Ketamine cardiovascular effects resemble sympathetic nervous system stimulation. Indeed, a direct negative cardiac inotropic effect is usually overshadowed by central sympathetic stimulation. HR and BP rise were similar between S(+)ketamine and racemic mixture.
Systemic blood pressure, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements all are increased after IV administration of ketamine cardiovascular effects . The cardiovascular-stimulating effects are blunted or prevented by prior administration of benzodiazepines or concomitant administration of inhaled anesthetics, including nitrous oxide.
Ketamine cardiovascular effects have a positive inotropic effect on myocardium albeit at low concentration. At low concentration (73 microM), S(+)ketamine increases isor.tric force, isotonic shortening, contractility more than R(-)ketamine. However, at higher concentrations (730 microM) a direct negative inotropic action occurs with ketamine and its isomers.
The failing myocardium exposed to ketamine cardiovascular effects has reduced ability to increase contractility even in the presence of increased beta-adrenergic stimulation. Tumour necrosis factor-alpha and interferon-gamma reduces post- stimulation intracellular cAMP levels, the second messenger for the beta-adrenergic receptor. By inhibiting these proinflammatory cytokines, ketamine improves blood pressure and cardiac output in sepsis and heart failure patients.
The effect of ketamine cardiovascular effects on cardiac rhythm is inconclusive. There is evidence that ketamine cardiovascular effects enhances the dysrhythmogenicity of epinephrine.
In the study by Aya et al. ketamine induced a concentration-dependent lengthening of the RR interval and slowed ventricular conduction and prolonged refractoriness without changing anisotropy or increasing dispersion of refractoriness. However, no arrhythmia could be induced by ketamine, regardless of its concentration.
Ketamine increases coronary blood flow. Studies demonstrated vasodilating capability of coronary arteries in vitro when administered in high concentrations.
There is a stereoselective difference with a stronger vasorelaxing effect of S(+) ketamine compared to racem-ic and R(-) ketamine. Ketamine has significant vasodilator activity in the pulmonary vascular bed which may in part be mediated by the activation of L-type calcium channels.