Atlas of Procedures in Neonatology parte 02

 

Congestive Heart Failure

 

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.

Decompensated CHF is commonly precipitated by

acute coronary syndrome (ACS), rapid atrial fibrillation,

acute renal failure, or medication and dietary noncompliance. Other important precipitants to consider are pulmonary embolus, uncontrolled hypertension, profound

anemia, thyroid dysfunction, and states of increased meta ­

bolic demand such as infection. Cardiotoxic drugs including alcohol, cocaine, and some chemotherapeutic agents

should also be considered.

CLINICAL PRESENTATION

� History

Patients most commonly present with shortness of breath

with exertion or at rest with severe exacerbations.

CHAPTER 15

Orthopnea, or dyspnea while lying flat, is common as a

result of the redistribution of fluid from the lower

extremities to the central circulation when the legs are

elevated. The increase in central circulation produces a

higher pulmonary capillary wedge pressure and secondary

pulmonary edema. Attempt to quantify the severity of the

orthopnea by asking on how many pillows the patient

sleeps and note any changes from baseline. Paroxysmal

nocturnal dyspnea occurs when sleeping patients awake

suddenly with marked shortness of breath with the need to

sit up and hang the legs over the side of the bed o r g o to a

window for air. In certain patients, pulmonary congestion

presents rather occultly with a persistent mild nocturnal

cough as the only symptom.

Patients may complain of peripheral edema, but this is

neither sensitive nor specific for CHF and should prompt

an investigation for alternative etiologies. Right upper

quadrant pain may occur in patients with hepatic congestion and can be confused with biliary colic.

Always obtain a detailed review of systems to try to

identify any possible precipitants of CHF. Specifically, ask

patients about antecedent or ongoing chest pain, palpitations, recent illnesses or infections, and medication or

dietary changes or noncompliance.

� Physical Examination

Quickly evaluate patient stability with a careful assessment

of vital signs and a focused physical exam. Check the respiratory rate, obtain a pulse oximetry, look for accessory

muscle use, and determine whether the patient can speak

in complete sentences to assess the severity of respiratory

distress. Decreased stroke volume and impaired cardiac

output may manifest as tachycardia, a narrowed pulse

pressure, or marked peripheral vasoconstriction. Recognize

hypotension and/or signs of hypoperfusion immediately

and treat as cardiogenic shock.

After the initial assessment, focus on signs of total body

volume overload. Patients with left ventricular failure typically present with pulmonary signs, including inspiratory

crackles, a persistent cough, or a "cardiac wheeze." Patients

with right ventricular failure show signs of systemic congestion. Check for peripheral edema, j ugular venous distention, and hepatojugular reflux (an increase in jugular

venous pressure with deep palpation of the right upper

quadrant) (Figure 15-1). Auscultate the heart for murmurs

or gallops. Although often difficult to appreciate in the

emergency department (ED), an S3 gallop is highly specific

for decompensated heart failure.

DIAGNOSTIC STUDIES

� Laboratory

Obtain a complete blood count to look for signs of anemia

and a serum chemistry to evaluate renal function and rule

out any electrolyte abnormalities (eg, hyperkalemia) that

.A. Figure 1 5-1. Jugular venous d istention.

may lead to cardiac irritability and impaired function.

Order cardiac enzymes to rule out ACS as the precipitating

event, although patients in decompensated CHF may

exhibit mild elevations in the absence of ACS because of

the excessive strain placed on the myocardium. Regardless

of etiology, patients in CHF with elevated cardiac enzymes

have a worse prognosis. Check thyroid function tests if

either hypothyroidism or thyrotoxicosis is thought to be

the source of heart failure.

Brain natriuretic peptide (BNP) is released from the ventricular myocytes in the presence of ventricular wall disten ­

tion. Measurement of serum BNP is especially helpful in

diff erentiating CHF from underlying pulmonary conditions

such as chronic obstructive pulmonary disease (COPD) or

pneumonia. Levels <100 ng/dL have a high negative pre ­

dictive value, whereas those >400 ng/dL are consistent with

decompensated CHF. Levels between 100 and 400 ng!dL

are neither sensitive nor specific for CHF and may be

indicative of pulmonary embolism, cor pulmonale, cirrhosis, or renal failure. Remember that heart failure is a clinical

diagnosis, and BNP measurement is most helpful in clinically indeterminate cases.

� Electrocardiogram

Obtain an emergent electrocardiogram (ECG) on all

patients with suspected CHF to look for evidence of new or

old myocardial injury, as well any precipitating arrhythmias.

Signs of atrial or ventricular hypertrophy may also be seen.

� Imaging

Obtain a chest x-ray ( CXR) in all patients. Findings consistent with CHF include cardiomegaly, bilateral pleural e ffusions, perihilar congestion, Kerley B lines (transverse

radio-opaque lines seen at the lung periphery), and vascular cephalization (Figure 1 5-2). CXR may reveal alternative

sources for the patient's dyspnea, including pneumonia,

CONGESTIVE HEART FAILURE

A B

.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

reduction

Sodium and water

excretion + initial

venodi latory

effects

Onset: 1 5-30 min

Same

Onset 10 min

Same

Onset 10 min

Same

Onset 5 min

Primarily Beta 1,

some Beta 2 &

alpha

Low dose: dopamine

intermed: Beta 1 & 2

High dose: alpha

Alpha, Beta 1

Adverse Effects

Hypotension,

tachycardia,

headache

Hypotension,

tachycardia,

headache

Hypotension,

cyanide &

thiocyanate

toxicity

Electrolyte

abnormal ities

Sulfa allergy

Ototoxicity

Same

Same

Same

Vasodilator

potential may

decrease BP

variabil ity in

dose-related

effects

vasoconstriction

Notes

Assess BP between doses.

Should not be used longer than

24 hours as tachyphylaxis/

tolerance develops.

Risk of toxicity increases with

prolonged use and larger

doses. Rebound vasoconstriction may occur.

Patients on chronic home therapy

or with renal insufficiency will

require higher dosing.

May be used with furosemide

allergy

May be used with sulfa allergy

Primarily inotropic, limited by

vasodi lation

May be used with dobutamine as

second agent in cardiogenic

shock

May be used with dobutamine as

second agent in cardiogenic

shock

The outpatient management of CHF includes treatment with angiotensin-converting enzyme inhibitors and

beta-blockers, as both have been shown to reduce patient

mortality. Of note, both of these agents are contraindicated

in patients with acute decompensation. Oral furosemide is

typically used for symptomatic relief, but no mortality

benefits have ever been demonstrated.

cases require an inpatient work-up including echocardiography and medication titration. All admitted patients require

education regarding medication compliance, as more than half

will be readmitted for the same within the next 6 months.

..... Discharge

Asymptomatic patients with stable vital signs and a negative

ED work-up may be safely discharged provided the precipi ­

tant for their presentation has been identified and adequately

addressed. Counsel these patients on the disease process and

the importance of medication and dietary compliance.

Provide appropriate discharge instructions, including r eturn

precautions, and arrange close outpatient follow-up.

DISPOSITION

..... Admission

The vast majority of patients with acute CHF exacerbations

require admission to a monitored unit Previously undiagnosed

CHAPTER 15

SUGGESTED READING

Collins S, Storrow AB, Kirk JD, et al. Beyond pulmonary edema:

Diagnostic, risk stratification, and treatment challenges of

acute heart failure management in the emergency department. Ann Emerg Med. 2008;5 1 :45.

Heart Failure Society of America, Lindenfeld J, Albert NM, et al.

HFSA 2010 Comprehensive Heart Failure Practice Guideline.

J Card Fail. 20 10;16:el.

Peacock WF. Congestive heart failure and acute pulmonary

edema. 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: 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.

Acute Coronary Syndromes

Ch ristopher Ross, MD

Key Points

• Consider acute coronary syndrome (ACS) in the initial

assessment of all patients presenting with chest pa in

and/or d ifficu lty breathing.

• Atypical presentations are common, especially in

women, the elderly, and diabetics.

• Obta in an emergent el ectroca rdiogram in all

patients with concern for ACS to ra pidly identify

INTRODUCTION

Acute coronary syndrome (ACS) encompasses a spectrum

of disease that includes unstable angina (UA), nonST-segment elevation myocardial infarctions (NSTEMI),

and ST-segment elevation myocardial infarctions (STEM!).

The distinction between the 3 is based on historical factors,

electrocardiogram (ECG) analysis, and cardiac biomarker

measurements. ACS is the leading cause of mortality in the

industrialized world and accounts for more than 25o/o of all

deaths in the United States. More than 5 million patients

per year present to U.S. emergency departments with

symptoms concerning for ACS, although fewer than lOo/o

will be diagnosed with acute myocardial infarctions (AMI).

That said, between 2o/o and 4o/o of all patients with ACS are

initially misdiagnosed and improperly discharged from the

ED, resulting in significant morbidity and mortality and

accounting for the leading source of malpractice payouts

in the United States.

The pathophysiology of myocardial ischemia can be

broken down into a simple imbalance in the supply and

demand of coronary perfusion. Atherosclerosis is responsible for almost all cases of ACS. This insidious process

begins with the deposition of fatty streaks in the coronary

50

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,

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

of gastrointestinal bleeding, and document a thorough

neurologic exam in patients who may require treatment

with anticoagulant or thrombolytic medications.

DIAGNOSTIC STUDIES

� Electrocardiogram

Obtain a 1 2-lead ECG immediately on presentation for

patients with symptoms concerning for ACS. The emergent identification of a STEM! ensures that definitive

therapy can be arranged as quickly as possible to limit

further myocardial loss. The use of prehospital ECG analysis has further reduced any delays in appropriate therapy.

Keep in mind that a single ECG provides only an isolated

snapshot of myocardial electrical activity, and as s uch, any

changes in clinical status should prompt repeat testing. In

addition, fewer than half of all AMis are of the STEM!

variety, and ECG interpretation may be completely normal

in the setting of NSTEMI or UA. ST-segment elevations

suggest the presence of an acute transmural infarction,

whereas ST-segment depressions suggest active myocardial

ischemia. The morphology of the ST-segment elevations

CHAPTER 14

Table 1 4-1. Anatomical reg ions of the hea rt

by ECG ana lysis.

Anatomic occluded Ischemic Reciprocal

Location Artery Leads Leads

Anterior wall LAD V2, V3, V4 II, Ill, aVF

Lateral wall LCX I, aVL, VS, V6 V1, V2

Inferior wall RCA, LCX II, Ill, aVF variable

Posterior RCA, LCX VB, V9 V1, V2

Right ventricle RCA V1, V4R Variable

with AMI is typically straight or convex upward ("tomb ­

stone") in appearance, whereas c oncave ST-segment elevations generally indicate a more benign etiology (left

ventricular hypertrophy, benign early repolarization, pericarditis). Concerning ST-segment changes with ACS,

whether elevations or depressions, should be seen in a

distinct anatomical region with corresponding reciprocal

changes (Table 14-1). Additional findings concerning for

cardiac ischemia include inverted and hyperacute T-waves

(wide-based asymmetric high-amplitude T-waves) . Q

waves indicative of myocardial necrosis generally appear

late in the course of patients with ACS and cannot be relied

on in the acute decision-making process.

The ECG analysis for ACS should always occur in a standard fashion based on the anatomic distribution of the coronary arteries (Figures 14-1 and 14-2). Of particular interest,

inferior wall AMis generally represent occlusion of the RCA.

ST-segment elevation that is more pronounced in lead III

versus lead II is a subtle clue for involvement of the right

ventricle (RV). Obtain a right-sided ECG (lead V4r, analogous to lead V 4 but placed on the right side of the sternum)

in these patients to better evaluate the RV, and use nitroglycerin very carefully to avoid precipitating hemodynamic collapse. Furthermore, as the posterior descending arteries (PDA)

of most patients arise directly from the RCA, acute occlu ­

sion of the RCA should raise concern for a concurrent posterior wall infarction. Findings on the ECG suggestive of a

posterior wall infarction include an R-wave amplitude

> S-wave amplitude in leads V1 and V2 along with corresponding ST-segment depressions and tall upright T-waves

Figure 1 4-1. Anterior wall myocardial infarction. This patient had a 1 00% occlusion of the left anterior descending artery .

.AFigure 1 4-2. I nferior wa ll myocardial infarction. Note the ST segment elevations in leads I I, Ill, and aVF. Elevation

in lead Ill is more pronou nced than lead I I, suggesting right ventricular wa ll involvement.

ACUTE CORONARY SYN DROMES

in leads V1-V4. Obtain a posterior ECG (leads V8 and V9)

in these patients.

Observe patients closely for the development of any

form of irritability, dysrhythmia, conduction delay, or

heart block (See Chapter 15 for further details). Highdegree AV block (second or third degree) is present in 6%

of patients with AMI. The incidence is higher in patients

with inferior wall infarctions (lSo/o) owing to the secondary increase in vagal tone or ischemia of the AV node.

Anterior wall infarctions can also produce AV blocks as a

result of ischemia of either the bundle of His or bilateral

bundle branches, resulting in a wide QRS complex bradydysrhythmia. The presence of a new left bundle branch

block in the appropriate clinical context should be considered and treated analogous to a STEMI.

..... Laboratory

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,

unfractionated heparin.

the infusion and administer IV fluid boluses to any

patients with signs of secondary hypotension. Patients

with infarctions that involve the right ventricle are particularly prone to hypotension given their preload dependent condition.

� Morphine

Administer IV morphine to all patients with persistent pain

despite treatment with nitroglycerin. Morphine reduces

myocardial 02 demand by decreasing vascular tone (preload)

ACUTE CORONARY SYN DROMES

and limiting the catecholamine surge that typically accompanies ACS. Avoid the use of morphine in hypotensive

patients.

� Antiplatelet Therapy

Begin immediate treatment with aspirin (ASA) in all patients

with presentations concerning for ACS. Give 2:162 mg of a

non-enteric-coated version. The first dose should be

crushed or chewed to improve absorption and more

quickly reach therapeutic blood levels. Aspirin alone

reduces mortality by 23o/o in STEM! patients. Minor con ­

traindications (remote history of peptic ulcer disease,

vague allergy, etc) should not preclude its use.

Clopidogrel, prasugrel, and ticagrelor all function to

inhibit platelet activation via blockade of the adenosine

diphosphate (ADP) receptors and therefore work in harmony with aspirin therapy. Clopidogrel has been the most

extensively researched of the 3 and, therefore, is the most

commonly used. A loading dose of 600 mg is recommended

for patients with STEM! undergoing emergent PCI, whereas

a 300-mg load is recommended for patients undergoing

reperfusion with thrombolytics and those with UNNSTEMI.

No loading dose is recommended in patients older than

75 years because of a concern for increased bleeding complications. Both prasugrel and ticagrelor produce a more

intense platelet inhibition, but do so at the expense of an

increase in major bleeding complications. Although there is

a legitimate concern for excessive bleeding in patients given

AD P-receptor antagonists who subsequently undergo coronary artery bypass grafting (CABG), the definite benefit of

platelet inhibition in patients with ACS far outweighs the

potential concern for bleeding in the very low number of

patients who actually require emergent CABG.

Glycoprotein lib/Ilia inhibitors represent the third class

of antiplatelet medications and function by inhibiting platelet aggregation via blockade of the surface binding sites for

activated fibrin. There are currently 3 available agents in this

class (abciximab, eptifibatide, and tirofiban), and their use in

patients with ACS has been extensively researched. These

agents have been associated with an increase in major bleed ­

ing complications, and current guidelines recommend their

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.

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.