Factors influencing pressure (P)
- Blood pressure. Intrachamber (left/right ventricular) pressure during systolic ejection is very close to the pressure in the aorta or pulmonary trunk. That means, in cases of systemic or pulmonary hypertension, elevation in ventricular pressure will automatically increase afterload. And visa versa, reduction in blood pressure will reduce afterload.
- Valvular stenosis interferes with chamber empting and causes accumulation of blood with subsequent increase in pressure (and volume)
- Congenital heart defects. E.g., atrial and ventricular septal defects, and patent ductus arteriosus increase pressure (and volume) load on the right chambers
- Valvular insufficiency leads to reverse blood flow with an increase in chamber volume
- Dilated cardiomyopathy
- Valvular stenosis (see above)
- Congenital heart defects (see above)
- Myocardial hypertrophy with an increase in sarcomere mass and reduction of wall stress
- Physiologic myocardial hypertrophy seen in athletes
- Pathologic myocardial hypertrophy as a compensatory process in patients with cardiovascular diseases, e.g., systemic hypertension
- Ventricular aneurysm, e.g., in old MI, with sclerosis and thinning of the wall
- Advanced heart failure with volume overload (thinning of the myocardial wall)
Amendment: Pharmacologic correction of afterload
- Vasodilators: reduction of blood pressure with subsequent afterload decrease
- Beta-blockers
- ACEI/ARBs
- Nitrites: potent venodilators, used in acute heart failure (e.g., pulmonary edema) to reduce preload
- Human BNP analogs: vasodilatory and diuretic effects
- Diuretics: reduction of volume of circulating blood and blood pressure with subsequent diminishing in afterload
- + preload reduction
To be continued
2 comments:
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