• Order a 1 2-lead electrocardiogram on stable patients

and address potentia l etiologies, including acute

coronary syndrome, electrolyte abnormal ities, toxic

ingestions, and medication side effects.

The normal electrocardiogram (ECG) waveform contains a P wave, QRS complex, and T wave. The P wave represents atrial depolarization. It is immediately followed by

the PR interval, which normally lasts between 1 20 and 200

msec in duration. The QRS complex represents ventricular

depolarization and is normally <100 msec in duration.

Delays in intraventricular conduction result in a widened

(> 100 msec) QRS complex. The ST segment represents the

plateau of ventricular depolarization and is normally iso ­

electric in appearance. Finally, the T wave represents ven ­

tricular repolarization. Of note, the segment extending from

the end of a T wave to the beginning of the next P wave,

known as the TP segment, should be used as the isoelectric

baseline when performing any type of ECG analysis.

Bradydysrhythrnias occur either because of depressed

sinus node activity or inhibited electrical signal conduction.

These are common in patients with structural heart damage,

excessive vagal tone, taking certain cardioactive medications,

or with specific electrolyte abnormalities (eg, hyperkalemia).

Tachydysrhythmias occur because of enhanced automaticity

from either the SA node or an ectopic focus and can originate

from both atrial and ventricular sources. Supraventricular

tachycardia (SVT) occurs when re-entry loops are present in

the AV node or accessory conduction pathways.

Rhythms with a wide QRS complex represent ventric ­

ular depolarization that occurs outside of the normal

CHAPTER 16

Table 1 6-1. PIRATES: Causes of atrial fibri l lation.

P PE, pneumonia, pericarditis

Ischemia (coronary artery disease and myocardial infarction)

R Rheumatic heart disease, respiratory failure

A Alcohol ("hol iday heart")

T Thyrotoxicosis

Endocrine (Ca), enlarged atria (mitral valve disease,

cardiomyopathy)

s Sepsis, stress (fever)

conduction system, whereas those with normal QRS durations originate from a focus either superior to or within

the AV node that then travel through standard conduction

pathways.

Cardiac dysrhythmias vary by etiology, severity, and

treatment. Atrial fibrillation (AF), for example, is common and has multiple causes (Table 1 6-1). Although

occasionally symptomatic and/or requiring emergent

intervention, many patients are typically unaware when

they are in AF. Asymptomatic bradycardia is also a very

common rhythm, especially in young, athletic patients. It

can be a normal fmding in some people or result from

medication use at therapeutic levels. Other bradydysrhythmias, such as third-degree heart block, always elicit

emergent concern. Tachydysrhythmias vary in a similar

manner, from an isolated asymptomatic atrial tachycardia

to an emergently life-threatening ventricular fibrillation,

the initial dysrhythmia for the majority of patients in

cardiac arrest.

 

Cydulka RK, Meckler GD. Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawHill, 20 1 1, pp. 405-414.

Silvers SM, Howell JM, Kosowsky JM, et al. Clinical policy:

Critical issues in the evaluation and management of adult

patients presenting to the emergency department with acute

heart failure syndromes. Ann Emerg Med. 2007;49:627.

Dysrhythmias

Marianne Haughey, MD

Key Points

• Qu ickly address airway, breath ing, and circu lation

(the ABCs), provide supplemental 02, secure intravenous access, and in itiate continuous cardiac monitoring.

• Rapidly disti nguish between stable versus unstable

presentations, as unstable patients requ ire immediate

intervention.

INTRODUCTION

The recognition of dysrhythmia is an essential skill for all

emergency physicians, as patients presenting with dysrhythmias are relatively common and have the potential

for rapid hemodynamic deterioration. Clinically, dysrhythmias are classified as stable or unstable based on the

presence or absence of adequate end-organ perfusion

(ie, systemic hypotension, cardiac ischemia, pulmonary

edema, or mental status changes). Dysrhythrnias are fur ­

ther divided by their rate into either bradydysrhythrnias

(heart rate [HR] <60) or tachydysrhythmias (HR >100).

An additional subset of dysrhythmia, atrioventricular

blocks, can present with any HR and represent a malfunction in electrical conduction between the sinoatrial (SA)

node, atrioventricular (AV) node, and bilateral ventricles.

A thorough understanding of the origins of normal cardiac rhythm and electrical conduction is essential to properly comprehend cardiac dysrhythmia. Normal cardiac

conduction originates in the SA node and conducts through

the atria to the AV node. In the majority of patients, the AV

node is the only site where electrical signals can transmit

between the atria and ventricles and therefore functions as

the ultimate "gatekeeper" to the ventricles. Impulses then

travel sequentially from the AV node to the bundle of His,

the right and left bundle branches, the Purkinje fibers, and

ultimately the ventricular myocardium.

63

 

.A Figure 1 5-2. A. Bilateral infiltrates, cardiomegaly and cephalization can be seen in this patient with pulmonary

edema. B. Kerley B Lines in patient with pulmonary edema (white arrowheads). (B: Reprinted with permission

from Schwa rtz DT. Chapter 1 -7. Congestive Heart Failure-Interstitial Lung Markings. In: Schwartz DT, ed. Emergency

Radiology: Case Studies. New York: McGraw-Hill, 2008.)

pneumothorax, or malignancy. Importantly, a normal

CXR does not exclude CHF, as radiographic findings can

lag the onset of clinical symptoms by up to 6 hours.

Echocardiography is often performed on an inpatient

basis to assess ventricular size and function and rule out

underlying valvular disease. Emergency practitioners

skilled in ultrasonography may use bedside e chocardiography to assess global cardiac function in the critically ill or

clinically indeterminate cases.

MEDICAL DECISION MAKING

Rapidly address any signs of respiratory distress. Mildly symp ­

tomatic patients require supplemental oxygen, whereas

patients in moderate to severe respiratory distress often

require some form of ventilatory assistance. After respiratory

stabilization, address the patient's hemodynamic status. A

hypotensive patient with signs of shock requires vasopressor/

inotropic support, whereas a hypertensive patient will benefit

from vasodilator and diuretic therapy. The differential diag ­

nosis of CHF is broad and includes many of its precipitants

such as ACS, cardiac dysrhythmias, pulmonary embolus, and

valvular disease. Bronchospastic disease and chronic pulmonary conditions (eg, COPD) may be difficult to distinguish

from acute CHF. A good history combined with ancillary

studies, including a BNP or CXR, may help with diagnosis

(Figure 15-3).

TREATMENT

The goals of treatment include symptom management,

hemodynamic stabilization, and reversal of precipitating

factors. Place all dyspneic and hypoxic patients on

supplemental oxygen via a nonrebreather mask and rap ­

idly escalate to noninvasive positive pressure ventilation

(NIPPV) (eg, bilevel positive airway pressure) in patients

who fail to respond. When initiated early, NIPPV will

reduce the need for endotracheal tube placement and

mechanical ventilation in patients with decompensated

CHF. The higher intrathoracic pressure improves oxygen ­

ation by recruiting additional alveoli and decreasing cardiac preload, thereby curtailing further pulmonary edema.

Contraindications to NIPPV include patients who are at

risk for aspiration, unable or too confused to cooperate, or

those with significant facial trauma. Endotracheally intubate and initiate mechanical ventilation in patients who do

not qualify for or fail NIPPV.

Patients with hypotension and/or signs of systemic

hypoperfusion are by definition in cardiogenic shock and

require immediate hemodynamic support. Initiate a dobutamine infusion for inotropic (cardiac pump) support, but

beware of worsening hypotension because of its vasodilatory properties. Most patients will require concurrent

dopamine or norepinephrine infusions to maintain an

adequate blood pressure. Aggressively seek the precipitating factor, keeping in mind that acute myocardial infarction

is the most likely culprit. Obtain early cardiology consultation to facilitate emergent bedside echocardiography and

admission to an intensive care unit/critical care unit setting

for further management.

The majority of patients in acute CHF present with

marked hypertension. In these patients, vasodilators are

the initial therapy of choice. Nitroglycerin is the preferred

agent as it rapidly decreases the ventricular preload and at

higher doses reduces the cardiac afterload, thereby improving overall cardiac output. Start with sublingual doses of

CHAPTER 15

Decompensated CHF (dyspnea,

orthopnea/PND, LE edema,

inspiratory crackles)

Preload reduction

• Nitroglycerin

• Nitroprusside

· Morphine

loop diuretics

Figure 1 5-3. CHF diagnostic a lgorithm. BiPAP, bilevel positive airway pressure; BP, blood pressure; CHF, congestive

hea rt failure; CXR, chest x-ray; 

 

ECG, electrocardiogram; LE, lower extremity; ICU, intensive care un it; IV, intravenous;

PND, paroxysmal nocturnal dyspnea.

0.4 mg every 5 minutes. Severe exacerbations warrant IV

nitroglycerin infusions. Start at a rate between 20 and 50

meg/min and rapidly increase in increments of 20-40

meg/min every 5-10 minutes. Titrate the infusion to

symptomatic relief or systemic hypotension. Consider

nitroprusside in patients who don't adequately respond, as

it is a more potent arterial vasodilator. It is important to

ask any patient requiring vasodilator therapy about the

current use of phosphodiesterase-S inhibitors (eg,

sildenafil, used in erectile dysfunction and pulmonary

hypertension), as the combination of agents may lead to

life-threatening drops in systemic blood pressure. Avoid

overaggressive vasodilation in patients with r ight ventricular infarction, aortic stenosis, and hypertrophic cardiomy ­

opathy, as all are preload dependent conditions.

Initiate IV loop diuretics (eg, furosemide) in all

patients with signs of volume overload. Furosemide is

not only a potent diuretic but also an effective venodilator, often producing symptomatic improvement long

before the onset of diuresis. Start the dosing at 40 mg IV

in patients naive to the drug, whereas those who take the

agent chronically should have their home dose doubled.

Evaluate patients who fail to diurese within 30 minutes

for any evidence of urinary obstruction and re-dose as

necessary. Bumetanide, torsemide, and ethacrynic acid

are alternative loop diuretics, with ethacrynic acid being

the agent of choice in patients with a history of severe

sulfa allergy.

A summary of medications used to treat acute CHF

exacerbations is listed in Table 15-1.

CONGESTIVE HEART FAILURE

Table 1 5-1. Med ications used in CHF.

Dosing Titration

Vasodilators

Nitroglycerin 0.4 mg SL Repeat q 3-5 min to

sublingual symptoms

Nitroglycerin IV 25-50 meg/min Titrate by 1 0-20 meg/min

q 3-5 min to symptoms.

Max: 400 meg/min

Nitroprusside IV 1 0-20 meg/min Titrate by 5-10 mcgjmin

q 5 min

Max: 400 meg/min

Loop Diuretiu

Furosemide 40-80 mg IV May re-dose at 30 min if no

diuresis, then q 12 hour

dosing

Max: 200 mg/ dose

Bumetanide 1 mg IV May re-dose at 2 hours

Torsemide 10 mg IV May re-dose at 2 hours

Ethacrynic acid 50 mg IV May be re-dosed at 8 hours

lnotropesjPressors

Dobutamine 2-5 meg/kg/min Titrate to effect,

Max: 20 meg/kg/min

Dopamine 3-5 meg/kg/min Titrate to effect,

Max: 20 meg/kg/min

Norepinephrine 2-5 meg/min Titrate to effect,

Max: 30 meg/min

Mechanism of

Action

Preload reduction

Preload reduction;

some afterload

reduction at

higher doses

Marked afterload

 

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 20 11, pp. 361-367.

Hollander J, Dierks D. Acute coronary syndromes: Acute myocardial infarction. In: Tintinalli JE, Stapczynski JS, Ma OJ,

Cline DM, Cydulka RK, Meckler GD. Tintinalli's Emergency

Medicine: A Comprehensive Study Guide. 7th ed. New York,

NY: McGraw-Hill, 20 1 1, pp. 367-385.

Congestive Heart Fail u re

Ta rlan Hedayati, MD

Negean Afifi, DO

Key Points

• A normal ejection fraction does not exclude congestive

heart failure (CHF), as CHF can occur secondary to either

systolic or diastolic dysfunction.

• Nitroglycerin is the initial treatment of choice because

it reduces both preload and afterload and rapidly

improves patient symptoms.

INTRODUCTION

Congestive heart failure ( CHF) is the leading cause of hospitalizations in the United States in patients older than 65 years.

Once symptomatic, up to 35% of patients will die within

2 years of the diagnosis, and more than 60% will succumb

within 6 years. The annual costs of treatment are more than

$27 billion and will only increase given the aging population.

Heart failure occurs when the myocardium is unable to

provide sufficient cardiac output to meet the metabolic

demands of the body. As the myocardium can no longer

keep up with the return of venous blood, pulmonary and

systemic vascular congestion occurs. Common causes of

CHF include myocardial infarction, valvulopathies, cardio ­

myopathies, and chronic uncontrolled hypertension.

Based on the underlying pathophysiology, heart failure

can be divided into systolic and diastolic s ubtypes. Systolic

heart failure develops when a direct myocardial injury

impairs normal cardiac contractility causing a secondary

decline in ejection fraction (eg, myocardial infarction).

Diastolic heart failure develops when impaired cardiac

compliance limits ventricular filling (preload) causing a

consequent drop in overall cardiac output ( eg, left ventricular hypertrophy).

In acute decompensated CHF, the global decrease in

cardiac output forces a compensatory increase in systemic

57

• Consider acute coronary syndrome as the primary

precipitant of CHF.

• CHF associated with cardiogenic shock maintains a

very high mortality rate despite appropriate medical

management.

vascular resistance (SVR) to maintain vital organ perfusion. This increase in SVR is actually counterproductive

and causes a further reduction in cardiac output as the

already compromised myocardium now faces an ever

higher afterload. The downward spiral continues as myo ­

cardial oxygen demand increases because of the increased

ventricular workload, resulting in further compromise of

the myocardium. Consequent elevations in left atrial and

ventricular pressures eventually beget pulmonary edema

and respiratory distress.

 

use only for patients with ACS undergoing PCI.

� Anticoagulation

Administer either unfractionated heparin (UFH) or lowmolecular-weight heparin (LMWH) in all patients with

ACS and no known contraindications. LMWH ( enoxaparin)

is generally preferred given its more predictable weightbased onset of activity, reduced tendency for immunemediated thrombocytopenia, and lack of requirement for

laboratory monitoring. That said, the longer half-life and

lack of easy reversibility of LMWH is problematic in

patients for whom invasive interventions are planned.

UFH is typically recommended for patients undergoing

PCI, whereas LMWH is preferred for patients with UA/

NSTEMI who are not undergoing emergent reperfusion.

Fondaparinux and bivalirudin (a direct thrombin

inhibitor) are two of the newer anticoagulant agents a vailable for the management of patients with ACS and will

likely have an expanding role in the near future. Both have

been shown to be equally effective with fewer bleeding

complications as compared with standard treatment with

UFH or LMWH in select patient populations.

� Beta-Blockers

Beta-blockers exhibit antiarrhythmic, anti-ischemic, and

antihypertensive properties. They reduce myocardial 0 2

demand via decreasing the heart rate, cardiac afterload,

and ventricular contractility. Current guidelines recommend the initiation of treatment in all ACS patients with

no contraindications (decompensated CHF, hypotension,

heart blocks, and reactive airway disease). Metoprolol can

be given in 5-mg N doses every 5 minutes for a total of

3 doses or as a single 50-mg oral dose if N treatment is not

required.

� Reperfusion Therapy

Patients with STEM! require immediate reperfusion

therapy with either PCI or thrombolysis. The American

College of Cardiology guidelines recommend a duration

of no more than 90 minutes between patient presentation and balloon inflation in those undergoing PCI and a

duration of no more than 30 minutes between presentation and treatment in those undergoing thrombolysis.

PCI is the preferred modality owing to a decreased risk of

bleeding complications, lower incidence of recurrent

ischemia and infarction, and improved rates of survivability. For patients with UA or NSTEMI, an early invasive approach (within 24-48 hours) utilizing PCI reduces

the risk of death, AMI, and recurrent ACS. Thrombolysis

is not recommended for patients with either UA or

NSTEMI.

DISPOSITION

� Admission

Admit all patients with suspected ACS to a monitored bed

for serial ECG testing and cardiac marker analysis. Highrisk patients including those with elevated cardiac markers,

ischemic ECG changes, and refractive symptoms warrant

admission to a critical care setting for early PCI. STEM!

patients require admission to a critical care setting after

appropriate reperfusion therapy (PCI or thrombolysis).

� Discharge

Patients at a very low risk for ACS (young healthy patient,

atypical history, normal ECG, and negative serial cardiac

markers) who remain symptom free during an emergency

department observation period of several hours can be

safely discharged home with early stress testing arranged in

the outpatient setting.

CHAPTER 14

SUGGESTED READING

Green G, Hill P. Chest pain: Cardiac or not. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

 

ST-segment elevation myocardial infa rctions

(STEM I).

• Patients with STEMI req uire immediate reperfusion

therapy with either thrombolytics or percutaneous

coronary intervention to salvage the maximum amount

of viable myocardium.

arteries of adolescent patients and progresses by early

adulthood to the formation of organized fibro-fatty

plaques. As plaques enlarge throughout adulthood, they

progressively limit coronary blood flow and may eventually induce the development of anginal symptoms with

exertion. In time, plaques can rupture, causing secondary

intraluminal thrombus formation and a sudden reduction

in coronary perfusion (ie, AMI).

UA is a clinical diagnosis that has no pathognomonic

ECG findings or confirmatory elevations in cardiac bio ­

markers. Patients with classic anginal symptoms that are

either new, accelerating in frequency or severity, or that

occur without exertion are considered to have UA. UA and

NSTEMI are very similar from a pathophysiologic standpoint with the latter being distinguished by the presence of

elevated cardiac biomarkers. Both conditions arise from

the non-complete occlusion of coronary blood flow with

the secondary development of ischemia and infarction,

respectively. Complete occlusions of the coronary arteries

typically result in transmural infarctions of the myocardium with associated ST segment elevation (STEM!) on

the ECG and increased biomarker levels. Of note, the mor ­

tality rates of patients with NSTEMI and STEM! are iden ­

tical at the 6-month follow-up point.

ACUTE CORONARY SYN DROMES

It is very important to understand the basic anatomy of

the coronary arteries to identify concerning ECG patterns

and predict clinical complications. The left coronary artery

(ie, left mainstem artery) arises from the aortic root and

branches almost immediately into the left anterior

descending artery (LAD) and left circumflex artery (LCX).

The LAD runs down the anterior aspect of the heart and

provides the main blood supply to the anterior left ventride and ventricular septum, whereas the LCX runs in the

atrioventricular (AV) sulcus between the left atrium and

left ventricle and provides blood to the lateral and posterior regions of the heart. The right coronary artery (RCA)

also arises directly from the aortic root. It runs in the AV

sulcus between the right atrium and right ventricle and

provides blood to the right side of the heart and inferior

portion of the left ventricle. The sinoatrial node is perfused

by the RCA, whereas the AV node is perfused by a combination of the RCA and LAD in most patients.

Risk factors predictive of underlying coronary artery disease (CAD) have been identified and include age >40 years,

 

Injury to myocardial tissue results in the release of unique

cardiac enzymes into the vascular space, which can be

readily measured via serum analysis. Keep in mind that

patients with ECG findings consistent with STEMI do not

require confirmatory testing with serum markers but

rather warrant immediate reperfusion therapy. That said,

serum markers are very useful in patients with nondiag ­

nostic ECGs to diagnose the presence of a NSTEMl. Of

note, there is no single cardiac marker analysis that has

sufficient accuracy to reliably identify or exclude AMI

within the first 6 hours of symptoms onset. Furthermore,

elevations can and do occur secondary to non-ACS-related

conditions, including myocarditis, decompensated CHF,

and acute pulmonary embolism.

The usual laboratory studies used for the diagnosis of

AMI are the troponins (both T and I subtypes). Troponin

(Tn) levels are the most specific marker for myocardial

necrosis and have become the gold standard for diagnosis.

Elevated levels can be detected within 3 hours of injury,

peak at 12 hours, and remain elevated for a period of 3-10

days. The degree of myocardial damage and mortality is

correlated with the degree of troponin elevation.

Creatinine kinase is found in all forms of muscle tissue,

but the MB subunit is far more specific for myocardial

injury. CK-MB elevations can usually be detected within

4-6 hours after symptom onset, peak at 24 hours, and

typically return to normal within 2-3 days. Myoglobin

assays are also in common use for the evaluation of AMI.

Although attractive in theory as significant elevations

can be detected within 1-2 hours of symptom onset, a

poor specificity limits the clinical utility of serum myoglo ­

bin analysis.

..... Imaging

Obtain an emergent chest x-ray in all patients who present with a chief complaint of chest pain or shortness of

breath. That said, there are no radiographic findings

specific for the diagnosis of ACS, and its role in this setting is primarily for excluding alternative diagnoses.

Acute CHF secondary to ACS may present with classic

radiographic fmdings.

MEDICAL DECISION MAKING

Order an ECG immediately on presentation to identify

patients with STEMI, as they require immediate and

aggressive reperfusion. Patients with cardiogenic shock,

acutely decompensated CHF, ventricular dysrhythmias,

and severe symptoms refractive to aggressive medical

therapy also typically warrant emergent percutaneous

coronary intervention (PCI). In patients with nondiagnostic ECGs, proceed with cardiac marker testing. Patients

with elevated cardiac markers should be treated as having

a NSTEMI. Those whose initial set of cardiac markers are

negative require serial ECG and biomarker testing. These

patients should be stratified to identify those who are at

high risk for adverse cardiovascular outcomes. Concerning

 

factors that may identify high-risk patients include

patients �65 years of age, the presence of at least 3 risk

factors for CAD, known prior coronary stenosis of �50%,

ST-segment deviations on ECG, elevated cardiac markers,

the use of aspirin within the prior 7 days, and at least 2

anginal episodes within the past 24 hours. Further treatment should be dictated by the patient's category of risk

(Figure 14-3).

TREATMENT

The proper management of ACS demands rapid and

aggressive care. These patients require treatment in an

area with ready access to resuscitation equipment including advanced airways and defibrillators. Address the

patient's airway and circulatory status and place the

patient on the cardiac monitor. Obtain N access and

administer supplemental oxygen to maintain an SpO 2

�94%. The immediate goals of therapy are to limit the

supply-demand mismatch by improving coronary perfusion while reducing myocardial oxygen demand. Further

treatment is dictated by condition into either STEMI or

UA/NSTEMI pathways.

..... Nitroglycerin

Nitroglycerin is widely used in patients with ACS and

provides benefit via several different actions. It decreases

myocardial oxygen demand by reducing the ventricular

preload, improves myocardial perfusion by dilating the

coronary vascular bed, and exhibits some mild antiplatelet properties. Start with sublingual doses of 0.4 mg in a

disintegrating tablet or spray. This can be repeated every

3-5 minutes as necessary for refractive pain provided that

the patient maintains a systolic blood pressure > 100 mmHg.

Chest pain that persists after 3-5 doses warrants the

initiation of IV therapy. Start an infusion at 1 0-20 meg/

min and rapidly titrate upward in 1 0-20 meg/min increments to achieve adequate pain control. Immediately stop

CHAPTER 14

Strong concern for myocardial

ischemia (new ST-segment

depressions or T-wave inversions)

UFH or LMWH, IV NTG,

IV 13-blocker + /­

clopidogrel load

• ST-segment depressions

• Elevated Tn

• Persistent chest pain

• Hemodynamic instability

• TIMI score �3*

No high-risk features

Admit to telemetry or

ccu bed for further

work-up

'' TIMI risk score for UA/NSTEMI equals the number of the following 7 risk factors that are present: Age

� 65, �3 CAD risk factors, known CAD, ASA use with in the past week, recent angina, elevated cardiac markers,

and ST-segment deviations � O.Smm. A score of 3 carries a 1 3% risk of an adverse cardiac event (AMI, death,

revascularization) within the next 14 days .

.&. Figure 1 4-3. ACS diagnostic algorithm. ACS, acute coronary syndrome; AMI, acute myocardial infarction;

ASA, aspirin; CAD, coronary artery disease; CCU, critical care unit; ECG, electrocard iogram; G PI, glycoprotein l ib/I l ia

inhi bitors; LBBB, left bundle branch block; LMWH, low-molecular-weight heparin; NTG, nitroglycerin; NSTEMI, nonST-segment elevation myoca rdial infa rction; PCI, percutaneous coronary intervention; STEM!, ST-segment elevation

myocardial infarction; TIMI, Thrombolysis In Myocard ial I nfarction; Tn, troponin; UA, unstable angi na; UFH,

 

male patients or postmenopausal females, hypertension,

dyslipidemia, diabetes mellitus, smoking, family history of

CAD, truncal obesity, and a sedentary lifestyle. It is important to remember that these risk factors are based on large

demographic analyses and cannot be used to predict the

presence or absence of CAD in a given patient. Approximately half of all patients presenting with ACS have no

identifiable risk factors outside of age and sex.

CLINICAL PRESENTATION

� History

A thorough history is the most sensitive tool for the detection of ACS, and an experienced clinician will always be

wary of its variable presentation. Chest pain is the most

common presenting complaint. Myocardial ischemia is

classically described as pressure-like or squeezing sensation

located in the retrosternal area or left side of the chest.

Inquire about the quality, duration, frequency, and in ten ­

sity of the pain. Determine whether there is radiation of

pain, associated symptoms, and provoking and palliating

factors. Symptoms commonly associated with myocardial

ischemia include nausea, diaphoresis, shortness of breath,

and palpitations. Anginal pain can radiate in almost any

direction depending on the individual patient and the

affected region of the heart, but radiation to the shoulder,

arm, neck, and jaw is most common. It should be noted

that the intensity of pain is not predictive of the overall

severity of the myocardial insult, and even minimal symptoms can correlate with significant mortality.

Up to a third of patients with ACS will present with

symptoms other than chest pain. Also known as "anginal

equivalents;' these presentations further complicate the

accurate diagnosis of ACS. Possible complaints include

dyspnea, vomiting, altered mental status, abdominal pain,

and syncope. Patients at an increased risk of atypical pre ­

sentations include the elderly, women, diabetics, polysubstance abusers, psychiatric patients, and nonwhite

minorities. These patients have a near 4-fold increase in

mortality owing to inherent delays in their diagnosis, treatment, and disposition. Always obtain a detailed social history and inquire about any recent and chronic substance

abuse. Habitual tobacco use has been proven to be an

independent risk factor for CAD, whereas cocaine use can

not only induce significant coronary spasm in the acute

setting, but also accelerate the atherosclerotic process when

chronically abused.

� Physical Examination

There are no physical findings specific for ACS, and the

exam is frequently normal. Obtain a complete set of vital

signs and closely monitor unstable patients. Bradycardia is

common with inferior wall ischemia owing to an increase

in vagal tone, whereas tachycardia may represent compensation for a reduction in stroke volume. Concurrent hypertension increases the myocardial 02 demand and may

exacerbate the underlying ischemia, whereas acute cardio ­

genic shock has an extremely poor prognosis.

Carefully auscultate the heart for any abnormal sounds.

Acute changes in ventricular compliance may result in an

S3, S4, or paradoxically split S2. The presence of a new

systolic murmur may signify either papillary muscle infarction with secondary mitral valve insufficiency or ventricu ­

lar septal infarction with secondary perforation. Look for

signs of acute congestive heart failure (CHF), including

jugular venous distension, hepatojugular reflux, and inspiratory crackles. Perform a rectal exam to look for evidence