Diagnosis and Management
Jon was diagnosed as having congestive heart failure (CHF) and was admitted to the hospital. His orders were bed rest, a salt restricted diet, and oxygen per nasal cannula at 2 L/min. His medications were digoxin 0.25 mg PO Q 6 hr times four doses then 0.25 mg, PO QD, furosemide 40 mg PO TID, and potassium chloride 20 mEq PO BID.
Discussion
Disease. The syndrome of congestive heart failure arises when the heart cannot supply sufficient oxygen to meet the metabolic demands of the tissues. The causes of heart failure are many, and some are consistent with Jon's history of angina pectoris, myocardial infarction, and longstanding hypertension with left ventricular hypertrophy. Although one can speculate that the recent change in propranolol with its adverse effect on inotropic function (beta blocker) may have compromised his left ventricular function. it is not likely without some evidence of his dependence on a sympathetic drive to maintain his cardiac function.
Jon complained of weakness, cough, dyspnea on exertion (DOE), nausea, loss of appetite, and paroxysmal nocturnal dyspnea (PND). Clinically, symptoms have been divided into those reflecting failure of the right or of the left ventricles or both. In right ventricle failure. the venous blood pools in the intestine causing gastrointestinal (GI) complaints (e.g.. nausea, loss of appetite, and bloating) and in the lower extremities causing pedal edema. When only the left ventricle fails, fluid accumulates in the lungs creating exertional shortness of breath and a non-productive cough, which sometimes is the initial complaint especially in the elderly. When Jon engaged in the activities of daily living, his heart could not supply enough oxygen-rich blood and he became short of breath (SOB). During sleep, fluid collected and redistributed to his lungs, causing him to awaken short of breath (i.e., paroxysmal nocturnal dyspnea). He also reported that he felt some relief in the semi-inclined position with his head elevated (i.e., orthopnea). Many patients with left ventricular failure report sleeping on pillows (e.g., 2 or 3 pillow orthopnea) with a fan blowing in their face or next to an open window to help them breathe.
In Jon, exam findings consistent with left ventricular failure include S3 gallop, bilateral diffuse moist crackles, wheeze, and an enlarged left ventricle evidenced by the PMI located at the level of the 6th intercostal space at the anterior axillary line, well outside its normal limits (i.e., 5th intercostal space, medial to midclavicular line). Left ventricular hypertrophy is noted on the ECG. Hypertension leads to left ventricular hypertrophy which leads to congestive heart failure. Exam findings consistent with right ventricular failure include positive hepatojugular reflux (which, combined with elevated liver enzymes, suggests hepatic congestion), hepatomegaly, jugular vein distention, and pitting pretibial edema to the knees. The Cheyne-Stokes pattern of breathing and peripheral cyanosis signify hypoxia (e.g., peripheral and central) and may or may not be present with congestive heart failure depending upon the severity of the failure.
Jon had several physical findings suggesting CHF. His heart was tachycardic (i.e., 120 beats/min) which was in response to sympathetic stimulation to supply more tissue oxygen.
Cheyne-Stokes respiratory pattern may be found in CHF and other diseases or drug-induced respiratory depression. Jon was breathing in a cyclic pattern of deep breathing followed by a period of apnea. As the heart enlarges. the apical impulse shifts to the left chest wall.
In the failing heart, rapid left ventricular filling accentuates the third heart sound. If the heartbeats are rapid, the sounds simulate a galloping horse. With less effective heart pumping, fluid accumulates in the lung bases (e.g., crackles) and sometimes wheezing may be heard. Engorgement of the liver is felt extending below the right costal margin. The neck jugular veins are distended. Firm hepatic palpation squeezes excess blood up the jugular vein, confirming hepatojugular reflux (HJR). Extracellular fluid is palpated in the ankles, extending up the legs. Poor blood oxygenation makes the skin appear bluish-purple (cyanosis). Jon demonstrated signs and symptoms of both right and left ventricle failure.
Management. The key to management of CHF is to reduce the workload on the heart, specifically to reduce the preload and afterload. This is accomplished by reducing intravascular volume with diuretics and restriction of fluids and salt. Further reduction of afterload with vasodilation is employed in some cases. Work of the heart is improved by increasing oxygenation, increasing inotropic forces, and decreasing preload and afterload. There are many different ways to manage CHF with various drug combinations. Decreasing intravascular volume and improving the cardiac output (i.e., work of the heart) would result in fluid moving from the alveoli of the lungs (e.g., crackles), the liver (e.g., hepatomegaly), the soft tissues (e.g.. pitting edema), the intravascular space (e.g., jugular distention, hepatojugular reflux) as diuresis occurs. With reversal of failure, the S3 gallop should disappear. The left ventricular hypertrophy will not change. Tissue oxygenation should improve with reversal of findings related to hypoxia.
Early treatment for a failing heart includes rest, along with restricted intake of fluids and salt. Sometimes, simply limiting activity can provide relief. The patient should rest in bed with the head of the bed elevated at 30°. Reassuring the patient often is calming and provides some relief. Diuresis can reduce excessive vascular volume, and water and salt must be consumed in moderation. Minor sodium restriction (e.g., avoiding salty foods and not adding salt during or after cooking) frequently is helpful. Daily fluid intake and output should be recorded.
If necessary, a diuretic is added to excrete excess fluid and control daily fluid buildup. The patient should be weighed daily at first and then periodically to judge response. Until symptoms improve, the patient should lose about 1 kg daily.
Furosemide was started in Jon. because a prompt diuresis was desirable to give quick symptomatic relief. Furosemide, a loop diuretic, diminishes vascular volume which reduces peripheral and pulmonary edema. It also reduces preload by vasodilation.
