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.