Changes which occur in the various body systems
Patients can present initially with very similar signs for both acutely occurring Gastric dilatation and acute gastric dilatation and torsion. With both conditions cardiorespiratory dysfunction occurs due to the increasing size of the gas filled stomach which puts an increased pressure on the diaphragm. This increased pressure results in reduced expansion of the diaphragm and reduced capacity of the lungs, resulting in hypoventilation which in turn will result in a ventilation-perfusion mismatch and arterial hypoxia as the stomach increases in size and the degree of respiratory dysfunction worsens. This in turn results in an increase in partial pressure of carbon dioxide will result in a respiratory acidosis which further complicates the patient’s condition.
Within the cardiovascular system the venous vessels which are under relatively low pressure, e.g. caudal vena cava, hepatic portal vein and splanchnic vessels located in the cranial abdomen become easily compressed as the stomach begins to dilate. This compression results in causing several negative effects on the patient, these include:
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A reduction in venous return
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will result in a reduction in cardiac output
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drop in systemic blood pressure
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Portal hypertension which leads to interstitial oedema and fluid leaking from the vascular spaces
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compromising circulating volume
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reduction in tissue perfusion
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myocardial injury
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risk of reperfusion injury occurring when the circulation is re-established during treatment.
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hypovolaemic shock.
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Reducing cardiac contractility is myocardial depressant factor. This factor is thought to arise due to reduced tissue perfusion in other organ systems, in particular the pancreas and intestines.
The cardiovascular effects are further compromised by the release of catecholamines, which increase peripheral resistance to compensate for the decrease in systemic blood pressure. This in turn will result in a further reduction in tissue perfusion which can result in severe reduction in renal perfusion and the loss of the intestinal mucosal barrier.
Gastric necrosis can develop as a result of torsion, occlusion and avulsion of the short gastric arteries which supply the greater curvature and fundus of the stomach. This may lead to ischaemia which can further develop to necrosis or large areas of the stomach that may well leak gastric contents.
During volvulus of the stomach, the spleen will also move with the greater curvature of the stomach. This can lead to splenic necrosis due to compromise of the splenic vasculature during volvulus.
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