Avoiding Common Errors in the Emergency Department - Book 1

60

DO NOT FORGET TO CONSIDER
NONTRADITIONAL RISK FACTORS
FOR CORONARY ARTERY DISEASE
IN PATIENTS WITH CHEST PAIN

THOMAS HARTKA, MD, MS

Emergency providers (EP) frequently evaluate patients with acute chest pain.
While most EPs rely on traditional risk factors for coronary artery disease
(CAD) to aid their evaluation, they should also be cognizant that there are
nontraditional risk factors that can impact the evaluation of patients with
acute chest pain. Failure to consider these nontraditional risk factors may
lead EPs to inappropriately determine that a patient is at low risk for an acute
coronary syndrome (ACS). These nontraditional risk factors include chronic
kidney disease (CKD), radiation therapy (RT), systemic lupus erythematosus
(SLE), rheumatoid arthritis (RA), corticosteroid therapy, and human
immunodeficiency virus (HIV).

CHRONIC KIDNEY DISEASE

Cardiovascular disease is the leading cause of death among patients with
CKD. CKD has been shown to be an independent risk factor for CAD. There
is a 40% to 50% rate of significant CAD on angiogram of patients with
recent-onset end-stage renal disease (ESRD). Even in mild renal impairment,
there is an increased risk of CAD and ACS. Patients with Stage IV CKD
have a staggering 5-year mortality of 45.7%. In fact, even in patients with
Stage II CKD, the 5-year mortality is 19.5%. Patients with any degree of
renal dysfunction should be considered to have an increased risk of CAD.

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RADIATION THERAPY

RT to the chest has been shown to be a risk factor for the development of
CAD. Chest RT is a common adjunct to chemotherapy in select lymphomas
and breast cancer. Risk factors for the development of radiation-induced
CAD include higher dose of radiation, younger age at time of exposure, and
traditional cardiac risk factors. A meta-analysis of patients from early trials
of adjunct RT for breast cancer demonstrated a 27% increase in mortality
from heart disease. It should be noted that radiation techniques have changed
substantially since these early studies and modern RT probably confer less
risk. In most cases, CAD does not develop until more than a decade after
exposure. Many patients may forget to report their distal radiation treatment.
It is important for EPs to inquire about RT to the chest, especially in patients
who have a history of breast cancer or lymphoma.

SYSTEMIC LUPUS ERYTHEMATOSUS

SLE is a common disorder that involves chronic inflammation in multiple
organ systems, which often includes the cardiovascular system. It is well
established that patients with SLE have an increased risk for myocardial
infarction (MI). This risk is especially elevated in young female patients with
SLE. A study using age-matched controls demonstrated a 50-fold increase in
the rate of MI in female SLE patients aged 35 to 44 years. From autopsy
studies, it is known that patients with SLE have an increased rate of
atherosclerosis compared to the general population. The common treatment
for SLE, chronic corticosteroid use, has also been associated with higher
rates of MI in this population. EPs should have a heightened suspicion for
ACS in patients with SLE, especially younger female patients.

RHEUMATOID ARTHRITIS

Inflammatory joint diseases (IJD), especially RA, are associated with a
substantially increased risk of CAD. Patients with IJD have a higher risk of
premature death compared to the general population, and most of this risk
can be attributed to CAD. A Dutch population-based study found that the
development of CAD in patients with RA was similar to that of patients with
diabetes mellitus (DM). A large meta-analysis showed patients with RA had
a relative risk of 1.48 for developing CAD compared to patients without RA.
Special care should be taken when evaluating patients with RA, or other IJD,
who present with acute chest pain, as these patients have an increased risk of

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CAD similar to that of patients with DM.

CORTICOSTEROID THERAPY

Long-term corticosteroid treatment is used for the management of several
conditions that include organ transplantation, inflammatory bowel disease,
SLE, and RA. Many of these conditions independently increase a patient’s
risk of developing CAD; however, corticosteroids themselves also increase
this risk. Long-term corticosteroid use is associated with metabolic and
hemodynamic changes that include hyperlipidemia, insulin resistance, weight
gain, and central obesity. A large case-controlled cohort study found a
relative risk of acute MI to be 1.42 for patients on long-term oral
corticosteroids compared to nonusers. Long-term corticosteroid should be
considered a risk factor for CAD due to its side effects and the underlying
disease for which they have been prescribed.

HUMAN IMMUNODEFICIENCY VIRUS

Patients infected with HIV have been shown to be at increased risk of CAD
and ACS, the etiology of which is likely multifactorial. Replication of HIV
appears to directly increase the risk of CAD. A study that compared
continuous with intermittent antiretroviral therapy (ART) showed a relative
risk of 1.5 for nonfatal cardiovascular events for patients in the intermittent
ART arm. ART is associated with hyperlipidemia, decreased high-density
lipoprotein, and insulin resistance. Several large cohort studies have shown
an increased rate of MI, specifically treatment with a protease inhibitor (PI).
However, two large cohort studies failed to show an increased rate of MI or
symptomatic heart disease in patients taking ART. Despite some conflicting
data, patients with HIV and AIDS are likely at a higher risk for CAD and
ACS.

KEY POINTS

Patients with any degree of CKD should be considered to have an
increased risk of CAD.
SLE confers a 50-fold increase in the rate of MI in female patients
aged 35 to 44 years.
Patients with IJD have a risk of CAD similar to that of patients with
DM.
Long-term corticosteroid use causes hyperlipidemia, insulin

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resistance, weight gain, and central obesity and is a risk factor for
CAD.
HIV patients may be at increased risk of CAD and ACS.

SUGGESTED READINGS

Baris A, Kultigin T, Adrian C, et al. An update on coronary artery disease and
chronic kidney disease. Int J Nephrol. 2014;2014:767424. Available at:
http://dx.doi.org/10.1155/2014/767424.

Darby SC, Cutter DJ, Boerma M, et al. Radiation-related heart disease: Current
knowledge and future prospects. Int J Radiat Oncol Biol Phys.
2010;76:656–665.

Mattu A, Petrini J, Brady WJ, et al. Premature atherosclerosis and acute coronary
syndrome in systemic lupus erythematosus. Am J Emerg Med.
2005;23:696–703.

Mishra RK. Cardiac emergencies in patients with HIV. Emerg Med Clin N Am.
2010;28:273–282.

Nurmohamed MT, Heslinga M, Kitas GD. Cardiovascular comorbidity in
rheumatic diseases. Nat Rev Rheumatol. 2015;11:693–704.

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61

DO NOT FORGET ABOUT THE NON-
ACS CAUSES OF CHEST PAIN

PATRICK SILER, MD AND J. JEREMY THOMAS, MD,
FACEP, FAAEM

Annually, almost 6 million patients present to the emergency department
with a chief complaint of chest pain. Thankfully, the majority will not have
an acute coronary syndrome (ACS) as the etiology of their symptoms. There
are numerous etiologies of chest pain that range from benign to life
threatening. The emergency provider (EP) should broaden the differential of
acute chest pain beyond simply ACS, in order to promptly recognize and
treat additional life-threatening etiologies of chest pain.

Life-threatening causes of acute chest pain include ACS, aortic
dissection, pulmonary embolism (PE), tension pneumothorax, cardiac
tamponade, and esophageal rupture. Delayed diagnosis of these etiologies is
associated with significant increases in patient morbidity and mortality. This
chapter discusses pearls and pitfalls from the history of present illness and
physical examination for the non-ACS causes of chest pain.

THORACIC AORTIC DISSECTION

The incidence of thoracic aortic dissection (TAD) is ~3 cases per 100,000
people per year. The incidence of TAD peaks at age 70 and is more common
in males. Patients commonly have a history of hypertension. Patients with
TAD who are younger than 40 years of age commonly have a history of
connective tissue disease (i.e., Marfan syndrome, Ehlers-Danlos syndrome),
chronically abuse cocaine, or have a history of a bicuspid aortic valve.
Pregnancy, especially in the third trimester, is an established risk factor for
TAD. Additional risk factors for TAD include a prior history of aortic

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surgery, aortic valve disease, or a family history of aortic valve disease.

The most common presenting symptom is the abrupt onset of severe
pain. In contrast to the textbook descriptions of “tearing” or “ripping” pain,
patients with TAD more commonly report the abrupt onset of sharp pain that
quickly reaches maximal intensity. TAD should also be considered in any
patient in whom symptoms cross the diaphragm (i.e., chest and abdominal
pain). Acute onset of thoracic back pain can be reported in patients with a
dissection of the descending aorta.

Classic physical examination findings in the patient with TAD include a
blood pressure differential between the extremities, an extremity pulse
deficit, an aortic insufficiency murmur, or a focal neurologic finding.
Importantly, these findings are variable. In fact, a systolic blood pressure
differential has been found to be both poorly specific and sensitive for TAD.
A normal physical examination should not exclude the diagnosis of TAD
when the history is strongly suggestive of this etiology.

Chest x-ray (CXR) abnormalities seen in patients with TAD include a
widened mediastinum and an abnormal aortic contour. These classic
findings, however, are infrequently found in the majority of cases. Computed
tomography (CT) angiography is commonly used to confirm, or exclude, the
diagnosis of TAD. In recent years, there have been numerous studies that
have attempted to validate the use of D-dimer in the evaluation of patients
with TAD. At present, a negative D-dimer is insufficient to exclude TAD in
low-risk patients.

PULMONARY EMBOLISM

The estimated incidence of PE continues to rise. Risk factors for PE are well
documented and include a history of hypercoagulability, recent surgery or
prolonged immobilization, connective tissue disease, and exogenous estrogen
use.

Patients with PE commonly report dyspnea, with or without exertion, and
acute chest pain. The chest pain of PE is typically described as pleuritic in
character. Other historical features that may guide the EP are the presence of
lower extremity or calf pain, unilateral lower extremity swelling, cough, or
hemoptysis.

Similar to TAD, physical examination findings are often absent in the
patient with PE. Vital sign abnormalities may raise the clinician’s suspicion,
but are not always present at the time of ED evaluation. Patients with PE can
have tachycardia, tachypnea, or hypoxia. With a massive PE, the patient may
present with hypotension and signs of shock. Fever, when present, is

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typically low grade and can mislead the EP toward a diagnosis of
pneumonia. Unilateral lower extremity swelling can suggest the diagnosis of
DVT and raise suspicion for PE.

The diagnostic evaluation for PE requires an understanding of current
clinical decision rules. The well-versed EP should be able to exclude PE in
low-risk patients with a combination of clinical gestalt and the Pulmonary
Embolism Rule-out Criteria. Beyond these low-risk patients, EPs must
understand and correctly apply the Well’s criteria or Revised Geneva Score
to calculate pretest probability and guide further evaluation with either a D-
dimer test or CT angiography of the chest.

TENSION PNEUMOTHORAX

The incidence of tension pneumothorax varies widely and is dependent on
the population studied. The EP should have a high index of suspicion for
tension pneumothorax in patients with a history of trauma or recent
instrumentation of the thorax, neck, or upper extremity regions. Tension
pneumothorax almost always presents with the combination of acute chest
pain and respiratory distress. Clinical features include unilateral or absent
breath sounds, hypotension, jugular venous distension, and tracheal
deviation.

Tension pneumothorax is a clinical diagnosis that requires rapid
intervention to prevent cardiac arrest and death. Bedside ultrasound can be
used to quickly confirm the diagnosis in patients with an equivocal exam.

CARDIAC TAMPONADE

In cardiac tamponade, a pericardial effusion increases pericardial pressure,
decreases right ventricular filling, and decreases cardiac output. Etiologies of
pericardial effusion include malignancy, trauma, infectious diseases,
pericarditis, uremia, and acute myocardial infarction. Patients with a
pericardial effusion with development of tamponade often report chest pain,
dyspnea, and fatigue. Diminished breath sounds or a pericardial friction rub
are heard in only one-third of patients. The classic triad of hypotension,
muffled heart sounds, and jugular venous distension is a late finding in
patients with tamponade. The electrocardiogram in patients with a pericardial
effusion can demonstrate low voltage, tachycardia, and electrical alternans.

Similar to tension pneumothorax, bedside ultrasound can be used to
quickly confirm the diagnosis. The presence of an effusion with diastolic
right ventricular collapse should lead to emergent pericardiocentesis.

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ESOPHAGEAL RUPTURE

Esophageal rupture is a rare diagnosis. Common precipitants of esophageal
rupture include iatrogenic (i.e., esophagogastroduodenoscopy), severe
emesis, trauma, caustic ingestion, and esophageal foreign body. Chest pain is
most often retrosternal, is severe, and frequently radiates to the back, neck,
shoulders, or abdomen. Additional historical features may include dysphagia,
dyspnea, and emesis. Patients with esophageal rupture can present in shock
with tachycardia, hypotension, and signs of poor perfusion. Physical exam
findings can include subcutaneous emphysema in the cervical and clavicular
region. Patients with an intra-abdominal rupture may present with signs of a
surgical abdomen.

Although a CXR can demonstrate a pneumothorax, pneumomediastinum,
or pleural effusion, the diagnosis of esophageal rupture is confirmed with CT
of the chest. CT findings of esophageal rupture can include periaortic or
periesophageal air, pleural effusions, or soft tissue stranding.

KEY POINTS

Patients with TAD more commonly report the abrupt onset of sharp
pain that quickly reaches maximal intensity.
Patients with PE may not present with tachycardia, tachypnea, or
hypoxia.
Tension pneumothorax remains a clinical diagnosis.
The classic triad of hypotension, muffled heart sounds, and jugular
venous distension is a late finding in patients with cardiac tamponade.
The most common etiology of esophageal rupture is iatrogenic.

SUGGESTED READINGS

Brown MD, Newman DH. Evidence-based emergency medicine. Can a negative
D-dimer result rule out acute aortic dissection? Ann Emerg Med.
2011;58:375–376.

Hagan PG, Nienaber CA, Isselbacher EM, et al. The international registry of acute
aortic dissection (IRAD). JAMA. 2000;283:897–903.

Kline JA, Kabrhel C. Emergency evaluation for pulmonary embolism, Part 1:
clinical factors that increase risk. J Emerg Med. 2015;48:771–780.

Kline JA, Kabrhel C. Emergency evaluation for pulmonary embolism, Part 2:
diagnostic approach. J Emerg Med. 2015;49:104–117.

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Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial disease: Diagnosis
and management. Mayo Clinic Proc. 2010;85(6):572–593.

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62

BE CAUTIOUS DIAGNOSING
“ANXIETY” OR “PANIC

DISORDER” IN PATIENTS WITH
CHEST PAIN AND ANXIETY

ADAM E. NEVEL, MD, MBA

Chest pain is a common complaint in emergency department (ED) patients.
Patients with acute chest pain often present with concomitant symptoms such
as dyspnea, diaphoresis, anxiety, nausea, or emesis. While these additional
symptoms can be helpful to the emergency provider (EP), caution should be
taken when relying on any one symptom. Specifically, the association of
anxiety or panic with a noncardiac cause of chest pain can be a risky
assumption. While some studies have shown a high prevalence of panic
disorder within an ED chest pain population (as high as 20%), anxiety and
panic itself are poorly specific findings.

Patients with acute life-threatening cardiac or pulmonary conditions
frequently present with feelings of panic or impending doom in association
with chest pain. This may even be in the setting of a stressful situation and
mislead the EP to feel confident that anxiolytic therapy and reassurance is all
that may be needed. These stressful situations can be the catalyst for a more
serious condition, as moments of high stress and anger have been associated
with an increased incidence of cardiovascular events. These events are
believed to occur from the catecholamine surge that is associated with acute
emotional distress. This can, in turn, lead to increased platelet aggregation
and subsequent rupture of an unstable intracoronary plaque. Furthermore,
multiple studies have shown a link between anxiety disorders and higher

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rates of cardiac risk factors. This suggests that patients with a psychiatric
history may be at higher risk for cardiac disease.

Unfortunately, misdiagnosis of a cardiopulmonary condition as anxiety is
a frequent occurrence. A recent survey-style study of emergency medicine
physicians found that nearly 10% of self-reported missed diagnoses consisted
of acute coronary syndrome (ACS), pulmonary embolism (PE), or aortic
dissection. In addition to the patient consequences of a missed or delayed
diagnosis, there are significant medicolegal implications as well. Roughly
7% of all malpractice claims for misdiagnosis are due to missed myocardial
infarction (MI) or PE. With that in mind, EPs should undoubtedly think twice
before excluding a life-threatening etiology of chest pain based primarily on
the concomitant symptoms of anxiety or panic.

A less common, but well-described, condition involving ACS and
emotional distress is takotsubo cardiomyopathy, also termed “broken-heart
syndrome.” Patients with takotsubo often present with chest pain in the
setting of recent emo tional event (i.e., loss of a loved one).
Electrocardiogram (ECG) findings in patients with takotsubo can be similar
to an acute anterior wall MI. These patients may even have elevations in
cardiac biomarkers and echocardiogram findings that support a diagnosis of
acute infarction. Cardiac catheterization, however, reveals no culprit
coronary lesions. Instead, dilatation of the left ventricle is seen with a
pathognomonic appearance that resembles pots used by Japanese fisherman
to catch octopi known as “takotsubo.” While these patients typically undergo
standard ACS treatment, ECG and ventricular function typically normalize
within several months of the initial presentation. Importantly, the incidence
of recurrence can be as high as 5% within 6 years.

In general, while “anxiety” and “panic disorder” will likely remain
frequent diagnoses for ED patients with chest pain, EPs must remain cautious
to not prematurely jump to these diagnoses before a thorough evaluation is
performed.

KEY POINTS

Misdiagnosis of a cardiopulmonary condition as anxiety is a frequent
occurrence.
Patients with acute life-threatening cardiac or pulmonary conditions
often present with feelings of panic or impending doom in association
with chest pain.
Moments of high stress and anger have been associated with an

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increased incidence of cardiovascular events.
Multiple studies have shown a link between anxiety disorders and
higher rates of cardiac risk factors.
Takotsubo cardiomyopathy is a reversible cardiomyopathy that occurs
in the setting of a severe emotional event.

SUGGESTED READINGS

Handberg E, Eastwood J, Eteiba W, et al. Clinical implications of the women’s
ischemia syndrome evaluation: interrelationships between symptoms,
psychosocial factors and cardiovascular outcomes. Womens Health (Lond
Engl). 2013;9:479–490.

Huffman J, Pollack M, Stern T. Panic disorder and chest pain: mechanisms,
morbidity, and management. Prim Care Companion J Clin Psychiatry.
2002;4:54–62.

Mostofsky E, Penner EA, Mittleman MA, et al. Outbursts of anger as trigger of
acute cardiovascular events: A systematic review and meta-analysis. Eur Heart
J. 2014;35:1404–1410.

Schiff G, Hasan O, Kim S, et al. Diagnostic error in medicine, analysis of 583
physician-reported errors. Arch Intern Med. 2009;169:1881–1887.

Sharma AK, Singh JP, Heist EK. Stress cardiomyopathy: diagnosis,
pathophysiology, management, and prognosis. Crit Path Cardiol.
2011;10:142–147.

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63

ONE AND DONE: RAPID RULE-
OUT PROTOCOLS

MAITE ANNA HUIS IN ‘T VELD, MD AND SEMHAR Z.
TEWELDE, MD

Chest pain is one of the most common patient complaints in the emergency
department (ED). In order to prevent unnecessary increases in morbidity and
mortality, it is imperative to rapidly identify patients with an acute coronary
syndrome (ACS). Electrocardiography (ECG) abnormalities or elevated
troponin values strongly suggest the presence of an ACS and the need for
further evaluation. Many ED patients with an ACS, however, lack these
characteristic abnormalities. Notwithstanding, it is expensive, potentially
harmful, and simply not feasible to admit all ED patients who present with a
complaint of chest pain. The challenge for the emergency provider (EP) is to
identify chest pain patients at low risk of an ACS and who, subsequently, can
be safely discharged from the ED.

Many authors have attempted to develop risk stratification systems to
identify ED patients with acute chest pain that can be discharged. The most
commonly referenced stratification systems are listed in Table 63.1. Of the
current systems, the HEART Score may be the most applicable tool for the
EP and is the focus of the remainder of this chapter.

TABLE 63.1 CHEST PAIN RISK SCORING SYSTEMS

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STEMI, ST-segment elevation myocardial infarction; NSTEMI, Non-ST
Elevation MI; CHF, congestive heart failure; CAD, coronary artery
disease.

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The HEART Score was derived from a retrospective cohort of patients
who presented to the ED with chest pain. These patients were followed for 6
weeks to measure the primary study end point of a major adverse cardiac
event (MACE). MACEs were defined as acute myocardial infarction (AMI),
primary coronary intervention (PCI), coronary artery bypass graft (CABG),
or death. Importantly, the HEART Score is the only stratification system that
incorporates the history of present illness (HPI) into the calculation. The
remaining components of the HEART Score are listed in Table 63.2. After
the initial study, the authors conducted a large validation trial. These results
are listed in Table 63.3. A more recent validation study was conducted by
Mahler et al., who compared the HEART Score to traditional care in ED
patients with chest pain. In this study, the HEART Score decreased cardiac
testing at 30 days by 12.1%, ED length of stay by 12 hours, and increased
early ED discharge by 21.3%. There were no MACEs reported in the early
discharge group at 30 days.

TABLE 63.2 HEART SCORE

TABLE 63.3 RESULTS OF INITIAL HEART STUDY AND VALIDATION
STUDY

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There are limitations to the HEART Score. The most notable is the
subjective component of the HPI. Another limitation is validation. Though
there have been several validation studies performed, there are currently no
studies that are adequately powered to detect a difference in MACE.
Furthermore, the validation study by Backus et al. reported a nonadherence
rate of 29% to the HEART Score in patients considered low risk for an ACS.

These scoring systems can be used to assist the EP in identification of
ED patients that can be safely discharged. The HEART Score has been
shown to be a reliable and valuable tool for low-risk ED chest pain patients.
Notwithstanding, future studies are needed to further validate the use of the
HEART Score in a larger group of patients.

KEY POINTS

Multiple risk scoring systems are available for evaluation of acute
chest pain.
The HEART Score is the only tool that was developed to assess ED
chest pain patients.
The HEART Score incorporates the patient’s HPI, ECG, age, risk
factors for coronary artery disease, and troponin value.
Patients with a HEART Score <3 have a <2% risk of MACE at 6
months.

SUGGESTED READINGS

Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients
with acute coronary syndromes without persistent ST-segment elevation.
Results from an international trial of 9461 patients. The PURSUIT

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Investigators. Circulation. 2000;101(22):2557–2567.
Lagerqvist B, Diderholm E, Lindahl B, et al. FRISC score for selection of patients

for an early invasive treatment strategy in unstable coronary artery disease.
Heart. 2005;91(8): 1047–1052.
Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the
HEART score. Neth Heart J. 2008;16(6):191–196.

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64

BEWARE OF THE “HIGHLY
SENSITIVE” TROPONIN

MAITE ANNA HUIS IN ‘T VELD, MD AND SEMHAR Z.
TEWELDE, MD

Acute chest pain accounts for ~5 million emergency department (ED) visits
annually in the United States (US). Cardiac enzymes are routinely used to
risk stratify ED patients with acute chest pain when there is concern for an
acute myocardial infarction (AMI) or acute coronary syndrome (ACS).
Troponins T and I are the current standard cardiac enzymes for the diagnosis
of AMI, with a sensitivity of ~85% for cardiac injury. Importantly, current
troponin assays may take several hours after the onset of AMI symptoms to
return abnormal. It is for this reason that many current ED chest pain
protocols obtain serial troponin values over the course of several hours to
exclude an AMI.

In 2009, “highly sensitive” troponin assays became available. These
assays can detect the presence of troponin at much lower serum levels
compared to traditional troponin assays. It is important to understand what is
meant by the term “highly sensitive.” For a troponin assay to be labeled as
“highly sensitive,” the following two criteria must be met:

1) The assay has to detect troponin in more than 50% of healthy patients.
Traditional assays do not detect troponin in healthy individuals who do
not have myocardial disease; therefore, any elevation in a traditional
troponin value is abnormal. This is not the case with “highly sensitive”
troponin values.

2) The analytic precision has to be high. Precision is measured with the
coefficient of variation (CV). The CV is calculated by performing the
same test on the same blood sample several different times. The

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standard deviation is then divided by the mean value of these results to
yield the CV. For the diagnosis of an ACS, the CV should be 10% or
less.
These “highly sensitive” troponin assays have a higher analytic
sensitivity compared with traditional assays. Theoretically, a single negative
“highly sensitive” troponin could be used to exclude AMI, decrease ED
length of stay, and reduce health care costs. It is important to note that
analytic sensitivity is vastly different from diagnostic sensitivity. Since their
introduction into clinical practice, the use of “highly sensitive” troponins has
remained controversial.

WHAT DOES A POSITIVE RESULT MEAN?

There are numerous cardiac and noncardiac etiologies for elevated troponin
values. These are listed in Table 64.1. Due to their increased sensitivity,
many more patients will have an elevated “highly sensitive” troponin
compared to a traditional assay. A positive “highly sensitive” troponin
should be considered a marker of myocardial injury, but not necessarily
diagnostic of an AMI. Not surprisingly, “highly sensitive” troponin assays
have decreased specificity compared with traditional assays. Unfortunately,
there are insufficient data to direct treatment for patients with a single
elevated “highly sensitive” troponin value. Repeat troponin values aid in the
diagnosis of AMI or ACS. Rising values suggest myocardial ischemia,
whereas stable values may indicate another disease process listed in Table
64.1.

TABLE 64.1 ETIOLOGIES OF POSITIVE TROPONIN VALUES

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WHAT DOES A NEGATIVE RESULT MEAN?

Initial studies on “highly sensitive” troponins reported a negative predictive
value for AMI between 99% and 100%. Recent studies have failed to
replicate these initial findings. A recent international study found that up to
23% of patients ultimately diagnosed with an AMI had an initial negative
“highly sensitive” troponin. Sensitivity and negative predictive value,
however, did improve when troponin values were obtained 6 or more hours
after symptom onset.

Troponin values should be used as a risk stratification tool. It is
imperative to recognize that a negative value does not exclude AMI, whereas
a positive troponin value is not always due to an AMI. The current literature
does not support the use of “highly sensitive” troponins as a single modality
to exclude or diagnose AMI. In many cases, repeat values are needed, similar
to the current utilization of traditional troponin assays. At present, the U.S.
Food and Drug Administration has not approved “highly sensitive” troponin
assays for use in clinical practice.

KEY POINTS

Troponin values should be used to risk stratify patients with acute

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chest pain.
There are numerous noncardiac etiologies for an elevated troponin
value.
“Highly sensitive” troponins have a higher sensitivity and negative
predictive value, but lower specificity, when compared with
traditional troponin assays.
Up to 23% of patients with an AMI may have an initial negative
“highly sensitive” troponin value.
There are insufficient data to support the use of a single “highly
sensitive” troponin to exclude AMI.

SUGGESTED READINGS

Body R, Burrows G, Carley S, et al. Rapid exclusion of acute myocardial infarction
in patients with undetectable troponin using a sensitive troponin I assay. Ann
Clin Biochem. 2015; 52:543–549.

Body R, Carley S, McDowell G. Rapid exclusion of acute myocardial infarction in
patients with undetectable troponin using a high-sensitivity assay. J Am Coll
Cardiol. 2011;58(13): 1332–1339.

de Lemos JA. Increasingly sensitive assays for cardiac troponins: a review. JAMA.
2013;309(21): 2262–2269.

Hoeller R, Rubini Giménez M, Reichlin T, et al. Normal presenting levels of high-
sensitivity troponin and myocardial infarction. Heart. 2013;99(21):1567–1572.

Rubini Giménez M, Hoeller R, Reichlin T, et al. Rapid rule out of acute myocardial
infarction using undetectable levels of high-sensitivity cardiac troponin. Int J
Cardiol. 2013;168(4): 3896–3901.

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65

WHEN GOOD VADS GO BAD

CHRISTINA LYNN TUPE, MD, RDMS

With the development of the ventricular assist device (VAD), patients with
end-stage cardiac failure now have an increased survival rate and improved
quality of life. There are currently three indications for placement of a VAD:
as a bridge to recovery in patients whose cardiac function is temporarily
diminished (i.e., myocarditis), as a bridge to cardiac transplantation, and as
destination therapy for patients who are not candidates for cardiac
transplantation. The left ventricular assist device (LVAD) is the most
common VAD in clinical practice, though a right ventricular assist device
(RVAD) and a biventricular assist device (BiVAD) are also available. A
well-coordinated multidisciplinary team manages VAD patients.
Notwithstanding, these patients will develop complications from the device
that require emergency department (ED) evaluation and treatment. As such,
it is imperative for the emergency provider (EP) to have a systematic
approach to the evaluation of these complex patients.

The ED evaluation of a VAD patient should begin with assessment of the
patient’s airway, breathing, and circulation. Current VA devices deliver a
continuous flow of blood to the patient. As a result, a pulse is often absent or
markedly diminished. Noninvasive systolic and diastolic blood pressure
measurements may be inaccurate or simply not obtainable. For VAD
patients, the mean arterial blood pressure (MAP) can be obtained with a
blood pressure cuff and Doppler ultrasound over the brachial or radial artery.
The cuff should be inflated until flow ceases on the Doppler device. The cuff
should then be slowly deflated. Auscultation of the first flow signal indicates
the patient’s MAP. The target range for MAP in VAD patients is 70 to 90
mm Hg. An arterial line should be considered in the VAD patient who
appears critical or moribund. It is also important to evaluate additional signs
of peripheral perfusion, such as mental status, skin color and warmth, and
urine output. The patient’s chest should be auscultated to determine the

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presence, or absence, of the continuous hum of the VAD. The absence of an
audible hum suggests catastrophic VAD dysfunction and the need for
immediate resuscitation.

Additional components of the VAD that should be included in the initial
assessment are the speed, flow, power, and battery life of the device. These
values are found on the VAD monitor. Once the initial assessment has
occurred, the patient’s VAD coordinator should be contacted to assist with
management.

Atrial or ventricular dysrhythmias can occur in up to 50% of VAD
patients. As such, it is important to obtain an electrocardiogram (ECG) in
most VAD patients. Common etiologies for dysrhythmias include
hypovolemia, electrolyte derangements, and myocardial ischemia. VAD
patients who are unstable due to a dysrhythmia should be cardioverted or
defibrillated. It is recommended to place the defibrillation pads in an anterior
and posterior position. VAD patients who are stable yet have a concerning
dysrhythmia can receive antiarrhythmic medications. These patients should
also receive intravenous fluids and, if necessary, electrolyte replacement.

Bedside echocardiography (echo) is an invaluable tool in the ED
evaluation of VAD patients, especially those who appear critically ill. Echo
can be used to evaluate for pump thrombosis, right ventricular (RV) failure,
and “suction” events. Pump thrombus occurs in up to 2% of patients within 2
years after VAD implantation. Pump thrombosis reduces cardiac output,
which results in an elevation in the pump power reading. VAD patients with
suspected thrombosis should receive anticoagulation with heparin. Acute RV
failure can occur in up to 25% of VAD patients and is usually seen soon after
implantation. VADs are preload-sensitive devices. In low-flow states, the
negative pressure produced by the VAD can cause leftward displacement of
the intraventricular septum and produce a “suction” event. Suction events
usually result from hypovolemia, but they can also occur with cardiac
tamponade, dysrhythmias, and malposition of the inflow cannula. Initial
management of a suction event includes intravenous fluids, echo, and
arrangement for transfer to a VAD center to evaluate the inflow cannula.

Bleeding is an important and common complication that occurs in up to
40% of VAD patients. All VAD patients are placed on anticoagulant and
antiplatelet medications to decrease the rate of thromboembolic events. In
addition, these patients develop an acquired von Willebrand syndrome in
response to shear forces from the VAD. Finally, the decreased pulse pressure
of the continuous flow contributes to arteriovenous malformations, especially
in the jejunum. VAD patients who are unstable due to hemorrhage should
receive blood products and agents to reverse anticoagulation.

373

Anticoagulation reversal in a stable VAD patient, however, should be done
in consultation with the patient’s VAD team.

VAD patients are at high risk for infection. Infection can occur anywhere
along the VAD including the surgical site, driveline, pump, or device pocket.
VAD infections can be caused by a variety of organisms, including gram-
positive organisms, especially coagulase-negative staphylococci and
Staphylococcus aureus, gram-negative organisms, and fungi. Critically ill
VAD patients should receive broad-spectrum antibiotics to cover both gram-
positive and gram-negative organisms.

Rarely, VAD patients may present in cardiac arrest. In these patients, the
controller should be quickly evaluated for battery life and proper
connections. Echo should be used to evaluate for pericardial effusion, left
ventricular (LV) function, or RV dilatation. Most VAD manufacturers state
that cardiopulmonary resuscitation (CPR) should be done only if absolutely
necessary, primarily due to concern of dislodgement of the inflow cannula
from the LV. The only literature that exists on CPR for the VAD patient is a
recent retrospective analysis of eight VAD patients who received CPR. In
this study, no patient experienced dislodgement of the device with a 50%
survival rate with good neurologic outcome.

VAD patients are a special challenge for the EP. Through a careful
assessment of the VAD, physical exam, MAP, ECG, and echo, the EP can
resuscitate the good VAD that has gone bad.

KEY POINTS

Contact the patient’s VAD coordinator as soon as possible.
Obtain an ECG early to evaluate for dysrhythmias.
Consider bleeding and sepsis in any critically ill VAD patient.
Use echo to assess for pump thrombosis, RV failure, and suction
events in the VAD patient.
CPR is reasonable in the VAD patient in cardiac arrest.

SUGGESTED READINGS

Partyka C, Taylor B. Review article: ventricular assist devices in the emergency
department. Emerg Med Australas. 2014;26(2):104–112.

Pratt AK, Shah NS, Boyce SW. Left ventricular assist device management in the
ICU. Crit Care Med. 2014;42:158–168.

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Shriner Z, Bellezzo J, Stahovich M, et al. Chest compressions may be safe in
arresting patients with left ventricular assist devices (LVADs). Resuscitation.
2014;85(5):702–704.

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66

DON’T STRESS THE STRESS TEST
IN SUSPECTED ACS

CHRISTINA LYNN TUPE, MD, RDMS

The evaluation of the emergency department (ED) patient with acute chest
pain centers on the history of present illness (HPI), physical examination,
and electrocardiogram (ECG). Often, the emergency provider (EP) utilizes
troponin values and the results of prior cardiac stress tests to further risk
stratify patients and determine the need for additional management. The role
of prior cardiac stress tests in the risk stratification of ED patients with
suspected acute coronary syndrome (ACS) is uncertain.

The goal of a cardiac stress test is to identify the patient with obstructive
coronary artery disease (CAD), typically defined as stenosis of 50% or more
of a coronary artery on angiography. Traditional stress tests include exercise
ECG (on a treadmill), echocardiography, or nuclear medicine studies. All
have rest and exercise phases. The exercise phases of echocardiography and
nuclear medicine studies can be performed with physical exertion or
chemically induced with medication such as adenosine or dobutamine.
Depending on the study, the test will detect ischemic ECG changes, wall
motion abnormalities, or diminished tracer update indicative of decreased
perfusion to regions of the myocardium. Test availability, the patient, and the
presence of comorbid conditions often determine the type of stress test that is
performed.

The pooled sensitivity for all cardiac stress tests range from 67% to 85%,
with specificity that ranges from 70% to 95%. Stress tests have higher
sensitivity in patients with multivessel CAD. Exercise ECG stress tests have
a sensitivity of 68% and a specificity of 77% for CAD. The presence of
multivessel disease increases the sensitivity to 81%. Importantly, the
sensitivity and specificity are lower in women than in men. Most

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cardiologists obtain an exercise ECG stress test as the initial outpatient test.
Recently, coronary computed tomography angiography (CCTA) has emerged
as a means of diagnosing CAD and defining coronary lesions. The pooled
sensitivity of CCTA ranges between 98% and 99%, with a specificity
between 82% and 89%. The positive predictive value of CCTA is reported to
be 85%, whereas the negative predictive value is ~92%.

The ED patient with acute chest pain is very different from the
asymptomatic patient who undergoes a routine outpatient cardiac stress test.
Nerenberg and colleagues reviewed the disposition of ED patients evaluated
for ACS. They authors found that a previous negative stress test did not
change the rate of hospital admission. Furthermore, there was no difference
in the rate of adverse events among patients with a positive stress test, a
negative stress test, or no previous stress test. In another series of ED
patients, Smith and associates found that ~5% of patients were diagnosed
with an acute myocardial infarction within 3 years of a negative stress test
result. Walker and colleagues reviewed the records of ED patients with chest
pain and a negative, or inconclusive, stress test result within the preceding 3
years. This study included treadmill and pharmacologic echocardiograms,
pharmacologic nuclear medicine studies, treadmill nuclear studies, and a
treadmill ECG-only evaluation. The authors defined CAD as a myocardial
infarction identified by positive cardiac enzymes, a subsequent positive stress
test, a cardiac catheterization that required intervention, coronary artery
bypass graft surgery, or death caused by cardiac arrest. Approximately 20%
of patients were diagnosed with CAD after a negative stress test within 3
years of the ED presentation. Of patients with significant CAD, 23.5% had a
negative stress test within 1 month before their ED presentation.

Cardiac stress test is a valuable tool for cardiologists to screen
outpatients for CAD. In an outpatient setting, stress tests are used to identify
fixed obstructions to coronary artery flow. In ED patients with acute chest
pain, however, the intent of testing is to identify acute plaque rupture and
thrombus formation. As such, cardiac stress tests have limited utility in the
ED evaluation of acute chest pain. The EP should not exclude an ACS in the
ED patient with acute chest pain based solely on a recent negative stress test
result. If the HPI is concerning, the EP should continue with the evaluation
and subsequent admission.

KEY POINTS

Cardiac stress tests have a pooled sensitivity of 67% to 85%.

377

The sensitivity of stress tests is higher in patients with multivessel
disease than in those with single-vessel disease.
The sensitivity and specificity of exercise ECG stress testing are lower
in women than in men.
A previous negative stress test should not be the basis for subsequent
decisions regarding hospital admission.
Significant CAD can be present despite a recent negative stress test
result.

SUGGESTED READINGS

Arbab-Zadeh A. Stress testing and non-invasive coronary angiography in patients
with suspected coronary artery disease: Time for a new paradigm. Heart Int.
2012; 7(1):e2.

Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for
exercise testing: Summary article: A report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2002;106(14): 1883–1892.

Nerenberg RH, Shofer FS, Robey JL, et al. Impact of a negative prior stress test on
emergency physician disposition in ED patients with chest pain syndromes. Am
J Emerg Med. 2007;25(1):39–44.

Smith SW, Jackson EA, Bart BA, et al. Incidence of myocardial infarction in
emergency department chest pain patients with a recent negative stress imaging
test. Acad Emerg Med. 2005;12(5):51.

Walker J, Galuska M, Vega D. Coronary disease in emergency department chest
pain patients with recent negative stress testing. West J Emerg Med.
2010;11(4): 384–388.

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67

REMEMBER TO OBTAIN A RIGHT-
SIDED ELECTROCARDIOGRAM IN A

PATIENT WITH AN INFERIOR
MYOCARDIAL INFARCTION

CARMEN AVENDANO, MD AND SEMHAR Z. TEWELDE,
MD

An acute inferior myocardial infarction (IMI) typically causes ST-segment
elevation (STE) in leads II, III, and aVF on the 12-lead electrocardiogram
(ECG). In addition to these findings, an IMI can also produce ST-segment
depression (STD) or T-wave inversion (TWI) in lead aVL. In fact, STD or a
new TWI in lead aVL is often the first ECG abnormality seen in patients
with an acute IMI. This underscores the importance of obtaining serial ECGs
in patients with a suspected acute coronary syndrome.

When an acute IMI is diagnosed, a right-sided ECG should be obtained
to exclude the presence of a concomitant right ventricular myocardial
infarction (RVMI). RVMIs can complicate 30% to 50% of acute IMIs. A
right-sided ECG is performed by taking leads V3 through V6 and placing
them on the right side of the chest. These leads are then labeled V3R through
V6R. STE of 0.5 mm or greater in one or more of leads V4R through V6R
has a sensitivity of 90% and specificity of 91% for an RVMI. In an RVMI,
STE is more commonly seen in lead V4R compared with leads V5R and
V6R. In fact, STE greater than 1 mm in lead V4R suggests a proximal
occlusion of the right coronary artery (RCA) and an increased risk for
atrioventricular block. Additional ECG findings that suggest an RVMI
include STE in lead V1, STE in lead III that is greater than the STE in lead

379

II, and an isoelectric ST segment in lead V1 with STD in lead V2.

It is important to diagnose an RVMI because it affects patient
management. Patients with an acute myocardial infarction commonly receive
nitrate medications in addition to other time-sensitive therapies. Patients with
an RVMI are preload dependent and require intravenous fluids to maintain
adequate perfusion. A precipitous decline in blood pressure can occur when
nitrates are administered to patients with an RVMI. Any medication that may
decrease preload should be avoided in the setting of an RVMI. Morphine has
been shown to increase infarct size and decrease coronary blood flow by up
to 13% in patients with an RVMI. Morphine should be avoided in patients
with an RVMI. Additional therapies for patients with an RVMI remain the
same as those for patients with non-RVMIs.

KEY POINTS

RVMI can complicate up to 50% of IMIs.
When an IMI is identified, a right-sided ECG should be obtained.
STE in lead V4R indicates a proximal occlusion of the RCA and an
increased risk for AVB.
STE in lead V1 with concomitant depression in lead V2 suggests an
RVMI.
Patients with an RVMI are preload dependent. Avoid nitrates and
administer intravenous fluids.

SUGGESTED READINGS

Chhapra D, Mahajan SK, Thorat ST. A study of the clinical profile of right
ventricular infarction in context to inferior wall myocardial infarction in a
tertiary care centre. J Cardiovasc Dis Res. 2013;4:170–176.

Inohara T, Kohsaka S, Fukuda K, Menon V. The challenges in the management of
right ventricular infarction. Eur Heart J Acute Cardiovasc Care.
2013;2:226–234.

Ondrus T, Kanovsky J, Novotny T, et al. Right ventricular myocardial infarction:
From pathophysiology to prognosis. Exp Clin Cardiol. 2013;18:27–30.

Waldo SW, Brenner DA, Li S, et al. Reperfusion times and in-hospital outcomes
among patients with an isolated posterior myocardial infarction: insights from
the National Cardiovascular Data Registry (NCDR). Am Heart J.
2014;167(3):350–354.

Wei EY, Hira RS, Huang HD, et al. Pitfalls in diagnosing ST elevation among
patients with acute myocardial infarction. J Electrocardiol. 2013;46:653–659.

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68

PITFALLS IN HYPERTENSIVE
EMERGENCIES

STEPHEN D. LEE, MD

Approximately 1% to 2% of patients with hypertension will present with a
hypertensive emergency, defined as organ dysfunction due to an elevated
blood pressure. Importantly, there is no specific blood pressure threshold that
identifies a patient with a hypertensive emergency. In a hypertensive
emergency, the initial pathophysiologic event is an abrupt increase in
systemic vascular resistance (SVR). The abrupt increase in SVR causes
endothelial injury and results in increased vascular permeability, platelet
activation, and fibrin deposition. This fibrin deposition causes microvascular
thrombi, vessel occlusion, organ ischemia, and ultimately organ dysfunction.

Patients with a hypertensive emergency should be treated with an
intravenous vasodilator medication. While patients with asymptomatic
hypertension can be safely treated with oral medications to slowly reduce
blood pressure, patients with organ dysfunction due to elevated blood
pressure should be given an easily titratable intravenous medication. This
allows for a safe, controlled, and appropriate reduction in blood pressure in
order to halt organ dysfunction.

Appropriate reduction in blood pressure is central to the management of
a hypertensive emergency. The target reduction in blood pressure depends on
the disease process and the specific organ involved. An abrupt and
aggressive reduction in blood pressure can cause further injury and ischemia,
as blood pressure can drop below the patient’s autoregulatory threshold.
Current literature recommends that the mean arterial blood pressure (MAP)
be lowered no more than 25% in the first 1 to 2 hours from the time of
diagnosis. Table 68.1 lists common hypertensive emergencies and the current
recommended blood pressure targets. Conditions that require more

381

aggressive MAP reduction in a shorter time period include aortic dissection,
intracerebral hemorrhage, and eclampsia. For these conditions, it may be
necessary to reduce MAP more than 25% in the first 2 hours in order to
minimize progressive organ injury. In contrast, it may be preferable to avoid
blood pressure reduction altogether for the patient with an acute ischemic
stroke, except in those patients with severe hypertension (>220/110 mm Hg)
or those receiving thrombolysis (>185/110 mm Hg). For patients with acute
myocardial infarction or acute pulmonary edema, MAP is reduced until
clinical symptoms improve.

TABLE 68.1 HYPERTENSIVE EMERGENCIES AND BLOOD PRESSURE
GOALS

There is currently limited data on the medications used to treat patients
with a hypertensive emergency. Medications are best chosen according to the
disease process. The most commonly used medications include calcium
channel blockers (e.g., nicardipine) and beta-blockers (e.g., labetalol).
Nicardipine is a second-generation calcium channel blocker that results in
coronary and cerebral vasodilation. Nicardipine is commonly used to treat
patients with a neurologic emergency, as it has little effect on intracranial
pressure. In contrast, sodium nitroprusside is an arterial and venous
vasodilator that can cause a coronary and cerebral “steal” phenomenon.
Nitroprusside should thus be avoided in patients with ischemic stroke or
acute myocardial infarction. Nitroprusside is also best avoided in patients
with eclampsia, as its by-product (cyanide) can accumulate with prolonged
use and may cause harm to the fetus. Beta-blockers (e.g., esmolol) should be
the first-line treatment for patients with an aortic dissection to reduce heart
rate. Once the target heart rate is reached, another vasodilator (e.g.,
nicardipine) can be administered to reduce the systolic blood pressure (SBP)
to 100 to 120 mm Hg. The direct vasodilator hydralazine should be avoided
in patients with a hypertensive emergency, as it can cause a reflex
tachycardia and has a duration of action that can exceed 10 hours.

382

It is important to consider secondary causes of hypertension in the
patient with a hypertensive emergency. Secondary causes of hypertension
include endocrine conditions (e.g., pheochromocytoma), drugs of abuse (e.g.,
cocaine, amphetamines, phencyclidine), and medication or drug withdrawal
syndromes. In these conditions, beta-blocker medications should be avoided
to prevent a catecholamine surge from unopposed alpha-adrenergic receptor
stimulation. The addition of other medications, such as a benzodiazepine or
clonidine, may prove beneficial in treating patients with these
hyperadrenergic states.

KEY POINTS

Hypertensive emergency is organ dysfunction due to elevated blood
pressure.
Lower the MAP by no more than 25% in the first 2 hours to avoid
hypoperfusion and organ ischemia.
Tailor your pharmacologic agent to the disease process.
Avoid reflex tachycardia in aortic dissection by using a beta-blocker
first.
Consider alternative sources for elevated blood pressure (e.g., cocaine,
pheochromocytoma).

SUGGESTED READINGS

Baumann B, Cline D, Pimenta E. Review article: Treatment of hypertension in the
emergency department. J Am Soc Hypertens. 2011;5:366–377.

Elliott W. Clinical features in the management of selected hypertensive
emergencies. Prog Cardiovasc Dis. 2006;48:316–325.

Muiesan M, Salvetti M, Pedrinelli R, et al. An update on hypertensive emergencies
and urgencies. J Cardiovasc Med. 2015;16(5):372–382.

Singh M. Hypertensive crisis-pathophysiology, initial evaluation, and management.
J Indian Coll Cardiol. 2011;1:36–39.

Vadhera R, Simon M. Hypertensive emergencies in pregnancy. Clin Obstet
Gynecol. 2014;57: 797–805.

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69

KNOW THE DIFFERENTIAL FOR ST-
SEGMENT ELEVATION: IT’S MORE

THAN JUST ACUTE CORONARY
SYNDROME

KATHLEEN STEPHANOS, MD AND SEMHAR Z. TEWELDE,
MD

Emergency providers (EPs) interpret electrocardiograms (ECGs) on a daily
basis for a variety of clinical scenarios. An ECG is most commonly obtained
for the emergency department (ED) patient with acute chest pain. In these
patients, it is imperative to diagnose an ST-segment elevation myocardial
infarction (STEMI), as emergent reperfusion therapy is indicated.
Notwithstanding, there are numerous conditions that cause ST-segment
elevation (STE) on an ECG that are not attributable to an acute coronary
syndrome. In order to avoid errors in diagnosis or management, it is
important for the EP to know the differential diagnosis for STE.

Early repolarization is a common cause of STE. It is typically seen in
males younger than 45 years of age and in athletic patients. Recent literature
has demonstrated that early repolarization is a risk factor for sudden cardiac
death, as it increases the risk for idiopathic ventricular fibrillation. Early
repolarization typically produces a notched J-point with STE that is <3 mm
on the ECG. There is currently no specific treatment for early repolarization.
Patients should be instructed to follow up with their primary care physician.
Cardiology referral is appropriate for patients who have a personal or family
history of sudden cardiac death or additional ECG findings that suggest the
presence of coronary artery disease.

384

Pericarditis is another condition that should be considered in the
differential diagnosis of STE. Patients typically present with acute chest pain
that is pleuritic and positional. Importantly, pericarditis produces diffuse STE
that is concave in appearance. The STE is most prominent in ECG leads I, II,
III, aVF, aVL, and V2 to V6. The presence of reciprocal ST-segment
depression or T-wave inversions is more consistent with the diagnosis of
STEMI. In addition, STE that is flat or horizontal should be considered an
STEMI until proven otherwise. PR-segment depression is commonly thought
to be pathognomonic for pericarditis; however, this finding can be transient
and can also be seen in patients with an STEMI. Rapid evolution of ST-
segment changes during the course of the ED evaluation is more suggestive
of an acute coronary syndrome in contrast to pericarditis. The ECG changes
seen in pericarditis typically occur over the course of several weeks.

Left bundle-branch block (LBBB), left ventricular hypertrophy (LVH),
and left ventricular aneurysm can all cause STE. In the setting of LBBB, the
ST segment is directly opposite to that of the main QRS complex vector. In
leads V1 to V3, the QRS vector is negative, thereby producing STE. This
discordant STE is typically less than 5 mm in the setting of LBBB. Patients
with a pacemaker will also demonstrate STE similar to a LBBB. LVH
produces discordant STE, with a deep S wave in leads V1 to V3 and a tall R
wave in leads I, aVL, V5, and V6. Patients with a left ventricular aneurysm
may have STE along with deep anterior or septal Q waves in leads V1 to V3.
Similar to pericarditis, LBBB, LVH, and left ventricular aneurysm do not
cause dynamic ECG abnormalities.

Hyperkalemia is often referred to as the “great imitator” of ECG
abnormalities. Hyperkalemia can produce numerous ECG findings that can
easily be misdiagnosed and incorrectly treated. It is well known to cause the
appearance of STE, as the T-wave is pulled to a peak. Additional signs of
hyperkalemia include peaked T-waves, bradydysrhythmias,
tachydysrhythmias, and widened QRS complexes.

Less common causes of STE include Prinzmetal angina and takotsubo
cardiomyopathy. Both of these clinical entities are often diagnosed as
STEMI in patients with acute chest pain. These diagnoses are often made
following emergent cardiac catheterization.

KEY POINTS

STEMI is not the only cause of STE.
Dynamic ECG abnormalities are more consistent with an acute

385

coronary syndrome.
Nonischemic causes of STE include early repolarization, LBBB,
LVH, pericarditis, and left ventricular aneurysm.
Hyperkalemia should be considered in the differential diagnosis of
STE.
The diagnosis of Prinzmetal angina or takotsubo cardiomyopathy is
often made following emergent cardiac catheterization for presumed
STEMI.

SUGGESTED READINGS

Hanna EB, Glancy DL. ST-segment elevation: Differential diagnosis caveats.
Cleve Clin J Med. 2015;82(6):373–384.

Huang HD, Birnbaum Y. ST elevation: Differentiation between ST elevation
myocardial infarction and nonischemic ST elevation. J Electrocardiol.
2011;44(5):494.e1–494.e12.

Toledano K, Rozin AP. Early repolarization: Innocent or dangerous? Am J Med
Sci. 2013; 346(3):226–232.

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70

DO NOT RELY ON A SINGLE ECG
TO EVALUATE CHEST PAIN IN THE

ED

KATHLEEN STEPHANOS, MD AND SEMHAR Z. TEWELDE,
MD

Chest pain is the second most common emergency department (ED)
complaint and accounts for over 8 million ED visits annually in the United
States. Fortunately, only a minority of patients will have a life-threatening
cause of their acute chest pain. Notwithstanding, it is critical to identify
patients with an acute coronary syndrome (ACS). At present, ~2% of ED
patients with an ACS are misdiagnosed, which leads to increased morbidity
and mortality.

The electrocardiogram (ECG) is a quintessential component of the
evaluation of ED patients with acute chest pain. It is one of the most
commonly utilized diagnostic tests in emergency medicine. Significant ST-
segment elevation with reciprocal changes in the patient with acute chest
pain is often easily recognized as an ACS. However, the initial ECG
frequently demonstrates nonspecific changes, or is normal, in the setting of
an ACS. As a result, it is important for the emergency provider to recognize
the limitations of a single ECG in the evaluation of ED patients with acute
chest pain.

Up to 20% of chest pain patients who ultimately require reperfusion
therapy have an initial ECG that is normal or displays nonspecific
abnormalities. Ischemic changes can occur rapidly and unbeknownst to the
clinician if an ECG is not repeated. Current guidelines from the American
Heart Association for the evaluation of low-risk ED patients with chest pain

387

recommend serial ECGs. Serial ECGs are also recommended in the most
recent AHA guideline for non–ST-segment elevation myocardial infarction.
Serial ECGs improve the sensitivity of identifying an ACS from 43% to
83%. Ideally, an ECG should be repeated every 5 to 10 minutes in
symptomatic patients or those who have a change in the character of their
chest pain. While this short time frame for a repeat ECG can be challenging
to meet in a busy ED, it can make a significant impact upon the delivery of
time-sensitive therapies. The initial, and repeat, ECGs should be compared
with any prior ECGs to identify subtle abnormalities such as new T-wave
inversions.

Currently, it is unclear how many ECGs should be obtained in the ED
patient with acute chest pain. Nevertheless, it is a high-yield diagnostic test
with minimal cost. For select patients, serial ECGs may make the difference
between life and death due to ACS.

KEY POINTS

Approximately 2% of patients with an ACS are missed.
The initial ECG in patients with an ACS is often nonspecific.
Serial ECGs improve the accuracy of an ACS diagnosis.
In symptomatic patients, obtain serial ECGs every 5 to 10 minutes.
Compare the current ECG to prior ECGs to detect subtle changes.

SUGGESTED READINGS

Amsterdam EA, Kirk JD, Bluemke DA, et al. Testing of low-risk patients
presenting to the emergency department with chest pain: A Scientific Statement
From the American Heart Association. Circulation. 2010;122:1756–1776.

Gibler WB, Young GP, Hedges JR, et al. Acute myocardial infarction in chest pain
patients with nondiagnostic ECGs: Serial CK-MB sampling in the emergency
department. The Emergency Medicine Cardiac Research Group. Ann Emerg
Med. 1992;21(5): 504–512.

Silber SH, Leo PJ, Katapadi M. Serial electrocardiograms for chest pain patients
with initial nondiagnostic electrocardiograms: Implications for thrombolytic
therapy. Acad Emerg Med. 1996;3(2):147–152.

388

71

KNOW HOW TO DIAGNOSE ACUTE
MI IN PATIENTS WITH AN LBBB

OR PACEMAKER

ANTHONY ROGGIO, MD

A left bundle branch block (LBBB) is generated on an electrocardiogram
(ECG) when an impulse is impeded as it passes down the conduction system
and attempts to innervate the left side of the heart. As a result, cardiac
myocytes are initially depolarized through the right bundle and then pass
through the septum to depolarize the left ventricle. This results in sequential
depolarization of the ventricles from right to left and creates an ECG pattern
characterized by a QRS complex >120 ms, a deep S wave in the anterior
leads V1 to V3, and a tall monophasic R wave in leads I, V5, and V6 (Figure
71.1). A similar ECG pattern can be seen in patients with a ventricular
pacemaker. The pacemaker leads first activate the myocytes of the right
ventricle, followed by depolarization of the left ventricle myocytes.

389

390

Figure 71.1 Left bundle branch block defining characteristics. Image
from Creative Commons, Left bundle branch block (LBBB). 2015.

In LBBB (with or without a ventricular pacemaker), there is discordance
between the QRS complex and the J-point. When the QRS complexes point
upward, the J-point should be below the isoelectric line. Conversely, when
the QRS complex points downward, the J-point should be above the
isoelectric line. This phenomenon is known as “appropriate discordance”
(Figure 71.2) and leads to difficulty in the diagnosis of an acute ST-segment
elevation myocardial infarction (STEMI). In fact, classic teaching states that
an acute STEMI cannot be diagnosed on ECG in the presence of an LBBB.
This has led to the common practice of administering emergent reperfusion
therapy (thrombolytic medication or cardiac catheterization) in patients who
have a new LBBB on ECG and symptoms that are consistent with a
myocardial infarction. However, recent literature has questioned the benefit
of emergent reperfusion therapy in patients with a new LBBB, where up to
86% of patients with an LBBB do not have an acute coronary artery

391

occlusion. As a result of recent literature, the finding of a new, or presumed
new, LBBB on the ECG has been removed from current guidelines as an
indication for emergent reperfusion therapy.

392

Figure 71.2 Examples of appropriate discordance.

Published in 2006, the Sgarbossa criteria are a set of validated ECG
criteria to help practitioners accurately diagnose an STEMI in the setting of
LBBB. These criteria are listed and illustrated in Figure 71.3. A score of 3 or
more points is associated with a sensitivity of >97% for the diagnosis of

393

acute myocardial ischemia. Since the initial publication of the Sgarbossa
criteria, multiple studies have shown that the last criterion (Rule 3) has the
lowest specificity for acute ischemia. In 2012, Smith and colleagues
proposed a modified version of the third Sgarbossa criteria. This
modification measures the ratio of the ST segment to the S wave (Figure
71.4). Acute ischemia is present if this ratio is >0.25. Both Cai and
colleagues and Gregg and colleagues evaluated this modification to the third
Sgarbossa criteria and demonstrated increased sensitivity with a specificity
that ranges from 90% to 95%.

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Figure 71.3 The Sgarbossa criteria. Rule 1: Concordant ST-segment
elevation ≥ 1 mm in any lead (5 points) (A). Rule 2: Concordant ST-
segment depression ≥ 1 mm in any one of leads V1 to V3 (3 points)
(B). Rule 3: Discordant ST-segment elevation ≥ 5 mm in any lead (2
points) (C).

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Figure 71.4 Smith-modified Sgarbossa criteria. Rule 3 Modified:
ST-segment elevation ≥ 25% size of QRS complex (ST/S ≥ 0.25).

KEY POINTS

The Sgarbossa criteria can be used to diagnose STEMI in the setting
of an LBBB.
A Sgarbossa score of 3 or more has a high sensitivity for acute
myocardial ischemia.
The third Sgarbossa criteria, discordance of the ST segment of more
than 5 mm, is the least specific for STEMI.
A modified version of the third Sgarbossa criteria, the ST-segment to
S-wave ratio, has a high sensitivity and specificity for acute ischemia.
Current guidelines recommend reperfusion therapy in patients with an
LBBB and:

Hemodynamic instability or evidence of acute heart failure
A Sgarbossa score of ≥ 3
A positive modified Sgarbossa criteria
Elevated troponin values, regional wall motion abnormalities on

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echocardiography that are suggestive of acute myocardial
infarction or have evolving ECG changes

SUGGESTED READINGS

Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the
2013 ST-elevation myocardial infarction guideline: From falsely declaring
emergency to denying reperfusion in a high-risk population. Are the Sgarbossa
Criteria ready for prime time? Am Heart J. 2013;166(3):409–413.

Gregg RE, Helfenbein ED, Babaeizadeh S. New ST-segment elevation myocardial
infarction criteria for left bundle branch block based on QRS area. J
Electrocardiol. 2013;46(6):528–534.

Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of
evolving acute myocardial infarction in the presence of left bundle-branch
block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen
Activator for Occluded Coronary Arteries) Investigators. N Engl J Med.
1996;334(8):481–487.

Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-elevation myocardial
infarction in the presence of left bundle branch block with the ST-elevation to
S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med.
2012;60(6):766–776.

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72

GETTING AHEAD OF CARDIOGENIC
PULMONARY EDEMA: AGGRESSIVE

NITROGLYCERIN USAGE

SEMHAR Z. TEWELDE, MD

The management of patients with acute decompensated heart failure (ADHF)
has historically focused on the administration of diuretic medications. In fact,
the 2013 American Heart Association/American College of Cardiology
Foundation Heart Failure Guidelines provide a Class Ia recommendation that
“patients with significant fluid overload should initially be treated with loop
diuretics given intravenously that should begin in the emergency department
without delay.” In recent years, there are increasing data that support the use
of high-dose vasodilator therapy as the initial treatment for patients with
ADHF. In 2007, the American College of Emergency Physicians published a
clinical policy on ADHF, which emphasized the use of vasodilator therapy in
the emergency department (ED) management of patients with ADHF.

Importantly, the majority of ED patients who present with ADHF are not
volume overloaded. Rather, their pulmonary congestion is due to volume
redistribution. The classic ED presentation for these patients includes acute
dyspnea, hypertension, and pulmonary edema. Often, these patients arrive to
the ED by ambulance and receive sublingual nitroglycerin therapy (0.4 mg
every 5 minutes) during their transport. Upon ED arrival, patients should be
continued on aggressive vasodilator therapy with nitroglycerin. In most
cases, nitroglycerin therapy is started at 50 mcg/min, a dose that is less than
what the patient received via the sublingual route with paramedics (80
mcg/min). Numerous studies have demonstrated the importance of initiating
a nitroglycerin infusion at a dose of 120 to 200 mcg/min. A report in the
American Journal of Cardiology noted that at least 120 mcg/min of

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nitroglycerin is required to produce a significant decrease in pulmonary
capillary wedge pressure. The nitroglycerin infusion can be rapidly increased
to 400 mcg/min based upon clinical effect and patient symptoms. Though
there have yet to be conclusive data that aggressive vasodilator use improves
long-term mortality, it has been shown to prevent intubation and mechanical
ventilation in this patient population.

The concomitant use of noninvasive ventilation (NIV) and high-dose
vasodilator has been shown to decrease intubation rates, intensive care unit
admissions, and hospital length of stay for patients with ADHF. NIV should
be initiated early in ED patients with ADHF. Once the patient improves
(decreased respiratory rate, decreased dyspnea, improved oxygenation,
improved blood pressure), diuretic therapy can be considered. Importantly,
diuretics require adequate renal perfusion in order to be effective. During the
initial ED evaluation and management when patients are in extremis, renal
perfusion is poor, and diuretics are ineffective. Though diuretic therapy is
eventually needed in all heart failure patients, they are not beneficial in the
initial resuscitation period. High-dose vasodilator therapy and NIV should be
the initial tenets of the ED management of patients with AHDF.

KEY POINTS

Diuretics should not be considered first-line therapy in the ED
treatment of patients with ADHF.
High-dose nitroglycerin therapy should be initiated early in ADHF,
especially in patients who are hypertensive.
Do not begin a nitroglycerin infusion at a dose less than that provided
by the sublingual route.
Nitroglycerin doses of at least 120 mcg/min are needed to reduce
capillary wedge pressure.
NIV should be administered early and in conjunction with high-dose
vasodilator therapy for patients with AHDF.

SUGGESTED READINGS

Collins SP, Storrow AB, Levy PD, et al. Early management of patients with acute
heart failure: State of the art and future directions—A consensus document
from the SAEM/HFSA acute heart failure working group. Acad Emerg Med.
2015;22(1):94–112.

den Uil CA, Brugts JJ. Impact of intravenous nitroglycerin in the management of

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