Why the study?
How does fluid challenge affect cardiorespiratory function in mechanically ventilated patients undergoing surgery for acute quadriplegia?
How does fluid challenge affect cardiorespiratory function in mechanically ventilated patients undergoing surgery for acute quadriplegia?
In patients with acute quadriplegia, left ventricular function is impaired, suggesting fluid replacement rather than peripheral vasoconstrictors should be used to optimize cardiac function during spinal shock.
Impaired left ventricular response to fluid challenge in acute quadriplegia; hypothesis-generating for volume optimization in spinal shock.
Cardiorespiratory function was assessed in 22 mechanically ventilated patients who underwent surgery within an average of 4.8 days following traumatic spinal cord injury at C3-7. A fluid challenge technique was used to derive right and left ventricular function curves and to assist in choice of therapy from four possible outcome responses. Both right and left ventricular stroke work increased but left ventricular stroke work was still lower than normal in six (27%) of 22 patients despite elevation of cardiac filling pressures. Pulmonary vascular resistance fell, but systemic vascular resistance was unchanged following fluid challenge. Respiratory function, including intrapulmonary shunt, lung/thorax compliance, dead space, and arterial pO2 and pCO2, were unchanged by fluid administration averaging 520 ml of plasma protein fraction in 12 minutes. The Bainbridge reflex was inoperative. There was no correlation between anesthetic agent, level or type of neurological deficit, and cardiorespiratory function. Left ventricular function was impaired so the use of peripheral vasoconstrictors that elevate systemic vascular resistance should be avoided in the management of spinal shock. Instead, myocardial depressants should be reduced and fluid replacement used to optimize cardiac function. Elevation of central venous or pulmonary capillary wedge pressures to 18 mm Hg should be used to reverse hypotension, acidosis, low venous pO2, or oliguria before institution of centrally acting inotropic therapy in the management of acute spinal cord injury.
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Mackenzie et al. (1985) studied this question.
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