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Information ⬇

[Section Outline]

Definition !!navigator!!

Abnormality of cardiac structure and/or function resulting in clinical symptoms (e.g., dyspnea, fatigue) and signs (e.g., edema, pulmonary crackles), hospitalizations, poor quality of life, and shortened survival. It is important to identify the underlying nature of the cardiac disease and the factors that precipitate acute HF.

Underlying Cardiac Disease !!navigator!!

Includes (1) states that depress systolic ventricular function with reduced ejection fraction (HFrEF; e.g., coronary artery disease [CAD], dilated cardiomyopathies, valvular disease, congenital heart disease); and (2) states of HF with preserved ejection fraction (HFpEF; e.g., restrictive cardiomyopathies, hypertrophic cardiomyopathy, fibrosis, endomyocardial disorders), also termed diastolic failure.

Acute Precipitating Factors !!navigator!!

Include (1) excessive Na+ intake, (2) noncompliance with HF medications, (3) acute MI (may be silent), (4) exacerbation of hypertension, (5) acute arrhythmias, (6) infection and/or fever, (7) pulmonary embolism, (8) anemia, (9) thyrotoxicosis, (10) pregnancy, (11) acute myocarditis or infective endocarditis, and (12) certain drugs (e.g., nonsteroidal anti-inflammatory agents).

Symptoms !!navigator!!

Due to inadequate perfusion of peripheral tissues (fatigue) and elevated intracardiac filling pressures (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema).

Physical Examination !!navigator!!

Jugular venous distention, S3 (in HFrEF/volume overload), pulmonary congestion (crackles, dullness over pleural effusion), peripheral edema, hepatomegaly, and ascites. Sinus tachycardia is common. In pts with HFpEF, S4 is often present.

Laboratory !!navigator!!

CXR may reveal cardiomegaly, pulmonary vascular redistribution, interstitial edema, pleural effusions. Left ventricular systolic and diastolic dysfunction are most readily evaluated by echocardiography with Doppler, and EF calculated or estimated. In addition, echo can identify underlying valvular, pericardial, or congenital heart disease, and regional wall motion abnormalities typical of CAD. Cardiac MR may be valuable in assessing ventricular structure, mass, volumes, and can help determine cause of HF (e.g., CAD, amyloid, hemochromatosis). Measurement of B-type natriuretic peptide (BNP) or N-terminal pro-BNP differentiates cardiac from pulmonary causes of dyspnea (elevated in the former).

Conditions That Mimic Chf !!navigator!!

Pulmonary Disease: Chronic bronchitis, emphysema, and asthma (Chaps. 131 Asthma and 133 Chronic Obstructive Pulmonary Disease); assess for sputum production and abnormalities on CXR and pulmonary function tests. Other Causes of Peripheral Edema: Obesity, varicose veins, and venous insufficiency do not cause jugular venous distention. Edema due to renal dysfunction is often accompanied by elevated serum creatinine and abnormal urinalysis (Chap. 38 Edema).

TREATMENT

Heart Failure

Aimed at symptomatic relief, prevention of adverse cardiac remodeling, and prolonging survival. Overview of treatment of chronic HF is shown in Table 126-1 Therapy for Chronic Heart Failure; notably, ACE inhibitors and beta blockers are cornerstones of therapy in pts with HFrEF. Once symptoms develop:

  • Control excess fluid retention: (1) Dietary sodium restriction (eliminate salty foods, e.g., potato chips, canned soups, bacon, salt added at table); more stringent requirements (<2 g NaCl/d) in advanced CHF. If dilutional hyponatremia present, restrict fluid intake (<1000 mL/d). (2) Diuretics: Loop diuretics (e.g., furosemide or torsemide [Table 126-2 Drugs for the Treatment of Chronic Heart Failure with Reduced EF]) are most potent and, unlike thiazides, remain effective when GFR <25 mL/min. Combine loop diuretic with thiazide or metolazone for augmented effect.
  • ACE inhibitors (Table 126-2 Drugs for the Treatment of Chronic Heart Failure with Reduced EF): Standard initial HF therapy that reduces mortality in pts with symptomatic HF, delays the onset of HF in pts with asymptomatic LV dysfunction, and lowers mortality when begun soon after acute MI. ACE inhibitors may result in hypotension in pts who are volume depleted, so start at lowest dosage (e.g., captopril 6.25 mg PO tid). Angiotensin receptor blockers (ARBs) (Table 126-2 Drugs for the Treatment of Chronic Heart Failure with Reduced EF) may be substituted if pt is intolerant of ACE inhibitor (e.g., because of cough or angioedema). For pts with persistent class II-III symptoms, consider converting ACE inhibitor or ARB to an angiotensin receptor-neprilysin inhibitor (Table 126-2 Drugs for the Treatment of Chronic Heart Failure with Reduced EF; hold ACE inhibitor for 36 hours prior to initiation).
  • Beta blockers (Table 126-2 Drugs for the Treatment of Chronic Heart Failure with Reduced EF), specifically metoprolol succinate, carvedilol, and bisoprolol, administered in gradually augmented dosage improve symptoms and prolong survival in pts with HF and reduced EF <40%. Begin at low dosage and increase gradually (e.g., carvedilol 3.125 mg bid, double q2weeks as tolerated to maximum of 25 mg bid [for weight <85 kg] or 50 mg bid [weight >85 kg]).
  • Aldosterone antagonist therapy (spironolactone or eplerenone [Table 126-2 Drugs for the Treatment of Chronic Heart Failure with Reduced EF]), added to standard therapy in pts with advanced HF reduces mortality. Such therapy should be considered in pts with class II-IV HF symptoms and left ventricular ejection fraction (LVEF) ≤35%. Should be used cautiously when combined with ACE inhibitor or ARB to avoid hyperkalemia.
  • Digoxin may be useful in HF due to (1) marked systolic dysfunction and (2) HF with atrial fibrillation (AF) and rapid ventricular rates. Unlike ACE inhibitors and beta blockers, digoxin does not prolong survival in HF pts but reduces hospitalizations. Digoxin is contraindicated in hypertrophic cardiomyopathy and in pts with AV conduction blocks.
    • Digoxin dosing (0.125-0.25 mg qd) depends on age, weight, and renal function and can be guided by measurement of serum digoxin level (maintain level <1.0 ng/mL).
    • Digitalis toxicity may be precipitated by hypokalemia, hypoxemia, hypercalcemia, hypomagnesemia, hypothyroidism, or myocardial ischemia. Early signs of toxicity include anorexia, nausea, and lethargy. Cardiac toxicity includes ventricular and supraventricular dysrhythmias and all degrees of AV block. At first sign of digitalis toxicity, discontinue the drug; maintain serum K+ concentration between 4.0 and 5.0 mmol/L. Bradyarrhythmias and AV block may respond to atropine (0.6 mg IV); otherwise, a temporary pacemaker may be required. Antidigoxin antibodies are available for massive overdose.
  • The combination of the oral vasodilators hydralazine (10-75 mg tid) and isosorbide dinitrate (10-40 mg tid) may be of benefit for chronic administration in pts intolerant of ACE inhibitors and ARBs and is also beneficial as part of standard therapy, along with ACE inhibitor and beta blocker, in African Americans with class II-IV HF.
  • Ivabradine, an inhibitor of the sinoatrial nodal If current, has been shown to reduce hospitalizations and cardiovascular endpoints in HF. It is a second-line agent (starting at 2.5-5.0 mg orally twice daily) for pts with LVEF ≤35%, in sinus rhythm with heart rate >70 bpm, already on maximally tolerated beta-blocker dose or have a contraindication to beta-blocker use.
  • For hospitalized pts with acute decompensated HF, use IV loop diuretics for volume overload, either by bolus or continuous infusion; obtain daily weights, aiming for loss of 1-1.5 kg/d. IV vasodilator therapy (Table 126-3 Drugs for Treatment of Acute Heart Failure) is often necessary. Nitroprusside is a potent mixed vasodilator for pts with markedly elevated systemic vascular resistance. It is metabolized to thiocyanate, which is excreted via the kidneys. To avoid thiocyanate toxicity (seizures, altered mental status, nausea), follow thiocyanate levels in pts with renal dysfunction or if administered for >2 days. IV nesiritide (Table 126-3 Drugs for Treatment of Acute Heart Failure), a purified preparation of BNP, is a vasodilator that reduces pulmonary capillary wedge pressure in pts with acutely decompensated CHF, but has neutral effects on mortality or sense of dyspnea. It should be considered only in pts with refractory HF.
  • IV inotropic agents (see Table 126-3 Drugs for Treatment of Acute Heart Failure) are administered to hospitalized pts for refractory symptoms or acute exacerbation of CHF to augment cardiac output, improve perfusion, and help relieve congestion. They are contraindicated in hypertrophic cardiomyopathy. Dobutamine augments cardiac output without significant peripheral vasoconstriction or tachycardia. Milrinone is a nonsympathetic positive inotrope and vasodilator that acts by inhibiting phosphodiesterase type 3.
  • The initial approach to treatment of acute decompensated HF can rely on the pt's hemodynamic profile (Fig. 126-1. Hemodynamic Profiles in Pts with Acute Heart Failure) based on clinical examination and, if necessary, invasive hemodynamic monitoring:
    • - Profile A “Warm and dry”: Symptoms due to conditions other than HF (e.g., acute ischemia). Treat underlying condition.
    • - Profile B “Warm and wet”: Treat with diuretic and vasodilators.
    • - Profile C “Cold and wet”: Treat with IV vasodilators and inotropic agents.
    • - Profile L “Cold and dry”: If low filling pressure (PCW <12 mmHg) confirmed, proceed with trial of volume repletion.
  • Consider implantable cardioverter defibrillator (ICD) prophylactically for chronic class II-III HF and LVEF <35%. Pts with LVEF <35%, refractory CHF (NYHA class III-IV), and prolonged QRS (especially left bundle branch with QRS ≥150 msec) are candidates for biventricular pacing (cardiac resynchronization therapy), often combined with an ICD. Pts with severe disease and very limited, short-term expected survival, and who meet stringent criteria, may be candidates for cardiac transplantation or prolonged-assisted mechanical circulation (see HPIM-20, Chap. 255).
  • Pts with HFpEF are treated with salt restriction and diuretics, and attention to underlying causes (e.g., treatment of hypertension). Beta blockers and ACE inhibitors may be of benefit in blunting neurohormonal activation, but have not been shown to lower mortality in this population.

Outline ⬆

Section 8. Cardiology