Heart failure is defined as a clinical syndrome caused by inability of the heart to pump enough blood to maintain fluid and metabolic homeostasis.
- Coronary heart disease.
- Valvular heart disease.
- COPD (cor pulmonale).
The American Heart Association/American College of Cardiology guidelines classify heart failure according to clinical syndromes, but alternative classification systems, including that of the New York Heart Association (NYHA), include functional severity, left-sided vs right-sided failure, and systolic vs non systolic failure (see Tables 1-2).
1) Systolic Dysfunction / Cardiac Failure With Reduced Ejection Fraction
A ↓ EF (< 40%) and ↑ left ventricular end-diastolic volumes. It is caused by inadequate left ventricular contractility or ↑ afterload. The heart compensates for ↓ EF and ↑ preload through hypertrophy and ventricular dilation (Frank-Starling law), but the compensation ultimately fails, leading to ↑ myocardial work and worsening systolic function.
S3 Heart Sound
S4 Heart Sound
- Exertional dyspnea that progresses to orthopnea, paroxysmal nocturnal dyspnea (PND), and finally dyspnea at rest.
- Chronic cough, fatigue, and peripheral edema may be reported.
- Exam: parasternal lift, an elevated and sustained left ventricular impulse, an S3/S4 gallop, JVD, rales on lung exam, and peripheral edema.
- Look for signs to distinguish left- from right-sided failure (see Table 3).
“The most common cause of right-sided heart failure is left-sided heart failure.”
- CHF is a clinical syndrome whose diagnosis is based on signs and symptoms.
- Diagnostic studies that may support diagnosis include the following:
- Best initial test: Echocardiogram (transthoracic echocardiogram). ↓ EF and ventricular dilation may help pinpoint underlying cause (ie, AF, old MI, or LVH).
- ECG: May show MI, heart block, arrhythmia.
- CXR: May show cardiomegaly, cephalization of pulmonary vessels, pleural effusions, vascular congestion, pulmonary edema, and prominent hila (see Figure 1).
- Lab abnormalities: Brain natriuretic peptide > 500 pg/mL, ↓ CBC (anemia), ↑ creatinine (sometimes), ↓ sodium in later stages, ↑ or ↓ TSH/T4 levels.
“Hyponatremia parallels severity of heart failure and is an independent predictor of mortality in these patients.”
CXR findings in CHF diagnosis—
Alveolar edema (“Bat’s wings”)
Kerley B lines (interstitial edema)
Dilated prominent upper lobe vessels
Acute CHF management—
Position (sit upright)
- Pharmacologic therapy (see Table 4):
- Loop diuretics (most commonly) for aggressive diuresis.
- ACEIs or ARB in combination with loop diuretics.
- β-blockers should be avoided during decompensated CHF but should be restarted once patient is euvolemic.
- Correct underlying causes such as arrhythmias, myocardial ischemia, and drugs (eg, CCBs, antiarrhythmics, NSAIDs, alcohol, anemia, thyroid and valvular disease, high-output states).
- Treat acute pulmonary congestion with LMNOP (see Acute CHF management mnemonic).
- Acute decompensated heart failure: Inotropic agents (eg, dobutamine) reduce left ventricular end-systolic volume for symptomatic improvement.
ACEIs/ARBs, ARNI, β-blockers, spironolactone or eplerenone, hydralazine/nitrates, and implantable defibrillator have mortality benefit in systolic dysfunction. Diuretics and digoxin (as well as other positive inotropic agents) are for symptomatic relief only and confer no mortality benefit. CCBs may ↑ mortality.
- Lifestyle: Control comorbid conditions, and limit dietary sodium and fluid intake.
- Pharmacologic therapy:
- β-blockers and ACEIs/ARBs: Help prevent remodeling of the heart and ↓ mortality for NYHA class II–IV patients. Avoid CCBs (can worsen edema).
- Low-dose spironolactone: Shown to ↓ mortality risk in patients with NYHA class III–IV heart failure.
- Diuretics (most commonly loop diuretics): Prevent volume overload.
- Digoxin: Symptomatic control of dyspnea and ↓ frequency of hospitalizations.
- Daily ASA and a statin are recommended if the underlying cause is a prior MI.
- Advanced pharmacologic therapy:
- Sacubitril/valsartan: angiotensin receptor-neprilysin inhibitor (ARNI) is a new drug class used in patients who continue to be dyspneic despite using the initial pharmacologic regimen. Provides mortality benefit for systolic dysfunction.
- Ivabradine: Reduces heart rate through SA nodal inhibition of the “funny channels.” Indicated in patients with systolic dysfunction if pulse is > 70 bpm or β-blockers are contraindicated.
c) Advanced treatments:
- Implantable cardiac defibrillator (ICD) in patients with an EF <35%. Shown to ↓ mortality risk.
- Biventricular pacemaker in patient with an EF < 35%, dilated cardiomyopathy, and widened QRS complex with persistent symptoms.
- Left ventricular assist device (LVAD) or cardiac transplantation may be necessary in patients who are unresponsive to maximal medical therapy and biventricular pacemaker failure.
2) Non-Systolic Dysfunction / Heart Failure With Preserved Ejection Fraction
Defined by ↓ ventricular compliance with normal systolic function. The ventricle has either impaired active relaxation (2° to hypertension, ischemia, aging, and/or hypertrophy) or impaired passive filling (scarring from prior MI; restrictive cardiomyopathy). Left ventricular end-diastolic pressure ↑, cardiac output remains essentially normal, and EF is normal or ↑.
Associated with stable and unstable angina, shortness of breath, dyspnea on exertion, arrhythmias, MI, heart failure, and sudden death.
- Best initial treatment: Diuretics (see Table 2.1-9).
- Maintain rate and BP control via β -blockers (first-line), ACEIs, ARBs, or CCBs.
- Digoxin and spironolactone are not beneficial in these patients.