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Pathophysiology of Heart Failure
Divided into systolic and diastolic dysfunction.
Systolic Dysfunction: heart failure that results from an abnormality of ventricular emptying. Results in decreased ability of ventricle to eject blood
Caused by impaired contractility or excessive afterload
Accounts for 2/3 of heart failure
Conditions that impaire CTY: MI, myocardial ischemia, volume overload (MR and AR),
Conditions that increase afterload: Aortic stenosis and hypertension
Etiology: Impaired contractility is caused by:
destruction of myocytes
abnormal myocyte function
Increased afterload is caused by pressure overload, which ↑ resistance to flow
Pathophysiology: a decrease in contractility causes a decrease in SV and an increase in end-systolic volume and pressure. During the next cardiac cycle, the ventricle receives a normal amount of blood from the lungs, resulting in an increased end-diastolic volume and pressure (increased preload.) Increased preload results in an increase in SV (Frank- Starling) and a reduction in end-systolic volume. However, increased preload cannot completely compensate for the decreased CTY and ejection fraction, so end-systolic volume remains higher than normal. The increased diastolic pressure is transmitted to the LA and the pulmonary veins and capillaries. If pulmonary capillary hydrostatic pressure rises above 20mmHg, then fluid collects in the interstitum of the lungs and causes pulmonary congestion.
↓ CTYÆ ↓ SVÆ ↑↑ ESVÆ ↑↑ preload Æ ↑ SVÆ ↓ ESV. However, ESV is still higher than normal, therefore: ↑ EDP and VÆ ↑ pulm hydrostatic P Æ congestion
For increased afterload, increased resistance to flow results in pressure overload, which causes a decrease in stroke volume and an increase in end-systolic volume and a subsequent increase in end-diastolic volume and pressure. Leads to increased pulmonary capillary hydrostatic pressure and pulmonary congestion.
↑ afterloadÆ ↑ resistanceÆ ↓ SVÆ ↑ ESVÆ ↑ EDV/ PÆ ↑ pulm hydrostatic PÆ congestion