Shock

• Shock is defined as inadequate tissue perfusion marked by decreased delivery of required metabolic substrate and inadequate removal of cellular waste products.
• Shock involves failure of oxidative metabolism that can involve defects of oxygen (O2) delivery, transport, and/or utilization.
• The initial cellular injury that occurs in shock is reversible, but the injury will become irreversible if tissue perfusion is prolonged or severe enough such that, at cellular level, compensation is no longer possible.
• Hypovolemic shock is a form of shock caused by fluid loss.
• Traumatic shock is a form of shock caused by physical injury.
• Vasodilatory (septic) shock is a form of shock caused by toxic infection.
• ADH is secreted in response to shock and remains elevated for approximately 1 week, which is seen as a result of increased water permeability in the distal tubule.
• Alpha2 receptors are found both in the brain and in the periphery.
• Alpha2 receptors determine both arteriolar resistance and venous capacitance, and thus blood pressure.
• Mesenteric vasodilation is also a result of ADH secretion in response to shock.
• Increase in sodium loss is also a result of ADH secretion in response to shock.
• Down regulation of alpha adrenergic receptors on the arterioles is also a physiological response to hypovolemia.
• Mesenteric vasoconstriction is a result of ADH secretion in response to shock.
• Vasoconstriction is one of the initial physiological responses to hypovolemia that is mediated by activation of alpha adrenergic receptors on the arterioles.
• Downregulation of beta adrenergic receptors at the arterioles is also a physiological response to hypovolemia.
• Activation of beta adrenergic receptors on the arterioles is a physiological response to hypovolemia.
• Alpha1 receptors are the classic postsynaptic alpha receptors and are found on vascular smooth muscle.
• Cardiogenic shock is a form of shock caused by heart disease.
• Obstructive shock is a form of shock caused by blockage.
• Neurogenic shock is a form of shock caused by nervous system disorder.
• End points in resuscitation are the points at which resuscitation efforts are discontinued.
• Hemorrhagic shock is a form of shock caused by blood loss.
• Shock can be classified into different categories based on the underlying etiology.
• The pathophysiology of shock involves tissue hypoperfusion and the developing cellular energy deficit leading to neuroendocrine and inflammatory responses.
• Septic shock, the most frequently encountered form of vasodilatory shock, is a by-product of the body’s response to disruption of the host-microbe equilibrium, resulting in invasive or severe localized infection.
• When this response is overly exuberant or becomes systemic rather than localized, manifestations of sepsis may be evident.
• Traumatic shock is a systemic response after trauma, combining the effects of soft tissue injury, long bone fractures, and blood loss, which is different from simple hemorrhagic shock.
• Causes of vasodilatory shock include systemic response to infection, noninfectious systemic inflammation, anaphylaxis, acute adrenal insufficiency, and prolonged, severe hypotension.
• Examples of traumatic shock include small volume hemorrhage accompanied by soft tissue injury, femur fracture, and crush injury.
• Decreased tissue perfusion can result directly from hemorrhage/hypovolemia, cardiac failure, or neurologic injury.
• Vasodilatory shock is characterized by peripheral vasodilation with resultant hypotension and resistance to treatment with vasopressors.
• Treatment of traumatic shock includes prompt control of hemorrhage, adequate volume resuscitation to correct O2 debt, debridement of nonviable tissue, stabilization of bony injuries, and appropriate treatment of soft tissue injuries.
• Vasodilatory shock is a dysfunction of the endothelium and vasculature secondary to circulating inflammatory mediators and cells or as a response to prolonged and severe hypoperfusion.
• Septic shock, the vasodilatory effects are due to the upregulation of the inducible isoform of nitric oxide synthase (iNOS or NOS 2) in the vessel wall.
• DAMPs activate the same set of cell surface receptors as bacterial products, initiating similar cell signaling.
• In the attempt to eradicate the pathogens, immune and other cell types (e.g., endothelial cells) elaborate soluble mediators that enhance macrophage and neutrophil killing effector mechanisms, increase procoagulant activity and fibroblast activity to localize the invaders, and increase microvascular blood flow to enhance delivery of killing forces to the area of invasion.
• Multiple organ failure, commonly associated with blunt trauma, can include acute respiratory distress syndrome (ARDS) and damage associated molecular patterns (DAMPs).
• Hyperfusion Deficit in Traumatic Shock is magnified by the proinflammatory activation that occurs following the induction of shock.
• Hypotension results from failure of the vascular smooth muscle to constrict appropriately in vasodilatory shock.
• Decreased tissue perfusion and cellular injury can then result in immune and inflammatory responses.