Bradycardia during reversible hypovolaemic shock: associated neural reflex mechanisms and clinical implications.

1. Heart rate response to reversible central hypovolaemia can be divided into three stages. In the first stage (corresponding to a reduction of the blood volume by approximately 15%) a modest increase in heart rate (< 100 beats/min) and total peripheral resistance compensate for the blood loss, and a near normal arterial blood pressure prevails (preshock). During the second stage, a reduction of the central blood volume by approximately 30% results in a decrease in heart rate, total peripheral resistance and blood pressure due to activation of unmyelinated vagal afferents (C-fibres) from the left ventricle. In the third stage, blood pressure falls further as haemorrhage continues and tachycardia (> 120 beats/min) is manifest. This stage may proceed into irreversible shock with death from cardiac arrest probably related to the formation of free oxygen radicals. 2. Recognition of the vasodepressor-cardioinhibitory reaction to a reduced circulating blood volume is important and suggests the need for immediate treatment with volume expansion in critically ill patients.