Q: What is the meaning of the term "vascular collapse"? A: Vascular collapse is commonly referred to as shock. It is an end result of many different injuries, which can often lead to shock, and, as a syndrome comprised of a wide spectrum of symptoms, signs, and laboratory findings. Vascular collapse is ultimately the result of an imbalance between tissue oxygen delivery and the metabolic needs of the body. Cardiac causes are common, but noncardiac causes also occur. Massive pulmonary embolism may also lead to vascular collapse when the embolic material (it is commonly a thrombus, but it may also consist of air, fat or tumor tissue) obstructs 30% more of the pulmonary vascular bed, ultimately resulting in right ventricular ischemia (the loss of blood supply to the right ventricle) and failure of the right ventricle of the heart. The result of vascular collapse is hypotension, resulting in inadequate blood flow to the organs, with ineffective perfusion of the tissues, cellular injury, and multiorgan dysfunction.
Hypovolemic shock is perhaps the most common type of shock and is due to a diminished circulating blood volume. This results in a decrease in the amount of blood returning to the heart and therefore a decrease in the volume of blood ejected at each cardiac cycle or stroke volume. The common clinical scenarios in which this is seen include gastrointestinal bleeding, massive vomiting, dehydration, trauma, severe burns, and ruptured aortic aneurysms. The individual is typically hypotensive and has a rapid heart rate and cool extremities, which may lead to pallor.
Vascular collapse due to distributive shock is the result of ineffective delivery and extraction of oxygen associated with inappropriate dilatation of peripheral blood vessels despite a normal cardiac output.
Traumatic shock, which is often associated with blood volume changes, can occur in combination with hypovolemic and distributive shock. A common result of these changes is multiple organ dysfunction syndrome. Acute lung injury frequently occurs and leads to impaired gas exchange, hypoxemia, and increased pulmonary workload, while injury of the kidneys results in acute renal failure. The pathogenesis of septic shock is complex and is associated with significant metabolic changes.
Tissue hypoperfusion, or decreased blood flow, and cellular hypoxia are the common consequence of vascular collapse. The underlying vascular mechanisms include: (1.) Endothelial cell injury due to decreased tissue perfusion with resultant increased vascular permeability. This results in escape of fluid from the vascular compartment into the extravascular compartment. (2.) A decrease in blood volume, venous return, and therefore cardiac output. (3.) Decreased perfusion of the myocardium, which leads to further decrease in the ability of the pump to function.
Management of vascular collapse should result in stabilization of the patient as well as restoration of circulation. A simultaneous attempt must be made to define the cause of the vascular collapse so that the cause may be treated.
Jagdish Butany Professor, University of Toronto Department of Laboratory Medicine and Pathobiology References: D. Annane, Corticosteroids for septic shock, Crit. Care Med., 29 (7 Suppl: S117-S120), July. 2001; T. Calandra, Pathogenesis of septic shock: Implications for prevention and Treatment, J. Chemother.,13;1:173-180, 2001; A.R. Bengur et al., Cardiogenic shock, New Horizons, 6(2):139-149,1998; R.P. Dellinger, Cardiovascular management of septic shock, Crit. Care Med., 31(3):946-955, March. 2003.