Articles Parts 3-4 and Class Notes
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| cardiogenic shock, nursing prevention | decrease infarction size: calm, reassuring, prompt pain relief, rest, supplemental oxygen
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| hypovolemic shock, nursing prevention | I&O/fluid status, daily weights, unmeasured fluid loss considered (insensible, sweat, drainage), decrease blood loss
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| minimizing blood/fluid loss | direct pressure at site, tell the doctor, replace IV fluids rapidly
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| neurogenic shock, nursing prevention | immobilization of spinal cord injuries ASAP, after spinal anesthesia HOB 15-20* elevated (so anesthesia doesnt get to medulla)
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| 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
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| septic shock, nursing prevention | strict asepsis (suctioning, dressing changes, wound care), check for inflammation (red, swell, warmth) and systemic infection, temp, WBC, BP
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| assesment of shock (4 major ones) | LOC, skin, UO, VS
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| reason for LOC changes | decreased cerebral BF, inadequate O2 delivery to brain ells
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| early shock LOC | subtle: restless, agitated, irritable
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| later shock LOC | confusion, personality change, loss of memory, altered sleep
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| shock latest stages LOC | responsive to verbal stimuli absent, thus pain response assessed (decreases from flexing to pain, then extanding, then flaccid/no response)
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| skin/mucous membrane assessment | color, temp, moistness, texture, turgor
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| early shock skin | cool, pale, sweat/clammy moist skin, reduced cap refill
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| sustained shock skin | cyanotic, cold, mottled
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| skin exceptions: sepsis | in hyperdynamic phase, warm, dry, and pink from early vasodilation
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| skin exceptions: liver ischemia/failure | jaundiced
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| skin exceptions: anaphylactic shock | flushed, macular/papular rashes
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| skin exceptions: hypovolemic shock from dehydration | very dry, poor skin turgor
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| skin exceptations: blood loss hypovolemic shock | mucous membranes pale
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| renal function: minimum hourly output | 20cc or 0.5cc/kg
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| UO, compensatory shock | volume decreased, osmolality increased (because kidneys can still excrete waste products but retain fluid as compensation for shock)
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| UO, shock progresses | volume low, concentration fixed or dilute (failing kidneys cant excrete waste products as well, lose ability to concentrate urine)
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| UO: early septic shock | inappropriate polyuria up to or over 100cc/hr (hypotension + polyuria r/t bacteria toxins causing renal vasodilation)
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| VS: initially | normal or elevated (compensation)
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| VS: progression of shock | systolic BP decreases (as CO decreases), diastolic normal (vasoconstriction) --> pulse pressure narrows
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| BP in shock | can be high, low, or normal depending on type, other conditions, compensation
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| 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
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| 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
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| Pulse in shock | rapid, rhythm poss irregular (d/t ishemic arrhythmias as progresses), amplitude reduced, quality thready
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| RR: early shock | rapid (>20 often), depth increased 2x
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| RR: shock progresses | respiratory muscles fatigue --> hypoventilation (shallow), rapid still
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| Lung sounds, shock progresses | moist crackles (from interstitial edema), expiratory wheezes if anaphylactic (from bronchial constriction)
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| Temperature in shock | decreased from slowed cellular met, decreased production of heat (except sepsis from inflammation or anaphylactic bc of allergic response)
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| 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)
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| nurse: lab testing, urine | elites, osmolality, creatinine clearance (for renal, metabolic probs)
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| nurse: other testing | radiographic, CT, ECG, U/S, pulmonary fxn, arteriograms, angiography
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| INTRODUCTION TO INVASIVE CATHETERS | I SKIPPED THIS IT WAS LONG AND BORING AND TMI
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| 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)
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| 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)
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| 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)
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| 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)
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| anaphylactic shock: hemodynamic changes | decreased filling pressures RAP and PAOP --> low CO and BP; PAP normal or low (from decreased BV)
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| hypovolemic hemodynamic simple | everything low except PAP any (high, low, or nomal)
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| cardiogenic hemodynamics simple | only one wiht high filling pressures (PAOP and RAP), low CO and BP, high PAP
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| neurogenic hemodynamics simple | low everything except for PAP low or normal
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| anaphylactic hemodynamics simple | same as neurogenic (everything low except poss normal PAP)
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| 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)
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| 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
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| 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
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| ominous sign | hypotension in the presence of shock
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| compensated shock | BP normal or high
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| decompensated shock | PB low, cardiopulmonary arrest is possibly imminent
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| shock | inadequate tissue perfusion, is present when CV dsyfxn --> inadequate perfusion of vital organs
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| most common causes (4) | severe dehydration, hemhorrage, progressive heart failure, sepsis
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| distributive/vasogenic shock | voume there, wrong place
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| most shock types | has elements from all types of shock
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| cardiogenic shock | volume there, pump isnt distributing it well; low CO and hypotension, clinical signs of inadequate BF to tissues
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| hypovolemic shock | loss of intravascular volume; amount lost = severity
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| hypovolemic shock management | early recognition (before hypotension or loss of 20-25%), correct underlying cause, rapid replace loss NS/LR, keep client calm
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| 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
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| open femur fracture | large bone full of BM, easily bleed so put immediate pressure
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| 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)
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| crystalloids vs colloids | crystalloids will leak into third space more, colloids have proteins in them and dont leak
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| cardiogenic shock management | limit/reduce cardiac damage, impove effectiveness of pumping action (drugs mostly, possibly elevate HOB)
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| cardiac output equation | CO = SV (SVR and ejection of heart) x HR
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| drugs/action for acute MI | aspirin, thrombolytics, angioplasty, nitroglycerine
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| 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
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| 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
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| 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
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| 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)
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| septic shock s/s | distributive, massive vasodilation, low SVR, capillary leak, organ failure, lactic acidosis despite high CO, systemic and pulmonary edema
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| 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
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| supportive management | ventilation, optimal intravascular adequate RBC volume, maintain metabolic state; O2 and nutrients becaue of hypermetabolic state/overdrive; check glucose
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| glucose in shock | increased BG when release stores early on, but later will drop when depleted
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| 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
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| lungs early compensation | rapid and deep RR: trying to get off CO2 (because met acidosis) and get more O2
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| lungs late compensation | still rapid RR but shallow --> risk for hypoxia at this point
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| 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)
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| decreased UO | kids <1cc/kg/hr adults <30cc/hr
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| 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
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| shock effects: CV s/s | HR changes, diminished pulse quality, decreased systolic and MAP, delayed cap refill
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| normal MAP | ??????
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| 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
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| ***intracranial hypertension and cerebral perfusion falling | CPP (cerebral perfusion flow) = MAP - ICP ?????????
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| shock effects: neuro s/s | changes in LOC often restless, agitated --> confusion, irritable, lethargy
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| 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)
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| liver damage | if reversed early, damage can be reversed cuz liver can regenerate itself
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| 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
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| phrophylactic treatment in stress situations | for ulcers eg nexium
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| 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
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| 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
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| skin when compensatory mechanisms fail | very cool, cyanotic, mottled
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| 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
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| if need to increase CO and pump action | give inotropic drugs (**but increae pump action and increase metabolic and oxygen consumption too)
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