Pathophysiology

• Potential predisposing factors:
  • GDV is most commonly seen in large and giant breed dogs although it can occur in small dogs and cats.
  • Breeds thought to be predisposed are deep chested with an increased thoracic depth:width ratio, a finding thought to be a main predisposing characteristic possibly due to prevention of appropriate eructation. Significant gas accumulation resulting in gastric distension is thought to occur due to aerophagia as well as from carbohydrate fermentation. Predisposed breeds may also have increased tone in their lower esophageal sphincter resulting in decreased pyloric outflow with subsequent gaseous accumulation.
• Additional predisposing factors may include:
  • Eating out of raised food bowls.
  • Highly stressed individuals.
  • Older age.
  • Having a first degree relative with a history of GDV.

• In the initial stages, dilatation begins with the accumulation of gas in the stomach through aerophagia and the fermentation of ingesta.
• Fluids from gastric and enteric secretions also accumulate and the gastric content is prevented from leaving the stomach by failure of the normal outflow mechanisms of eructation, vomiting and, less importantly, pyloric outflow.
• The syndrome may progress no further than simple dilatation or the stomach may begin to rotate about its esophageal attachment in a clockwise or anticlockwise direction as viewed from below.
• Rotation between 90° and 270° in a clockwise direction is the most common form of volvulus.
• In this configuration the pylorus moves across the abdominal floor and comes to lie alongside the esophagus on the left abdominal wall. The fundus moves to the right around the esophageal axis and then ventrally. The spleen moves dorsally and to the right, making contact with the liver or diaphragm.
• Venous return to the heart is dramatically reduced as a result of compression of the caudal vena cava and portal vein during volvulus by distended stomach.

Concurrent pathophysiological changes

• Dilation of the stomach occurs with or without torsion. Distension leads to compression of the caudal vena cava, portal vein and splanchnic vessels thus causing reduced preload, decreased cardiac output and hypotension. Torsion and distension of the stomach may result in trauma to the short gastric and epiploic vessels resulting in hemorrhage which further contributes to decreased cardiac output and hypotension. Gastric distension, gastric acidity and gastric hypoperfusion causes mucosal damage that may lead to bacterial translocation, gastrointestinal necrosis and/or perforation leading to peritonitis Peritonitis and possibly sepsis Shock: septic. Splenic congestion may occur resulting in splenomegaly that may progress to splenic thrombus or even torsion.

• Significant gastric distension prevents normal excursion of the diaphragm resulting in an increased respiratory rate and effort. Hypoxemia Hypoxemia may occur due to inadequate ventilation associated with gastric distension and impaired diaphragmatic motion, aspiration pneumonia Lung: aspiration pneumonia , acute respiratory distress syndrome Acute Respiratory Distress Syndrome (ARDS) or even hemorrhage from DIC Disseminated intravascular coagulation. Respiratory acidosis may occur due to inappropriate ventilation and retention of carbon dioxide.
• Hypovolemic shock develops through the sequestration of large volumes of blood in the portal circulation. Venous return decreases together with central venous pressure, cardiac output, stroke volume and arterial pressure.
• Electrolyte abnormalities are common, the most consistent and serious being the hypokalemia caused by loss of potassium into the gastric lumen.
• Acid-base abnormalities arise inconsistently since the tendency to acidosis caused by the anaerobic changes in the ischemic areas of the gut is often countered by the alkalosis developing from sequestration of acidic gastric content.
• Gastric necrosis develops through torsion and occlusion of the short gastric vessels supplying the greater curvature and fundic areas of the stomach. The gastric mucosa in these areas is particularly vulnerable to acute ischemia which leads to necrosis of large areas of the stomach and, in some cases, perforation.
• Cardiac arrhythmias are seen in about 40% of patients with GDV. Cardiac arrhythmias result from myocardial ischemia, hypoxia and reperfusion injury arising from decreased venous return during the first few hours of the condition. In addition, pancreatic hypoxia is thought to contribute subsequently to the problem, releasing the so-called myocardial depressant factor (MDF) and further compromising cardiac function. Approximately half of all GDV cases will develop dysrhythmias during the first 48 hours. Abnormalities include premature ventricular contractions and ventricular tachycardia.
• Endotoxemia may develop as gram-negative organisms proliferate in the ischemic stomach and their toxins are permitted to move across the gut wall into the circulation, further complicating the shock syndrome. Sepsis may occur secondary to bacterial translocation associated with portal hypertension. Gastric distension increases portal hydrostatic pressure thus preventing appropriate blood flow and resulting in hepatic and gastrointestinal congestion. These changes allow for bacterial translocation and may result in septicemia. Sepsis can also occur due to gastric necrosis and perforation.
• Disseminated intravascular coagulation (DIC) may occur due to gastric necrosis, dilutional coagulopathy from aggressive fluid resuscitation, as a consequence of septicemia, hemorrhage, ischemia-reperfusion injury, severe hypertension and/or severe tissue hypoxia and endotoxemia.
• Enzyme changes include raised ALT, SAP, blood urea and creatinine concentrations.
• Also: increased intra-abdominal pressure → decreased ventilation → ventilation/perfusion mismatch → hypoxia. Increased intra-abdominal pressure is the prime cause of decreased venous return and decreased cardiac output.
• Ischemic reperfusion injury occurs when resuscitation restores perfusion to previously hypoperfused organs. During ischemia, ATP is degraded resulting in the formation of reactive oxygen species (ROS). ROS damages DNA, RNA, proteins and cell membranes eventually leading to cell death.

Timecourse

• Rapid.