Haemodynamic changes in trauma

Trauma is the leading cause of death during the first four decades of life in the developed countries. Its haemodynamic response underpins the patient’s initial ability to survive, and the response to treatment and subsequent morbidity and resolution. Trauma causes a number of insults including haemorrhage, tissue injury (nociception) and, predominantly, in military casualties, blast from explosions. This article discusses aspects of the haemodynamic responses to these insults and subsequent treatment. ‘Simple’ haemorrhage (blood loss without significant volume of tissue damage) causes a biphasic response: mean arterial blood pressure (MBP) is initially maintained by the baroreflex (tachycardia and increased vascular resistance, Phase 1), followed by a sudden decrease in MAP initiated by a second reflex (decrease in vascular resistance and bradycardia, Phase 2). Phase 2 may be protective. The response to tissue injury attenuates Phase 2 and may cause a deleterious haemodynamic redistribution that compromises blood flow to some vital organs. In contrast, thoracic blast exposure augments Phase 2 of the response to haemorrhage. However, hypoxaemia from lung injury limits the effectiveness of hypotensive resuscitation by augmenting the attendant shock state. An alternative strategy (‘hybrid resuscitation’) whereby tissue perfusion is increased after the first hour of hypotensive resuscitation by adopting a revised normotensive target may ameliorate these problems. Finally, morphine also attenuates Phase 2 of the response to haemorrhage in some, but not all, species and this is associated with poor outcome. The impact on human patients is currently unknown and is the subject of a current physiological investigation.