Initial stage of shock occurs at the cellular level and is not clinically apparent o Metabolic changes aerobic anaerobic lactic acid build up Body activates neural hormonal and biochemical compensatory mechanisms o Attempt to overcome complications of anaerobic metabolism maintain homeostasis STAGES OF SHOCK COMPENSATROY STAGE CLINICAL MANIFESTATIONS Neurologic o Oriented to person place and time o Restless apprehensive confused o Change in LOC Cardiovascular o Sympathetic nervous system response Decreased CO and narrowing of pulse pressure hypotension baroreceptors activate SNS vasoconstriction release of epinephrine and norepinephrine blood is diverted to heart and brain away from GI skin kidneys and lungs oxygen demand and SNS stimulation myocardium response HR and contractility increased O2 demand coronary arteries dilate o Coronary artery dilation o Narrowed ulse pressure o Decreased BP but adequate to perfuse vital organs heart and brain Respiratory o Decreased blood flow to the lungs Physiologic dead space Physiologic dead space anatomic dead space decreased gas exchange units and any inspired air that cannot participate in gas exchange ventilation perfusion mismatch o Areas of the lung not perfused will not participate in gas exchange Ventilation perfusion mismatch Hyper ventilation Minute ventilation Gastrointestinal o Blood supply o GI motility o Hypoactive bowel sounds o Risk for paralytic ileus Renal o Renal blood flow renal perfusion renin release angiotensin produces angiotensin I angiotensin II arterial and venous vasoconstriction increases venous return to the heart increases BP Angiotensin II also aldosterone sodium and water reabsorption and potassium excretion ADH release increases water reabsorption increasing blood volume increased CO and BP o Renin resulting in release of angiotensin vasoconstrictor o Aldosterone resulting in Na and water reabsorption o Antidiuretic hormone resulting in water reabsorption Hepatic o None Hematologic o None Temperature o Normal or abnormal Skin o Pale and cool o Warm and flushed early onset of septic shock Key Laboratory Findings o blood glucose o pH o PaO2 o Pa CO2 o If not progressive stage PROGRESSIVE STAGE Begins as the compensatory mechanisms fail CLINICAL MENIFESTATIONS Neurologic o Mental status changes are the most important findings o cerebral perfusion o cerebral blood flow o Listless or agitated o responsiveness to stimuli Cardiovascular If the cause of shock is corrected at this stage there is little to no residual aftereffects o CO begins to fall decrease in BP and perfusion altered capillary permeability fluid and protein leakage into interstitial space anasarca o capillary permeability systemic interstitial edema o cardiac output BP and HR o MAP 60 or drop of 40 from baseline o coronary perfusion dysrhythmias myocardial ischemia myocardial infarction o peripheral perfusion ischemia of distal extremities diminished pulses and capillary refill o End result is complete cardiovascular deterioration Respiratory o First system to show dysfunction o ARDS o capillary permeability pulmonary interstitial edema bronchoconstriction and decreases residual capacity alveolar edema and decreases surfactant o Pulmonary vasoconstriction increase pulmonary arterial pressure pulmonary capillary blood flow worse ventilation perfusion mismatch o Diffuse infiltrates o RR o compliance o Moist crackles o Overall increase in work of breathing Gastrointestinal o Vasoconstriction and perfusion ischemic gut Erosive ulcers GI bleeding Translocation of GI bacteria Impaired absorption of nutrients o Normal mucosa barrier become ischemic risk for ulcers and bleeding Renal o Renal tubules become ischemic acute tubular necrosis acute renal failure o urine output o BUN creatinine ratio o urine sodium o urine osmolality specific gravity o urine potassium o Metabolic acidosis from inability to excrete lactic acid and reabsorb bicarbonate Hepatic o Failure to metabolize drugs and waste products o Cell death increased liver enzymes o Jaundice decreased clearance of bilirubin o NH3 and lactate o Increased risk of bacteremia o DIC bleeding from orifices GI lungs puncture sites Thrombin clots in microcirculation Consumption of platelets and clotting factors with secondary fibrinolysis Hematologic Temperature o Hypothermia o Sepsis hypo or hyperthermia Skin o Cold and clammy Key laboratory findings o liver enzymes ALT AST GGT o Bleeding times o Thrombocytopenia IRREVERSIBLE STAGE metabolism Decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic Once one organ system fails many other soon follow lactic acid capillary permeability and dilation fluid and plasma proteins to leave vascular space interstitial space blood pools in capillary beds worsens hypotension tachycardia and coronary blood flow myocardial depression further decline in CO cerebral ischemia CLINICAL MANIFESTATIONS Neurologic o Unresponsive o Areflexia loss of reflexes o Pupils nonreactive and dilated Cardiovascular o Profound hypotension o Decreased cardiac output o Bradycardia and irregular rhythm o Decreased BP inadequate to perfuse vital organs Respiratory o Severe refractory hypoxemia o Respiratory failure Gastrointestinal o Ischemic gut Renal Hepatic o Anuria Hematologic o DIC progresses Temperature o Hypothermia Skin o Mottled cyanotic Key Laboratory Findings o blood glucose o NH3 lactate and K also urea and ammonia o Metabolic acidosis LABORATORY ABNORMAILITES RBC can be normal increased or decreased DIC screen o Metabolic changes from accumulation of waste products NH3 lactate CO2 o Fibrin split products o Fibrinogen level o Platelet count o PTT and PT o Thrombin time o D dimer Creatinine kinase Troponin BUN Creatinine early or Glucose Serum electrolytes o early or Sodium o or early Potassium Arterial blood gases o Respiratory alkalosis early r t hyperventilation o Metabolic acidosis late r t anaerobic metabolism lactic acid Blood cultures growth of organisms Lactic acid Liver enzymes ALT AST GGT