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AHIV - ch 34

QuestionAnswer
Shock sequence Local infection -> Systemic infection (early sepsis) -> SIRS (systemic inflammatory response) -> Organ failure (severe sepsis) -> MODS (Multiple organ system failure) -> Death
Shock Widespread abnormal cellular metabolism that occurs when gas exchange with oxygenation & tissue perfusion needs are not met sufficiently to maintain cell function
What can start the syndrome of shock? Any problem that impairs perfusion (the cardiovascular system delivers oxygen to all tissues) & gas exchange (the lungs bring oxygen into the body) to tissues & organs can start the syndrome of shock & lead to a life-threatening emergency
Hypovolemic shock Occurs when too little circulating blood volume decreases MAP, resulting in inadequate total body perfusion & gas exchange
Hypovolemic shock causes/risk factors Hemorrhage, trauma, GI ulcer, surgery, clotting, hemophilia, liver disease, cancer therapy, anticoagulation therapy, dehydration, vomiting, diarrhea, heavy diaphoresis, diuretic therapy, nasogastric suction, & diabetes insipidus
Cardiogenic shock Direct pump failure (fluid volume not affected)
Cardiogenic shock causes/risk factors Myocardial infarction, cardiac arrest, ventricular dysrhythmias, cardiomyopathies, myocardial degeneration, & cardiac tamponade
Distributive shock When blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs; includes septic shock, neurogenic shock, & anaphylactic shock
Distributive shock causes/risks Neural induced, pain, anesthesia, stress, spinal cord injury, head trauma, chemical induced, anaphylaxis, sepsis, capillary leak, burns, extensive trauma, liver impairment, & hypoproteinemia
Obstructive shock Cardiac function decreased by noncardiac factor (indirect pump failure); total body fluid not affected, although central volume is decreased
Obstructive shock causes/risk factors Cardiac tamponade, arterial stenosis, pulmonary embolus, pulmonary hypertension, constrictive pericarditis, thoracic tumors, & tension pneumothorax
S/S of shock Symptoms result from physiologic adjustments (compensatory mechanisms) that the body makes in the attempt to ensure continued perfusion of vital organs; see chart on pg. 733
Mean arterial pressure (MAP) Perfusion is related to this; factors that influence: total blood volume, cardiac output, & size & integrity of the vascular bed; total blood volume & cardiac output are directly related (increase in both = increase in MAP, same with decrease); norm: > 65
Stages of shock 1) Initial stage 2) Compensatory stage 3) Progressive stage 4) Refractory stage
Initial stage Baseline MAP decreased by < 10; increase in HR (from adaptive responses of vascular constriction), RR, & slightly in diastolic BP (may be your only signs of shock in this stage)
Compensatory stage MAP decreases by 10 - 15; kidney & hormonal adaptive mechanisms are activated (decreased urine output), tissue hypoxia in nonvital organs, acidosis & hyperkalemia, O2 90 - 95%, & increased anxiety; reversible stage
Progressive stage MAP decrease > 20; compensatory mechanisms functioning, but can no longer deliver sufficient oxygen, even to vital organs, impending doom; altered mental status, rapid, weak pulse, low BP, cyanosis, cool, anuria, increased thirst, O2 75 - 80%
Refractory stage Slow shallow respirations, dusky extremities, nonpalpable pulse; can’t be saved
Multiple organ dysfunction syndrome (MODS) The sequence of cell damage caused by the massive release of toxic metabolites & enzymes
First sign of shock Increased heart rate (to keep cardiac output & MAP at normal levels, even though the actual stroke volume per beat is decreased)
Assessment in shock Cardiac: increased HR & BP Resp: increased RR, shallow resp, decreased PaCO2 & O2 stat Renal: decreased urine -> anuria, risk for AKI & kidney failure Skin: Cyanosis & clammy CNS: thirsty, change in LOC Skeletal: weak & in pain
Labs during shock Decreased pH (acidosis) Decreased PaO2 Increased PaCO2 Increased Lactic acid (norm: 3 - 7 mg/dL) Decreased H&H (anemic) Increased potassium
Initial & compensatory stage interventions Blood transfusion, O2, & fluids
Nonsurgical management of shock Oxygen, IV therapy (fluids; 18 - 20g), drug therapy (see chart on pg. 740), monitoring vital signs & LOC, & hemodynamic monitoring
Surgical management of shock Vascular repair, surgical hemostasis of major wounds, closure of bleeding ulcers, & chemical scarring (chemosclerosis) of varicosities
Sepsis An extreme response to infection that can cause tissue damage, organ failure, & death if not treated promptly & appropriately; infection in bloodstream
Septic shock Subset of sepsis that is associated with a much higher risk of death than is sepsis alone; associated with both systemic inflammatory response syndrome (SIRS) & sepsis with multiple organ dysfunction syndrome (MODS); uncontrolled bleeding occurs (DIC)
Septic shock can be identified in patients who… - Require vasopressor therapy to maintain a MAP of at least 65 - Have a lactate level greater than 18 mg/dL
Sepsis/septic shock health promotion & maintenance - Prevention - Evaluate risk - Aseptic technique - Early detection of sepsis
Conditions predisposing to sepsis & septic shock See table 34.4 on pg. 743
Sepsis/septic shock assessment Cardio: cardiac output & BP are low; inadequate clotting -> DIC Resp: ARDS Skin: cool & clammy with pallor, mottling, or cyanosis; petechiae from DIC Kidney: low urine output Psych: impending doom; LOC Labs: C&S (draw lactate while waiting)
Interventions for sepsis & septic shock Focus on identifying the problem as early as possible, correcting the conditions causing it, & preventing complications
Hour-1 bundle for management of sepsis - Measure lactate level - Blood cultures before administering antibiotics - Administer broad-spectrum antibiotics - Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate > 4 - Apply vasopressors if hypotensive
Specific interventions for sepsis/septic shock O2, drug therapy to enhance cardiac output & restore vascular volume, antibiotics, adrenal support via corticosteroids, insulin to maintain blood glucose, heparin, & blood replacement therapy
Sepsis S/S Increased WBCs (shift to the left), vasodilation (increased HR, decreased BP), decreased urine output, increased temp, impaired clotting, decreased capillary refill time, hypoxia, hyperglycemia, cool & clammy. Late signs: petechiae & decreased HR
Sepsis labs C&S, H&H, lactic acid, D-dimer, & platelets (150 - 400)
Lactic acid Chemical your body produces when your cells break down carbohydrates for energy; it assists in cell respiration, glucose production, & molecule signaling
Created by: tatianalopez03
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