cardio 267 Flashcards
Stroke volume
stroke volume affected by contractility, After-load and Preload.
SV increases:
increase contractility(e.g. anxiety, exercise)
decrease pre load(e.g early pregnancy)
decrease after-load
A failing heart has decrease SV(systolic and/or diastolic dysfunction
Contractility
contractility and(SV) increases with: catecholamines(inhibition of phospholamban--increase Ca2+ entry into sarcoplasmic reticulum--increase Ca2+ induced Ca2+ release) increase intracellular Ca2+ decrease extracellular Na+( decrease activity of Na+/Ca2+ exchanger) Digitalis (blocks Na+/K+ pump)-- increase intercellular Na+--decrease Na+/Ca2+ exchanger activity--increase intracellular Ca2+)
contractility
contractility and (SV) decreases with Beta blockade (decrease cAmp) HF with systolic dysfunction Acidosis hypoxia/hypercapnia(decrease po2/increase pco2) non-dihydropyridine Ca2+ channel blockers
Pre-load
pre load approximated by ventricular EDV; depends on venous tone and circulating blood volume
Venodilators (e.g nitroglycerin) decreases pre load
After-load
After-load approximated by MAP
increase afterload- increase pressure-increase wall tension per laplaces law.
LV compensates for increase afterload by thickening( hypertrophy) in order to decrease wall tension
Vasodilators (e.g hydralazine) decrease aferload (arteria)
ACE inhibitors and ARBS decrease both pre load and after load.
chronic hypertension (increase MAP)–LV hypertrophy
Ejection fraction
EF=SV/EDV=EDV-ESV/EDV
left ventricular EF is an index of ventricular contractility; normal EF is > 55%
EF is decrease in systolic HF
EF is normal in diastolic HF
Myocardial oxygen demand
increase myocardial oxygen demand is increase by:
increase contractility
increase after load(proportional to arterial pressure)
increase heart rate
increase diameter of ventricle (increase wall tension)
wall tension follows laplace’s law
wall tension= pressure x radius/2 x wall tension
Starling curve
force of contraction is proportional to end- diastolic length of cardiac muscle fiber( pre load)
increase contractility with catecholamines, positive inotropes (eg, digoxin)
decrease contractility with loss of myocardium (eg, MI), beta-blockers(acutely, non- dihydropyridine Ca2+ channel blockers, dilated cardiomyopathy.