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209 Cards in this Set
- Front
- Back
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Which of the following causes a decrease in Cardiac Output
a) excessive metabolism b) hypovolemia c) abnormal tissue perfusion d) decreased vascular tone e) obstruction of blood flow |
hypovolemia
decreased vascular tone obstruction of blood flow |
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Which of the following has NO effect on Cardiac Output?
a) excessive metabolism b) hypovolemia c) abnormal tissue perfusion d) decreased vascular tone e) obstruction of blood flow |
excessive metabolism
abnormal tissue perfusion |
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T/F All types of shock lead to inadequate delivery of nutrients and inadequate removal of waste products in tissues
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True
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How much blood loss must be appreciated before cardiac output and arterial pressure will be effected?
a) 10% b) greater than 10% c) 35 - 40% d) 50% |
35 - 40% when reflex intact
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The CNS Ischemic response kicks in when systolic arterial pressure reaches?
a) 60 mmHg b) 50 mmHg c) 40 mmHg d) 30 mmHg |
50 mmHg
an extreme SNS response occurs due to lack of O2 and increase of CO2 |
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T/F A pt can have a low arterial pressure but still have normal tissue perfusion and NOT be in shock?
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True
d/t body compensation |
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Non-progressive shock
a) needs extrinsic help b) needs NO extrinsic help c) aka compensated shock d) aka uncompensated shock |
needs NO extrinsic help
aka compensated shock |
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The factors that assist a person from recovering from compensated shock are
a) negative feedback processes b) positive feedback processes |
negative feedback processes
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Which of the following are factors that help in compensated shock
a) Baroreceptor b) vasomotor failure c) Angiotensin d) Vasopressin e) CNS ischemic response |
Baroreceptor
Angiotensin Vasopressin CNS ischemic response |
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Angiotensin
a) helps in nonprogressive shock b) constricts veins & arteries c) constricts peripheral arteries d) decreases urine output |
helps in nonprogressive shock
constricts peripheral arteries decreases urine output |
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Describe Reverse Stress Relaxation
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When there is a lack of blood volume, this reflex causes blood vessels to contract around the vessel so that the blood available fills the space
found in compensated shock |
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Progressive shock
a) aka uncompensated shock b) requires extrinsic help c) involves positive feedback mechanisms |
aka uncompensated shock
requires extrinsic help involves positive feedback mechanisms |
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T/F The heart has a tremendous reserve capacity which allows it to pump up to 300 - 400% more blood than usual
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True
but only works in Early stage of shock in Late shock heart is exhausted |
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In order for vasomotor tone to remain what arterial pressure must remain?
a) 20 mmHg b) 30 mmHg c) 40 mmHg d) 50 mmHg |
30 mmHg
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What is sludging of the blood in shock caused by
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sluggish flow (low perfusion pressure)
accumulation of carbonic & lactic acid |
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What toxin is released from the GI tract in sepsis that leads to cardiac depression?
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Endotoxin it increases cellular metabolism which causes cardiac depression
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As shock becomes progressively worse what happens in the liver?
a) Na & Cl excretion from cells b) Na & Cl retention in cells c) K excretion from cells d) decreased mitochondrial activity e) release of hydrolases |
Na & Cl retention in cells
K excretion from cells decreased mitochondrial activity ( INSULIN not produced anymore) release of hydrolases ( from Lysosomes) that cause deterioration |
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Why is there increased capillary permeability in shock?
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B/C of hours of HYPOXIA, lack of nutrients. Fluid moves to tissues to try to feed them
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Tissue Necrosis in shock happens where?
a) arterioles b) venuoles |
venuoles, b/c there is poor nutrition in these areas because blood flow is not making it that far d/t increased capillary permeability
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Acidosis in shock
a) poor O2 delivery to tissues b) anaerobic metabolism c) high lactic acid d) lack of removal of CO2 |
poor O2 delivery to tissues
anaerobic metabolism high lactic acid lack of removal of CO2 (leads to formation of carbonic acid) |
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Irreversible Shock
a) no therapy works b) depletion of phosphate reserve c) death |
no therapy works (even if CO & Art. Press. nml)
depletion of phosphate reserve (adenosine converted to uric acid) death |
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T/F Sympathetic Reflexes maintain arterial pressure by causing vasoconstriction
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True
Arteriole constriction = inc. PVR Veins/ reservoir constriction = adequate venous return Increased HR ( as high as 160 - 180) |
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How much blood loss is tolerable if Sympathetic Reflexes are intact?
a) 15 - 20% b) 30 - 40% c) 50 - 60 % |
30 - 40%
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How much blood loss is tolerable if Sympathetic Reflexes are NOT intact?
a) 15 - 20% b) 30 - 40% c) 50 - 60 % |
15 - 20%
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Sympathetic Reflexes have more control over
a) Cardiac Output b) Arterial Pressure |
Arterial Pressure
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T/F A person who is hemorrhaging will maintain their Arterial Pressure longer than their Cardiac Output
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True
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Does increasing Peripheral Vascular Resistance increase Cardiac Output in hemorrhagic shock?
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NO!!!!
Vasopressors don't work in hemorrhaging patients |
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Sympathetic Stimulation
a) cerebral vasoconstriction b) coronary vasoconstriction c) no effect on cerebral vessels d) no effect on coronary vessels |
no effect on cerebral vessels
no effect on coronary vessels BLOOD FLOW TO THESE AREAS MAINTAINED BY AUTO-REGULATION if pressure NOT < 70 mmHg |
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Neurogenic Shock
a) loss of vasomotor tone b) increased vascular capacity c) inadequate filling of vessel without blood loss |
loss of vasomotor tone
increased vascular capacity inadequate filling of vessel without blood loss |
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Cause(s) of Neurogenic Shock
a) Deep General Anesthesia b) Spinal Anesthesia c) Brain Damage |
Deep General Anesthesia (vasomotor paralysis)
Spinal Anesthesia (sympathetic outflow blocked) Brain Damage ( ischemia > 5 - 10 mins) |
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Anaphylaxis
a) immediate reaction to antigen b) decreased cardiac output c) decreased arterial pressure d) all of the above |
immediate reaction to antigen
decreased cardiac output decreased arterial pressure |
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Histamine Shock
a) venous dilation b) arteriole dilation c) increased capillary permeability d) all of the above |
venous dilation
arteriole dilation increased capillary permeability |
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T/F Hemorrhage is the #1 cause of Hypovolemic shock
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True
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T/F Septic Shock is the #2 cause of death?
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True
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What makes Septic Shock different than other shocks?
a) increased temp b) increased cardiac output c) sludging of blood d) DIC |
increased temp
increased cardiac output sludging of blood DIC (micro blood clots, b/c clotting factors used up) |
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What is the best blood product for Hemorrhage?
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Whole Blood
very expensive and not really used that often never the less it is the best treatment |
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What is the best treatment for Dehydration?
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Crystalloids
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T/F Plasma cannot restore HCT?
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True, but body can handle a HCT of 1/2 normal if cardiac output is adequate
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Plasma substitutes
a) Dextran b) Hespan c) Albumin d) exert osmotic pressure |
Dextran
Hespan Albumin exert osmotic pressure (keeps fluids intravascular) |
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Sympathomimetic Drugs
a) Treat Neurogenic Shock b) Treat Anaphylactic Shock c) Norepi d) Epi |
Treat Neurogenic Shock
Treat Anaphylactic Shock Norepi Epi |
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Glucocorticoids in Shock
a) can inc. heart strength in late shock b) prevent lysosomes from opening c) aid in metabolism of glucose |
can inc. heart strength in late shock
prevent lysosomes from opening (no release of hydrolases) aid in metabolism of glucose |
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T/F Anesthetic Gases can cause Circulatory Arrest?
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True when combined with low flow O2
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Circulatory Arrest greater than 5 - 8 minutes
a) a small amount of permanent brain damage b) large amount of permanent brain damage c) no permanent brain damage |
a small amount of permanent brain damage
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Circulatory Arrest greater than 10 -15 minutes
a) a small amount of permanent brain damage b) large amount of permanent brain damage c) no permanent brain damage |
large amount of permanent brain damage
blood becomes Sluggish = clots |
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T/F Trauma is the #1 cause of death in the first 35 years of life
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True
ETOH/Drug abuse is common 50% die immediately 30% die in first 1 - 2 hours |
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Trauma patient profile
a) full stomach b) Cervical spine injury c) hypovolemic d) hypothermic |
full stomach
Cervical spine injury hypovolemic hypothermic |
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T/F Hypotension must be assumed to be secondary to hypovolemia until proven otherwise
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True
TREATMENT IS VOLUME!! |
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T/F Hypoventilatory Hypoxia is ALWAYS accompanied by Hypercarbia
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True
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When pt is hypoxic & hypercapnic what order do signs & symptoms show up
a) HTN, Inc. HR, Lethargy, Coma, Death b) Inc. HR, Lethargy, HTN, Coma, Death c) Lethargy, HTN, Inc. HR, Coma, Death d) Inc. HR, HTN, Lethargy, Coma, Death |
Inc. HR
HTN Lethargy Coma Death |
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Highest risk to injured brain
a) Hypoxia b) HOTN c) Hypercapnia |
HOTN
Hypoxia is second highest |
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T/F Keep MAP 90 mmHg until see what brain "looks" like
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True
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Which has more effect on Brain Edema
a) colloidal osmotic pressure b) osmolality |
osmolality
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Trauma Pack...
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6 u PRBCs
4 u FFP 10 u Platelets |
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Goals of Volume Resuscitation
a) Tissue perfusion, oxygenation b) HR < 100 c) Pulse Pressure > 30 mmHg d) UOP > 0.5 - 1 ml/kg/hr e) Resolving acidosis/no acidosis |
Tissue perfusion, oxygenation
HR < 100 Pulse Pressure > 30 mmHg UOP > 0.5 - 1 ml/kg/hr Resolving acidosis/no acidosis |
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1 unit PRBCs
a) Hct 70 - 80 b) increases Hgb by 1 gm/dl c) increases Hgb by 2 gm/dl d) Hct 50 - 60 |
Hct 70 - 80
increases Hgb by 1 gm/dl |
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FFP
a) factor VIII only b) fibrinogen + platelets c) All coag factors d) All coag factors EXCEPT platelets |
All coag factors EXCEPT platelets
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Cryo
a) factor VIII only b) fibrinogen + platelets c) All coag factors d) All coag factors EXCEPT platelets |
factor VIII only (FIBRINOGEN)
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T/F Dilutional Thrombocytopenia is MOST COMMON cause of coagulopathy
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True ( platelets are diluted out which leads to clotting problems)
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T/f Hypofibrinogenemia is the second most common cause of coagulopathy
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True (fibrinogen is diluted out r/t high PRBC transfusions)
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Massive PRBC transfusions
a) decrease in serum Ca b) TRALI or ARDS c) thrombocytopenia d) Hypofibrinogenemia |
decrease in serum Ca
TRALI or ARDS (d/t debris in packed cells) thrombocytopenia Hypofibrinogenemia |
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Lactated Ringers
a) hypotonic solution b) isotonic solution c) contains Ca d) can cause metabolic alkalosis e) can lead to acidosis |
hypotonic solution
contains Ca can cause metabolic alkalosis |
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Your pts blood pressure remains low even though you have given enough PRBC's and Crystalls to replace their volume, what drug would you want to give?
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Calcium = increased contractility
Ionized Ca may be low d/t calcium binding with citrate in blood product |
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Gold Standard for intubation in a Trauma pt?
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RSI with Sux (Roc if need to)
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Why would you not want to use Atracurium, & Morphine in a trauma patient?
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Histamine releasers
Even tho Sux is as well, its effects are much shorter lived than the other drugs |
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You have drawn an ABG and are trying to determine if the FiO2 you have the pt on is sufficient. How would you do that?
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Using the formula
FiO2 x 5 = PaO2 will help determine if need to increase or decrease FiO2 Normal PaO2 = 80 - 100 mmHg |
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T/F Acidosis is effected by hydration and organ perfusion
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True
with adequate hydration and organ perfusion acidosis will improve |
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Lactate Level
a) reflects metabolic function b) direct measure of tissue perfusion c) indirect measure of tissue perfusion |
reflects metabolic function
direct measure of tissue perfusion |
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T/F Base Deficit is the amount of base required to titrate 1 liter of whole blood to a normal pH assuming a normal PaO2, PaCO2 and Temp
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True
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T/F Base Deficit is an indicator of metabolic dysfunction r/t hypovolemic shock
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True
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Base Deficit - 2 to - 5
a) mild hypovolemia b) moderate hypovolemia c) severe hypovolemia |
mild hypovolemia
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Base Deficit - 6 to - 14
a) mild hypovolemia b) moderate hypovolemia c) severe hypovolemia |
moderate hypovolemia
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Base Deficit < - 14
a) mild hypovolemia b) moderate hypovolemia c) severe hypovolemia |
severe hypovolemia
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What is the ratio of FFP to PRBCs that should be given
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2 units FFP : 1 unit PRBC
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When you give Bicarb why would your ETCO2 go up?
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HCO3 + H2O = H2CO3 + CO2
will need to adjust ventilation to blow off excess |
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Hypothermia
a) left shift in OxyHgb curve b) right shift in OxyHgb curve c) dec. plt function d) inc. blood viscosity |
left shift in OxyHgb curve
dec. plt function inc. blood viscosity |
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Platelet Plugs
a) formed in bone marrow b) 1/2 life 8 - 12 days c) cleared by spleen d) help repair small capillaries |
formed in bone marrow
1/2 life 8 - 12 days cleared by spleen help repair small capillaries |
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What is formed in response to ruptured vessel or damage to blood
a) platelet plug activator b) prothrombin activator c) fibrinogen activator |
prothrombin activator which converts prothrombin into thrombin to form a clot
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Where is thrombin formed?
a) Kidney b) Liver c) Spleen |
Liver
It is dependent on Vit K levels and liver function |
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Fibrinogen
a) plasma protein b) made in liver c) forms clots d) dissolves clots |
plasma protein
made in liver dissolves clots |
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Coumadin competes with Vit K for receptor and blocks formation of
a) Prothrombin b) Factor V c) Factor VII d) Factor IX e) Factor X |
Prothrombin
Factor VII Factor IX Factor X |
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What is given to reverse effects of Coumadin?
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FFP (contains all factors except platelets)
Vit K (takes 3 - 6 hours) |
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A platelet count
a) quantitative only b) qualitative only c) both quantitative and qualitative |
quantitative only
Bleeding rarely occurs unless plt count < 50 -70 thousand BOARD QUESTION |
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Ivy Bleeding time
a) quantitative only b) qualitative only c) both quantitative and qualitative |
both quantitative and qualitative
BOARD QUESTION |
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Which of the following X-rays clears a C-spine
a) Flexion b) Extension c) Flexion, Extension d) Flexion, Extension, Lateral |
Flexion, Extension
Results must be written in chart |
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T/F Tension pneumothorax worsens with positive pressure ventilation
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True
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Signs of Renal Failure
a) ↑ K, ↑ Mg b) ↓ Ca c) ↓K, ↓ Mg d) ↑ Ca |
↑ K, ↑ Mg
↓ Ca |
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Donor Selection for Kidney transplant
a) Must be ABO match b) Cross ABO group OK c) cadaver d) living |
Cross ABO group OK (but there is an increased risk of rejection)
cadaver (can be iced for 24 - 36 hours) living |
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Anesthesia for Kidney transplant
a) RSI b) Nimbex c) CVP 12 - 15 d) avoid direct acting vasopressors |
RSI
Nimbex CVP 12 - 15 avoid direct acting vasopressors |
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What do Mycin Antibx do to NDMRs?
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Potentiate them
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Clinical signs of Heart Failure
a) EF <10 - 15% b) Acidosis c) ↓ SvO2 d) Systemic/Pulmonary Congestion |
EF <10 - 15%
b) Acidosis c) ↓ SvO2 d) Systemic/Pulmonary Congestion |
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Pt selection for Heart Transplant
a) < 60 yrs b) No infections c) life expectancy > 1 yr d) compliance |
< 60 yrs
No infections life expectancy > 1 yr compliance |
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Contraindications to Heart Transplant
a) ↑ pulmonary resistance b) irreversible kidney/ liver dz c) Severe PVD d) Malignancy |
↑ pulmonary resistance
irreversible kidney/ liver dz Severe PVD Malignancy |
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T/F When choosing a donor for a Heart Transplant it's OK for the donor to have brain tumor?
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True, They CANNOT have any other type of tumor but a brain tumor is OK
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Heart Donors
a) must be ABO compatible b) males < 35 yrs c) females < 40 d) must be lymphocytic crossmatch negative |
must be ABO compatible
males < 35 yrs females < 40 must be lymphocytic crossmatch negative |
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Denervated Hearts
a) pump dependent b) volume dependent |
volume dependent
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Post CBP the denervated heart
a) slow, chaotic pumping b) is the 2nd P-wave on EKG c) is the 1st P - wave on EKG d) junctional rhythm |
slow, chaotic pumping
is the 2nd P-wave on EKG junctional rhythm |
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Which drugs will the heart rate of the Denervated Heart not respond to
a) Isuprel b) Digoxin c) Neostigmine d) Atropine e) Dopamine |
Digoxin
Neostigmine Atropine Must use direct acting drugs to get any response from Heart |
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The treatment of Pulmonary HTN in a Post Pump Heart transplant patient is best accomplished by?
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Primacor (pulmonary vasodilator)
Levophed ( vasoconstrictor) |
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T/F The Non-Cardiac surgery post Heart transplant patient will NOT have chest pain when ischemic
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True
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Functions of Liver
a) Carb Metabolism b) Fat Metabolism c) Protein Metabolism d) Protein Synthesis e) Synthesis of clotting factors f) Drug Metabolism |
Carb Metabolism (store glycogen)
Fat Metabolism (lipoproteins) c) Protein Metabolism (removal ammonia, amines) d) Protein Synthesis (drug binding, coagulation) e) Synthesis of clotting factors( thromb, fibrinogen, V, VII, IX, X) f) Drug Metabolism |
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Liver Failure
a) ↑ ammonia b) ↓ Na, ↓ K, ↓ glucose c) ↑ Na, ↑ K, ↑ glucose d) ↓ ammonia |
↑ ammonia
↓ Na, ↓ K, ↓ glucose |
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Portal Vein delivers what % of blood to liver
a) 20% b) 40% c) 50% d) 70% |
70% (but won't in Liver failure d/t stenosis) So will have Portal HTN
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T/F In liver failure a Hyperdynamic state is seen?
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True Cardiac Output can increase to 15 - 18
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In Kidney transplants the donor urine output should be kept
a) 0.5 ml/min b) 1 ml/min c) 2 ml/min d) there is no specific u/o requirement for a Donor kidney |
2 ml/min
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Must a Liver Transplant donor be ABO compatible?
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NO but it is preferred
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Is it OK for a Liver Transplant donor to have a malignancy?
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Yes as long as it is a BRAIN malignancy only
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Does size matter when it comes to hearts and livers?
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Yes!!
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What happens during Anhepatic phase
a) coags get ugly b) acidosis worsens c) need large volume replacement d) Calcium replacement |
coags get ugly
acidosis worsens need large volume replacement (20 - 100L blood loss) Calcium replacement (r/t blood transfusions) |
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Which transplant is the only one that Normosol is used for maintenance fluids?
a) Kidney b) Kidney/Pancreas c) Heart d) Liver |
Liver
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What are the transfusion goals
a) Hgb > 7 but < 10 b) Hgb > 7 c) Plt count > 100,000 d) Plt count < 100,000 |
Hgb > 7 but < 10
Plt count < 100,000 |
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What does a TEG (thromboelestography) measure?
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Total clotting time
using this measurement helps unnecessary blood transfusions from happening. TEG can tell you what you need to give |
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Normal CMRO2
a)1 ml/100g/ min b) 3 - 3.5ml/100g/ min c) 5 - 5.5 ml/100g/miin |
3 - 3.5ml/100g/ min
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Brain CMRO2
a) 20% of total b) 40% of total c) 60% of total d) 80% of total |
20% of total
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Metabolic activity CMRO2
a) 20% of total b) 40% of total c) 60% of total d) 80% of total |
40% of total
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Neuronal activity CMRO2
a) 20% of total b) 40% of total c) 60% of total d) 80% of total |
60% of total
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Which uses the most CMRO2
a) white matter b) gray matter |
gray matter
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T/F There is no reserve capacity in the brain
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True, that's why hypoxia injury is rapid and leads to death with low CBF
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What is the glucose consumption per minute
a) 1 mg/100g/min b) 5 mg/100g/min c) 8 mg/100g/min |
5 mg/100g/min
glucose is primary energy source and low & high levels are bad |
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Cerebral Blood Flow (choose 2)
a) 25ml/100g/min b) 50ml/100g/min c) 15 - 20% Cardiac Output d) 5 - 10% Cardiac Ouput |
50ml/100g/min
15 - 20% Cardiac Output |
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CBF < 20 - 25 ml/100g/min
a) slow EEG, cerebral impairment b) Flat EEG c) Irreversible damage |
slow EEG, cerebral impairment
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CBF < 15 ml/100g/min
a) slow EEG, cerebral impairment b) Flat EEG c) Irreversible damage |
Flat EEG
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CBF < 10 ml/100g/min
a) slow EEG, cerebral impairment b) Flat EEG c) Irreversible damage |
Irreversible damage
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What factors determine CBF
a) CO2 b) auto-regulation c) venous pressure d) temperature e) oxygen |
CO2
auto-regulation venous pressure temperature oxygen (but only if PaO2 < 50mmHg) |
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CO2
a) dilates cerebral vessels b) constricts cerebral vessels c) inc. resistance d) decreases resistance e) increases CBF f) decreases CBF |
dilates cerebral vessels
decreases resistance increases CBF |
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How much will CBF change for every 1 mmHg change in PaCO2
a) 1 ml/100g/min b) 2 ml/100g/min c) 3 ml/100g/min |
1 ml/100g/min
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T/F Hypoxia & Hypercapnia are synergistic
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True, CBF will increase more with both factors than it would alone
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T/F Cerebral auto-regulation occurs at small arteriolar level
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True
Auto-Regulation 50 - 150 mmHg |
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Your patient has Chronic HTN which way would the auto-regulation curve be shifted?
a) left b) right |
RIGHT
will require higher pressures to maintain perfusion (80 - 180) |
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Can Trauma, Hypoxia and some anesthesia agents abolish auto-regulation
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yes
CBF will change in direct proportion to CPP Resistance will be constant at max dilation/constriction |
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When auto-regulation abolished what happens to the sensitivity to CO2 effects on CBF
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they are decreased
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How much will a 1 degree change in temperature effect CBF?
a) 1 - 2% b) 3 - 4% c) 5 - 7% |
5 - 7%
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At what temperature does the EEG become Isoelectric?
a) 10 degrees Celsius b) 20 degrees Celsius c) 30 degrees Celsius |
20 degrees Celsius
CMRO2 will continue to fall |
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Volatile Agents
a) decrease CMRO2 b) cerebral dilators @ 0.6 MAC c) dose dependent inc. CBF d) constrictors @ 0.6 MAC |
decrease CMRO2
cerebral dilators @ 0.6 MAC dose dependent inc. CBF |
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Forane + Hyperventilation = ?
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increased CBF (r/t dilation and decreased resistance) With NO EFFECT ON ICP
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T/F Desflurane + Hyperventilation acts as Forane does in regards to CBF and ICP
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False!! there will be an mild increase in ICP
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T/F N20 is a cerebral vasodilator
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True
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Barbiturates & Opioids
a) increase CBF b) decrease CBF c) increase ICP d) decrease ICP |
decrease CBF
decrease ICP (r/t vasoconstriction) |
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Luxury perfusion
a) increase CBF without increased CMRO2 b) Increased CBF in normal brain tissue but at cost to ischemic tissue c) blood flow favors ischemic areas with hyperventilation & hypocapnia |
increase CBF without increased CMRO2
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Steal
a) increase CBF without increased CMRO2 b) Increased CBF in normal brain tissue but at cost to ischemic tissue c) blood flow favors ischemic areas with hyperventilation & hypocapnia |
Increased CBF in normal brain tissue but at cost to ischemic tissue (VOLATILES do this)
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Robin Hood Steal (aka reverse steal)
a) increase CBF without increased CMRO2 b) Increased CBF in normal brain tissue but at cost to ischemic tissue c) blood flow favors ischemic areas with hyperventilation & hypocapnia |
blood flow favors ischemic areas with hyperventilation & hypocapnia
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Cerebral Spinal Fluid
a) 150ml total circulating b) 20ml/hr produced c) 500 ml/day produced |
150ml total circulating
20ml/hr produced 500 ml/day produced |
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Where is the CSF produced
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In the Choroid Plexus (lateral ventricles)
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Where is the CSF absorbed?
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In the Arachnoid Villi
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Normal ICP
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10 mmHg (measured at level of ear)
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Cranial Vault rigid, fixed volume what % does the Brain take up?
a) 8% b) 12% c) 80% |
80%
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Cranial Vault rigid, fixed volume what % does the Blood take up?
a) 8% b) 12% c) 80% |
12%
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Cranial Vault rigid, fixed volume what % does the CSF take up?
a) 8% b) 12% c) 80% |
8%
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How do you decrease ICP
a) Hyperventilation b) CSF Drainage c) Hyperosmotic Drugs d) Barbiturates |
Hyperventilation (25 - 30 mmHg)
CSF Drainage Hyperosmotic Drugs Barbiturates |
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How long do the effects of hyperventilaton last on ICP?
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6 - 12 hours
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EEG
a) MAC doesn't effect b) MAC effects keep @ 0.5 c) Barbs & opioids don't effect d) Barbs & opioids effect |
MAC effects keep @ 0.5
Barbs & opioids effect |
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BAER
a) MAC doesn't effect b) MAC effects keep @ 0.5 |
MAC doesn't effect
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Somatosensory Evoked Potential
a) sensory pathway monitor b) neuronal function monitor c) descending pathway monitor d) cerebral perfusion |
sensory pathway monitor
neuronal function monitor |
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Motor Evoked Potential
a) sensory pathway monitor b) neuronal function monitor c) descending pathway monitor d) cerebral perfusion |
descending pathway monitor
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BAER
a) sensory pathway monitor b) neuronal function monitor c) descending pathway monitor d) cerebral perfusion |
sensory pathway monitor
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T/F A rapid increase in BP with failed auto-reg = cerebral edema, increased CBF and ICP
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True will rupture an aneurysm
a rapid decrease will cause ischemia |
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What are the most stimulating times during a crani?
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Laryngoscopy
Pin Placement Skin Incision Bone Flap elevation |
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Benign Tumors
a) astrocytoma b) meningioma c) medulloblastoma d) acoustic neuroma |
meningioma
acoustic neuroma |
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Malignant Tumors
a) astrocytoma b) meningioma c) medulloblastoma d) acoustic neuroma |
astrocytoma
medulloblastoma |
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What is the main factor that can determine whether an aneurysm will rupture?
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SIZE (La Place)
LOCATION, AGE are NOT factors |
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T/F Venous Air Embolism happen when operative site is ABOVE heart
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True
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Pathway of venous air embolism
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venous sinus
jugular vein SVC RA RV PA to microcirculation |
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What is used to detect VAE?
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Doppler transducer over RIGHT heart
TEE |
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Signs of a VAE
a) sudden decrease in ETCO2 b) increased PAP, CVP c) HOTN d) tachycardia, murmur |
sudden decrease in ETCO2
increased PAP, CVP HOTN tachycardia, murmur |
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Subdural Hematoma
a) arterial/ sudden b) venous/ slow c) between dura & arachnoid d) between skull & dura |
venous/ slow
between dura & arachnoid |
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Epidural Hematoma
a) arterial/ sudden b) venous/ slow c) between dura & arachnoid d) between skull & dura |
arterial/ sudden
between skull & dura |
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Your patient with an Epidural Hematoma has a high BP what should you treat it with?
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DON'T TREAT IT SILLY! as soon as it's evacuated it will come down
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Trigeminal Neuralgia
a) aka Tic Douloureux b) sudden, brief, intense pain c) tx with anticonvulsant d) surgical ablation or decompression |
aka Tic Douloureux
sudden, brief, intense pain tx with anticonvulsant surgical ablation or decompression |
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T/F Chiari Malformation is the
downward placement of tonsillar portion of the cerebellum/medulla |
True
it will transend down thru Foramen Magnum into the upper spinal cord |
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Spinal Cord Transection
a) above C2 - C4 = death b) has 2 phases c) below C4 has decreased Exp. Reserve Volumes |
above C2 - C4 = death
has 2 phases below C4 has decreased Exp. Reserve Volumes |
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Early Transection of Spinal Cord
a) spinal shock b) flaccid paralysis c) lasts 1 - 3 weeks d) morbidity is r/t inability to clear secretions |
spinal shock
flaccid paralysis lasts 1 - 3 weeks morbidity is r/t inability to clear secretions |
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Chronic phase of Spinal Cord Transection
a) return of reflexes b) Overstimulation SNS c) thermoregulation is a problem d) autonomic hyperreflexia |
return of reflexes
Overstimulation SNS thermoregulation is a problem autonomic hyperreflexia |
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Autonomic Hyperreflexia happens when spinal cord transection is
a) above C4 b) above T6 c) below T6 |
above T6
85% of people with this transection will have Autonomic Hyperreflexia |
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Diaphragmatic innervation is wiped out in a
a) C2 - C4 transection b) below C4 transection |
C2 - C4 transection
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Autonomic Hyperreflexia
a) vasconstriction above injury b) vasconstriction below injury c) HTN above injury d) HTN below injury |
vasconstriction below injury
HTN below injury Baroreceptors will receive message but cant send message below injury d/t transection |
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How do you treat Autonomic Hyperreflexia?
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Nipride, or NTG and alpha blockers
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T/F In a Spinal cord transection below C4 the patient will have adequate Tidal Volumes
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True
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Your quad patient foley catheter becomes kinked and suddenly he becomes Bradycardic, HTN, and has flushed extremities. What the HECK is going on?
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They are exhibiting the HALLMARK signs of autonomic hyperreflexia
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Autonomic Hyperreflexia is evident in
a) spinal shock phase b) Chronic phase |
Chronic phase
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T/F Autonomic Hyperreflexia is unlikely in a T10 or below transection
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True
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Sux when is it OK to use it in a Spinal Cord Transection?
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In the first 24 hours would be the best time, after that worry about increased extrajunctional receptors, elevated K and all that
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Major Burn
a) full thickness >10% BSA b) partial thickness > 25% BSA c) child > 20% BSA |
full thickness >10% BSA
partial thickness > 25% BSA child > 20% BSA |
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1st degree
a) destruction of dermis b) both epidermis & dermis involved c) epidermis, dermis & subQ tissue |
destruction of dermis
NO BLISTERS |
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2nd degree
a) destruction of dermis b) both epidermis & dermis involved c) epidermis, dermis & subQ tissue |
both epidermis & dermis involved
dermis has 2 layers |
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3rd degree
a) destruction of dermis b) both epidermis & dermis involved c) epidermis, dermis & subQ tissue |
epidermis, dermis & subQ tissue
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2nd degree
a) cherry red b) no blisters c) blisters d) require skin graft |
cherry red
blisters require skin graft (if basement membrane not intact) |
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1st degree
a) blisters b) no blisters c) heal on own d) require grafts |
no blisters
heal on own Harmless |
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4th degree
a) destruction of dermis b) both epidermis & dermis involved c) epidermis, dermis & subQ tissue d) all layers may involve muscle, down to bone |
all layers may involve muscle, down to bone
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Which of the following burn calculating scales CANNOT be used on Peds
a) Lund & Broweder b) Rule of Nines |
Rule of Nines
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What is the #1 cause of death in burns?
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Infection
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The extent of an electrical burn is dependent on
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Voltage & duration of contact
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Of the following which is the most common
a) electrical burns b) thermal injury c) inhalation injury d) chemical burns |
thermal injury
happen around house age extremes |
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Supraglottic Inhalation injury
a) tissue edema b) decrease ciliary movement c) rapid airway obstruction d) decrease surfactant production |
tissue edema
rapid airway obstruction |
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Infraglottic Inhalation injury
a) tissue edema b) decrease ciliary movement c) rapid airway obstruction d) decrease surfactant production |
decrease ciliary movement
decrease surfactant production as well as increased cap. permeability and edema |
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Carbon Monoxide Poisoning
a) shifts OxyHgb to left b) shifts OxyHgb to right c) SaO2 appears normal d) SaO2 85% |
shifts OxyHgb to left
SaO2 appears normal 200x more affinity for Hgb than O2 |
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Formula for fluid resuscitation for burn patients
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4ml / kg/ % TBSA
4 x 50 kg x 40% = 8000 50% over 1st 8 hrs (4000) 50% over next 16 hours (4000) |
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Which type of fluids are given in 1st 24 hours of fluid resuscitation in a burn patient
a) crystalloids b) colloids |
crystalloids
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In 2nd 24 hours of fluid resuscitation in a burn patient
a) crystalloids b) colloids |
colloids
Crystalloids are continued as well |
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Burn Shock Phase
a) loss of plasma proteins in 1st 36 hours b) catechol surge c) myocardial depressant factor released |
oss of plasma proteins in 1st 36 hours
catechol surge myocardial depressant factor released |
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In Major burns Pulmonary edema happens when
a) in first 24 hours b) after 48 hours c) will always show symptoms d) may or may not show symptoms |
after 48 hours
may or may not show symptoms May have pulm edema if overhydrated in 1st 24 hours |
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What is the gold standard for assessing renal function?
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Urine output
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Treatment of Myoglobinuria involves
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Administration of Na Bicarb
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T/F Curlings Ulcer is common in burn patients d/t a negative nitrogen balance
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True, treat with H2 blockers and antacids
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Caloric need in burn patients is increased
a) 50% b) 100% c) 200% d) 300% |
100% insert dobhoff and start insulin gtt ASAP
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Ileus is common in TBSA
a) 10% b) 20% c) 40% d) 50% |
20% d/t release of mediators and narcotics
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Tangential Debridement
a) good cosmetically b) bad cosmetically c) high blood loss d) minimal blood loss |
good cosmetically
high blood loss eschar is shaved away |
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Full Thickness Debridement
a) good cosmetically b) bad cosmetically c) high blood loss d) minimal blood loss |
bad cosmetically
minimal blood loss eschar cut away with bovie |
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Drugs in burns
a) increased narcotic requirement b) decreased narcotic requirement c) increased NMBD d) decreased NMBD |
increased narcotic requirement
increased NMBD (increase dose by 30% for up to 60 days) |
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T/F Blood loss is 2 - 3% of blood volume for each 1% TBSA
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True
TBSA x 3% = % % x Total Blood Vol = blood loss ie: Total blood volume = 5 L 20% TBSA x 3% = 60% 60% (0.6) x 5 L = 3000ml blood loss |
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If normal Hct is 35 % and a unit of blood has a Hct of 70% and the patient loses 700ml (2 units of blood) how would you replace it?
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I unit PRBCs (350 ml) Hct 70%
+ crystalloids for rest of volume |
