Cardiac Tag's Archives

Pathophysiology of Circulatory Failure

circulatory failure
Circulatory failure, or the inability of the heart to provide sufficient cardiac output to sat­isfy tissue metabolic requirements, is the most important and most common cause of altered pharmacokinetics during cardiac emergencies. Circulatory failure may result from decreased myocardial contractility, arrhythmias that allow insufficient time for diastolic filling or impair atrioventricular synchrony, circulatory stresses such as increased afterload or hypovolaemia, valvular dysfunction, tamponade, or a variety of less common insults.

Regardless of the aetiology, circulatory fail­ure elicits characteristic compensatory haemodynamic adjustments, mediated in large part by activation of the sympathetic nervous system [Peniel & Benowitz 1984; Benowitz & Meister 1978]. Enhanced sympathetic tone in­creases cardiac contractility and peripheral vas­cular resistance, both of which serve to main­tain arterial blood pressure. The increase in peripheral vascular resistance, however, is not uniform among different vascular beds.

General Anaesthetic Agents

The mechanism by which anaesthetic drugs produce unconsciousness is still unknown. Meyer in 1899 and Overton in 1901 noted that within any group of drugs, anaesthetic potency correlates well with lipid solubility, and most modern theories agree that the site of action is probably the lipid bilayer of nerve cell mem­branes, or possibly a protein receptor in this sit­uation, but further knowledge is limited.

Inhalational Agents

Anaesthesia Inhalational
Anaesthetic practice is unique in that a high proportion of the drugs are administered by the inhalational route. Such agents must either be gaseous, or the vapour of volatile liquids (Vari­ous Authors 1984).
Of the original three inhalational agents – ni­trous oxide, ether and chloroform – the first two are still used widely.