Congestive heart failure pathophysiology

Congestive Heart Failure Microchapters
Home
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
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
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

• Cardiac output can be maintained if LV dilation occurs and stroke volume is preserved even though the LVEF is low.
• As LV dilation occurs, functional mitral regurgitation (MR) may develop despite an anatomically normal mitral valve.
• The ejection fraction is usually below 35% in symptomatic patients.
• 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 at lower pressures.
• Hypoperfusion at rest is suggested by cool extremities, altered mentation, and declining renal function.
• As part of the diagnostic maneuvers check the serum TSH and iron levels. Check TSH particularly in those e patients treated with amiodarone.
• Decompensation; most often is non compliance with therapeutic regimens.
• Atrial fibrillation is a major target of therapy. It occurs in 20% of patients with congestive heart failure.

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

• 
  HEART: Congestive heart failure, hydropic change
• 
  HEART Congestive heart failure, hydropic change
• 
  Spleen, congestion, congestive heart failure