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-acute, life-threatening allergic reaction to a sensitizing substance
-the reaction causes massive vasodilation, release of vasoactive mediators, and increases capillary permeability, causing fluid to leak into the interstitial space
-respiratory distress d/t laryngeal edema, bronchospasm, and circulatory failure
-dizziness, chest pain, incontinence, swelling of lips and tongue, wheezing, stride, flushing, pruritus, urticaria, and angioedema, anxiety, confusion, sense of impending doom -presence of sepsis with hypotension despite adequate fluid resuscitation, inadequate tissue perfusion
-when microorganism is introduced, normal immune and inflammatory response are activated, but in septic shock the response is exaggerated
-inflammation and coagulation increase, fibrinolysis decreases
-endotoxins stimulate release of cytokines, tumor necrosis factor (TNF), interleukin-1, and other pro inflammatory mediators
-platelet-activating factors leads to micro-thrombi being formed
-endothelium is damaged, vasodilation, increased capillary permeability, neutrophil and platelet aggregation to the endothelium
-vasodilation, maldistribution of blood flow, and myocardial depression
-relative hypovolemia
-ventricles dilate to maintain the stroke volume, and resolves over 7-10 day
-respiratory failure: hyperventilation and respiratory alkalosis at first, when can no longer compensate, then respiratory acidosis
-respiratory failure and ARDS can develop -the body attempts to overcome the consequences of anaerobic metabolism and to maintain homeostasis
-a drop in blood pressure (d/t decrease in CO) is sensed by the baroreceptors in the carotid and aortic bodies, and they activate the SNS
-SNS: vasoconstriction, epinephrine and norepinephrine are potent vasoconstrictors, blood flow is maintained to brain and heart, but shunted from GI tract, skin, and lungs
-SNS stimulates heart rate and contractility, increasing myocardial oxygen consumption,
-ventilation-perfusion mismatch, blood flow is decreased to the lungs and not as much air goes through gas exchange, respirations will increase in rate and depth
-blood is shunted from the GI tract, resulting in impaired mobility, decreased peristalsis, risk for paralytic ileus
-blood is shunted from the sin, skin is cold and clammy
-blood shunted from the kidneys, activates renin-angiotensin system, angiotensin II causes arterial and venous vasoconstriction, aldosterone causes sodium & water rentention and potassium excretion, stimulates ADH to increase water absorption from the kidneys, trying to increase CO and BP -compensatory mechanisms begin to fail
-decrease in perfusion to the heart, brain, and periphery
-altered capillary permeability, allows leakage of fluid and protein out of the blood vessels and into the surrounding areas
-edema all over the body, further decreases tissue perfusion
-cardio: weak peripheral pulses, dysrhythmias, myocardial ischemia, MI
-respiratory: pulmonary arterioles constrict and increases PA pressures, worsening ventilation-perfusion mismatch, fluid moves from the pulmonary blood vessels to the interstitial space, causing interstitial edema, eventually moves into the fluid and causes alveolar edema and decreases surfactant production, decreased compliance, tachypnea, crackles, increased work of breathing
-GI: mucosal barrier in the GI tract becomes ischemic, predisposes patient to GI ulcers and bleeding, risk that bacteria will travel from the GI tract into the blood, decreased ability to absorb nutrients
-renal: renal tubular ischemia, acute tubular necrosis that may lead to AKI, made worse by nephrotoxic drugs, decreased urine output, elevated BUN and serum creatinine, metabolic acidosis because the kidneys cannot excrete lactic acid or reabsorb bicarb
-liver: can't metabolize and produce wastes like lactate and ammonia, jaundice as bilirubin builds up, liver enzymes increase as liver cells die
-hematologic: risk for DIC, when all platelets and clotting factors are consumed and bleeding occurs from many orifices
-need to intervene aggressively to prevent MODS -low doses have a beta-adrenergic agonist action with cardiac stimulation, bronchodilation, and peripheral vasoconstriction, increases HR, contractility, and CO, decreases SVR
-high doses have an alpha-adrenergic agonist with peripheral vasoconstriction, increases stroke volume and SVR, increases systolic and decreases diastolic BP, increases CVP and PAWP
-low doses are used for cardiogenic shock, anaphylactic shock, and septic shock
-high doses for cardiac arrest, pulseless ventricular tachycardia, ventricular fibrillation, and asystole -ABCs
-tissue perfusion: vital signs, LOC, peripheral pulses, capillary refill, skin temperature, color, and moisture, and urine output
-obtain a brief history, such as time of onset and duration of symptoms, health history (medications, allergies, date of last tetanus vaccination, recent travel) -patients who are older, immunocompromised, or have a chronic illness are at a higher risk for shock
-for patient with MI, limit the infarct size, restore coronary blood flow, rest, analgesics, and sedation
-confirm all allergies before giving medications, premedicate if patients have a high risk of reaction
-monitor fluid balance to prevent hypovolemic shock, I&Os, daily weights
-decrease number of invasive catheters, use aseptic technique during invasive procedures, pay attention to hand washing 