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Harrison’s Manual of Medicine



Heart Failure
Cor Pulmonale
DEFINITION   Heart failure is a condition in which the heart is unable to pump sufficient blood for metabolizing tissues or can do so only from an abnormally elevated filling pressure. It is important to identify the underlying nature of the cardiac disease and the factors that precipitate acute CHF.
UNDERLYING CARDIAC DISEASE   Includes states that depress ventricular function (coronary artery disease, hypertension, dilated cardiomyopathy, valvular disease, congenital heart disease) and states that restrict ventricular filling (mitral stenosis, restrictive cardiomyopathy, pericardial disease).
ACUTE PRECIPITATING FACTORS   Include (1) increased Na intake, (2) noncompliance with anti-CHF 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, and (11) acute myocarditis or infective endocarditis.
SYMPTOMS   Due to inadequate perfusion of peripheral tissues (fatigue, dyspnea) and elevated intracardiac filling pressures (orthopnea, paroxysmal nocturnal dyspnea, peripheral edema).
PHYSICAL EXAMINATION   Jugular venous distention, S3, pulmonary congestion (rales, dullness over pleural effusion, peripheral edema, hepatomegaly, and ascites).
LABORATORY   CXR can reveal cardiomegaly, pulmonary vascular redistribution, Kerley B lines, pleural effusions. Left ventricular contraction can be assessed by echocardiography or radionuclide ventriculography. In addition, echo can identify underlying valvular, pericardial, or congenital heart disease, as well as regional wall motion abnormalities typical of coronary artery disease.
CONDITIONS THAT MIMIC CHF   Pulmonary Disease   Chronic bronchitis, emphysema, and asthma (Chap. 128 and Chap. 130); look for sputum production and abnormalities on CXR and pulmonary function tests.
Other Causes of Peripheral Edema   Liver disease, varicose veins, and cyclic edema, none of which results in jugular venous distention. Edema due to renal dysfunction is often accompanied by elevated serum creatinine and abnormal urinalysis (Chap. 17).

Aimed at symptomatic relief, removal of precipitating factors, and control of underlying cardiac disease. Overview of treatment shown in Table 116-1; notably, ACE inhibitor should be begun early, even in pts with asymptomatic LV dysfunction. Once symptoms develop:

Table 116-1 Therapy for Heart Failure

Decrease cardiac workload: Reduce physical activity; include periods of bed rest. Prevent deep venous thrombosis of immobile pts with heparin 5000 U SC bid.

Control excess fluid retention: (a) 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). (b) Diuretics (see Table 17-1): Loop diuretics (e.g., furosemide 20–120 mg/d PO or IV) are most potent and unlike thiazides remain effective when GFR <25 mL/min. Combine loop diuretic with thiazide or metolazone for augmented effect. Potassium-sparing diuretics are useful adjunct to reduce potassium loss; should be used cautiously when combined with ACE inhibitor to avoid hyperkalemia.
During diuresis, obtain daily weights aiming for loss of 1–1.5 kg/d.

Vasodilators (Table 116-2): ACE inhibitors recommended as standard initial CHF therapy. ACE inhibitors are mixed (arterial and venous) dilators and are particularly effective and well tolerated. They, and to a lesser extent the combination of hydralazine plus nitrates, have been shown to prolong life in pts with symptomatic CHF. ACE inhibitors also have been shown to delay the onset of CHF in pts with asymptomatic LV dysfunction and to lower mortality when begun soon after acute MI. Vasodilators may result in significant hypotension in pts who are volume depleted, so start at lowest dosage (e.g., captopril 6.25 mg PO tid); pt should remain supine for 2–4 h after the initial doses. Angiotensin receptor blocker (Table 124-4) may be substituted if pt is intolerant of ACE inhibitor (e.g., cough, angioedema).

Table 116-2 Vasodilators for Treatment of CHF

In sicker, hospitalized pts, IV vasodilator therapy (Table 116-2) is monitored by placement of a pulmonary artery catheter and indwelling arterial line. Nitroprusside is a potent mixed vasodilator for pts with markedly elevated SVR. It is metabolized to thiocyanate, then excreted via the kidneys. To avoid thiocyanate toxicity (seizures, altered mental status, nausea), follow thiocyanate levels in pts with renal failure or if administered for more than 2 d.

Beta blockers administered in gradually augmented dosage improve symptoms and prolong survival in patients with moderate (NYHA class II– III) heart failure. Begin at low dosage and increase gradually [e.g., carvedilol 3.125 mg bid, double q2 weeks as tolerated to maximum of 25 mg bid (for weight < 85 kg) or 50 mg bid (weight > 85 kg)].

Digoxin is useful in heart failure due to (a) marked systolic dysfunction (LV dilatation, low ejection fraction, S3) and (b) heart failure associated with atrial fibrillation and rapid ventricular rate. Unlike ACE inhibitors, digoxin does not prolong survival in heart failure pts. Not indicated in CHF due to pericardial disease, restrictive cardiomyopathy, or mitral stenosis (unless atrial fibrillation is present). Digoxin is contraindicated in hypertrophic cardiomyopathy and in pts with AV conduction blocks.
Digoxin loading dose is administered over 24 h (0.5 mg PO/IV, followed by 0.25 mg q6h to achieve total of 1.0–1.5 mg). Subsequent dose (0.125– 0.25 mg qd) depends on age, weight, and renal function and is guided by measurement of serum digoxin level. The addition of quinidine increases serum digoxin level; therefore, digoxin dosage should be halved. Verapamil, amiodarone, propafenone, and spironolactone also increase serum digoxin level.
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 extrasystoles and ventricular tachycardia and fibrillation; atrial tachycardia with block; sinus arrest and sinoatrial block; all degrees of AV block. Chronic digitalis intoxication may cause cachexia, gynecomastia, “yellow” vision, or confusion. 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. Digitalis-induced ventricular arrhythmias are treated with lidocaine or phenytoin (Chap. 115). Antidigoxin antibodies are available for massive overdose.

The aldosterone antagonist spironolactone, 25 mg/d, added to standard therapy in patients with advanced heart failure has been shown to reduce mortality. Its diuretic properties may also be beneficial, and it should be considered in patients with class IV heart failure symptoms.

IV sympathomimetic amines (Table 121-2) are administered to hospitalized pts for refractory symptoms or acute exacerbation of CHF. They are contraindicated in hypertrophic cardiomyopathy. Dobutamine [2.5–10 (µg/ kg)/min], the preferred agent, 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 greater than 10 (µg/kg)/min. Amrinone [5–10 (µg/kg)/min after a 0.75 mg/kg bolus] is a nonsympathetic positive inotrope and vasodilator. Vasodilators and inotropic agents may be used together for additive effect.
Patients with severe refractory CHF with <6 months expected survival, who meet stringent criteria, may be candidates for cardiac transplantation.

Right ventricular enlargement resulting from primary lung disease; leads to RV hypertrophy and eventually to RV failure. Etiologies include the following:

Pulmonary parenchymal or airway disease. Chronic obstructive lung disease (COPD), interstitial lung diseases, bronchiectasis, cystic fibrosis (Chap. 130 and Chap. 133).

Pulmonary vascular disease. Recurrent pulmonary emboli, primary pulmonary hypertension (PHT), vasculitis, sickle cell anemia.

Inadequate mechanical ventilation. Kyphoscoliosis, neuromuscular disorders, marked obesity, sleep apnea.
SYMPTOMS   Depend on underlying disorder but include dyspnea, cough, fatigue, and sputum production (in parenchymal diseases).
PHYSICAL EXAMINATION   Tachypnea, cyanosis, clubbing are common. RV impulse along left sternal border, loud P2, right-sided S4. If RV failure develops, elevated jugular venous pressure, hepatomegaly with ascites, pedal edema.
LABORATORY   ECG   RV hypertrophy and RA enlargement (Chap. 113); tachyarrhythmias are common.
CXR   RV and pulmonary artery enlargement; if PHT present, tapering of the pulmonary artery branches. Pulmonary function tests and ABGs characterize intrinsic pulmonary disease.
Echocardiogram   RV hypertrophy; LV function typically normal. RV systolic pressure can be estimated from Doppler measurement of tricuspid regurgitant flow. If imaging is difficult because of air in distended lungs, RV volume and wall thickness can be evaluated by MRI. If pulmonary emboli suspected, obtain radionuclide lung scan.

Aimed at underlying pulmonary disease and may include bronchodilators, antibiotics, and oxygen administration. If RV failure is present, treat as CHF, instituting low-sodium diet and diuretics; digoxin must be administered cautiously (toxicity increased due to hypoxemia, hypercapnia, acidosis). Loop diuretics must also be used with care to prevent significant metabolic alkalosis that blunts respiratory drive. Supraventricular tachyarrhythmias are common and treated with digoxin or verapamil (not beta blockers). Chronic anticoagulation with warfarin is indicated when pulmonary hypertension is accompanied by RV failure. In selected pts, inhalation of nitric oxide and infusion of prostacyclin reduce pulmonary hypertension and are undergoing evaluation for this purpose.


For a more detailed discussion, see Braunwald E: Heart Failure, Chap. 232, p. 1318; and Cor Pulmonale, Chap. 237, p. 1355, in HPIM-15.

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