Shock Interventions for Clients with Shock Hope Knight MS RN
TYPES OF SHOCK • Functional Impairment • Hypovolemia • Cardiogenic • Distributive • Obstructive • Site of Origin • Hypovolemic • Cardiogenic • Vasogenic • Septic
Key Features of Shock • Cardiovascular • Respiratory • Neuromuscular • Renal • Integumentary • Gastrointestinal
SHOCK - FLUID THERAPY • Crystalloids • Blood/Blood Products Whole/Packed Red Blood Cells Colloids Hetastarch/Hextend Albumin Dextran
SHOCK – DRUG THERAPY • Dopamine • Dobutamine • Milrinone • Epinephrine • Norepinephrine • Phenylephrine • Nitroglycerine • Sodium Nitroprusside
STAGES OF SHOCK • Initial Stage • Nonprogressive Stage (Compensatory Stage) • Progressive Stage (Intermediate Stage) • Refractory Stage (Irreversible Stage) • Multiple Organ Dysfunction Syndrome (MODS)
Initial Stage • Baseline MAP i <10mm/Hg • Cellular changes = h anaerobic metabolism h lactic acid • compensation: vascular constriction & h HR • MAP maintained • difficult to detect
Nonprogressive Stage • MAP <10-15mm/Hg from baseline • Release of renin, antiduiretic hormone (ADH), aldosterone, epinephrine, and norepinephrine. • Renin eiurine output,hNA+ reabsorption • ADH ehWater reabsorption,hblood vessel constriction • Compensate: keep volume in central blood vessel • Cellular: acidosis, hyperkalemia
Progressive Stage • MAP >20mm/Hg from baseline • Compensatory mechanisms do not function use > amount of oxygen • Vital organs eanoxic & ischemic epoor oxygenation & htoxic metabolites esevere cell damage/death • Life threatening emergency • Immediate intervention • Look at pre-existing health • Correct shock conditions within 1 hour
Refractory Stage • Too much cellular death & tissue damage • Vital organs overwhelming damage • Therapy NOT effective even if MAP returned to normal • Cell damage in vital organs continues
Multiple Organ Dysfunction Syndrome e Cycle of more dead cells break open and release harmful metabolites. • microthombi e damage more cells • Liver, heart, brain & kidney septic shock involves lungs also • Heart muscle harmed by ischemic pancreas releases myocardial depressant factor
Hypovolemic Shock • Etiology • Causes • Assessment • Manifestations • Cardiovascular • Skin • Respiratory • Renal • CNS • Musculoskelatal • Psychosocial Assessment • Interventions
Situation #1 • Client admitted post abdominal surgery. BP 120/70, Tele: SR 95, RR 20 reg, skin pale, AAO, output 40ml/hr. c/o thirst. • BP 85/65, Tele: ST 120 w/PVCs, RR 34 & shallow, skin pale, output 20ml the last hour, c/o very thirsty, cap refill >4 sec • BP 70/45, Tele: ST 150 with burst V-tach, RR 44 & very deep, bilat crackles, confused, mottled, lethargic, weak in all extremeties, no cap refill noted
Cardiogenic Shock • Etiology • Necrosis of more than 40% of heart occurred. • Causes • MI, structural problem, or arrhythmia • Assessment • Tachycardia, iBP, narrow pulse pressure, hworkload on heart • Medical Management • Chapter 41 page 854
Situation #2 61 y/o male admitted with MI 2 days ago. Vitals: BP 100/60, RR 20. Tele: SR 80 w/PVC’s. Skin pink, no c/o SOB or pain at this time, pulses 2+ bilat. B/P 90/65, Tele: ST 100 couplets PVCs, RR 34 & shallow, skin pale & diaphoretic, anxious, output dark, pedal pulses 1+ bilat. BP 75/50, Tele: ST 150 with run 5-8 v-tach, RR 48 & shallow, skin cyanotic/mottled, pedal pulses not palpable, restless & confused, output 20m/hr, wife crying beside in chair in corner.
Distributive Shock • Causes • Neural-Induced • Pain, spinal cord injury, head trauma • Chemical Induced • Anaphylaxis • Sepsis • Capillary Leak Syndrome • Predisposing Factors to Sepsis-induced Shock • Health Promotion
Anaphylaxis • Rarely occurs with 1st encounter • Histamines move rapidly into blood • Massive blood vessel dilation • Increased capillary leak • Severe hypovolemia & vascular collapse • Decreased cardiac contraction & dysrhythmia • Antigen-antibody rxn in bronchial tissue esevere edema and obstruction ereduced gas exchange • Without intervention = death
Situation #3 • 21 y/o male admitted from ED post fall from ladder. AAO, BP 120/65, HR 70, Temp 99, RR 24 & reg, pulses 2+ radial and pedal, voids per urinal, skin warm & dry, c/o pain between shoulder blades, skin warm pink. • Anxious, restless, BP 80/40, HR 50, Temp 92, RR 12 & deep, pulses 4+ radial and pedal, skin cool and dry, client states ” I have to get to the store!!” family trying to keep him in bed,
Sepsis-Induced Distributive Shock • Assessment • Clinical Manifestations • Cardiovascular • Respiratory • Psychosocial Assessment • Interventions • O2, drugs (DIC & clotting),activated protein C • Community Based Care • Evaluating Outcomes
Phase 1/hyperdynamic/”warm shock” • Endotoxins react w/WBC & vessel walls e inflammatory rxn,e stimulate heart ehCO e tachycardia, hSV, hBP, e vasodilation, e pink mucous membrane, e warm skin e bounding peripheral pulses RR & depth h e resp alkalosis, ecrackles & i breath sounds
Phase 1/hyperdynamic/”warm shock” progresses Endotoxins & inflammatory rxn e damage endothelial cell of blood vessels e thousands of small clots form in capillaries of liver, kidney, brain, spleen & heart e ioxygenation e hypoxia & ischemia e metabolism anaerobic e possible hemorrhage e phase 2!!
Phase 2/hypodynamic/”cold shock” iclotting factors & fibrinogen(DIC disseminated intravascular coagulation)eblood vessels dilatedeCOiBPipulse pressureiperipheral pulseseuse of doppler for Bpeskin cool/clammyecap refill slow or absent Respiratory: ARDS may occur caused by SIRS (systemic inflammatory response syndrome)eformation of oxygen free radicalsedamage lung cells Presence of ARDS in Septic Shock = h mortality rate
SITUATION #4 • 84 y/o female admitted from outlying nursing home. Anxious, alert, BP 100/60, HR 110, Radial and Pedal pulses 1+, RR 30 rapid and deep, skin warm & flushed, Temp 101, c/o chills. Incontinent diarrhea. • Lethargic & not following commands, BP 80/40, HR 130 irreg, radial and pedal pulses not palpable, RR 40 shallow with periods of apnea, skin cool, pale and edema noted in hands and feet, foley placed with scant thick whitish yellow urine, temp 96.