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

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

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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

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.
  • EKG often shows low voltage. The differential diagnosis of low voltage on the EKG includes amyloid.
  • Poor R wave progression in the precordial leads and LBBB are both common with both ischemic and non-ischemic causes.
  • Since the LV often dilates in the anteroposterior direction, the cardiac silhouette may appear deceptively normal. Once the heart failure is advanced, the enlarged right ventricle forms the left border of the cardiac silhouette.
  • The presence of enlargement of vessels to the upper lobes, per bronchial cuffing, and pulmonary interstitial and alveolar edema are all indicative of pulmonary venous hypertension.
  • 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.

References

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