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
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
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
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
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)
Biology Lab Midterm
