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

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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.