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52 Cards in this Set
- Front
- Back
Define shock:
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Progression of a cascade of events that begins when cells/ tissues are deprived of oxygen resulting in an accumulation of waste products, failure of energy dependant functions, cellular enzyme release, calcium accumulation, and reactive oxygen species accumulation which leads to cellular death.
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3 major factors affecting blood flow:
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circulating volume, cardiac pump function, vasomotor tone (peripheral vascular resistance)
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what is the equation determining blood flow to tissues?
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Cardiac output = stroke volume x heart rate
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what affects stroke volume?
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Preload (amount of blood returning from the body entering the heart), cardiac contractility (muscular function of the heart), afterload (ABP required to push blood from into the pulmonary valves and aorta)
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Causes of decreased preload:
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loss of volume, hypovolemia, decreased vasomotor tone, vasodilation
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Cardiac out put equations:
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CO = SV x HR or CO= BP / total peripheral vascular resistance
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Classes of shock:
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Hypovolemic shock (volume deficit due to hemorrhage, 3rd space loss, severe dehydration) cardiogenic shock (stroke volume is inadequate to maintain perfusion because of cardiac muscle failure) distributive shock (loss of vasomotor tone results in loss of blood pressure and decreased venous return)
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Define transcapillary fill:
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Precapillary sphincter tone lowers capillary hydrostatic pressure which favors movement of fluid from the interstitium to the capillary beds
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Effect of transcapillary fill:
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Interstitial fluid deficit which can restore circulating fluid losses of less than 15%
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Hypodynamic shock:
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Compensatory mechanisms are insufficient to maintain ABP and perfusion of organ with blood loss greater than 15%.
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Consequences of hypodynamic shock:
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Ischemia to vital organs, cellular function failure, accumulation of waste products, acidosis
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Categories of shock based on clinical signs:
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Mild (class 1) blood loss < 15% body is capable of restoring volume with compensatory mechanisms. Hyperdynamic (early class 2) blood loss of 15-30% body can compensate but only is losses stop. Decompensatory shock (classes 3 and 4) blood loss > 30% failure of compensatory mechanisms and cycle of decreased CO, BP, and tissue perfusion results in circulatory collapse.
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Determinates of oxygen delivery:
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Concentration of oxygen in the blood (Hb & saturation of Hb) and the amount of blood perfusing tissues
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What are the negative consequences of isotonic (rapid) fluid therapy?
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80% of volume will diffuse to interstitial and intracellular spaces resulting in replacement volumes being 4-5 greater than loss. Excess fluid administration results in excess total body water, excess lytes, excerbating fluid movement out of vascular space. Cellular effects trigger inflammatory response, compartment syndrome, ARDS, CHF, dilutional coagulopathy
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goal of fluid therapy:
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restore perfusion, improve oxygen delivery
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what is the difference between replacement and maintenance fluid?
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Replacement fluids electrolyte composition closely approximates extracellular electrolyte composition
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What is the method of administering isotonic fluids for hypovolemic shock?
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Calculate fluid deficit, administer in doses of 10-20 m/kg then reassess parameters
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Mechanism of hypertonic saline:
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Pulls fluid primarily from intracellular space, expands capillaries, blunts neutrophil activation, alters balance between inflammatory & anti-inflammatory cytokines
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What is the dose of hypertonic saline?
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2-4 mL/kg
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what are the benefits of colloids?
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Large molecules retained in the intravascular space, exert an oncotic pressure opposing hydrostatic pressure to retain fluid or draw fluid to vascular space
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What is normal COP?
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20 mmHg
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Examples of natural colloids:
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Plasma, whole blood, bovine albumin
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Benefits of natural colloids:
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Provide albumin, clotting factors, antibodies, other plasma proteins
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Examples of synthetic colloids:
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Hydroxyethyl starch, dextran
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What is the COP of HES?
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30 mmHg
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how is HES eliminated?
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Renal and extravasation
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What is the dose for HES?
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10 ml/kg/day
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how long is HES active?
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At least 120 hours
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Complications of HES:
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Increased cutaneous bleeding times and decrease in vWF antigen with 20 mL/kg doses
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Advantages of whole blood:
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Clotting factors, prevents dilutional coagulopathy, improves oxygen content, proteins help retain fluid in vascular space
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Disadvantages of whole blood:
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Difficult to store/ have available, can not be rapidly infused
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benefits of dobutamine in shock resuscitation:
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b1 adrenoreceptor, weak b2 & a adrenoreceptor has positive ionotropic (increase contractility) action, improves splanchnic perfusion
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dose of dobutamine:
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1-5 ug/kg/min
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benefits of norepinephrine:
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strong b1 & a adrenorecptor increases vasoconstriction, cardiac contractility
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what are methods to monitor response to shock therapy?
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Repetitive PE, CRT, CVP, urine output, ABP, lactate, oxygen extraction, PvO2, CO, regional perfusion
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What does CVP assess?
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Cardiac function, blood volume, vascular resistance
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What is normal CVP?
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7-12 mmHg with a catheter in the right atrium, catheter in jugular vein will be higher
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what is normal urine production?
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1 mL/kg/ hr or more
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What level of urine production requires treatment?
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< 0.5 mL/kg/hr
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when does BP record below normal?
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With a 30% or more decrease in blood volume
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What BP is treatment aimed at maintaining?
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>65 mmHg
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examples of direct BP measurement:
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catheterization of transverse facial(adults & foals), metatarsal, radial, or auricular artery (foals)
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locations for indirect BP measurement:
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coccygeal or metatarsal arteries
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what is normal indirect coccygeal systolic BP?
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80-144 mmHg
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how is oxygen extraction calculated?
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Difference between central venous saturation and arterial oxygen saturation
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What is normal oxygen extraction?
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20-30%
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what is normal jugular PvO2?
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40-50 mmHg
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how is CO estimated?
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Pulmonary thermodilution, lithium dilution, transesophgeal or transthoracic Doppler
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What is the goal of hypotensive resuscitation?
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Prevent or minimize further blood loss by administering fluids to maintain a mean BP of 40-60 mmHg (or systolic BP of 80-90 mmHg)
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what occurs with prolonged catecholamine release?
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Long term increased peripheral vascular resistance and tissue ischemia
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Triggers of cortisol release:
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Catecholamines, vasopressin, angiotensin II, norepinephrine, endotoxin
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Results of cortisol release:
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Na & H2O retention (edema), insulin resistance, gluconeogenesis, lipolysis, protein catabolism
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