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Basic Pharmacology And Physiology Of Congestive Heart Failure (CHF) Drugs

October 23, 2020Category : Public Health
Basic Pharmacology And Physiology Of Congestive Heart Failure (CHF) Drugs

It has been estimated that 6.3 million Americans suffer from heart failure. Heart failure is a heterogeneous clinical syndrome stemming from cardiac overload and injury that leads to considerable morbidity and mortality.

Despite advances in diagnosis and treatment of heart failure (HF), it remains a growing disease state in the United States, annually affecting millions of people that causes well over a million hospitalizations, contributing to more than 50,000 deaths, and consuming billions of dollars in health care spending.

Although all segments of the population are affected, this growing burden of HF is especially evident in certain populations. This disease burden is further amplified by the fact that the beneficial impact of new treatment advances has been limited by slow penetration of evidence‐based therapy into the broader community setting of clinical practice.

This too is especially evident in certain special populations. Thus, the health and economic burden of HF continues to grow and affects certain underserved populations in a disproportionate manner.

 Cognitive impairment has been described as a consequence of heart failure in numerous studies spanning the last three decades. When optimal medical therapy and cardiological interventions have failed to improve a patient’s condition, surgical intervention may be a valid option in order to improve cardiac function. Surgical treatment of end-stage chronic heart failure encompasses different treatment modalities like surgical revascularization of ischemic territories using coronary artery bypass grafting (CABG), alleviating functional mitral valve insufficiency (using restrictive mitral annuloplasty) and reconstructing left ventricular geometry and thereby improving contractility in patients that suffered from a large myocardial infarction resulting in a scarred and dilated left ventricle.

Ultimately, left ventricular function can be replaced by performing orthotopic heart transplantation or by implantation of a left ventricular assist device (LVAD). These surgical options have improved clinical outcome.

 Unfortunately, heart failure surgery is associated with an increased risk on vasoplegia, also named vasodilatory shock. This syndrome is characterized by hypotension and the continuous need of vasopressors, despite a normal or high cardiac index. The incidence of vasoplegia ranges from 11 to 31% in patients undergoing heart failure surgery.

The prognosis of vasoplegia is poor. Prolonged hypotension and the accompanying hypoperfusion lead to end-organ dysfunction and is associated with an increased morbidity. An earlier study showed that the 90-day survival rate after heart failure surgery is decreased in vasoplegic patients compared with non-vasoplegic patients

The remodeling process initiates an inexorable cycle of worsening left ventricular function, leading to progressive cardiac enlargement, increased hemodynamic and wall stresses, mitral valve dysfunction, further maladaptive neurohormonal activation, and ventricular irritability, all of which beget progressive cardiac dysfunction, sudden cardiac death and, ultimately, end‐stage HF and pump failure death.

This process may be associated with impaired systolic function, as evidenced by reduced left ventricular ejection fraction (LVEF); with normal to mildly impaired LVEF with or without diastolic abnormalities; or with what is considered to be essentially preserved ejection fraction, generally defined clinically as LVEF ≥40%, and presumably with abnormalities of relaxation (“diastolic dysfunction”). Myocardial (ventricular) remodeling is described as being either physiological or pathological.

Patients must initially be taught that heart failure is a chronic and ongoing disease to comprehend the need for lifestyle changes and management of life problems.

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Randomized controlled trials have demonstrated the benefits of guideline-directed medical therapy in the outpatient setting for treatment of chronic heart failure. However, the benefits of continuation (or discontinuation) of major chronic heart failure therapies when treating acute heart failure during hospitalization are less clear.

Real and anticipated worsening renal function, hyperkalemia and hypotension are the three major reasons for discontinuation of renin-angiotensin-aldosterone system inhibitors during hospitalization, and a failure to resume renin-angiotensin-aldosterone system inhibitors before discharge could worsen cardiovascular outcomes.

 Available data, mostly observational, shows that continuation or initiation of renin-angiotensin-aldosterone system inhibitors appears efficacious, safe, and well tolerated in majority of acute heart failure patients during hospitalization.

Worsening renal function portends poor prognosis only if associated with congestion in acute heart failure, and clinicians should not de-escalate diuretic therapy routinely for worsening renal function. Because adherence is a key determinate of clinical outcomes, promoting patient adherence with medications is a major focus for clinicians working with patients with heart failure. Various diagnostic tests are explained as well as the treatment of heart failure. Treatment includes pharmacologic, nonpharmacologic, and surgical interventions.

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