Hypovolaemic ShockBMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g1139 (Published 07 March 2014) Cite this as: BMJ 2014;348:bmj.g1139
- Jerry P. Nolan1,
- Rick Pullinger2
- Royal United Hospital Bath, UK
- John Radcliffe Hospital Oxford, UK
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After haemorrhage, the systolic blood pressure of healthy adults may not decrease until 30–40% of their blood volume has been lost.
Stop the bleeding as rapidly as possible.
Blood will be required rapidly if the patient is exsanguinating.
In the severely injured patient, maintain a haemoglobin concentration in the range 8–10 g/dL depending on the specific circumstances and the patient's known co-morbidity.
Warm all fluids: hypothermia increases mortality.
In massive haemorrhage, give fresh frozen plasma and platelets early.
Hypovolaemic shock is a clinical state in which loss of blood or plasma causes inadequate tissue perfusion. Compensatory responses to haemorrhage are categorised into immediate, early and late. The loss of blood volume is detected by low-pressure stretch receptors in the atria and arterial baroreceptors in the aorta and carotid artery. Efferent output from the vasomotor centre triggers an increase in catecholamines, which causes arteriolar constriction, venoconstriction and tachycardia. Early compensatory mechanisms (5–60 min) include movement of fluid from the interstitium to the intravascular space and mobilisation of intracellular fluid. Long-term compensation for haemorrhage occurs by several mechanisms: reduced glomerular filtration rate; salt and water reabsorption (aldosterone and vasopressin); thirst; increased erythropoiesis.
Haemorrhagic shock causes a significant lactic acidosis; once the mitochondrial PO2 is less than 2 mmHg, oxidative phosphorylation is inhibited and pyruvate is unable to enter the Krebs cycle. Instead, pyruvate undergoes anaerobic metabolism in the cytoplasm, a process that is relatively inefficient for adenosine triphosphate (ATP) generation. ATP depletion causes cell membrane pump failure and cell death. The …