The cardiovascular consequences of burn injury

Abstract

This thesis is concerned with the cardiovascular changes which occur in the first 90 minutes after burn injury. In these studies, a full thickness burn injury of the skin was induced in anaesthetised rats using a method based on those of Arturson (1960) and Philpot (1981). 

Burn injury leads to many physiological changes, including falls in the cardiac output, the stroke volume of the heart and the peripheral vascular conductance, but only small changes in blood pressure and heart rate. It has been suggested that the loss of plasma volume due to leakage from damaged or dilated capillaries, leads to a decrease in venous return (i.e. preload on the heart) and therefore to a decrease in stroke volume. This thesis, however, presents evidence that the initial event leading to these cardiovascular responses is a decrease in myocardial contractility. 

The role of angiotensin II during the early post-burn period was investigated using captopril to block the renin-angiotensin system. Captopril protected against the falls in stroke volume and peripheral conductance. This dependence of stroke volume on peripheral conductance is most easily explained if myocardial function is impaired at the time. 

To obtain evidence for this hypothesis I measured cardiac function in the rat directly. I developed a measuring system which uses a fluid-filled blood pressure transducer and a BBC microcomputer to obtain measurements directly from the heart of the rat. Also, I used signal processing techniques to correct for resonance and damping artifacts inherent in such measurements. A new technique called the 'drop test' was devised for measuring the resonance and damping properties of the system. Several pressure-based indices of heart muscle performance were computed from blood pressure measurements recorded from inside the left ventricle of the rat. 

The physiological relevance of these indices was then verified by measuring the reproducibility, sensitivity and preload/afterload dependence of the indices. In these studies, the indices derived from the second differential of left ventricular pressure were found to give the most specific indication of changes in contractility. 

These indices of myocardial contractility, heart rate, stroke volume and arterial blood pressure were monitored before and after burn injury. The majority of the indices of contractility were depressed by 30-40% at 20 minutes post-burn. This depression was greatest at 30 minutes post burn, but disappeared by 60 minutes post-burn. 

A possible cause of the myocardial depression was investigated in two further studies. Plasma taken from a rat 5 minutes after a burn injury caused a fall in cardiac output when transfused into a recipient rat. This plasma also caused a significant deterioration in the contractile function of an isolated heart muscle preparation.

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