ICU Primary PrepCast Epi 89 - ICU Primary Snippet 32 - Effect of sudden and sustained increase in afterload on LV.
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May 7, 2024 Exploring the impact of sudden and sustained increase in afterload on the Left ventricle, including volume, pressure, work, coronary perfusion, reflexes, heart rate, and cardiac output. Importance of structured thinking in medical scenarios and using a structured approach to problem-solving.
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Acute Afterload Raises Volumes, Then Frank‑Starling Compensates
- A sudden increase in afterload reduces myocyte shortening velocity, causing early aortic valve closure and lower stroke volume.
- Increased end-systolic and end-diastolic volumes recruit the Frank-Starling mechanism to restore stroke volume in a healthy left ventricle.
Afterload Raises Myocardial Work and Ischemia Risk
- Increasing afterload raises myocardial oxygen demand and myocardial work acutely.
- Coronary autoregulation matches flow initially but sustained afterload risks subendocardial ischemia from hypertrophy.
Baroreflex Determines Net Heart Rate Response
- Baroreceptor reflexes only activate if afterload elevation raises arterial pressure, and then reduce sympathetic drive.
- Heart rate may increase or decrease depending on whether stroke volume falls (low BP) or arterial pressure rises (baroreflex-mediated slowing).