Anesthesia+&+Cardiovascular+Response

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=Cardiovascular Responses to Anesthesia = All volatile anesthetic agents have a direct depressant effect on the myocardium. Therefore they reduce myocardial contractility, and many also reduce sympathetic stimulation of the vascular system.

Decreased CO -> vasodilatation -> hypotension -> compromised vital organ perfusion (esp. during induction of a hypovolemic patient).

Propofol
Most induction agents are cardiovascular depressants. The greatest effect is seen with propofol, which may cause a marked fall in blood pressure, systemic vascular resistance and heart rate, the latter due to central vagal stimulation.

Thiopental
Thiopental has similar effects, but less pronounced, and presence of reflex tachycardia mediated by the baroreceptor reflex. This can result in increased myocardial oxygen consumption and a consequent increase in coronary blood flow.

Etomidate
Etomidate provides the most cardiovascular stability, with only slight hemodynamic changes. It has little effect on myocardial oxygen balance.

Ketamine
Ketamine, on the other hand, is a potent cardiovascular stimulant by increasing sympathetic nervous discharge, although its direct effect on the myocardium is negatively inotropic. On induction there is a marked rise in heart rate and blood pressure caused by central nervous stimulation and an increase in circulating catecholamines.

Volatile Anesthetics
Volatile anesthetic agents reduce discharge from the SA node. This can lead to junctional rhythms, when the AV node takes over as the pacemaker, associated with an absent P wave on the ECG. All decrease SVR, except for halothane.

Halothane
During halothane anesthesia systemic vascular resistance is unchanged and, due to vagal stimulation, bradycardias and nodal rhythms are common. Halothane sensitizes the heart to the arrhythmogenic effects of catecholamines as well as ventricular ectopy. High catecholamine levels can lead to VT/VF.

<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Ether
<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Ether causes sympathetic stimulation, catecholamine release and vagal nerve blockade. Therefore, there is an increase in cardiac output, heart rate and systemic vascular resistance, so blood pressure is well maintained.

<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Local Anesthetics
<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Local anesthetic agents depress conduction of the cardiac impulse. This effect can be therapeutic, for example in the treatment of ventricular arrhythmias. However, at higher concentrations local anesthetics can cause cardiac arrest - it is vital to avoid accidental intravenous injection when using these agents.

<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Positive Pressure Ventilation
<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Controlled ventilation in a paralyzed patient has many effects. Firstly, it increases intra-thoracic pressure which reduces venous return and preload, causing a fall in cardiac output. Secondly, changes in the partial pressure of carbon dioxide (PaCO2) resulting from changes in ventilation will also have cardiovascular effects. A low PaCO2, which commonly occurs during controlled ventilation, causes peripheral vasoconstriction by a direct effect. This increases systemic vascular resistance, increases afterload and can result in a fall in cardiac output. It also causes cerebral vasoconstriction, thereby, reducing cerebral blood volume. A high PaCO2 usually occurs in the anesthetized patient during spontaneous breathing, and causes vasodilatation and increased sympathetic activity, leading to increased cardiac output. However, the heart will be more likely to develop arrhythmias, particularly when using volatile agents

<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Neuraxial Anesthesia
<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Spinal and epidural anesthesia blocks sympathetic nerves as well as sensory and motor fibers. This can lead to marked hypotension due to arteriolar and venous dilation because the sympathetic nerves to the lower extremities are blocked. Cardiac sympathetic nerve fibres, which arise from the high thoracic spinal cord, may also be blocked, allowing an unopposed vagal action on the heart. In this case there will not be an appropriate increase in cardiac output, and blood pressure will fall further with a bradycardia.

<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Take Home Message
<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">For patients with coronary artery disease, it is important to use an anesthetic technique which does not cause further myocardial ischemia. The important principle is to ensure that myocardial oxygen supply is greater than myocardial oxygen demand. The balance between these two variables is influenced by the following factors:

<span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Diastolic Time ||< <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Heart Rate <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Tachycardia || <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Aortic DBP <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Ventricular EDBP ||< <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Ventricular Wall Tension <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Preload (EDV) <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Afterload || <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Arterial oxygen partial pressure <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Hemoglobin concentration ||< <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Contractility ||
 * ~ <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Myocardial Oxygen Supply ||~ <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Myocardial Oxygen Demand ||
 * < <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Heart Rate
 * < <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Coronary Perfusion Pressure
 * < <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Arterial Oxygen Content
 * < <span style="display: block; font-family: Arial,Helvetica,sans-serif; text-align: left;">Coronary Artery Diameter ||<  ||

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