Miller Inhaled Anesthetics: Cardiovascular Flashcards
Volatile anesthetics produce dose-related depression of left ventricular (LV), right ventricular, and left atrial myocardial contractility, LV diastolic function, and LV-arterial coupling in the normal heart.
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• The negative inotropic effects of volatile anesthetics are related to alterations in intracellular calcium homeostasis within the cardiac myocyte.
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• Volatile anesthetics are relatively weak coronary vasodilators that are not capable of producing coronary steal at typically used clinical concentrations, even in patients with steal-prone coronary artery anatomy
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• Nitrous oxide causes direct negative inotropic effects, does not substantially affect LV diastolic function, and produces modest increases in pulmonary and systemic arterial pressure via a sympathomimetic effect. These actions are dependent to some degree on the baseline anesthetic.
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The negative inotropic actions of all volatile anesthetics are exacerbated by hypocalcemia, calcium channel blockers, and β 1 -adrenoceptor antagonists and may be reversed by administration of exogenous calcium (Ca 2+ ), cardiac phosphodiesterase fraction III inhibitors, β 1 -adrenoceptor agonists, Ca 2+ channel agonists, and myofilament Ca 2+ sensitizers.
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Volatile anesthetics also depress contractile function by inhibiting Na + -Ca 2+ exchange and reducing intracellular Ca 2+ concentration independent of the voltage-dependent Ca 2+ channel in vitro.
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Definitions of heart failure based solely on contractile dysfunction are inadequate because LV function during diastole significantly influences overall cardiac performance. The heart serves dual roles, propelling blood into the high-pressure arterial vasculature during systole and collecting blood from the low-pressure venous circulation during diastole. Thus, heart failure may occur not only from impaired contractility but also from altered LV diastolic function
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