Congestive heart failure pathophysiology and etiology: Difference between revisions
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== Pathophysiology & Etiology== | == Pathophysiology & Etiology== | ||
*There are several general causes of heart failure. Heart failure may be of pericardial origin such as [[tamponade]] and [[pericardial constriction]], valvular such as aortic or [[mitral regurgitation]]; myocardial such as [[idiopathic dilated cardiomyopathy]], [[familial dilated cardiomyopathy]], [[ischemic cardiomyopathy]], and valvular cardiomyopathy; coronary vascular such as acute ischemic episodes, and rhythm disturbances such as [[tachycardia-induced heart failure]]. | *There are several general causes of heart failure. Heart failure may be of pericardial origin such as [[tamponade]] and [[pericardial constriction]], valvular such as aortic or [[mitral regurgitation]]; myocardial such as [[idiopathic dilated cardiomyopathy]], [[familial dilated cardiomyopathy]], [[ischemic cardiomyopathy]], and valvular cardiomyopathy; coronary vascular such as acute ischemic episodes, and rhythm disturbances such as [[tachycardia-induced heart failure]]. | ||
Revision as of 12:10, 10 June 2009
| Heart failure | |
| ICD-10 | I50.0 |
|---|---|
| ICD-9 | 428.0 |
| DiseasesDB | 16209 |
| MedlinePlus | 000158 |
| eMedicine | med/3552 |
| MeSH | D006333 |
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Pathophysiology & Etiology
- There are several general causes of heart failure. Heart failure may be of pericardial origin such as tamponade and pericardial constriction, valvular such as aortic or mitral regurgitation; myocardial such as idiopathic dilated cardiomyopathy, familial dilated cardiomyopathy, ischemic cardiomyopathy, and valvular cardiomyopathy; coronary vascular such as acute ischemic episodes, and rhythm disturbances such as tachycardia-induced heart failure.
- 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.
- Other secondary causes include anemia, obesity, drugs [(such as first generation calcium channel blockers, disopyramide, and sotalol, NSAIDs (may cause fluid retention), beta blockers (may cause heart failure with their negative inotropic effects)].