Emergency Medicine 2
Table 2A.1. JNC-VI classification of blood pressure in adults
Category Systolic BP Diastolic BP
Optimal <120 <80
Normal <130 <85
High-Normal 130-139 85-89
Hypertension
Stage 1 140-159 90-99
Stage 2 160-179 100-109
Stage 3 >180 >110
Table 2A.2. Hypertensive emergencies
Hypertensive encephalopathy
Stroke (ischemic or hemorrhagic)
Myocardial infarction or unstable angina
Pulmonary edema/congestive heart failure
Aortic dissection
Acute renal failure
Preeclampsia/eclampsia
Microangiopathic hemolytic anemia
Catecholamine excess
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Hypertensive Encephalopathy
• When the acutely elevated blood pressure exceeds the CNS’s ability for autoregulation,
uncontrolled cerebral blood flow occurs. This results in vasospasm, vascular damage and
leakage, and potential cerebral hemorrhage, ischemia, and/or edema.
• Patient complaints include headache, vomiting, drowsiness, confusion, visual changes,
or focal neurologic changes. Papilledema is present and severe retinopathy is often present.
• Untreated, patients will progress to coma and death.
• Treatment involves the acute lowering of blood pressure with titratable IV medications.
By definition, patients with hypertensive encephalopathy lack cerebral autoregulation.
Precipitous lowering of the systemic blood pressure may cause a dangerous
fall in cerebral perfusion pressure, leading to further cerebral ischemia. Therefore,
careful monitoring of patients is necessary to evaluate for neurologic deterioration.
Systemic blood pressure reduction should be done slowly with published guidelines of
approximately 15-20% reduction in diastolic pressure within 1 h or a diastolic pressure
of 110 mm Hg as therapeutic goals.
Hypertensive Stroke
• Severe, uncontrolled hypertension is frequently an etiologic factor in patients with
strokes. Patients with this degree of hypertension have cerebral autoregulatory set points
changed to accommodate the degree of chronic hypertension. Therefore, overaggressive
lowering of blood pressure may cause a dangerous lowering of cerebral perfusion
pressure and extend ischemic zones of the brain.
• Patients with hemorrhagic infarctions may present with severe hypertension as a response
to the bleed, as well as an etiology of the infarction. This may resolve without
treatment.
• With the above considerations, there is debate in the literature regarding the appropriate
management of severe hypertension in stroke. Many authors recommend lowering
for diastolic pressures >120, while others recommend that blood pressure never needs
acute lowering in the emergency setting.
Hypertension with Ischemic Coronary Syndromes
• Severe hypertension is an etiologic factor in atherosclerotic heart disease. Many patients
presenting with acute coronary syndromes (myocardial infarction or unstable
angina) have chronic hypertension which may be severe or uncontrolled. Acute elevations
in blood pressure may exacerbate coronary ischemia by increasing ventricular
strain and myocardial oxygen demand.
• Decreasing afterload with the use of IV nitrates decreases myocardial work. IV ²-blockers
also decrease myocardial work by decreasing blood pressure and heart rate.
• The use of direct vasodilators, which may cause a reflex tachycardia, is contraindicated
in the setting of ischemia.
Hypertension with Pulmonary Edema or Congestive Heart Failure
• Severe hypertension is an etiologic factor for congestive heart failure but may also be
secondary to the catecholamine response to pulmonary edema.
• Treatment for these patients includes nitroglycerin and diuretics but may also require
the addition of morphine sulfate and nitroprusside. The use of morphine sulfate is
effective in decreasing the catecholamine response to heart failure. Both nitroglycerin
and nitroprusside produce vasodilatation in the capacitance vessels thus improving
cardiac hemodynamics. Nitroprusside has a more pronounced effect on arterioles,
thus reducing afterload. However, a reflexive tachycardia and increased inotropy may
counteract the decrease in afterload and even lead to an increase in cardiac workload.
Nitroprusside may also cause coronary steal in patients with coronary artery disease. It
is therefore not the first line drug in cardiac failure with severe hypertension.
Cardiovascular Disorders 19
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Aortic Dissection
• The control of hypertension is essential in the emergency stabilization of a patient
with an aortic dissection.
• The use of both ²-blockers and nitroprusside is recommended to both decrease the systemic
blood pressure and to decrease the shearing force of the systolic pulse on the weakened
aortic wall. Standard medications used are nitroprusside plus labetolol or esmolol.
• Blood pressure should be decreased to the lowest possible level without exacerbating
ischemic symptoms.
Hypertension and Acute Renal Failure
• Patients with long-standing uncontrolled hypertension often develop renal failure.
Acute elevations in blood pressure may lead to intrarenal vascular injury, glomerular
ischemia, and subsequent hematuria, proteinuria and loss of renal function.
• The management of acute renal failure secondary to acute hypertension is focused
on maintaining normal volume status, renal perfusion, and minimizing secondary
complications.
• IV ²-blockers or calcium channel blockers are the drugs of choice. They must be used
with caution, and euvolemia must be maintained in order to not decrease renal perfusion
to a level which exacerbates instead of alleviating renal damage. The use of diuretics
may be either beneficial, if used in hypervolemic or euvolemic patients to increase
GFR, or problematic if used in hypovolemic patients. Nitroprusside, while effective for
decreasing blood pressure, is problematic in patients with renal dysfunction because the
thiocyanate metabolite of the drug may accumulate, leading to cyanide toxicity.
• Dialysis may be needed in severely symptomatic or hypertensive patients.
Preeclampsia/Eclampsia
• Preeclampsia and eclampsia represent diffuse end-organ damage secondary to pregnancy
induced hypertension.
• Most patients with preeclampsia/eclampsia are vasoconstricted and hypovolemic.
• Hydralazine is the standard antihypertensive used in preeclampsia. However, IV
²-blockers or calcium channel blockers may also be used.
• Careful management of volume status is important as these patients have renal and often
cerebral vascular injury and are therefore prone to develop edema with overaggressive
hydration. The treatment for preeclampsia/eclampsia is delivery of the fetus and placenta
and close communication with an obstetric specialist is required.
Microangiopathic Hemolytic Anemia
• The endovascular damage associated with hypertensive crises results in fibrin deposition
in arterioles and ultimately fibrinoid necrosis. This fibrin deposition may lead to a
hemolytic anemia which is diagnosed by the presence of schistocytes on peripheral
blood smear. This anemia is rarely seen in isolation in hypertensive emergencies and
management is based on end-organ damage in other organ systems.
Catecholamine Excess
• Excess catecholamines may lead to hypertensive emergencies. Causes include pheochromocytomas;
ingestions of stimulant medications or drugs, such as cocaine or amphetamines;
withdrawal syndromes as seen in the rebound hypertension with clonidine
withdrawal; or the ingestion of tyramine rich foods while taking MAOIs. These conditions
all result in an increased ±-adrenergic tone.
• Treatment requires ± blockade with phentolamine. B-blockade alone is contraindicated
as it leads to unopposed ± stimulation. In the case of stimulant drug ingestions,
anxiolytics such as lorazepam or valium may be effective in lowering blood pressure as
well as treating associated hyperactivity.
20 Emergency Medicine
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Medications Used to Treat Hypertensive Emergencies
and Urgencies
Pharmacologic treatment of hypertensive emergencies requires medications which
are rapid acting, easily titratable, and which lack significant side effects. Intravenous
medications are the most appropriate for true emergencies. Patients must be closely
monitored during the use of these medications for adverse reactions including hypotension
or worsening of the underlying condition.
In hypertensive urgencies, the blood pressure may be reduced slowly. Oral medications
may be appropriate in these situations.
Sodium Nitroprusside
• Nitroprusside is the drug of choice for most hypertensive emergencies.
• Nitroprusside decreases both afterload and preload by direct arterial and venous dilatation.
The blood pressure response is dose dependent.
• It is administrated as a light-sensitive IV solution at doses beginning at 0.25 mcg/
kg/min. Onset of action is within 1-2 min. The half-life is 3-4 min which allows
the pharmacologic effect to be quickly discontinued in patients with adverse reactions.
• As discussed above, nitroprusside may have multiple cardiovascular complications including
an increase in cardiac work as well as coronary steal in atherosclerotic coronaries.
However, in patients with congestive heart failure, nitroprusside has been shown
to be effective in increasing cardiac output.
• Theoretically, nitroprusside may adversely effect cerebral perfusion. Nitroprusside’s
potent vasodilatation may cause dilation in the cerebral vasculature, thus increasing
cerebral blood flow and intracerebral swelling. However, the decrease in systemic blood
pressure counteracts this effect, making nitroprusside the drug of choice in patients
with hypertensive encephalopathy.
• Nitroprusside is metabolized into thiocyanate and may therefore lead to cyanide toxicity
if administered for a prolonged time or to patients with either liver or kidney
disease.
Nitroglycerin
• Nitroglycerin is a direct vasodilator that acts predominantly on the venous circulation.
At higher doses it has some effect on arterial tone.
• Doses begin at 5 mcg/min. Onset is within 1-5 min.
• Nitroglycerin dilates coronary arteries and thus, it is used primarily as an anti-anginal
medication in patients with acute coronary syndromes. Nitroglycerin decreases preload
which improves cardiac mechanics in failing hearts.
• Nitroglycerin may cause hypotension, especially in the face of hypovolemia, as well as
headache, flushing and nausea.
Labetolol
• Labetolol produces both ± and ² blockade.
• It can be given both IV and PO. Therapeutic effect can be seen in approximately 2-5
min and peaks in approximately 10 min. Initial loading dose of 20 mg over 2 min can
be repeated in 10 min intervals until a response is noted.
• IV labetolol produces orthostatic hypotension.
• It does not cause a decrease in cerebral or peripheral blood flow and is safe in patients
with coronary artery disease.
• Contraindications are those for all ²-blockers as a group and include bronchospasm,
CHF, or heart block. Labetolol may also cause postural hypotension.
Cardiovascular Disorders 21
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Esmolol
• Esmolol is an ultra-short acting ²-blocker with a rapid onset of action and cessation of
action when discontinued.
• It is used IV and is most suitable for relatively unstable patients with supraventricular
dysrhythmias or aortic dissection.
• Contraindications include those previously mentioned for ²-blockers.
Nicardipine
• Nicardipine is a titratable IV calcium channel blocker which may also be given orally.
• The onset is 5-15 min with duration of action approximately 30 min. The starting
dose is 5-15 mg/h.
• Nicardipine decreases afterload without reducing heart rate or cardiac output. It has a
favorable effect on failing hearts by improving ejection fraction and acts as an
anti-anginal by dilating coronary arteries.
• Adverse effects include hypotension, headache, and nausea.
Hydralazine
• Hydralazine produces direct vasodilatation and is the drug of choice in hypertensive
emergencies associated with pregnancy.
• As with all direct arterial dilators, hydralazine causes a reflex tachycardia causing an
increase in cardiac work. Hydralazine is therefore not used in patients with cardiac
ischemia and severe hypertension
Phentolamine
• Phentolamine is an IV short acting ±-adrenergic blocker with rapid onset.
• It is given as an initial bolus of 5-10 mg and repeated as necessary.
• Adverse effects include the development or exacerbation of coronary ischemia.
• Its use is limited to settings with catecholamine excess.
Nifedipine
• Oral nifedipine was used commonly in the treatment of hypertensive emergencies.
• It causes a potent arteriole dilatation 5-10 min after administration. Unfortunately,
this reduction in blood pressure is often uncontrolled, leading to adverse effects on
cerebral blood flow as well as adverse cardiac effects secondary to reflexive tachycardia.
It is contraindicated in hypertensive emergencies because of these dangers.
Table 2A.3. Medications for hypertensive emergencies
Medications Contraindicated
Emergency of Choice Medications
Hypertensive Nitroprusside
Encephalopathy
Stroke Medication
not indicated
Ischemic coronary Nitroglycerin Hydralazine
syndromes
CHF/Pulmonary edema Nitroglycerin
Aortic dissection Nitroprusside plus Hydralazine
²-blocker, Esmolol
Acute renal failure Nicardipine ²-blocker
Preeclampsia/Eclampsia Hydralazine
Catecholamine excess Phentolamine, ²-blocker alone
Lorazepam
22 Emergency Medicine
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Clonidine
• Clonidine is a central acting ± antagonist.
• Reductions in blood pressure can be seen 30 min after oral administration with maximal
effect in 2-4 h.
• While it appears to be safe, it has a slower onset than the IV drugs listed above. It is
also not easily titratable and thus may be dangerous if adverse effects occur.
• Clonidine also causes drowsiness and thus difficulties in monitoring mental status.
Common Effects of Anti-Hypertensive Medications
Anti-hypertensive medications are prescribed commonly. A functional knowledge
of the use and side-effect profile of these drugs is important when managing patients
taking these medications.
Diuretics
• Diuretics are an excellent choice for initial therapy in hypertension. If they are not the
initial medication used, they are indicated as a secondary medication as they have an
additive effect on blood pressure when used in combination. They are especially effective
in African Americans.
• The most common side effects of the diuretics are due to their effect on fluid and
electrolyte balance. Dehydration is the most obvious side effect. Hypokalemia and
hyperkalemia may both occur depending on the agent used.
• Diuretics may also cause increases in uric acid and thus precipitation of gouty arthritis.
Beta Blockers
• Beta blockers are recommended as monotherapy for hypertension. They are especially
useful in patients with ischemic heart disease, tachydysrhythmias, essential tremor, or migraines.
• Beta blockade may cause exacerbation of asthma or other bronchospastic diseases. It
may worsen CHF or cause heart block especially when combined with calcium channel
blockers. Beta blockade may mask the symptoms of hypoglycemia in diabetics.
Depression and sexual dysfunction may also occur.
Calcium Channel Blockers
• Calcium channel blockers are especially effective in African Americans.
• Vasodilatation by calcium channel blockade may precipitate orthostatic hypotension
or peripheral edema, especially in the elderly. CHF may be worsened by the negative
inotropic effect of these medications. Heart block may also occur.
ACE Inhibitors
• ACE inhibitors are recommended as initial therapy in diabetics, patients with heart
failure and patients with renal insufficiency (creatinine <3 mg/dl).
• ACE inhibitors may cause angioedema or cough. Hyperkalemia may also occur as well
as worsening of renal failure especially in patients with renal artery stenosis.
Suggested Reading
1. Abdelwahab W, Frishman W, Landau A. Management of hypertensive urgencies and
emergencies. Journal of Clinical Pharmacology August 1995; 35(8):747-62.
2. Grossman E, Ironi AN, Messerli FH. Comparative tolerability profile of hypertensive
crisis treatments. Drug Safety August 1998; 19(2):99-122.
3. Jackson R. Hypertensive emergencies. In: Tintinalli JE, Kelen GT, Stapczynski JS, eds.
Emergency Medicine. A Comprehensive Medicine Study Guide. McGraw-Hill, 2000.
4. Kitiyakar C, Guzman NJ. Malignant hypertension and hypertensive emergencies. Journal
of the American Society of Nephrology January 1998; 9(1):133-42.
Cardiovascular Disorders 23
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5. Mathews J. Hypertension. In: Marx JA, Hockberger RS, Walls RM, eds. Emergency
Medicine. Concepts and Clinical Practice. Mosby, 2002:2.
6. Murphy C. Hypertensive emergencies. Emergency Medicine Clinics of North America
November 1995; 13(4):973-1007.
7. Thach AM, Schultz PJ. Nonemergent hypertension. New perspectives for the emergency
medicine physician. Emergency Medicine Clinics of North America November
1995; 13(4):1009-35.
8. Tietjen CS, Hurn PD, Vlatowski JA et al. Treatment modalities for hypertensive patients
with intracranial pathology: Options and risks. Critical Care Medicine February 1996;
24(2):311-22.
9. The sixth report of the joint national committee on prevention, detection, evaluation,
and treatment of high blood pressure. Archives of Internal Medicine November 1997;
157(21):2413-46.
10. Varon J, Marik P. The diagnosis and management of hypertensive crises. Chest July
2000; 118:214-227.
11. Vaughn CJ, Delanty H. Hypertensive emergencies. Lancet July 2000;
356(9227):411-7.
Part B: Acute Coronary Syndromes
Coronary artery disease is the most common cause of death in the United States,
accounting for approximately 600,000 deaths annually. Of 6.0 million ED visits per
year for chest pain, about 1.2 million people are diagnosed with myocardial infarction
and another million with unstable angina. It has been estimated that the overall
cost of coronary artery disease exceeds 100 billion dollars annually in the U.S. There
is also a significant cost in terms of malpractice claims, with missed myocardial infarction
and acute coronary syndromes continuing to constitute a large percentage of
both claims and costs. Mortality and morbidity continue to decrease with advances
in therapy. There was a 54% reduction in age-adjusted mortality from myocardial
infarction in the U.S. from 222/100,000 in 1963 to 101/100,000 in 1990.
Definitions
• Coronary artery disease (CAD) is a spectrum of disease that ranges clinically from
asymptomatic or “silent” to one of the following clinical syndromes: stable angina,
variant angina or acute coronary syndrome.
• Stable angina is episodic, exertional chest pain lasting approximately 5-15 min. EKG
changes occur <50% of the time. Cardiac enzymes are not elevated.
• Variant or Prinzmetal angina is uncommon and occurs primarily at rest without provocation,
typically at the same time of the day. ST elevation can be seen on EKG.
• Acute coronary syndromes comprise the entire spectrum of disease from unstable angina
through to myocardial infarction.
• Unstable angina is defined as new onset angina or angina that is increasing in frequency,
intensity, duration, sensitivity to exercise or nitroglycerin (NTG) requirement.
EKG changes occur in 50% or more of patients and cardiac troponin may be
mildly elevated.
• Acute myocardial infarction (AMI) occurs when there is frank necrosis of myocytes.
Chest pain is usually sustained >20 min. EKG changes occur in 50% or more of cases
and cardiac serum markers are elevated. AMI is classically divided into transmural
(Q-wave) or subendocardial (non Q-wave) MI, although there is significant overlap
between these entities. A more important classification of AMI in the ED is to distinguish
ST elevation MI (STEMI) from non-ST elevation MI (non-STEMI).
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Pathophysiology
• In most cases, coronary artery disease is caused by atheromatous plaques in the
lumina of the epicardial vessels. However, other sources of occlusion include thrombus
formation associated with arterial dissections as well as thrombi from heart chambers
and prosthetic valves. Inflammatory processes, such as those associated with
Kawasaki disease and systemic lupus erythematosis are uncommon causes of coronary
artery disease.
• Stable angina is caused by chronic, fixed nonulcerating plaques. Angiography usually
reveals 50-75% obstruction.
• Variant angina is primarily due to vasospasm. Angiography reveals normal coronaries
in one-third of the cases and CAD in conjunction with vasospasm in the remaining
two-thirds.
• Acute coronary syndromes share the common pathophysiology of a fissuring or “unstable”
plaque (often with <50% occlusion) that becomes a nidus for the aggregation
of platelets and fibrin. Vasospasm at the site of the fissured plaque also occurs.
• Mechanisms of cardiac ischemia and infarction independent of coronary artery obstruction
include those from metabolic, hematologic and toxicologic conditions. Hypoxia,
anemia, hypotension and carbon monoxide toxicity all tend to result in injury
in a global cardiac distribution rather than in the distribution of a particular epicardial
artery, but may manifest first in territories of vessels with preexistent CAD.
Risk Factors
• Major risk factors for CAD include age, male gender, diabetes mellitus, chronic hypertension,
family history of premature CAD, cigarette smoking, hyperlipidemia and
lack of hormone replacement after menopause.
• Because these well known risk factors are based on lifelong risks in populations, they are
less important in the ED than they are in the primary care setting. In the ED, the
individual patient’s presenting symptoms (e.g., “crushing retrosternal chest pain versus
sharp, intermittent pain”) and the appearance of the 12-lead EKG (e.g., ST segment/T
wave changes versus normal) overshadow any predictive value of the classic risk factors.
Diagnosis and Evaluation
History
• The classic presentation of symptomatic CAD is that of left-sided or retrosternal
chest pain of a pressure-like nature. However, many variations exist including burning
pain, pain akin to indigestion (approximately 20% of patients) and sharp, stabbing
pain (5-20% of patients). Pain may radiate to the jaw, neck, back or down
either upper extremity, corresponding to the C8-T5 dermatomes. It is important to
note that lack of classic characteristics of pain cannot be used to rule out CAD as a
cause for chest pain.
• The temporal pattern of pain and its relation to activity will help to classify the presentation
into one of the clinical categories outlined above.
• Common associated symptoms include nausea and vomiting (especially with inferior
wall ischemia), diaphoresis, shortness-of-breath and lightheadedness.
• In diabetic and elderly patients, chest pain itself may be absent. In some of these cases an
“anginal equivalent” such as shortness-of -breath, lightheadedness or nausea may be present.
In the oldest subset of patients, CAD may present very nonspecifically with weakness,
malaise or simply with the complications of an acute coronary event such as congestive
heart failure (CHF), dysrhythmia or cerebrovascular accident.
• 5-15% of AMIs are completely asymptomatic or “silent”. These occur mostly in elderly
and diabetic patients.
Cardiovascular Disorders 25
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Physical Examination
• Physical examination is rarely diagnostic of symptomatic CAD. Although signs such
as the new onset of an S4 gallop and a paradoxical spilt of S2 have been described with
AMI, these are unreliable.
• The physical examination serves two other important roles:
• The exclusion of other life-threatening causes of chest pain such as pneumothorax
(asymmetrical resonance to percussion), aortic dissection (asymmetry of pulses, neurological
signs) and pulmonary embolus (signs of right-sided heart strain)
• The identification of complications of myocardial ischemia and infarction such as
CHF (jugular venous distension, S3 gallop, rales, edema, hypotension), acute papillary
muscle rupture and myocardial rupture (new onset murmur with signs of
severe CHF) and pericarditis (friction rub).
EKG Findings
• The EKG remains the most important diagnostic tool in the evaluation of acute chest
pain and guides the early management of patients with CAD. A 12-lead EKG should be
obtained as soon as possible.
• There is a great degree of variability in the patterns of change on the 12-lead EKG
during symptomatic CAD. In unstable angina and subendocardial MI, when a partial
obstruction to flow in a coronary artery exists, T wave inversions and ST segment
depressions are most commonly seen. ST elevations in the vascular territory of a particular
epicardial artery (see above) is characteristic of transmural MI, when there is
complete obstruction.
• Because of the time-dependent nature of revascularization treatments for STEMI, the
most important distinction that must be made in the initial evaluation of a patient
with symptomatic CAD is that between those patients with significant ST elevation
and those without.
• Since ST elevation may not be present on the initial EKG, it is important to obtain
frequent serial EKGs, especially when there is a dynamic nature to the patients presenting
symptoms. Conversely, ST elevation on the initial EKG may completely resolve
with medical therapy, again with major implications on therapy. For similar
Table 2B.1. Relationship of EKG leads to location of ischemia related
epicardial vessel
Location of
EKG Lead Ischemia/Infarction Epicardial Vessel
II, III, and AVF Inferior Wall Right Coronary Artery
V1, V2 Septal Wall Left Anterior Descending Artery
Posterior Wall* Right Coronary Artery (in most cases)
I,AVL, V5 and V6 Lateral Wall Left Circumflex Artery
V1, V2,V3,V4,V5 Anterior Wall Left Anterior Descending Artery
Special Leads
V8, V9 Posterior Wall Right Coronary Artery
RV4 Right Ventricle Right Coronary Artery
* Note: In posterior wall ischemia/infarction, changes in leads V1 and V2 will be opposite
to those expected in other leads. Because ST segment changes in leads V1 and V2 can
represent both STEMI in the posterior wall as well as non-STEMI in the anterior and septal
locations, additional leads (e.g., V8 or V9) or an echocardiogram may be obtained to help
clarify the situation. The presence of a tall R wave in lead V1 is the equivalent of a Q wave
in the other infarct locations.
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reasons, a previous EKG tracing of the patient prior to the acute episode may be
extremely valuable in making emergency management decisions.
• Although variable, the typical progression of EKG changes in STEMI begin with the
brief (minutes) appearance of giant or “hyperacute” T waves, followed by ST elevations
in the distribution of the occluded or “infarct-related” vessel. With time (typically
several hours), there is the development of Q waves. T wave changes are variable.
• The presence of a left bundle branch block (LBBB) is extremely important in the
evaluation of ACS. Its presence indicates a poor prognosis and the need for more
aggressive management. If the LBBB is documented or presumed to be new in onset,
the treatment of ACS follows similar lines as that of STEMI.
• The progression of nonSTEMI is even more variable than with ST elevation MI. Q
waves do not usually occur.
• The distribution of ischemia/infarction within the heart is important to predict likely
complications as well as to predict prognosis.
• The additional leads V8 and V9 may be placed when there is suspicion for acute
posterior wall MI, in which case ST segment elevation in these leads will be seen.
Suspicion for posterior wall MI exists when there are changes suggestive of ischemia in
leads V1 and V2.
• The additional lead RV4 may be placed when there is suspicion for acute right ventricular
MI. Acute RV infarction is confirmed by the presence of ST segment elevation.
Right ventricular MI may be suspected either on clinical grounds (e.g., because
of an exaggerated hypotensive response to preload reduction therapy such as nitrates)
or when ischemic changes are present in the inferior leads (II,III and avL).
• Changes of a dynamic nature (e.g., changes from previous EKG recordings on the
same patient or changes over serial EKGs in the ED during the initial hours of the
presentation) are more suggestive of ACS and predict a higher mortality and need for
aggressive therapy.
• A normal EKG cannot be used to rule out the presence of ACS or AMI. However, in
those patients with normal or minimally abnormal EKGs, the risk of mortality and
complications is much lower.
Serum Cardiac Markers
• Cardiac markers have a role in the diagnosis as well as the risk stratification of patients
with ACS.
• At the present time, no perfect marker of ACS exists, although there ongoing advances in
technology and research continue to improve the utility of cardiac markers.
Figure 2B.1. The placement of additional leads V8, V9 and RV4 (the 15-lead EKG)
Cardiovascular Disorders 27
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• Most institutions have a protocol for the serial measurement of cardiac markers in the
evaluation of possible ACS. Regardless of the protocol used, a knowledge of the benefits
and limitations of each marker is important.
• Myoglobin, CK and cardiac troponin are all released into the blood after cardiac cell
injury and death. Table 2B.2 compares the temporal characteristics of these markers
in AMI.
• Myoglobin is elevated quickly and is very sensitive. However, its total lack of specificity
limits its diagnostic value.
• CK-MB assays are generally less specific and less sensitive than cardiac troponin, although
differences in technique account for significant variations in reported accuracy.
• To date, cardiac troponin I and T are the most cardiac specific markers and have been
adopted by many institutions in the U.S.
• Before the advent of cardiac troponin, the commonly accepted definition of AMI
included an elevation in CK-MB. A new group of patients has been identified in
whom there is a mild elevation of cardiac troponin without an increase in CK-MB,
making the precise definition of AMI less clear. However, identification of this group
of patients with ACS and “microinfarction” has proved important clinically, because
they have poorer outcomes than patients with no marker elevations and warrant more
aggressive management strategies.
• Although there is some degree of elevation of cardiac troponin in renal failure, it still
appears to have prognostic value.
• In certain cases it may be helpful to combine markers because of their different temporal
profiles. For example, the addition of CK to cardiac troponin may be helpful to
detect early reinfarction in the week following an AMI when troponin values are still
elevated from the initial event.
Other Laboratory Values
• When suspicion for ACS is high, additional laboratory investigations are appropriate
and may include CBC, basic chemistry, urine toxicology and blood typing (when
fibrinolytic or invasive procedures are contemplated).
Imaging Studies
• Emergent portable chest X-ray helps to rule out other important causes of chest
pain such as aortic dissection and pneumothorax. Many institutions have protocols
to ensure that a chest X-ray is reviewed prior to the administration of fibrinolytic
therapy so that signs suggestive of aortic dissection are not overlooked. Chest X-ray
is also important to detect cardiomegaly and other signs of congestive heart failure
that may complicate or coexist with ACS.
Table 2B.2. Serum markers in acute coronary syndromes*
Time to Time to Time to
Elevation Peak Normalization
Marker (hours) (hours) (days)
Myoglobin 2 8 1
CK (creatine phosphokinase) 6-8 24-30 3-4
CK-MB isoenzyme 3-4 18-24 2
Cardiac troponin I and T 3-6 18-24 7-14
*The above figures are estimates. Characteristics of individual assays, as well as normal
and diagnostic values, vary with technique and manufacturer. Laboratories will be able to
provide specific information on marker assays used in individual institutions.
28 Emergency Medicine
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• Emergent echocardiography has an important role in cases where the diagnosis of
ACS or MI is still in question after the initial assessment and EKG.
Echocardiography gives a great deal of information that may guide management,
including an assessment of the global functioning if the heart (ejection fraction),
assessment of regional wall motion and the function of the cardiac valves.
Figure 2B.2. Important EKG findings in acute coronary syndromes. A) Acute anterior MI
showing ST elevations in the precordial leads, with reciprocal ST depression in the inferior
leads (reciprocal changes increase diagnostic certainty of AMI and also indicate a
graver prognosis). B) Deep, symmetrically inverted T waves in the anterior leads in setting
of cardiac symptoms are strongly suggestive of proximal left anterior descending
obstruction and carry a poor prognosis without prompt therapeutic intervention. Although
emergent cardiology referral and admission to the CCU are appropriate, this
patient does not meet criteria for the administration of fibrinolytics. C) A 15-lead EKG
performed in a patient with ST segment depressions in leads V1 and V2. In this case, the
finding of ST elevation in leads V8 and V9 confirms that the changes in V1 and V2
actually represent an acute posterior infarction rather than only septal ischemia—this
patient now meets criteria for revascularization therapy with fibrinolytics or percutaneous
coronary intervention (PCI)
Cardiovascular Disorders 29
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• In the setting of ACS with cardiogenic shock, echocardiography is also useful to rule out
mechanical complications such as papillary muscle, septal and free-wall rupture that
mandate emergent surgical consultation. At present, bedside ultrasound by EPs is limited
to the detection of pericardial effusion, which may by itself be helpful in some cases.
ED Management
• As with every patient in the ED, management begins with the primary survey and
emergent resuscitation as required.
• All patients being evaluated for ACS must be placed on a cardiac monitor with a pulse
oximeter. IV access should be obtained in all patients. Intubation and resuscitation
equipment, including an external pacer and defibrillator, must be checked and ready
for use at the bedside.
• Treatment of symptomatic CAD is tailored in each case to the severity of the presenting
syndrome. All patients with presumed ACS receive the most basic treatments,
with the most aggressive therapies reserved for massive STEMIs. In general:
• The treatment of STEMI or ACS with presumed new LBBB focuses on immediate
revascularization therapy with fibrinolytics, percutaneous coronary intervention
(PCI) or surgery.
• The treatment of non-STEMI ACS focuses on reduction in myocardial necrosis
and the prevention and treatment of complications.
• The treatment of patients with stable angina or chest pain of uncertain etiology
focuses on the elimination of ACS from the differential diagnosis and risk stratification
for future coronary events.
Oxygen
Oxygen should be given to all patients. It may be provided as 2-4 L/min by nasal
cannula or by face mask in the presence of hypoxia.
Aspirin (ASA)
Aspirin (ASA) decreases platelet aggregation by inhibition of cyclooxygenase, which
results in decreased production of thromboxane A2.
• ASA is the single most effective medication in treatment of CAD and reduces mortality
by over 20% in ACS. All patients should receive ASA except those with true allergies
or active hemorrhage. Concurrent antacid use can decrease GI upset.
• The dose in ACS is 160-325 mg PO (lesser doses may be acceptable for chronic therapy,
but not for ACS)
• Ticlopidine (Ticlid) and clopidogrel (plavix) are alternative agents for patients with
severe (anaphylactoid) reactions to ASA. These agents have a slower onset of action,
more adverse reactions and are more expensive than ASA. Their role in the ED is very
limited at this point, although an additive benefit of clopidogrel to ASA therapy was
identified in one recent trial.
Nitrates
Nitrates cause vasodilatation of coronary arteries, relieve vasospasm, and decrease
preload and afterload, which in turn decreases myocardial oxygen demand.
• Evidence for their benefit in ACS is indirect at best. Nonetheless, nitrates have an
important role in relieving symptoms and improving hemodynamics in ACS.
• Patients with systolic BP>90 Hg mm and ongoing chest pain should be treated with
nitroglycerin (NTG).
• Caution should be exercised when using the sublingual dose (0.4 mcg SL Q3-5 min)
because it can cause profound hypotension, especially in right ventricular infarction.
• Nitrates are contraindicated when sildenafil (Viagra®) has been used in the preceding
48 h.
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• If pain continues after the initial 3 doses of sublingual NTG, it may be administered
by IV infusion, starting at 10 mcg/min and quickly titrated upward to resolution of
pain while maintaining systolic BP >90.
• If symptoms are mild, NTG may be given by paste applied to the chest wall. Doses
range from 1/2-2 inches of topical paste.
Morphine
Morphine is a potent analgesic and sedative. Evidence for its effectiveness in AMI
is indirect, but it is very effective at decreasing patient anxiety and fear. Similar to
nitrates, caution is advised when systolic BP is low. Even small doses (e.g., 2 mg)
may be beneficial.
Beta-Blockers
Beta-blockers exert their effects by decreasing afterload, contractility, overall myocardial
oxygen demand and myocardial irritability.
• Studies have shown that early use of ²-blockers in AMI reduces infarct size and reduce
mortality significantly.
• Beta-blockers should be administered to all patients without contraindications, which
include cardiogenic shock, hypotension (systolic BP<90), reactive airway disease (asthma
and COPD), allergy, advanced (2nd or 3rd degree) AV blocks and bradycardia
• Atenolol and metoprolol are B1 selective IV agents and are preferred. Metoprolol
can be given in 5mg increments IV q 5min, to a usual total dose of 15 mg. Esmolol,
which is an IV titratable agent with a half-life of under 10 min, can be given in cases
where reversibility is desired (e.g., in the presence of relative or uncertain
contraindications)
Unfractionated Heparin (UFH) and Low Molecular Weight Heparins
(LMWH)
UFH and LMWH are antithrombin agents. Their effectiveness in ACS and
AMI is supported by some studies but is controversial. In addition, the benefits of
antithrombin agents appear to disappear once they are discontinued. UFH and
LMWH are also not without risk, with a very significant incidence of
life-threatening bleeding complications. Because of the potential for hemorrhage,
risk/benefit ratios for the use of these agents must be considered in each individual
case.
• Although some experts recommend their use in all cases of ACS in the absence of a
specific contraindication, they may be more appropriately limited to a subset of patients
at highest risk for mortality and complications (e.g., those with significant EKG
changes) as a “bridge” to more definitive revascularization therapy.
• Unfractionated heparin (UFH) is administered according to ideal body weight with
the usual dose of 60 ¼/kg bolus followed by an infusion of 12 ¼/kg/h (maximum
4,000 u bolus and 1,000 ¼/h infusion). PTT must be monitored regularly starting at
4-6 h after the initiating of the infusion) with a goal of maintaining PTT at 2x the
upper limit of normal.
• Low molecular weight heparins (LMWH) have been used in many trials. They are
as effective as UFH and have several advantages, including ease of administration
(subcutaneous injections versus IV infusion), more consistent therapeutic effects,
and a lack of need for routine therapeutic monitoring. It is also possible to use
LMWH in patients for whom PCI is anticipated, although heparin is still preferred
by some in this setting because of its easier titratability. A commonly used LMWH
is enoxaparin, with a dose of 1mg/kg SQ q12h.
Cardiovascular Disorders 31
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Glycoprotein IIb/IIIa Receptor Inhibitors
Glycoprotein IIb/IIIa receptor inhibitors (abciximab, eptifibatide, tirofiban) are
very potent anti-platelet agents that block the final common pathway of platelet
aggregation (the formation of fibrinogen bridges between platelets). They are administered
as IV infusions in ACS.
• Currently, there is good evidence that these agents are beneficial in high-risk ACS patients
who are undergoing PCI, including those who receive a stent. Their use in patients
not receiving interventional therapy is controversial at this time and they are not recommended
for general use in patients with unstable angina or nonSTEMI.
Fibrinolytic (Thrombolytic) Agents
Fibrinolytic (thrombolytic) agents promote clot lysis through activation of plasminogen.
Available agents include streptokinase (SK), tissue plasminogen activator
(t-PA), anistreplase (APSAC), reteplase and tenecteplase (TNK-t-PA)
• Fibrinolytic therapy is indicated in STEMI and LBBB of new onset in the clinical
setting of ACS, when the duration of symptoms is <12 h. In some cases, when the
onset of symptoms is unclear or symptoms are stuttering in nature, it may be possible
to extend this window.
• Specific EKG criteria for ST segment elevation include the presence of at least 1 mm of
elevation in two leads of the same vascular territory (2 mm in the precordial leads).
• Benefit is greatest with early administration (<30 min), with progressively less efficacy
as each h passes after the onset of symptoms.
• The similarities among these agents are greater than the differences—the efficacies of
the various available agents are all comparable. The choice of agent is more likely
dependent on the institutional and departmental availability and practice, and the
ease and safety of the protocol is an important consideration in this choice.
• SK and APSAC may cause immune reactions and hypotension—they should be avoided
in patients with allergy or recent exposure to either agent.
• Absolute contraindications to fibrinolytic therapy include active internal bleeding,
known intracranial malignancy, previous hemorrhagic CVA, ischemic CVA in the last
12 mo and suspected or known aortic dissection.
• Relative contraindications include uncontrolled hypertension (>200/110 mm Hg),
pregnancy, active peptic ulcer, internal bleeding within the last 4 wk, recent major
trauma or surgery, recent puncture of a major noncompressible vessel, current use of
anticoagulants, proliferative diabetic retinopathy, history of prior CVA and the presence
of occult blood on rectal examination.
• Because of the potent nature and serious consequences of adverse reactions, protocols
for fibrinolytic administration should be in place in every ED, including drug preparation
instructions, dosing schedules and a checklist to ensure that no contraindications
are overlooked prior to the initiation of the protocol. Informed consent should be
obtained after a discussion of the risks and potential benefits of therapy with the patient
and family members.
• Patients undergoing fibrinolytic therapy require extremely close monitoring for resolution
of symptoms and 12-lead EKG changes, dysrhythmias, bleeding complications
(especially intracranial hemorrhage) and other adverse reactions.
• During the reperfusion phase, an accelerated idioventricular rhythm (usual rate
100-120) is often seen which usually does not require therapy. All other arrhythmias
should be treated according to ACLS protocols.
• In the event of life-threatening hemorrhage or any suspicion of intracranial hemorrhage
(sudden severe headache, focal neurologic signs or decreasing level of consciousness),
fibrinolytic and heparin infusions must be discontinued immediately.
Emergent brain CT and neurosurgery consultation should be obtained. Fibrinogen
32 Emergency Medicine
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may be replaced by cryoprecipitate (10-20 ¼ IV) and coagulopathy may be reversed
with fresh frozen plasma (2-4 units FFP IV). Protamine can be used to reverse
heparin (dosing varies with amount of heparin infused). Platelets, beginning with 1
single-donor unit can also be infused. In refractory cases, aminocaproic acid, a fibrinolysis
inhibitor, may be used.
Primary Percutaneous Coronary Intervention (PCI)
PCI is becoming increasingly popular in U.S. centers and in experienced hands
provides outcomes superior to fibrinolytic therapy for STEMI, particularly when
coronary stenting is employed.
• Primary PCI has an advantage over fibrinolytic therapy when cardiogenic shock complicates
AMI. It may be the only option for revascularization when there are absolute
contraindications to fibrinolytic therapy. It also may be preferred in patients >75 yr of
age who have higher rates of complications with fibrinolytics.
• The most important factor in outcome remains time to revascularization. Therefore,
any benefit of PCI may be lost if there is significant delay in bringing the patient to the
catheterization laboratory. A delay of more than 90 min is not likely warranted, and if
such a delay is anticipated, administration of fibrinolytics should proceed. A reasonable
goal is to perform revascularization by interventional or pharmacological means
within 60 min or less from the time that the patient arrives in the ED.
• In some cases, PCI may be considered after fibrinolytics, especially when there is a
poor response to therapy.
Complications
The two complications of ACS responsible for the majority of deaths are
dysrhythmias and congestive heart failure/cardiogenic shock.
Arrhythmias
• Arrhythmias are very common after an ischemic event. The incidence of premature
ventricular contractions (PVCs) is virtually 100% and sinus tachycardia has an incidence
of 40-60%. Ominous rhythms such as ventricular tachycardia and/or ventricular
fibrillation have an incidence of 5-10%.
• The risk of a life-threatening dysrhythmia complicating ACS generally increases with
infarct size and is greatest in infarcts of the left anterior descending artery (anterior)
distribution.
• Anterior wall MIs are more likely to be complicated by severe bradydysrhythmias
(e.g., Mobitz II and third degree AV block) due to injury of the conducting system.
These rhythms may not respond to atropine and preparations for external and/or
invasive pacing should be made immediately.
• Inferior wall MIs are often complicated by less severe bradydysrhythmias (e.g., first
degree AV block or Wenkebach patterns) due to an increase in vagal tone. These are
usually transient and responsive to IV atropine.
• Tachydysrhythmias increase myocardial oxygen demand and should be treated according
to ACLS protocols.
• It should be noted that the presence of low-grade ectopy in ACS, such as intermittent
premature ventricular contractions (PVCs), is not routinely treated with
antidysrhythmic agents as was once common practice.
Left Ventricular Failure/ Cardiogenic Shock
• Left ventricular failure and cardiogenic shock are more common after anterior wall
AMI because of the typically larger infarct size.
Cardiovascular Disorders 33
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• Vasoactive catecholamines such as dopamine, dobutamine, epinephrine and norepinephrine
all have a role in management, but all increase cardiac irritability and oxygen
consumption, making them less than optimal treatment modalities. An arterial line
and Swan-Ganz catheter should be used to guide therapy when these agents are used.
• Intra-aortic balloon pump (IABP) is another important tool that may be used in cases of
refractory shock, especially as a bridge to revascularization or transplantation surgery.
• Ventricular septal defect and papillary muscle rupture should be sought as causes of
shock and sudden decompensation; 50% of all cases occur in the first 5 days of an MI
and 90% in the first 14 days. If these are suspected, emergent cardiovascular surgical
consultation is indicated.
Disposition
• All patients with suspicion for ACS should be admitted to telemetry or a chest pain
unit for observation.
• For those patients in whom AMI is ruled out by serial cardiac markers and EKGs
(usually over a time period of 8-12 h), the diagnosis of unstable angina is still a possibility.
In the case of a patient with significant risk factors for CAD or typical symptoms,
further risk stratification can occur with provocative testing, such as stress
echocardiography or nuclear medicine studies, on an inpatient basis. For those patients
with atypical presentations of chest pain with few or no risk factors for CAD
that are felt to have a very low likelihood of occlusive disease, timely outpatient follow-up
(2-3 days) with a primary care provider is appropriate.
• Patients with a confirmed diagnosis of AMI should be admitted to a cardiac or intensive
care unit (CCU or ICU).
Suggested Reading
1. Aufderheide TP, Brady WJ, Gibler WB. Acute ischemic coronary syndromes. In: Marx
JA, Hockberger RS, Walls RM, eds. Emergency Medicine. Concepts and Clinical Practice.
Mosby, 2002:2.
2. Brady WJ. ST segment elevation: Causes and diagnostic accuracy. J Emerg Med 1998;
16:797.
3. Hamm CW et al. Emergency room triage of patients with acute chest pain by means of
rapid testing for cardiac troponin T or troponin I. N Engl J Med 1997; 337:1648.
4. Hollander JE. Acute coronary syndromes: Unstable angina, myocardial ischemia, and
infarction. In: Tintinalli JE, Kelen GT, Stapczynski JS, eds. Emergency Medicine. A
Comprehensive Medicine Study Guide. McGraw-Hill, 2000.
5. Hunink MGM et al. The recent decline in mortality from coronary heart disease, 1980-1990.
The effect of secular trends in risk factors and treatment. JAMA 1997; 227:535.
6. Kirk JD et al. Evaluation of chest pain in low-risk patients presenting to the emergency
department: The role of immediate exercise testing, Ann Emerg Med 1998; 32:1.
7. Lee T et al. Acute chest pain in the emergency room: Identification and examination of
low risk patients. Arch Intern Med 1985; 1456:65.
8. McCarthy BD et al. Missed diagnoses of acute myocardial infarction in the emergency
department: Results from a multicenter study. Ann Emerg Med 1993; 22:579.
9. Marin MM, Teichman SL. Use of rapid serial sampling of creatine kinase MB for early
detection of myocardial infarction in patients with acute chest pain. Am Heart J 1992;
123:354.
10. The CAPTURE Investigators: Randomized placebo-controlled trial of abciximab before
and during coronary intervention in refractory unstable angina: The CAPTURE study.
Lancet 1997; 349:1429.
11. The GUSTO Angiographic Investigators: The effects of tissue plasminogen activator,
streptokinase, or both on coronary-artery patency, ventricular function, and survival
after acute myocardial infarction. N Engl J Med 1993; 329:1615.
34 Emergency Medicine
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Part C: Congestive Heart Failure
Congestive heart failure (CHF) is one of the most commonly encountered entities
in the Emergency Department. Because the prevalence of CHF increases with
age, the enormous burden of this disease is also on the increase. Currently, CHF
costs the health care system about $20 billion per year in the U.S. and it accounts
for more hospitalizations than any other disease in patients older than 65.
Definitions
• Congestive heart failure (CHF) exists when the heart is unable to pump sufficient
blood to meet the metabolic requirements of the body’s tissues. Because of natural
compensatory mechanisms in response to heart failure, it most commonly is associated
with abnormal retention of fluid.
• CHF is classified in many ways. Although in some respects, these classifications
are artificial because they do not exist as independent entities, they are nonetheless
very helpful distinctions to make in the evaluation and treatment of CHF
patients:
• High output failure versus low output failure: In low output failure there is an
inherent problem with the contractility of the heart. In high output failure, an
intact myocardium is unable to keep up with excess functional demands secondary
to hypermetabolic states such as thyrotoxicosis, anemia or AV shunts. Low output
failure is much more common.
• Left-sided versus right-sided failure: Left-sided failure is usually due to mechanical
overload or ischemia. The most common cause of right-sided failure is pulmonary
hypertension secondary to left-sided failure.
• Systolic versus diastolic failure: Systolic failure is more common and is due to impaired
contractility during systole. Diastolic failure occurs when impaired relaxation
prevents adequate filling of the ventricles during diastole. Diastolic failure is
less well understood and appears to be due to hypertension, as well as other less
common causes such as restrictive cardiomyopathy or aortic stenosis.
• Backward versus forward failure: Backward failure refers to the accumulation of fluid
behind the ventricles (e.g., edema and hepatic congestion in right-sided failure, pulmonary
edema in left-sided failure). Forward failure refers to the failure of the heart to
provide adequate perfusion of the tissues, which is usually manifested by some degree
of hypotension, whether relative or absolute.
• Acute and chronic heart failure essentially involve the same process, although when
heart failure develops over a short period of time, it tends to involve more forward
failure and hypotension and less accumulation of fluid. In chronic failure, there is
more time for the evolution of compensatory processes.
• Cardiogenic pulmonary edema refers to the accumulation of fluid in the interstitial
and alveolar spaces as a result of CHF. It is a severe form of left-sided CHF.
Epidemiology
At the present time, nearly 5 million patients are diagnosed with CHF in the U.S.
with 500,000 new cases identified each year. Almost 300,000 patients die from
CHF or its complications every year.
Pathophysiology
• The most common underlying pathology in CHF is ischemic heart disease. Other causes
of low output failure include valvular disease, myocarditis, chronic hypertension and
cardiomyopathies (such as those caused by ethanol and cocaine abuse). Anemia and
thyrotoxicosis are causes of high output failure. Table 2C.1 lists common processes that
Cardiovascular Disorders 35
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can precipitate CHF. The causes in the first column are especially important to identify
because they have specific therapy that can be initiated in the ED.
• In CHF, elevated left ventricular filling volumes exceeds the threshold over which
increased preload increases efficiency and instead, the heart begins to pump more
inefficiently, with decreasing stroke volume. This relationship is described by the
Frank-Starling curve. Decreasing stroke volume leads to the clinical effects of both
backward and forward failure.
• Neurohormonal compensatory responses play an important role in the pathophysiology
of CHF. Alterations in adrenergic tone redistribute blood flow to the brain and
heart and reduce flow to other organs. The reduction in flow to the kidneys increases
stimulation of renin-angiotensin-aldosterone axis which leads to an increased secretion
of ADH, renin and angiotensin II. This leads to increased sodium and water retention
and a rise in both preload and afterload. Increased adrenergic tone leads to arteriolar
vasoconstriction, which also contributes to increased afterload.
Diagnosis and Evaluation
Clinical Features
• Left-sided failure symptoms include dyspnea (particularly with exertion), orthopnea,
paroxysmal nocturnal dyspnea, fatigue and nocturia.
• Physical examination features in left-sided failure include tachypnea, tachycardia, pulmonary
rales and/or wheezing (“cardiac asthma”), dullness to percussion, diaphoresis,
poor peripheral perfusion causing pale and cool extremities, S3 and S4 gallop rhythms
and in severe pulmonary edema secondary to CHF, abnormal breathing patterns, such
as Cheyne-Stokes.
• Right-sided failure symptoms include lower extremity edema and right upper quadrant
pain and anorexia due to liver congestion.
• Examination features in right-sided failure include jugular venous distention,
hepatojugular reflux, hepatomegaly, RUQ abdominal tenderness, and peripheral edema.
Diagnostic Studies
• In addition to establishing the diagnosis of CHF, the EP must focus on the identifying
and correction of its underlying causes. Important precipitating causes are listed in
Table 2C.1.
• Chest X-ray (CXR) findings are mostly a function of left-sided failure, which results in
increased pulmonary venous pressures.
• Because of the higher resistance to flow in the lower regions, blood flow is initially
shunted to the upper pulmonary vasculature. This appearance of engorged vessels in
the upper lung fields is known as “cephalization” and is the earliest finding of CHF on
the chest X-ray.
• As the vascular pressure increases, fluid starts to move to the gravity-dependent lower
zones of the lungs, which is known as “caudalization”
• Interlobular edema creates short horizontal linear markings in the lung periphery at
the bases which are known as Kerley B lines.
Table 2C.1. Common precipitants of congestive heart failure
Myocardial infarction/ischemia Dietary and fluid excesses
Dysrhythmia Valvular heart disease
Infection Non-compliance with medications
Thyrotoxicosis Uncontrolled hypertension
Pulmonary embolism
36 Emergency Medicine
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• With increasing severity, a bat-wing pattern may be seen, representing interstitial
edema in both upper and lower regions of the lungs
• In its most severe form, edema fluid spills from the interstitial spaces into the airspaces,
causing opacification of the lung fields on CXR
• Cardiomegaly is usually evident on the CXR, especially in patients with chronic CHF.
In those cases where CHF occurs acutely in a previously healthy individuals, the EP
must distinguish cardiogenic from noncardiogenic causes of pulmonary edema, such
as the adult respiratory distress syndrome (ARDS)
• Pleural effusion may also be seen in CHF. It is often bilateral.
• A 12-lead EKG should be obtained immediately in patients presenting with signs and
symptoms suggestive of CHF because an important precipitant of CHF is ischemia
and infarction.
• In chronic CHF, changes such as ventricular hypertrophy and conduction abnormalities
can be seen. These changes invariably make the identification of acute coronary syndromes
(ACS) more difficult, underscoring the importance of performing serial EKGs
in the ED and obtaining previous EKGs for comparison. The presence of dynamic or
new changes in the 12-lead EKG should raise the suspicion for ACS.
• Bedside echocardiography performed by EPs may be very valuable in ruling out the
presence of a pericardial effusion in the setting of a patient with signs of failure and an
enlarged heart on CXR. Formal echocardiography yields a great deal of valuable information
to help guide the management of patients with CHF but is not necessarily
required during the course of ED management.
• Basic laboratory investigations such as CBC, electrolytes, urea and creatinine are indicated
in CHF. Anemia is an important contributing factor in CHF. Electrolyte disturbances
are common and potentially life-threatening. These are often the result of chronic
diuretic therapy and renal insufficiency associated with CHF.
• In most cases, serum troponin or other cardiac markers should be measured during the
ED evaluation because of the strong association between CHF and ischemic heart disease.
• A digitalis level should be obtained in those patients receiving digoxin therapy.
• B-type natriuretic peptide (BNP) is an endogenous cardiac peptide produced in the
ventricles that is released from the heart in response to fluid overload. Recently, an
assay of BNP has been introduced to assist in the diagnosis of CHF. It is both sensitive
and specific for the presence of CHF; however, its clinical role has yet to be determined.
At present, it appears that this test may have a role in a limited subset of
patients in whom the diagnosis of CHF may be clouded by coexisting pulmonary
disease such as chronic obstructive pulmonary disease (COPD) or sleep apnea.
ED Management
Emergency Resuscitation
• In severe cases, emergent management may involve aggressive intervention to maintain
airway, breathing and circulation.
• All patients require vascular access, cardiac monitoring and pulse oximetry.
• All patients should be placed on oxygen therapy. The specific technique of delivery
(nasal cannula, face mask, non-rebreather mask) should be guided by the severity of
presentation and pulse oximetry values.
• Aggressive airway management should be initiated in the setting of severe respiratory
distress, with or without hypoxia. Endotracheal intubation will be necessary in patients
who become so somnolent that they are unable to protect their airway or in those who
have tired of breathing and may have begun to have periods of apnea.
• Noninvasive ventilation techniques such as continuous positive airway pressure (CPAP)
or biphasic positive airway pressure (BiPAP) have been used in many instances where
Cardiovascular Disorders 37
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intubation and mechanical ventilation were once considered inevitable. They are used
as a bridging therapy in the patient with severe cardiogenic pulmonary edema until
pharmacologic therapy takes effect. These devices provide continuous or biphasic positive
airway pressure through a tight-fitting face mask. This positive pressure improves
cardiac output by decreasing venous return and excessive preload. It also improves
oxygenation by increasing alveolar recruitment and decreases the work and metabolic
requirement of breathing.
• Heart rate is extremely important in CHF and both inappropriately slow and fast rates
will decrease the ability of the heart to work efficiency. Brady- and tachydysrhythmias
should be treated according to ACLS guidelines in the setting of CHF.
• When frank shock is present, vasopressor therapy may need to begin immediately. An
inotropic agent such as dopamine is preferred. These agents all increase myocardial
oxygen consumption and ischemia, creating an additional risk for dysrhythmias.
• Although pressors may raise arterial blood pressure, this alone does not guarantee sufficient
perfusion, if cardiac output is too low. Adequate perfusion must always be assessed
by using clinical indicators such as urine output, skin appearance and mental status.
• Interventional therapies may be possible in the event that acute exacerbation is due to
ACS (e.g., percutaneous coronary intervention) or a related structural problem (e.g.,
valvular or myocardial rupture repair).
• Intra-aortic balloon counterpulsation (IABP) can be used as a bridge to other
interventional therapies such as cardiac transplantation.
Specific Pharmacotherapy
• The use of pharmacotherapeutic agents is aimed at improving the unfavorable hemodynamics
of acute CHF. In general, these agents share the ability to precipitate or
worsen hypotension. As each successive agent is introduced (at a pace commensurate
with the severity of symptoms), close attention must be paid to vital signs, fluid balance
and symptomatic response to therapy.
• Nitrates cause both arterial and venous vasodilatation, reducing both preload and
afterload. Nitroglycerin (NTG) is the initial agent of choice in acute CHF.
• Nitrates can be administered through many routes including sublingual, transdermal,
and intravenous.
• Caution should be exercised with sublingual NTG because of its ability to cause
precipitous drops in blood pressure.
• Transdermal paste (1/2-2 inches applied to chest wall) gives a slower, lower dose
release of NTG but may not be effective in severe CHF when cutaneous perfusion
is compromised.
• IV dosing is required in severe CHF, and IV infusions may be started at 10-20 mcg/
min and titrated to relief of symptoms while maintaining systolic BP
<90 mm.
• Nitrates predictably cause headache, which will often require treatment with analgesics.
• Diuretics reduce volume overload. Loop diuretics are the preferred class, and initial
treatment should begin with furosemide (Lasix) 20-80 mg IVP, depending on the
patient’s previous exposure and severity of symptoms. Even with IV administration,
full effect may take up to 30 min, underscoring the importance of using diuretics
together with nitrates. Adverse effects of diuretics include electrolyte imbalances,
prerenal azotemia, contraction alkalosis and hypotension.
• ACE inhibitors decrease afterload. Because of several trials that demonstrate reduction
in morbidity and mortality in CHF, ACE inhibitors should be used in the treatment
of chronic CHF unless a contraindication exists. Several agents can be given in the
ED, however, captopril (Capoten) 6.25-12.5 mg PO q8h is preferred because it is the
38 Emergency Medicine
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fastest acting of the various agents available. Angiotensin II receptor blockers (ARBs)
inhibit the effects of angiotensin II. They decrease afterload and improve diuresis.
Currently, they should only be used in place of ACE inhibitors in patients who are
intolerant or allergic to ACE inhibitors.
• Morphine decreases catecholamine levels by decreasing anxiety, theoretically causing a
decrease in preload and afterload. However, little evidence for the effectiveness of
morphine exists and its use is controversial. Respiratory depression with morphine
may result in unnecessary intubation—a small dose (e.g., 2 mg IV) may be beneficial
without impairing respiratory effort.
• Beta-blockers have been shown in multiple well-designed, randomized studies to improve
the symptoms and altered hemodynamics in chronic CHF. They inhibit the neurohormonal
cascade and improve symptoms, especially in the setting of cardiac ischemia.
They have also been shown to decrease mortality. However, they are not generally indicated
in the treatment of acute heart failure and may result in acute decompensation.
When CHF occurs within the setting of AMI, the decision to add ²-blockers to therapy
should be made with the guidance of a cardiologist.
• Digoxin enhances contractility and reduces afterload by blunting the cardiac sympathetic
response. It also causes AV nodal blockade which may be beneficial in patients
with atrial dysrhythmias. Currently, there are no conclusive data to show that digoxin
reduces mortality in CHF although it may reduce hospitalizations and improve quality
of life. Because it is slow to act, its use in the ED for CHF is on the decline. IV
loading may be initiated in the ED with 0.25 mg followed by further IV or PO doses
over the next several hours.
• Calcium channel blockers are not currently recommended in the ED treatment of CHF,
unless they are required for rate control in accordance with ACLS guidelines.
• Dobutamine is a synthetic catecholamine that unlike other pressor agents causes vasodilatation
in addition to inotropy. For this reason, it is the one vasoactive catecholamine
sometimes used in treatment of CHF in the absence of cardiogenic shock.
Dobutamine must be given with close hemodynamic monitoring and may initially
result in hypotension.
• Nesiritide (Beta natriuretic peptide) is an endogenous substance that acts both a vasodilator
and a diuretic. It has recently been demonstrated to be effective in the treatment
of acute CHF. However, its effects are more prolonged and it is less titratable
than NTG. Its role as a first-line agent in the treatment of CHF and superiority over
NTG has yet to be demonstrated.
Prognosis
Prognosis in CHF decreases proportionately with severity. Two commonly used
classification systems for severity of heart failure are given in (Table 2C.2). Both
classifications demonstrate the typical progression of chronic CHF from backward
to forward failure.
Disposition
Patients diagnosed with acute heart failure or acute exacerbation of chronic
heart failure most commonly require admission to hospital. Moderate or severe
presentations require admission to the cardiac care unit (CCU) or monitored unit.
Mild exacerbations may be admitted to unmonitored settings in the absence of
suspected ACS. It may also be appropriate to admit patients with mild exacerbations
to short-stay or observational units or even to discharge them home with
close follow-up when no acute serious underlying pathology is suspected and symptoms
have resolved.
Cardiovascular Disorders 39
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Suggested Reading
1. Cairns CB. Heart failure and pulmonary edema. In: Tintinalli JE, Kelen GT, Stapczynski
SJ, eds. Emergency Medicine. A Comprehensive Medicine Study Guide. McGraw-Hill,
2000.
2. Falk JL, O’Brien JF, Shesser R. Heart Failure. In: Marx JA, Hockberger RS, Walls RM,
eds. Emergency Medicine. Concepts and Clinical Practice. Mosby, 2002:2.
3. Hunt SA, Baker DW, Chin MH et al. ACC/AHA guidelines for the evaluation and
management of chronic heart failure in the adult: A report of the American College of
Cardiology/ American Heart Association Task Force on Practice Guidelines. 2001 American
College of Cardiology Web site: Available at http://www.acc.org/clinical/guidelines/
failure/hf_index.htm. (Accessed 3/28/2002.).
4. Packer M, Cohn JN. Consensus recommendations for the management of chronic heart
failure. AM J Cardiol 1999; 83:1A-38A.
5. The ELITE II Investigators. Effect of losartan compared with captopril on mortality in
patients with symptomatic heart failure. Randomized trial—The Losartan Heart Failure
Study ELITE II. Lancet 2000; 355:1582-1587.
6. The SOLVD Investigators. Effect of enalapril on mortality and the development of heart
failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl
J Med 1992; 327:685-691.
7. Tsutamoto T, Wada A, Maeda K et al. Attenuation of compensation of endogenous
cardiac natriuretic peptide system in chronic heart failure: Prognostic role of plasma
brain natriuretic peptide concentration in patients with chronic symptomatic left ventricular
dysfunction. Circulation 1997; 96:509-516.
Part D: Endocarditis
Epidemiology/Pathophysiology
• Endocarditis is an infection of the heart valves which can present either acutely or as a
chronic disease. It is a life threatening infectious disease that is difficult to diagnose
with certainty in the Emergency Department.
• Intravenous drug abusers, immunocompromised patients, patients with a history of
rheumatic heart disease, and patients who have undergone valve replacement are at
heightened risk for developing endocarditis. Other patients at risk include those with
intracardiac devices (pacemakers, defibrillators), those with a history of endocarditis,
Table 2C.2. Classification of heart failure severity and prognosis
Killip Classification 1 yr
(Clinical) Definition Incidence (%) Mortality (%)
Class I No signs of pulmonary 30 5
edema
Class II Mild failure (rales, S3) 40 15-20
Class III Frank pulmonary edema 10 40
Class IV Cardiogenic shock 20 80
Diamond-Forrester
Classification (Based Cardiac Index Pulm. Artery Wedge 1 yr
on invasive monitoring) (L/min/m2) Pressure (mm Hg) Mortality (%)
Class I >2 <18 3
Class II >2 >18 9
Class III <2 <18 23
Class IV <2 >18 51
40 Emergency Medicine
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those with mitral valve prolapse and regurgitation, and patients with certain congenital
heart defects.
• Streptococci are the most common cause of native valve endocarditis.
• Staph species are responsible for the majority of IVDU-related endocarditis and coagulase
negative Staph is responsible for the majority of prosthetic valve endocarditis.
• Other etiologic agents include Enterococcus, Gram-negative bacteria, the HACEK organisms
(Haemophilus, Acetinobacillus, Cardiobacterium, Eikenella, and Kingella species),
Candida and Aspergillus.
Diagnosis and Evaluation
• Diagnosis of endocarditis has traditionally been based on clinical findings and bacteriologic
criteria from blood cultures. The development and increased utilization of
echocardiography has provided increased ability to diagnose endocarditis. The Duke
criteria describes clinical, bacteriological and echocardiographic diagnostic criteria for
endocarditis.
History and Physical Exam
• Endocarditis presents with a variety of clinical complaints.
• The triad of fever, anemia, and a heart murmur is highly suggestive of endocarditis but
is not routinely present.
• Fever, malaise and altered mental status are common historical features.
• Patients may also present with embolic sequelae, which occur in approximately
25-50% of patients with endocarditis. 65% of emboli involve the central nervous
system, usually in a MCA distribution.
• Physical findings include heart murmurs, most commonly of the mitral and aortic
valves. However, less than one-third of IVDU patients with endocarditis will have
murmurs.
• Osler’s nodes, painful erythematous nodules found on the palmar fingertips, are rarely
found. Janeway lesions, flat nontender macular areas on the palms are also rarely seen.
Laboratory and Studies
• Laboratory findings include positive blood cultures as discussed above and a mild
anemia. Most patients have microscopic hematuria as well.
• Echocardiography is a powerful tool to aid in the diagnosis of endocarditis.
• Transthoracic echo has a poor sensitivity (approximately 60%) but excellent specificity
if vegetations are seen.
• Transesophageal echocardiography is more sensitive (>85% sensitivity) for visualization
of vegetations.
ED Management
• Blood culture results are often unavailable to the Emergency Physician and thus
empiric antibiotic coverage is required. Blood cultures should be drawn before beginning
antibiotics as antibiotics reduce the bacterial recovery rate of cultures by
approximately one-third.
• Patients with an acute presentation of endocarditis, a history of IVDU or a prosthetic
heart valve should receive vancomycin, an aminoglycoside (gentamycin), and rifampin.
Patients with a subacute course and native heart valves should receive either penicillin and
an aminoglycoside or a penicillinase-resistant penicillin (nafcillin) and an aminoglycoside.
• Occasionally, patients may require surgical therapy. Indications for surgery include
severe congestive heart failure, recurrent emboli, fungal endocarditis, and failure of IV
antibiotic therapy.
Cardiovascular Disorders 41
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• Patients with conditions predisposing them to endocarditis should receive antibiotic
prophylaxis prior to dental, GI, or GU procedures. Amoxicillin or erythromycin should
be given 1 h before the procedure for proper prophylaxis.
Suggested Reading
1. Bayer A et al. Diagnosis and management of infective endocarditis and its complications.
Circulation Dec 1998; 98(25).
2. ACC/AHA guidelines for the management of patients with valvular heart disease. A
Report of the American College of Cardiology/American Heart Association Task Force
on practice guidelines. J Am Coll Cardiol 1998; 32(5):1486-588.
3. Cline D. Valvular Emergencies and Endocarditis. In: Tintinalli JE, Kelen GT, Stapczynski
JS, eds. Emergency Medicine. A Comprehensive Medicine Study Guide. McGraw-Hill,
2000.
4. Dunmire S. Infective Endocarditis and Acquired Valvular Heart Disease. In: Marx JA,
Hockberger RS, Walls RM, eds. Emergency Medicine. Concepts and Clinical Practice.
Mosby, 2002:2.
Part E: Pericardial Diseases
Pericardial disease is an important consideration in patients presenting with cardiopulmonary
symptoms. The understanding of pericardial disease is important as
these diseases not only cause significant morbidity, but they may also mimic other
diseases which may require alternative treatment.
Definitions
• Pericarditis is an inflammation of the pericardial layer surrounding the heart.
• A pericardial effusion is an abnormal accumulation of fluid in the pericardial space.
• Cardiac tamponade refers to an impairment of cardiac output caused by a pericardial
effusion.
• Scarring and thickening of the pericardium may cause constrictive pericarditis, a rare
complication of pericarditis.
Table 2D.1. The Duke criteria for the diagnosis of endocarditis
Major Criteria Positive blood cultures with typical microorganisms consistent with
endocarditis
Evidence of endocardial involvement with a positive echocardiogram
or new valvular regurgitant murmur
Minor Criteria Predisposing heart condition or IVDU
Fever
Vascular phenomena including emboli, Janeway lesions, pulmonary
infarctions, mycotic aneurysms, or, splinter hemorrhages
Immunologic phenomena including Osler’s nodes, Roth spots,
glomerulonephritis
Blood cultures suggestive of endocarditis but not meeting
the major criteria
Echocardiographic evidence suggestive of endocarditis but not
meeting major criteria
The presence of 2 major criteria, 1 major criterion and 3 minor criteria, or 5 minor criteria
establishes a diagnosis of endocarditis.
42 Emergency Medicine
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Epidemiology/Pathophysiology
• Pericarditis has multiple etiologies including infection, malignancy, uremia, connective
tissue disorders, trauma, myocardial infarction, or medications. Pericarditis may also be
idiopathic, but it is unclear if these represent undiagnosed viral pericarditis.
• Pericarditis that occurs post myocardial infarction is called Dressler’s syndrome.
• Dressler’s syndrome is associated with large, anterior infarctions and may indicate a
poor long-term prognosis.
• Pericardial inflammation causes an increase in pericardial fluid beyond the 15-50 ml
normally present. As pericardial fluid accumulates, intrapericardial pressure increases
exponentially.
• Cardiac tamponade occurs when intrapericardial pressures rise to a level such that
diastolic filling of the heart is impaired. This leads to an increase in central venous
pressure and a decreased cardiac output.
• Constrictive pericarditis may lead to similar hemodynamic abnormalities as cardiac
tamponade.
Diagnosis and Evaluation
History and Physical Examination
• Pericarditis may be asymptomatic. Presenting symptoms correlate with the etiology of
pericarditis.
• Acute viral pericarditis typically presents with fevers, myalgias, and fatigue.
• Chest pain is common in acute pericarditis. The pain is classically sharp and pleuritic.
It is often exacerbated by leaning forward and relieved by supine positioning. Radiation
of the pain to the trapezius ridge is a specific finding.
• As a pericardial effusion enlarges and tamponade begins, symptoms of increased venous
pressure and decreased cardiac output (dyspnea, orthopnea, syncope) present.
• A pericardial friction rub is the classic physical finding of pericarditis. Friction rubs
have been described in many ways such as “creaky” or “velcro-like.” They are best
heard with the bell of the stethoscope and can be heard anywhere over the pericardium.
Friction rubs are transient and change in quality over time. Thus, the absence of
a friction rub does not rule out pericarditis.
• As cardiac tamponade develops, signs of increased venous pressure (JVD, hepatomegaly)
and decreased cardiac output (hypotension) develop.
• Beck’s triad of hypotension, JVD, and muffled heart sounds is specific for cardiac
tamponade, but rarely present.
• Pulsus paradoxus, a decrease of systolic blood pressure of at least 10 mm Hg during
inspiration, is another sign of cardiac tamponade, but its presence is not sensitive
enough to rule out the diagnosis.
Laboratory and Studies
• Laboratory tests do not play a major role in the evaluation of pericardial disease.
• An increased ESR is a nonspecific test that is usually elevated in pericarditis.
• Cardiac enzymes may be elevated in pericarditis indicating a concurrent inflammation
of the underlying myocardium.
• The electrocardiogram is an important tool in the evaluation of patients with pericardial
disease. As these patients often present with chest pain that may not be indistinguishable
from ischemic chest pain, subtle differences in the EKG may dramatically
change treatment.
• The EKG typically evolves through four stages in acute pericarditis:
• Stage 1, hours to days after symptom onset, demonstrates a diffuse concave upward
elevation of the ST segment in all leads but AVR and V1. The PR segment is depressed
in 80% of patients. There are generally no T-wave abnormalities.
Cardiovascular Disorders 43
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• In stage 2 there is a normalization of the above ST and PR segments
• Stage 3 demonstrates diffuse deep, symmetric T-wave depressions.
• Stage 4 is a normalization of the T-wave depressions.
• Electrical alternans, the finding of changing QRS polarity with every other beat, is a specific
finding for large, chronic pericardial effusions most commonly caused by malignancy.
• Chest X-ray may demonstrate cardiomegaly or a “water bottle” heart with large pericardial
effusions.
• Echocardiography is a fast, reliable method to diagnose pericardial effusions.
Echocardiography can detect as little as 15 ml of fluid and can be done at bedside in
unstable patients. Echocardiography is a sensitive test for signs of cardiac tamponade
including right ventricular diastolic collapse and IVC dilation with lack of inspiratory
collapse.
ED Management
• Treatment of acute pericarditis includes pain control and control of inflammation
with NSAIDS. Treatment may continue on an outpatient basis in stable patients, but
may require inpatient management in patients with severe pain, significant pericardial
effusions, or any signs of hemodynamic instability.
• Treatment of pericardial effusions is dependent on the etiology. Uremic pericarditis
with effusion, for example, is an indication for dialysis.
• Cardiac tamponade is treated with drainage of pericardial fluid via pericardiocentesis
or operative drainage.
• Constrictive pericarditis is treated with operative removal of the pericardium.
Suggested Reading
1. Fowler N. Cardiac Tamponade, a clinical or an echocardiographic diagnosis? Circulation
1993; 87:5.
2. Pawsat D, Lee J. Inflammatory disorders of the heart. Pericarditis, Myocarditis, and
Endocarditis. Emerg Med Clin North Am 1998; 16:3.
3. Reddy P, Curtiss E. Cardiac tamponade. Cardiology Clinics November 1990; 8:4.
4. Shabeti R. Acute pericarditis. Cardiol Clin 1990; 8:4.
5. Spodick D. Pathophysiology of cardiac tamponade. Chest 1998; 113:5.
Part F: Structural Heart Disease
The Emergency Physician must be comfortable managing patients with structural
heart disease. Although the incidence of rheumatic fever has decreased, thus decreasing
the incidence of rheumatic heart disease, many patients with structural heart disease
of other etiologies are being increasingly recognized and living longer. These patients
have special needs that the Emergency Physician must include in the criteria for urgent
or emergent operative repair and the need for prophylactic antibiotics for procedures.
This section discusses the presentation and treatment of structural heart disease
as well as the potential complications of prosthetic valves.
Aortic Stenosis
Epidemiology/Pathophysiology
• Aortic stenosis is caused by rheumatic heart disease or valvular calcification. Calcific
aortic stenosis presents in the fifth to sixth decade of life in patients with a congenital
bicuspid valve and in the seventh to eighth decade of life in patients with normal
tricuspid valves.
• The pathophysiology of aortic stenosis is due to a narrowing of the cardiac outflow
with compensatory increase in left ventricular size and subsequent diastolic dys44
Emergency Medicine
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function. The progressive narrowing of cardiac outflow leads to a decrease in cardiac
output with progressive systolic dysfunction causing the classic symptom triad
of angina, syncope, and heart failure.
• Angina—Left ventricular hypertrophy leads to increased myocardial oxygen demand,
causing angina despite normal coronary arteries; 50% of patients with aortic
stenosis and angina have coexisting significant coronary artery disease.
• Syncope—The inability to increase cardiac output past a stenotic valve leads to
exertional dizziness and ultimately syncope. Other explanations include a dysfunction
of ventricular baroreceptors leading to inappropriate peripheral dilatation despite
decreased cardiac output.
• Heart failure—Symptoms of heart failure are secondary to diastolic dysfunction
from a hypertrophied left ventricule. Only late in the disease does systolic function
decompensate to a pathologic level. The inability to increase cardiac output during
times of exertion will also cause dyspnea on exertion.
Diagnosis and Evaluation
• Classic presentation of critical aortic stenosis includes the above trilogy: angina, syncope,
and heart failure.
• Other symptoms of aortic stenosis include symptoms of atrial fibrillation or sudden
cardiac dysrhythmias.
• The murmur of aortic stenosis is classically described as a crescendo-decrescendo systolic
best heard at the right upper sternal border and radiating to the carotids. A single
second heart sound is present and there is a delayed carotid upstroke.
• Echocardiography is the test of choice for patients with symptoms or signs suggestive of
aortic stenosis. It can delineate the severity of outflow obstruction, discover concurrent
valvular abnormalities (80% of patients with aortic stenosis have concurrent aortic regurgitation),
and evaluate left ventricular response to the stenotic valve.
ED Management
• Treatment of aortic stenosis is surgical.
• Medical treatment is reserved for treating concurrent diseases (i.e., coronary artery
disease) and the routine use of antibiotics for endocarditis prophylaxis.
• Valve replacement is indicated for patients with symptomatic aortic stenosis. Without
surgical correction, the 2-yr survival rate is <50%.
Aortic Insufficiency
Epidemiology/Pathophysiology
• Aortic insufficiency may be acute or chronic.
• Acute aortic insufficiency is due to aortic root disease with dissection or valvular destruction
secondary to endocarditis. Acute aortic insufficiency causes a rapid increase
in cardiac afterload secondary to the regurgitant blood volume as well as an acute
increase in pulmonary vascular pressure. Symptoms include severe dyspnea with signs
of pulmonary edema. Other symptoms are those of the underlying disease such as
tearing chest pain in patients with aortic dissection.
• Chronic aortic insufficiency is most likely secondary to rheumatic heart disease. The
damaged valve leads to a backflow of blood during diastole, thus increasing the stroke
volume. This increases afterload as the ventricle attempts to push the increased blood
volume against the regurgitant flow. Preload is also increased as the regurgitant flow
significantly increases the volume load of the left ventricle. Early in the disease, the left
ventricle is able to compensate with hypertrophy and dilatation, with minimal symptoms.
However, as the disease progresses, the ventricle is unable to compensate, ejection
fraction decreases, and symptoms of heart failure develop. Other symptoms include
Cardiovascular Disorders 45
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anginal chest pain as the hypertrophied heart outgrows its blood supply or palpitations
from the increased systolic outflow.
Diagnosis and Evaluation
• The murmur of aortic insufficiency is a “blowing” diastolic murmur heard best at the
left sternal border of the heart. There may be an accompanying systolic ejection murmur
heard as the increased volume is expelled during systole. Other findings include a
“water-hammer” pulse with a fast upstroke and an abrupt collapse.
• The electrocardiogram is variable in acute disease, often reflecting the underlying cause.
Chronic aortic insufficiency will cause signs of LVH to be present on the EKG.
• The diagnostic test of choice is the echocardiogram, which can assess the severity of
the valvular dysfunction as well the left ventricular function. In acute disease, the
echocardiogram is also important for evaluation of concurrent life threatening complications
of the underlying disease, especially pericardial tamponade associated with
aortic dissections.
ED Management
• Treatment of aortic insufficiency is surgical.
• Acute disease is a cardiothoracic surgical emergency requiring immediate operative
repair of both the valve and often the aortic root.
• Chronic disease develops over years with surgical correction suggested for most symptomatic
patients and most patients with severe disease and/or concurrent left ventricular
dysfunction despite clinical symptoms.
• Medical management includes the use of afterload reducing agents in order to decrease
the regurgitant volume, hopefully retarding the onset of left ventricular dysfunction.
However, medical management is not a replacement for surgical valve replacement
or repair. Other medical management issues include the treatment of
concurrent diseases including coronary artery disease, atrial fibrillation, and the prevention
of endocarditis.
Mitral Stenosis
Epidemiology/Pathophysiology
• The most common cause of mitral stenosis is rheumatic heart disease.
• The mitral valve becomes thickened, calcified, and fused. The increased pressure required
to force blood across the stenotic valve leads to an elevation of left atrial pressures
and subsequent left atrial dilatation. With progression of disease, the pressure
column backs into the pulmonary circulation, leading to pulmonary hypertension,
tricuspid valve dysfunction, and right heart failure. The disease progresses slowly over
years but may be accelerated by conditions increasing the demand for flow across the
damaged valve, such as atrial fibrillation, pregnancy, infection, or other stressors.
Diagnosis and Evaluation
• Mitral stenosis presents with symptoms of congestive heart failure and pulmonary
hypertension usually in the fifth to sixth decade of life.
• Patients may also present with complications of previously unrecognized disease. This
includes atrial fibrillation in 30-40% of patients, hemoptysis secondary to pulmonary
hypertension and erosion of bronchial veins, chest pain (despite the lack of concurrent
coronary artery disease), or embolic disease in 10-20% of patients.
• The murmur of mitral stenosis is a low-pitched diastolic rumble best heard at the apex
of the heart. Other findings include an opening snap. Auscultatory findings are best
heard with the patient in the left lateral position with the bell of the stethoscope.
• Electrocardiographic findings include “P-mitrale,” a widened p-wave in the limb leads.
46 Emergency Medicine
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• Echocardiography is the test of choice to visualize the abnormal mitral valve, assess the
severity of valvular obstruction and evaluate its effect on the pulmonary circulation.
ED Management
• Treatment for mitral stenosis is surgical via mitral valve replacement or balloon valvotomy.
• Medical treatment is reserved for the treatment of concurrent diseases including atrial
fibrillation with rate control medications and anticoagulation, as well as antibiotic
prophylaxis against endocarditis.
Mitral Regurgitation
Epidemiology/Pathophysiology
• Mitral regurgitation may be acute or chronic.
• Acute mitral regurgitation is secondary to infective endocarditis with erosion of the valve
or acute ischemia of the chordae tendinae/papillary muscle support system. Acute mitral
regurgitation causes an abrupt increase in the pulmonary vascular pressure leading to
acute pulmonary edema. This often progresses to cardiogenic shock and cardiac arrest.
• Chronic mitral regurgitation has multiple etiologies, most commonly rheumatic heart
disease. Chronic mitral regurgitation leads to a compensatory enlargement of both the
left atrium and ventricle in order to handle the regurgitant blood volume. Early in the
course of the disease, the contractile force of the left ventricle is preserved and stroke
volumes are supranormal with both the normal stroke volume and the regurgitant
volume expelled during systole. With disease progression, the left ventricle enlarges to
a point that compromises the contractile function, lowering the ejection fraction. The
decrease in forward flow leads to an increase of pulmonary pressures and symptoms of
heart failure.
Diagnosis and Evaluation
• The murmur of mitral regurgitation is holo-systolic at the apex of the heart that radiates
to the axillae. In acute mitral regurgitation, the murmur is typically harsh with
signs of pulmonary edema present. In chronic mitral regurgitation, there may also be
a diastolic murmur heard at the apex indicative of the increased regurgitant flow across
the valve.
• Physical signs of cardiac enlargement are usually present.
• The electrocardiogram typically demonstrates LVH and LAE in mitral regurgitation.
However, these may be absent in cases of acute valvular dysfunction.
• The diagnostic test of choice is the echocardiogram, which can assess the severity of
the valvular dysfunction as well as the left ventricular function.
ED Management
• Treatment of acute mitral regurgitation is surgical.
• Medical support is geared toward treatment of acute pulmonary edema and the underlying
etiology of the dysfunction (i.e., ischemia).
• Surgical repair is indicated in most patients with decompensated chronic mitral
regurgitation.
• Medical treatment options for patients with chronic mitral regurgitation are complex.
Afterload reduction with ACE inhibitors and other vasodilators may reduce the regurgitant
flow and thus decrease symptoms and prolong the time between diagnosis and
the need for operative repair. Medical treatment is also geared toward the prophylaxis
and treatment of potential complications including atrial fibrillation and endocarditis.
Cardiovascular Disorders 47
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Mitral Valve Prolapse
Epidemiology/Pathophysiology
• Mitral valve prolapse is the most common form of valvular disease.
• Etiologies include congenital valve degeneration and connective tissue disorders.
• The overall prognosis for most patients with mitral valve prolapse is excellent, with
most symptoms being benign.
• Sudden death is a rare complication, occurring in 1-2% of patients.
Diagnosis and Evaluation
• The presentation of mitral valve prolapse is diverse. Patients are usually asymptomatic,
with the diagnosis made on auscultatory findings alone.
• Common symptoms include chest pain and palpitations. The chest pain is often times
atypical, nonanginal type chest pain but can occasionally have angina-like characteristics.
The palpitations of mitral valve prolapse are usually due to occasional premature
ventricular complexes but can occasionally be due to more troubling dysrhythmias
such as SVT or rarely ventricular tachycardias.
• Mitral valve prolapse is also associated with autonomic hyperactivity symptoms. Patients
may present with anxiety, panic attacks, or other symptoms of concurrent psychiatric
disease.
• Neurologic complications such as TIAs and migraine headaches are also associated
with mitral valve prolapse.
• The auscultatory finding of mitral valve prolapse is a midsystolic click. Mitral valve
prolapse can progress to significant mitral regurgitation at which time the systolic
murmur of MR is heard.
• Diagnosis is confirmed by echocardiography.
ED Management
• Treatment is focused on the relief of symptoms and the prevention of complications.
Beta-blockers are used to control palpitations and anxiety symptoms.
• Antibiotics are used for the prevention of endocarditis.
• Aggressive rhythm control is required for patients with more severe dysrhythmias.
Tricuspid Valve Disease
Epidemiology/Pathophysiology
• Tricuspid valve disease is usually found with concurrent left-sided valvular diseases
and pulmonary hypertension.
• Congenital abnormalities and endocarditis, seen most commonly in abusers of intravenous
drugs, cause isolated right-sided valvular disease.
• Weight loss medications may also result in tricuspid valve disease.
Diagnosis and Evaluation
• In patients with tricuspid disease and associated left-sided valve dysfunction or pulmonary
hypertension, symptomatology is dominated by the concurrent diseases.
• Isolated tricuspid disease presents with symptoms of right-sided heart failure including
hepatomegaly, ascites, and peripheral edema.
• The murmur of tricuspid regurgitation is pansystolic at the left lower sternal border.
Tricuspid stenosis inconsistently produces a high-pitched diastolic murmur. Prominent
jugular venous pulsations are present in both abnormalities.
• Diagnosis is confirmed by echocardiography.
48 Emergency Medicine
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ED Management
• Treatment is geared toward concurrent disease processes and prevention of complications
such as endocarditis.
• Surgical correction may be needed.
Prosthetic Valve Dysfunction and Complications
• Valve replacement surgery is very common with more than 40,000 replacements done
per year.
• Prosthetic heart valves are either bioprosthetic (usually bovine, porcine, or human
cadaveric) or mechanical.
• The evaluation of a patient with a prosthetic valve begins with an understanding of
the type of valve placed and the reason for placement. Patients are instructed to carry
a card describing the prosthetic valve.
• Mechanical valves have a mechanical click and systolic murmurs. Bioprosthetic valves
normally have only slight murmurs.
• Any change in clinical status or auscultatory findings in patients with prosthetic valves
requires an evaluation of the valve including echocardiography.
• Complications of prosthetic valves include valve thrombosis, infection, and degeneration
of the valve or surgical site.
• Thrombosis of a prosthetic valve can be acute or chronic and is much more common
in mechanical valves. Acute valvular thrombosis is a cardiothoracic surgical
emergency, presenting with acute heart failure and cardiogenic shock. Thrombi
may also occur chronically and present with either progressive valvular dysfunction
and symptoms of worsening valvular disease, or with embolic phenomena. Treatment
includes valve replacement but may also include fibrinolytic therapy.
• Endocarditis is common in prosthetic valves. Within the first 2 mo after placement,
Staph species are common. After the first 2 mo, the etiology is similar to
native valve endocarditis. Treatment with antibiotics as in patients with native valve
endocarditis is required. Surgical valve replacement may be required.
• Valve dysfunction occurs more commonly with bioprosthetic valves with approximately
30% requiring replacement within 10 yr. All prosthetic valves have some
regurgitation and stenosis inherently. Degeneration of the valve itself, the perivalvular
surgical site, or the diseased myocardium can lead to worsening regurgitation or
stenosis. Valve failure presents with symptoms of either the stenosis or regurgitation
of the diseased valve. It is often difficult to distinguish valve dysfunction from progression
of underlying cardiac disease in these patients, thus requiring liberal use of
echocardiography in the evaluation of these patients.
• Mechanical prosthetics may also cause chronic hemolysis and subsequent anemia.
Hemolysis from mechanical valves or perivalvular degeneration is usually compensated
and asymptomatic. Severe dysfunction may lead to a more severe anemia and
subsequent symptoms.
Suggested Reading
1. Otto C. Aortic Stenosis: Clinical evaluation and optimal timing of surgery. Cardiol Clinics
1998; 16:3.
2. Bruce C, Nishimura R. Clinical assessment and management of mitral stenosis. Cardiol
Clinics 1998; 16:3.
3. Quinones M. Management of mitral regurgitation: Optimal timing for surgery. Cardiol
Clinics 1998; 16:3.
4. Bonow R. Chronic aortic regurgitation: Role of medical therapy and optimal timing for
surgery. Cardiol Clinics 1998; 16:3.
5. Safi H, Vinnerkvist A, Subramaniam M et al. Management of the patient with aortic
root disease and aortic insufficiency. Cardiol Clinics 1998; 16:3.
Cardiovascular Disorders 49
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6. Barbetseas J, Zoghbi W. Evaluation of prosthetic valve function and associated complications.
Cardiol Clinics 1998; 16:3.
7. Blaustein A, Ramanathan A. Tricuspid valve disease: Clinical evaluation, physiopathology,
and management. Cardiol Clinics 1998; 16:3.
8. Carabello B, Crawford F. Medical progress: Valvular heart disease. New Engl J Med
1997; 337.
9. ACC/AHA Guidelines for the management of patients with valvular heart disease. A
report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines. J Am Coll Cardiol 1998; 32(5):1486-588.
10. Cline D. Valvular Emergencies and Endocarditis. In: Tintinalli JE, Kelen GT, Stapczynski
JS, eds. Emergency Medicine. A Comprehensive Medicine Study Guide. McGraw-Hill,
2000.
11. Dunmire S. Infective Endocarditis and Acquired Valvular Heart Disease. In: Marx JA,
Hockberger RS, Walls RM, eds. Emergency Medicine. Concepts and Clinical Practice.
Mosby, 2002:2.
Part G: Aortic Emergencies
Diseases of the aorta are occurring more frequently with the aging of the population.
Imaging with CT and ultrasound has led to increased recognition of aortic
pathology. These diseases present in both dramatic and subtle ways, but left untreated
they are almost universally fatal. Therefore, the Emergency Physician must
be aware of the various presentations of aortic emergencies and have a complete
understanding of their management.
Aortic Dissection
Epidemiology/Pathophysiology
• The most important cause of aortic dissection is long-standing systemic hypertension.
The forceful ejection of the cardiac output results in repeated sheer stress on the intimal
wall, ultimately leading to the wall disruption that causes dissection.
• Patients with Marfan’s syndrome or Ehlers-Danlos syndrome have a congenitally weakened
aortic wall, thus predisposing these patients to aortic dissection.
• Dissection of the thoracic aorta is caused by a disruption of the intimal wall of the
aorta. Blood is transmitted through the tear creating a false lumen in the aortic wall.
Once the medial wall is weakened by the false lumen, the dissection can rupture through
the remainder of the outer wall, rupture through the side branches of the aorta, or
rarely rupture back into the true lumen of the aorta.
• Occasionally, dissections of the ascending aorta may also damage the coronary arteries
or the aortic valve.
Diagnosis and Evaluation
History and Physical Exam
• The presentation of aortic dissection usually involves the acute onset of severe chest
pain. Classically, the pain is described as “tearing” and is most severe at its onset.
• Occasionally, dissections will present with pain in other locations due to the migration
of the dissection and damage to side branch vessels.
• Neurologic symptoms may also be present if the carotid or spinal arteries are involved.
• Syncope may be a presenting symptom and is usually associated with ascending aorta
dissections.
• On clinical exam, hypertension is usually present, unless there are pulse deficits in the
arms being measured.
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• Hypotension in the face of an aortic dissection is indicative of a dissection into the
pericardium causing tamponade or severe hypovolemia secondary to hemorrhage.
• Pulse deficits may be present on exam and should be sought initially and on reexamination
to check for propagation of the dissection.
• If the dissection spreads proximally, dissection through the aortic valve may occur, resulting
in the findings of acute aortic insufficiency and congestive heart failure.
• As mentioned above, neurologic deficits may be present.
Laboratory and Studies
• Laboratory results are variable in aortic dissections; the only lab test of true importance
is the type and cross.
• The electrocardiogram usually indicates evidence of long-standing hypertension. Proximal
dissections may disrupt coronary blood flow, thus causing myocardial infarctions
with related EKG changes. Most commonly, the right coronary artery is involved,
leading to inferior myocardial infarctions.
• The chest X-ray is almost always abnormal. Most commonly, mediastinal widening is
present. Other X-ray signs include obliteration of the aortic knob, right-sided deviation
of a nasogastric tube, depression of the left mainstem bronchus, or a small left-sided
pleural effusion, or a left apical cap.
• Definitive diagnosis of an aortic dissection involves direct imaging of the aorta. The
gold standard remains aortography, which allows complete aortic visualization but is
being rapidly replaced by other modalities.
• Contrast CT scanning allows visualization of the extent of the dissection, as well as
pericardial and pleural effusions. CT scanning does not precisely localize intimal tears,
unreliably demonstrates side branch involvement, and is not able to define aortic regurgitation.
Furthermore, the contrast load needed for the CT scan is substantial and
can have adverse consequences, especially for patients with renal insufficiency.
• Transesophageal echocardiography (TEE) is highly accurate for proximal aortic dissections.
Benefits of TEE include speed and safety. TEE is also able to quickly evaluate for
aortic insufficiency and pericardial effusions and evaluate myocardial function. Drawbacks
to TEE include the need for an experienced operator and the inability to evaluate
the descending aorta in its entirety or the side branch arteries.
ED Management
• The anatomic location of a dissection is the major determinant for therapy. Two classification
schemes are widely used to describe dissections, the Stanford and DeBakey
classifications.
• The Stanford classification labels dissection as type A if the ascending aorta is involved
and type B if there is no ascending aorta involvement.
• The DeBakey classification describes dissections as Type I involving both the ascending
and descending aorta, Type II if the dissection involving the ascending
aorta only, and Type III involving the descending aorta only.
• The treatment of an aortic dissection begins with control of hypertension. These patients
can be very sensitive to blood pressure manipulation. Short acting, titratable
medications are therefore appropriate in this setting. ² blockade (esmolol, labetolol,
or propranolol are appropriate) is used to decrease the sheer stress placed on the aorta
by the systolic pulse. Nitroprusside is used in conjunction with ² blockade to control
hypertension. The goal of blood pressure control is to lower the blood pressure to the
lowest level which still allows organ perfusion.
• Definitive treatment is based on anatomy.
• Dissections involving the ascending aorta are treated surgically with replacement of
the involved segment. Concurrent aortic insufficiency or coronary insufficiency
can be corrected surgically during the procedure.
Cardiovascular Disorders 51
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• The treatment of isolated dissections of the descending aorta is intensive blood
pressure control alone. Indications for surgical management include uncontrollable
hypertension, rupture, or involvement of a major aortic branch with subsequent
end-organ ischemia.
Aortic Aneurysm
Epidemiology/Pathophysiology
• Aneurysms are defined as dilatation of an aortic segment >3 cm.
• They are true aneurysms, indicating a dilatation of all three layers of the aortic wall.
• Men older than 70, smoking, hypertension, and a family history of aneurysms are
predisposing factors.
• Most aortic aneurysms are diagnosed in the seventh decade of life.
• Abdominal aortic aneurysms (AAA) are most commonly located in an infrarenal location,
but may occur at any level of the aorta.
• Aneurysms enlarge at a rate of 0.5 cm per year on average, with larger aneurysms
enlarging at a faster rate.
• The risk of aneurysm rupture is largely based on size. While small aneurysms may
rupture, the risk of rupture increases dramatically as aneurysms enlarge to >5cm.
• The mortality rate of ruptured aortic aneurysms is approximately 90% with over half
of patients dying before reaching the hospital.
Diagnosis and Evaluation
History and Physical Examination
• The most important factor in diagnosing AAA is entertaining the diagnosis.
Middle-aged patients presenting with abdominal or flank pain should always have the
diagnosis entertained.
• Unruptured aneurysms are usually asymptomatic.
• Chronic abdominal pain, back pain, and ureteral colic-like symptoms are common
presentations of aneurysms.
• Physical exam findings may include palpation of a pulsatile abdominal mass, but this
finding is neither sensitive nor specific enough to rule in or out aneurysmal disease.
• A ruptured aneurysm classically presents with pain, hypotension and a pulsatile mass.
However, many patients present without these findings. The location and quality of
pain is variable, most commonly presenting as acute, severe abdominal, back, or flank
pain. Hypotension is a late and grave finding. Other presentations include syncope
and altered mental status.
Laboratory and Studies
• Lab work is not helpful except for a type and cross which is imperative in cases of
ruptured AAA.
• Imaging studies are indicated and the choice of study is largely dependent on the
clinical stability of the patient.
• Plain films of the abdomen can be helpful if positive but are not sensitive enough to
rule out aneurysms. Calcification of the aortic wall can be seen with obvious enlargement
of the aorta. These studies are almost universally available and can be
done rapidly in the case of an unstable patient.
• Ultrasound is the test of choice to detect aneurysmal disease. It is very sensitive and
can evaluate the size of an aneurysm as well as identify intraperitoneal free fluid
indicative of rupture. Bedside ultrasound can be done rapidly, making it especially
useful for unstable patients. Drawbacks of ultrasound include operator-dependent
accuracy and difficulty in visualization of the aorta in patients with excess bowel gas
or obesity.
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• CT scanning is almost 100% sensitive for the detection of AAA. It has better sensitivity
than ultrasound for the detection and location of rupture and is better in
defining the surrounding anatomy. IV contrast is helpful, but not imperative for
the examination. The main disadvantage of CT scanning is the inability to monitor
critically ill patients during the exam.
ED Management
• Treatment of AAA depends on the stability of the patient. Asymptomatic aneurysms
discovered during physical exam or during evaluation for other problems may be referred
for further evaluation and treatment. Generally, aneurysms <5 cm. are observed
with repeat ultrasound evaluation and elective surgical management based on patients’
concurrent illnesses and the size of the aneurysm.
• Newer intravascular stent techniques are beginning to be used and are appropriate for
a select group of patients.
• Treatment of ruptured AAA includes rapid medical resuscitation with blood products
as needed.
• Definitive treatment is surgical and arrangements for surgery should be made as quickly
as possible.
• Complications of AAA repair include infection, thrombosis, erosion, and dilation of
the graft. These are often life-threatening.
• Infections may occur immediately postoperatively or from hematogenous spread of
other infections later in life. Staph species are generally responsible. Treatment includes
IV antibiotics and removal and repair of the infected graft.
• Thrombotic complications present in multiple ways with embolic phenomena or
ischemic symptoms. Evaluation includes visualization of the aorta and anticoagulation
and repair as necessary.
• Erosion of the graft may lead to rupture and/or fistula formation. Aorto-enteric
fistulae are caused by erosion into the GI tract. The duodenum is the most common
site of fistulae. Fistulae present with GI bleeding and can range from a slow,
chronic process, to an acute life-threatening hemorrhage. Many patients with
aorto-enteric fistulae also have septic complications necessitating antibiotics. Treatment
for fistulae is surgical.
Suggested Reading
1. Rebel R. Diseases of the thoracic aorta. Heart Aug 2001; 86(2).
2. Pretre R, Segesser L. Aortic dissection. Lancet 1997; 349:1461-64.
3. Dmowski A, Carey M. Aortic dissection. Am J Emerg Med 1999; 17(4).
4. Hals G, Pallaci M. The clinical challenges of abdominal aortic aneurysm: Rapid, systematic
detection and outcome-effective management. Emerg Med Reports 2000; 21(12).
5. Thompson MM, Bell PRF. Arterial aneurysms. Brit Medl J 2000; 320(7243).
6. Hallett J. Management of abdominal aortic aneurysms. Mayo Clin Proc 2000; 75(4).
7. Glover J. Thoracic and abdominal aortic aneurysms. In: Tintinalli JE, Kelen GT,
Stapczynski JS, eds. Emergency Medicine. A Comprehensive Medicine Study Guide.
McGraw-Hill, 2000.
8. Bourland M. Aortic Dissection. In: Marx JA, Hockberger RS, Walls RM, eds. Emergency
Medicine. Concepts and Clinical Practice. Mosby, 2002:2.
9. Bessen H. Abdominal Aortic Aneurysm. In: Marx JA, Hockberger RS, Walls RM, eds.
Emergency Medicine. Concepts and Clinical Practice. Mosby, 2002:2.
CHAPTER 1
CHAPTER 3
Emergency Medicine, edited by Sean Henderson. ©2006 Landes Bioscience.
Pulmonary Emergencies
Deborah B. Diercks, Steven Offerman, Mark Thoma and Peter E. Sokolove
Basic Anatomy and Physiology
• The trachea, bronchi, and bronchioles are the conducting airways and consist of a
series of branching tubes that become narrower and shorter as they penetrate into the
lungs. These airway structures have no diffusion capacity and represent about 150 ml
of lung volume. Eventually the terminal bronchioles lead to the alveoli that form the
actual gas-exchange interface. The alveolar surface consists of approximately 3000 ml
of lung volume.
• The walls of the conducting airways contain smooth muscles which, when contracted,
cause airway narrowing and increased resistance to airflow. These smooth muscles
respond to both sympathetic and vagal input. Beta2-receptor stimulation causes muscle
relaxation, while ±-receptor and vagal stimulation result in bronchoconstriction. Constriction
is also reflexive and may be initiated by irritants, temperature, and psychogenic
causes.
• Contraction of the diaphragm and intercostal muscles increases the volume of the
thoracic cavity creating a negative intrathoracic pressure. This bellows action draws air
into the airways and alveoli by bulk flow. Expiration is a passive process that occurs as
the elastic lung tissue returns to its preinspiratory volume.
Part A: Acute Respiratory Failure (ARF)
• Definition: ARF is an impairment of oxygen (O2) or carbon dioxide (CO2) gas exchange
that results in immediate or impending breakdown of cell metabolism. There
are two fundamental mechanisms (see Table 3A.1):
• Failure to oxygenate: Room air PaO2 <60 mm Hg.
• Failure to ventilate: PaCO2 >50 mm Hg.
• An increased work of breathing may signal impending ventilatory failure prior to the
development of hypercarbia or hypoxia.
• Patients who chronically retain CO2 have baseline elevation of their PaCO2 but usually
have a normal pH via metabolic compensation. In these patients, ventilatory failure is
identified by an increase in PaCO2 above baseline and a corresponding decrease in pH.
Diagnosis
• Dyspnea is the most common symptom and is almost universal in awake patients.
• Crucial aspects of the physical evaluation include general appearance, vital signs, and
pulmonary examination.
• General appearance
• Signs of increased work of breathing include diaphoresis, tripod positioning,
intercostal muscle retractions, nasal flaring, and audible grunting. Patients may
be unable to speak full sentences. Significant increases in work of breathing indicate
acute or impending respiratory failure. Agonal respirations are slow, shallow
breaths that identify impending respiratory arrest.
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• Altered mental status (AMS) is an important indicator of ARF. Confusion, somnolence
and agitation may occur secondary to hypoxia and/or hypercarbia. The
presence of decreased mentation in patients with respiratory distress indicates
the need for immediate intervention.
• Vital signs
• Respiratory rate (RR) is typically abnormal and may be elevated or depressed.
Tachypnea occurs secondary to stimulation of central respiratory centers in
patients with hypoxia or hypercarbia. Hypopnea results from drug ingestion,
stroke, seizures, hypothyroidism, and other causes of impaired brainstem
function.
• Patients with ARF usually have tachycardia as a result of underlying hypoxia and/
or an adrenergic response. However, severe hypoxia may also cause bradycardia.
• Pulse oximetry: all patients with oxygen saturation <90% should be considered
severely hypoxic (see following section for full discussion).
• Pulmonary examination
• Stridor is associated with upper airway obstruction (larynx or trachea) and is
audible without a stethoscope. Inspiratory stridor is classically seen with supraglottic
obstruction and expiratory stridor with subglottic pathology.
• Wheezes are associated with lower airway obstruction. Bronchspasm is the most
common cause but other etiologies include foreign body and pulmonary edema.
Some patients with bronchospasm or airway obstruction may have little or no
wheezing if airflow is severely reduced.
• Rhonchi occur with airflow through areas narrowed by inflammation, smooth
muscle contraction, or mucous.
• Rales are suggestive of alveolar inflammation or fluid.
• Decreased or absent breath sounds may signify nonventilated lung segments,
pleural effusion or pneumothorax.
• Pulse Oximetry (Pox) provides rapid, noninvasive measurement of oxygenation and
correlates well with measured PaO2. A Pox reading of 90% corresponds to a PaO2 of
approximately 60 mm Hg. Carbon monoxide (CO) poisoning may result in falsely
elevated readings. Dark nail polish, peripheral vascular disease, hypoperfusion, and
anemia may cause falsely depressed readings. Note that a normal Pox does not rule out
the presence of hypercapnia.
