Congestive heart failure pathophysiology: Difference between revisions
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==Pathology== | ==Pathology== | ||
== | ==Microscopic Pathology== | ||
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] | [http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] |
Revision as of 03:40, 2 November 2011
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 could result from an abnormality of any one of the anatomical structures of the heart; the pericardium, myocardium, endocardium or 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.
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.
- 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.
Pathology
Microscopic Pathology
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HEART: Congestive heart failure, hydropic change
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HEART: Congestive heart failure, hydropic change
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HEART: Congestive heart failure, hydropic change
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HEART: Congestive heart failure, hydropic change
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HEART: Congestive heart failure, hydropic change
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HEART: Congestive heart failure, hydropic change
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Lung, congestion, heart failure cells (hemosiderin laden macrophages)
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Lung, Congestive Heart Failure, bone marrow embolus
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Lung, pulmonary edema in patient with congestive heart failure due to heart transplant rejection
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HEART: Congestive heart failure, hydropic change
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HEART Congestive heart failure, hydropic change
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Spleen, congestion, congestive heart failure