateral circulation, and the metabolic
7
and death within 3 months. There is a high risk of death demands placed on the myocardium. Usually the ventricle
Cardiovascular Alterations and Management 217
wall is affected, with a small infarction often resulting in
a dyskinetic wall (altered movement), whereas a large TABLE 10.1 The PQRST criteria for assessing
infarction may result in akinesis (no movement). chest pain 110
The location and impact of the infarction will depend on
which coronary artery has been obstructed: P Precipitating Exercise and activity
Stress and anxiety
● Left anterior descending (LAD) affects the function of Cold weather
the left ventricle and interventricular septum, includ- Palliating Stop activity
ing ventricular conduction tissue. Patients with antero- Rest
septal MI are at high risk of heart failure, cardiogenic Nitroglycerin
shock and mortality due to pump deficits. Q Quality Heavy, tight, choking, vice-like,
● Circumflex (CX) affects the left ventricle lateral and constricting
5
posterior walls and the SA node in 50% of people. R Region, Radiation Left side of chest, shoulder, arm and jaw
The impact on pump efficiency of lateral and posterior Retrosternal and radiating to the neck
wall necrosis is not as severe as anteroseptal infarcts, S Severity Rate pain on scale of 1 (no pain) to 10
although patients are at more risk of arrhythmias. (worst pain possible)
● Right coronary artery (RCA) affects the inferior wall of
the left ventricle and the right ventricle, as well as the T Time Pain lasts longer than 10 minutes
despite nitroglycerin
AV node in most patients and the SA node in 50% of Pain comes and goes but lasts longer
people. There is potentially severe impact on ventricu- than 20 minutes
lar function if both the inferior wall and the right Hudak CM, Gallo BM, Morton PG. Critical care nursing, A holistic approach.
ventricle are affected, as well as a high risk of arrhyth- (7 Ed) Philadelphia: Lippincott 1998.
th
mias due to SA and AV node involvement.
Clinical Features
Patients with AMI most often present with chest pain. delayed diagnosis and treatment and a higher mortality
7
This pain is described as central crushing retrosternal (50%) than with typical symptoms (18%). Differentiat-
pain, which lasts longer than 20 minutes and is not ing this pain from any previous pain is also useful. The
relieved by nitrate therapy. The pain may radiate to the brief history should include a short cardiovascular risk
neck, jaw, back and shoulders and is often accompanied profile: (a) previous cardiac history such as angina, MI,
by ‘feelings of impending doom’, sweating and pallor. revascularisation; and (b) family history, smoking, hyper-
Nausea is often associated with the pain, due to vagal tension, diabetes.
nerve stimulation. Depending on the size and location of
the AMI, patients may also present as sudden death and Practice tip
with varying degrees of syncope and heart failure. Women
may present with different symptoms. Because of changes in neuroreceptors, older patients and dia-
betic patients may not describe the typical anginal pain.
Patient Assessment and Diagnostic Features Women also may not describe classic angina symptoms and
4
A key feature of assessment of the patient with chest pain may use different descriptors from men. Be alert for prodromal
is the use of protocols and guidelines to promote rapid symptoms, such as increased shortness of breath, weakness
assessment so that revascularisation procedures such as and fainting.
thrombolysis and percutaneous coronary intervention
(PCI) can be implemented as soon as possible. This
means that assessment may begin as early as in the ambu-
lance, with ECG transmission to hospital ED where rapid, A more complete history, which includes detailed infor-
9
early triage models of care are in place. Additionally mation about risk factors, can be acquired when the
assessment also needs to determine whether there are any patient is stabilised. This information will be essential to
contraindications for thrombolysis. guide patient education, rehabilitation and to plan dis-
The assessment method used depends on the condition charge. Recurrent chest discomfort requires urgent reas-
of the patient but should occur within 10 minutes of sessment, including immediate ECG.
7
arrival. This initial history will focus on the nature of
symptoms such as pain. Pain assessment is complex, and Physical examination
the use of an acronym such as PQRST (see Table 10.1) is Physical appearance varies and depends on the impact of
useful to incorporate precipitating and palliative factors, pain, size and location of the infarction in the individual.
qualitative descriptors, location, radiation and length of Heart rate and blood pressure may be raised due to
time. A pain scale is included to help rate the intensity of anxiety. Impaired left ventricular function may result in
pain. Asking patients for descriptive words is useful in dyspnoea, tachycardia, hypotension, pallor, sweating,
assessment as many patients will deny pain and instead nausea and vomiting. Impaired right ventricular function
use words such as pressure, tightness or constriction. It is may be indicated by jugular vein distension and peri-
essential not to ignore other presentations, as patients pheral oedema. Abnormalities in heart sounds may be
with atypical symptoms, such as women, often have a present, including a muffled and diminished first heart
218 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
sound due to decreased contractility. A fourth heart sound electrodes, V7–V9, may be placed over the posterior of
is common, whereas a third heart sound is uncommon. the left chest to view the posterior wall. Other indicative
Many patients develop a pericardial rub after about 48–72 signs of posterior wall damage are a small r wave in V1
hours due to an inflammatory response to the damaged and/or ST depression in V3 and V4 as these may be recip-
myocardium. Additional findings occur with complica- rocal changes. The endocardial surface of the posterior
tions, and these are discussed in that specific section wall faces the praecordial leads of the ECG so the signs
below. of ischaemia and infarction are reversed or reciprocal
such as ST depraession or a small r wave. If these signs
Electrocardiographic examination are present a left-sided ECG, V7–V9, should be done to
Patients with chest discomfort should be assessed by an confirm or rule out a posterior infarction.
appropriately qualified person and have an ECG recorded Continuous ECG monitoring is essential to detect arrhyth-
within 5 minutes of arrival at a healthcare facility to mias, which often accompany AMI and are a common
determine the presence and extent of myocardial isch- cause of death. The arrhythmia may be due to poor perfu-
aemia, the risk of adverse events and to provide a baseline sion of the conduction tissue. More often, arrhythmias
7
for subsequent changes. Most importantly, the ECG is occur because ischaemic tissue has a lower fibrillatory
essential to determine whether emergency reperfusion is threshold and ischaemia is not being managed. Arrhyth-
required, and is recommended as the sole test for select- mias also result from left ventricular failure.
ing patients for PCI or thrombolysis. Where ST segment
monitoring is available, this should be continuous. Alter- Typical ECG evolution pattern
natively, if chest discomfort persists, ECGs should be
repeated every 15 minutes. Even when chest pain resolves The initial ECG features of myocardial infarction are ST
it is important to record a series of 12-lead ECGs during segment elevation with tall T-waves recorded in leads
admission to determine changes over time. (The normal overlying the area of damaged myocardium. These changes
ECG is covered in Chapter 9, whereas this section gradually change, or evolve, over time, with ST segments
addresses ischaemic changes in the ECG.) returning to baseline (within hours), while Q waves
develop (hours to days) and T waves become inverted
Myocardial ischaemia, injury or infarction cause cellular (days to weeks). The time course for the evolutionary
10
alterations and affect depolarisation and repolarisation. changes is accelerated by reperfusion, e.g. PCI, throm-
Myocardial ischaemia may be a transient finding on the bolysis or surgery. Thus an almost fully-evolved pattern
ECG. Ischaemia results in T wave inversion or ST segment may be seen within hours if successful reperfusion has
11
depression in the leads facing the ischaemic area. Isch- been undertaken (see Figures 10.2–10.4 for an example).
aemic T waves are usually symmetrical, narrower and Given the expected time course for evolution, it is possi-
more pointed. ST segment depression of 1 mm for 0.08 ble to approximate how recently infarction has occurred,
seconds is indicative of ischaemia, especially when which is essential in determining management:
12
forming a sharp angle with an upright T wave. These
changes are reversible with reduction in demand (e.g. by ● acute (or hyperacute): there is ST elevation but Q
rest, nitrates). waves or T inversion have not yet developed (see
Figure 10.5).
On acute presentation, myocardial injury (infarction) is
most commonly associated with ST segment elevation on ● recent: Q waves have developed. ST segment elevation
the ECG, although this is not universal. In addition, a may still be present. Evolution is underway. The infarc-
typical pattern of ECG changes over time (evolution of tion is more than 24 hours old.
the ST segments, Q wave development and T wave inver- ● old (fully evolved): Q waves and T inversion are
sion) are often seen (described below), but these changes present. ST segments are no longer elevated. Infarction
too are not universal. The distinction between the various occurred anything from a few days to years ago.
acute coronary syndromes, including ST elevation acute
coronary syndrome (STEACS), ST elevation myocardial Biochemical markers
infarction (STEMI) and non-ST elevation myocardial Intracellular cardiac enzymes enter the blood as ischaemic
infarction (non-STEMI), is important for ensuring appro- cells die, and elevated levels are used to confirm myocar-
13
priate assessment and protocol-based treatment for the dial infarction and estimate the extent of cell death. The
various presentations. cardiac troponins T and I (cTnT and cTnI) have been
The location and extent of ischaemia or infarction may found to be both sensitive and specific measures of cardiac
14
be evident on the ECG leads overlying the affected area, muscle damage. Troponin I is rapidly released into the
as follows: bloodstream, so it is especially useful for the diagnosis
and subsequent risk stratification of patients presenting
● anteroseptal wall of left ventricle, V1–V4; with chest pain in the early stages. Troponin I is also a
● anterior wall of the left ventricle, V1-V6, I and aVL; more appropriate marker to use in postoperative and
● lateral wall of left ventricle, I, aVL,V5 and V6; trauma patients than creatine kinase–MB (CK-MB), as
● inferior wall of left ventricle, II, III and aVF.
CK-MB levels will be affected by muscle damage. However,
Additional leads are needed to view the right ventricle CK-MB is less costly and more readily available, and so
and posterior wall. Chest electrodes can be placed on the is still often used, particularly in the presence of a non-
right chest wall using the same landmarks as the left chest diagnostic ECG. C-reactive protein assays may prove to
to view the right ventricle (see Chapter 9). Further be useful, as baseline and discharge levels are predictive
Cardiovascular Alterations and Management 219
FIGURE 10.2 Acute inferoposterior infarction: ST elevation in indicative leads II, III and aVF. The ST segment depression in I and aVL is reciprocal to the
inferior infarction. As well, ST depression in anterior leads (V1–V3) is reciprocal to posterior wall infarction. Posterior leads (not shown here) were recorded
and revealed ST elevation in V7, V8 and V9. This patient had acute (100%) obstruction at the ostium of the right coronary artery.
FIGURE 10.3 The same patient as above, recorded only 1 hour later, after stenting of the right coronary artery with an evolving inferoposterior infarction.
Note the ST segments in II, III and aVF are still elevated but returning to baseline. The reciprocal ST depression is likewise diminishing and can now be
seen only in aVL, V1 and V2. Q waves have already developed in inferior leads.
of subsequent cardiac events. However, the laboratory arteries and manoeuvred into the ostium of each coronary
facilities are not readily available. artery. Contrast media is then injected and images are
Coronary angiography and left taken from several views to provide detailed information
on the extent, site and severity of coronary artery lesions
heart catheterisation and the blood flow into each artery. This flow is graded
Coronary angiography gives a detailed record of coronary using the Thrombolysis in Myocardial Infarction (TIMI)
artery anatomy and pathophysiology. Specially designed studies system (see Table 10.2). Typically, a left ventricu-
15
catheters are advanced with the assistance of a guidewire lar angiogram is performed during the same procedure to
into the ascending aorta via the femoral or brachial assess the appearance and function of the left ventricle,
220 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
FIGURE 10.4 The same patient again, recorded a further 21 hours later. An almost fully evolved pattern is now present. Note the ST segments inferiorly
have almost completely returned to baseline (as have the reciprocal changes). The Q waves remain, and T waves have now inverted inferiorly.
FIGURE 10.5 Acute anterolateral infarction in a patient with left anterior descending coronary artery obstruction. Note the ST elevation and tall (hyper-
acute) T waves across the chest leads V1–V6. ECG recorded on admission.
mitral and aortic valves. If CHD is present, treatment is positive for CHD if there is 1 mm or more of reversible
16
determined as appropriate according to the severity (PCI, ST segment depression. False-positive tests are more
coronary artery bypass grafting or medical therapy). The common in populations with a lower incidence of CHD,
nursing care for coronary angiography is similar to PCI, including women. 17
and is covered under that section.
Chest radiography
Exercise test An initial chest X-ray film is useful to exclude other causes
Exercise testing with ECG monitoring forms part of the of chest pain, such as pneumonia, pneumothorax and
diagnostic screen for patients suspected of stable angina. aortic aneurysm, and to assess whether heart failure and/or
The Bruce protocol is used most often and considered pulmonary congestion are present. If the diagnosis is
Cardiovascular Alterations and Management 221
Thrombolytic therapy
TABLE 10.2 Thrombolysis in Myocardial Infarction Thrombolytic therapy has been demonstrated to show a
(TIMI) flow grades in coronary arteries 15 significant reduction in mortality in the high-risk group
20
described above. The greatest reduction in mortality
TIMI 0 No perfusion and no antegrade flow beyond the occurs if the reperfusion occurs within the first ‘golden’
occlusion.
20
hour of presentation. Thrombolysis can be delivered
TIMI 1 Penetration with minimal perfusion, and contrast does effectively in many settings where other methods of
not opacify the entire bed distal to the stenosis during reperfusion are not available.
the picture run.
Clots formed in response to injury normally dissolve
TIMI 2 Partial perfusion and contrast opacifies the entire
coronary bed distal to the stenosis, although entry to using the body’s fibrinolytic processes as tissue repair
this area is slower than with unaffected coronary beds. takes place. This requires the presence of the proenzyme
plasminogen, which is converted into the enzyme plasmin
TIMI 3 Complete perfusion and filling and clearance of contrast
is rapid and comparable to other coronary beds. when activated by macrophages and degrades the clot.
Thrombolytic agents, including streptokinase and tissue-
type plasminogen activator (tPA), have been developed
that trigger conversion of plasminogen to plasmin and
therefore break down clots. It is essential to screen patients
clearly ACS or AMI, this step can wait until after thromboly- for contraindications to thrombolysis quickly but thor-
sis or PCI. oughly so that therapy can be commenced as soon as
possible. Contraindications are given in the National
Collaborative Management of Angina and Health Foundation of Australia (NHFA) Guidelines.
Acute Coronary Syndrome
The management of stable angina patients is aimed at: Streptokinase and tenecteplase are the most commonly
prescribed thrombolytic agents. Streptokinase is pre-
(a) secondary prevention of cardiac events; (b) symptom pared from beta-haemolytic streptococci and is a potent
control with medication; (c) revascularisation; and (d) plasminogen activator. Streptokinase is not thrombus-
21
rehabilitation (see Figure 10.6). (Revascularisation by specific, so plasmin is released into the general circula-
coronary artery bypass graft is reviewed in Chapter 12; tion that may break down any recent clot formed as a
revascularisation by percutaneous coronary angioplasty is result of surgery, injection or healing, leading to a poten-
reviewed in the next section.) tial increase in haemorrhagic episodes. Streptokinase is
Treatment of acute coronary syndrome aims at rapid bacterial in origin, so it is antigenic. Most individuals
diagnosis and prompt re-establishment of flow through have been exposed to beta-haemolytic streptococci so
the occluded artery to ensure myocardial perfusion antibodies are often present, which means a higher dose
and reduce size of infarction. In addition, treatment may be required owing to the destruction of some of the
aims to: 18 enzyme when administered. Occasionally an escalated
allergic response will occur and will need urgent treat-
● minimise the area of myocardial ischaemia by increas- ment. This is more likely if streptokinase has been
ing coronary perfusion and decreasing myocardial administered in the previous 6 months. Streptokinase is
workload given intravenously over 60–90 minutes, because it has a
● maximise oxygen delivery to tissues short half-life.
● control pain and sympathetic stimulation
● counter detrimental effects of reperfusion The drug tissue-type plasminogen activator (tPA) is avail-
● preserve ventricular function able as alteplase, tenecteplase and reteplase. These agents
● reduce morbidity and mortality. are of human origin, made by recombinant DNA tech-
niques. The drug activates only plasminogen present in
22
The ideal place to manage ACS or MI patients is in the blood clots, so the risk of haemorrhage is decreased.
coronary care unit, where continuous, specialised nursing Unlike streptokinase, tPA can be given repeatedly without
19
care is available and there is rapid access to treatments. risk of anaphylactic reaction. However, tPA costs about 10
Secondary prevention of cardiac events includes the pro- times as much as streptokinase, so it is occasionally still
vision of medications, such as antiplatelet therapy and reserved for patients who have recently received streptoki-
lipid-lowering therapy. nase or are at risk of allergic reaction. Often patients with
anterior ischaemic changes are treated with tPA (alteplase)
Reperfusion therapy based on the GUSTO-1 trial that showed improved out-
23
Reperfusion therapy includes coronary angioplasty, comes in terms of reduction of ischaemia. Alteplase is
ideally with stent and thrombolytic therapy (also termed usually given by infusion, whereas reteplase, which has a
fibrinolysis). Patients fast-tracked for reperfusion therapy longer half-life, can be given in two bolus injections.
have one or more of the following indications: (a) isch- Nursing management of patients post-thrombolysis
aemic or infarction symptoms for longer than 20 minutes; focuses on monitoring and detection of bleeding compli-
(b) onset of symptoms within 12 hours; (c) ECG changes cations and/or return of ischaemia. Care is as follows:
(ST elevation of 1 mm in contiguous limb leads, ST eleva-
tion of 2 mm in contiguous chest leads; left bundle ● Observations. Assess neurological state including ori-
branch block). entation, any IV sites and urinalysis for the presence
222 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
FIGURE 10.6 Management of acute coronary syndromes (© 2011 National Heart Foundation of Australia), http://www.heartfoundation.org.au/acute-coronary-syndrome.)
Cardiovascular Alterations and Management 223
of bleeding. Along with vital signs, these are attended patients presenting with chest pain who meet the indica-
every 15 minutes for the first hour, half-hourly for an tions for reperfusion when: (a) facilities are available and
hour, and then hourly according to the patient’s con- can be achieved within 60 minutes; (b) there are contra-
dition, however, patients are advised to report any indications to fibrinolytic therapy described above; (c)
bleeding postdischarge as well. ischaemia would result in large anterior AMI within 4
● ECG monitoring. This includes 12-lead ECG on return hours; or (d) haemodynamic instability or cardiogenic
and ongoing ECG monitoring and chest pain assess- shock are present.
ment to detect reocclusion. Patients need to be
requested to inform nursing staff of any chest pain or A stent is usually inserted to prevent abrupt closure and
26
discomfort. maintain patency for longer. The structure of the stent
● IV anticoagulants such as heparin and/or oral anti- within the vessel enlarges the lumen and prevents vessel
platelet drugs, such as clopidogrel or ticlopidine, may stricture. Restenosis due to intimal hyperplasia is a
be given following thrombolysis to prevent reocclu- relatively common complication, occurring 10–12 weeks
sion in the stent. Assess International Normalised postimplantation. In response to this problem, drug-
Ratio (INR), prothrombin (PT) and partial thrombo- eluting stents have been developed. The drug coatings
plastin time (PTT), as bleeding is more likely to occur include sirolimus, a macrolide antibiotic that has been
if anticoagulants are above the therapeutic range. demonstrated to effectively decrease hyperplasia and
27
prevent reduction of flow. Paclitaxel has also shown
Coronary angioplasty promise in a series of studies. In addition to dactino-
28
Coronary angioplasty (PTCA) procedures are being used mycin, these drugs are undergoing approval processes.
about twice as frequently as coronary artery bypass graft Nursing management of patients post-PTCA includes care
surgery, with 155 PTCA procedures performed for every of the puncture site to prevent bleeding and detect arterial
2
100,000 population in Australia in 2008–09. PTCA rates changes (including clot and aneurysm). The process
29
have grown dramatically in patients aged over 75 years. used to create and maintain access for insertion of the
In this procedure, a catheter is introduced by the brachial catheters can damage the blood vessel(s) and alter perfu-
or femoral artery into the coronary arteries and advanced sion to the limb. The sheath used to aid insertion and
into the area of occlusion or stenosis under the guidance maintain access is usually maintained for 1–2 hours post-
of imagery and specifically designed catheters. A balloon procedure for emergency access. Care is as follows:
attached to the end of the catheter is then inflated to
widen the lumen of the artery by stretching the vessel ● Observations. Observe access site for haemorrhage
wall, rupturing the atheromatous plaque and cracking the and haematoma, assess perfusion to the lower limb,
intima and media of the artery (see Figure 10.7). including colour, warmth and pulses. This monitoring
needs to be done often in the first few hours, when
PTCA tends to be reserved for patients with single- or
double-vessel disease as assessed on coronary artery complications are most likely to occur.
angiograms. Angioplasty provides better symptom relief ● ECG monitoring. This includes 12-lead ECG on return
than medication alone, but there is no evidence of sur- and ongoing ECG monitoring and chest pain assess-
vival benefits. Primary angioplasty results in a higher ment to detect reocclusion. Patients need to be
24
rate of patency of the affected artery in AMI (>90%), lower requested to inform nursing staff of any chest pain or
rates of CVA and reinfarction and higher short-term sur- discomfort.
vival than thrombolysis. PTCA is recommended in all ● Vital signs. These are recorded every 15 minutes for
25
the first hour, half-hourly for one hour, and then
hourly according to the patient’s condition.
● Removal of sheath. This is usually performed by
medical or specially trained nursing staff.
● Achievement of haemostasis. Use either application of
pressure for at least 5 minutes or vascular sealing. 29
● Pressure application can be by a manual compres-
sion device (such as Femostop, RADI Medical
Systems, Uppsala, Sweden) and less often digital,
to maintain a pressure of about 20 mmHg.
● Vascular sealing uses a device such as the Angioseal
1 2 3 4 5
Vascular Closure Device (St Jude Medical Inc, St
Paul, MN). This includes a collagen plug and a
small biodegradable plate inside the artery, which
is held in place by a small suture, tamping tube
and small spring on the exterior. The tension spring
is removed and the suture trimmed half an hour
after application. This enables the patient to mobil-
ise and reduces nursing time. 30
● Assess International Normalised Ratio (INR), pro-
thrombin (PT) and partial thromboplastin time (PTT),
FIGURE 10.7 PTCA procedure. as bleeding is more likely to occur if anticoagulants
106
224 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
are above the therapeutic range. Weight-adjusted treatment of complications, comfort and pain control, psy-
heparin (100 units/kg) is usually used during PTCA to chosocial support and teaching and discharge planning.
prevent thrombus formation, and glycoprotein IIb/ Reduction of myocardial workload includes ensuring the
IIIa inhibitors such as abciximab may be used to patient has bedrest, providing support with activities and
prevent platelet aggregation and thrombus formation limiting stress. A calm, caring manner during nursing care
for patients at high risk of occlusion. is essential to lower patient and family stress levels. Indi-
● Bedrest (2–6 hours) is used to discourage the patient vidual evaluation of the patient and the family is neces-
from moving the joint of the insertion site to prevent sary to determine the most appropriate management of
clot displacement and haematoma formation. Ini- visiting. ECG monitoring (preferably including ST moni-
tially the patient should lie relatively flat if femoral toring) and evaluation of heart rate, shortness of breath,
artery access has been used, then progress to sitting. chest discomfort and blood pressure are essential to deter-
The period of rest has been demonstrated to be safely mine ischaemia, treatment effects, myocardial workload
reduced to 1 hour in low-risk patients (normotensive and complications. This monitoring should occur hourly
and normal platelet count). 29 during the acute phase, reducing as the patient recovers.
● Pain relief is used primarily to promote comfort for Provision of oxygen by mask or nasal cannulae in the
patients who find bedrest to cause pain and discomfort. first 6 hours is standard practice to raise SaO 2 levels in
● Urine output. Adequate urine output is essential as the myocardium, although there is no evidence of patient
radiographic IV contrast is cleared by the kidneys, so benefit if heart failure is not present. Oxygen saturation
it is vital that nurses ensure good hydration and levels should be routinely assessed concomitantly.
monitor initial urine output.
● Oral antiplatelet drugs, such as clopidogrel or ticlopi- Symptom relief should be provided, including analgesia
dine, may be given prior to the procedure to prevent for pain. Analgesia management should be conducted by
later reocclusion in the stent. Usually patients will be nurses because of their continued contact and thus more
18
discharged on this medication to continue for up to accurate assessment and treatment of pain. It is essential
3 months while endothelium lines the stent/injured to treat pain, not only for the distress it causes patients
area. Unless contraindicated, all patients will take but also because pain causes stimulation of the sympathetic
aspirin for the rest of their lives. 30,31 nervous system (SNS). SNS responses include elevated
heart rate and potential for arrhythmias, peripheral vaso-
constriction and increased myocardial contractility and,
Practice tip therefore, an overall increase in myocardial oxygen
demand. Effective treatments for pain include IV morphine
Increased hydration can aggravate problems with urination and nitrates. The IV route is preferable, as absorption is
when on bedrest, particularly in older men with prostate predictable and additional punctures in thrombolysed
enlargement. If a femoral access site is used in these patients, patients are not required. Morphine has the additional
it is easier for the patient to urinate while turned on the side, benefit of reducing anxiety in a distressing situation and
using pillow support to maintain the position. should be initially provided at a dose of 2.5–5 mg at 1 mg/
min, followed by 2.5 mg doses as indicated. While there
is little randomised controlled trial evidence to support
Practice tip this particular practice, it is generally accepted to be appro-
priate. A standardised method of pain evaluation and
If a femoral access site has been used, bleeding may track charting should be used to ensure consistent assessment
between the patient’s legs and pool, and this will be invisible and treatment. An antiemetic such as metoclopramide
to a cursory inspection, particularly if the patient is obese. should be given concurrently to lessen and prevent nausea.
Always move the patient’s thigh during regular inspections. Other drugs, such as beta-blockers and nitrates, decrease
myocardial workload, contributing to pain reduction.
Many patients find the PTCA procedure and confirmation Nursing care for thrombolysis
32
of CHD diagnosis stressful. It is an important nursing Patients receiving thrombolytics require constant obser-
role to provide patients with preparatory information vation, regular non-invasive blood pressure measurement
about the procedure and care required during recovery. for hypotension, and monitoring for allergic reactions
As family members provide valuable support and remind- to streptokinase. Continuous ECG monitoring for
ers about recovery, these people should be included in arrhythmias and ST segment changes is essential. Some
any information sessions. The patient and family need to arrhythmias, particularly idioventricular arrhythmias, are
be provided with information about the possibility of associated with reperfusion and tend to be benign. ST
restenosis, mobility restrictions at home and the lifestyle segment monitoring and assessment of pain help evalu-
changes needed to reduce the risk of worsening CHD. ate the effectiveness of the thrombolysis. Thrombolysis is
considered to have failed if the patient is still in pain and
Nursing management of ACS and MI the ST segment has not resolved within 60–90 minutes.
18
The nursing role in patients with ACS and MI includes reduc- If thrombolysis fails, patients are at high risk for other
ing myocardial workload and maximising cardiac output, interventions, so repeat thrombolysis is often the only
provision of treatments, careful monitoring to determine treatment option. Salvage or rescue angioplasty may be
the effects of treatment and detect complications, rapid undertaken if available at the site.
Cardiovascular Alterations and Management 225
TABLE 10.3 Medications used in the treatment of ACS
Agent Action Side effects/caution Comments
Antiplatelet agents
aspirin Prevents platelet synthesis of thromboxane Gastrointestinal irritation & Noted to reduce the risk of AMI
A2, a vasoconstrictor and stimulant of platelet bleeding; use enteric-coated by 50%, although often
30
aggregation. tablets to minimise. underutilised. Lifelong use is
33
May provide benefits from anti-inflammatory recommended in angina patients.
properties in reducing plaque rupture. 31
clopidogrel Adenosine diphosphate (ADP) receptor agonist; Inhibits P450 liver enzyme; care Clopidogrel produces fewer GI effects
prevents the binding of ADP to its platelet is required when delivering than aspirin and is more effective in
receptor, thus inhibiting platelet aggregation. with other drugs and other patients with recent stroke, MI and
anticoagulants. 22 peripheral vascular disease. 34
ticlopidine As for clopidogrel. Severe side effects including
neutropenia.
tirofiban, Glycoprotein IIb/IIIa receptor antagonists prevent the Bleeding, thrombocytopenia, Early decreases in mortality in ACS
eptifibatide, final step of platelet aggregation; used most nausea, fever and headache ; and MI, particularly when given in
22
lamifiban, commonly to inhibit thrombus formation in acute doses need to be reduced in combination with aspirin and
abciximab 36 coronary syndrome angina. 35 renal failure. heparin, have been seen.
Beta-blockers
Reduce cardiac workload (↓heart rate and force of Contraindications include Recommended for patients during the
contraction) by blocking beta-adrenergic receptors, significant AV block, acute MI phase, reducing risk of
preventing sympathetic stimulation of the heart. bradycardia, hypotension, further MI. 37
history of asthma or
uncontrolled heart failure.
Nitrates
glyceryl Potent peripheral vasodilators, particularly in venous Reflex tachycardia, hypotension, Tolerance to the vasodilator effect
trinitrate (IV, capacitance vessels, thereby reducing preload and syncope and migraine-like occurs, so intermittent treatment is
sublingual to a lesser extent afterload, to reduce myocardial headache; generally occur in most effective. In the case of
and spray), workload. first few days of treatment, transdermal delivery, if treatment is
isosorbide Dilate normal and atherosclerotic coronary blood then subside. Blood pressure withheld for 8–12 hours in every 24
mononitrate vessels to increase myocardial oxygen supply. should be monitored. hours, therapeutic activity is
Used to manage unstable angina and reduce blood restored. 22
pressure in the critical care setting, where there is
some evidence for symptomatic relief. 38
Lipid-lowering statins
atorvastatin, Inhibit 3-hydroxy-3-methylglutaryl-coenzyme-A Headache, gastrointestinal To lower and maintain cholesterol at
simvastatin, (HMG-CoA) reductase, the enzyme that limits the upset, inflammation of 5 mmol/L, evidence that statin
fluvastatin, rate of cholesterol synthesis in the liver, thereby voluntary muscles and altered medications can reduce mortality
39
pravastatin reducing plasma cholesterol. 22 liver function; taking statins for up to 5 years after AMI.
with food may reduce GI Education needs to include
symptoms. monitoring for muscle soreness and
regular GP visits for liver function
tests.
Medications are usually commenced unless contraindicated. Calcium
Provision of medications and assessment of the effective- channel blockers may be used in patients who do not have
ness of treatment is a major component of the nurse’s cardiac failure or heart block. (These medications are
role in caring for the cardiac patient. Many of the medica- described in the next section.) The choice of medication
tions are accompanied by side effects and interactions may depend on how acceptable the patient finds the reduc-
with other drugs, which the nurse must monitor. An array tion in symptoms and the presence of side effects. Patients
of medications is used to treat AMI patients, including need to take antianginal agents continuously, regardless of
aspirin, lipid-lowering agents, beta-blockers and organic symptoms. Patients should also be encouraged to take sub-
nitrates (see Table 10.3). lingual GTN prophylactically.
Angina may also be managed by avoiding situations that
Symptom control trigger angina. Education needs to be directed at aware-
Control of anginal symptoms with medication usually ness of symptoms and management of unstable angina
includes sublingual glyceryl trinitrate (GTN) for immediate and AMI symptoms, and the need for emergency care.
symptom control and one or more antianginal medica- Although these patients are at low risk of further cardio-
18
tions for sustained symptom management. Beta-blockers vascular events in the short term, in the medium to long
226 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
term, risk may accumulate. Patients with angina are ● communicating with patients and families, while
encouraged to attend cardiac rehabilitation programs to reducing conversation demands as excessive conversa-
learn how to deal with symptom management. 41 tion by patients may unnecessarily raise heart rate 45
● restricting the number and type of visitors in the acute
Angiotensin-converting enzyme (ACE) inhibitors have
been recommended for all post-AMI patients while in hos- phase is customary, but many patients feel safer if a
pital, with review of prescription at 4–6 weeks postdis- family member is present
charge. Patients with left ventricular failure should be ● provision of comprehensive information to families,
maintained on ACE inhibitors. Similarly, diuretics provide with more concise information in understandable
the mainstay of the management of left ventricular failure language for patients.
if it is present (see Chapter 19). Diabetic patients have a Nurses need to monitor patients for signs of excessive
higher mortality after AMI in both acute and long-term anxiety, including facial expressions and behavioural
phases. Provision of an insulin-glucose infusion for BSL changes. However, overt behaviours may be controlled by
>11 mmol/L during the acute phase, followed by subcutane- the patient, so careful conversation and/or use of specific
ous injections for at least 3 months, has been demonstrated assessments may be necessary to detect anxiety. The move
to significantly reduce mortality up to 3 years post-AMI. 42 to the step-down or general ward may also be stressful to
Transfer to a step-down unit or general ward usually occurs the patient and family. This move needs to be planned
when the patient is pain-free and is haemodynamically and discussed, and promoted as a sign of recovery.
stable. Stability means that patients are not dependent on
IV inotropic or vasoactive support and have no arrhyth- Cardiac rehabilitation
mias. Discharge home after AMI varies, but usually occurs Coronary heart disease is a chronic disease process, which
at day 3 for low-risk patients. 18 often presents with acute events such as ACS or AMI. Like
all chronic illnesses, it has implications for patients in
Independent Practice terms of lifestyle change, uncertainty of long-term out-
Emotional responses and patient comes, functional changes and social and economic
and family support alterations. Cardiac rehabilitation aims to address these
issues. The World Health Organization describes cardiac
ACS or AMI is usually accompanied by feelings of acute rehabilitation as ‘the sum of activities required to influ-
anxiety and fear, as most patients are aware of the signifi- ence favourably the underlying cause of the disease, as
cant threat posed to their health. For many patients it well as to ensure the patients the best possible physical,
18
may also be the first experience of acute illness and asso- mental and social conditions so that they may, by their
ciated aspects such as ambulance transport, emergency own efforts, preserve, or resume when lost, as normal a
care and hospitalisation, so they may experience shock place as possible in the life of the community’. Systematic,
46
and disbelief as well. Fast-track processes require patients individualised rehabilitation and secondary prevention
and their families to process a large amount of informa- need to be offered to all AMI patients. Participation in
tion and make decisions quickly, and this, added to an well-structured, multidisciplinary programs has been
alien environment, full of unfamiliar technology and per- demonstrated to reduce mortality by up to 30%. Addi-
47
sonnel, can be quite distressing. However, the environ- tional benefits have been shown for improvements in
ment can also promote a feeling of security for patients exercise tolerance, symptoms, serum lipids, psychological
and their families. Patients’ perceptions of the CCU envi- wellbeing and cessation of smoking. 48-50
ronment have been linked to recovery. 43
Cardiac rehabilitation is structured around four phases,
Anxiety is a common response to the stress of an acute beginning with phase I, during admission. The compo-
50
cardiac event and leads to important physiological and nents of phase I include:
44
psychological changes. The sympathetic nervous system
is stimulated, resulting in increased heart rate, respiration ● information regarding the disease process, the prog-
and blood pressure. These responses increase the workload nosis, and an optimal approach to recovery, early
of the heart and therefore myocardial oxygen demand. mobilisation and discharge planning
In an acute cardiac event, these demands occur when ● assessment of patients’ understanding of their diagnosis
perfusion is already poor and may lead to worse out- and treatment as a foundation for self-management
comes, including ventricular arrhythmias and increased ● discharge planning which incorporates discussions on
myocardial ischaemia. Therefore, staff working in emer- adaptation to the functional and lifestyle changes
gency and coronary care should employ strategies to needed for secondary prevention – dietary intake of
reduce a patient’s anxiety. lipids, exercise, smoking cessation, stress management
and symptom monitoring, and management of acute
Increasing a patient’s sense of control, calm and confi- symptoms
dence in care reduces the patient’s sense of vulnerability, ● early mobilisation as an inpatient to encourage a
44
whether it is realistic or not. This can be achieved by: positive approach to recovery with monitoring of
● providing order and predictability in routines, allow- the response to activity in heart rate, shortness of
ing the patient to make choices, providing informa- breath and chest pain to determine the rate of prog-
tion and explanations, and including the patient in ress. (Most hospital units use an activity progress
decision making chart for this purpose based on metabolic equiva-
● using a calm, confident approach lents [METs]).
Cardiovascular Alterations and Management 227
The phases that follow, from II to IV, are managed in the and/or corticosteroids. Approximately 1–5% of AMI
outpatient setting and begin with assessment, liaison patients develop pericarditis as a late complication, 2
18
with multidisciplinary professionals and health educa- weeks to a few months post-AMI. Usually this late-onset
tion. Phase II occurs in the immediate postdischarge pericarditis is associated with Dressler’s syndrome and
period and includes liaison with community-based carers may be an autoimmune response to myocardial injury.
and services and further assessment. In phase III, tailored, This is a chronic condition requiring systemic corticoste-
supervised exercise programs are usually conducted and roid treatment.
there is a range of psychosocial interventions, such as
support sessions and stress management. Finally, in phase Structural defects
IV the focus is on chronic disease management and main- Myocardial tissue death may be catastrophic if it is exten-
taining risk modification behaviours. All phases require sive or results in rupture of ventricular or papillary muscle.
incorporation of the principles of adult learning to maxi- These conditions are rare and symptoms develop rapidly.
mise learning and behaviour change. These principles Intraventricular septal rupture is usually associated with
50
include recognition of ‘readiness to learn’. Adults are anterior MI. The patient develops progressive dyspnoea,
ready to learn most effectively when they are physically tachycardia and pulmonary congestion, as well as a loud
and emotionally stable and are aware of the problem or systolic murmur associated with a thrill felt in the para-
need to learn. Nurses, because of their expertise and con- sternal area. If a pulmonary artery catheter is present,
tinual presence, are best placed to assess and provide blood samples from the right atrium and right ventricle
education at optimal times. will reveal a higher than usual oxygen content. Diagnosis
Complications of Myocardial Infarction must be confirmed by cardiac catheterisation, and urgent
Cardiogenic shock surgery is required.
Papillary muscle rupture most often occurs 2–7 days after
Cardiogenic shock occurs as a complication of MI in
about 5–10% of patients and is the most common cause MI. Patients experience a sudden onset of pulmonary
50
of death in hospitals. It arises from loss of contractile oedema secondary to pulmonary hypertension and car-
force, and generally occurs when ventricular damage is diogenic shock. Additional heart sounds and a systolic
more than 40% and ejection fraction less than 35%. Car- murmur will be heard. Urgent surgery is required, as the
54
diogenic shock and the related management are described mortality rate for papillary muscle rupture is 95%.
in more detail in Chapter 12. Cardiac rupture most often occurs within 5 days of MI
and is commonest in older women. The patient experi-
Arrhythmias ences continuous chest pain, dyspnoea and hypotension
Arrhythmias often occur in ACS and AMI and are often as tamponade develops. Symptoms may worsen rapidly
the cause of death in the prehospital phase. Management and result in pulseless electrical activity (PEA) unless
of the prehospital phase centres on community educa- surgery is undertaken immediately.
tion and an effective, rapidly responsive ambulance
51
service, as exemplified in Seattle in the USA. Arrhyth- HEART FAILURE
mias may be generated by poorly perfused tissue and In normal circumstances, the heart is a very effective,
electrolyte alterations, and increased sympathetic tone efficient pump with reserve mechanisms available to
during infarction, but are more often due to a failing left allow output to meet changing demands. These mecha-
ventricle. They may also complicate reperfusion after suc- nisms include (a) increasing heart rate to increase total
52
cessful revascularisation. It is essential to rapidly and cardiac output, (b) dilation to create muscle stretch and
effectively treat arrhythmias in the ACS and AMI context. more effective contraction, (c) hypertrophy of myocytes
The goal of treatment is to maintain cardiac output while over time to generate more force, and (d) increasing
reducing workload. Arrhythmias and management are stroke volume by increasing venous return and increased
described in Chapter 11.
contractility. Heart failure is a complex clinical condition
Pericarditis that is characterised by an underlying structural abnor-
Pericarditis is an inflammation of the visceral and parietal mality or dysfunction that results in the inability of the
ventricle to fill with or eject blood. The condition is also
55
layers of the pericardium that cover the heart. This inflam- known as congestive cardiac failure, a term commonly
mation occurs in approximately 20% of AMI patients used in the USA but not in Australia. Chronic heart failure
10
within the following 2–3 days. The patient experiences (CHF) describes the long-term inability of the heart to
chest pain, which may be confused with ischaemic pain. meet metabolic demands.
This confusion with an ischaemic event may be com-
pounded by the additional presence of ST segment eleva- The burden of disease associated with heart failure is on
tion on the ECG. However, pericardial pain increases with the rise due to our ageing population, the prevalence of
deep inspiration and a pericardial rub is often present. coronary heart disease and hypertension, the decrease in
Electrocardiographically, the elevated ST segments of fatality from acute coronary syndrome and improved
55
pericarditis are typically concave upwards (saddle-shaped) methods of diagnosis. Survival rates and prognosis for
and often widespread, contrasting with convex ST segment heart failure patients are extremely poor. Approximately
elevation limited to the distribution of a single coronary 50% of patients diagnosed with heart failure will die
53
artery in infarction. Pericarditis normally responds to within five years of diagnosis. 56-58 When compared with
anti-inflammatory treatment by aspirin, indomethacin those patients with cancer, heart failure patients have the