Cardiovascular effects of inhalation anesthetics occur on all aspects of cardiovascular function, namely, inotropic, chronotropic, dromotropic and lusitropic state of the heart. Their effects are as follows:
a) Myocardial
b) Coronary circulation
c) Conduction
d) Circulation
Cardiovascular effects of inhalation anesthetics produce dose-related myodial depression of LV, RV and LA contractility as well LV diastolic function and LV-arterial coupling in the nonnI heart in the following order. Halothane = Enflurane > Isoflurane
Desflurane = Sevoflurane Patients with userlying contractile dysfunction are more sensitive to negative inotropic effects. The negative inotropic effects are related to alterations in intracellular Ca homoeostasis within the cardiac myocyte.
The LV afterload is the ratio of mean arterial pressure to cardiac output is affected by volatile anaesthetics. Systemic haemodynamic effects are due u actions on myocardial, vascular (venous and arterial) and the autonomic nervous system this having a cardiovascular effects of inhalation anesthetics
Volatile anaesthetics produce direct coronary vasodilatation but are not capable of producing steal at clinical concentrations, Halothane > Isoflurane > Desflurane > Sevoflurane. Xenon has no effects.
Cardiovascular effects of inhalation anesthetics conduction is affected by volatile anaesthetics, they slow the rate of sinoatrial discharge by direct effects on SA node. They have the potential to produce bradycardia. Halothane, isoflurane and enflurane prolong Qt interval in humans; so patients with long Qt syndrome may be at a greater risk of developing torsades-de-pointes tachycardia.
For cardiovascular effects of inhalation anesthetics , Arrhythmias may occur due to sensitization of the heart as a result of interaction between volatile anaesthetics and catecholamines. There is a reduction in the threshold for atrial and ventricular arrhythmias. During myocardial ischaemia or infarction, they may be cardioprotective and prevent arrhythmias. Depending on concentration of the agent and extent of injury, the actions may be due to activation of intracellular signal. conduction pathways.
The circulatory cardiovascular effects of inhalation anesthetics are a direct action on smaller arteries and veins resulting in reduction in systemic vascular resistance: Halothane> Enflurane> Isoflurane> Sevoflurane> Desflurane. Nitrous oxide has direct negative inotropic effect but increases pulmonary and systemic pressures via a sympathomimetic effect. Volatile agents depress baroreceptor reflex control of arterial pressure of varying degree. Xenon is devoid of cardiovascular effects of inhalation anesthetics