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Shock: Diagram showing Complications of Shock Shock is a clinical state of cardiovascular collapse due to the disparity of blood volume and the capacity of circulatory bed (systemic hypoperfusion). Clinically, shock is characterized by the falling blood pressure, rapid pulse, tachycardia, cold, clammy and cyanotic skin, oliguria etc. Types of shock: 1. Cardiogenic shock: Myocardial infarct, ventricular rupture, arrhythmia, massive pulmonary embolism causes the failure of myocardial pump, due to intrinsic myocardial damage or extrinsic pressure or obstruction to outflow, resulting in shock. 2. Hypovolemic shock: It is due to hemorrhage, fluid loss (vomiting, diarrhea, extensive burns, crush injury, fracture), and acute abdomen (pancreatitis, peritonitis, intestinal obstruction, perforation) produce shock due to inadequate blood or plasma volume. 3. Septic shock : Overwhelming microbial infection causes endotoxic shock. Gram-positive septicemia or fungal sepsis causes peripheral vasodilation and pooling of blood producing endothelial activation and injury, resulting in leukocyte induced damage leading to Disseminated intravascular coagulation. Septic shock is also caused by systemic gram-negative microbial infections. Mechanism of septic shock: Gram-negative bacterial wall consists of Lipopolysaccharide (LPS) containing lipid A and O antigen. Gram-positive bacteria and wall of fungi contain bacterial protein "super antigen", similar to LPS. Lipopolysaccharide combines with serum protein and bind to CD14 of leukocytes (especially monocytes and macrophages, endothelial cells and other cells), liberating cytokines (TNF, IL-1). -With mild infection: LPS activate complement, monocyte/macrophage and adhesion molecule producing local inflammation, with removal of bacteria. -With moderate infection: High LPS causes high secretion of cytokines and direct capillary endothelial injury and activate coagulation cascade. -With severe infection: High LPS causes high level of secretion of cytokines and secondary mediators causing: - Systemic vasodilation (hypotension) - Decreased myocardial contractibility. -Widespread endocardial injury and activation with systemic leukocyte adhesion and pulmonary alveolar capillary damage (adult respiratory distress syndrome-ARDS). -Activation of the coagulation system causes disseminated intravascular coagulation. Rarer causes of shock: 4. Neurogenic shock: Neurogenic shock is due to loss of vascular tone causing peripheral pooling of blood - Example: anesthetic accident, spinal cord injury. 5. Anaphylactic shock: (IgE mediated hypersensitivity).
Prognosis: Prognosis varies with the cause and duration of shock. Treatment targets the underlying cause but is otherwise mainly supportive. Most (80 to 90%) young and healthy patients with hypovolemic shock survive with appropriate management. Cardiogenic shock due to extensive myocardial infarction and septic shock have mortality rates of up to 75%.
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Summary of Pathogenesis: Shock is initiated by one of the two principal events: pump failure, or “cardiogenic shock” ; and loss of circulatory volume, also called “hypovolemic shock”. Hypovolemic shock follows internal fluid loss, such as that in endo toxemia, burns, trauma, or anaphylaxis, or from external fluid loss such as that caused by hemorrhage, diarrhea, and dehydration. The effects of both events is decreased cardiac output and decreased tissue perfusion. The resulting anoxic cell injury sets into motion several vicious cycles. Metabolic acidosis (renal failure, increased anaerobic glycolysis) and heart failure lead to a further decline in cardiac output. Endothelial damage increases vascular permeability and decreases effective blood volume, reducing venous return and decreasing cardiac output. |
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