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.

Chest Pain

Jonathon D. Pa lmer, MD

Key Points

• Chest pain is a very common complaint in emergency

department patients.

• A rapid electrocardiogram and chest x-ray will help distinguish between multiple emergent causes of chest pain.

INTRODUCTION

Chest pain is one of the most common presenting complaints in the emergency department (ED). As several fatal

�

onditions present with chest pain, it is imperative to rapIdly and thoroughly evaluate these patients to distinguish

between emergent and nonemergent causes. Approach

chest pain with a broad differential diagnosis and utilize

your history, physical exam, and ancillary testing to narrow

down the etiology.

The pathophysiology of chest pain will vary tremendously depending on the specific etiology. Regardless of

the source, pain sensation ultimately occurs owing to

stimulation of either visceral or somatic nerve fibers.

Somatic nerve fibers innervate the skin and parietal pleura.

Patients will typically complain of a pain that is sharp in

nature and easily localized. Potential etiologies include

pulmonary embolism, pneumothorax, musculoskeletal

injury, herpes zoster infection, pneumonia, and pleurisy.

Conversely, visceral nerve pain is often vague in quality,

poorly localized, and will frequently radiate to nearby

structures. Patients may deny the actual sensation of "pain"

and rather describe their condition as a heaviness, pressure, or simple discomfort. Potential etiologies include

acute coronary syndrome (ACS), aortic dissection, gastro ­

esophageal reflux, and pericarditis.

46

• The exclusion of life-threatening sources of chest pain

should be the emergency physicia n's chief diagnostic

concern.

CLINICAL PRESENTATION

� History

A detailed history is essential when evaluating patients

with chest pain, as no single element in isolation is sensi ­

tive or specific enough to determine either the etiology or

the severity of the complaint. Ascertain the character of the

pain to help determine a somatic or visceral source. For

example, a sharp and stabbing pain is less likely in patients

with ACS, but rather common in patients with pulmonary

embolism. Identify the exact location of the pain and

whether there is any associated radiation. Prototypical

ischemic chest pain presents either just beneath the sternum or on the left side and radiates to either the left arm

or jaw, whereas a mid-thoracic "tearing type" pain radiating straight through to the back is classically associated

with aortic dissection. Determine the severity and duration

of the pain. A mild, sharp pain lasting only seconds in

duration is rarely associated with a serious pathology,

whereas pain lasting greater than 10 minutes may suggest a

more serious etiology. Recurrent pain that lasts for many

hours or days per episode is unlikely to be cardiac.

In patients with a known history of heart disease, ascertain whether or not their symptoms mirror prior presenta ­

tions. Patients with pain that is either similar to or more

severe than a previous myocardial infarction (MI) have a

markedly increased likelihood of ACS. Identify exacerbating or relieving factors, as this can quickly impact manage ­

ment. Patients with potential cardiac presentations

frequently complain of pain that is worse with exertion

and improved with rest. Pain that is worse with cough or

deep inspiration (pleuritic pain) is typically associated

with either pleurisy, a musculoskeletal etiology, or pulmo ­

nary embolism. Epigastric pain that is worse with meals

usually signifies a gastrointestinal etiology. Pain that is

aggravated by emotional stress may point to an underlying

psychiatric etiology. Finally, inquire about any associated

symptoms. For example, nausea and diaphoresis have been

associated with a higher likelihood for ACS.

Unfortunately, the long-term risk factors for underlying

heart disease (high cholesterol, smoking, hypertension, diabetes, family history) have not been shown to help in the

differentiation of acute chest pain patients in the ED. Nonetheless, this history should be taken. A history of an underlying hypercoagulable state ( eg, pregnancy, malignancy) should

alert you to a possible pulmonary embolism (PE), whereas a

history of an underlying connective tissue disorder ( eg,

Marfan syndrome) should prompt an evaluation for aortic

dissection. Ask about any illicit drug habits, as cocaine use

has been associated with accelerated atherosclerosis, acute

MI, and aortic dissection.

� Physical Examination

Note the general appearance of the patient. Those with

ACS or other serious etiologies may be clutching their

chest and frequently appear anxious, pale, and diaphoretic.

This "sick vs not sick" mentality will guide the rapidity of

your examination. As with all emergency patients, assess

the vital signs and ensure adequate airway, breathing, and

circulation (ABCs). Note abnormal vital signs to help

guide your differential diagnosis. A detailed examination

of the heart, lungs, abdomen, extremities, and neurologic

systems will ensure that no emergent causes of chest pain

are overlooked. Listed next are some emergent presenta ­

tions matched with potential physical exam findings.

ACS. Vital signs will vary widely depending on the re ­

gion of ischemia or infarction. For example, an inferior

wall MI may present with bradycardia and hypotension

owing to increased vagal tone. Murmurs and abnormal

heart sounds such as an S3 or S4 may be present. I nspiratory crackles on 1 ung exam are consistent with secondary

pulmonary edema.

Tension pneumothorax. Look for the classic signs of

decreased breath sounds, tracheal deviation, and res piratory distress. Consider spontaneous pneumothorax in

young, thin patients with an acute onset of chest pain

and shortness of breath.

Pericardia! tamponade. Although usually limited to

patients in extremis, patients may exhibit the classic

signs of Beck's triad (hypotension, diminished heart

CHEST PAIN

sounds, and jugular venous distension). Pulsus paradoxus > 10 mmHg has shown a high sensitivity but low

specificity for tamponade, as any condition causing increased intrathoracic pressure may demonstrate this.

Pulmonary embolism. Dyspnea is the most common

complaint of patients with PE. They may also describe a

pleuritic-type chest pain, especially those with segmental

PEs that cause secondary infarction of the parietal pleura.

Patients with significantly large (massive or submassive)

PE are generally ill-appearing and hemodynamically unstable owing to the sudden severe increase in pulmonary

vascular resistance. A detailed examination of the heart

and lungs may reveal rales, gallops, or a prominent P2.

Lower extremity exam may reveal unilateral swelling consistent with a deep venous thrombosis.

Aortic dissection. The pain is often most severe at onset

and typically extends above and below the diaphragm.

These patients are often hypertensive and may have a

pulse deficit in either the radial and/or femoral arteries.

A marked discrepancy in blood pressure compared between each arm (>20 mmHg) is highly suggestive.

DIAGNOSTIC STUDIES

Perform an electrocardiogram (ECG) within 10 minutes of

presentation for all patients who complain of chest pain or

have signs and symptoms concerning for ACS. Obtain cardiac

markers including a troponin assay ± CK-MB analysis in all

patients with suspected ACS. D-dimer can aid the evaluation

of low-risk patients in whom PE is a diagnostic possibility.

CXR should be ordered on most patients in the ED with

chest pain. Posteroanterior and lateral views are ideal, but a

portable anteroposterior view is sufficient for patients who

require continuous cardiac monitoring. Acute aortic dissection may present with a widened mediastinum or abnormal

aortic contour. Pneumothoraces and subcutaneous air are

readily identified. Pneumomediastinum ± a left-sided pleural

effusion (owing to the relative thinness of the left esophageal

wall) is seen with esophageal rupture (Boerhaave syndrome).

Newer generation CT angiography is the modality of

choice to diagnose pulmonary embolism and aortic dissection and may have an evolving role in the evaluation of

patients with potential coronary artery disease.

Transthoracic echo is often readily available and clinically useful to evaluate for possible pericardia! effusions

and tamponade physiology, ventricular hypokinesis in

patients with ACS, and right ventricular strain in patients

with massive PE. A bedside transesophageal echo is very

sensitive for diagnosing acute aortic dissection in patients

who are not candidates for CT angiography.

MEDICAL DECISION MAKING

A detailed history and physical exam in combination with

an ECG and/or chest radiograph may provide sufficient

evidence to exclude a myriad of emergent conditions.

CHAPTER 13

Patient presenting with

chest pain

Rapidly address ABC's, IV access,

supplemental 02 and cardiac mon itor

Immediate ECG and CXR

Absent breath

sounds with

shock

Pain radiates to

the back with wide

mediastinum on CXR

ECG with ischemia

or positive troponin

Pleuritic CP,

hypoxia, + CT

angiogram

History of vomiti ng,

mediastinal air on

CXR

Hypotension,

JVD, muffled

heart tones

.&. Figure 13-1. Chest pain diagnostic algorithm. BMP, basic metabolic panel; BP, blood pressure; CBC, complete blood

count; CP, chest pain; CT, computed tomography; CXR, chest x-ray; ECG, electrocardiogram; JVD, jugular venous distention.

When this is not adequate, a thoughtful use of laboratory

studies combined with the pretest probability of disease

will guide decision making (Figure 13-1).

TREATMENT

� Acute Coronary Syndrome

Provide supplemental 0 2, administer a loading dose aspirin

(162-365 mg), and begin sublingual nitroglycerin (0.4 mg

every 5 minutes) on all ACS patients without known contraindications (eg, allergy, hypotension). Further antithrombotic

(eg, clopidogrel) and anticoagulation (eg, low-molecularweight heparin) therapy will differ by institution and cardiologist. Of note, the preceding interventions are often only

temporizing measures, as early revascularization is definitive,

especially in those patients presenting with an ST -elevation MI.

� Aortic Dissection

Patients with an aortic dissection require an immediate

and aggressive reduction in both heart rate and blood pressure. The goal of treatment is to maintain a heart rate

<60 bpm and systolic blood pressure < 100 mmHg. There

are multiple medication options for this purpose, and

often concurrent infusions are required to meet the pre ­

ceding targets. When utilizing dual therapy, it is of utmost

importance to control the heart rate before dropping the

blood pressure to avoid a "reflex tachycardia" and conse ­

quent expansion of the underlying dissection.

� Pulmonary Embolism

Treatment will vary based on the hemodynamic impact of

the embolism. Anticoagulate stable patients with either

low-molecular-weight or unfractionated heparin. Hemo ­

dynamic instability may necessitate the use of thrombolytic

therapy.

..... Boerhaave Syndrome

Esophageal rupture is uncommon and classically presents

with the sudden onset of chest pain after vomiting. Initiate

broad-spectrum antibiotic coverage while arranging for

definitive surgical repair.

..... Pneumothorax

Place all patients with a pneumothorax on s upplemental 02

via a nonrebreather mask. Those with a tension pneumothorax require immediate needle decompression followed

by chest tube thoracostomy. Simple pneumothoraces can be

treated with tube thoracostomy or simple observation.

..... Pericardia! Tamponade

The recognition of tamponade is much easier in the age of

bedside ultrasonography. Perform immediate pericardio ­

centesis in unstable patients while arranging for an operative pericardia! window via cardiothoracic surgery.

DISPOSITION

...,_ Admission

Admit all patients with concerning presentations to a

monitored bed. The following chapters discuss the

CHEST PAIN

disposition of patients with specific conditions m

greater detail.

..... Discharge

Many patients with chest pain can be discharged with close

primary care follow-up and a list of strict indications for

reevaluation. Take care to exclude emergent causes and

discharge only those cases with a clear nonemergent etiology (eg, chest wall pain, zoster, dyspepsia). If clinical doubt

exists, it is certainly prudent to err on the side of caution

and admit for inpatient observation.

SUGGESTED READING

Anderson JL, Adams CD, Antman EM, et al. ACC/ AHA 2007

Guidelines for the management of patients with unstable

angina/non ST-elevation MI: A report of the ACC/AHA

task force of practice guidelines. Circulation. 2007;116:

el48.

Fesmire FM, Brown MD, Espinosa JA, et a!. Critical issues in the

evaluation and management of adult patients presenting to

the emergency department with suspected pulmonary embolism. Ann Emerg Med. 20 1 1;57:628-652.

Green GB, Hill PM. Chest pain: Cardiac or not. I n: 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. 36 1-367 .

Swap CJ, Nagumey JT. Value and limitations of chest pain his ­

tory in the evaluation of patients with acute coronary syn ­

dromes. JAMA. 2005;294:2623-2639. 

Shock

La u ren M. Smith, MD

Nihja 0. Gordon, MD

Key Points

• Do not wait for hypotension to diagnose shock.

• Early ide ntification and i n itiation of aggressive

therapy can significantly improve patient

survival.

INTRODUCTION

More than 1 million patients present to U.S. emergency

departments annually with shock, and despite continued

advances in critical care, mortality rates remain very high.

Shock occurs when the circulatory system is no longer able

to deliver enough 02 and vital nutrients to adequately meet

the metabolic demands of the patient. Although initially

reversible, prolonged hypoperfusion will eventually result

in cellular hypoxia and the derangement of critical bio ­

chemical processes. From a clinical standpoint, shock can

be divided into the following subtypes: hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic

shock results from an inadequate circulating blood volume

owing to either profound dehydration or significant hemorrhage. Traumatic hypovolemia is the most common type

of shock encountered in patients <40 years of age.

Cardiogenic shock occurs when the heart is unable to provide adequate forward blood flow secondary to impaired

pump function or significant dysrhythmia. Myocardial

infarction is the leading cause of cardiogenic shock and

typically occurs once -40% of the myocardium is dysfunctional. Obstructive shock results from an extracardiac

blockage of adequate venous return of blood to the heart

( eg, pericardia! tamponade, tension pneumothorax, and

massive pulmonary embolism [PE) ). Finally, distributive

shock occurs secondary to an uncontrolled loss of vascular

tone (eg, sepsis, anaphylaxis, neurogenic shock, and adrenal

42

• I n itiate early goa l-directed therapy in patients with

septic shock.

• Early revascu larization is key to improving outcome in

patients with cardiogenic shock.

crisis). Neurogenic shock most commonly occurs in

trauma patients with high cervical cord injuries and a

secondary loss of sympathetic tone and should always be

considered a diagnosis of exclusion. Classically these

patients will present with hypotension and a paradoxical

bradycardia. Suspect septic shock in elderly, irnmunocompromised, and debilitated patients who are toxic appearing

despite only vague symptoms. The prognosis for patients

with cardiogenic and septic shock remains grave, with

mortality rates between 30% and 90%.

The pathophysiology of shock can be divided into

3 basic categories: a systemic autonomic response, endorgan cellular hypoxia, and the secretion of proinflammatory mediators. The autonomic system initially responds

to widespread tissue hypoperfusion by globally increasing

the overall cardiac output. As tissue perfusion continues

to decline, the body shunts circulating blood away from

less vital structures including the skin, muscles, kidneys,

and splanchnic beds. Reflexively, the kidneys activate the

renin-angiotensin axis, prompting the release of various

vasoactive substances, with the net effect to preserve perfusion to the most critical organs, namely the brain and

the heart.

When the preceding response is inadequate despite

maximal tissue 02 extraction, cellular hypoxia forces a conversion from aerobic to anaerobic metabolism. By nature,

anaerobic metabolism cannot produce enough adenosine

triphosphate to maintain regular cellular function. Tissue

lactate accumulates, resulting in systemic acidosis, and

eventually this breakdown in cellular metabolism leads to

widespread tissue death. Injured and dying cells prompt

the production and secretion of harmful inflammatory

mediators, resulting in the development of the systemic

inflammatory response syndrome, defined by the presence

of fever, tachycardia, tachypnea, and leukocytosis.

CLINICAL PRESENTATION

� History

Vague complaints such as fatigue and malaise may be the

only presenting symptoms, especially in elderly patients.

Friends, family, and emergency medical service personnel

will be vital in obtaining a history in patients with altered

mental status. The past medical history including a list of

active medications might reveal risk factors such as immunosuppression, underlying cardiac disease, and potential

allergic reactions.

� Physical Examination

Although hypotension and tachycardia are the cardinal

features of shock, many patients will presents with normal

vital signs owing to physiologic compensation. Because of

the unmet metabolic demands of the central nervous sys ­

tern, altered mental status is not uncommon. Jugular

venous distention, cardiac murmurs, and pulmonary rales

often accompany cardiogenic shock. A careful skin examination can be invaluable, as patients in distributive shock

frequently exhibit warm hyperemic extremities, whereas

those in cardiogenic, hypovolemic, and obstructive shock

will present with cool mottled extremities secondary to

profound systemic vasoconstriction. Furthermore, abnormal findings such as diffuse urticaria, pronounced erythema, or widespread purpura may help identify the t ype

and source of shock. The abdominal exam should focus on

careful palpation and looking for signs of peritonitis or a

pulsatile mass. Measure urine output, as low volumes indicate an absolute or relative volume deficiency and may help

guide resuscitation.

DIAGNOSTIC STUDIES

� Laboratory

No single laboratory test is diagnostic of shock. Complete

blood count testing may reveal an elevated, normal, or

low white blood cell (WBC) count. No matter the absolute WBC count, a bandernia >10% suggests an ongoing

infectious process. Comprehensive metabolic panel analysis will assess both kidney and liver function and acidbase status. An elevated anion gap may indicate underlying

lactic acidosis, uremia, or toxic ingestion. Blood gas

analysis is useful to determine the serum pH, lactate

level, and base deficit. Serum lactate is a highly sensitive

marker for tissue hypoperfusion and predictive of overall

SHOCK

mortality in septic shock. Lactate levels >4 rnmol!L are

significant and indicate ongoing cellular hypoxia. Other

tests useful in the appropriate clinical scenario include

cardiac markers, urinalyses, coagulation profiles, toxicologic screens, and pregnancy testing. Obtain blood and

urine cultures (and possibly cerebrospinal fluid) if sepsis

is a concern.

� Imaging

No single radiologic test is diagnostic of shock. Chest

x-ray may reveal evidence of an infiltrate (sepsis),

enlarged cardiac silhouette (cardiac tamponade), subdiaphragmatic free air (sepsis), pulmonary edema (cardiagenic shock) or pneumothorax. Bedside ultrasound can

guide the work-up, treatment, and disposition of patients

in shock in multiple clinical situations including sepsis,

blunt abdominal trauma, pregnancy, abdominal aortic

aneurysm, and pericardia! tamponade. Furthermore,

ultrasonographic inferior vena cava measurement can

help guide appropriate fluid resuscitation. Computed

tomography imaging has become the modality of choice

for diagnosing PE, aortic dissection, and intra-abdominal

pathology.

PROCEDURES

Endotracheal intubation may be required in patients with

profound shock to reduce the work of breathing and systemic metabolic demands. Central venous line placement

can expedite fluid or blood product infusion, vasopressor administration, and central venous pressure (CVP)

analysis.

MEDICAL DECISION MAKING

Once shock is recognized, rapidly attempt to identify both

the subtype and inciting factor to determine the appropriate therapy (Table 1 2-1). Time is truly of the essence in

these patients, and any delay will significantly impact

patient outcome. Concurrently address the patient airway,

breathing, and circulation (ABCs) and stabilize all severely

ill patients. Use the ancillary laboratory and imaging studies mentioned previously to guide the diagnosis and treatment (Figure 12-1).

Table 1 2-1. SHOCK: differentia l diagnosis.

Shock Mnemonic

S Septic, spinal (neurogenic)

H Hypovolemic, hemorrhagic

0 Obstructive (pulmonary embol ism, tamponade)

c Cardiogenic

K Kortisol (adrenal crisis), AnaphylaKtic

Continued volume resuscitation,

identify and control ongoing

hemorrhage

CHAPTER 12

Early goal directed therapy

for sepsis

Epineph rine, antih istamines

& steroids and removal of

inciting agent for ana phylaxis

Dopamine and atropine for

neurogenic shock

Pericard iocentesis for

tamponade

Fibrinolysis for

massive PE

Needle thoracostomy

for tension PTX

ACLS care for dysrhythmia

control

Inotropic support with

dobutamine + dopamine

Immediate reperfusion

with PCI

.&. Figure 1 2-1. Shock diagnostic algorithm. ACLS, advanced cardiac life support; PCI, percutaneous coronary

intervention PE, pulmonary embol ism; PTX, pneumothorax.

TREATMENT

The goal of treatment is 2-fold, namely to restore normal

cellular function and reverse the inciting factor. Place all

patients on supplemental 02 and consider early mechanical

ventilation in those with markedly elevated metabolic

demands, as hyperactive respiratory muscles can steal away

up to 50% of normal cerebral blood flow. Place a minimum

of 2 large-bore peripheral N lines in all patients and con ­

sider central line placement in those who will require multiple infusions, vasopressor support, or CVP monitoring.

Administer boluses of normal saline to replenish an absolute

or relative vascular depletion. Transfuse red blood cells as

needed to augment circulating 02 delivery. Initiate vasopressor support in patients who either fail to respond or have a

contraindication ( eg, cardiogenic shock) to repeated fluid

boluses. Place a Foley catheter to accurately measure urine

output. The management of specific types of shock is discussed next.

� Hypovolemic Shock

Restore adequate tissue perfusion by rapidly expanding the

intravascular volume. Infuse several liters of normal saline

followed by several units of packed red blood cells in hemorrhagic patients who fail to respond. Patients with simple

dehydration will improve rapidly. Of note, avoid overly

aggressive volume expansion in trauma patients, as this

may trigger recurrent hemorrhage at previously clotted

sites. Titrate therapy in these patients to a goal mean arte ­

rial pressure (MAP) of 60 mmHg and restoration of nor ­

mal mental status.

� Distributive Shock

Sepsis

Begin early goal-directed therapy in all patients with septic

shock. Monitor the CVP to guide fluid resuscitation in these

patients. Begin treatment by aggressively bolusing several

liters of normal saline to achieve a goal CVP between 8 and

12 mmHg. Initiate vasopressor support with a norepinephrine infusion in patients who remain hypotensive and

titrate to a goal MAP >65 mmHg. Start broad-spectrum

antibiotics targeted at the proposed source and pursue s urgical drainage/debridement when indicated.

Neurogenic Shock

Address all other potential causes of shock first, as neuro ­

genic shock is a diagnosis of exclusion. Aggressively expand

the circulating blood volume by bolusing several liters of

normal saline. Initiate a dopamine infusion for vasopressor

support in all patients who fail to respond. Use small doses

ofN atropine (eg, 0.5 mg) to treat symptomatic bradycardia refractive to the previously mentioned measures.

Anaphylaxis

Anaphylactic shock can be rapidly fatal and requires

immediate treatment. Administer normal saline boluses,

N antihistamines, and N corticosteroids to all patients.

Give intramuscular epinephrine (1:1,000 solution) in 0.3-

to 0.5-mg doses as needed to maintain systemic perfusion.

In patients refractive to the preceding, administer 0.3- to

0.5-mg doses of N epinephrine (1:10,000 solution) over a

2- to 3-minute duration. Actively search for and remove

any ongoing allergen exposure ( eg, retained soft tissue bee

stinger).

SHOCK

� Obstructive Shock

Cardiac Tamponade

Administer 1-2 L of normal saline followed by emergent

bedside pericardiocentesis. Perform an emergency department

thoracotomy in patients with penetrating thoracic trauma

who fail to respond.

Pulmonary Embolism

Administer small boluses of normal saline (250-500 mL)

followed by vasopressor support in unstable patients.

Fibrinolysis is the treatment of choice for massive PE presenting with profound hypotension (MAP <60), severe

refractive hypoxemia (Sp02 <90 despite supplemental 02),

or cardiac arrest.

Tension Pneumothorax

Administer 1-2 L of normal saline while performing

emergent needle thoracostomy followed by chest tube

placement.

� Cardiogenic Shock

The goal of treatment is to improve cardiac output while

at the same time reducing myocardial workload.

Administer IV fluids judiciously to avoid undesired elevations in the left ventricular preload and secondary pulmonary edema. Begin inotropic and vasopressor support in

patients who remain hypotensive despite IV fluids. Firstline therapy is often a combination of dopamine and

dobutamine (as dobutamine monotherapy will exacerbate

hypotension), with norepinephrine reserved for patients

who fail to respond. Of note, all of the aforementioned

modalities are temporizing measures pending definitive

revascularization (ie, percutaneous coronary intervention

or fibrinolysis).

DISPOSITION

Admit all patients in shock to a critical care bed.

SUGGESTED READING

Cherkas D. Traumatic hemorrhagic shock: Advances in fluid

management. Emerg Med Pract. 20 1 1;13:1-20.

Dellinger, RP, Levy, MM, et al. Surviving Sepsis Campaign:

International guidelines for management of severe sepsis and

septic shock: 2008. Grit Care Med. 2008;36:296-327.

Otero RM, Nguyen HB, Rivers EP. Approach to the patient in

shock. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ,

Cydulka RK, Meckler GD, eds. Tintinalli's Emergency

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

NY: McGraw-Hill, 201 1.

Reynolds HR, Hochman ]S. Cardiogenic shock: Current concepts

and improving outcomes. Circulation. 2008;1 17: 

Airway Management

Theresa M. Schwab, MD

Key Points

• Rapid-sequence intubation (RSI) is the preferred method

for endotracheal tube placement in the emergency

department.

• The decision to intubate should always be made on

clinical grounds. Time permitting, assess for factors

predictive of a difficult airway before RSI.

INTRODUCTION

Successful airway management depends on the prompt

recognition of an inadequate airway, the identification of

risk factors that may impair successful bag-valve-mask

(BVM) ventilation or endotracheal t ube (ETT) placement,

and the use of an appropriate technique to properly secure

the airway. The decision to intubate is a clinical one and

should be based on the presence of any 1 of 3 major conditions: an inability to successfully protect one's airway

against aspiration/occlusion, an inability to successfully

oxygenate the blood (hypoxemia), or an inability to successfully clear the respiratory byproducts of cellular

metabolism (hypercapnia). Additional indications including the desire to decrease the work of breathing (sepsis),

the need for therapeutic hyperventilation (increased intracranial pressure [ICP]), and the need to obtain diagnostic

imaging in noncooperative individuals (altered mental

status) should be taken into account on a patient-bypatient basis.

Techniques for the management of unstable airways

range from basic shifts in patient positioning to invasive

surgical intervention. Standard basic life support recommendations such as the head-tilt chin-lift maneuver may

open a previously occluded airway. Oropharyngeal and

nasal airway adjuncts are both simple to use and highly

37

• General criteria for endotracheal intubation include a

failure to protect the airway, a failure to adequately

oxygenate, and a fa ilure to expire accumulating co r

• Pursue alternative techniques (eg, cricothyrotomy) in

patients when the in itial airway intervention has fa iled

and the patient cannot be adequately ventilated.

effective in this setting, but are unfortunately often underutilized. Failure to respond to these measures warrants the

placement of an ETT. Rapid-sequence intubation (RSI)

combines the careful use of pretreatment interventions with

the administration of induction and paralytic agents to create the ideal environment for ETT placement and is the

preferred method in the emergency department (ED).

A patient who cannot be intubated within 3 attempts is

considered a failed airway. This scenario occurs in -3-5%

of all cases. Numerous alternative devices including laryn ­

geal mask airways (LMA), introducer bougies, and fiberoptic instruments have been developed to facilitate airway

management in these situations. That said, these methods

are not failsafe, and roughly 0.6% of patients will require a

surgical airway. Emergent cricothyrotomy is the preferred

surgical technique for most ED patients.

CLINICAL PRESENTATION

.... History

The need for immediate airway intervention in emergency

situations always supersedes the need for a comprehensive

history and physical exam. Time permitting, perform a

rapid airway assessment to identify any risk factors predictive of a difficult airway, inquire about any current

CHAPTER 11

medication use and known drug allergies, and try to ascertain the immediate events leading up to ED presentation.

Risk factors predictive of a difficult airway include

those that impair adequate BVM ventilation and those that

preclude successful placement of an ETT. Examples of the

former include patients with facial trauma and distorted

anatomy, obese patients with excessive cervical soft t issue,

and asthmatic patents with excessively high airway resistances. Examples of the latter include patients with a his ­

tory of degenerative changes of the spine that limit cervical

mobility ( eg, rheumatoid arthritis, ankylosing spondylitis),

patients with underlying head and neck cancers that distort the normal cervical anatomy, and those with excessive

swelling of the airway and surrounding tissues (eg,

angioedema).

..... Physical Examination

Rapidly examine the airways of all critically ill patients.

Always consider the presence of concurrent cervical spine

injury in victims of trauma and immobilize as appropriate.

Carefully examine the face, noting any signs of significant

facial trauma and the presence of a beard, both of which

frequently impair adequate BVM ventilation. Inspect the

oropharynx, noting the presence of dentures; the size of

the teeth and presence of a significant overbite; visibility of

the soft palate, uvula, and tonsillar pillars (ie, Mallampati

classification); and the presence of significant airway swelling. The pooling of blood or secretions in the oropharynx

indicates an inability to properly protect the airway. A good

adage to remember when assessing the airway is the 3-3-2

rule. The inability to open the mouth 3 finger breaths, a

distance from the tip of the chin to the base of the neck less

than 3 finger breaths, or a distance between the mandibular floor and the prominence of the thyroid cartilage of less

than 2 finger breaths all predict more difficult ETT place ­

ment. Assess the range of motion of the cervical spine,

provided there is no concern for occult injury.

DIAGNOSTIC STUDIES

..... Laboratory

Although abnormalities on either blood gas analysis (hypercapnia) or pulse oximetry (hypoxemia) may be indicative of

an inadequate airway, normal values on either of these studies should not j ustify the delay of definitive intervention in

the appropriate clinical scenario. Progressive abnormalities

on serial testing (increasing PaC02

, decreasing Pa02

) in

patients who are clinically decompensating indicates the

need for airway intervention.

..... Imaging

Imaging studies should not be used to predict the need for

airway intervention. Obtain a chest x-ray (CXR) in all

patients after intubation to confirm proper ETT placement.

The tip of the ETT should be visualized approximately

2 em above the carina. Deeper insertion results in placement into the right mainstem bronchus.

MEDICAL DECISION MAKING

Consider all rapidly reversible causes of airway compromise

(eg, hypoglycemia, opioid overdose) before pursuing endotracheal intubation. Proper intervention may transform a

comatose patient with a rather tenuous airway into an awake

coherent individual with adequate airway protection.

Identify patients who are likely to present a difficult airway

and those who require specialized approaches ( eg, head

trauma precautions, hypotension, cervical spine injury) and

proceed accordingly (Figure 1 1-1).

PROCEDURES

..... Bag-Valve-Mask Ventilation

Proper BVM ventilation requires an open airway and an

airtight seal between the mask and the patient's face. Use

the head-tilt chin-lift technique (jaw-thrust maneuver in

trauma victims) to open the airway and insert oropharyngeal or nasal adjuncts as necessary to maintain patency.

Avoid the use of oral adjuncts in patients with intact gag

reflexes and nasal adjuncts in patients with significant

mid-face trauma. With proper technique and a high-flow

oxygen source, this method can provide an Fi02 of

approximately 90% ( Figure 1 1-2).

..... Rapid-Sequence Intubation

Preoxygenate all patients with a high-flow oxygen source

(eg, nonrebreather [NRB] mask) for several minutes as

time permits before RSI. Avoid positive pressure ventilation

(eg, BVM) to prevent insufflation of the stomach, which

can increase the patient's risk for aspiration. Use this time

to prepare and check your equipment. Ensure adequate N

access and proper function of the suction device. Remove

patient dentures, significant loose teeth, and any oral debris.

Choose the appropriate size ETT. Tube sizes range in diameter from 2.5-9 mm. A size 7.5- or 8.0-mm tube is appropriate for most adult female and male patients respectively.

Inflate the balloon to check for leaks and insert a stylet.

Uncuffed ETTs have been historically preferred in patients

younger than 8 years of age as the narrowest portion of

their airways lies inferior to the vocal cords at the level of

the cricoid ring. That said, most practitioners now prefer

cuffed ETTs for all patients. To determine the appropriate

size of the ETT in pediatric patients, either use the formula

Size = (Age/4) + 4 for uncuffed tubes or (Age/4) + 3 for the

cuffed variety, or use a tube that is equal in diameter to the

child's fifth finger .

Check the light on your laryngoscope blade to ensure

that it works. Laryngoscope blades range in size from 0-4

and come in 2 major varieties. The Macintosh blade is

curved in shape and meant to indirectly lift the epiglottis

away from the vocal cords. It is also designed with a special

AIRWAY MANAGEMENT

Airway management indicated:

Failure to oxygenate, venti late, or

protect the airway

Rapid airway eva luation to identify

findings indicative of a difficult airway

Difficult airway

predicted

No difficult airway

predicted

Modified approach including:

• "Awake look" intubation

• Difficult airway adjuncts

(LMA, bougie, fiberoptics, etc.)

Figure 1 1-1. Airway diag nostic algorithm. LMA, laryngeal mask airways; RSI, rapid-sequence intubation.

ridge meant to sweep the tongue to the side during insertion

to improve visualization of the vocal cords. The Miller blade

is straight in appearance and meant to directly lift the

Figure 1 1-2. Proper method of BVM ventilation.

epiglottis away from the vocal cords. It is of particular benefit in patients with very anterior airways and those with a

large "floppy" epiglottis. A size 3 or 4 Macintosh blade is

appropriate for most adult ED patients (Figure 1 1-3).

Certain clinical scenarios warrant unique modifications to standard RSI to attenuate the adverse physiologic

responses to endotracheal intubation. Pretreat head injury

patients with lidocaine (1.5 mg/kg) and a "defasciculating"

dose of a nondepolarizing neuromuscular blocker ( eg,

pancuronium 0.01 mg/kg) to limit the potential spike in

ICP that may accompany ETT placement. Pretreat most

pediatric patients with an anticholinergic agent ( eg, atro ­

pine 0.02 mg/kg) to prevent reflex bradycardia. Pretreat

patients in whom rapid elevations in either blood pressure

or heart rate would be catastrophic (eg, aortic dissection)

with an opioid analgesic ( eg, fentanyl 3 meg/kg) to limit

excessive catecholamine surges. Of note, the clinical utility

of many of these pretreatment regimens has recently come

under considerable debate.

Outside of the pretreatment agents listed previously,

the remaining RSI medications can be divided into either

CHAPTER 11

Figure 1 1-3. Equi pment needed for orotracheal

intubation in an adu lt. From left to right, laryngoscope

handle attached to Macintosh 3 blade, Maci ntosh

4 blade, Miller 4 blade, end-tidal C02 detector,

1 0-ml syringe, and endotracheal tube with stylet.

induction agents or paralyzing agents. Induction agents are

designed to elicit extremely rapid sedation to facilitate ETT

placement. A variety of medications are available, including etomidate (0.3 mg/kg), propofol (1 mg/kg), ketamine

(2-3 mg/kg), and midazolam (0.05-0. 1 mg/kg). Of these,

etomidate is used most frequently in the ED because of its

rapid onset and offset and relative hemodynamic neutrality. Avoid the use of benzodiazepines and propofol in

hypotensive patients and ketamine in patients with paten ­

tial traumatic brain injury.

Paralytic agents can be divided into depolarizing and

nondepolarizing categories. Succinylcholine ( 1.5 mg/kg) is

the lone agent in the depolarizing class and the most commonly used paralytic for RSI because of its rapid onset and

short duration of activity. Most patients achieve r elaxation

within 1 minute, complete paralysis by the 2- to 3-minute

mark, and a return of motor function within 10 minutes.

Avoid succinylcholine in patients with known hyperkale ­

mia and those with pathologically denervated tissues (eg,

spinal cord injuries, burns) as it can precipitate life-threatening ventricular dysrhythmias. Given the longer duration

of paralysis for most nondepolarizing agents (eg, atracurium), their use is generally avoided in RSI.

Certain patients predicted to have difficult airways may

benefit from intubation via the use of lower than normal

doses of induction agents without concurrent paralytics.

Also known as the "awake look;' this limits the all too real

potential for creating the scenario of a paralyzed and,

therefore, not breathing patient who cannot be intubated.

Finally, apneic patients or those in cardiac arrest are not

Anterior

Vocal cords

.6. Figure 1 1-4. Laryngoscopic view. (Reproduced with

permission from Kempe CH, Si lver HK, O'Brien 0,

(editors): Current Pediatric Diagnosis Er Treatment. 4th ed.

lange, 1 976.)

candidates for RSI. Their condition does not allow time for

either preoxygenation or pretreatment, and being unconscious, they do not require RSI medications to facilitate

ETT placement. Temporize these patients with BVM venti ­

lation pending their emergent intubation.

To visualize the vocal cords, hold the laryngoscope in

the left hand and carefully insert the blade into the oropharynx directed downward along the tongue and into the

throat. Gentle upward traction should lift the epiglottis

from tl1e larynx and reveal the vocal cords (Figure 1 1-4).

Concurrent external laryngeal manipulation may shift the

patient's vocal cords into better view. Keep in mind that

pediatric airways are typically more anterior than those of

adults and that their relatively large tongues and floppy

epiglottis often necessitate the use of a Miller blade.

Insert the ETT and maintain visualization until the balloon has clearly passed the vocal cords. Advance the ETT

until the depth (at the teeth) is at 3 times the diameter of the

tube. Keep in mind this is only an estimate, and all patients

require a postprocedural CXR to document the depth of

ETT placement. Proper insertion can be inlmediately con ­ firnled at the bedside by auscultating for Synlffietric bilateral

breath sounds and via the use of color-change capnography.

Gentle downward pressure applied to the cricoid cartilage (Sellick's maneuver) at the onset of induction and

paralysis has been historically advocated to limit the potential for aspiration. A growing body of literature has begun to

question the utility of this maneuver as it not only fails to

prevent aspiration but can limit adequate visualization of

the vocal cords and impair successful insertion of the ETT. If

cricoid pressure is applied, release inlmediately if the patient

begins to vomit to prevent secondary esophageal rupture.

� Difficult Airway Adjuncts

Multiple devices have been designed to assist with the

management of difficult airways. Laryngeal mask airways

AIRWAY MANAGEMENT

Figure 1 1-5. Schematic demonstrati ng use

of bougie.

(LMA) conform to the natural curvature of the oropharynx and are designed for blind insertion into the supraglottic region. Proper insertion creates an airtight seal over

the larynx, allowing for mechanical ventilation. LMA

insertion does not prevent aspiration, though, and is not

considered a definitive airway.

Introducer bougies are very useful in patients whose

vocal cords cannot be adequately visualized. They are

essentially long flexible rubber sty lets with a distal curve at

their tip, which, when blindly inserted along the inferior

margin of the epiglottis, will naturally angle upward into

the larynx and through the vocal cords. Successful endotracheal placement can be detected as the tip of the bougie

skips along the tracheal rings. The ETT is then inserted

blindly over the bougie and into the airway (Figure 1 1-5).

Cricothyrotomy is performed by making a percutane ­

ous incision in the cricothyroid membrane through which

a tracheostomy or small ETT can be placed (Figure 1 1-6).

This can be a life-saving intervention in the crashing

patient when less invasive techniques to secure the airway

have failed. Common indications include massive facial

trauma and angioedema. Cricothyrotomy is contraindi ­

cated in children <8 years of age and should be replaced

with needle cricothyrotomy.

Additional difficult airway adjuncts include blind nasatracheal intubation, lighted stylets, Combitubes, fiberoptic

intubation, retrograde wire-guided tracheal intubation,

and percutaneous translaryngeal ventilation.

DISPOSITION

Admit all patients who require airway management to an

intensive care unit setting.

Figure 1 1-6. Cricothyrotomy. A. An 11 blade

scalpel is used to cut the cricothyroid membrane. B. A

skin hook opens the incision and lifts the thyroid

carti lage su periorly so that the tracheostomy tube or

ETT can be inserted into the ai rway. (Reprinted with

permission from Bai l itz J, Bokhari F, Scaletta TA, et al.

Emergent Management of Trauma. 3rd ed. New York:

McGraw-Hill Education, 201 1 .)

SUGGESTED READINGS

Hedayati T, Ross C, Nasr N. Airway procedures. Rapid sequence

intubation. In: Simon RR, Ross CR, Bowman SH, Wakim PE.

Cook County Manual of Emergency Procedures. 1 st ed.

Philadelphia, PA: Lippincott Williams & Wilkins, 201 2, pp.

14-2 1.

Roman AM. Noninvasive airway management. In: Tintinalli JE,

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

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 20 11, pp. 183-190.

Vissers RJ, Danzl DF. Tracheal intubation and mechanical venti ­

lation. In: Tintinalli JE, Stapczynski JS, Ma OJ, Clince DM,

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

Comprehensive Study Guide. 7th ed. New York, NY: McGrawHill, 20 l l, pp. l 98-2 15.