Congestive heart failure pathophysiology

	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
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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
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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

Underlying Anatomic Abnormalities

Heart failure may result from an abnormality of any one of the anatomical structures of the heart:

Pericardium
Myocardium
Endocardium
Valvular heart disease or
Disorders of the great vessels (e.g. pulmonary hypertension)

Systolic versus Diastolic Dysfunction

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

In heart failure, there is a failure of blood to move forward (forward failure) and a tendency of blood to move back ward (backward failure).
Normally, with respect to the left side of the heart, blood flows from the lungs, into the pulmonary veins, into the left atrium, through the mitral valve, and finally into the left ventricle. When the left ventricle cannot be normally filled during diastole, blood will back up into the left atrium and, eventually, into the lungs. The result is a higher than normal pressure of blood within the vessels of the lung. As a result of hydrostatic forces, this high pressure leads to leaking of fluid (i.e. transudate) from the lung's blood vessels into the air-spaces (alveoli) of the lungs. The result is pulmonary edema, a condition characterized by difficulty breathing, inadequate oxygenation of blood, and, if severe and untreated, death.

Compensatory Mechanisms

Left ventricular systolic dysfunction is associated with a reduction in stroke volume, the amount of blood the heart ejects with each heart beat.
The reduction in stroke volume leads to a reduction in cardiac output which is the stroke volume multiplied by the heart rate.
There are two compensatory mechanisms to preserve forward cardiac output (the product of stroke volume and heart rate):

Dilation of the left ventricle to increase the stroke volume and
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, contractility drops, and functional mitral regurgitation (MR) may develop despite an anatomically normal mitral valve.
Left ventricular enlargement 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.

Pulmonary Edema

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 lungs at lower pressures.

End Organ Hypoperfusion

The reduction in forward cardiac output leads to hypoperfusion at rest which is suggested by :*cool extremities

confusion and altered mentation
Impaired renal perfusion 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

HEART: Congestive heart failure, hydropic change
HEART: Congestive heart failure, hydropic change
HEART: Congestive heart failure, hydropic change

HEART: Congestive heart failure, hydropic change
HEART: Congestive heart failure, hydropic change
HEART: Congestive heart failure, hydropic change

Lung, congestion, heart failure cells (hemosiderin laden macrophages)
Lung, Congestive Heart Failure, bone marrow embolus
Lung, pulmonary edema in patient with congestive heart failure due to heart transplant rejection