Systolic heart failure is a failure of the heart to work well as a pump. Your Physician Assistant Exam will expect you to know about this type of heart failure. On an echocardiogram, you see this failure as a reduced ejection fraction. Assuming that the heart has a normal ejection fraction of 65 percent, anything less than 50 percent is thought to represent some degree of a pump problem.
Common causes of systolic heart failure include ischemia due to CAD (that is, an ischemic cardiomyopathy), hypertension, and other causes of cardiomyopathy, especially a dilated cardiomyopathy (which you read about later in “Muscling In on the Cardiomyopathies”).
On the PANCE, you’ll be asked not only about the medications for treating systolic heart failure but also about key side effects and potential drug-drug interactions. Here’s a list of meds typically used in treating systolic heart failure:
Furosemide: Furosemide (Lasix) is used to help treat the volume overload and pulmonary edema associated with congestive heart failure. It can be given intravenously or orally. Before it does its main job — facilitating a diuresis — it works in the pulmonary circulation to decrease preload. Side effects of this medication and other loop diuretics include hypokalemia, hypomagnesemia, and metabolic alkalosis.
ACE inhibitors and ARBs: Angiotensin converting enzyme inhibitors and angiotensin receptor blockers prolong morbidity and mortality in systolic CHF. The medications can cause remodeling of cells of the left ventricle and decrease left ventricular hypertrophy. Side effects include a cough and hyperkalemia. An uncommon side effect of an ACE inhibitor is angioedema. If used, you need to check a blood chemistry panel for the serum creatinine and potassium levels.
Digoxin: Digoxin (Lanoxin) improves systolic heart failure symptoms and morbidity, but it doesn’t improve mortality. In CHF, digoxin has been shown to help reduce sympathetic tone. This medication is also an atrioventricular nodal blocker that can be used in managing rate control for atrial fibrillation. Digoxin is renally eliminated, so in cases of chronic kidney disease or acute kidney failure, the dosing needs to be greatly reduced or held.
Watch for symptoms of digoxin toxicity. When the digoxin level is very high, symptoms of toxicity include nausea, vomiting, dizziness, and palpitations. On an ECG, you can see many types of arrhythmias, including junctional rhythm. The most common arrhythmia you see with digoxin toxicity is paroxysmal atrial tachycardia with block.
Note that hypercalcemia can make digoxin toxicity worse, as can hypokalemia. You treat digoxin toxicity by using Fab antibody fragments (Digibind) that bind digoxin. Because digoxin is heavily protein-bound, it can’t be removed by hemodialysis.
Beta blockers: Beta blockers are used in treating chronic systolic heart failure. They improve morbidity and mortality. They can reduce sympathetic tone, as can digoxin. Beta blockers also have a mortality benefit in treating the post-MI patient. Commonly prescribed medications include metoprolol (Lopressor) and carvedilol (Coreg).
Spironolactone: Spironolactone (Aldactone) is added after a person is on digoxin, an ACE inhibitor, a beta blocker, and a loop diuretic. Spironolactone can help with survival in patients with CHF. It also can help reverse left ventricular hypertrophy, as can an ACE inhibitor.
Spironolactone has to be carefully dosed in patients with a glomerular filtration rate (GFR) < 30 mL/min. It’s contraindicated in advanced kidney disease because it can cause hyperkalemia. The kidney function and potassium levels need to be watched, especially if the person is also on an ACE inhibitor.
In general, treating heart failure involves more than just using the meds described here. The patient should get daily exercise and adhere to a diet that is low in sodium (1,500–2,000 mg/day limit) and high in fruits and vegetables. Fluid restriction is often recommended.
Avoiding medications like NSAIDs is also important, because they can cause high blood pressure and salt and water retention and can blunt the effect of loop diuretics. NSAIDs can also cause hyperkalemia and acute kidney failure.