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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.
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)
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)
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.
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.
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)
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)
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).
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.
What are the main complications of shock?
- Acute respiratory distress syndrome.
- Acute renal failure.
- Disseminated intravascular coagulation.
- Multiple organ dysfunction syndrome.
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.
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.