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Shock
types of shock
| Question | Answer |
|---|---|
| pathophysiology of shock | alterations in at least 1 of 4 components: blood volume, contractility, blood flow, vascular resistance |
| cardiogenic shock | pump failure results in hemodynamic changes decreased cardiac output and decreased tissue perfusion |
| precipitating factors of cardiogenic shock | MI, cardiomyopathy, blunt cardiac trauma, cardiac tamponade, pulmonary hypertension, dysrhythmias |
| early manifestations of cardiogenic shock | tachycardia, hypotension, increased myocardial O2 consumption |
| physical assessment of cardiogenic shock | tachypneic, cool, clammy skin, decreased capillary refill, crackles in lungs, confusion, agitation, decreased renal perfusion, decreased urine output |
| management of cardiogenic shock | treat dysrhythmias, cardiac catheterization to restore flow, intraaortic balloon pump, VAD device |
| medications- positive inotropes to help contract heart | dopamine, dobutamine, digoxin, milrenon |
| medications to help decrease preload | diuretics, vasodilators, nitrates |
| when to know if vasodilators are effective | if patient is pink and warm |
| medications to help decrease afterload | ACE inhibitors, positive inotropes and vasodilators |
| hypovolemic shock | inadequate circulating volume creates hemodynamic changes including decreased preload decreased stroke volume decreased cardiac output |
| manifestations of hypovolemic shock | anxious, increased RR, increased HR, cardiac output decreased, decreased stroke volume, decreased urine output |
| management of hypovolemic shock | determine and treat underlying cause, stop loss of fluid, replace fluids (monitor urine output) |
| neurogenic shock | massive vasodilation without compensation due to loss of SNS vasoconstriction tone |
| causes of neurogenic shock | SCI, trauma, depression of medulla - opiods / drugs |
| clinical manifestations of neurogenic shock | decreased blood pressure, decreased HR, inability to regulate temperature, dry skin |
| management of neurogenic shock | atropine (increases HR) fluids |
| anaphylactic shock | acute, life-threatening hypersensitivity (allergic) reaction |
| causes of anaphylactic shock | drugs, vaccines, food, insect venom |
| clinical manifestations of anaphylactic shock | hypotension, respiratory distress, dizziness, chest pain, wheezing, swelling |
| management of anaphylactic shock | prevention!!!!!! epinephrine IM benadryl, steroids, vasopressors, bronchodilators possible ET intubation |
| septic shock | presence of sepsis with hypotension despite fluid resuscitation |
| causes of septic shock | gram negative and positive bacteria |
| clinical manifestations of septic shock | hypoxia, increased coagulation, inflammation, vasodilation, increased RR, decreased ejection fraction, decreased urine output |
| management of septic shock | find the cause and start antibiotics but must get cultures first fluids and vasopressors |
| obstructive shock | physical impairment to adequate circulatory blood flow |
| possible causes of obstructive shock | cardiac tamponade, pulmonary embolism, tension pneumothorax |
| clinical manifestations of obstructive shock | hypoxia, jugular vein distention, chest pain, pulmonary edema |
| management of obstructive shock | mechanical decompression, chest tube, thrombolytics, radiation or removal of mass |
| Shock: stage 1 | initiation: hypoperfusion- inadequate delivery or extraction of oxygen causes lactic acid buildup- no obvious clinical signs |
| shock stage 2 | compensatory sustained reduction in tissue perfusion ANS releases norepinephrine and cortisol RAAS system initiated CM- decrease in BP, increased HR, RR, and decreased urine output |
| shock stage 3 | progressive compensatory mechanisms fail- all organs compromised CMs: AKI, ARDS, change in mental status, decreased cardiac output, increased RR, crackles, MI, GI bleed |
| shock stage 4 | refractory anaerobic metabolism due to decreased perfusion blood and fluid leave intravascular space hypotension and hypoxemia unresponsive to therapy |
| CNS assessment | decreased LOC, blurred vision, confusion, restlessness and anxious |
| pulmonary early stage assessment | increased ventilation, perfusion mismatch hyperventilation tachypnea |
| pulmonary late stage assessment | pulmonary vasoconstriction increased capillary permeability alveolar edema moist crackles |
| GI assessment | decreased intestinal activity decreased blood supply |
| hepatic assessment | failure to metabolize drugs and waste (buildup of lactic acid and ammonia) increased susceptibility to toxicity |
| integumentary assessment | pale and cool to mottled and blue |
| diagnostic findings | CBC, coagulation studies, BMP, serum lactate acid level (5-20), EKG, CXR, hemodynamic monitoring |
| cardiogenic shock diagnostics | cardiac enzymes, echo, cardiac catheter, CT scan |
| hypovolemic shock diagnostics | type and crossmatch, fecal occult, EGD |
| septic shock diagnostics | blood, urine, and wound cultures |
| medical management of shock | treat cause, fluid resuscitation, nutrition (within first 24 hrs), optimize oxygen delivery and O2 demands |
| crystalloids | 0.9 NS, or LR |
| colloids | albumin when volume is lost due to loss of plasman vs loss of blood |
| vasopressors are used when | after fluid resuscitation keep MAP > 65 vasopressin |
| vasodilators are used to | break cycle of widespread vasoconstriction nitroglycerin |
Created by:
ebrewer12
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