Shock and Multiple Organ Dysfunction Syndrome (MODS) chapter 14 Review Complete

Shock and Multiple Organ Dysfunction Syndrome (MODS) chapter 14  Shock: Definition • Life-threatening condition • Results from inadequate tissue perfusion  Prevents adequate oxygen delivery to cells • Effects all body systems • May develop rapidly or slowly→ progression is neither linear nor predictable • Rapid assessment and response by nursing is essential to patient recovery • Although all shocks are different but all have the same result  decrease perfusion • Normal EF 55%-70%: indicator of perfusion, CO, oxygenation • Know diff fluid type: hypo, hyper, iso  Shock: Overview • Adequate blood flow requires (need an effective pump) o Effective cardiac pump o Effective vasculature (circulatory system) o Adequate blood volume (assist with organ perfusion) o If pt is losing blood (H&H, O2 sat decreases) • Shock results in: o Cellular hypoxia (cell not getting enough o2, passed normal body compensation) → Cell death→ progresses to organ dysfunction→ Death • No adequate volume at least 60 mEq for kidney to perfuse  bun/cr, & K build up once kidney shut down • If you don’t have flow, pt develop shock shake  Shock: General Physiologic Responses • Regardless of the initial cause of shock, physiological responses are common to all types of shock: o Hypoperfusion of tissues o Hypermetabolism (increase demand) o Activation of inflammatory response • Prognosis o Depends on body’s ability to effectively respond • Failure of compensatory mechanisms to respond o End Organ Dysfunction o If pt losing a lot of blood tacky occur to compensate then decrease when it can no longer compensate o Also, a decrease in bp  Pathophysiology: Cellular Responses • Cellular swelling occurs • Cell membrane becomes more permeable • Fluid & electrolytes seep into the cell • Mitochondria & lysosomes are damaged • Cell death occurs  Pathophysiology: Cellular Responses • Cellular changes that occur with shock: o Inadequate blood supply therefore, cell produce energy in anaerobic (w/o O2) metabolism due to the changes cell function ceases (cell death) o Hyperglycemia occur (secondary to stress state) [doesn’t mean pt is diabetic] o Biochemical mediators (cytokines) stimulate vasoconstriction or vasodilation o Insulin resistance (not good since pts are already hyperglycemic) o Organ failure • BP regulation requires adequate 1. Blood volume (Tank) 2. Cardiac pump (Pump) 3. Vasculature (Pipes)  Pathophysiology: Coagulopathic Responses • Fibrinolysis o In healthy individual removal of fibrin o Inflammation initiates coagulation cascade o In severe sepsis, endothelial injury  production that impairs fibrinolysis • Over time & if untreated can  DIC  Pathophysiology: Inflammatory Responses • Inflammation 1. Neutrophils 2. Myocardial depressant factor 3. Cytokine release  pro-coagulation 4. Vasodilation 5. Excessive inflammation & coagulation damage endothelium dysfunction & capillary leak  fluid shift into tissue (edema)  How is BP regulated? MAP= CO x PVR (peripheral vascular resistance) • Cardiac Output o What components make up the cardiac output? HR & SV o What influences these components? SNS; preload, contractility, & afterload • Peripheral Vascular Resistance o Diameter of arterioles • Causes of increased PVR? Arteries constriction • Causes of decreased PVR? Arteries dilation • What physiologic responses change our BP? Stress, exercise, weight… o MAP 65 mm Hg decreases oxygen and nutrients delivered to cells (must exceed 65 mm Hg for cells to receive o2 & nutrients needed to metabolize energy in amounts sufficient to sustain life)  Blood Pressure Regulation: pressure Receptors • Baroreceptors (located in carotid sinus & aortic arch; responsible for monitoring circulatory volume & regulating neural & endocrine activities) o How does the body restore BP? • BP decreases→ release of catecholamine's (epinephrine, norepinephrine) →increased HR and vasoconstriction of vasculature • Chemoreceptors o BP and RR regulation→ Responds to changes in O2 and CO2  Blood Pressure Regulation: RAA (kidney regulator, slowest system yet safest) • Release of renin→ converts angiotensin 1 to angiotensin 2 (potent vasoconstrictor) • Aldosterone release→ Retention of Na+ and Water • ADH release (from increase Na) → Kidneys retain water in effort to raise blood volume/BP→ May take hours to days  3 Stages of Shock 1. Compensatory 2. Progressive 3. Irreversible  Compensatory Stage of Shock • SNS causes vasoconstriction, increased HR/increased heart contractility o BP remains normal (by the time BP drops, damage has already been occurring at the cellular & tissue levels pt at risk for shock must be assess & monitor closely before BP falls) • Body shunts blood from skin, kidneys, GI to brain, heart, & lungs to ensure good blood supply to vital organs o Clinical manifestations: Normal body temp & Normal bp build up lactic acid from anaerobic metabolism result in Metabolic acidosis HR increase 100 Increase RR 20 (compensatory resp alkalosis, blowing off CO2) PaCO2 decrease 35 Skin is cold & clammy BS is hypoactive U/O decrease (oliguria) even after multi L of fluid has been given Decrease mentation, confusion & agitation • Inadequate tissue perfusion o Acidosis occurs from anaerobic metabolism o Respiratory rate increases as a compensatory mechanism. • Labs: NA & glucose increase in response to aldosterone & catecholamines; blood culture for infection (tx w/ antibiotics as order) • Medical management: Id & correct underlying cause (o2, fluid replacement, & med therapy to maintain BP & reestablish & maintain tissue perfusion) • Nursing management: monitor tissue perfusion (LOC, VS, U/O, & labs), reducing anxiety, & promoting safety  Progressive Stage of Shock • Mechanisms that regulate BP can no longer compensate o BP and MAP decrease (if you don’t have enough volume or circulation, nothing to constrict) o All organs suffer from hypoperfusion o Vasoconstriction continues further compromising cellular perfusion • Clinical manifestations? • Addressing MAP is the best way to address systolic bp, MAP (65 at least) tell you if you have good perfusion  Progressive Stage of Shock • Pulmonary system fails o Clinical manifestations? • SOB, rapid & shallow resp (decrease O2 & increase CO2), crackles, hypoxemia, pulmonary edema leading to acute lung injury, ARDS • Mechanical vent needed • Cardiac system fails o Clinical manifestations? • Lack of blood flow lead to chest pain, d/r & ischemia, rapid HR 150, MI • Troponin I level increase • Neurological manifestation: mental status deteriorates, agitation, confused, signs of delirium, lethargy increases • Renal system fails o Clinical manifestations? • AKI characterized by elevate bun/cr, toxin, no flow or urine outputoliguric • GI function decreases o Clinical manifestations? • Ileus, necrotic bowel, stress ulcer risk for bleeding, bloody diarrhea, bac translocation may occur & organ d/f (bac toxin enter bloodstream thru lymphatic system) • Hematologic function is altered o Clinical manifestations? • DIC, bruises (ecchymoses), petechiae, • PT & APtt prolonged, decrease in plt • Liver function is altered o Clinical manifestations? • Less able to metabolized med or waste product (ammonia & lactic acid) • Susceptible to infection r/t liver fails to filter blood • AST & ALT, bilirubin elevated pt become jaundice • Medical management: IV fluid & med to restore tissue perfusion, early enteral nutritional support, tx hyperglycemia w/ IV insulin (maintain glc to 180mg/dL), antacid, histamine2 blocker or antipeptic med to reduce risk of GI ulcer & bleeding • Nursing man