Haemodynamic changes in XXXX .

@entity1 @entity548 @entity190 @entity1457 @entity651 @entity591 @entity551 @entity1286 @entity204 @entity1168 @entity130
@entity130 is the leading cause of @entity204 during the first four decades of life in the developed countries. Its haemodynamic response underpins the @entity1 's initial ability to survive, and the response to treatment and subsequent morbidity and resolution. @entity130 causes a number of insults including @entity548 , 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' @entity548 ( @entity190 without significant volume of tissue damage) causes a biphasic response: mean arterial blood pressure (MBP) is initially maintained by the baroreflex ( @entity591 and increased vascular resistance, Phase 1), followed by a sudden decrease in MAP initiated by a second reflex (decrease in vascular resistance and @entity1168 , 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 @entity548 . However, hypoxaemia from @entity651 limits the effectiveness of @entity551 resuscitation by augmenting the @entity1457 state. An alternative strategy ('hybrid resuscitation') whereby tissue perfusion is increased after the first hour of @entity551 resuscitation by adopting a revised normotensive target may ameliorate these problems. Finally, @entity1286 also attenuates Phase 2 of the response to @entity548 in some, but not all, species and this is associated with poor outcome. The impact on @entity1 @entity1 is currently unknown and is the subject of a current physiological investigation.
