Multisystem alterations shocks

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Multisystem alterations shocks
2014-11-29 19:45:19

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  1. what is the common factor of all types of shocks?
    • The common factor is hypoperfusion and impared cellular oxygen utilization.
    • May result from (5 types) trauma, fluid loss, CV failure, infection, and spinal cord injury. (TFCIS)
    •  It always begins at the cellular level and progresses to organ failure and death. 
  2. Circulatory shock chts? Tx? types and etiologies of each? Patho?
    • It is the inability of the circulation to adequately perfuse the body tissues.
    • Imbalace b/t Osupply and O demand, which causes inadequate perfusion to vital organs. 
    • Tx: treat the underline probs, and improve CO and perdusion.
    • Types: Cardiogenic: inadequate cardiac output; MI, CHF, cardiomyopathy, etc -- Obstructive: Circulatory blockage; PE. Hypovolemic: Loss of volume; Hemorrhage, burns. Distributive: inappropriate vasodilation; 3 types: Anaphylactic (allergic rxn vasodilataion), Neurogenic (loss of either para or symp enovation), Septic (masive vasodilation bc of bacteria's secretion)
    • Patho: Inadequeate cellular oxyganation may result from decreased CO (MI, CHF) , maldistribution of blood (vasodilation), reduced blood oxygen content (PE)
  3. what is the main goal of the compensatory responses? what are the clinical stages of shock? define compensated stage and CM.
    • the compensatory responses main goal is to restore tissue perfusion and oxygenation.
    • Stages: compensated, progressive, refractory.
    • Compensatory: Main goal is to maintaing BP bc of the decrease of CO and perfussion, the body increases cardiac contractility, rate, and peripheral vasoconstriction; Capillary pressure decreases allowing fluid shifting; initiation of RAA (retention of fluids).
    • CM: Narrow pulse pressure w or w/o hypotension(110/90) -- tachycardia (the body trying to pump more blood) -- Fast and deep respirations (try to maintain amt of O) -- Decreased UO (RAA activation, retention of fluid) -- Increased in uringe specific gravity (increased of concentration of urine) -- cool, clammy skin (bc of vasoconstriction) -- altered mentation(less perfussion of the brain) -- Dilated pupils (dilatation in the eye)
  4. what is the progressive and irreversible stage of the compensatory mechanism? CM?
    • Progressive: Can no longer compensate for the decrease of CO and are unable to maintain normal BP. -- U need to help them maintain normal BP, usually drugs. -- progressive tissue hypoxia from tissue constriction -- change from aerobic to anaerobic respiration which results in metabolic acidosis.
    • CM: Hypoxia, tachycardia, Acute renal failure (oliguria, increased BUN and Creatinine) -- ATM: acute tubular necrosis.
    • Irreversible: The shock is refractory to treatment and results in death.
    • * look at slide 16  and 17 to see the graph summarizing.
  5. Cardiogenic chock chts? Dx? etiologies? Patho? CM?
    • Inadequate tissue perfusion from cardiac dysfunction.
    • Dx features: Decreased CO -- elevated Lt ventricule end-diastolic pressure (canulating the pt can give you these first 2) -- S3 heart sound -- Pulmonary edema.
    • Etiology: all of them have to do w contractility probs; MI, Cardiomyopathy, CHF, etc. 
    • Patho: Adequate volume but inadequate perfusion. Then u get probs at the cellular level. They heart can't move the blood through the body bc of the decreased in contractility.
    • CM: hypotension, tachycardia w weak, thready pulse, Cardiac arrhythmias, Crackles, Tachypnea, JVD, cool, moist skin.
  6. Hypovolemic shock chts? etiologies? patho? CM?
    • Loss of blood volume which decreased CO and contractility which in turn decreases tissue perfusion.
    • Need to abt 15 to 20% to show signs.
    • Low CO, n intracardiac pressures lead to SNS activation = elevated HR, vasoconstriction, increased contractility.
    • Etiologies: Hemorrhage, dehydration from vomiting n diarrhea, overuse of diuretics, burns, and pancreatitis (pts can't eat n they are digesting themselves).
    • Patho: Loss of circulating volume causes and inadequate MAP.
    • CM: Thrist and Oliguria, and all the others (tachy, pallor, restless, confusion episodes, hypotension, etc)
  7. Obstructive shock chts? etiologies? patho? CM?
    • mechanical obstruction that prevent effective cardiac filling and stroke volume.
    • Etiology: PE, Cardiac tamponade, tension Pneumothorax, Dissecting aortic aneurysm, DVT.
    • Patho: Ventricle do not fill or empty appropriately, cardiac preload decreases, increase pressure on the Rt side of the heart and inadequate blood return.
    • CM: Pericardial friction rub, and all the rest (hypotension, tachy w dyspnea, JVD, pallor, chest pain, oliguria, etc)
  8. Distributive shock chts? types? explain each w etiologies, patho, and CM?
    • Characterized by excessive vasodilatation which result in peripheral pooling and relative hypovolumia (bc the blood is not coming back).
    • Preload and stroke V can't maintain perfusion.
    • Types: Anaphylactic shock, neurogenic shock, and sptic shock.
    • Anaphylactic: Mast cells realease vasodilatory mediators resulting in severe hypotension -- etiologies: antibiotics, food, insect bites, etc -- patho: exposure to an antigen produces antibody rxn, large amts of histamine, which increase vasodilatation and permeability, causing a fluid change, and edema. -- CM: sever itching and difficulty swallowing, urticaria (wells).
  9. Describe neurogenic shock, and septic shock w etiologies, patho, CM?
    • Neurogenic: Results from loss of sympathetic activation of arteriolar smooth muscle. -- etiologies: spinal cord trauma, drug overdose, brain injury. -- patho: parasympatetic stimulation is unchecked allowing peripheral vasodilatation to occurs, therby decreasing MAP and causing hypotension, peripheral pooling and decrease CO and PL. -- CM: Bradycardia followed by tachycardia, hypothermia, and the others (oliguria, hypotension, and LOC varies)
    • Septic shock: overwhlming systemic infection, usually from gram-negative, but could be gram-positive or fungal. It causes high CO, but still have insufficient blood volume. Therapy: aim to improve the distribution of blood. -- Etiologies: bacteremia (presence of bacteria in the blood); deptesimia: the bacteria have realeased toxins. -- patho: endotoxins in bacteria cells stimulate massive IS action, inflammation. This leads to peripheral vasodilation w hypotension. which causes cell hyoxia and increases capillary permeability. -- CM: Normotensive, and the others, tachy, tachypsnea, hyperthermia, shivering, N & V, etc.
  10. What are the main complications of shock?
    • Acute respiratory distress syndrome.
    • Acute renal failure.
    • Disseminated intravascular coagulation.
    • Multiple organ dysfunction syndrome.
  11. 1) What is acute respiratory distress syndrome, ARDS? 2) Disseminated intravascular coagulation complication, DIC?
    • 1) ARDS: Lethal form of respiratory failure, most commonly associated w septic shock.
    • Alveolar wall get severally impaired, resulting in capillarity permeability and fluid accumulation. Lungs become solid and noncompliant, not enough echange of O2 and CO2, cell injury and death.
    • 2) DIC: Microcirculation obstructions lead to ischemic tissure damage.
    • Widespread clot formation soncumes platelets and clotting factors.
    • Platelets cound and fibrinogen levels are low.
    • Obstruction of blood by small clots lead to ischemic tissure.
    • Clot formation consumes platelets which leaves the pt vulnerable fro sever bleeding.
  12. What is acute renal failure and multiple organ dysfunction syndrome complications?
    • ARF: bc of the hypoperfussion, ATN (acute tubular necrosis) occurs due to hypoxia of the renal tubules.
    • Decrease in UO (waste products)
    • MODS: It has very high mortality, due to ongoing inflammation which will destroy the organ. Overactive immune mechanism that are destructive.
    • sepsis and septic shock are the most common causes.