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Shock, SHOCK 2. Cardiogenic Pump failure of left ventricle->circulatory collapse -most often a result of myocardial infarction->reduced CO ->venous blood pooling upstream of failing ventricle -cool extremities, SHOCK 1. Hypovolemic Acute reduction in circulating blood->circulatory collapse -Due to: 1. Severe hemorrhage or fluid loss from skin -from extensive burns, severe trauma 2. Loss of fluid from GI tract -from severe vomiting or diarrhea -cool extremities, SHOCK Other Types Hypoadrenal - adrenocortical insufficiency ->hyposecretion of cortisol Traumatic - loss of blood volume into interstitium of injured tissues->relative hypovolemia, Leading cause of death in ICUs Systemic response to severe infection -Most commonly from endotoxin-producing gram-negative bacteria -Also due to superantigen of Staph. aureus->"toxic shock syndrome" Course: 1. Initial vasodilation increases blood flow 2. Increased vascular permeability ->pooling of blood in extremities, relative hypovolemia 3. Cytokines (TNF-α, IL-1, IL-6, IL-8), complement, kinins, NO released 4. Endothelial injury (from NO) + released PAF -> ->Disseminated Intravascular Coagulation (DIC) Do our pts have this? YES, but without the infection. Induced Cytokine Storm. -TNF-α dramatically increased w/in 1 hr of infusion -Followed by elevated IL-2,6,10, IFN-α w/in 4 hrs -w/ TNF-α->increased vasc. permeability, vasodilatation -activate monocytes -Storm resolved after hydrocortisone, prednisone -Inhibit Phospholipase A2, COX->fewer leukotrienes, prostaglandins Where did the cytokines come from? Activated T cells - nonspecifically activated by TXT00009 Activated Macrophages - activated by T cells, Acute reduction in circulating blood->circulatory collapse -Due to: 1. Severe hemorrhage or fluid loss from skin -from extensive burns, severe trauma 2. Loss of fluid from GI tract -from severe vomiting or diarrhea -cool extremities Do our pts have this? Yes, kind of - Relative Hypovolemia secondary to systemic inflammation, Due to trauma, especially of high cervical spinal cord ->interrupt sympthetic vasomotor input -->arteriolar dilatation, venodilation -warm extremities Do our pts have this? No - No trauma., SHOCK General Features Circulatory collapse->multisystem end-organ hypoperfusion -Clnical indicators: Reduced mean arterial pressure (MAP) (ឬmmHg) Tachycardia, Tachypnea Cool skin, extremities (except in neurogenic) Usually Hypotension Results in tissue hypoxia -> lactic acidosis, SHOCK Stages 1. Nonprogressive (early) stage - Compensatory mechanisms maintain perfusion -increased HR, increased peripheral resistance 2. Progressive stage - Tissue hypoperfustion->circulatory and metabolic imbalance -metabolic acidosis from lactic acidemia - Compensatory mechanisms not adequate. 3. Irreversible stage - organ damage and metabolic disturbances incompatible w/ life, Pump failure of left ventricle->circulatory collapse -most often a result of myocardial infarction->reduced CO ->venous blood pooling upstream of failing ventricle -cool extremities Do our pts have this? No - Healthy, young men with unremarkable PMH, SHOCK 3. Septic Leading cause of death in ICUs Systemic response to severe infection -Most commonly from endotoxin-producing gram-negative bacteria -Also due to superantigen of Staph. aureus->"toxic shock syndrome" Course: 1. Initial vasodilation increases blood flow 2. Increased vascular permeability ->pooling of blood in extremities, relative hypovolemia 3. Cytokines (TNF-α, IL-1, IL-6, IL-8), complement, kinins, NO released 4. Endothelial injury (from NO) + released PAF -> ->Disseminated Intravascular Coagulation (DIC)