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Shock Articles/Notes

Articles Parts 3-4 and Class Notes

QuestionAnswer
cardiogenic shock, nursing prevention decrease infarction size: calm, reassuring, prompt pain relief, rest, supplemental oxygen
hypovolemic shock, nursing prevention I&O/fluid status, daily weights, unmeasured fluid loss considered (insensible, sweat, drainage), decrease blood loss
minimizing blood/fluid loss direct pressure at site, tell the doctor, replace IV fluids rapidly
neurogenic shock, nursing prevention immobilization of spinal cord injuries ASAP, after spinal anesthesia HOB 15-20* elevated (so anesthesia doesnt get to medulla)
anaphylactic shock, nursing prevention caution when IV drug admin especially first time giving, when giving blood blood type and Rh matched, monitor for s/s (flushing, pruritis, edema, hypotension, dyspnea) and stop if occur leaving IV patent with isotonic fluids
septic shock, nursing prevention strict asepsis (suctioning, dressing changes, wound care), check for inflammation (red, swell, warmth) and systemic infection, temp, WBC, BP
assesment of shock (4 major ones) LOC, skin, UO, VS
reason for LOC changes decreased cerebral BF, inadequate O2 delivery to brain ells
early shock LOC subtle: restless, agitated, irritable
later shock LOC confusion, personality change, loss of memory, altered sleep
shock latest stages LOC responsive to verbal stimuli absent, thus pain response assessed (decreases from flexing to pain, then extanding, then flaccid/no response)
skin/mucous membrane assessment color, temp, moistness, texture, turgor
early shock skin cool, pale, sweat/clammy moist skin, reduced cap refill
sustained shock skin cyanotic, cold, mottled
skin exceptions: sepsis in hyperdynamic phase, warm, dry, and pink from early vasodilation
skin exceptions: liver ischemia/failure jaundiced
skin exceptions: anaphylactic shock flushed, macular/papular rashes
skin exceptions: hypovolemic shock from dehydration very dry, poor skin turgor
skin exceptations: blood loss hypovolemic shock mucous membranes pale
renal function: minimum hourly output 20cc or 0.5cc/kg
UO, compensatory shock volume decreased, osmolality increased (because kidneys can still excrete waste products but retain fluid as compensation for shock)
UO, shock progresses volume low, concentration fixed or dilute (failing kidneys cant excrete waste products as well, lose ability to concentrate urine)
UO: early septic shock inappropriate polyuria up to or over 100cc/hr (hypotension + polyuria r/t bacteria toxins causing renal vasodilation)
VS: initially normal or elevated (compensation)
VS: progression of shock systolic BP decreases (as CO decreases), diastolic normal (vasoconstriction) --> pulse pressure narrows
BP in shock can be high, low, or normal depending on type, other conditions, compensation
Taking BP in shock using cuff normally inaccurate and may underestimate arterial pressure by 15-30; may not even hear so have to palpate arterial pulse distal to cuff to estimate systolic BP or use U/S flow meter
Taking pulses in shock tell about peripheral BF, do major arteries (carotid, brachial, radial, ulnar, femoral, popliteal, dorsalis pedis, posterior tibial); assess rate, rhythm, amplitude, quality
Pulse in shock rapid, rhythm poss irregular (d/t ishemic arrhythmias as progresses), amplitude reduced, quality thready
RR: early shock rapid (>20 often), depth increased 2x
RR: shock progresses respiratory muscles fatigue --> hypoventilation (shallow), rapid still
Lung sounds, shock progresses moist crackles (from interstitial edema), expiratory wheezes if anaphylactic (from bronchial constriction)
Temperature in shock decreased from slowed cellular met, decreased production of heat (except sepsis from inflammation or anaphylactic bc of allergic response)
nurse: lab testing, blood frequent blood samples: ABGs, elites, glucose, enzymes (CPK, SGOT, amylase: tell organ/tissue destruction), BUN/creatinine/bili/ammonia (renal, hepatic fxn), CBC and coag studies (test covert bleed, coag prob)
nurse: lab testing, urine elites, osmolality, creatinine clearance (for renal, metabolic probs)
nurse: other testing radiographic, CT, ECG, U/S, pulmonary fxn, arteriograms, angiography
INTRODUCTION TO INVASIVE CATHETERS I SKIPPED THIS IT WAS LONG AND BORING AND TMI
hemodynamic changes in shock arterial BP, PAP (pulm artery pressure), PAOP (pulm artery occlusion pressure, RAP (R atrial pressure), CO (changes vary depending on type and progression)
hypovolemic shock: hemodynami changes ­­decreased venous return, low ventricular filling pressures, R atrial pressure and PAOP low, SV and CO low, PAP normal or reduced (low volume) or elevated (vasoconstriction)
cardiogenic shock: hemodynamic changes filling pressure RAP and PAOP increased (d/t ventricles not emptying), CO decreased (impaired contractility), arterial BP low, PAP increased (from increased L heart pressures into pulm circ)
neurogenic shock: hemodynamic changes venous return falls (blood pooling, vasodilation massive), RAP and PAOP low, low CO and BP (heart doesnt fill enough), PAP normal or low (vasodilation, relative hypovolemia)
anaphylactic shock: hemodynamic changes decreased filling pressures RAP and PAOP --> low CO and BP; PAP normal or low (from decreased BV)
hypovolemic hemodynamic simple everything low except PAP any (high, low, or nomal)
cardiogenic hemodynamics simple only one wiht high filling pressures (PAOP and RAP), low CO and BP, high PAP
neurogenic hemodynamics simple low everything except for PAP low or normal
anaphylactic hemodynamics simple same as neurogenic (everything low except poss normal PAP)
septic hemodynamics simple early (decreased everything except for increased or normal CO), late (increased or decreased filling pressures RAP and PAOP, decreased CO and BP, increased PAP)
septic shock, early/warm phase hemodinamics massive vasodilation --> decreased venus return --> RAP and PAOP decreased; CO nnormal or increased (from low SVR and afterload); BP decreased in spite of CO increase (massive vasodilation and lowerered peripheral vascular resistance); PAP normal or low
sepsis late/cold/hypodynamic phase hemodynamics cap permeability increase --> less volume; CO low (impaired contractility, inadequate filling); PAOP and RAP can be decreased (less venous return) usually increased (myocardial dysfxn, incomplete V. emptying), BP low; PAP eventually increases
ominous sign hypotension in the presence of shock
compensated shock BP normal or high
decompensated shock PB low, cardiopulmonary arrest is possibly imminent
shock inadequate tissue perfusion, is present when CV dsyfxn --> inadequate perfusion of vital organs
most common causes (4) severe dehydration, hemhorrage, progressive heart failure, sepsis
distributive/vasogenic shock voume there, wrong place
most shock types has elements from all types of shock
cardiogenic shock volume there, pump isnt distributing it well; low CO and hypotension, clinical signs of inadequate BF to tissues
hypovolemic shock loss of intravascular volume; amount lost = severity
hypovolemic shock management early recognition (before hypotension or loss of 20-25%), correct underlying cause, rapid replace loss NS/LR, keep client calm
injuries where in wrong place, stopping bleeding never move something if it is not in the proper location and it hurts/doesnt move easy, because it can cause damage, cut off blood supply, cause nerve damage, etc
open femur fracture large bone full of BM, easily bleed so put immediate pressure
rapid replacement of fluids in hypovolemic shock start off with crystalloids (NS, LR) but if there is a lot will shift to blood products (colloids: albumin, parked RBC, blood)
crystalloids vs colloids crystalloids will leak into third space more, colloids have proteins in them and dont leak
cardiogenic shock management limit/reduce cardiac damage, impove effectiveness of pumping action (drugs mostly, possibly elevate HOB)
cardiac output equation CO = SV (SVR and ejection of heart) x HR
drugs/action for acute MI aspirin, thrombolytics, angioplasty, nitroglycerine
IV fluid in cardiogenic shock be cautious because if give the pump has to work harder, cant pump it out, backs up from R sided HF (seen as SOB, jugulovenous distensiton, backup into body and edema --> eventual L sided HF and pulm edema); however, give 1st bolus when undetermined shock
inotropics for cardiogenic shock: dopamine given primarily to imporve renal function (in low doses) dilates kidney vessels; not usually for cardiac sstem just to sustain kidneys when in shock; then another drug is given for cardiac support
anaphylactic shock distributive, may show symptoms w/in 20 minutes of exposure, early symptoms are ???? later symptoms are ?????; the earlier you catch the easier it is to fix
anaphylaxis managment ID/remove causative agent, reverse effects of chemical mediators (epinephrine stops vasodilation and opens up airways, given SQ or IV), then reverse infammation next (salumedrol, steroids/corticosteroids, benadryl, etc)
septic shock s/s distributive, massive vasodilation, low SVR, capillary leak, organ failure, lactic acidosis despite high CO, systemic and pulmonary edema
septic shock management early recognition key, optimize CO, control O2 demand; can take up to a week after resolved to stop edema because giving fluids and third spacing
supportive management ventilation, optimal intravascular adequate RBC volume, maintain metabolic state; O2 and nutrients becaue of hypermetabolic state/overdrive; check glucose
glucose in shock increased BG when release stores early on, but later will drop when depleted
shock effects: pulmonary capillary perfusion increases (lungs fluffy/fluid on xray) --> leaks, alveoli flooded; endothelial liining damage --> less surfactant, alveolar collapse --> fibrotic changes/scarred lungs
lungs early compensation rapid and deep RR: trying to get off CO2 (because met acidosis) and get more O2
lungs late compensation still rapid RR but shallow --> risk for hypoxia at this point
shock effects: renal reduced GFR, blood shunted from outer to inner cortex --> renin/angiotensin system sense less BF, activated --> decreased O2/ATP cause cellular sloughing and ATN --> w/ATN cant excrete waste products --> faulure (decreased UO is clinical sign)
decreased UO kids <1cc/kg/hr adults <30cc/hr
shock effects: CV blood shunts to central circulaiton, vital organs; myocardial O2 demand increases --> tachycardia (when compensation); late shock comp fails --> CO/BP falls; decreased coronary perfusion
shock effects: CV s/s HR changes, diminished pulse quality, decreased systolic and MAP, delayed cap refill
normal MAP ??????
shock effects: neuro blood shunted to brain early (up to 5x); once MAP <60 autoreg responses fail (cant breathe, no reflexes, etc), cerebral cells become ischemic and lactate accumulates; intracranial hypertension and cerebral perfusion pressure falls
***intracranial hypertension and cerebral perfusion falling CPP (cerebral perfusion flow) = MAP - ICP ?????????
shock effects: neuro s/s changes in LOC often restless, agitated --> confusion, irritable, lethargy
shock effects: hepatic liver fails from anaerobic met; hepatocytes cant generate ATP during anaerobic met, so cellular membrane damage w/loss of liver fxn; liver enzymes elevate (ALT, AST, >>> phosphatase), ammonia and lactate accumulate (ammonia --> encephalopathy)
liver damage if reversed early, damage can be reversed cuz liver can regenerate itself
shock effects: GI system one of the earlier systems to take a hit; blood redirected from gut through vasoconstriction of splanbchic vessesl; reduced BF --> damage to epithelial lining --> decreased gastric motility, paralytic ileus; predisposed to ulcers, GI bleed
phrophylactic treatment in stress situations for ulcers eg nexium
shock effects: hematologic sluggish BF --> microemboli --> microishcemias --> cell death --> lactic acidosis, other bad stuff; hypoperfusion of liver --> decreased clotting factors made --> coagulopathies, cant stop bleeding; poss leukopenia from leukocytosis
shock effects: integument one of first affected; peripheral vasoconstriction --> pale, cool, clammy skin, mottled if severe*** for a long time and really bad cuz means ishemia already happened is purply looking; if distributive skin is warm dry and flushed
skin when compensatory mechanisms fail very cool, cyanotic, mottled
vasoactive inotropic drug therapy increase HR if too slow, increase CO if inadequate, increased cardiac contractility, redistribute CO, manipulate vascular resistance, administered IV continuous and titrated to effect (always) most places standing orders to titrate so nurses can do
if need to increase CO and pump action give inotropic drugs (**but increae pump action and increase metabolic and oxygen consumption too)
Created by: hanalin2 on 2008-03-17



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