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52 Cards in this Set

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