Michael Roscoe is Chair/Program Director and Associate Professor, Andrew Lampkins is Associate Professor, Sean Harper is Assistant Professor, and Gina Niemeier is Associate Program Director and Assistant Professor, in the PA Department at the University of Evansville in Indiana.
The authors have no financial relationships to disclose.
The body’s neurohormonal system, including the RAAS and the sympathetic nervous system, is activated to compensate for the insufficient cardiac performance found in HF. However, activation of these systems contributes to worsening HF, deterioration of quality of life, and poor outcomes.22 Therefore, therapies that suppress these responses can reduce the progression of HF.
Treatment of HF is generally divided into symptom-relieving treatment and disease-modifying/life-prolonging treatment.1 Symptom relief is similar in both systolic and diastolic HF. However, most evidence-based, disease-modifying treatment focuses on systolic HF; guidelines for disease-modifying treatment of diastolic HF are minimal.1
Treatment of reversible causes
Since HF is caused by something else, the primary focus of management is addressing underlying causes. The primary goal is to relieve symptoms while improving functional status—which should lead to a decrease in hospitalization and premature death.
The first step is to evaluate patients’ use of medications that can contribute to a worsening of HF.9 The most common offending medications are calcium-channel blockers with negative inotropy (non-dihydropyridine calcium-channel blockers, eg, verapamil and diltiazem); some antiarrhythmic drugs (eg, amiodarone); thiazolidinediones (glitazones); and NSAIDs.9 If identified as a possible contributor to HF symptoms, these agents should be stopped (if possible) or replaced.
Nonpharmacotherapy
Effective counseling and education of patients with HF may help with long-term adherence to treatment plans. Patients can be taught to monitor their weight at home and to adjust the dosage of diuretics as advised: A sudden increase in weight (> 2 kg in one to three d), for example, should alert a patient to alter treatment or seek advice.23
Diet modificationis a multifactorial recommendation. Proper nutrition is critical because HF patients are at increased risk for malnutrition due to poor appetite, malabsorption, and increased nutritional requirements.23 Weight reduction in obese patients helps reduce cardiac workload. Patients should be placed on salt restriction (2 to 2.6 g/d of sodium).9,23
Exercisehas been shown to relieve symptoms, provide a greater sense of well-being, and improve functional capacity. It does not, however, result in obvious improvement in cardiac function.22
Alcohol consumption should be restricted because of the myocardial depressant properties of alcohol and its direct toxic effect on the myocardium.22 Smokingshould be discouraged because it has a direct effect on coronary artery disease.
Influenza and pneumococcal vaccination should be considered in all patients with HF.23 Heart failure predisposes patients to, and can be exacerbated by, pulmonary infection and exacerbation of chronic obstructive pulmonary disease.
Evaluation and management of obstructive sleep apnea should be performed. Sleep-disordered breathing, an umbrella term that covers obstructive and central sleep apneas, has been found to increase the risk for poor prognosis in HF.24 All patients with HF should be tested for obstructive sleep apnea because, often, only the patient’s bed partner is aware of disordered sleep. For unknown reasons, patients with HF do not report subjective sleepiness.25
