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Information ⬇

Definition !!navigator!!

Abnormality of cardiac structure and/or function resulting in clinical symptoms (e.g., dyspnea, fatigue) and signs (e.g., edema, rales), 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 CHF.

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 heart failure 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 heart failure medications, (3) acute MI (may be silent), (4) exacerbation of hypertension, (5) acute arrhythmias, (6) infections 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, verapamil).

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 (rales, 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 can be assessed 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 heart failure (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. 129. Asthma and 131. 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. 36. Edema).

Treatment: Heart Failure

Aimed at symptomatic relief, prevention of adverse cardiac remodeling, and prolonging survival. Overview of treatment shown in Table 124-1; 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 124-2]) are most potent and, unlike thiazides, remain effective when GFR <25 mL/min. Combine loop diuretic with thiazide or metolazone for augmented effect.

    During acute diuresis, obtain daily weights, aiming for loss of 1-1.5 kg/d.

  • ACE inhibitors (Table 124-2): Recommended as standard initial CHF therapy. They prolong life in pts with symptomatic CHF, delay the onset of CHF in pts with asymptomatic LV dysfunction, and lower 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 124-2) may be substituted if pt is intolerant of ACE inhibitor (e.g., because of cough or angioedema). Consider hydralazine plus an oral nitrate instead in pts who develop hyperkalemia or renal insufficiency on ACE inhibitor.
  • Beta blockers (Table 124-2) administered in gradually augmented dosage improve symptoms and prolong survival in pts with heart failure 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 124-2]), added to standard therapy in pts with advanced heart failure reduces mortality. Such therapy should be considered in pts with class II-IV heart failure symptoms and LVEF ≤35%. Should be used cautiously when combined with ACE inhibitor or ARB to avoid hyperkalemia.
  • Digoxin may be useful in heart failure due to (1) marked systolic dysfunction (LV dilatation, low EF, S3) and (2) heart failure with atrial fibrillation (AF) and rapid ventricular rates. Unlike ACE inhibitors and beta blockers, digoxin does not prolong survival in heart failure pts but reduces hospitalizations. Not indicated in CHF due to pericardial disease, restrictive cardiomyopathy, or mitral stenosis (unless AF is present). 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 heart failure.
  • Ivabradine, an inhibitor of the sinoatrial nodal If current, has been shown to reduce hospitalizations and cardiovascular endpoints in heart failure and was recently approved for that purpose. It is a second line agent that can be prescribed (starting at 2.5-5.0 mg orally twice daily) to pts with left ventricular ejection fraction (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.
  • In sicker, hospitalized pts, IV vasodilator therapy (Table 124-3) 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 124-3), 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 heart failure.
  • IV inotropic agents (see Table 124-3) are administered to hospitalized pts for refractory symptoms or acute exacerbation of CHF to augment cardiac output. They are contraindicated in hypertrophic cardiomyopathy. Dobutamine augments cardiac output without significant peripheral vasoconstriction or tachycardia. Dopamine at low dosage (1-5 [µg/kg]/min) facilitates diuresis; at higher dosage (5-10 [µg/kg]/min) positive inotropic effects predominate; peripheral vasoconstriction is greatest at dosage >10 (µg/kg)/min. Milrinone (0.1-0.75 [µg/kg]/min after 50-µg/kg loading dose) is a nonsympathetic positive inotrope and vasodilator. The above vasodilators and inotropic agents may be used together for additive effect.
  • The initial approach to treatment of acute decompensated heart failure can rely on the pt's hemodynamic profile (Fig. 124-1) based on clinical examination and, if necessary, invasive hemodynamic monitoring:
    • - Profile A “Warm and dry”: Symptoms due to conditions other than heart failure (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, consider trial of volume repletion.
  • Consider implantable cardioverter defibrillator (ICD) prophylactically for chronic class II-III heart failure and LVEF <35%. Pts with an LVEF <35%, refractory CHF (NYHA class III-IV), and QRS >120 ms may be candidates for biventricular pacing (cardiac resynchronization therapy), typically in combination 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-19, Chap. 281, p. 1516).
  • Pts with predominantly diastolic heart failure are treated with salt restriction and diuretics. Beta blockers and ACE inhibitors may be of benefit in blunting neurohormonal activation.

Outline

Outline ⬆

Section 8. Cardiology