228 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
poorest five-year survival rate, with the exception of lung ● Diastolic heart failure (or heart failure with preserved
59
cancer. In Australia during 2001–2002, 41,874 patients systolic function [HFSF]): indicates normal systolic
were hospitalised with a primary diagnosis of CHF (0.7% function with a normal ejection fraction but impaired
60
of all hospitalisations). Internationally, heart failure is relaxation so there is a resistance to filling with increased
the most common cause of hospitalisation in patients filling pressures. Diastolic dysfunction usually occurs
55
aged over 70 years. Approximately 40% of patients in conjunction with systolic dysfunction and is more
admitted to hospital with heart failure will be readmitted common in the elderly.
or die within one year. 61 ● Low cardiac output syndrome: this occurs in response
to hypovolaemia and/or hypertension. Severe vasocon-
Over 50% of patients newly diagnosed with heart failure
have concurrent ischaemic heart disease, hypertension is striction further reduces the cardiac output.
present in 65% and idiopathic dilated cardiomyopathy ● High cardiac output syndrome is the result of an
55
(5–10% of cases). The causes of heart failure can be cate- increase in metabolic demands causing a decrease in
gorised according to (a) myocardial disease, (b) arrhyth- SVR leading to an increase in stroke volume and
mias, (c) valve disease, (d) pericardial disease and (e) cardiac output. Burns and sepsis are the main causes.
congenital heart disease. Myocardial disease may be ● Left sided heart failure: occurs when there is a reduced
62
caused by myocardial infarction and fibrosis from pro- left ventricular stroke volume resulting in accumula-
longed ischaemic heart disease which accounts for tion of blood in the pulmonary system.
approximately two-thirds of systolic heart failure causing ● Right sided heart failure: is the congestion of blood in
systolic dysfunction and a reduced ejection fraction. the systemic system due to the inability of the right
ventricle to expel its blood volume.
Arrhythmias, including both brady- and tachyarrhyth-
mias, may cause heart failure due to changes in filling RESPONSES TO HEART FAILURE
time affecting preload and resultant cardiac output. Myo- When heart failure occurs, several adaptive responses are
cardial oxygen demand is increased and if the heart is initiated by the body in an attempt to maintain normal
poorly perfused, muscle contraction will be affected. perfusion (see Figure 10.8). These mechanisms are suc-
Frequent premature contractions and atrial fibrillation cessful in the normal heart, but contribute to decreased
disturb mechanical coordination so that the ventricles effectiveness in the failing heart. The compensatory mech-
may not be adequately filled for efficient contraction. anisms include:
Heart failure patients are also at high risk of sudden
cardiac death due to ventricular fibrillation or tachycar- ● sympathetic nervous system response
dia. Valvular disease causing heart failure usually involves ● renin-angiotensin-aldosterone system (RAAS)
valves on the left side of the heart (mitral and/or aortic ● Frank-Starling response
valves). Aortic stenosis results in an increase in afterload ● neurohormonal response.
and ventricular hypertrophy develops with reduced dia- The sympathetic nervous system is the first response to
stolic compliance resulting in a reduced ejection fraction. be stimulated in heart failure. It occurs within seconds
Mitral stenosis is usually due to rheumatic heart disease. of a reduction in cardiac output and the parasympathetic
Valvular incompetence results in a dilated ventricle to system becomes inhibited. The baroreceptor reflexes
accommodate the regurgitant volume. Stroke volume are activated in response to a reduced arterial pressure.
increases in an attempt to empty its contents and ven- The beta-adrenergic receptors located in the heart are
tricular muscle mass increases. However, over time the activated resulting in an increase in heart rate and cont-
ventricle is unable to maintain the increased workload ractility to increase stroke volume and cardiac output.
and heart failure develops. Valvular heart disease and Sympathetic nervous system response in the peripheral
treatment is described in more detail in Chapter 12.
vascular system results in vasoconstriction which increase
There are several terms used to describe the pathology systemic venous return (SVR) and mean systemic filling
and signs and symptoms of heart failure. These include: pressures. This results in an increase in venous return,
preload and afterload (see Figure 10.8). The consequence
● Backward failure: refers to the systemic and pulmo- of this activation is increased myocardial oxygen demand.
nary congestion that occurs as a result of failure of Although blood flow to essential organs is maintained,
the ventricle to expel its volume. perfusion to the kidneys, gastrointestinal system and
● Forward failure: is due to an inadequate cardiac output skin is reduced and peripheral resistance increased.
and leads to decrease in vital organ perfusion. Chronic activation of vasoconstrictors contributes to the
● Acute heart failure: includes the initial hospitalisation progression of cardiac failure through increased resis-
for the diagnosis of heart failure and exacerbations tance and effects on cardiac structure, causing hypertro-
of chronic heart failure. phy and fibrosis and downregulation of beta-adrenergic
● Chronic heart failure: develops over time as a result of receptors and endothelial dysfunction. Chronic poor
the inability of compensatory mechanisms to maintain perfusion to skeletal muscles may contribute to changes
an adequate cardiac output to meet metabolic demands. in muscle metabolism, resulting in further reductions in
● Systolic heart failure: refers to the inability of the exercise tolerance.
ventricle to contract adequately during systole resulting
in a reduced ejection fraction and an increased The next compensatory mechanism to be activated is the
end-diastolic volume. This is the most common form RAAS. This is stimulated within minutes, in response to
of heart failure. a decrease in kidney perfusion resulting in a decrease in
Cardiovascular Alterations and Management 229
Activation of sympathetic
nervous system
Coronary artery disease
Hypertension Heart failure Decreased cardiac output Body fatigue
Valvular disease Weakness
Activation of renin–
angiotensin system
Increased retention of sodium and water Oedema
Weight gain
Increased venous pressure
Symptoms of right-sided failure Symptoms of left-sided failure
SYSTEMIC CONGESTION Increased venous congestion PULMONARY CONGESTION
Anorexia and nausea Dyspnoea
Pain in upper right quadrant Orthopnoea
Oliguria during day Paroxysmal nocturnal dyspnoea
Polyuria at night Cough and wheezing
PHYSICAL SIGNS
Cardiomegaly (hypertrophy)
Gallop rhythm
Hepatomegaly
Peripheral oedema
Ascites
104
FIGURE 10.8 Flowchart of the pathophysiology of heart failure.
glomerular filtration rate. Activation of this response
results in an increase in SVR and sodium and water reab-
sorption which then increases the circulating blood
volume, systemic filling pressures and venous return B
enhancing preload and afterload (see Chapter 9).
The Frank-Starling response is also activated. As the end-
diastolic volume increases (preload) in response to sym- A
pathetic nervous system stimulation ventricular dilatation
Compensated Heart Failure
occurs stimulating the Frank-Starling response. As the Cardiac Output Litres/Minute 5 C
myocardial fibres are stretched during diastole the force of
contractility also increases to expel the increasing preload. Normal
This is a major mechanism of the heart to maintain a Hyperfunction D
normal cardiac output. Optimal contractility occurs when Decompensated Heart Failure
63
the diastolic volume is 12–18 mmHg. However, when
the ventricle is damaged, such as in MI, the sympathetic
nervous system increases heart rate and contractility
further increasing cardiac workload and exacerbating
myocardial dysfunction which increases end-diastolic 12 mmHg 20 mmHg
volume (preload) and ventricular dilatation further and Left Ventricular End-Diastolic Filling Pressure
heart failure progresses. As ventricular dilatation contin- (Wedge Pressure)
ues, ventricular hypertrophy results. The myocardium also FIGURE 10.9 Function curves of left ventricular pressure during various
increases its muscle mass in an attempt to increase contrac- stages of heart failure.
109
tility called ventricular remodelling. However, overtime
ventricular hypertrophy results in changes to end-diastolic has a depressant effect of ventricular compliance, heart
compliance and contractility due to the thickened ven- rate and contractility resulting in an increase in end-
tricular wall, impaired muscle function and growth of diastolic pressure with no associated increase in contractil-
collagen. These result in further impairment of ventricular ity. As the pulmonary artery pressures increase, pulmonary
function (see Figure 10.9). Ventricular hypertrophy also oedema and cardiogenic shock develop.
230 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
The final compensatory mechanism to be activated is the exists when the ventricle has an ejection fraction of less
neurohormonal response which takes days to be activated. than 40%, resulting in increased end-diastolic volume
64
This response involves the activation of vasopressin and and increased intraventricular pressure. The left atrium is
atrial natriuretic peptide (ANP). Vasopressin is a potent unable to empty into the left ventricle adequately and
vasoconstrictor and also an antidiuretic hormone. ANP is pressure in the left atrium rises. This pressure is reflected in
important in the regulation of cardiovascular volume the pulmonary veins and causes pulmonary congestion.
homeostasis. It is released from the atria in response to When pulmonary venous congestion exceeds 20 mmHg,
atrial stretching due to an increased circulating blood fluid moves into the pulmonary interstitium. Raised pul-
volume. ANP blocks the effect of the sympathetic nervous monary interstitial pressure reduces pulmonary compli-
system, RAAS and vasopressin. It reduces tachycardia via ance, increases the work of breathing and is experienced
the baroreceptors and reduces circulating blood volume by the patient as shortness of breath. Increased blood
by increasing salt and water excretion in the kidneys. volume in the lung also initiates shallow, rapid breathing
Plasma ANP is increased in acute heart failure but depleted and the sensation of breathlessness. Patients also experi-
in chronic heart failure. ence orthopnoea (dyspnoea while lying flat) and paroxys-
Whilst in the healthy heart, these compensatory mecha- mal nocturnal dyspnoea (PND), because when lying,
nisms would result in an adequate cardiac output, in blood is redistributed from gravity-dependent areas of the
heart failure they do not, depending on the aetiology. In body to the lung. Sitting upright or standing, and sleeping
64
ischaemic heart failure the damaged myocardium is with additional pillows, relieves breathlessness at night.
unable to respond adequately to the Frank-Starling Acute pulmonary oedema results when pulmonary capil-
response and ventricular remodelling develops. Heart lary pressure exceeds approximately 30 mmHg, and then
failure caused by hypertension or valvular heart disease fluid from the vessels begins to leak into the alveoli (see
results in persistent pressure or volume overload which Figure 10.10). This fluid leak decreases the area available
63
is exacerbated by the Frank-Starling response and sympa- for normal gas exchange and severe shortness of breath
thetic nervous system compensatory mechanisms. This results, often accompanied by pink, frothy sputum and
causes ventricular remodelling and depletion of norepi- noisy respirations. This causes patients to experience severe
nephrine and a reduction of inotropic response to the anxiety and decreased oxygen levels. Pulmonary oedema
cardiac sympathetic nervous system. These all exacerbate is a medical emergency and requires urgent treatment.
the reduction in circulating blood volume and kidney In addition to pulmonary symptoms, patients with left
perfusion. Many patients with heart failure often have a ventricular failure experience signs and symptoms related
high plasma renin activity due to the continual activation to decreased left ventricular output, including weakness,
of the RAAS compensatory mechanism.
fatigue, difficulty in concentrating and decreased exercise
In heart failure patients the inadequate cardiac output tolerance. These symptoms may be present for some time
results in signs and symptoms of hypoperfusion (oliguria, before an accurate diagnosis of heart failure is made,
cognitive impairment and cold peripheries) and conges- because they are non-specific and are consistent with
tion of the venous and pulmonary systems (acute pulmo- other diagnoses such as depression. Other signs that are
nary oedema, dyspnoea, hypoxaemia, peripheral oedema useful in diagnosis include the presence of S3 (ventricular
and liver congestion). Classification of signs and symp- gallop), crackles over lung fields that do not clear with a
toms is usually considered in the context of left or right cough, cardiomegaly and the presence of pulmonary
ventricular failure. vessels on chest X-ray.
LEFT VENTRICULAR FAILURE RIGHT VENTRICULAR FAILURE
Left ventricular failure (LVF), compared with other forms Right ventricular failure (RVF) does not usually occur in
of heart failure, is characterised by breathlessness, orthop- isolation, except in the presence of severe lung disease,
noea and paroxysmal nocturnal dyspnoea, irritating such as chronic obstructive pulmonary disease, pulmo-
60
cough and fatigue (see Table 10.4). Left ventricular failure nary hypertension or a massive pulmonary embolus. In
TABLE 10.4 Clinical manifestations of failure of right and left sides of the heart
Left ventricular failure Right ventricular failure
Signs Symptoms Signs Symptoms
Tachypnoea Dyspnoea Peripheral oedema Fatigue
Tachycardia Orthopnoea Raised jugular venous pressure Weight gain
Bibasal crackles Paroxysmal nocturnal dyspnoea Raised central venous pressure Anorexia
Haemoptysis Fatigue Ascites
Cough Nocturia Hepatomegaly
Pulmonary oedema
Raised pulmonary artery pressure
S3 heart sound
Cardiovascular Alterations and Management 231
Alveolus
Proteins
A Capillary Lymphatics B
FIGURE 10.10 Pathophysiology of pulmonary oedema. As pulmo-
nary oedema progresses, it inhibits oxygen and carbon dioxide
exchange at the alveolar–capillary interface. (A) Normal relation-
ship. (B) Increased pulmonary capillary hydrostatic pressure causes
fluid to move from the vascular space into the pulmonary intersti-
tial space. (C) Lymphatic flow increases and pulls fluid back into the
vascular or lymphatic space. (D) Failure of lymphatic flow and wors-
ening of left-sided heart failure causes further movement of fluid C D
106
into the interstitial space and then into the alveoli.
this case, right ventricular failure is due to resistance to ● palpation of the praecordium and apical impulse:
outflow. The right ventricle can adapt to fairly large This may be displaced laterally and downward to the
changes in volume; however, when cardiac output left due to an increased heart size.
decreases, end-diastolic volume increases, and the right ● auscultation of a third heart sound (S3 gallop): This
atrium is unable to empty adequately. Right atrial pres- occurs due to a low ejection fraction and diastolic
sure rises and is reflected into the venous system. Jugular dysfunction. A fourth heart sound may also be present
vein distension occurs, and the veins are usually visible due to a decrease in ventricular compliance.
above the clavicle. Symptoms of right heart failure are not ● assessment of jugular venous pressure (JVP): This is to
as specific as left ventricular failure, and are mostly related estimate the degree of venous volume. If raised it
to low cardiac output and raised venous pressure (see reflects hypervolaemia, right ventricular failure, and
Table 10.4). Ascites and oedema tend to progress insidi- reduced right ventricular compliance. It can also be
ously, and dependent oedema in the feet and ankles is raised in the presence of tricuspid valve disease. The
often most prominent. Weight gain is an important sign hepatojugular reflex is also assessed by pressing on the
as one kilogram of weight gain equals one litre of excess liver and observing an increase in JVP. This results in
fluid. Liver congestion may result in tenderness, ascites an increase in blood flow to the right atrium.
and jaundice. Nausea and anorexia may be present and ● blood pressure: Lying and standing blood pressure are
are a result of an increased intra-abdominal pressure. measured to assess postural hypotension due to a low
Many signs are not readily distinguishable from left ven- cardiac output and also the prescribing of beta-
tricular failure, including extra heart sounds. adrenergic blocking agents and ACE inhibitors.
● peripheries: Look for the presence of cyanosis which
PATIENT ASSESSMENT, DIAGNOSTIC may be due to vasoconstriction. Assess the fingers for
PROCEDURES AND CLASSIFICATION clubbing which indicates long-term cyanosis usually
Assessment and diagnosis are summarised in a diagnostic as a consequence of congenital heart disease. Also
algorithm (see Figure 10.11). A full assessment and history assess the patient for ankle oedema. Peripheral oedema
is essential to determine the cause(s) of CHF and to assess up to the midcalves indicates a moderate amount of
the severity of the disease. A careful physical assessment excess fluid and the patient may require a bolus dose
is important for initial diagnosis and to evaluate the effec- of diuretic medication.
tiveness of treatments and progress of the disease. The Pulmonary assessment includes chest auscultation for
depth and time taken to conduct the assessment depend inspiratory crepitations that do not clear with coughing.
on the severity of symptoms. The physical examination They are initially heard in the bases but as congestion
of the patient focuses on cardiovascular and pulmonary increases they become diffuse. General assessment of the
assessment. patient includes daily weighing, looking for signs of
cachexia (usually associated with severe chronic heart
Cardiovascular assessment includes: failure), anaemia and dizziness.
● pulse rate and rhythm: The pulse rate is generally Heart failure is usually classified according to the severity
elevated due to a low cardiac output. However, if the of symptoms. In chronic heart failure, the New York Heart
patient is prescribed beta-adrenergic blocking agents Association (NYHA) Functional Classification is com-
and/or angiotensin converting enzyme (ACE) inhibi- monly used to classify patients on the basis of the activity
tors, the pulse rate may be low. level that initiates symptoms (see Table 10.5).
232 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
Suspected CHF
Shortness of breath
Fatigue
Oedema
Clinical history
Physical examination
Initial investigations
Pulse rate and rhythm
Symptoms of CHF Blood pressure
Dyspnoea Elevated JVP
Orthopnoea Cardiomegaly
PND Cardiac murmurs
Fatigue Lung crepitations
Oedema Hepatomegaly
Palpitations/syncope Oedema
Past cardiovascular
disease Electrocardiogram
Angina/MI Chest x-ray
Hypertension Other blood tests: full blood
Diabetes count, electrolytes, renal
Murmur/valvular disease function, liver function,
Cardiomyopathy thyroid function
Alcohol/tobacco use Consider BNP or
Medications N-terminal proBNP test
Clinical diagnosis of CHF
Echocardiogram
Structural diagnosis Pathophysiological diagnosis
E.g. myopathic, valvular Systolic dysfunction (LVEF <40%)
Diastolic dysfunction (LVEF >40%)
Consider specialist referral Proceed to treatment guidelines
for further investigation
BNP = B-type natriuretic peptide
JVP = jugular venous pressure
LVEF = left-ventricular ejection fraction
MI = myocardial infarction
PND = paroxysmal nocturnal dyspnoea
55
FIGURE 10.11 Diagnostic algorithm for CHF. Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand.
Cardiovascular Alterations and Management 233
● urinalysis for specific gravity and proteinuria.
TABLE 10.5 New York Heart Association functional ● myocardial ischemia and viability need to be assessed
classification of heart failure 64 in patients with heart failure and coronary artery
disease. These can be assessed by a stress ECG, stress
Class Definition echocardiography or a stress nuclear study. Coronary
angiography is useful to determine the contribution
I Normal daily activity does not initiate symptoms.
There are no limitations on activity of coronary artery disease in these patients.
● natriuretic peptides includes plasma ANP and B-type
II Ordinary activities initiate onset of symptoms, but natriuretic peptide (BNP). BNP or N-terminal proBNP
symptoms subside with rest. Slight limitation of
daily activities. is not recommended to be used to diagnose chronic
heart failure as an elevated BNP may be due to other
III A small amount of activity initiates symptoms; causes. However, it is useful to differentiate between
55
patients are usually symptom-free at rest.
Marked limitation of activity. dyspnoea due to chronic heart failure and dyspnoea
due to chronic obstructive pulmonary disease.
IV Any type of activity initiates symptoms, and ● endomyocardial biopsy should be conducted if there
symptoms are present at rest.
is a suspicion of cardiomyopathy.
NURSING MANAGEMENT
Diagnostic Tests Treatment of CHF is lifelong and multifactorial, requiring
Tests used to diagnose heart failure include: a well-coordinated, multidisciplinary approach. The goals
of heart failure treatment are to identify and eliminate
● trans-thoracic echocardiography is the most useful the precipitating cause, promote optimal cardiac func-
investigation to confirm diagnosis. This is the gold stan- tion, enhance patient comfort by relieving signs and
dard diagnostic test for heart failure and should always symptoms, and help the patient and family cope with any
be undertaken when possible. This test is vital, as it can lifestyle changes. Clinical practice guidelines have been
distinguish systolic dysfunction (left ventricular ejec- developed to guide the treatment of heart failure on the
tion fraction [LVEF] <40%) from diastolic dysfunction, basis of ventricular dysfunction and grade of symptoms
55
and therefore help determine treatment. Information (see Figures 10.12–10.14). 55
on left and right ventricular size, volumes, left ventricu-
lar thrombus and ventricular wall thickness and motion Planning for hospital discharge begins early in the
can be provided. Assessment of valve structure and admission and aims to promote quality of life for the
function as well as intracardiac and pulmonary pres- patient and prevent unnecessary admissions. Several
sures can be determined, without the need for invasive health care services have been implemented to support
techniques. Pulsed-wave Doppler and tissue Doppler the transition from hospital to home as it is during the
studies can be used to determine diastolic dysfunction. first 30 days post-discharge that nearly 20% of heart
65
● assessment of cardiac function can also be done failure patients are readmitted to hospital. There are
by invasive techniques (e.g. coronary angiography) currently over 70 outreach heart failure programs
and nuclear cardiology tests (e.g. gated radionuclide throughout Australia that support heart failure patients
66
angiocardiography). post-discharge. The main goals of these programs are
● ECG should be done as an initial investigation. Most to reduce symptom burden, improve functional capacity
common abnormalities include ST-T wave changes, and minimise hospital readmissions. These programs
left bundle branch block, left anterior hemiblock, left range from in-hospital visits to facilitate discharge plan-
ventricular hypertrophy, atrial fibrillation and sinus ning, nurse-led heart failure outpatient clinics, home
tachycardia. visit programs and heart failure specific exercise pro-
● chest X-ray for cardiomegaly and pulmonary mark- grams. Several meta-analyses of home visit programs
ings, including evidence of interstitial oedema: perihi- have shown a reduction in hospital admissions and
lar pulmonary vessels, small basal pleural effusions mortality 67,68 and these programs are now standard care
55
obscuring the costophrenic angles, Kerley B lines for heart failure patients. Home visit heart failure pro-
(indicating raised left atrial pressure). grams involve a heart failure nurse visiting the patient at
● full blood count for anaemia and mild thrombo- home and providing education to the patient and carer,
cytopenia. Any signs of anaemia should be further assessing their symptoms and educating the patients and
investigated. their carers about self-management strategies. Nurse-led
● urea, creatinine and electrolytes for dilutional hypona- outpatient clinics also reduce hospital admissions and
traemia, hypokalaemia, hyperkalaemia, low magne- mortality 69,70 and play an important role in the manage-
sium, and glomerular filtration rate. These should be ment of heart failure patients post-discharge.
closely monitored if there are any changes in clinical Management of heart failure post the acute phase is based
status and/or drug therapy such as ACEIs and diuretics. on three principles: self-care management, long-term life-
● liver function tests for elevated levels of AST, ALT, LDH style changes and adherence to pharmacotherapy. Man-
and serum bilirubin. agement of self-care is the key to non-pharmacological
● thyroid function tests particularly in patients with no management of heart failure. Self-care refers to the
history of coronary artery disease and who develop decision-making process of patients concerning their
atrial fibrillation. choice of healthy behaviour and response to worsening
234 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
Mild-moderate symptomatic CHF
(NYHA Class II – III)
Correct/prevent acute Pharmacological Non-pharmacological
precipitants management management
Non-compliance Multidisciplinary care**
Acute ischaemia/infarction Exercise/conditioning program
Arrhythmia* Low-salt diet
Fluid management
Fluid overload
Yes No
Diuretic*** ACEI****
+
ACEI
Persistent oedema Improved Add beta-blocker
Add spironolactone Add beta-blocker
(Class III)
+/- digoxin
+/- angiotensin II
receptor antagonists
Improved
Add beta-blocker
* Patients in atrial fi brillation (AF) should be anticoagulated with a target INR of 2.0 – 3.0. Amiodarone may be used to control
AF rate or attempt cardioversion. Electrical cardioversion may be considered after 4 weeks if still in AF. Digoxin will slow
resting AF rate.
** Multidisciplinary care (pre-discharge and home review by a community care nurse, pharmacist and allied health personnel)
with education regarding prognosis, compliance, exercise and rehabilitation, lifestyle modifi cation, vaccinations and
self-monitoring.
*** The most commonly prescribed fi rst-choice diuretic is a loop diuretic e.g. frusemide; however there is no evidence that loop
diuretics are more effective or safer than thiazides.
**** If ACEI intolerant, use angiotensin II receptor antagonists instead.
FIGURE 10.12 Pharmacological treatment of systolic heart failure. Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia
55
and New Zealand.
Cardiovascular Alterations and Management 235
Severe symptoms (NYHA Class IV)
Identify/treat acute Non-pharmacological Pharmacological
precipitant treatment treatment
Acute ischaemia/ Multidisciplinary care*
infarction Salt/fl uid restriction
Arrhythmia Exercise/conditioning
Non-compliance program
Diuretic
+ ACEI**
No improvement Improved
Add spironolactone Add beta-blocker
+/- digoxin
+/- angiotensin II receptor
antagonists
No improvement Improved
Add hydralazine/nitrate Add beta-blocker
Consider heart (irrespective of NYHA
transplantation Class***)
Not tolerated Tolerated
Consider heart Continue medical
transplantation if age treatment
<65 years + no major
comorbidity
* Multidisciplinary care (pre-discharge and home review by a community care nurse, pharmacist and allied health personnel)
with education regarding prognosis, compliance, exercise and rehabilitation, lifestyle modifi cation, vaccinations and
self-monitoring.
** If ACEI intolerant, use angiotensin II receptor antagonists instead.
*** Patients with NYHA Class IV CHF should be challenged with beta-blockers provided they have been rendered euvolaemic
and do not have any contraindication to beta-blockers.
FIGURE 10.13 Pharmacological treatment of refractory systolic heart failure. Courtesy National Heart Foundation of Australia and the Cardiac Society
55
of Australia and New Zealand.
236 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
Management of HFPSF
Is there fl uid overload?* Is there an identifi able cause?
Yes No
Diuretic Treat cause
Hypertension CHD Diabetes** Cardiomyopathy
Anti-hypertensive Investigate Hypertrophic Restrictive
therapy*** suitability for cardiomyopathy — cardiomyopathy
to target revascularisation Investigate family
history
Pharmacological Pharmacological Endomyocardial
treatment treatment biopsy for
ACEI**** Beta-blocker infi ltrative diseases
Beta-blocker Calcium antagonist e.g. sarcoidosis,
Calcium antagonist amyloidosis
If no specifi c cause
found, consider
constrictive
pericarditis
Surgical
pericardiectomy
* With rare exception, patients with diastolic heart failure present with symptoms and signs of fl uid overload, either pulmonary
or systemic congestion or both.
** Better diabetes control.
*** Choice of therapy will vary according to clinical circumstances, e.g. thiazide diuretic — elderly, systolic hypertension;
ACEI — LV hypertrophy, diabetes, CHD; beta-blocker — angina.
**** If ACEI intolerant, use angiotensin II receptor antagonist instead.
55
FIGURE 10.14 Management of HFPSF. Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand.
Cardiovascular Alterations and Management 237
symptoms when they occur. It involves cognitive decision heart failure physical activity should be undertaken under
making, requiring the recognition of signs and symptoms the supervision of trained heart failure specialists, e.g.
that indicate a change in condition, which is based on physiotherapist or exercise physiologist, who can tailor
knowledge and prior experiences of deterioration. 71-73 the level of exercise to the degree of severity of symptoms.
Many CHF patients have co-morbidities such as arthritis,
Lifestyle Modification and Self-care which make exercise programs difficult, but maintaining
Management general activity should be encouraged.
Patient education is the key to self-management and Dietary sodium intake should be reduced to 2 g/day for
must include family members to be effective. Patient edu- patients with moderate to severe heart failure and to 3 g/
cation should include information on the following: day for mild heart failure. Reduction in sodium intake
55
● the disease process. This involves discussing what helps reduce fluid retention, diuretic requirements and
heart failure is, signs and symptoms and why they potassium excretion. A large proportion of an individu-
occur, and strategies to improve their symptoms al’s sodium intake can come from processed foods, so
● lifestyle changes patients are encouraged to read nutrition labels and
● medications and side effects reduce the intake of these foods. Salt intake can also be
● self-monitoring and acute symptoms reduced by avoiding adding salt in cooking or to meals.
● the importance of adherence to their medications and As CHF patients who are overweight increase demands
management plan. on their heart, weight loss by lowering dietary fat intake
may improve symptoms and quality of life. These patients
Restriction of fluid to 1–1.5 L/day is one of the most may require referral to a dietician for weight loss manage-
important strategies that patients can adhere to in order ment. In patients with moderate to severe heart failure,
to improve their symptoms. Patients are encouraged to cardiac cachexia and anaemia are common which further
weigh themselves daily and to identify any increase in exacerbate weakness and fatigue. These patients will
weight as an increase of 1 kg equals 1 litre of excess fluid. require a referral to a dietician for nutritional support.
National guidelines stipulate that if their weight increases Other lifestyle changes are: smoking cessation, ideally no
by 2 kg over 2 days they need to see their local doctor as alcohol otherwise limit alcohol to less than 2 standard
55
soon as possible. Patients that adhere to their manage- drinks/day (alcohol is a myocardial toxin and reduces
ment plan and closely monitor their daily weight may contractility), limit caffeinated drinks to 1–2 drinks/day
self-manage their volume status by using a flexible diuretic (to decrease risk of arrhythmias), control diabetes, annual
action plan as developed by their cardiologist. In addi- vaccinations for influenza and regular pneumococcal
tion, patients should be advised of early warning signs of disease vaccinations. 55
excess fluid volume and decompensation, such as increas-
ing dyspnoea, fatigue and peripheral oedema. Palliative care may be more appropriate for patients
with end-stage heart failure who are experiencing signifi-
Sleep apnoea also occurs commonly in CHF patients. cant symptoms, prescribed maximal pharmacotherapy,
There are two types: obstructive sleep apnoea and central frequent hospital admissions and poor response to
sleep apnoea. Obstructive sleep apnoea occurs due to treatment.
airway collapse and is associated with obesity. It can be
treated with weight reduction and night-time continuous
positive airway pressure (CPAP). The use of CPAP for Practice tip
obstructive sleep apnoea results in an improvement in
LVEF due to an increase in left ventricular filling and When considering if a patient is suitable for palliation, discus-
emptying rates, and a decrease in systolic blood pressure sion also needs to include deactivation of their pacemaker
74
and left ventricular chamber size. Central sleep apnoea or implantable cardioverter defribillator (ICD).
(Cheyne-Stokes respirations) occurs due to pulmonary
congestion and high sympathetic stimulation in patients
with severe heart failure and may be treated with CPAP. Pharmacotherapy in patients with heart failure is vital,
However, the benefits of oxygen therapy have not been and includes an array of drugs that require careful man-
proven. However, exercise is equally important, to prevent agement. In Australia and internationally, nurse practitio-
the deconditioning of skeletal muscle that occurs in CHF. ners are authorised to titrate some heart failure medications,
Exercise training – including walking, exercise bicycle and including diuretics and beta-adrenergic blocking agents.
light resistance – has been shown to improve functional Pharmacists also provide essential patient education, and
capacity, symptoms, neurohormonal abnormalities, support the optimisation of medication treatments and
64
quality of life and mood in CHF. The Heart Foundation management of complex medication schedules. Some
of Australia recommends that all stable CHF patients, major hospitals have a pharmacist outreach program
regardless of age, should be considered for referral to a where a pharmacist visits the patient at home.
tailored exercise program (preferably a heart failure spe-
cific exercise program) or modified cardiac rehabilitation Medications
55
program. Heart failure exercise programs comprise Pharmacological management relies on the following
resistance training and have been shown to improve func- categories of drugs: ACE inhibitors, beta-adrenergic
tional capacity, heart failure symptoms and survival and blocking agents, angiotension receptor blocking agents
75
reduced hospitalisations. In patients with symptomatic (ARBs), diuretics, digoxin and antiarrhythmic drugs.
238 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 10.6 Common medications for the treatment of heart failure 55,64,107,108
Drug/example Action Major adverse effects
First line pharmacotherapy
ACE inhibitor Decrease systemic vascular resistance by stopping angiotensin conversion Symptomatic hypotension
Captopril I to II; decreased sodium and water retention. Hyperkalaemia
Enalapril Unproductive cough
Renal failure
Rash
Loop diuretics Increase urine volume by decreasing reabsorption of chloride and sodium. Hypokalaemia
Frusemide Ototoxicity
Rash
Thiazide diuretics Increase urine volume by decreasing reabsorption of sodium. Hypokalaemia
Chlorothiazide Hyperglycaemia
Hydrochlorothiazide Sensitivity: rash
Beta-adrenergic blockers Reduce systemic vascular resistance and heart rate by blocking Hypotension
Bisoprolol adrenoreceptors in arteries and heart. Bronchoconstriction
Carvedilol
Metoprolol CR/XL
Potassium-sparing Increase urine volume by aldosterone blocking and sodium retention. Hyperkalaemia
diuretics Rash
Spironolactone Gynaecomastia
ARB Block the angiotensin II receptor that responds to angiotensin II Symptomatic hypotension
Candesartan stimulation; decreased sodium and water retention. Alternative to ACEI. Hyperkalaemia
Irbesartan Renal failure
Second line pharmacotherapy
Cardiac glycosides Increase myocardial contractility and decrease heart rate by inhibiting Tachycardia
Digitalis sodium pump in myocytes. AV block
Nausea and vomiting
Disorientation
Visual disturbances
(Beta-adrenergic blocking agents and antiarrhythmic the workload of the heart without affecting heart rate or
drugs are reviewed on page 266). The main actions and cardiac output.
adverse effects of these drugs in heart failure are sum- Common adverse effects of ACE inhibitors primarily
marised in Table 10.6. result from hypotension, including dizziness and head-
ache. Other side effects include hyperkalaemia, deteriora-
Angiotensin-converting enzyme inhibitors tion of renal function, and an unproductive cough, which
ACE inhibitors are the cornerstone of CHF treatment, as may respond to asthma prophylactic medications. Initial
they have been demonstrated to prolong survival, improve doses of ACE inhibitors should be low, as severe – though
patient symptoms and exercise tolerance, prevent transient – symptomatic hypotension can occur, worsen-
hospitalisation and improve ejection fraction in CHF ing of renal function and hyperkalaemia. The dose of ACE
patients. 76,77 All patients with symptomatic systolic LV inhibitors needs to be gradually increased to maximum
dysfunction should be prescribed ACE inhibitors. 55,61 dose over 2–3 months to optimise the survival and func-
Drugs in this group (captopril, enalapril, lisinopril) act tional capacity benefits. This group of drugs is contrain-
on the renin–angiotensin system by specifically prevent- dicated in patients with bilateral renal artery stenosis due
78
ing the conversion of angiotensin I into angiotensin II. to the danger of developing renal failure. One important
As a result, systemic vascular resistance (afterload) is adverse effect of ACEIs is that it cannot be taken in con-
decreased. This is particularly important in preventing the junction with NSAIDs as NSAIDs reduce the action of
progression of CHF, because blockade of the renin– ACE inhibitors. 79
angiotensin system prevents further development of sys-
tolic dysfunction. In addition, because angiotensin II also Practice tip
stimulates the release of aldosterone, sodium and water
retention are decreased (preload). This may also be ben- A dry, non-productive cough is often associated with the intro-
eficial when ACE inhibitors are prescribed with diuretics, duction of ACE inhibitor medication, but is often mistaken for
as potassium loss is limited. Further, ACE inhibitors a symptom of other conditions, so patients may not report the
inhibit the breakdown of bradykinin (a vasodilator), symptom as new. The cough usually begins within 1–2 days of
which also contributes to decreasing vascular resistance. commencing therapy and uptitration of dose.
The total reduction of systemic vascular resistance reduces
Cardiovascular Alterations and Management 239
increased concentrations are present in the loop, attract-
Practice tip ing more water and increasing urine volume. Intrave-
nous administration of frusemide is often used to
Heart failure is a disease of the elderly. Many elderly patients manage preload in acute exacerbations. In fluid-
have arthritis. However, elderly patients with heart failure must overloaded patients, the aim is to achieve increased urine
avoid taking NSAID medications especially when taking ACEIs output and a weight reduction of 0.5–1 kg daily, until
as NSAIDs counter the action of ACE inhibitors. In such cases clinical euvolaemia is achieved. Hypokalaemia is a
we usually recommend taking glycosamine for relief from common adverse effect, and patients on long-term
arthritis pain. diuretics need regular monitoring and may require
potassium supplements. Hyponatraemia may also
Beta-adrenergic blocking agents occur at high doses, and needs careful management in
All patients with symptomatic systolic left ventricular dys- heart failure patients. Ototoxicity, presenting as tinnitus,
vertigo and deafness, can occur at high doses, so IV deliv-
function should be prescribed a beta-adrenergic blocking ery of frusemide should be no faster than 4 mg/min.
agent. Beta-adrenergic blocking agents (carvedilol, meto- ● Thiazide and thiazide-like diuretics: These drugs (chlo-
prolol, bisoprolol) are used in CHF to inhibit the adverse rothiazide, hydrochlorothiazide, chlorthalidone) act
effects of chronic activation of the sympathetic nervous on the ascending loop of the nephron and decrease
system and improve ventricular function (see Chapter 10). sodium reabsorption. As a result, the fluid in the col-
In heart failure beta-2 receptors predominate with beta-1 lecting ducts is more concentrated and attracts more
receptors being downregulated. In heart failure beta- water. Thiazides also cause peripheral arteriole vasodi-
adrenergic blocking agents reduce this neurohormonal lation, which may be beneficial in hypertensive patients.
activity. The addition of a beta-adrenergic blocker has Adverse effects are similar to loop diuretics due to
been demonstrated to reduce symptoms, reduce hospi- potassium and sodium loss, and supplementation may
talisations and prolong survival in patients. 80,81 Similar to be necessary. When ACE inhibitors are prescribed con-
ACE inhibitors the dose of beta-adrenergic blocking agents currently, there is less potassium loss (details below).
needs to be gradually increased. Once the patient is euro- Hyperglycaemia can occur, so diabetics need monitor-
volaemic they should be commenced on low dose and ing. Impotence may also occur, as well as sensitivity
gradually increased to maximal dose over several months. due to the presence of sulphonamide in the drug
In patients with COPD, selective beta-1 blockers are pre- structure.
scribed. Patients will require close monitoring for signs ● Aldosterone antagonists: These are potassium-sparing
of deterioration of their COPD. Other adverse events are: diuretics and include spironolactone. Aldosterone
55
symptomatic hypotension, bradycardia and worsening acts on the distal convoluted tubule of the nephron to
heart failure. Also during the up-titration of beta-adrenergic cause sodium retention and thus water retention,
blocking agents many patients complain of feeling vague although potassium is lost. Antagonists stop this
in the morning; this usually disappears after 2–3 weeks. action, so potassium is not lost and not as much
Angiotensin receptor blocking agents sodium retained, thus there is minor diuresis. Spirono-
lactone is particularly useful in chronic heart failure
The primary use of angiotensin receptor blocking agents because there is excessive aldosterone production,
(ARBs) is in patients who are intolerant of ACE inhibitors causing oedema. There is the potential that spironolac-
such as ACEI cough. They have a similar action as ACE tone, by blocking aldosterone systemically, may prevent
inhibitors, however, ARBs block the angiotensin II recep- the negative effects of aldosterone on the heart, such
tor that responds to angiotensin II stimulation. ACE as fibrosis, hypertrophy and arrhythmogenesis. Adverse
inhibitors on the other hand act on the enzyme that effects include hyperkalaemia, which may occur more
78
produces angiotensin II. They have similar benefits as readily in CHF patients because of renal failure, and
ACE inhibitors, improving survival, LVEF and heart failure because of its potentially lethal effects requires regular
symptoms and a reduction in hospitalisations. 82,83 Similar monitoring. Other effects include hyponatraemia and
to ACE inhibitors, ARBs are commenced on a low dose feminisation effects such as gynaecomastia. Spirono-
and gradually up-titrated to optimal dose over two lactone is recommended for use in patients with severe
months. Adverse effects are: deterioration in renal func- symptomatic (NYHA class III–IV) systolic heart failure
tion, hyperkalaemia and symptomatic hypotension. 61 in addition other pharmacotherapy such as ACE inhib-
Diuretics itors. Aldosterone antagonists have additional survival
84,85
Diuretics are one of the mainstays of management of benefits and reduce hospital readmission.
heart failure, primarily to decrease the sodium and water Inotropic agents
retention response to the low cardiac output state. A com- This category of drugs increases cardiac contractility. The
bination of diuretics may be used if oedema persists on group includes cardiac glycosides (digoxin) and dopa-
one diuretic. Most often diuretics will be used in combi- mine agonists (dopamine, dobutamine), sympath o-
nation with ACE inhibitors. mimetics (adrenaline, noradrenaline), and calcium
● Loop diuretics: These drugs (frusemide, ethacrynic acid sensitising agents (levosimendan). Inotropes are used as
and bumetanide) act on the ascending limb of the loop IV infusions in severe heart failure, acute exacerbations of
of Henle of the nephron. They prevent the reabsorption chronic heart failure and for palliative care or bridging to
of chloride and sodium ions from the loop, so that transplant in very severe chronic heart failure. These drugs
240 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
have both inotropic and chronotropic actions, so that cardiopulmonary bypass and left ventricular assist devices
cardiac contractility and heart rate are both increased to (LVADs) may be used. In appropriate candidates, cardiac
improve cardiac output. Continuous ambulatory infu- transplant may also be an option. These procedures are
sion of inotropic agents such as dobutamine are admini- covered under cardiac surgery.
stered in patients with severe heart failure as a bridge to
transplantation which allows these patients to be dis- Acute Exacerbations of Heart Failure
charged home with support from a home visit nurse. Acute exacerbations of CHF usually occur as episodes of
Cardiac glycosides decompensation due to progression of the disease or
87
non-adherence to their management plan. Acute epi-
Cardiac glycosides such as digitalis inhibit the sodium sodes usually present as congestive heart failure with
pump such that the exchange between sodium and associated pulmonary oedema, cardiogenic shock (see
calcium is impaired. This results in calcium stores being Chapter 21) or decompensated CHF. Patients with
55
released and intracellular calcium levels rising. As more severe dyspnoea due to pulmonary congestion should be
calcium is available for contraction, contractility and administered oxygen therapy. If their hypoxaemia does
cardiac output increase. These changes in ion movement not improve then they may benefit from bilevel positive
and additional affects, which enhance parasympathetic airway pressure (BiPAP) to support ventilation and gas
stimulation, result in decreased impulse generation by exchange. The use of continuous positive airway pressure
the sinoatrial (SA) node. This is known as a negative ventilation (CPAP) or BiPAP in acute pulmonary oedema
chronotropic effect. Conduction is also slowed through will reduce the need for intubation and mechanical
the atrioventricular (AV) node and ventricles, allowing ventilation.
more filling time, and therefore having a positive effect
on cardiac output. The negative chronotropic effects are The mainstay of treatment of an acute exacerbation is
particularly beneficial in patients with the atrial fibrilla- pharmacological, so a combination of the medications
tion that is so common in CHF. Digitalis may also affect is given, usually comprising diuretics, morphine and
cardiopulmonary baroreceptors to reduce sympathetic nitrates. The nitrates and morphine cause vasodilatation.
tone, which may be a valuable offset to excessive sympa- Morphine also reduces the respiratory drive and respira-
thetic stimulation in CHF. tory workload. Nitrates also cause epicardial artery dilata-
tion and reduce preload which also helps to relieve
The most important adverse effects of digoxin are caused symptoms of pulmonary congestion particularly at night
by changes in conduction: tachycardia, fibrillation and AV when filling pressures are increased due to the recumbent
block. Digoxin may also cause nausea and vomiting by position of sleeping. Diuretics should be administered
55
direct brain effects and gastrointestinal irritation. Digi- intravenously to optimise the excretion of intra and extra-
talis has a narrow margin of safety, a long half-life, and vascular cellular fluid to reduce circulating blood volume
side effects can be fatal, so assay of plasma drug levels to reduce cardiac workload. Fluid restriction, usually to
must be conducted regularly and at initiation and change 1–1.5 L in 24 hours, is begun. A urinary catheter may need
of treatment. Excessive digoxin causes disorientation, hal- to be inserted so that accurate, continuous measures of
lucinations and visual disturbances. Potassium levels urine output can be gained and an accurate fluid balance
directly alter the effect of digoxin, so that low levels calculated. This is necessary, along with consistent daily
enhance effects and high levels reduce effects. weighing, to determine the effectiveness of diuretic therapy
Arrhythmias are common in heart failure and need to be and renal status. Various positive inotropes may be admin-
treated. The agent must be carefully selected, as chronic istered (e.g. IV dobutamine causes vasodilatation; IV
heart failure patients often have complex medication regi- dopamine to improve renal function) to improve contrac-
mens and interactions may occur. Also, some ventricular tility and reduce systemic venous return. Various mechani-
antiarrhythmics, like class 1 agents (e.g. flecainide), are cal devices are also available, e.g. intra-aortic balloon
associated with sudden death in CHF. Implantable pump, LVAD (discussed in Chapter 12). CRT with or
cardioverter-defibrillator (ICD) therapy may be more without an ICD may be implanted. CRT is recommended
effective in treating ventricular arrhythmias. ICDs reduce in NYHA class III–IV patients on optimal pharmacologi-
86
mortality by 20–30% and are first-line therapy in patients cal therapy, LVEF ≤35%, QRS duration > 120 ms, and
55
with a history of VF or sustained VT, LVEF ≤30% at least sinus rhythm. All of these criteria must be fulfilled. Cri-
one month post myocardial infarction or three months teria for implantation of an ICD include: symptomatic
post CABGs and symptomatic heart failure and LVEF patients (NYHA class II–IV) and LVEF ≤35%, LVEF <30%
55
≤35%. Cardiac resynchronisation therapy (CRT) (also one month post AMI or three months post CABGs, spon-
known as biventricular pacing) is also indicated in patients taneous VT with structural CHD, or survived a cardiac
with symptomatic heart failure to reduce asynchronous arrest due to VT or VF which was not due to a reversible
pacing of the left ventricle (QRS duration > 150 ms). cause. If a patient is to have an ICD implanted then exten-
Systolic function is improved when the left and right sive counselling pre- and post-implantation must be
ventricles are paced simultaneously. Often patients with undertaken with the patient and carer to ensure they are
a prolonged QRS will have a combination of an ICD with aware of the painful and unexpected shocks that may be
55
CRT therapy. ICDs and CRT are discussed in more detail delivered. Figure 10.15 provides an overview of the esca-
in Chapter 11. lation of treatment for acute heart failure. 55
In severe heart failure, when patients do not respond to Most patients in acute heart failure have poor perfusion
pharmacological treatment, mechanical measures such as of the gastrointestinal system and, combined with
Cardiovascular Alterations and Management 241
Ventricular assist devices
Intra-aortic balloon counterpulsation
Assisted ventilation
CPAP
Positive inotropes
Morphine
Vasodilators
Diuretics
Oxygen
FIGURE 10.15 Emergency therapy of acute heart failure. Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and
55
New Zealand.
dyspnoea, a resultant limited appetite. Small, easily Diagnosis
ingested meals are best. While the patient is on bedrest, Many of the features of DCM are non-specific. Heart
nursing care to prevent problems related to immobility failure, as mentioned, is present with typical symptoms
is important. Skin care is particularly important, as poor of dyspnoea, fatigue, peripheral oedema and cardiomeg-
skin perfusion and oedema place the CHF patient at aly. S3 and S4 heart sounds may be present on ausculta-
higher risk of skin breakdown.
tion. Atrial and ventricular arrhythmias are common,
SELECTED CASES particularly atrial fibrillation, ventricular tachycardia,
ventricular fibrillation and torsades de pointes. Left
bundle branch block (LBBB) is often present, which
worsens systolic performance and shortens survival, espe-
CARDIOMYOPATHY cially when the QRS is markedly prolonged. Echocar-
88
diography demonstrates the defining abnormalities and
As the term implies, the cardiomyopathies are primary
disorders of the myocardium in which there are systolic, may be useful in revealing atrial thrombus. Occasionally,
diastolic or combined abnormalities. Classification of the endocardial biopsy is undertaken to differentiate from
commonest forms of cardiomyopathy is made on the myocarditis or rarer causes of cardiomyopathy.
basis of the dominant abnormality, which may be dila- Management
tion, hypertrophy, or restricted filling. However, each has
different haemodynamic effects and therefore require dif- Treatment for DCM is similar to that of heart failure and
ferent treatment. includes beta-adrenergic blocker therapy, ACEIs, diuretics
and antiarrhythmic therapy where indicated or, if neces-
DILATED CARDIOMYOPATHY sary, an ICD for recurrent haemodynamically significant
88
Dilated cardiomyopathy (DCM) is the most common ventricular arrhythmias. The use of cardiac resynchroni-
form of cardiomyopathy and is characterised by ventricu- sation therapy (CRT) has produced significant clinical
lar and atrial dilation and systolic dysfunction. All four improvements and is recommended for DCM patients
88
chambers become enlarged which is not in proportion to with NYHA functional class III–IV, optimal medical
the degree of hypertrophy. It presents as heart failure of therapy, LVEF ≤35%, and sinus rhythm with QRS greater
variable severity, sometimes complicated by thromboem- than 120 msec. 61,90 Cardiac transplantation is considered
bolism, at least partly due to atrial fibrillation, which is when standard therapies fail to influence clinical progres-
common. Conduction abnormalities are common in sion and left ventricular assist devices and ICDs may be
DCM further exacerbating AV dyssynchrony and left ven- used as a bridge to transplantation.
tricular dysfunction. DCM is the most common cause of
sudden cardiac death due to ventricular arrhythmias. HYPERTROPHIC CARDIOMYOPATHY
Annual mortality from DCM ranges from 10–50%. Idio- Hypertrophic cardiomyopathy (HCM) is a genetic abnor-
89
pathic DCM is the most common cause of heart failure in mality that gives rise to inappropriate hypertrophy espe-
young people. Aetiology of DCM includes coronary heart cially in the intraventricular septum with preserved or
disease, myocarditis, cardiotoxins, genetics and alcohol. hyperdynamic systolic function. The main abnormality
242 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
with HCM is diastolic rather than systolic as in DCM. The patient with HCM deteriorates and is hospitalised, posi-
hypertrophy is not a compensatory response to excessive tive inotropes, chronotropes and nitrates worsen LVOTO
load, such as in aortic stenosis or hypertension. Left ven- and should be avoided. However, beta-adrenergic block-
tricular hypertrophy of variable patterns is seen, occasion- ers, amiodarone and calcium antagonists such as verapra-
88
ally with disproportionate septal hypertrophy, which mil are indicated. Due to the familial nature of HCM,
causes left ventricular outflow tract obstruction (LVOTO) relatives aged 12–18 years also need to be screened
in which HCM progresses to hypertrophic obstructive for HCM.
cardiomyopathy, or HOCM. In HCM the muscle mass is
large and hypercontractile, but the left ventricular cavity RESTRICTIVE CARDIOMYOPATHY
is small. The increase in left ventricular systolic pressure Restrictive cardiomyopathies (RCMs) limit diastolic dis-
and the altered relaxation cause diastolic dysfunction tensibility or compliance of the ventricles. The stiff ven-
and impaired ventricular filling. Mitral regurgitation is tricular walls feature diastolic dysfunction and there is
common. These abnormalities combine to produce impaired ventricular filling. Infiltrates into the intersti-
pulmonary congestion and dyspnoea due to a raised end- tium and the replacement of normal myocardium with
diastolic pressure. Sudden cardiac death, often after exer- abnormal tissue hamper this relaxation. Initially, sys-
88
tion or other increases in contractility, is sometimes seen tolic function and wall thickness are normal. However, as
in HCM and is thought to be partly attributable to outflow the disease progresses systolic dysfunction occurs. RCM
91
obstruction. It is the most common cause of death in is commonly caused by myocardial infiltration, as in
athletes. 63
amyloidosis, sarcoidosis, fibrosis or cardiac metastases, or
88
may be idiopathic. Endomyocardial disease is more
Diagnosis common in tropical countries, but in the Western world,
Echocardiography will confirm the presence and pattern RCMs are the least common form of cardiomyopathy. 88
of hypertrophy and the presence (or absence) of an
outflow tract gradient. Examination findings include car- Diagnosis
diomegaly and pulmonary congestion. An S4 heart sound Clinically there is heart failure (increase in JVP, dyspnoea,
is common, and the ECG shows left ventricular hypertro- S3 and S4 heart sounds, and oedema), particularly right
phy and often ventricular arrhythmias. When the obstruc- ventricular, and infiltration of the conduction system may
tive form (HOCM) is present, a systolic murmur, mitral cause conduction defects and heart block. Low-voltage
regurgitation murmur and deep narrow Q waves on ECG, ECGs are commonly seen. Patients commonly present
88
may be present. The majority of patients are asymptom- with decreased exercise tolerance due to the impaired
atic and when they present to hospital it will be in severe ability to increase heart rate and cardiac output because of
symptoms of dyspnoea, angina and syncope. Angina is reduced ventricular filling. Restrictive cardiomyopathy
the result of an imbalance between oxygen supply and must be distinguished from constrictive pericarditis (which
demand due to the increased myocardial mass and not it may closely resemble), as pericarditis may be easily
due to atherosclerosis. managed. If echocardiography demonstrates a restrictive
88
pattern then a myocardial biopsy may be undertaken to
Management determine its aetiology, especially in the case of systemic
Treatment for HCM is aimed at the prevention of sudden infiltrative disease. 88
cardiac death and pharmacotherapy to increase diastolic
filling and to reduce the LVOTO. Pharmacotherapy Management
includes beta-adrenergic blocker or calcium channel There is no treatment for RCM so the aim of therapy is
blocker therapy, as these decrease contractility and lessen to relieve symptoms. This includes diuretics, corticoste-
outflow tract obstruction. Care is necessary with medica- roids and pacing. The use of nitrates should be done with
tion selection, as vasodilation may worsen obstruction, caution as the filling defect can be worsened by decreased
88
causing haemodynamics to suffer. The impact of atrial venous return or hypovolaemia. Generally, prognosis is
fibrillation, by worsening the ventricular filling defect, poor with many dying within 1–2 years of diagnosis. 92
can be dramatic in HCM patients and will require antiar-
rhythmics and anticoagulation. If ventricular arrhythmias HYPERTENSIVE EMERGENCIES
are present, or there is a family history of sudden cardiac
92
death, treatment with an ICD should be considered. For Acute, uncontrolled hypertension is often divided into
severely symptomatic patients or those worsening despite two categories: hypertensive emergencies and hyperten-
maximal drug treatment, surgical myectomy to reduce sive urgencies. In hypertensive emergencies blood pres-
the size of the septum and lessen obstruction may be sure needs to be reduced within one hour to prevent
necessary and can result in a marked improvement of end-organ damage, such as hypertensive encephalopathy,
93
92
symptoms. Septal ablation with alcohol injected into papilloedema or aortic dissection. Immediate blood
the first septal branch of the left anterior descending pressure reduction with IV agents under critical care moni-
artery is a less invasive alternative, a procedure that is toring is needed. By contrast, hypertensive urgencies are
usually undertaken with pacemaker insertion as AV block those in which end-organ damage is not occurring, and
is produced. Although surgical myectomy remains the although prompt management is required, this can be
gold standard, both treatments provide effective symptom approached more gradually with oral antihypertensive
92
relief and improvement in heart failure severity. If the agents under close supervision, without necessarily
Cardiovascular Alterations and Management 243
93
requiring admission to a critical care unit. Previous INFECTIVE ENDOCARDITIS
hypertension is not always present, but because of chronic
adaptive vascular changes may provide some level of pro- Infective endocarditis remains a potentially life-threatening
98
tection against acute tissue injury. Symptoms may not disorder, with mortality remaining as high as 20–25%
develop until the blood pressure exceeds 220/110 mmHg, even in this era of relative rheumatic fever control. This
whereas in patients without previous hypertension, same era, however, sees other means of developing endo-
hypertensive emergencies may occur at levels of even carditis, with factors such as longer life, IV drug use,
94
160/100 mmHg. When the diastolic pressure is persis- prosthetic valves, greater rates of cannulation during hos-
tently above 130 mmHg, there is risk of vascular damage pitalisation, cardiac surgery, resistant organisms, and
and must be treated. increased numbers of immunocompromised patients
from immunosuppressant drugs and HIV/AIDS. 99,100
Diagnosis Infection of the endocardium, often with involvement of
A thorough history is taken, including any hypertension the cardiac valves, occurs most commonly due to staphy-
management, known renal or cerebrovascular disease, lococcal, streptococcal and enterococcal bacteraemia. 99,100
eclampsia in previous pregnancies if gravid, or use of stim- The definition of infective endocarditis now also includes
ulants or illicit drugs such as cocaine. Patient assessment an infection of any structure within the heart such as
should include evidence of end-organ damage, such as prosthetic valves, implanted devices and chordae tendin-
101
back pain (aortic dissection), neurological damage: head- eae. Infective endocarditis can be acute or subacute.
ache, altered consciousness, confusion, visual loss, stupor Acute infective endocarditis progresses over days to weeks
or seizure activity (encephalopathy); cardiac damage: chest with destruction of valves and metastatic infection. Sub-
pain, ST segment changes, cardiac enlargement, or the acute infective endocarditis occurs over weeks to months
development of heart failure or pulmonary oedema; and and is milder than acute infective endocarditis. Endothe-
93
renal damage: oliguria and azotaemia. Serum urea, creati- lial damage occurs in the endocardium. Platelet-fibrin
nine, electrolytes, urinalysis, ECG and chest X-ray should deposits form and a lesion develops. Bacterial colonisa-
be performed. tion then occurs and vegetation adheres to the endocar-
dial lesion. Many of the signs and symptoms of infective
Management endocarditis are due to the immune response to the
microorganism. The patient presents with fever, and
More severe, or malignant, hypertension may cause retinal general features of febrile illness, which may include
haemorrhage or papilloedema, and emergency treatment septic shock. Joint pain is common and septic arthritis is
should immediately be instituted. Other contexts in sometimes seen. Cardiac symptoms develop when there
which there is a need for rapid treatment of severe hyper- is valvular involvement, which may manifest as erosion
tension include intracranial bleeding, acute myocardial through valve leaflets producing regurgitation, fusing of
infarction, phaeochromocytoma, recovery from cardiac valve leaflets or vegetations (outgrowths from valve struc-
surgery, and bleeding from vascular procedure sites. tures), producing valvular stenosis or regurgitation. The
100
Hypertensive emergencies in pregnancy threaten both the mitral valve is more commonly affected, but aortic valve
mother and the fetus. 95
98
involvement carries a worse prognosis. Conduction
The aim of treatment is to acutely lower the blood pres- system involvement manifests as arrhythmias and con-
sure, but neither too quickly nor too dramatically. duction defects. Embolic complications are relatively
Recommendations vary, but an initial aim of 150/110– common and multifactorial. Septic emboli, embolisation
160/100 mmHg within 2–6 hours, or a 25% reduction in of atrial thrombi when atrial fibrillation is present, and
mean arterial pressure within 2 hours, has been fragmentation of vegetations may all give rise to pulmo-
described. 96,97 Continuous direct arterial pressure moni- nary and systemic emboli. These most often present as
toring should be in place during treatment. Intravenous splenic infarction, stroke, peripheral vascular occlusion
sodium nitroprusside, a rapidly acting arterial and venous and renal failure. 98
dilator, is most frequently used, at doses of 0.25–10 µg/kg/
97
min. Weaning of nitroprusside is undertaken after the Diagnosis
later introduction of oral antihypertensives. Care is Diagnosis of infective endocarditis is based on the modi-
required to avoid hypotension during treatment, as well as fied Duke criteria. This is based on the presence of micro-
rebound hypertension as nitroprusside is withdrawn. organisms (identified in blood cultures), pathological
Rapidly acting beta-adrenergic blocking agents with short lesions (vegetation or abcess present), and clinical crite-
half-lives such as IV esmolol may be used at doses of 50– ria. The clinical criteria are based on two major criteria or
100 µg/kg/min (or higher) in patients without standard one major and three minor criteria or five minor criteria.
contraindications to beta-adrenergic blockers (asthma, Major clinical criteria are:
97
heart failure). Glyceryl trinitrate infusions at 10–100 µg/ ● positive blood culture
min or higher are used for combined venous and arterial ● evidence of endocardial involvement (positive echo-
97
dilation, especially if there is angina. Intravenous cardiography, abscess, partial dehiscence of a pros-
frusemide may be introduced during the acute phase. After thetic valve, or new valvular vegetation)
intravenous therapies have been established and progress
towards target pressures is made, oral agents are intro- Minor clinical criteria include:
duced. These include oral beta-adrenergic blockers, ● fever with body temperature ≥38°C
calcium channel blockers, ACE inhibitors and diuretics. ● predisposing heart condition or intravenous drug use
244 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
● vascular signs: arterial emboli, intracranial haemor- Artery
rhage, Janeway lesions (erythematous spots on the
palms and feet) or conjunctival haemorrhages
● immunological signs: Osler nodes (painful, red-
dened nodules on the fingers and the feet), or
glomerulonephritis 98
A
Echocardiography may reveal vegetations, abscess and Fusiform area
valvular abnormalities, but endocarditis is more a clinical Artery
diagnosis based on the appearance of febrile illness, posi-
tive blood cultures with organisms known to cause endo-
carditis, new murmur and vascular features.
Management
B Sacculated area
Prosthetic valve endocarditis must be aggressively
100
managed, as mortality may be as high as 65%. Impaired
valvular opening, even obstruction, may occur or the Torn intima
100
prosthetic valve may become unseated. Reoperation to False
replace the affected valve should be undertaken when Blood channel
valvular dysfunction is present. Antibiotic therapy is pro- flow created
vided empirically until blood culture and sensitivities are
established. Cardiac failure, if present, is managed along C
standard lines (see section on Nursing management of Ruptured area with
acute heart failure). Observations during endocarditis clot covering the
should be directed at detecting embolic complications opening
involving the brain, kidneys, or spleen; development and
progress of heart failure; progress of the febrile illness, Blood
flow
including hydration and dietary status.
D
Prophylactic antibiotic coverage should be undertaken
for at-risk patients 1 hour before dental procedures are to FIGURE 10.16 Aneurysm. Major types of aneurysm: (A) fusiform aneu-
be performed, in particular for those with previous rheu- rysm has an entire section of an artery dilated, occurring most often in the
101
matic fever or endocarditis, or prosthetic valves. Anti- abdominal aorta due to atherosclerosis; (B) sacculated aneurysm affects
biotic prophylaxis for genitourinary and gastrointestinal one side of an artery, usually in the ascending aorta; (C) dissecting aneu-
procedures is no longer recommended. 101 rysm results from a tear in the intima, causing blood to shunt between the
intima and media; (D) pseudoaneurysm usually results from arterial
trauma, such as intra-aortic balloon pump catheter or an arterial intro-
AORTIC ANEURYSM ducer; the opening does not heal properly and is covered by a clot that
106
can burst at any time.
The aorta is the major blood vessel leaving the heart. An
aneurysm is a local dilation or outpouching of a vessel
wall and comes in several forms (see Figure 10.16). Most into the left retroperitoneum which may contain the
aortic aneurysms are fusiform and saccular, and occur in rupture. However, the other 20% rupture into the perito-
102
the abdominal aorta. A fusiform aneurysm is uniform in neal cavity and uncontrolled haemorrhage results.
shape with symmetrical dilation that involves the whole Patients often experience no symptoms until the aneu-
102
circumference of the aorta. A saccular aneurysm has rysm is extensive or ruptures. Clinical presentation varies
dilation of part of the aortic wall so the dilation is very and depends on the location and expansion rate. Aneu-
102
localised. A dissecting aneurysm occurs when the layers rysms of the ascending aorta tend to affect the aortic root
of the wall of the aorta continue to separate and fill with and cause valve regurgitation. Expansion of the aneurysm
blood, resulting in obstructed blood flow. The aorta is may also compress the vena cavae, leading to engorged
particularly susceptible to aneurysm formation because neck and superficial veins, or compress the large airways,
of constant stress on the vessel wall and the absence of causing respiratory distress. The first symptom most
penetrating vasa vasorum that normally provide perfu- patients experience is pain, which may be steady and
sion to the adventitia. As the blood flows through the continuous from local compression or sudden and severe
aneurysm it becomes turbulent and some blood may in the case of dissection or rupture usually in the lower
stagnate along the walls allowing a thrombus to form. back. In this case, the pain is usually associated with
This thrombus in addition to atherosclerotic debris may syncope and is an acute emergency. Depending on the
embolise into the distal arteries compromising their cir- site of the aneurysm, there is usually an absence or
culation. Atherosclerosis is the commonest cause of aneu- decrease in the pulses below the site of the aneurysm,
rysm, because plaque formation erodes the vessel wall. most commonly in the limbs. The renal arteries may be
Other causes include syphilis, infection, inflammatory affected, resulting in decreased urine output and renal
diseases and trauma. Aneurysms occur most often in men failure. The spinal blood flow may also be affected, result-
and in people with the risk factors of hypertension or ing in paraplegia, and if the carotid arteries are affected
smoking. Approximately 80% of aortic aneurysms rupture there may be altered consciousness. Infrarenal aneurysms
Cardiovascular Alterations and Management 245
are the most common form of aortic aneurysms and are perfusion and maintain appropriate blood volume is also
located below the renal arteries. Bruits can also be heard essential. Finally, preparation for surgery is necessary, and
over the aneurysm. must include the patient and family.
Diagnosis VENTRICULAR ANEURYSM
A chest X-ray is usually the first investigation, and may Less than 5% of patients post-STEMI, particularly a
reveal a widened mediastinum or enlarged aortic knob. transmural anterior infarction, develop a left ventricular
Some aneurysms will be hidden, so normal chest X-ray aneurysm. Post-STEMI, dyskinetic or akinetic areas of
103
does not exclude the diagnosis. If available, a CT scan, the left ventricle are common and known as regional
using contrast dye, provides accurate information on the wall motion abnormalities. It is in these areas that
location and size of the aneurysm. Transoesophageal there is a risk of an aneurysm developing. Ventricular
echocardiography (TOE) provides an accurate diagnosis aneurysms are more likely to develop post anterior
and is the preferred investigation in dissecting aneurysms. STEMI with a totally occluded LAD with poor collateral
TOE can clearly identify the tear/flap, to enable classifica- circulation.
tion of the aneurysm. There are some limitations in
viewing the ascending aorta, and patients with respiratory Aneurysms form when the intraventricular tension
dysfunction may have difficulty with lying flat for the stretches the dyskinetic area and a thin weak layer of
procedure and having a light anaesthetic. necrotic muscle and fibrous tissue develops and bulges
with each contraction of the ventricle resulting in a reduc-
Management tion in stroke volume. Aneurysms range from 1–8 cm in
Management of asymptomatic aneurysms is conservative, diameter and are four times more likely to occur at the
unless the size of the aneurysm is >1.5 times the normal apex and anterior wall rather than the inferoposterior
103
102
size of the aortic segment or the situation is acute. The wall. Large ventricular aneurysms may result in a reduc-
primary aim is to lower hypertension and prevent increases tion in stroke volume causing an increase in myocardial
in thrombus size and emboli through the administration oxygen demand (MvO 2 ) resulting in angina and heart
of aspirin. Usually the patient has regular monitoring to failure. The mortality rate in people with ventricular aneu-
assess the aneurysm and to determine the timing and need rysms is four times higher than those with no aneurysm
for surgical repair. due to a higher risk of tachyarrhythmias and sudden
cardiac death. Unlike aortic aneurysms these aneurysms
Acute and dissecting aortic aneurysms are life-threatening rarely rupture so their management is usually conserva-
emergencies, and surgery is often the only option. The tive. Diagnosis of a ventricular aneurysm is by echocar-
development of new or worsening lower back pain may diography. Ventricular aneurysm should be considered
indicate impeding rupture and they may have a palpable when ST segment elevation persists beyond 1 week after
pulsatile abdominal mass. The faster treatment is initiated, myocardial infarction.
the higher the chances of survival with optimal recovery.
The primary goal is to control blood pressure. If hyperten- Management
sive, beta-adrenergic blockers or sodium nitroprusside are Management of a left ventricular aneurysm consists of
used to reduce further arterial wall stress. If the patient is aggressive management of STEMI and reperfusion therapy.
hypotensive, IV fluid and inotropes may be necessary. Long term anti-coagulation therapy with warfarin is
Nursing management of dissecting aortic aneurysm required. A complication of a ventricular aneurysm
involves the following: includes the development of an intraventricular thrombus
within the aneurysmal pocket which, if mobilised,
● support during the diagnostic phase; becomes arterial emboli. Also due to the high risk of
● assessment of pain and provision of analgesia; tachyarrhythmias, antiarrhythmic therapy is indicated. An
● stabilising and monitoring the clinical condition; ICD may also be necessary if antiarrhythmic therapy is
● providing psychological support to patient and family; unsuccessful in suppressing tachyarrhythmias. Surgical
and aneurysmectomy may also be required, if heart failure and
● preparation for surgery and long-term care. angina become severe, and is usually successful.
Assessment of the patient’s symptoms and effects of the SUMMARY
aneurysm is essential. This includes careful assessment and
recording of symptoms, including pain level and intensity, Compromise of the cardiovascular system, as either a
peripheral pulses, oxygen saturation levels, blood pressure primary or secondary condition, is a common problem
in both arms, and neurological symptoms to assist with that necessitates admission of patients to a critical care
diagnosis and detect progression. Intravenous analgesia is area. Prompt and appropriate assessment and treatment
essential to control the severe pain, and an antiemetic is is required to ensure adequate oxygen supply to the
useful to prevent opiate side effects. Opiates may also tissues throughout the body. The commonest cardiovas-
contribute to a sedative effect and slight vasodilation, cular problems experienced by patients include coronary
which are both beneficial. Oxygen therapy via mask should heart disease, arrhythmias and cardiogenic shock, however
be administered as indicated by oxygen saturation levels. heart failure, and selected conditions such as cardio-
Blood pressure control is vital, and usually IV medications myopathies, hypertensive emergencies, endocarditis and
are titrated to a narrow MAP range of 60–75 mmHg. Close aortic aneurysm also occur. Appropriate assessment
observation of fluid balance to detect changes in renal and management is essential to prevent secondary
246 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
complications arising. Important principles covered in ● Heart failure:
this chapter are summarised below. ● May affect either the left, right or both ventricles,
● Coronary heart disease: resulting in different symptoms being displayed by
● Incorporates myocardial ischaemia, angina and the patient.
acute coronary syndrome. ● Diagnosis is usually made on the basis of echo-
● Early patient assessment and diagnosis is essential cardiography, ECG, chest X-ray, full blood count,
electrolytes, liver function tests and urinalysis.
to facilitate prompt intervention. ● In acute heart failure, CPAP or BiPAP may be neces-
● Initial diagnosis is based on history, clinical assess- sary to improve hypoxaemia
ment, electrocardiographic and biochemical exam- ● Pharmacological therapy of acute heart failure con-
ination, with coronary angiography, exercise testing sists of: morphine, nitrates and diuretics. Positive
and chest radiography available to provide later inotropes may also be used such as IV dopamine
detail. and dobutamine to improve renal perfusion and
● Early restoration of blood flow – including reperfu- contractility
sion therapy and coronary angioplasty – to reduce ● Many patients with heart failure will also have a
myocardial damage is a core component of pacemaker with cardiac resynchronisation therapy
treatment. and/or a defibrillator to improve cardiac function
● Other goals of care include reducing plaque and and reduce the incidence of sudden death
clot formation in coronary arteries, reducing the ● Patient care must be lifelong and coordinated
workload of the heart, controlling symptoms, between all members of the healthcare team. Broad
providing psychosocial support to the patient interventions, including medications, diet and life-
and family, and educating the patient about the style modification, may be appropriate for some
disease process, lifestyle and future responses to patients, while palliative care might be more
illness. appropriate for other patients.
Case study
Mrs See is a 69-year-old woman who presented to the emergency had a slightly globular configuration. There was no evidence of a
department with intermittent chest pain. She presented to her pericardial effusion.
general practitioner (GP) two days ago complaining of chest pain
lasting 2–3 hours. An ECG was done showing old q waves anteriorly Within a short time her acute pulmonary oedema was stabilised
and ST depression V5 & V6. A troponin-I was done by her GP that and so she was considered for a primary PTCA. Coagulation profiles
was 0.16 µg/L. and a brief history of, and contraindications to, fibrinolytic treat-
ment were collected. Preparation for PTCA included locating,
Her past medical history included: smoker for the past 50 years of assessing and marking peripheral pulses in both right leg and right
10–20 cigarettes a day, diabetes mellitus type 2, infrarenal abdomi- arm. The coronary angiogram report stated: moderate to severe
nal aortic aneurysm, asthma/COPD, peripheral vascular disease, reduction in left ventricular function, ejection fraction 30%; intact
left internal carotid artery aneurysm, hypercholesterolaemia and left circumflex artery, intact left main coronary artery with minor
hypertension. Her medications consisted of: diamicron 60mg daily, irregularities (30%) in left anterior descending artery; and severe
glargine 26 units nocte, perindopril 5 mg daily, seretide and ven- localised 70–80% stenosis within the proximal third of the right
tolin puffers and lipitor 20 mg daily. coronary artery and collaterals from the left coronary artery. Her
right coronary artery was the dominant vessel. This stenosis was
Two days after visiting her GP, she presented to emergency depart- dilated by PTCA with resulting TIMI 3 flow, and a paclitaxel drug-
ment with further intermittent chest pain. Initial 12-lead ECG eluting stent was placed.
showed ST elevation in leads II, III and aVF. She was also feeling
tired and nauseated at times. She denied any chest pain. She was Post-PTCA, Mrs See was admitted to CCU with oxygen via mask,
afebrile, BP 143/96, pulse 120 bpm and regular, respiratory rate PTCA access site and sheath in her right groin. Her observations
33 bpm, and O 2 sat 93% on room air. Her respirations were laboured included: BP 100/60 mmHg, HR 80 beats/min, RR 20/min. She was
and her skin was cool and clammy. On chest auscultation there free of pain. Her ECG was normal except for T inversion in lead III
were bibasal crackles to midzones. Her jugular venous pressure with a generalised widened QRS (200 msecs). Post PTCA she expe-
was +6 and peripheral oedema to mid calves. She had dual heart rienced short runs of ventricular tachycardia. These were initially
sounds (S1S2) and a third heart sound (S3). Blood test results: thought to be due to reperfusion arrhythmias. However, the short
U&E-Na 134 mmol/L, K 5.1 mmol/L, urea 5.2 mmol/l, creatinine intermittent runs of ventricular tachycardia continued. Her blood
86 µmol/L, ctroponin-I 2.0 µg/L, CK 590 U/L and random glucose test results were: Na 137 mmol/L, K 4.6 mmol/L, urea 8.8 mmol/L,
10.6 mmol/L. Her FBE and LFTs were normal. Fast-track treatment creatinine 99 μmol/L, calcium 2.37 mmol/L, magnesium
was commenced, including administering aspirin 300 mg orally, 0.96 mmol/L. Fasting cholesterol profile: total cholesterol
oxygen via face mask, glyceryl trinitrate patch, morphine 2.5 mg 4.3 mmol/L, HDL-C 1.91 mmol/L, LDL-C 2.1 mmol/L, triglycerides
IV, metoclopramide 10 mg IV and frusemide 40 mg IV. Chest X-ray 0.7 mmol/L, cholesterol/HDL-C 2.3 mmol/L. Her liver function and
showed horizontal linear interstitial opacities at both bases, which full blood examination tests were normal. She was commenced on
were not present on a previous X-ray taken six months ago, which an intravenous amiodarone infusion and considered for an ICD
was consistent with the clinical impression of pulmonary oedema. with CRT, in light of her newly diagnosed heart failure (evident on
There was also a marked increase in size of the heart which also coronary angiogram) and NYHA class III symptoms.
Case study, Continued
Post-ICD-implantation, her hospital stay was uneventful. Her fluids 5 mg daily, perindopril 5 mg daily, spironolactone 25 mg daily,
were restricted to 1.5 L/day, weighed daily, commenced a beta- co-plavix 100/75 mg daily, spirivia 18mcg daily, seretide 250/25 mg
adrenergic blocking agent and diuretic and provided with educa- BD, lantus 36 units nocte, amiodarone 200 mg BD, gliclazide MR 60
tion concerning heart failure and coronary artery disease. Her mg mane, frusemide 80 mg mane and midi, and GTN spray. She
husband was also included in the education sessions. She was was also referred to a heart failure management program and a
transferred from CCU to the ward and then a few days later dis- cardiac rehabilitation program.
charged home. On discharge her medications were: bisoprolol
Research vignette
Body R, Carley S, Wibberley C, McDowell G, Ferguson J, Mackway- the preceding 24 hours presenting to the ED, excluding other
Jones K. The value of symptoms and signs in the emergent diagnosis primary presenting diagnoses, chest trauma, pregnant women and
of acute coronary syndromes. Resuscitation. 2010; 81(3): 281–6. people with insufficient English to consent. ED doctors used a spe-
Abstract cifically designed yes/no checklist of 21 signs and symptoms on
Objective first assessment and prior to troponin-T testing and were therefore
Patient history and physical examination are widely accepted as blinded to the results. Patients received all usual care and were
cornerstones of diagnosis in modern medicine. This research followed up at 48 hours, 30 days and 6 months, with no patients
aimed to assess the value of individual historical and examination lost to follow-up. Adverse events included death, AMI or the need
findings for diagnosing acute myocardial infarction (AMI) and pre- for urgent revascularisation and AMI was determined by troponin-t
dicting adverse cardiac events in undifferentiated Emergency levels. Interobserver reliability of the checklist was also assessed in
Department (ED) patients with chest pain. 44 cases by two ED doctors and near-perfect agreement occurred
for pain being previously diagnosed as ischaemic, ischaemic ECG
Methods features, sweating observed and rest pain whereas only slight
Patients were prospectively recruited patients presenting to the ED agreement occurred for pain character dull, any radiation, reported
with suspected cardiac chest pain. Clinical features were recorded sweating and paraesthesia.
using a custom-designed report form. All patients were followed-up
for the diagnosis of AMI and the occurrence of adverse events Of the 796 patients eligible and recruited in the study, 18.6% had
(death, AMI or urgent revascularisation) within 6 months. AMI during the index admission and 22.9% went on to have an
adverse event during follow-up. After adjusting for age, gender
Results
AMI was diagnosed in 148 (18.6%) of the 796 patients recruited. and presence of ischaemic ECG changes, the odds of an AMI diag-
Following adjustment for age, sex and ECG changes, the following nosis were increased significantly for central pain, pain duration of
characteristics made AMI more likely (adjusted odds ratio, 95% more than 1 hour, radiates to right and both shoulders/arms,
confidence intervals): pain radiating to the right arm (2.23, 1.24–4), reported vomiting and observed sweating. Importantly, several of
both arms (2.69, 1.36–5.36), vomiting (3.50, 1.81–6.77), central the symptoms identified in the international guidelines, neck and
chest pain (3.29, 1.94–5.61) and sweating observed (5.18, 3.02– arm pain and symptoms occurring at rest, were not useful includ-
8.86). Pain in the left anterior chest made AMI significantly less ing pain radiating to the left side of the chest, which actually
likely (0.25, 0.14–0.46). The presence of rest pain (0.67, 0.41–1.10) reduced the odds of having an AMI diagnosis. Of the significant
or pain radiating to the left arm (1.36, 0.89–2.09) did not signifi- predictors identified above, by far the strongest positive predictors
cantly alter the probability of AMI. of AMI were observed sweating, reported vomiting and hypoten-
sion. In terms of adverse events within 6 months follow-up the
Conclusions results were very similar with the addition of worsening angina and
The results challenge many widely held assertions about the value hypotension as significant predictors with hypotension, reported
of individual symptoms and signs in ED patients with suspected vomiting and pain radiating to both arms the strongest positive
acute coronary syndromes. Several ‘atypical’ symptoms actually predictors.
render AMI more likely, whereas many ‘typical’ symptoms that are
often considered to identify high-risk populations have no diag- Several limitations are relevant to the study including the single
nostic value. site and lack of inclusion of people who were unable to speak
Critique English. The latter may most limit generalisability as the authors
This study investigated the relative importance of the patients’ note that symptoms have been noted to vary between different
history and examination in diagnosing AMI and predicting adverse ethnicities. Furthermore symptoms could only have a yes/no
cardiac events in the following six months in patients presenting response when clinicians may be most influenced by the intensity
to the ED with chest pain. While international guidelines recom- of the individual symptom. Regardless, the results challenge clini-
mend that these factors, in particular the presence of central chest cians to reconsider the value of so-called typical versus atypical
pain radiating to the left side of the chest, neck and arm, or symp- symptoms and that associated symptoms such as vomiting and
toms occurring at rest, are included in determination of diagnosis sweating may be far more important to consider. In this respect as
there has been little recent research to determine their value. nurses are closely involved in triage, history and examination of
patients with chest pain both in ED and other critical care environ-
The study was performed at single hospital in the UK and enrolled ments, nurses must be encouraged to consider an array of symp-
patients over 25 years of age with suspected cardiac chest pain in toms and undertake careful assessments.
248 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
Learning activities
1. Discuss the various categories included under the umbrella 7. Discuss the compensatory mechanisms that are activated in
‘acute coronary syndrome’, including their identifying and dif- heart failure and their effect on the cardiovascular system.
ferentiating features. 8. Why did the patient in the case study meet the criteria for
2. Differentiate common versus prognostic symptoms of acute implantation of an ICD with CRT?
coronary syndrome. 9. In the case study, when the patient was discharged from hos-
3. Describe the nursing care for a patient undergoing primary pital, why were they prescribed perindopril, bisoprolol, spi-
PTCA. ronolactone and frusemide? Include in your answer the reason
4. Identify the common complications of myocardial infarction in for prescribing these medications and their actions and major
the early recovery period. side effect.
5. Why is silent ischaemia more common in patients with CHD 10. Observe an echocardiograph and ask the sonographer to
and diabetes? explain what is visualised on the screen, particularly in Doppler
6. In the case study, what is the significance of an S3 heart sound mode. Ask them to identify areas of hypokinesis or akinesis and
in the clinical setting of heart failure? any evidence of dyssynchrony between the ventricles.
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National Heart Foundation of Australia, <www.heartfoundation.com.au> 18. Moser D, Riegel B. Care of patients with acute coronary syndrome: ST-segment
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Cardiac Rhythm Assessment
and Management 11
Malcolm Dennis
David Glanville
Learning objectives Key words
After reading this chapter, you should be able to: arrhythmia
● describe the various arrhythmogenic mechanisms sinoatrial
implicated in the development and propogation of cardiac atrial
arrhythmias atrioventricular
● recognise the features of the various commonly observed junctional
arrhythmias and discuss the aetiological factors that ventricular
predispose to the development of each bradycardia
● discuss the actual or potential haemodynamic tachycardia
consequences and prognostic implications of each of the anti-arrhythmic
commonly observed arrhythmia types
● describe the general and specific assessment and treatment pacemaker
strategies applicable to each of the various arrhythmia threshold
types failure to sense
● discuss the principles and indications for pacemaker failure to capture
therapy failure to pace
● recognise abnormal pacemaker activity on ECG and discuss oversensing
the causes and corrective actions for complications during implantable cardioverter defibrillator
temporary pacing antitachycardia pacing
● describe the principles and benefits of cardiac cardiac resynchronisation therapy
resynchronisation therapy (CRT), including the factors ablation
which limit the effectiveness of the therapy cardioversion
● discuss the principles and indications for treatment of
arrhythmias including ablation therapies, permanent
pacing, cardioverter defibrillators, cardioversion and
defibrillation.
compromising arrhythmias is effectively the same as the
outcomes of shock from other aetiologies, and includes
reduced oxygen delivery and consumption, increased
INTRODUCTION oxygen extraction and lactic acidosis. This chapter
describes the major arrhythmias encountered in critical
Many critically ill patients experience cardiac arrhyth- care, their causes, ECG features, impact and management.
mias. These typically compromise cardiovascular perfor- Electrical therapies (temporary pacing, permanent pacing,
mance to a greater or lesser extent and may be temporary, implantable cardioverter defibrillator therapies, arrhyth-
recurrent, or permanent. Symptomatic impact ranges mia ablation procedures and external cardioversion) are
from lethargy, exercise intolerance, dyspnoea, lighthe- described, along with their electrocardiographic and
adedness and palpitations, to marked haemodynamic clinical assessments and patient management.
instability and syncope. Brady-asystolic arrhythmias and
tachyarrhythmias may present as, or progress to, cardiac THE CARDIAC CONDUCTION SYSTEM
arrest. Physiological effects of tachyarrhythmias include
increased myocardial oxygen demand at the same time The normal heartbeat sequence occurs through rhythmic
that reduced oxygen delivery is occurring, with scope for stimulation of the heart via its specialised conduction
resultant myocardial ischaemia. The metabolic impact of system. The sinoatrial node, located superiorly in the 251
252 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
right atrium, spontaneously generates an activation dispersion). Slow conduction through a region of the
current that conducts across preferential right and left heart may allow enough time for other tissues which have
atrial pathways (producing a P wave on the surface ECG) already been depolarised to recover, and then to be
and then to the atrioventricular node at the lower inter- re-excited by the arrival of the slowly-conducting wave-
atrial septum. After a brief physiological slowing of the front. Once this pattern of out-of-phase conduction and
current (to allow the ventricles to be optimally ‘pre- repolarisation is established, a current may continue to
loaded’), the impulse travels to the Bundle of His in the circulate back and forth between adjacent areas, or around
upper interventricular septum before spreading down a re-entry circuit. Each ‘lap’ of the circuit gives rise to
4,6
through the ventricles via the right and left bundle another depolarisation (P wave or QRS complex). The
branches. These terminate distally as branching Purkinje ultimate rate of the tachycardia depends on the size of
fibres which penetrate and activate the ventricles. This the circuit (micro versus macro reentry) and the conduc-
ventricular activation (or depolarisation) sequence pro- tion velocity around the circuit.
duces a QRS complex on the surface ECG and subsequent
repolarisation gives rise to an electrocardiographic T ARRHYTHMIAS AND ARRHYTHMIA
wave. Pathophysiological processes may disrupt this MANAGEMENT
sequence, giving rise to arrhythmia production. 1,2
Arrhythmias may arise from myocardial or conduction
ARRHYTHMOGENIC MECHANISMS system tissue, and may represent inappropriate excitation
Arrhythmias result from three primary electrophysiologi- or depression of automaticity, altered refractoriness
cal mechanisms; abnormal automaticity, triggered activ- resulting in micro-reentry arrhythmias, or may involve
ity and reentry, each of which is described below. reentry on a larger scale, as between the atria, AV node
and/or ventricles. 3
Abnormal Automaticity The clinical impact of tachyarrhythmias is highly variable
and is influenced by the rate and duration of the
The action potential of sinus and atrioventricular con-
ducting tissue differs from that of the myocardium in that arrhythmia, the site of origin (ventricular vs supraven-
phase 4 of their action potentials are less stable and tricular), and the presence or absence of underlying
possess the property of spontaneous automaticity and cardiac disease. As a result, arrhythmias may require no
consequent depolarisation. This is an important property treatment, at least in the short term, or at worst may
that allows these tissues to assume the role of electro- present as cardiac arrest and require treatment according
physiological pacemaker dominance. However, in some to advanced life support algorithms (as described in
circumstances, such as myocardial ischaemia or cardio- Chapter 24).
stimulatory influences, regional levels of spontaneous Bradyarrhythmias may be due to failure of sinus node
automaticity can be abnormally accelerated, stimulating discharge (sinus bradycardia, pause, arrest, or exit block)
subsidiary pacing cells (such as those within the AV or to failure of AV conduction (second- or third-degree
junction and ventricular Purkinje fibres) to override the AV block). In any of these contexts, junctional or ventricu-
normal sinus rate. 3,4 lar escape rhythms may make their appearance. Failure
of escape foci may result in asystole or ventricular
Triggered Activity standstill.
Arrhythmias may occur through the occurrence of abnor-
mal oscillations within the early and late repolarisation ARRHYTHMIAS OF THE SINOATRIAL
stages of the cardiac action potential that lead to the NODE AND ATRIA
propagation of aberrant ‘triggered’ arrhythmic events. In health, the sinus node controls the heart rate according
Such oscillations are classified as either ‘early after depo- to metabolic demand, responding to autonomic, adrenal
larisations’ that occur during phases 2 and 3 of the action and other inputs, which vary according to exertion or
potential or late after depolarisations, which occur during other stressors. In response to needs, the sinus node
phase 4. Digitalis toxicity, ischaemia, hypokalaemia, discharge rate typically varies from as low as 50 beats/min
hypomagnesaemia and elevated catecholamine levels are to as high as 160 beats/min. In the conditioned heart
5
the more common causes of triggered activity. Excessive (e.g. in athletes), this range extends perhaps down to as
prolongation of the action potential duration enhances low as 40 beats/min, and to as high as 180 beats/min.
the risk of such triggered activity and as such these mech- Peak activity in the elite athlete may even achieve sinus
anisms are implicated in the development of certain rates of 200/min, though this represents the extreme end
subtypes of ventricular tachyarrhythmias, in particular of the sinus rate. Sinus rhythm is illustrated in Figure 11.1.
torsade de pointes (refer to description later in this
chapter). Sinus Tachycardia
In adults, a sinus rate of greater than 100/min is termed
Reentry sinus tachycardia and may occur with normal exertion
7,8
The most common cause of tachyarrhythmias is reentry, (see Figure 11.2). When sinus tachycardia occurs in the
in which current can continue to circulate through patient at rest, reasons other than exertion must be sought
the heart because of different rates of conduction and and include compensatory responses to stress, hypoten-
repolarisation in different areas of the heart (temporal sion, hypoxaemia, hypoglycaemia or pain, in which there
Cardiac Rhythm Assessment and Management 253
FIGURE 11.1 Sinus rhythm, rate 78/min. All P waves are followed by QRS complexes of normal duration after a P-R interval of around 0.16 sec.
FIGURE 11.2 Sinus tachycardia. The rhythm is slightly irregular and varies between 105/min and 115/min.
FIGURE 11.3 Sinus bradycardia. The rhythm is regular and at a rate of 50/min. Borderline first-degree AV block: the P-R interval is 0.20 sec.
is increased neurohormonal drive. Many drugs such as accompanies beta-blocker, antiarrhythmic or calcium
9
inotropes and sympathomimetics also accelerate the channel blocker treatment. Treatment of sinus bradycar-
sinus rate. Sinus tachycardia should therefore be regarded dia reflects the treatment of AV block and is covered
as a response to a physiological stimulus rather than an below under the management of atrioventricular block.
arrhythmia arising from sinus node dysfunction. Treat-
ment is directed at the trigger for the tachycardia, not the Sinus Arrhythmia
tachycardia itself. As sinus tachycardia may point to covert When the rhythm is clearly sinus in origin but is irregular,
events such as internal bleeding or pulmonary embolism, then the term sinus arrhythmia may be used (see Figure
there should be thorough investigation for unexplained, 11.4). Generally, a gradual rise and fall in rate can be
persistent sinus tachycardia. appreciated in synchrony with respiration. The gradual
rise and fall in rate is important: it distinguishes sinus
Sinus Bradycardia arrhythmia from the abrupt prematurity with which atrial
A sinus rate of less than 60 beats/min is termed sinus ectopic beats make their appearance, or the abrupt
7,8
bradycardia (see Figure 11.3). In general terms the slowing of the sinus rate seen in sinus pause and sinus
slower the rate, the more likely it is to produce symptoms arrest. Sinus arrhythmia may accompany sinus node dys-
related to low cardiac output. Slowing of the rate to less function but is seen also in the normal heart. Of itself,
than 50/min is commonplace during sleep, especially sinus arrhythmia does not require treatment.
in the athletic heart, but is otherwise uncommon. Brady-
cardia may accompany myocardial ischaemia (especially Sinus Pause and Sinus Arrest
when due to right coronary artery disease), conduction Abrupt interruption to the sinus discharge rate has
system disease, hypoxaemia, and vagal stimulation spawned a variety of descriptive terms, based partly
(e.g. nausea, vomiting, or painful procedures). It also on physiology and partly on severity. Sinus pause is
254 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 11.4 Sinus arrhythmia with marked rate variation in synchrony with respiration. The rhythm is clearly sinus but is irregular, accelerating from
75 to 120/min before slowing back to 75/min by the end of the strip.
N N N M N
FIGURE 11.5 Sinus pause and sinus arrest. Sinus rhythm at 60/min followed by an abrupt rate drop. Using 3 sec as a cut off between sinus pause and
sinus arrest, the first long interval of 2.5 sec would qualify as sinus pause whereas the next interval (3.2 sec) would be classified as sinus arrest.
FIGURE 11.6 Sinus exit block. An abrupt rate drop follows the first three sinus beats. As the P-P interval spanning the pause is exactly twice the P-P interval
of the preceding beats, the pause here could be due to sinus exit block. It could equally simply be a sinus pause.
self-descriptive: during a period of sinus rhythm, there occasion the electrocardiographic distinction between
is a sudden pause during which the sinus node does atrial flutter, atrial tachycardia and atrioventricular nodal
9
not fire. The heart rate abruptly drops, during which reentry tachycardia may be difficult to make, and it
time there may be bradycardic symptoms. Sinus arrest may be useful in that context to use the more general
tends to be used as a descriptor when the sinus pause is term SVT. Supraventricular arrhythmias may occur as
longer rather than shorter (usually above 3 seconds) single-beat ectopics arising from atrial or junctional
(see Figure 11.5). The longer the period of sinus arrest, tissue, or runs of consecutive premature beats, and
the greater the likelihood of symptoms, and syncope is thus be termed supraventricular tachycardias. SVTs
9
possible. Sinus pause may be indistinguishable from may be self-limiting (paroxysmal) or sustained (until
sinus exit block (in which there is sinus discharge that treatment), recurrent or incessant (sustained despite
fails to excite the atria), as both result in missing P waves. treatment).
The distinction is academic, however, as both arrhyth-
mias arise from the same groups of causes, and are sig- Atrial Ectopy
nificant only when they cause symptomatic bradycardia. Impulses arising from atrial sites away from the sinus
Pauses in which the P–P intervals spanning the pause are node (atrial foci) conduct through the atria in different
multiples of the pre-pause P-P interval favour the diagno- patterns to sinus beats, and so give rise to P waves of dif-
5
sis of exit block (Figure 11.6). Recurrent syncopal pauses ferent morphologies. These altered P waves define atrial
may require acute responses for symptomatic bradyar- ectopy, and their prematurity, or faster discharge rate, sees
rhythmias (see AV block treatment below). If episodes them more completely described as premature atrial
continue, consideration should be given to permanent beats. A characteristic P wave morphology cannot be pro-
pacemaker implantation.
vided, as ectopy may arise anywhere within the atria,
ARRHYTHMIAS OF THE ATRIA AND causing upright, inverted or biphasic P waves. Ectopic P
waves are often so premature that they become hidden
ATRIOVENTRICULAR NODE within the preceding T wave. At such times evidence of
The term supraventricular tachycardia (SVT) is often their presence can be concluded only because they deform
used to group the tachyarrhythmias which arise from the T wave, and because premature QRS complexes of
tissues above the ventricles. In its more common usage, normal morphology follow, suggesting a supraventricular
SVT is thus an umbrella term, to include any of the origin of those beats. Premature atrial beats most com-
tachyarrhythmias arising from the sinus node, the atrial monly conduct normally, although they may conduct
10
tissue or the atrioventricular node. However, when a aberrantly, or not at all, depending on their degree of
specific arrhythmia can be classified, the specific term prematurity and the state of AV nodal and intraventricular
is used rather than the more general term SVT. On conduction (see Figure 11.7).
Cardiac Rhythm Assessment and Management 255
FIGURE 11.7 Sinus rhythm with frequent atrial ectopics. The notched P waves at a rate of 75–80/min are the Ps of the dominant sinus rhythm, while the
more rapidly firing P waves with peaked configurations are the atrial ectopic beats. Note that the ectopic P waves have some variability in their shapes
and firing rate. They should therefore be described as multifocal atrial ectopics.
FIGURE 11.8 Atrial tachycardia. In this narrow complex tachycardia the rhythm is very regular and the rate close to 210/min. It is not possible to clearly
identify P waves within the T waves.
FIGURE 11.9 Multifocal atrial tachycardia. After 3 beats of sinus rhythm, the rate abruptly rises during a paroxysm of multifocal atrial tachycardia, which
spontaneously reverts. The resultant tachycardia is irregular, and P waves of varying shapes can sometimes be clearly seen while others can be gleaned
only by the deformity of T waves.
Atrial Tachycardia AV Conduction During Supraventricular
A rapidly firing atrial focus or (more commonly) the pres- Tachyarrhythmias
ence of an atrial reentry circuit may give rise to a rapid The rapid atrial rates associated with some atrial arrhyth-
rate, which is termed atrial tachycardia. Rates range from mias exceed the conduction capability of the AV node,
140–230 beats/min and the rhythm is typically very with the result that not all of the atrial impulses can be
5
regular. P waves may be difficult to identify, as they conducted (see Figures 11.10 and 11.11). This usually
become hidden in T waves. At such times, the presence occurs when the atrial rate exceeds 200/min. Thus during
of narrow QRS complexes, confirming supraventricular atrial flutter, or rapid atrial tachycardia, it is common to
conduction, aid diagnosis and discrimination from ven- see 2 : 1 block or greater. During atrial fibrillation the
tricular tachycardia. Distinction from other supraventric- ventricular response rate rarely exceeds 170/min.
ular arrhythmias may rely on the absence of characteristic
features of other SVTs (e.g. the sawtooth baseline of Atrial Flutter
flutter, the irregularity of fibrillation, or the pseudo-R Atrial flutter is a rapid, organised atrial tachyarrhythmia
waves and onset pattern of atrioventricular nodal reentry (see Figure 11.11). The atrial rate may be anywhere
tachycardia). When the atrial rate exceeds the conduction between 240 and 430/min, but most commonly the rate
capability of the AV node, varying degrees of AV block is close to 300/min. At these rates the atrial depolarisa-
9
occur. Atrial tachycardia may be paroxysmal, sustained or tion waves (flutter waves) run together to produce the
incessant (see Figure 11.8). Symptoms vary and are partly characteristic ECG feature of this arrhythmia: the so-called
dependent on the rate of the arrhythmia, and the pres- ‘sawtooth’ baseline, because of its resemblance to the
ence or absence of myocardial dysfunction. teeth of a saw. This sawtooth baseline is generally best
shown in the inferior leads. By contrast, in lead V1 the
Multifocal Atrial Tachycardia flutter waves usually appear more like discrete P waves,
When multiple atrial sites participate in generating atrial whilst in leads I and aVL, it may appear more like fibril-
ectopic beats at a rapid rate, the term multifocal atrial latory waves. The atrial rate of close to 300/min rarely
tachycardia is used (see Figure 11.9). The different foci conducts on a 1 : 1 basis to the ventricles. Rather 2 : 1, 3 : 1,
produce P waves of varying morphology, and typically the 4 : 1 or variable levels of AV block intervene to limit the
9
strict regularity seen during atrial tachycardia is lost. ventricular response rate, often to between 75 and 150/
9
Multifocal atrial tachycardia in particular complicates min. When the AV block is variable, beats at 3 : 1, 4 : 1 or
chronic obstructive pulmonary disease (COPD), as well other ratios are seen together in a single strip. When there
as other pulmonary diseases as part of the cor pulmonale is 2 : 1 block, the flutter waves are often concealed within
spectrum. 11 the QRS and/or T wave, and so definite identification may
256 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 11.10 Atrial tachycardia with high-degree block (many consecutive P waves do not conduct). The atrial rate is around 190/min, but because there
is variable AV block (3 : 1 to 4 : 1) the resultant ventricular rate is between 50 and 60/min. This patient had digitalis toxicity.
FIGURE 11.11 Atrial flutter with variable block. Note the sawtooth baseline, which characterises atrial flutter. The atrial rate is regular and is a little faster
than 300/min, while the ventricular rate is irregular because of the variable block. At times the ventricular rate is close to 150/min (when there is 2 : 1 block)
and at other times close to 100/min (when there is 3 : 1 block).
FIGURE 11.12 A narrow complex tachycardia at a rate of 150/min in the top strip could be any number of supraventricular rhythms, among them atrial
flutter with 2 : 1 block. Administration of IV adenosine produces momentary high-degree AV block (middle ⅔ of the lower strip), during which flutter waves
at a rate of 300/min become apparent. Carotid sinus massage or other vagal manoeuvres may produce the same diagnostic impact via transient AV block.
be difficult (see Figure 11.12). At such times, the presence
of a narrow QRS tachycardia at a fixed rate close to 150/ Atrial Fibrillation
min is particularly suggestive of atrial flutter with 2 : 1 Atrial fibrillation is a chaotic atrial rhythm in which
block. The tendency for flutter waves to appear as discrete multiple separate foci either discharge rapidly or par-
P waves in lead V1 may also be useful, as they may be ticipate in reentry circuits, resulting in rapid and irregular
more easily visualised in this lead. Vagal manoeuvres, or depolarisations that are not able to gain complete
7,9
adenosine administration, may increase the degree of control of the atria. Discrete P waves (representing
block and so reveal the flutter waves (Figure 11.12). 7,8 the coordinated depolarisation of the atria) are therefore
Cardiac Rhythm Assessment and Management 257
FIGURE 11.13 Atrial fibrillation with a rapid (uncontrolled) ventricular response. The rate is around 170/min and the rhythm clearly irregular. Because of
the rapid rate there is little opportunity to identify the fibrillatory baseline, but enough can be seen for confirmation.
not seen; rather there is a continuous undulation of Atrioventricular Nodal Reentry Tachycardia
the ECG baseline (fibrillatory waves at a rate between Atrioventricular Nodal Reentry Tachycardia (AVNRT) is
300 and 500/min), reflecting the continuous erratic the most common type of paroxysmal supraventricular
electrical activity within the atria. This erratic, uncoor- tachycardia (PSVT), accounting for greater than 50% of
dinated electrical activity results in uncoordinated cases of PSVT. (Note that PSVT as used here does not
5
contraction, and the atria can be seen not so much include atrial flutter or fibrillation). AVNRT is more
to contract but to quiver continuously. It is this quiv- common in women (75% of cases), more often in
ering (fibrillatory) motion that gives atrial fibrillation younger than older patients, and in some individuals
its name.
there is an identifiable link to stress, anxiety or stimu-
The irregularity of the atrial rate results in an irregular lants. As the name suggests the arrhythmia arises because
arrival of impulses at the AV node and, as a result, con- of reentry involving the AV node. Normally, atrial
duction to the ventricles at irregular intervals. Thus, a impulses reach the AV node via both slow and fast AV
7
hallmark of atrial fibrillation is the marked irregularity nodal pathways which link the atria to the AV node
of the ventricular rhythm. The ventricular response rate proper. The resultant PR interval is <0.20 sec. In AVNRT,
to the rapid atrial rate is determined by the state of AV the trigger mechanism is a premature atrial ectopic which
nodal conduction, and in patients with normal AV con- is blocked by the fast pathway because of refractoriness.
duction is often in the range of 140–180/min (rapid or Conduction into the AV node and to the ventricles is still
uncontrolled atrial fibrillation) (see Figure 11.13). Alter- possible by the slow AV nodal pathway, but the resultant
natively, when AV conduction is impaired, or limited by PR interval will be quite long (AV delay plus slow conduc-
drug effect, slower ventricular rates are seen. When atrial tion into the AV node). Following this atrial ectopic with
fibrillation is accompanied by a ventricular rate less than its long PR interval is the onset of the tachycardia. 13
100/min, it may be termed slow (or controlled) atrial
fibrillation. Atrial fibrillation is a common significant The tachycardia develops because the initiating impulse,
arrhythmia and, while not usually immediately life- the atrial ectopic, is delayed in reaching the AV node.
12
threatening, it contributes significantly to morbidity, Once it does reach the AV node it conducts to the ven-
especially in patients with existing cardiac failure. The tricles, but also now finds the previously refractory fast
loss of organised atrial contraction (atrial kick) as well pathway recovered and able to conduct retrogradely back
as rapid rates deprive the ventricles of adequate filling, to the atria. There is now a functional circuit for reentry
and so hypotension and low cardiac output may result. between the atria and the AV node. Impulses conduct
Consequent pooling of blood in the atria enhances the slowly into the AV node, lengthening the PR interval, but
risk of emboli formation and stroke. In addition, the on reaching the AV node conduct just as quickly to atria
incomplete atrial emptying results in congestion of first as to the ventricles. As a result, the P waves appear at
13
the atria and then the pulmonary circulation, and con- much the same time as the QRS. In some instances of
tributes to dyspnoea, increased work of breathing, and AVNRT it is not possible to identify P waves at all because
hypoxaemia. Patients with left ventricular failure rely they are hidden within the QRS. Often, however, the P
more heavily on atrial kick, and so symptoms and the waves can be seen distorting the final part of the QRS
severity of their heart failure typically worsen during atrial complex, appearing as small R waves in V1 and small S
fibrillation. At times, atrial fibrillation is debilitating in waves in lead II. Because they are P waves rather than part
this group, and shock and/or acute pulmonary oedema of the QRS, the ECG appearance has been dubbed ‘pseudo
13
may develop. R waves’ in V1 and ‘pseudo-S waves’ in lead II
(Figure 11.14). AVNRT is typically regular, and most com-
Antiarrhythmic therapy aims at reverting atrial fibrilla- monly at rates between 170 and 240/min but may be
tion, or to limiting the ventricular rate (rate control) even slower. The QRS is narrow unless there is concommitant
12
if fibrillation is persistent. For patients with chronic bundle branch block. AVNRTs sometimes respond well
atrial fibrillation in whom adequate rate control cannot to vagal manoeuvres, including coughing, bearing down,
be achieved pharmacologically, it is sometimes necessary and carotid sinus massage. Adenosine may interrupt
to perform radiofrequency ablation of the AV node itself. the arrhythmia, and other AV blocking drugs or antiar-
Permanent pacemaker implantation is therefore also rhythmics may be necessary to prevent recurrence. Elec-
necessary. tive cardioversion is sometimes necessary, and if the
258 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
N N N N S S S S
FIGURE 11.14 Atrioventricular Nodal Reentry Tachycardia. Lead V1. There is sinus rhythm initially. A premature atrial ectopic (arrow) conducts with a long
PR interval (0.36 sec), initiating onset of AVNRT at a rate of 140/min. Note the P waves during the tachycardia can be seen distorting the end of the QRS
(the ‘pseudo R wave in V1’ of AVNRT) which is not present before the tachycardia. Note also the monitor designations above each beat: N = normal, S =
supraventricular.
arrhythmia is chronically troublesome, slow pathway ● increased parasympathetic activity: vagal stimu-
ablation may be undertaken. 5,13 lation such as nausea, vomiting, carotid sinus
pressure, increased abdominal pressure, femoral
Nursing Management of Atrial Arrhythmias manipulation.
General symptoms of atrial tachyarrhythmias include: In the absence of stimulation by the SA node, other
palpitations, dyspnoea/tachypnoea, fullness in the throat/ tissues within the conduction system and myocardium
neck, fatigue, lightheadedness, syncope, chest pain and can generate cardiac rhythms at rates slower than the
angina symptoms and nausea and/or vomiting. Manage- normal sinus rate. Thus sinus node failure need not
ment of atrial tachyarrhythmias includes: (a) searching severely compromise the patient, as the inherent auto-
for and correction of the cause; (b) rate control limiting maticity of the AV node can generate a (nodal) rhythm
the ventricular response, even if the arrhythmias cannot at a rate of 40–60 beats/min. Similarly, should the AV
be suppressed; 14,15 (c) reversion of the arrhythmias by node fail and the ventricles receive no stimuli, there
vagal manoeuvres, medication, cardioversion or over- is an additional layer of protection, as the ventricles
16
drive pacing; (d) ablation; (e) prophylactic anticoagu- themselves can generate (ventricular) rhythms at rates of
lation; and (f) prevention of recurrence using cardiac 20–40 beats/min. 7
resynchronisation therapies such as biventricular pacing. 17
Junctional Escape Rhythms
BRADYARRHYTHMIAS AND This term describes the AV node response to bradycardia.
ATRIOVENTRICULAR BLOCK When sinus bradycardia falls to a rate slower than the
Bradycardia, a slowing of the ventricular rate to less than inherent automatic rate of the AV node, then the junc-
7,9
60 beats/min, may occur in the form of slowing of the tional tissues fire. Typical rates are 40–60/min but may
sinus node rate or failure of conduction at the level of the be slower, as the cause of the primary bradycardia may
AV node. As the rate slows, escape rhythms should inter- also suppress the firing of escape foci. In traventricular
vene, limiting the severity of the bradycardia. However, conduction usually follows the same pattern as had been
these may also fail, rendering the patient asystolic or with present before junctional rhythm and so the QRS is
catastrophic bradycardia. 18,19 unchanged from how it was previously, although occa-
sionally aberrant ventricular con duction may occur, wid-
Bradycardic Influences ening the QRS complex. P waves may or may not be
Conduction system depression may occur with abnormal evident and are often inverted because of retrograde con-
duction, as atrial activation spreads from the AV node and
autonomic balance (increased vagal or decreased sympa- upwards through the atria. These P waves may at times
thetic tone), decreased endocrine stimulation (reduced be seen in advance of the QRS (at shorter than normal
catecholamine or thyroid hormone secretion), or from P–R intervals), within the ST segment, or may be hidden
pathological influences such as conduction system within the QRS complexes (see Figure 11.15).
disease, or congestive, ischaemic, valvular or cardiomyo-
pathic heart diseases. Many biochemical and pharmaco- Ventricular Escape Rhythms
logical factors cause conduction system depression with
18
resultant bradycardia. The causes of bradycardia and AV When either the sinus or AV node fails, and stimulation
block include: 18 of the ventricles does not occur, the ventricles can auto-
excite themselves, usually at a rate of 20–40 beats/min
● drugs: virtually all antiarrhythmics, calcium channel (Figure 11.16). Symptoms of bradycardia commonly
or beta-blockers, and digitalis preparations may con- accompany these idioventricular rates, and acute rate res-
tribute to bradycardia and AV conduction disturbance toration may be necessary. However, true cardiac arrest
to a greater or lesser extent requiring cardiopulmonary resuscitation is less common,
● decreased sympathetic activity, or blockade of neural with the escape rhythm providing sufficient cardiac
transmission (e.g. spinal injury, anaesthetic or recep- output to sustain vital functions in the short term. ECG
tor blockade) features of idioventricular escape beats include:
Cardiac Rhythm Assessment and Management 259
FIGURE 11.15 Sinus bradycardia followed by onset of junctional escape rhythm. Note that the sinus rate is initially around 37/min. It then slows into the
escape rate range of the AV node, which then discharges at 35/min. The junctional beats are not preceded by P waves: the more slowly discharging sinus
node probably has its P waves hidden first in the QRS of the second-last beat and then distorts the ST segment of the last beat.
FIGURE 11.16 Ventricular escape rhythm (idioventricular rhythm). Note that after the first sinus beat, the slow rate allows the ventricular escape rhythm
to emerge. The resultant rhythm is at a rate of 35/min, with wide QRS complexes and absent P waves.
I I
I I
FIGURE 11.17 Accelerated Idioventricular Rhythm (AIVR) following reperfusion in myocardial infarction. An accelerated ventricular focus emerges at
65/min, taking over from the slower sinus rate of 60/min. It then accelerates gradually until settling at a rate of 85/min by the end of the second strip. This
display of rate ‘warm-up’ at onset is a characteristic of arrhythmias due to increased automaticity. The distortion of the ST segment from the third beat of
AIVR onwards is due to retrograde conduction to the atria, and explains the absence of the sinus P waves.
● single ventricular ectopic beats occurring after a pause thus often indicating successful revascularisation follow-
in the dominant rhythm, or as groups of beats at the ing PCI or thrombolytic therapy. 20,21 It may therefore
slow escape rate imply therapeutic success rather than mishap, and
● QRS >0.12 sec, often notched, larger in amplitude and usually needs no treatment. The arrhythmia is commonly
bizarre due to increased automaticity and as with other auto-
● ST segment and T wave, often in the opposite direction maticity arrhythmias may show a ‘warm-up’ in rate, i.e.
to the major QRS direction. it may commence and then gradually accelerate and
settle at a faster rate. This behaviour can be useful in
When these beats occur at a rate of 20–40/min the rhythm differentiating arrhythmias from reentry which typically
is termed ventricular escape, or idioventricular rhythm. have an abrupt change in rate as their onset. When it
Under excitatory influences the ventricular pacemaker occurs outside of the context of reperfusion, AIVR should
cells may increase their firing rate to between 60 and be regarded as inappropriate ventricular excitation
100/min (accelerated idioventricular rhythm) or to faster (Figure 11.17).
than 100/min (ventricular tachycardia). 20
Accelerated Idioventricular Rhythm Atrioventricular Conduction Disturbances
Accelerated idioventricular rhythm (AIVR) has assumed Atrioventricular conduction disturbances make their
a special place in cardiology because of its relatively appearance as delayed or blocked conduction from atria
common appearance during postinfarction reperfusion, to ventricles, and thus appear as altered P–QRS (or P–R)
260 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 11.18 Sinus rhythm with first-degree AV block. Rhythm is regular, rate 100/min, 1 : 1 AV conduction, with a P-R interval of 0.24 sec.
* * *
PR prolonged dropped
FIGURE 11.19 Sinus rhythm with second-degree AV block type I. Every third P wave is not conducted (3 : 2 conduction). The P–R interval can be seen to
lengthen before the dropped beats(*). After the dropped beats the cycle starts with a P–R interval of 0.18 sec. It then extends to 0.25 sec before again
dropping a beat.
* * * * * * *
FIGURE 11.20 Second degree AV block type II. A non conducted beat confirms the second degree block. There is no progressive prolongation of the P–R
interval before the dropped beat (*), rather, the uniformity of all P–R intervals distinguishes this as type II.
relationships. The conventional classifications for AV ● Second-degree AV block type I (Wenckebach): A cycli-
block are based purely on the patterns of conduction. The cal pattern of AV conduction is seen in which the
classification as first-, second- and third-degree partially conducted P waves show a progressive lengthening of
represents the severity of AV node or His-bundle dysfunc- the P–R interval until one fails altogether to be con-
7,9
tion. AV block may complicate heart disease but is also ducted (blocked, or dropped, P waves). Cycles begin
seen commonly with drug therapy (e.g. digitalis, calcium with a normal or (often) prolonged P–R interval,
channel blockers, beta-blockers and other antiarrhyth- which then extends over succeeding beats until there
20
mics). It may occur abruptly following vagal stimula- is a dropped beat. After the dropped beat the cycle
tion. When accompanying myocardial infarction, it is recurs, commencing with a P–R interval equivalent to
63
more likely to be transient following inferior infarction; that commencing previous cycles (Figure 11.19). The
whereas its appearance following anterior infarction is frequency of dropped beats partially represents the
more likely to be permanent. severity of AV block. When, for example, every fifth P
wave is not conducted, 5 : 4 conduction is said to be
Degrees of Atrioventricular Block present. If AV conduction deteriorates further, more
frequent P waves fail to be conducted (4 : 3, 3 : 2
First-degree AV block conduction).
All atrial impulses are conducted to the ventricles but ● Second-degree AV block Mobitz type II: Dropped
conduction occurs slowly, with a P-R-interval >0.20 sec. beats (non-conducted P waves) are also present,
1 : 1 AV conduction is maintained (see Figure 11.18). but the conducted beats show a uniform P–R interval
9
rather than any progressive lengthening (Figure
11.20). The dropping of beats may be regular, e.g.
Second-degree AV block every fourth P wave (termed 4 : 1 block), progressing
This is an intermediate level of block in which some P to 3 : 1, or even 2 : 1 block as AV nodal, or more com-
waves conduct to the ventricles while others do not. Thus monly, His-Bundle conduction, worsens. Alterna-
there are periodic non-conducted P waves, or ‘dropped’ tively, the dropping of beats may be more irregular
beats. A further distinction is usually made into either (variable block), with combinations of 2 : 1, 3 : 1, 4 : 1
type I or type II second-degree AV block, as follows: or other levels of block evident in a given strip. The
Cardiac Rhythm Assessment and Management 261
FIGURE 11.21 Sinus rhythm with high degree AV Block. At the beginning and end of the strip there is second degree block (2 : 1). Alternate P waves fail
to conduct, qualifying as at least second degree AV block. The appearance of consecutive non-conducted P waves in the middle of the strip (5 in a row),
however, escalates the classification to ‘high degree’ block.
* * * * * * * *
FIGURE 11.22 Sinus rhythm with third-degree AV block. Note the P waves (asterisks) at a rate of 90–100/min and the ventricular rate of 40/min. The P
waves bear no relationship to the QRS complexes – they are dissociated. (The seventh asterisked P wave is premature and different in morphology from
the others, and is therefore possibly an atrial ectopic P wave).
more frequent the dropped beats, the slower the ven- Patients need to be on rest in bed, provided with reassur-
tricular rate and the greater the likelihood of symp- ance and oxygen by mask or nasal prongs. If the patient
toms. Second-degree Type II AV block is often is hypotensive, IV fluids should be administered and the
asso ciated with intraventricular conduction delay, patient laid flat. Standardised protocols for bradycardia
with corresponding widening of QRS complexes. should be applied if the patient is symptomatic, and
When this is seen it represents conduction impair- these usually include: 18
ment not just of the AV node but of intraventricular ● atropine sulphate 0.5–1.0 mg IV 25
conduction as well. Progression to complete AV block ● isoprenaline hydrochloride in 20–40 mcg incre-
is more common. 9
26
ments, with an infusion at 1–10 mcg/min
A final form of second-degree block is ‘high-degree’ AV ● transthoracic pacing (usually with sedation)
block, in which conducted P waves show a uniform P–R ● possibly low-dose adrenaline infusion.
interval but, rather than single periodic dropped beats,
multiple consecutive non-conducted P waves can be seen If the patient is pulseless or unconscious, standard
(Figure 11.21). advanced life support should be administered (see
Chapter 24). Persistent or recurrent symptomatic brady-
cardia or AV block may require permanent pacemaker
Third-degree (complete) AV block implantation. 18,19
None of the atrial impulses are conducted to the ventri-
cles, resulting in a loss of any relationship between P
waves and QRS complexes (AV dissociation). Usually a VENTRICULAR ARRHYTHMIAS
lower pacemaker assumes control of the ventricular rate, Ventricular ectopic rhythms may either occur as a response
and this focus may be either junctional (narrow QRS, at to slowing of the dominant cardiac rhythm (escape beats
a rate of 40–60/min) or ventricular (wide QRS, at a rate or escape rhythms) or may emerge at faster rates than the
of 20–40/min) (Figure 11.22). 9 dominant rhythm (as premature ectopic beats, couplets,
9
or ‘runs’ of ventricular tachycardia). Escape rhythms
(occurring after a pause) should be regarded as physio-
Nursing Management During AV Block logical, as they protect against otherwise severe bradycar-
AV block may be progressive in nature, and may worsen dia (see Figure 11.16), whereas premature beats and rapid
with advancing heart disease or after introduction, or ventricular ectopic rhythms (occurring in advance of
dose modification of drugs that depress AV conduc- the dominant rhythm) occur when pathology gives rise
tion. 23,24 Thus monitoring should include P–R interval to increased automaticity or reentry behaviour (Figure
7,9
measurement, and where the P–R interval becomes pro- 11.23). Single ectopic beats may be benign occurrences,
longed there should be an increase in vigilance directed often seen in the absence of heart disease. However, their
towards further prolongation or the development of new appearance accompanying cardiac or systemic disease
dropped beats, to signify advancing AV block. Treatment may precede the development of more serious arrhyth-
of AV block and bradycardia includes immediate assess- mias, such as ventricular tachycardia or fibrillation, and
ment of cardiovascular status or other symptoms, includ- thus warrant close monitoring. Ectopic beats, whether
ing chest pain, dyspnoea, conscious state and nausea. The premature or late (escape), show characteristic features as
cause should be identified and treated where possible. follows:
262 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 11.23 Sinus rhythm with premature ventricular ectopic beats occurring bigeminally. The second, fourth and sixth beats arise prematurely, appear-
ing in advance of the dominant rhythm, and are clearly wider than the intervening supraventricular beats.
● QRS complexes are wide (>0.12 sec) and of different
morphology (large and bizarre in shape) 27 BOX 11.1 Patterns suggesting higher
● Notching of the QRS is common. risk of arrhythmia
● ST segments and T waves are usually in the opposite
direction to the major QRS deflection. ● Increasing frequency of ectopy
● Trigeminy, bigeminy
Ectopic beats may occur as single or coupled beats, or ● Polymorphic ectopics (multiple QRS shapes), regarded as
in runs of consecutive beats. Ventricular tachycardia is more important than monomorphic ectopics (single QRS
defined as greater than 3 consecutive ventricular beats shape)
occurring at a rate greater than 100/min. 5 ● Two ectopic beats in a row
Causes of ventricular tachyarrhythmias include: 3,8,28 ● Three or more beats in a row (defined as ventricular
tachycardia)
● myocardial disease ● R-on-T ectopics
● myocardial ischaemia, infarction ● Bradycardia-dependent ectopics when the Q-T interval is
● cardiomyopathies/cardiac failure long
● hypertrophy
● myocarditis
● other causes of excitation
● biochemistry: hypokalaemia, hypomagnesaemia, pH
derangements
● hypoxaemia, hypoglycaemia arrhythmia varies in its clinical impact, but when sus-
● shock, hypotension tained is typically symptomatic with some degree of
● excitatory pharmacology haemo dynamic compromise. Ventricular tachycardia
● adrenaline, isoprenaline, dobutamine, dopamine, often presents as cardiac arrest, with the patient pulseless
levosimendan, atropine.
and unconscious, and is one of the major mechanisms
Patterns of Ectopy of sudden cardiac death. The severity of symptoms
Some patterns of ectopic frequency and morphology may depends partly on the rate (which may be 100–250/min),
the duration of the arrhythmia, the presence of cardiac
warn of increasing risk for the development of serious disease (ischaemic, congestive, hypertrophic, cardiomyo-
arrhythmias such as ventricular tachycardia or fibrilla- pathic), and the presence of co-morbidities. 9,32 When it
tion, and therefore earn a particular mention in monitor- develops, VT may be categorised as self-limiting (termi-
ing. Historically, ectopic patterns have been graded nating without treatment), sustained for some period of
according to their pre-emptive risk of serious arrhythmia time (minutes or longer), incessant (persisting until or
29
development or 2-year mortality. Studies undertaken in despite treatment) or intermittent. Additional defining
2003 and 2005 did however call into question the predic- terminology includes monomorphic (all beats of the
tive status of certain ‘high risk’ ectopic patterns (such as same morphology) or polymorphic (in which the rhythm
‘R on T’ ectopy), instead postulating that other factors conforms to the other features of VT but there is vari-
such as a patient’s underlying left ventricular function ability in the QRS shapes). ECG features of ventricular
and level of autonomic responsiveness may play a more tachycardia: 14,32,33
significant role in the generation of life threatening ven-
tricular tachyarrhythmias, independent of the prior pres- ● Rate >100/min, rarely >240/min.
ence or pattern of ectopy present. 30,31 However, in the ● Rhythm typically regular; there may be minor irregu-
critical care context it is reasonable to respond to certain larity, especially on commencement and sometimes
patterns (as shown in Box 11.1) by investigating and preceding self-termination.
managing potential contributing causes. If the patient can ● P waves may be absent. Atrial activity, whether disso-
be seen to be advancing through stages of increased ciated or retrograde, is usually difficult to identify
arrhythmic complexity consideration for antiarrhythmic electrocardiographically.
therapy should be given. ● Morphology: QRS is wide (>0.12 sec). QRS often
notched or bizarre in shape.
Ventricular Tachycardia ● Any axis is possible (normal axis, left or right axis
Ventricular tachycardia (VT) is described as a ‘run’ of deviation). An axis in the range of −90 to −180 degrees
three or more consecutive ventricular ectopic beats, (‘no man’s land’) provides strong support for the diag-
12
at a rate greater than 100/min (Figure 11.24). The nosis of ventricular tachycardia, as it implies the QRS
Cardiac Rhythm Assessment and Management 263
FIGURE 11.24 Sinus rhythm at 65/min before onset of ventricular tachycardia. Note a ventricular ectopic emerges from the T wave of the third sinus beat
(R-on-T ventricular ectopic), precipitating ventricular tachycardia (VT). The VT is then sustained at a regular rate of 220/min, with the characteristic wide
QRS and ST/T in opposite direction to the QRS.
FIGURE 11.25 Probable ventricular flutter. The complexes are broad, regular and monomorphic (one shape), but it is difficult to know which is the QRS
deflection and which is the T wave. This feature plus the very fast rate of 300/min or more are the typical defining characteristics of this uncommon but
serious arrhythmia, recorded during recovery from tricyclic antidepressant overdose in a 16-year-old female.
originates at the apex and spreads through the ven- waves, ventricular flutter has earned its own classifica-
tricles upwards and to the right. tion. An example is shown in Figure 11.25. The diagnos-
32
● ST segment and T wave displacement is in opposite tic separation from other types of VT is clinically
direction to the major QRS direction. unimportant, and treatment should follow normal guide-
lines for VT.
If VT is not self-limiting, treatment depends on the sever-
ity of the symptoms. If the patient becomes pulseless
and unconscious, advanced life support is initiated (see Ventricular Fibrillation
Chapter 24). If the patient is conscious and has a pulse, During ventricular fibrillation there is no recognisable
therapy can be undertaken more cautiously. Occasionally, QRS complex. Instead, there is an irregular and wholly
5,9
robust coughing may revert VT in the cooperative patient. disorganised undulation about the baseline. There
Antiarrhythmic therapy (at slower administration rates are deflections, which at times approach rates of 300–
than during cardiac arrest) is usually undertaken first, 500/min, but these are typically of low amplitude and
along with biochemical normalisation. If unsuccessful, none convincingly resemble QRS complexes (Figure
sedation and elective cardioversion may be necessary. 11.26). In the absence of organised QRS complexes the
Consideration for internal cardioverter defibrillator (ICD) patient becomes immediately pulseless, and uncon-
implantation should be given to patients surviving sciousness follows within seconds. Immediate defibrilla-
ventricular tachycardia or fibrillation. 34,35 tion is required. If VF persists treatment occurs according
to standing basic and advanced life support guidelines.
Practice tip Polymorphic Ventricular Tachycardias
These forms of VT do not have a single QRS morphology.
Initial tolerance of VT may be evident, only to be followed by Rather, the QRS complexes during the rhythm vary from
abrupt deterioration when reserves or compensatory mecha- one shape to another, either alternating on a beat-to-beat
nisms are exhausted. Emergency responses should always be basis or switching between groups of beats, with first one
activated on initial identification. 9,32
morphology and then another (bidirectional VT). The
more common form of polymorphic VT is Torsades de
Pointes (TdP), in which the QRS undergoes a gradual
Ventricular Flutter transition from one QRS pattern to another. The descrip-
This uncommon arrhythmia is most likely just a subset tive French term, literally ‘twisting of the points’, refers to
of ventricular tachycardia, but because of its rapid rate (at the appearance of the ‘points’ (QRS direction), which is
times up to 300/min or more) and the appearance of QRS first positive and then negative, usually with an ill-defined
complexes that are largely indistinguishable from the T transition between the two (Figure 11.27). 28,36,37
264 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 11.26 Ventricular fibrillation. Rapid, irregular and wholly disorganised deflections from the baseline are present, and produce nothing resembling
QRS complexes.
FIGURE 11.27 Torsades de pointes polymorphic ventricular tachycardia. After 3 beats of sinus rhythm a ventricular ectopic beat emerges from the T wave
and precipitates onset of a rapid and sustained polymorphic ventricular rhythm. The characteristic sinusoidal twisting around the baseline and changing
direction of the QRS is clearly apparent, and along with the rate of 300/min defines this as torsades de pointes.
ECG features of Torsades de Pointes are: 28,36,37 ● a search for and correction of causes, including
● ischaemia: ECG for AMI/ischaemia, cardiac
● QRS polymorphic, with the transitions between enzymes
polarity as described above. ● biochemical: potassium derangement, hypomag-
● rate often very rapid, in the range of 300/min. nesaemia
● regularity: the evident complexes are often regular, but ● metabolic: hypoxaemia, pH derangement,
particularly within the transition between QRS direc- hypoglycaemia
tions there may be irregularity. ● drug effect: inotrope, chronotrope, recreational
● often self-limiting but recurrent. drugs
● Q–T prolongation evident during normal rhythm (see ● pulmonary artery or intracardiac catheters 40
Research vignette) ● cardiomyopathy, hypertrophy
● often precipitated by R-on-T ectopic beats. ● long QT interval and QT prolonging influences
● commonly pause-dependant, with bradycardia or ● proarrhythmia from antiarrhythmic drugs
single beat pauses precipitating onset. ● immediate CPR and cardioversion/defibrillation
Because of the very rapid rate, syncope and cardiac arrest for pulseless, unconscious ventricular arrhythmias
38
are common, and advanced life support practices (cardiac arrest). In conscious patients, initial treat-
required. A thorough search for possible causes of Q–T ment is usually pharmacological, and, if necessary,
prolongation should be undertaken. Causes include: cardioversion is applied under the influence of short-
class Ia (procainamide, quinidine, disopyramide) or class acting anaesthetics (e.g. propofol)
5,9
III (amiodarone, sotalol) antiarrhythmics, erythromy- ● antiarrhythmic therapy
cin, antidepressants, hypocalcaemia, hypokalaemia and ● immediately: IV amiodarone, lignocaine, sotalol, 38
32
hypomagnesaemia. Congenital long Q–T syndromes ● ongoing: oral amiodarone, sotalol, procainamide
36
also exist. Apart from the general ventricular arrhythmia flecainide, beta-blockers 41
management principles listed below, the treatment of ● heart failure management, which needs to be aggres-
TdP includes cessation of Q–T prolonging agents, a sive if contributory
greater emphasis on IV magnesium, and the use of iso- ● electrophysiological (EP) testing, which should be
prenaline and/or pacing to shorten the Q–T interval and performed for serious arrhythmias to identify foci or
prevent bradycardia. 38 pathways and confirm effectiveness of treatment 41
● pacing strategies
Bradycardia in patients with long QT requires special ● cardiac resynchronisation therapy using biventric-
mention as Torsades de Pointes is so often bradycardia, ular pacemaker, which may be beneficial in heart
or pause, dependent. Pauses prolong the QT and favour failure 42
ectopy which more easily find the T wave, triggering TdP. ● overdrive pacing therapy: antitachycardia pacing
The role of pacing and isoprenaline are to both prevent strategies as part of implantable cardioverter
pauses, and to shorten the QT interval. 36,39 defibrillator 34,35
● implantable cardioverter defibrillator therapy, which
should be considered for all survivors of sudden
Management of Ventricular Arrhythmias cardiac death, 34,35 especially those with low ejection
The emergency management algorithm for life- fraction and recurrent sustained ventricular
threatening ventricular arrhythmias is described in the arrhythmias 41
chapter on resuscitation. In general terms, the manage- ● where a myocardial scar can be confirmed as the
ment of ventricular arrhythmias should include the arrhythmic focus, surgical resection may sometimes
following: 38 be undertaken.
Cardiac Rhythm Assessment and Management 265
other class III drugs (e.g. sotalol) and class IA agents,
TABLE 11.1 Antiarrhythmic classifications 43 there is a risk of Q–T interval prolongation and the devel-
opment of Torsades de Pointes. 41,48 Although sotalol
Class Action Drugs carries the greatest risk of this arrhythmia, it may be
selected when amiodarone side effects need to be avoided,
IA Sodium channel blockers: quinidine
action potential prolongation procainamide or when combined antiarrhythmic–beta-blocker therapy
disopyramide is desired, (e.g. arrhythmias postinfarction or in the
setting of heart failure). Lignocaine, the front-line ven-
IB Sodium channel blockers: lignocaine
accelerate repolarisation; mexiletine tricular antiarrhythmic for many years, lacks the efficacy
shorten action potential of amiodarone, but is well tolerated and effective in the
49
duration setting of the ischaemic myocardium. Whatever the
IC Potent sodium channel flecainide choice of antiarrhythmic, additional attention should
blockers: little effect on always be directed to biochemical correction, in particu-
repolarisation lar serum magnesium, potassium and pH. 38
II Beta-blockers: depress metoprolol
automaticity (prolong phase propanolol
4); indirect prolongation esmolol CARDIAC PACING
phase 2
Artificial cardiac pacing is most commonly used to
III Potassium (outward) channel amiodarone
blockers: prolong duration of sotalol (beta-blocker provide protection against bradycardia and/or atrioven-
action potential (prolonged with class II actions) tricular (AV) block. Slow heart rates can be sustained at
repolarisation) more physiological rates by repetitive electrical stimula-
IV Calcium channel blockers verapamil tion, delivered by a pacemaker at a programmed rate.
diltiazem Temporary pacing may be provided as an emergency
intervention, providing rhythm protection whilst revers-
ible factors are overcome (biochemical or drug influence,
myocardial ischaemia or infarction) or as support until
confirmation of the need for permanent pacemaker
50
implantation. Separate from such bradycardia protec-
ANTIARRHYTHMIC MEDICATIONS tion, pacing may be undertaken to improve haemody-
Antiarrhythmic drugs are classified partly on the basis of namic status, or to treat or suppress arrhythmias.
beta-receptor or membrane channel activity, and partly
by their physiological effects on the cardiac action poten- PRINCIPLES OF PACING
tial. This is well represented by the Vaughan Williams A complete electrical circuit is achieved via a pacemaker
39
classification system (see Table 11.1). However, as action connected in series with pacing leads to (and from) the
potential abnormalities cannot be expediently identified myocardium. Electrical current is delivered to the heart
at the bedside, matching antiarrhythmic agents to cellular via the negative electrode of the circuit, whilst the positive
physiology cannot realistically be undertaken. Instead, electrode completes the electrical circuit and enables
antiarrhythmics are chosen partly on the basis of their sensing (detection) of the patient’s intrinsic cardiac
known efficacy, by their suitablity to atrial or ventricular rhythm. 51,52 Electrical impulses of sufficient strength
arrhythmias, and after consideration of side effects and stimulate the myocardium to depolarise (and then to
contraindications to known comorbidities in a given contract) at a rate selected by the operator.
patient. 41,42
Pacing leads (or pacing electrodes) may be positioned in
Table 11.2 depicts the classification of the major acute
antiarrhythmics in use in Australia and New Zealand, contact with the endocardium via transvenous access, or
along with doses, arrhythmic indications, precautions attached to the epicardium when the heart is exposed at
53
and side effects. Class I agents all slow phase 1 (depolari- the time of cardiac surgery. For epicardial pacing, two
sation) and so may slow down conduction and prolong separate leads or ‘wires’ are usually attached to each
the QRS. The subgroups of class I agents denote strength chamber paced, with one wire connected to each of the
(A = weakest, C = strongest) and affect repolarisation, negative and positive terminals of the pulse generator
with class IA (prolonging), IB (shortening) and IC (not (pacemaker). For transvenous pacing, a single lead is
affecting) repolarisation duration. The class II agents advanced to the apex of the right ventricle. These leads
(beta-blockers) depress automaticity, slowing the heart have a pacing electrode at their tip and a circumferential,
rate and prolonging the action potential. The class III or ‘ring’, sensing electrode slightly proximal to this. In an
agents notably prolong repolarisation, action potential emergency, these transvenous ventricular pacing wires
duration and the Q–T interval. Class IV agents slow can be inserted promptly and at least establish a support-
54
inward calcium channel flux, decreasing automaticity and ive ventricular rate. Temporary transvenous pacing is
prolonging the action potential. 37 almost always undertaken for ventricular pacing only.
While there are transvenous leads available for temporary
In the modern era, amiodarone ranks as the most effec- atrial pacing, they are more difficult to position, and their
tive agent in converting arrhythmias, but its use must be use is very infrequent. By contrast, in the cardiac surgical
weighed against its considerable side effects. 46,47 As with patient, where direct lead attachment is straightforward,
266 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 11.2 Acute antiarrhythmic characteristics 41,44,45
Arrhythmic
Agent Dose indication Considerations Side effects
quinidine (class IA) Oral treatment only Supraventricular Avoid hypokalaemia QRS prolongation
WPW Increased risk torsades Q-T prolongation
following elective Hypotension
cardioversion GI intolerance
procainamide 50 mg increments per minute Supraventricular Potentiates class IA QRS prolongation
(class IA) IV (up to 10 mg/kg) Ventricular and class III Hypotension
WPW Q-T prolongation
AVB
lignocaine (class IB) 1 mg/kg over 2 min; 1–4 mg/ Ventricular If hepatic/renal dysfunction: Hypotension, bradycardia,
min infusion 24 hours dose modification AVB
necessary to avert toxicity CNS disturbance
Avoid hypokalaemia
flecainide (class IC) IV 1–2 mg/kg over 10 min; Supraventricular Proarrhythmia more marked Hypotension
infusion 0.150–0.025 mg/ Ventricular in structural heart disease Bradycardia, AVB
kg/min WPW Proarrhythmia
QRS prolongation
esmolol (class II) 0.5 mg/kg/min over 1 min, Supraventricular Hypotension
followed by decremental Bradycardia, AVB
infusion protocol Symptom provocation in
asthma, COAD, diabetes,
metoprolol (class II) Supraventricular peripheral vascular disease
sotalol (class III + 5 mg increments per min up Supraventricular Potentiation of class IA and Q-T prolongation ++ (sotalol)
beta-blocker, to 80 mg total; maintenance Ventricular III agents
class II) 160–280 mg/day
amiodarone (class 150–300 mg (over 2 min in Supraventricular Slow GI absorption Hypotension
III, also strong cardiac arrest, otherwise Ventricular Long half-life 25–110 days Bradycardia, AVB
class I, with some over 20 min); maintenance Potentiation of digoxin, Q-T prolongation
class II and IV 400–800 mg/day warfarin, class IA, Thyroid, hepatic dysfunction
activity) class III effects Pulmonary fibrosis
verapamil (class IV) 5–10 mg IVI Supraventricular Potentiates digoxin Hypotension
Selected use in Bradycardia
ventricular AVB
adenosine (class 6–12 mg rapid IVI bolus Supraventricular Experience may be Transient AVB/ventricular
IV-like) followed by flush disturbing. Consider standstill
(repeatable) presedation.
Half-life 10 sec
AVB = atrioventricular block; WPW = Wolff–Parkinson–White syndrome; GI = gastrointestinal; CNS = central nervous system; COAD = chronic obstructive airway
disease.
pacing may be undertaken as single chamber (atrial or MAJOR PACEMAKER CONTROLS
ventricular) or dual chamber (atrial and ventricular).
All devices give the operator control over pacing rate,
Importantly, temporary transvenous wires are particularly pacemaker output (strength of the applied electrical
53
vulnerable to movement. Unlike permanent pacing stimulus), sensitivity (to intrinsic rhythm), and (in dual-
leads which are ‘fixed’ in some manner to the myocar- chamber modes) the AV interval. Additional controls
55
dium, temporary leads are simply blunt-ended leads such as mode selection, output pulse width, upper track-
which rely on lodging in muscular folds (trabeculae) near ing rate and the post ventricular atrial refractory period
the apex to hold the lead in position. Activity limitation (for DDD mode) are available on some temporary and
and strict rest in bed are therefore recommended for the all permanent devices. Table 11.3 describes the major
pacemaker-dependent patient. parameters that can be directly controlled on most tem-
The details and descriptions of pacing in this section porary devices.
apply equally to temporary and permanent pacing;
however, the strategies for the correction of problems are PACING TERMINOLOGY
oriented more towards temporary pacing, because it is To aid in communication when discussing pacing func-
with temporary pacing that critical care nurses have a tions, international agreement on terminology has been
56
more direct and immediate role. Additional features and reached (see Table 11.4). A 5-letter code describes the
issues related to permanent pacing are provided at the pacing (and/or defibrillation) capabilities of any given
end of this section. device in terms of chambers involved in pacing, sensing,
Cardiac Rhythm Assessment and Management 267
TABLE 11.3 Pacemaker controls and settings
Control Function
Base rate Sets the rate at which the pacemaker will discharge: pacing occurs at this rate unless the patient’s own rate is faster
and is sensed by the pacemaker. Typically set at 60–100/min.
Ventricular output The size, or strength, of the stimulus delivered to the ventricles. In temporary devices this is an adjustable current
(measured in milliamperes [mA]). Output is increased until capture (successful stimulation) is achieved. The
minimum current required to achieve capture is termed the output threshold. Impulses delivered below the
threshold value will not capture the myocardium. Temporary pacemakers have an adjustable output range of
0.1–25 mA.
Atrial output The size or strength of the stimulus delivered to the atria. Range 0.1 to 20 mA.
Atrial and ventricular Not adjustable on all devices. Allows adjustment of the duration for which the pacemaker output is applied to the
pulse width myocardium. Selectable range typically 1.0–2.0 milliseconds (msec) in 0.25 msec increments. Increasing the pulse
width enhances ability to gain capture.
Atrioventricular delay The interval between the delivery of the atrial and ventricular pacing stimuli. Normally this is set in the same range
as normal P–R intervals (between 0.12 and 0.20 sec).
Sensitivity Affects the ability of the pacemaker to detect the presence of spontaneous cardiac activity. Sensitivity settings can
be adjusted between 1.0 and 20 millivolts (mV). Set at 1.0 mV the device is very sensitive (able to sense small
electrical signals from the heart). Set at higher values, the device becomes less sensitive (higher voltage signals
required to be detected), with the risk that QRS complexes or P waves will not be sensed.
TABLE 11.4 Pacemaker terminology 56
Antitachyarrhythmia
Chamber paced Chamber sensed Response to sensing Programmable functions functions
O, none O, none O, none O, none O, none
A, atrium A, atrium T, triggered P, simple programmable P, pacing
V, ventricle V, ventricle I, inhibited M, multi-programmable S, shock
D, dual (A & V) D, dual (A & V) D, dual (T & I) C, communicating D, dual (P & S)
R, rate modulation
FIGURE 11.28 Ventricular pacing at 86/min. There is capture on the first five beats but none of the remaining pacing spikes are followed by the expected
wide QRS of capture. Note: while there is capture, the patient’s own rhythm is suppressed. When capture is lost, the patient’s slower rate emerges.
Consistent capture needs to be re-established, by either increasing the pacemaker output or correcting factors that depress myocardial responsiveness.
or other functions such as rate responsive pacing capabili- by a P wave or a QRS complex, ‘failure to capture’ is said
ties. A pacemaker designated as VVIR, for example, is to be occurring and requires immediate corrective action
capable of Ventricular Pacing, Sensing of Ventricular (see Figure 11.28).
activity, Inhibiting pacing in response to sensing of ven-
tricular activity, as well as possessing Rate responsiveness. Output and Threshold
While the first three positions in the terminology relate The strength of the pacing stimulus applied is termed the
to all types of pacing, the fourth and fifth letters relate pacing ‘output’, which is adjustable by the operator. On
only to permanent pacing and have not been used initiation of pacing, output is typically increased gradu-
through this chapter. ally until 100% capture is achieved. The minimum output
required to achieve capture is termed the output thresh-
Capture old. Threshold may vary significantly with changes in
A ventricular pacing stimulus that successfully generates biochemistry, arterial pH, myocardial perfusion, drugs
a QRS complex is said to have ‘captured’ the ventricles. and other factors. 53,57-59 To accommodate potential thresh-
The same applies when an atrial pacing stimulus ‘cap- old changes, output settings on the pulse generator are
tures’ the atrium. It is important to verify that all of the set with a ‘safety margin’, i.e. at least double the threshold
stimuli cause capture. If pacing stimuli are not followed value. 58
268 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 11.29 Demand ventricular pacing at a rate of 60/min. The patient’s rate increases after the first two paced beats and inhibits the pacemaker.
It then slows to below 60/min and the pacemaker recommences ‘on demand’.
FIGURE 11.30 Intermittent asynchronous pacing due to incomplete sensing. Set pacing rate 66/min. The 1st, 3rd and 4th beats are sensed and appro-
priately inhibit pacing. However, a pacing spike can be seen at the apex of the T wave of the 2nd beat, which does not cause arrhythmia. The next pacing
spike, just after the apex of the T wave of the 5th beat, arrives during the period of increased excitability in the action potential and precipitates ventricular
tachycardia.
Demand versus Asynchronous Pacing pacing at elevated rates (usually 90–100/min) only whilst
Pacing can be configured in either demand (sensing), or the magnet is in place. The appropriateness of continuing
asynchronous (non-sensing) modes. in an asynchronous mode should always be reconsidered
if the patient’s rate re-emerges in competition with the
Demand pacing pacing due to the risk of arrhythmia.
The most common approach to pacing are the so-called
‘demand’ modes. In these modes, pacing is provided only
on demand: that is, when the heart rate falls below a Practice tip
nominated level (demand rate) (Figure 11.29). Demand
pacing requires pacemaker detection of the patient’s Asynchronous pacing is not commonly applied. However, it
intrinsic cardiac rhythm. If intrinsic rhythm is sensed, it should be considered when there is risk of oversensing in a
‘inhibits’ the pacemaker from delivering a pacing stimu- patient who has no underlying rhythm. Patient transport may
lus. The demand modes ensure that pacing is provided expose pacing systems to movement and electrical field inter-
only when needed, and also protect against pacing during ference not normally seen in critical care units. Pacemaker
arrhythmically vulnerable moments in the cardiac cycle. inhibition in the asystolic patient may be catastrophic. A team
Ventricular pacing delivered at the time of the T wave may discussion should address this issue prior to transporting
induce ventricular tachyarrhythmias (Figure 11.30), whilst patients with temporary pacing.
atrial pacing during atrial repolarisation (shortly after the
P wave) may precipitate atrial tachyarrhythmias. 60
Ventricular Pacing
Asynchronous pacing Stimulation of just the ventricles results in the generation
Pacing may be delivered in an asynchronous mode, that of a ventricular ectopic rhythm. Functionally this will be
is, without the capability of sensing the heart’s inherent no different from an intrinsic ventricular rhythm. There
activity. When in an asynchronous mode, the pulse gen- will be loss of atrioventricular synchrony, and the loss
erator will pace perpetually at the set rate, irrespective of of effective atrial kick may cause low cardiac output
whether the patient is generating his/her own rhythm. and hypotension. To offset the loss of atrial kick, ventricu-
The main applications of non-sensing (asynchronous) lar pacing is sometimes undertaken at slightly higher
modes are: (a) when there is oversensing, or risk of over- rates than normally seen in the resting patient (e.g.
sensing, such as in environments with strong electromag- 70–80/min, rather than 50–60/min).
netic fields; and (b) when patients would otherwise be The delivered pacing stimulus should be followed imme-
asystolic or critically bradycardic if pacing were inter- diately by a QRS complex which is wide (>0.12 sec) and
rupted (pacemaker-dependent). 51,61,62 In demand modes often notched. Pacing from near the apex will produce
of pacing, false sensing of electromagnetic interference is an ECG which closely resembles left bundle branch
able to inappropriately inhibit pacing, returning patients block morphology, with left axis deviation. Repolarisa-
to their own unreliable rhythm. Temporary reprogram- tion abnormalities are also seen, with ST segments and T
ming to non-sensing modes (AOO, VOO, DOO) is waves displaced in the opposite direction to the major
commonly undertaken during surgery to prevent false QRS direction in each lead. 57
pacemaker inhibition by electrocautery. For permanent
pacing this is achieved by reprogramming, or by magnet Ventricular pacing provides protection against bradycar-
application over the device, which causes asynchronous dia or AV block by stimulating the ventricles at a set
Cardiac Rhythm Assessment and Management 269
FIGURE 11.31 Onset of ventricular pacing. At the start of the strip the patient’s heart rate is around 70/min. The pacemaker is then turned on with the
rate set at 80/min. Capture is achieved immediately, and because the pacing rate is faster there is suppression of the patient’s own rhythm. Note the wide
QRS and ST elevation during pacing. This is the expected appearance.
FIGURE 11.32 Commencement of atrial pacing. The patient’s own sinus rhythm is around 65/min at the start of the strip. Pacing is turned on at a rate of
around 70/min, and causes suppression of the slower sinus rhythm. Note: the commonly seen changes during pacing compared with sinus rhythm are
present here – paced P waves are lower in amplitude than the sinus beats, and the P-R interval prolongs slightly during pacing.
(programmable) rate (Figure 11.31). Temporary, emer- pressure. In this respect atrial pacing is superior to ven-
gency, ventricular pacing may also be undertaken to tricular pacing.
prevent bradycardia-dependant tachyarrhythmias such as Atrial pacing tends to produce low-amplitude P waves,
63
TdP. Pacing provides protection by both reducing the which vary from the typical P waves seen during sinus
QT interval, as well as preventing pauses which give rise rhythm (Figure 11.32). They may at times be difficult to
to ectopy and onset of TdP. 63
identify on the ECG. Appropriate lead selection is impor-
tant to reveal the atrial depolarisation and confirm atrial
capture. It is common for the AV interval (P–R interval)
to extend slightly (e.g. to 0.20–0.22 sec) during atrial
Practice tip pacing compared with sinus rhythm, as the time taken
If haemodynamic status is suboptimal during ventricular pacing for atrial impulses to traverse the atria from the pacing
(low blood pressure and/or cardiac output), consider changing focus is longer than the sinus-to-AV node conduction
the pacing rate. A faster pacing rate may offset the loss of atrial interval.
kick and so restore cardiac output despite low stroke volume.
Alternatively, turning down the pacing rate may reveal an Atrial Pacing and AV Block
underlying (slower) sinus rhythm that produces improved Any degree of AV block is possible during atrial pacing
cardiac output. and is rate dependent. 64,65 Thus the severity of AV block
may be worsened, not only by AV node dysfunction but
also by changes in the atrial pacing rate. A patient with
ATRIAL PACING first-degree block may develop second-degree block if the
atrial pacing rate is increased, without this implying wors-
Atrial pacing alone is indicated when there is sinus node ening AV node function. Conversely, AV block developing
dysfunction in the presence of reliable AV conduction. 50,62 during atrial pacing may be lessened or overcome by
The characteristic arrhythmias of such patients are symp- reducing the atrial pacing rate. An example of such rate-
tomatic sinus bradycardia and/or sinus pause/arrest dependent AV block behaviour is demonstrated in Figures
which may be syncopal. For atrial-only pacing to be 11.33 to 11.35 which are sequential strips from the same
undertaken, there needs to be confidence that AV conduc- patient.
64
tion is intact, and that it will remain intact in the future
as the annual incidence of progression to AV block is 1%
65
in these patients. If there is AV block, atrial pacing alone DUAL-CHAMBER PACING
is unsuitable, and dual-chamber pacing should be con- Pacing of both the atria and ventricles offers the benefit
sidered. 50,62,64 The reliability of AV conduction is some- of atrial kick as well as a guarantee of a ventricular
times assessed by pacing the atria rapidly (e.g. at rates of response. Thus it provides protection against bradycardia
up to 120 to 150/min). If AV block does not develop at and AV block. As with either atrial or ventricular pacing,
these faster rates there can be confidence that AV conduc- demand modes have been preferred in dual-chamber
tion is reliable. The advantage of atrial pacing over ven- pacing, unless either oversensing or pacemaker depen-
tricular pacing is the provision of atrial kick which may dence warrant asynchronous pacing. Over the past decade,
contribute substantially to cardiac output and blood however, particular features of the DDD pacing mode
270 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 11.33 Atrial pacing at 70/min with first-degree AV block. Note the long P–R interval, at almost 0.4 sec; particular caution is warranted in increasing
the rate, as, although AV conduction is 1 : 1, it is already very slow. See the next 2 figures for worsening of AV block as the atrial rate is increased.
PR longer dropped PR longer dropped PR longer dropped
FIGURE 11.34 Second-degree AV block type I with 3 : 2 conduction. The same patient as above, with worsening AV block after increasing the atrial pacing
rate to 80/min. Note: the 1 : 1 conduction has been lost and there are dropped beats. After each of the dropped beats the P–R is 0.30 sec, which extends
to 0.46 sec on the next beat, before dropping of the 3rd beat of each cycle.
FIGURE 11.35 The same patient again, now with the atrial pacing at 86/min. At the faster atrial rate, AV conduction has worsened further. There is now
a 2 : 1 block yielding a ventricular rate of 43/min.
have made it the predominant mode in both permanent ventricular conduction produces a contractile pattern
and temporary epicardial pacing. which is superior to the contraction from ventricular
pacing. This may result in better haemodynamics than
Pacing stimuli are delivered to the atria and ventricles at when the ventricles are paced. There has been increasing
a selected rate. After delivery of the atrial stimulus there interest in permitting native AV conduction because of
is a delay of usually 0.16–0.24 seconds (equivalent to a these above reasons, and also on the basis of recent data
P–R interval) before delivery of the ventricular pacing from the DAVID trial which revealed that chronic ven-
stimulus (Figure 11.36). If the patient is able to conduct tricular pacing induces negative ventricular remodelling
the atrial depolarisation to the ventricles themselves and worsening of heart failure. Prolonging AV delays to
66
before the ventricular pacing is due, then the pacemaker permit native conduction has become commonplace, but
senses the resultant QRS and inhibits ventricular pacing.
carries some slight arrhythmic risk (Figure 11.37).
67
DDD Pacing: The ‘Universal’ Pacing Mode
Practice tip The introduction of the DDD mode of pacing added an
important new dimension to dual-chamber pacing, that
If AV block is encountered during atrial pacing and is causing
significant bradycardia, consideration should be given to is, the ability to synchronise ventricular pacing to spon-
62
reducing the atrial pacing rate to see whether the severity of taneous atrial activity in patients with AV block. In addi-
the AV block can be reduced. tion to the normal bradycardia and AV block protection,
the DDD mode features a ‘triggered’ function. If the pace-
maker detects a P wave but a QRS does not follow within
the preset AV interval (AV block), the pacemaker will be
A dual-chamber pacemaker may demonstrate AV pacing triggered to provide ventricular pacing at the end of the
at the set rate and the set AV delay as described above, or programmed AV interval. This means that the ventricular
may operate as simply atrial pacing if normal AV node rate can be brought back under control of the sinus node,
conduction occurs before the programmed AV delay has even though there is AV block. Consequently, in a DDD
elapsed. Deliberately prolonging the programmed AV pacemaker it is common to see ventricular pacing at a
delay provides greater opportunity for patients to conduct range of different rates as it responds to sinus activity.
to the ventricles by themselves. In some patients intrinsic This triggered behaviour of the DDD device is sometimes
Cardiac Rhythm Assessment and Management 271
FIGURE 11.36 Dual-chamber pacing at a rate of 72/min. Note: the atrial spikes are followed by P waves (atrial capture), then after an AV interval of 0.20 sec
there is a ventricular spike, followed by a QRS complex (ventricular capture).
FIGURE 11.37 AV pacing with prolongation of the AV delay to permit native conduction. There is initially AV pacing at a rate of 75/min, with an AV delay
of 0.16 sec. The AV delay is then increased to 0.30 sec, during which the patient can be seen to conduct spontaneously through to the ventricles to produce
spontaneous narrow QRS. These are sensed by the pacemaker and inhibit the ventricular pacing.
III aVF V3 V6
FIGURE 11.38 ECG excerpt from a patient with sinus rhythm and 2 : 1 AV block. The non-conducted P waves are partially concealed but can be seen
distorting the T waves (arrows). Although the sinus node can generate a rate of 75/min, the patient is rendered bradycardic by the AV block.
III aVF V 3 V 6
FIGURE 11.39 The same patient as above, 2 hours later. A DDD pacemaker has been inserted, and although some of the pacing spikes are difficult to see,
all QRSs are paced beats. The sinus rate is again close to 75/min, and atrial tracking ensures that a paced QRS follows each P wave. The ventricular rate
has been brought back under control of the sinus node. Note: although set to a backup rate of 60/min, the pacemaker is pacing much faster than this
because of the triggered behaviour of DDD.
called ‘P-synchronous ventricular pacing’, although ‘atrial pacing can be provided, (how fast it may track the atria
tracking’ is a more practical term as the ventricular pacing at a 1 : 1 ratio). This is typically set to around 120–130
‘tracks’ the atrial rate. per minute. In younger patients it may be set higher, e.g.
140–150/min.
Atrial tracking allows the pacemaker to pace the ventricles
in response to the atrial rate sensed by the pacemaker. This triggering of ventricular pacing in response to sensed
This is desirable when the atrial rate is controlled by the P waves is intended to mimic the behaviour of the AV
sinus node, but is inappropriate during atrial arrhyth- node. It ensures that a QRS follows each P wave and
mias. Atrial tracking at a 1 : 1 rate during atrial flutter brings the ventricular rate back under the control of the
would produce an intolerable ventricular rate of 300/ sinus node (see Figures 11.38 and 11.39). Pacing will be
min, and during atrial fibrillation the tracking rate could seen at a wide range of rates, as the ventricular pacing
be even higher. For this reason, an ‘upper rate’ for atrial follows the normal speeding and slowing of the sinus rate
tracking is programmed in the DDD pacemaker. The in response to such conditions as pain, fever and activity.
upper rate controls the maximal rate at which ventricular If the atrial rate exceeds the upper rate for tracking, then
272 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 11.40 Intermittent failure to capture. The 1st, 2nd, 6th and 7th spikes gain ventricular capture but the rest do not. Note the significant pause
during failure to capture, in which there is atrial but not ventricular activity. Symptoms during failure to capture depend on the rate of any underlying
rhythm.
1 2 3 4 5 6 7 8
FIGURE 11.41 Atrial pacing with intermittent failure to capture (output set at 14 mA). Note: capture is evident following the 1st, 3rd, 5th, 7th and 8th
pacing spikes, but not the others. Fortunately, here the patient has an underlying sinus rhythm, so that the impact of failure to capture is of no great
consequence.
it is no longer possible for all of the atrial beats to be Failure to capture
tracked. DDD pacemakers will start ‘dropping’ beats in a The event in which pacing spikes do not successfully
manner analagous to the behaviour of the AV node. stimulate the heart is termed ‘failure to capture’. Pacing
spikes are evident on the ECG but are not followed by
External (‘Transcuataneous’) Pacing either QRS complexes (in ventricular pacing) or P waves
Emergency pacing may be undertaken noninvasively (in atrial pacing) (see Figures 11.40 and 11.41). Failure to
via external pacing electrodes, and is termed ‘external’, capture may occur when the myocardial responsiveness
‘transthoracic’, or ‘transcutaneous’ pacing. Standard, self- (threshold) worsens, or when impulses do not reach
adhesive defibrillation pads are applied in either the responsive myocardium. Note that dislodgement of a
antero-posterior (preferred), or standard right parasternal- lead from the myocardium will still show pacing spikes
apical positions as per defibrillation. These are connected on the ECG as long as the lead is in contact with body
to a defibrillator with additional pacing capability. Pacing fluids or tissue. Repositioning of leads must therefore be
stimuli of large current (10–200 mA) are necessary to included in considerations during management.
achieve myocardial capture, and frequently also cause
uncomfortable or painful skeletal muscle stimulation. Its Failure to capture may present as a clinical emergency and
use is therefore usually reserved for highly symptomatic/ requires immediate attention. With failure to capture,
life-threatening bradyarrhythmias, and only as a short- patients are left to generate their own rhythm, which may
term bridge to invasive pacing. Sedation is typically be unacceptably slow. Failure to capture may be complete
required in the conscious patient. (all spikes not capturing) or intermittent (with only some
spikes achieving capture). Even if there are only occa-
External cardiac pacing provides ventricular pacing only, sional spikes that fail to capture, immediate attention
and the patient should be assessed not only for reliable is required, as complete failure to capture may ensue
capture, but also for an adequate pulse and blood pres- (see Case Study at the end of this Chapter). Causes and
sure during pacing. Pacing may be in either demand management of failure to capture 51,58,59,68,69 are listed in
or asynchronous mode, usually at rates of 40–80 beats Table 11.5.
per minute.
Failure to Sense
COMPLICATIONS OF PACING Sensing of the intrinsic cardiac rhythm is necessary to
Effective pacing may be disturbed by problems related achieve demand pacing. If rhythms are not sensed, then
to pacing leads, myocardial responsiveness, programmed pacing will proceed at a fixed rate and in competition
values, the pulse generator itself (including power with the native rhythm (Figures 11.42 and 11.43). Pacing
sources), and interactions between any of these spikes delivered during the excitable period of the action
factors. 56-61 Four major disturbances to pacing are potential may trigger tachyarrhythmias (see Figure
described below. These provide the bulk of pacing prob- 11.30). The risk of arrhythmias is greatest when ven-
lems encountered, and because they may either interrupt tricular pacing spikes are delivered just after the peak of
pacing or precipitate serious arrhythmias, critical care the T wave, especially when there is myocardial isch-
nurses need to be competent in their recognition and aemia or infarction, or hypokalaemia. Immediate resto-
management. ration of appropriate sensing needs to be undertaken.
Cardiac Rhythm Assessment and Management 273
FIGURE 11.42 Ventricular pacing with failure to sense. At the start of the strip there is ventricular pacing. A junctional rhythm appears at a slightly faster
rate than the ventricular pacing, but despite this the pacemaker continues to fire, delivering the spikes into the ST segment and T wave. Appropriate
sensing of the last three beats of the strip would have caused inhibition of these pacing spikes.
FIGURE 11.43 Atrial failure to sense. The first three beats show atrial pacing. Then there are two spontaneous P waves (4th and 5th beats). These P waves
should have inhibited the atrial pacing, but pacing spikes can be seen at the start of the QRS of the 4th beat and in the ST segment of the 5th beat.
TABLE 11.5 Failure to capture: causes and BOX 11.2 Failure to sense: causes and
management management
Causes Management Causes:
● Sensitivity set too low (too high a number)
● Output too low ● Increase output.
● Increase pulse width if available. ● Set in asynchronous mode (AOO, VOO or DOO)
● Altered threshold (lead maturation)
● Changing capture ● Check for and treat ischaemia, ● Lead movement/dislodgement
threshold hyperkalaemia, acidosis or
alkalosis. Management:
● Lead maturation.
● Increase sensitivity (to a lower number)
● Antiarrhythmic drugs ● Consider dose modification. ● Check connections
● Reverse the polarity of the electrodes if appropriate for the
● Lead migration/ ● Reposition wire if able.
dislodgement ● Reverse polarity of leads pacing wires (reverse connections of positive and negative
(epicardial wires) electrodes)
● Position patient on left side ● Increase the pacer rate to overdrive the competing rhythm
(transvenous wires). ● If underlying rhythm satisfactory, consider turning pace-
● Consider unipolar pacing via
application of a skin suture maker off
● Treat the resultant rhythm (e.g. ● Consider placement of an alternative sensing electrode
atropine, isoprenaline). (skin suture) to create unipolar pacing.
● Place another wire.
● Consider external pacing.
Causes and management of failure to sense 60,68,70,71 are Failure to pace
detailed in Box 11.2. Remember, however, that sensing Failure to pace is an imperfect term that is used to describe
controls are inverse: lowering numerical settings (e.g. the event where the pacemaker does discharge but the
from 5 to 2 mV) increases the sensitivity whilst increas- impulse fails to reach the patient. In this sense it may be
ing the value (from 1 to 4 mV) makes the pacemaker useful to regard failure to pace as resulting from an
less sensitive. incomplete electrical circuit. The flashing pace indicators
274 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 11.44 At the start of the strip there is ventricular pacing at a rate of around 85/min. However, the pacing spikes abruptly cease and the patient
is left to generate his/her own slower rate. Spikes do reappear but these are at a slower than programmed rate. This could be either failure to pace or
oversensing during ventricular pacing, and differentiation cannot be made absolutely from this strip. Rather, pacing indicators need to be examined to
aid this differentiation. This was a case of ventricular failure to pace due to a poor connection of the pacing leads to the bridging cable.
FIGURE 11.45 Atrial pacing with failure to pace. There is sudden disappearance of the pacing spikes after the first three beats. From this strip alone, failure
to pace or oversensing cannot be separated as possibilities. However, the pacing indicator was flashing through such pauses, rather than the sensitivity
indicator, confirming failure to pace. The connection between the pacing wires and the bridging cable needed tightening and immediately corrected the
problem.
on temporary pacemakers confirm that pacing has
occurred but the spikes fail to appear on the ECG. Most BOX 11.3 Failure to pace: causes and
commonly, failure to pace is due to a loose connection management
in the lead system or a fractured lead or bridging cable.
Electrocardiographically, failure to pace appears as failure Causes
of the pacing spikes to appear when expected. As with ● Disconnected lead/loose connections – commonest cause
failure to capture, this leaves patients with whatever ● Pacemaker turned off or dysfunctional
rhythm they can generate themselves, which may or may ● Output turned off
not be adequate. Failure to pace (also termed ‘failure to ● Battery depleted
output’ in some literature) may present as complete loss ● Fractured lead (may be internally fractured but outwardly
of pacing, or just pacing at a slower rate than set (see intact)
Figures 11.44 and 11.45). If the patient’s rhythm is very
slow, then failure to pace can be a clinical emergency. Management
Even if there is an adequate rhythm, the situation requires ● Check that pacemaker is turned on.
immediate attention. Causes and management of failure ● Check all connections and leads, and tighten/replace if
to pace 22,51,68-71 are detailed in Box 11.3. necessary.
● Change battery.
● Change the connecting lead.
● Ensure output is turned on.
Practice tip ● Complete circuit with skin suture to positive terminal of the
pacemaker, and try each of the existing wires in the nega-
The ECG usually does not help to distinguish between over- tive terminal.
sensing and failure to pace, and instead – at least with tempo- ● Differentiate from oversensing.
rary pacing – the distinction is made from inspection of the ● Assess and support rhythm and haemodynamics.
flashing pacing indicators. If the pacing indicator continues to
flash during periods where the spikes do not appear, then the
problem is failure to pace (an interrupted electrical circuit).
Alternatively, if the sense indicator is flashing during a period
where the spikes do not appear, then the problem is device will respond as if these are genuine signals and
oversensing. inhibit pacing. Oversensing is a common event during
temporary pacing and electrocardiographically may be
indistinguishable from failure to pace, as both appear as
Oversensing missing spikes.
As in failure to pace, pacing spikes may fail to appear Oversensing may result in momentary interruptions to
when oversensing occurs. Rather than sensing intrinsic pacing (pauses) or complete cessation of pacing. The
cardiac activity, the pacemaker may sense electrical signals clinical impact depends on the duration of oversensing,
(electromagnetic interference) from other sources. The and on the patient’s ability to generate an underlying
Cardiac Rhythm Assessment and Management 275
● identification of return of spontaneous rhythm
BOX 11.4 Oversensing: causes and ● assessment of haemodynamic adequacy during both
management paced and spontaneous rhythms (BP, CO, perfusion,
symptoms)
Causes: ● strip documentation of rhythm 6-hourly and daily
● Muscle potentials other than QRS complexes: 12-lead ECG
● Cardiac: T waves, U waves, P waves ● daily chest X-ray to confirm position of wire/absence
● Non-cardiac: shivering, fasciculations, seizure activity, of complications
any skeletal muscle movement ● checking and tightening of all connections (leads to
● External electrical interference: bridging cable, bridging cable to pulse generator) at
● Electrocautery, TENS machines commencement of shift and during all pacing adverse
● Electrical devices (rare) events
● Movement of the connecting pins at the connection to the ● confirmation of battery status each shift
pulse generator (common). ● performance of pacemaker threshold assessment each
shift or daily.
Management:
● Reduce sensitivity (turn sensitivity to higher number)
● Consider disabling the sensitivity altogether (i.e. asynchro- Protection Against Microshock
nous, VOO, AOO, DOO mode) Patients with temporary pacemakers require microshock
● Consider reversing the polarity of the wires (positive to protection. Normally, small electrical stimuli (e.g. static
negative) electricity applied to the body) dissipate through body
● Remove the source of interference where it can be tissues and never reach sufficient current density at the
identified. heart to produce arrhythmias. However, pacing wires
provide a direct route to the heart, so that even minor
electrical sources may achieve sufficient current density at
the heart to precipitate arrhythmias. Protection strategies
include nursing patients in body- and cardiac-protected
rhythm. Electromagnetic interference resulting in over- areas, insulating external connector pins when pacing is
sensing may arise from a variety of causes, originating not in use, and using rubber gloves at all times when
from the patient (muscle movement) or external sources handling pacing wires. 70
(devices). The sources of oversensing 22,51,70,71 may be dif-
ficult to establish clinically but should be sought and
corrected where able. Causes and management of over- Battery Depletion in a Temporary Pacemaker
sensing are detailed in Box 11.4. A standard 9V battery might be expected to power a tem-
porary pacemaker for up to a week, although this is vari-
An important distinction must be made between failure able depending on the device, the mode, rate, and output
to pace and oversensing (see Figures 11.44 and 11.45). settings, the percentage paced, and the impedance of the
In both complications the pacing spikes do not appear pacing leads. Additionally it is often not known whether
when expected and may therefore be indistinguishable a new battery was inserted into the pacemaker at the
from each other. Clearly the management of the two commencement of treatment for the current patient.
complications is different, and so prompt, accurate
differentiation is important to ensure appropriate Temporary pacemakers provide indications of depleting
management. battery status; these are usually displayed when there is
less than 24 hours of battery life remaining: (a) flashing
NURSING PRACTICE battery icons may appear on the digital screens of newer
Care, monitoring and management of the patient and the generation devices; (b) on both new and older non-
pacing system largely fall to the nursing staff of critical digital screen devices, the pacemakers will stop supplying
care units. Nurses must ensure ongoing monitoring of power to the flashing sense/pace LEDs. Battery replace-
pacing performance and the detection of pacing abnor- ment should be undertaken as soon as reasonably pos-
malities, the integrity of the pacing system, the avoidance sible as these indicators are not obvious until looked
of clinical situations or physical changes that may alter for, so some time may have elapsed before detection
pacing effectiveness, patient safety, and the prevention of by staff.
complications. Changing the battery on a temporary device carries the
risk of interrupting pacing which may be disastrous in the
Nursing responsibilities in the care of the patient with a
pacemaker include: pacemaker-dependent patient. Although the time taken
to change a battery may be brief, additional significant
● pacemaker site inspection for inflammation/swelling/ time may be lost if the device ‘powers down’ during the
haematoma battery change. It is worth noting, however, that tempo-
● avoidance of hip flexion and rest in bed if femoral rary pacemakers carry a small stored charge which is
insertion enough to sustain pacing for about 10 seconds. If a well-
● vital signs, circulatory observations, etc. at intervals rehearsed procedure is undertaken, battery change can be
appropriate to the overall patient context performed without interrupting pacing for even a single
● confirmation of capture and sensing beat. An understanding of the behaviour of the device in
276 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
1. Store current values in memory (for devices with memory). If rhythm difficulty is encountered
during testing, these original settings can be immediately re-established by depressing the
stored values mode selector.
2. Test for underlying rhythm. Gradually decrease rate in 10 beat/min steps until evidence of
underlying rhythm (ULR) emerges:
(a) If ULR present, observe whether sensing is now occurring.
(b) If still pacing at 50/min (no emergence of ULR), return to initial settings; do not continue to
test sensitivity or output thresholds.
(c) Document attempt and ULR less than 50/min.
If underlying rhythm is haemodynamically acceptable, continue.
3. Test sensitivity threshold. Having confirmed haemodynamically adequate underlying rhythm:
(a) Turn pacing rate to half the patient’s rate.
(b) Turn output to minimum (not off).
(NB: Sensitivity testing requires that failure to sense is created for a brief period, so steps 3a
and 3b are designed to minimise danger of arrhythmias.)
While observing the sense indicator on the pacemaker:
• decrease sensitivity (increasing the number) until failure to sense (the sense indicator
stops flashing — pacing indicator will now be flashing);
• increase sensitivity (decreasing the number) until sensing resumes;
• note the value at which sensing returns — this is the threshold value for sensing; and
• set sensitivity to half this value minus 1 mV.
4. Test output threshold (continuing from step 3 above the pacing will now be set at a low rate,
and at minimum output):
• Increase the pacing rate to 10 greater than underlying rhythm.
While watching the monitor:
• gradually increase the output until capture is achieved;
• note the value at which capture occurs — this is the threshold value; and
FIGURE 11.46 Routine temporary • set output to double this value plus 1 mA.
pacemaker testing protocol: underly- 5. Store new values in memory and document settings.
ing rhythm, output and sensitivity
threshold test.
use should be established before undertaking battery undertaken and to report any sensations of lightheaded-
replacement. ness, dyspnoea or other discomfort.
Pacemaker Function Testing Pacemaker testing in the unstable
Routine pacemaker performance checks should be under- pacemaker-dependent patient
taken regularly in the patient with a temporary pace- Greater caution must be applied in the testing of pace-
maker. Temporary pacing leads and wires are prone to maker functions if the patient has marked haemody-
movement and therefore to sensing and capture thresh- namic instability or has little or no underlying rhythm.
old variation. Variations may also be marked when there It is common for pacemaker testing to be avoided
is myocardial, biochemical and haemodynamic volatility altogether in such circumstances although this may be
as often seen in the critically ill patient. Pacemaker tests misguided. Routine testing of pacemaker function as
are performed to reveal the return of underlying rhythm described in Figure 11.46 may not be suitable, but testing
which may be being concealed by pacing, and to measure for underlying rhythm, and some level of testing of
thresholds for both capture and sensing, as these values capture threshold so as to be confident of safety margins
typically change with time and in response to changing is beneficial. For the patient with haemodynamic insta-
myocardial responsiveness. 54,58,62,68 Regular checking bility and/or inotrope use, testing for underlying rhythm
allows detection of threshold changes, and setting of becomes of even greater important as pacing may either
sensing and output safety margins, in order to minimise prevent or conceal the return of sinus rhythm capability,
the development of acute failure to capture or failure and cardiac output may be as much as 50% greater with
to sense.
the atrial kick of sinus rhythm than during pacing (see
The practices employed to test temporary pacemakers Figure 11.47). It may take several seconds for the sinus
vary widely across Australia, as do attitudes to whether node to ‘warm up’ and express itself, so decrease the rate
this may or may not be undertaken by nurses. The sample gradually and only to reasonable levels (sinus rates of less
protocol shown in Figure 11.46 provides an organised than 50 are unlikely to be beneficial). Be sure to gain
approach to testing during which safety has been empha- agreement from the multi-disciplinary team before
sised. Because of the varying attitudes to nursing respon- undertaking testing in this context.
sibilities, the use of this approach should be ratified at
individual institutions before use. Threshold testing in the pacemaker-dependent patient is
also contentious as loss of capture during testing may be
Testing pacemaker thresholds is performed daily or on poorly tolerated. If the capture threshold is not measured,
each shift, but not if the patient is unstable, using the however, a rising threshold and loss of safety margins
steps described in Figure 11.46. The test should be carried cannot be identified, and may only become apparent
out promptly, with attention to avoiding undue bradycar- upon development of acute failure to capture, possibly
dia or periods of asynchronous pacing. The patient with outputs already set to maximum and therefore no
should be advised that pacemaker assessment is being scope for recovering capture. An alternative approach to
Cardiac Rhythm Assessment and Management 277
68 60
85/50
70
125/65
FIGURE 11.47 Unveiling haemodynamically superior underlying rhythm (strips are continuous). Initially there is ventricular pacing at a rate of 68/min. No
atrial activity can be seen and the blood pressure is 85/50 mmHg with noradrenaline support at 8 mcg/min. Across the top strip the paced rate is reduced,
allowing P waves to emerge at a rate of 60/min (arrow) and then accelerate to around 70/min across the lower strip. Note the impressive BP increase to
2
125/65 mmHg allowing discontinuation of noradrenaline infusion. (Note also: cardiac index recorded during V pace 1.7 L/min/m , during sinus rhythm
2
2.3 L/min/m ). Importantly, there was no suggestion of sinus capability until the pacing rate was reduced.
testing thresholds in this context is useful. Rather than dysfunction are more likely to have rate responsive pacing
formally measuring threshold by creating loss of capture, enabled so that the pacemaker can adjust pacing rates to
the output may be decreased to a value which confirms activity and exercise. Single chamber pacing of the atria
safety margins are still possible, but without having lost only (AAI mode) is uncommon as it provides no protec-
capture at any point, e.g. decreasing output to 10 mA on tion against the future development of AV block. 63
a device with an output capability of 20 mA. If there
is still capture at 10 mA then further reductions can A pulse generator is positioned in a pre-pectoral pocket
be avoided because a 10 mA safety margin has been and leads advanced into the heart either through subcla-
demonstrated. vian vein puncture (from within the pocket), or via
cephalic vein cutdown. The cephalic approach avoids the
PERMANENT PACING intrathoracic complications such as pneumothorax which
For bradyarrhythmias which are not due to temporary, may accompany subclavian puncture. Typical pacemaker
reversible factors, or are likely to be sustained or longevity is 8–12 years.
recurrent, permanent pacemaker implantation may be Permanent pacing leads differ from temporary pacing
undertaken. Indications vary, but syncopal events, symp- wires in that for chronic stability over a lifetime of activity
tomatic bradycardia, pauses greater than 3 seconds, the leads must be ‘fixed’ in some manner to the myocar-
and bradycardia-dependent tachyarrhythmias are general dium. ‘Active fixation’ leads have an extendable helix that
63
indications for permanent pacing. Dual chamber pacing is screwed into the myocardium at the time of implanta-
27
is usually provided unless the patient has chronic atrial tion, much like a corkscrew. ‘Passive fixation’ leads by
fibrillation as it is not possible to capture the atria during contrast are not directly secured to myocardium but have
fibrillation. For such patients rate responsive ventricular soft tines similar to the barbs of a spear, near the lead tip.
55
pacing (VVIR) is the most common mode. 27,72 A dual The lead is positioned where these tines can embed within
chamber pacemaker may still sometimes be implanted if muscle infoldings (trabeculae) at the ventricular apex or
there is anticipation of possible future reversion of atrial in the right atrial appendage. Both types of leads have
fibrillation, and the device programmed to DDI or VVI good chronic performance in terms of sensing and stimu-
in the interim. Alternatively the device may be implanted lation thresholds. However, an inflammatory response
55
in DDD mode allowing the device to Automatically Mode does develop at the lead–tissue interface and contributes
Switch to DDI or VVI whilst the patient is in atrial fibril- to an increase in capture thresholds. This is most marked
lation and then automatically switch back to DDD if in the first month (acute threshold phase) during which
atrial fibrillation reverts. the threshold may double or triple, before settling at a
55
The most common mode of pacing with dual chamber lower chronic threshold. Steroid-tipped leads are now
devices is DDD, unless the patient has recurrent atrial universal and limit the local inflammatory response,
55
tachyarrhythmias in which a non-tracking mode (e.g. reducing the magnitude of the acute threshold increase.
DDI) may be selected. 72,73 Patients with sinus node Because of the expected threshold change during the first