Shock Interventions for Clients with Shock Hope Knight MS RN.
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Transcript of Shock Interventions for Clients with Shock Hope Knight MS RN.
Shock
Interventions for Clients with ShockHope 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 CellsColloids
Hetastarch/HextendAlbuminDextran
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 <10mm/Hg• Cellular changes = anaerobic
metabolism lactic acid compensation: vascular constriction
& HR MAP maintained difficult to detect
Nonprogressive Stage
MAP <10-15mm/Hg from baselineRelease of renin, antiduiretic hormone
(ADH), aldosterone, epinephrine, and norepinephrine.
Renin urine output,NA+ reabsorptionADH Water reabsorption,blood vessel
constrictionCompensate: keep volume in central blood
vesselCellular: acidosis, hyperkalemia
Progressive StageMAP >20mm/Hg from baselineCompensatory mechanisms do not function
use > amount of oxygenVital organs anoxic & ischemic
poor oxygenation & toxic metabolites severe cell damage/death
Life threatening emergency Immediate intervention Look at pre-existing healthCorrect shock conditions within 1 hour
Refractory StageToo 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
Cycle of more dead cells break open and release harmful metabolites.
microthombi 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, BP, narrow pulse pressure,
workload 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
AnaphylaxisRarely occurs with 1st encounter Histamines move rapidly into bloodMassive blood vessel dilation Increased capillary leakSevere hypovolemia & vascular collapseDecreased cardiac contraction & dysrhythmiaAntigen-antibody rxn in bronchial tissue
severe edema and obstruction reduced 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 wallsinflammatory rxn,stimulate heart CO
tachycardia, SV, BP, vasodilation,pink mucous membrane, warm skin bounding peripheral pulses
RR & depth resp alkalosis, crackles & breath sounds
Phase 1/hyperdynamic/”warm shock” progresses
Endotoxins & inflammatory rxn damage endothelial cell of blood vessels thousands of small clots form in capillaries of liver, kidney, brain, spleen & heartoxygenation hypoxia & ischemia metabolism anaerobic possible hemorrhage phase 2!!
Phase 2/hypodynamic/”cold shock”clotting factors & fibrinogen(DIC
disseminated intravascular coagulation)blood vessels dilatedCOBPpulse pressureperipheral pulsesuse of doppler for Bpskin cool/clammycap refill slow or absent
Respiratory: ARDS may occur caused by SIRS (systemic inflammatory response syndrome)formation of oxygen free radicalsdamage lung cells
Presence of ARDS in Septic Shock = 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.