Heart patient intervention.
Most commonly, HF is classified as low cardiac output (CO) secondary to impaired cardiac function. It also can be classified as high output, with an inordinate increase in the body's metabolic demands leading to an increase in CO of a normally functioning heart.
HF is characterized by progressive fatigue, shortness of breath, cough and pulmonary congestion, which are related to the inadequate perfusion of vital organs during exertion and often to the retention of fluid. The condition's primary cause is an impairment of the heart's ability to fill or empty the left ventricle properly.
The growing prevalence of HF, in part, may be related to better treatment of patients with acute myocardial infarctions (MI), or heart attacks, who survive only to develop HF later in life. It may also be due to the increasing proportion of older adults who have ever received the diagnosis. HF affects adults over age 60 who have other comorbidities such as coronary artery disease (CAD), renal insufficiency, and diabetes.
Ischemic HF accounts for 70% of the cases caused by CAD, hypertension and dilated cardiomyopathy. HF also can be designated as non-ischemic, caused by hypertension, viral illnesses, thyroid disease, excessive alcohol use, familial congenital disease and valvular disorders.
In addition, HF can be classified based on the main component of the cardiac cycle leading to impaired ventricular function. Abnormal ventricular filling (diastolic dysfunction) and/ or ventricular contraction (systolic dysfunction) can result in a decrease in CO leading to HF symptoms. Most HF is associated with left ventricular systolic dysfunction evidenced by a reduced ejection fraction (EF). Some patients have a combination of both systolic and diastolic dysfunction.
Several drugs have been shown to precipitate or exacerbate HF. Agents causing negative inotropic effect including antiarrhythmics (e.g. disopyramide) and calcium channel blockers (e.g. verapamil). Certain chemotherapy agents--such as doxombicin, daunomycin and cyclophosphamide --may be toxic to the myocardium. Lastly, agents that cause sodium and water retention--including NSAIDs, COX-2 inhibitors, glucocorticoids, androgens, estrogens, salicylates and thiazolidinedione--can also exacerbate HF.
Nonpharmacologic management modalities are crucial for patients to adopt in self-management of HF. These strategies may include dietary modification, such as sodium and fluid restriction; risk factor reduction, such as smoking cessation; timely immunization; oxygen supplementation; supervised regular physical activity; and management of such concomitant conditions as sleep apnea, insomnia, depression and sexual dysfunction.
Patients should be urged to keep a daily log of their weight and bring it to each clinical visit. Those with a weight gain of three pounds in a day or five pounds over five days should be referred to their HF care provider, especially if they are symptomatic.
Dietary sodium restriction (2 to 3 grams daily) is recommended for patients with mild to moderate symptoms, and further restriction (2 grams daily) should be considered in severe HF. Restriction of daily fluid intake to 2 liters is recommended in patients with severe hyponatremia (serum sodium <130 mEq/L) and should be considered for all patients demonstrating fluid retention that is difficult to control despite high doses of diuretic and sodium restriction.
Finally, pneumococcal and annual influenza vaccinations are recommended in all patients with HF in the absence of known contraindications.
Pharmacologic treatment is focused on agents that relieve symptoms only (e.g. diuretics) and that modify the course of the disease (renin-angiotensin-aldosterone inhibitors). In early stages, antihypertensives and lipid-lowering agents should be utilized when appropriate to decrease stroke and MI in HF.
The goal for those with mild to moderate HF is to prevent or slow disease progression by interfering with the neurohormonal pathways that cause cardiac damage. In such patients, ACE inhibitors or ARBs and beta-blockers are the mainstay of therapy. In patients with more advanced HF (EF <40%), the goal is to reduce fluid retention, minimize disability, and reduce the risk of hospitalization and death. In such patients, treatment focuses on a combination of loop diuretics and neurohormonal antagonists. Aldosterone antagonists and digoxin are often added as cardiac function declines. Patients intolerant to ACE inhibitors from hyperkalemia or renal insufficiency are likely to experience the same side effects with ARBs. hi these cases, the combination of hydralazine and an oral nitrate should be considered.
Pharmacists can play a crucial role in the management of HF patients. Pharmacists can identify potential reversible causes of HF exacerbations, including prescription and nonprescription drug therapies, dietary indiscretions and medication adherence. Pharmacists in community and ambulatory care settings also can identify patients not following their therapy and provide timely feedback and patient education.
Darrell Hulisz, R.Ph., Pharm.D., is associate professor of family medicine at the Case Western Reserve University School of Medicine. Lubna Kousa, M.S., is a pharmacy intern at the University of Findlay.