Key Clinical Updates in Heart Failure
In patients with heart failure and preserved left ventricular ejection fraction (45% or greater), sacubatril/valsartan did not significantly improve the outcome of total heart failure hospitalizations and cardiovascular death in the PARAGONHF trial.
ESSENTIALS OF DIAGNOSIS
LV failure: Either due to systolic or diastolic dysfunction. Predominant symptoms are those of low cardiac output and congestion, including dyspnea.
RV failure: Symptoms of fluid overload predominate; usually RV failure is secondary to LV failure.
Assessment of LV function is a crucial part of diagnosis and management.
Optimal management of chronic heart failure includes combination medical therapies, such as ACE inhibitors, aldosterone antagonists, and beta-blockers.
Heart failure is a common syndrome that is increasing in incidence and prevalence. Approximately 6.5 million patients in the United States have heart failure, and there are around 960,000 new cases each year, with 8 million or more patients projected to have heart failure by 2030. Each year in the United States, 900,000 patients are discharged from the hospital with a diagnosis of heart failure. It is primarily a disease of aging, with over 75% of existing and new cases occurring in individuals over 65 years of age. Seventy-five percent of heart failure patients have antecedent hypertension. The prevalence of heart failure rises from less than 1% in individuals below 60 years to nearly 10% in those over 80 years of age.
Systolic function of the heart and resulting cardiac output is governed by four major determinants: the contractile state of the myocardium, the preload of the ventricle (the end-diastolic volume and the resultant fiber length of the ventricles prior to onset of the contraction), the afterload applied to the ventricles (the impedance to LV ejection), and the heart rate.
Cardiac function may be inadequate as a result of alterations in any of these determinants. The primary derangement is often depression of myocardial contractility caused either by loss of functional muscle (due to MI, etc) or by processes diffusely affecting the myocardium. However, the heart may fail as a pump because preload is excessively elevated, such as in valvular regurgitation, or when afterload is excessive, such as in aortic stenosis or in severe hypertension. Pump function may also be inadequate when the heart rate is too slow or too rapid. Whereas the normal heart can tolerate wide variations in preload, afterload, and heart rate, the diseased heart often has limited reserve for such alterations. Finally, cardiac pump function may be supranormal but nonetheless inadequate when metabolic demands or requirements for blood flow are excessive. This situation is termed high-output heart failure and, though uncommon, tends to be specifically treatable (eFigure 10–75). Causes of high output include thyrotoxicosis, severe anemia, arteriovenous shunting (including dialysis fistulas), Paget disease of bone, and thiamine deficiency (beriberi).
High-output heart failure secondary to ...