Cardiology Flashcards
Define stroke volume, preload, contractility, and afterload.
SV = EDV - ESV, and depends on preload, contractility, and afterload.
Preload is the left ventricular end-diastolic pressure = the pressure required to distend the ventricle to its EDV
Contractility is the stroke work generated at a given preload, and describes the inotropic state of the myocardium. By the Frank-Starling law, as preload increases, contractility also increases. The inotropic state is quantified by ejection fraction (EF = SV/LVEDV).
Afterload is the resistance against which the heart contracts, usually measured as systolic BP.
What happens to preload, contractility, and ejection fraction in systolic heart failure?
The heart usually has decreased contractility, so a poorer inotropic state, and there is a lower ejection fraction. To maintain the same stroke volume at a lower EF, since EF = SV/LVEDV, LVEDV must increase, which would increase the preload (LVEDP). This is hard to do, and SV normally ends up decreasing because LVEDV does not increase ENOUGH. Decreased SV means there is decreased cardiac output.
With decreased cardiac output in systolic heart failure, how does the RAAS and sympathetic nervous system respond?
RAAS and sympathetics respond to increase preload through mechanisms including vasoconstriction for a higher afterload, salt and fluid retention for a higher preload, and then myocardial hypertrophy in order to help decrease stress on the wall of the LV. The LVEDP increases, which leads to production of BNP from the ventricles, since BNP usually decreases systemic resistance and causes natriuresis. Ultimately, this process spirals into dilatation of the ventricles and ventricular failure.
What is the physiologic abnormality in diastolic heart failure, and what does that do to contractility, preload, and afterload?
The ventricle has decreased compliance, so the heart does not fill with blood as easily, leading to a high LVEDP (preload) at a given EDV. That pressure backs up into the pulmonary vasculature, leading to pulmonary congestion. Contractility is normal or can be increased to compensate. Afterload may be high, especially if hypertension is the underlying cause.
