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  <10mm/Hg Cellular changes =  anaerobic metabolism  lactic acid  compensation: vascular constriction &  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   urine output,  NA+ reabsorption ADH   Water reabsorption,  blood 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  anoxic & ischemic  poor oxygenation &  toxic metabolites  severe 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  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

Anaphylaxis  Rarely occurs with 1 st 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  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 walls  inflammatory 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 & heart   oxygenation  hypoxia & ischemia  metabolism anaerobic  possible hemorrhage  phase 2!!

Phase 2/hypodynamic/”cold shock”  clotting factors & fibrinogen(DIC disseminated intravascular coagulation)  blood vessels dilated  CO  BP  pulse pressure  peripheral pulses  use of doppler for Bp  skin cool/clammy  cap refill slow or absent Respiratory: ARDS may occur caused by SIRS (systemic inflammatory response syndrome)  formation of oxygen free radicals  damage 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.