Congestive heart failure pathophysiology

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Congestive Heart Failure Microchapters

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Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Systolic Dysfunction
Diastolic Dysfunction
HFpEF
HFrEF

Causes

Differentiating Congestive heart failure from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Clinical Assessment

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

Cardiac MRI

Echocardiography

Exercise Stress Test

Myocardial Viability Studies

Cardiac Catheterization

Other Imaging Studies

Other Diagnostic Studies

Treatment

Invasive Hemodynamic Monitoring

Medical Therapy:

Summary
Acute Pharmacotherapy
Chronic Pharmacotherapy in HFpEF
Chronic Pharmacotherapy in HFrEF
Diuretics
ACE Inhibitors
Angiotensin receptor blockers
Aldosterone Antagonists
Beta Blockers
Ca Channel Blockers
Nitrates
Hydralazine
Positive Inotropics
Anticoagulants
Angiotensin Receptor-Neprilysin Inhibitor
Antiarrhythmic Drugs
Nutritional Supplements
Hormonal Therapies
Drugs to Avoid
Drug Interactions
Treatment of underlying causes
Associated conditions

Exercise Training

Surgical Therapy:

Biventricular Pacing or Cardiac Resynchronization Therapy (CRT)
Implantation of Intracardiac Defibrillator
Ultrafiltration
Cardiac Surgery
Left Ventricular Assist Devices (LVADs)
Cardiac Transplantation

ACC/AHA Guideline Recommendations

Initial and Serial Evaluation of the HF Patient
Hospitalized Patient
Patients With a Prior MI
Sudden Cardiac Death Prevention
Surgical/Percutaneous/Transcather Interventional Treatments of HF
Patients at high risk for developing heart failure (Stage A)
Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B)
Patients with current or prior symptoms of heart failure (Stage C)
Patients with refractory end-stage heart failure (Stage D)
Coordinating Care for Patients With Chronic HF
Quality Metrics/Performance Measures

Implementation of Practice Guidelines

Congestive heart failure end-of-life considerations

Specific Groups:

Special Populations
Patients who have concomitant disorders
Obstructive Sleep Apnea in the Patient with CHF
NSTEMI with Heart Failure and Cardiogenic Shock

Congestive heart failure pathophysiology On the Web

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US National Guidelines Clearinghouse

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FDA on Congestive heart failure pathophysiology

CDC on Congestive heart failure pathophysiology

Congestive heart failure pathophysiology in the news

Blogs on Congestive heart failure pathophysiology

Directions to Hospitals Treating Congestive heart failure pathophysiology

Risk calculators and risk factors for Congestive heart failure pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Saleh El Dassouki, M.D [3], Atif Mohammad, MD

Overview

Heart failure may result from an abnormality of any one of the anatomical structures of the heart; the pericardium, the myocardium, the endocardium, valvular heart disease or disorders of the great vessels. Heart failure was once thought to be secondary to a depressed left ventricular ejection fraction. However, studies have shown that approximately 50% of patients who are diagnosed with heart failure have a normal ejection fraction (diastolic dysfunction). Patients may be broadly classified as having heart failure with depressed left ventricular ejection fraction (systolic dysfunction) or normal/preserved ejection fraction (diastolic dysfunction). Systolic and diastolic dysfunction commonly occur in conjunction with each other.

Pathophysiology

  1. Dilation of the left ventricle to increase the stroke volume and
  2. Increase in heart rate
  • Dilation of the left ventricle increases volume and increases contractility up to a point (see Frank-Starling law of the heart). As further LV dilation occurs, however, functional mitral regurgitation (MR) may develop despite an anatomically normal mitral valve.
  • Left ventriular enlargment and lack of forward cardiac output can lead to left atrial enlargement. Left atrial dilation may lead to atrial fibrillation which occurs in 20% of patients with congestive heart failure. Atrial fibrillation diminishes left ventricular filling through the loss of the atrial kick (the atrial contraction) and due to an increase in the heart rate which reduces the time available for the left ventricle to fill.
  • The reduction in forward cardiac output leads to a rise in the pulmonary capillary wedge pressure. Rales usually develop if the pulmonary capillary wedge pressure is >25 mm Hg. Rales may not be present in the patient with chronic heart failure. Rales may develop at even lower pressures if LV function deteriorates suddenly.
  • Dyspnea and orthopnea occur due to interstitial edema within the lungsat lower pressures.
  • The reduction in forward cardiac output leads to hypoperfusion at rest which is suggested by cool extremities, altered mentation, and declining renal function.

Pathology

Microscopic Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology




References

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