Shock Concept Map PDF

^Epi i nc OFTn»ESOF£MOC ©2016 DEANNEA. BLACH, MSN, RN ^ Hvpovolemic -> loss of intravascular volume. Cardioeenic -> cardiac pump failure. Distributive -> maldistribution of circulating blood volume. Classified as: a Septic-> microorganisms entering body. o Anaphvlactic -> severe antibody- Hypovolein...

^Epi i nc OFTn»ESOF£MOC ©2016 DEANNEA. BLACH, MSN, RN ^ Hvpovolemic -> loss of intravascular volume. Cardioeenic -> cardiac pump failure. Distributive -> maldistribution of circulating blood volume. Classified as: a Septic-> microorganisms entering body. o Anaphvlactic -> severe antibody- Hypovolein 1c Cardio loss of sympathetic tone. ^^ PA7HOPHYSIOLOGY- STAGESOFSt ' Administerfluids (crystalloids, colloids) for ^ A dynamic physiologic phenomenon results in Initialstage:CO ^, tissue perfusionthreatened. Compensatory stage: Almost immediately, body's homeostatic mechanisms attempt to maintain CO, BP, & tissue perfusion. Mechanisms are mediated by SNS. - Neural response: 1^ HR & contractility, vasoconstriction, & shunting of blood to vital preload from intravascular volume depletion.. Measure preload responsiveness with respiratory or positional variation in pulse pressure, systolic pressure, & SV. Ensure sufficient H/H levels. Blood administration Compensatory mechanisms begin to fail if Hgb critically ^, but restrictive transfusion practice 4^ mortality from transfusion-related ^ ^ Cardiac Output acute lung injury.. Sodium bicarb not recommended in treatment of shock-related lactic acidosis.. Implement individualized enteral nutritional support therapy within 24-48 hrs.. ^ Tissue Perfusion ^ Acute Circulatory Failure organs. - Hormonal response: Activation of reninangiotension-aldosterone-ADH mechanism -> sodium and water retention. Secretion of ^ Risk for MODS & Death. Targetglucose at 140-180mg/dLto ^ infection, ACTH -> production ofglucocorticoids -> ^ blood glucose. Release of epi & norepi -> renal failure, sepsis, & death. Provide comfort and emotional support. Institute evidence-based practice protocols to prevent complications. Assess response to therapy. Death vasoconstriction. Progressive staee: -> 4/ tissue perfusion, ->. Occurs Successful lactic acidemia. Vasodilation & T vascular permeability -> ^ intravascular volume, tissue edema, & further \1/ tissue perfusion -> SIRS -> Prevent and maintain surveillance for complications. PATIENT irreversible cell damage & cellular death -> cells OUTCOMES unable to use oxygen. Every system in the body is affected. Refractory stape: Shock unresponsive to therapy & irreversible. As the individual organ systems Perfusion SAVINGTHE LIFEOFTHE PATIENTIN SHOCK die, MODSoccurs -^ patient death. DEMONSTRATEADEQUATE TISSUEPERFUSION: - Hemodynamic values within normal (CO, DlAC »IS Indicators of systemic perfusion and tion Serum lactate, arterial base deficit, serum bicarb, & central or mixed venous 02saturation levels. Inadequatecellular oxygenation with anaerobic metabolism & /[~ metabolic lactate production /I^serum lactate level. BP, HR, CVP, PAP, PCWP) - Electrolytes and H/H within normal range - Maintain 02 Sat of 90% or greater Mental clarity, skin warm/dry Urine output > 60 mL/hr RR within normal, clear breath sounds I I I.... Identify underlying cause & treat accordingly. Ensure adequate organ & extremity perfusion. Identify and correct cause of lactic acidosis. Support oxygen delivery.