Heart Failure
Pathogenesis
Coronary Disease diminihes oxygen availability to the tissues
Hypertension makes the hearxt work harder.
Heart failure is due to dysfunction of normal relaxation and filling (diastolic HF) or contractile ability (systolic HF) of the ventricles.
The term “congestive” refers to abnormal fluid retention resulting from this loss of relaxation/contractility. [Explain How]
less frequent with the onset of right ventricular (RV) failure and tricuspid regurgitation.
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Heart failure occurs when cardiac output is inadequate to provide the oxygen needed by the body*.
HF can involve one or both sides of the heart. Right-sided failure results in increased systemic venous pressures and subsequent peripheral edema, while left-sided failure causes increased pulmonary venous pressures and subsequent pulmonary edema.
Two major types of failure may be distinguished.
Approximately 50% of younger patients have systolic failure, with reduced mechanical pumping action (contractility) and reduced ejection fraction (HFrEF).
The remaining group has diastolic failure, with stiffening and loss of adequate relaxation playing a major role in reducing filling and cardiac output. Ejection fraction may be normal (preserved, HFpEF) in diastolic failure even though stroke volume is significantly reduced. The proportion of patients with diastolic failure increases with age. Because other cardiovascular conditions (especially myocardial infarction) are now being treated more effectively, more patients are surviving long enough for heart failure to develop, making heart failure one of the cardiovascular conditions that is actually increasing in prevalence in some countries.
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Heart failure is a progressive disease that is characterized by a gradual reduction in cardiac performance, punctuated in many patients by episodes of acute decompensation, often requiring hospitalization. Treatment is therefore directed at two somewhat different goals: (1) reducing symptoms and slowing progression as much as possible during relatively stable periods and (2) managing acute episodes of decompensated failure. These factors are discussed in Clinical Pharmacology of Drugs Used in Heart Failure.
Although it is believed that the primary defect in early systolic heart failure resides in the excitation-contraction coupling machinery of the myocardium, the clinical condition also involves many other processes and organs, including the baroreceptor reflex, the sympathetic nervous system, the kidneys, angiotensin II and other peptides, aldosterone, and apoptosis of cardiac cells. Recognition of these factors has resulted in evolution of a variety of drug treatment strategies (Table 13–1) that constitute the current standard of care.