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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 -also due to ventricular arrhythmias, extrinsic compression, outflow obstruction (PTE) -cool extremities, Leading cause of death in ICUs - mortality up to 75% Systemic response to severe infection-results from spread to blood -Most commonly from endotoxin-producing gram-negative bacteria(70%) -Also due to superantigen of Staph. aureus->"toxic shock syndrome" Endotoxin+circulating blood protein complex->activate WBCs, endoth via CD14 -low doses->local inflammation; -moderate doses (more NO, PAF) - acute phase reactants->fever, systemic effects -high doses->low CO, low TPR, vessel injury->DIC, ARDS(alv cap dmg) ->multiorgan system failure (liver, kidneys, CNS)->death Course: 1. Initial vasodilation increases blood flow (warm extremities) 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) Tx underlying infx, control LPS Presentation Skin warm and flushed, SHOCK Other Types Hypoadrenal - adrenocortical insufficiency ->hyposecretion of cortisol Traumatic - loss of blood volume into interstitium of injured tissues->relative hypovolemia Anaphylactic - generalized IgE-mediated hypersenstivity ->widespread vasodilation and not enough blood to fill, 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, 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 Presentation Hypotension Weak, rapid pulse Tachypnea Cool, clammy, cyanotic skin, SHOCK Stages 1. Nonprogressive (early) stage - Compensatory mechanisms maintain perfusion -increased HR, increased peripheral resistance, renal fluid conservation -baroreceptor reflexes, epi/noepi release, renin-AT axis, ADH release -coronary, cerebral maintain constant flow (no constriction) 2. Progressive stage - Tissue hypoperfustion->circulatory and metabolic imbalance -dominated by renal insufficiency -metabolic acidosis from lactic acidemia - Compensatory mechanisms not adequate. -lower pH blunts vasomotor response->peripheral pooling -confused pt, urine output declines 3. Irreversible stage - organ damage and metabolic disturbances incompatible w/ life -complete renal shutdown due to acute tubular necrosis, NO->MI, GI flora to blood, SHOCK General Features Circulatory collapse->multisystem end-organ hypoperfusion Final common Pathway for many lethal clinical events via drop in CO of blood volume -Clnical indicators: Reduced mean arterial pressure (MAP) (ឬmmHg) Tachycardia, Tachypnea Cool skin, extremities (except in neurogenic, early septic) Usually Hypotension Results in tissue hypoxia -> lactic acidosis, SHOCK General Features 1. Nonprogressive (early) stage - Compensatory mechanisms maintain perfusion -increased HR, increased peripheral resistance, renal fluid conservation -baroreceptor reflexes, epi/noepi release, renin-AT axis, ADH release -coronary, cerebral maintain constant flow (no constriction) 2. Progressive stage - Tissue hypoperfustion->circulatory and metabolic imbalance -dominated by renal insufficiency -metabolic acidosis from lactic acidemia - Compensatory mechanisms not adequate. -lower pH blunts vasomotor response->peripheral pooling -confused pt, urine output declines 3. Irreversible stage - organ damage and metabolic disturbances incompatible w/ life -complete renal shutdown due to acute tubular necrosis, NO->MI, GI flora to blood, SHOCK 4. Neurogenic Due to trauma, especially of high cervical spinal cord ->interrupt sympthetic vasomotor input -->arteriolar dilatation, venodilation -warm extremities, SHOCK 3. Septic Leading cause of death in ICUs - mortality up to 75% Systemic response to severe infection-results from spread to blood -Most commonly from endotoxin-producing gram-negative bacteria(70%) -Also due to superantigen of Staph. aureus->"toxic shock syndrome" Endotoxin+circulating blood protein complex->activate WBCs, endoth via CD14 -low doses->local inflammation; -moderate doses (more NO, PAF) - acute phase reactants->fever, systemic effects -high doses->low CO, low TPR, vessel injury->DIC, ARDS(alv cap dmg) ->multiorgan system failure (liver, kidneys, CNS)->death Course: 1. Initial vasodilation increases blood flow (warm extremities) 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) Tx underlying infx, control LPS