Cardiovascular Effect of Volatile Anesthetics Flashcards
Cardiovascular Effects of Volatile Anesthetics: dose dependent myocardial depression
- alterations in intracellular Ca homeostasis
- inhibition of Na/Ca exchange
- LV diastolic dysfunction?
- LV after load effects
- LA myocardial depression
Cardiovascular Effects of Volatile Anesthetics: dose dependent decrease in SBP
- halothane and enflurane reduce myocardial contractility and cardiac output
- isoflurane, desflurane and seovflurane decrease arterial blood pressure primarily as a result of reductions in LV after load
Cardiovascular Effects of Volatile Anesthetics:SVR
decrease
Cardiovascular Effects of Volatile Anesthetics: direct negative chronotropic effects
- depress SA node
- baroreceptor reflex activity
Cardiovascular Effects of Volatile Anesthetics: SA node discharge
all agents slow rate of SA discharge via direct and indirect effects on SA node automaticity
-potential to produce bradycardia and AV conduction abnormalities
Cardiovascular Effects of Volatile Anesthetics: arrhythmogenicity
- halothane, enflurane, and isoflurane are cardioprotective against ventricular fibrillation reduced by coronary artery occlusion and repercussion
- halothane to a lesser extent, other volatile anesthetics sensitize myocardium to the arrhythmogenic effects of epinephrine
- des, iso, and sevo do not sensitive the heart to ventricular extra systoles
Cardiovascular Effects of Volatile Anesthetics: in vitro
direct coronary artery vasodilation
Cardiovascular Effects of Volatile Anesthetics: invivo
coronary artery constriction
-reduction in determinants of myocardial oxygen consumption (MVo2), including HR, preload, after load, inotropic state, produced by anesthetics via metabolic auto regulation
Cardiovascular Effects of Volatile Anesthetics: myocardial O2 extraction and ratio of myocardial o2 delivery to MVo2 revealed
coronary artery vasodilation
- halothane and isoflurane decreed myocardial O2 extraction and increased ratio of O2 delivery to consumption in isolated beating hearts
- indicating volatile anesthetics produce direct coronary vasodilation in isolated hearts because myocardial O2 delivery exceeds MVo2 and coronary sinus O2 tension increases
coronary steal
doesn’t occur