Cardiovascular responses to anaesthesia

All anaesthetic agents have a direct depressant effect on the myocardium. Therefore they reduce myocardial contractility, and many also reduce sympathetic stimulation of the vascular system. The result is a decreased cardiac output accompanied by vasodilation, causing hypotension. This fall in blood pressure can compromise perfusion of vital organs, especially at induction of anaesthesia in the hypovolaemic patient. In contrast, agents such as ketamine and ether increase sympathetic activity, which opposes the direct depressant effect. Thus cardiac output and blood pressure are maintained despite the direct myocardial depressant action.

Volatile anaesthetic agents reduce discharge from the sinoatrial node. This can lead to junctional rhythms, when the atrioventricular node takes over as pacemaker, associated with an absent P wave on the ECG. Local anaesthetic agents depress conduction of the cardiac impulse. This effect can be therapeutic, for example in the treatment of ventricular arrhythmias with lignocaine. However, at higher concentrations local anaesthetics can cause cardiac arrest - it is vital to avoid accidental intravenous injection when using these agents.
Controlled ventilation in a paralysed patient has many effects. Firstly it increases intrathoracic 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, reducing cerebral blood volume ( Cerebral blood flow, Update in Anaesthesia 1998;8). A high PaCO₂ usually occurs in the anaesthetised patient during spontaneous breathing, and causes vasodilation and increased sympathetic activity, leading to increased cardiac output. However, the heart will be more likely to develop arrhythmias, particularly when using volatile agents.

Spinal and epidural anaesthesia blocks sympathetic nerves as well as sensory and motor fibres. 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.

For patients with coronary artery disease, it is important to use an anaesthetic technique which does not cause further myocardial ischaemia. 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:

This article contained links to the following additional information:

 The autonomic nervous system
 Intracranial pressure and cerebral blood flow

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