ITE QBANK Misc 3 Flashcards
Early adult onset ventilator assoc. PNA is typically d/t _____
MSSA
TCAs primary MOA is the inhibition of presynaptic neurotransmitter uptake _______ and _______
Norepi and serotonin
Treatment for TCA toxicity with ECG showing wide QRS interval
Sodium bicarb
Common metabolic changes seen with TPN (6)
- Hypercarbia
- Hyperglycemia
- Hyperinsulinemia
- Hypophosphatemia
- Hypokalemia
- Hypomagnesemia
*NOT sodium
Can hepatic steatosis be seen in TPN?
Yes - common
- liver will store excess sugar as fat in liver
Can hypocarbia or hypocapnia occur with TPN infusion?
No - HYPERcarbia or HYPERcapnia
- Pt will metabolize excess carbs into sugar and increase CO2 production.
Can hypernatremia occur with TPN?
Unlikely
- more common in pts not receiving enough free water (calculate deficit and give as free water bolus)
Is low dose corticosteroids good for tx of septic shock?
No - not Recommended unless pt is unresponsive to fluids and vasopressors
No mortality benefit, but does reduce dependence of vasopressors and speed resolution of shock
____________ is defined as intrapulmonary vascular dilatations and increased A-a oxygen gradient, in the setting of end-stage liver disease
Hepatopulmonary syndrome
*Pts with hepatic failure have excessive circulating levels of NO –> excessive pulmonary vasodilators.
In hepatopulmonary syndrome, hypoxia is _____ when the pt lies flat, and ______ when the pt stands
Improved (platypnea)
worsened (orthodeoxia)
*worsened by increasing VP mismatch
Mean PAP > __ mmHg in a liver failure pt is suggestive of high perioperative mortality risk.
Mean PAP > __ mmHg is an absolute contraindication to liver transplantation.
> 35 mmHg
> 50 mmHg
Septic shock is a dyregulated response to infection, causing a metabolic _______ with compensatory ______
acidosis
respiratory alkalosis
Phosgene (chemical warfare agent) exposure can cause severe ________, which can cause significant morbidity and mortality
pulmonary edema
*targets type I and II pneumocytes
Inflammatory mediators cause:
- Prostaglandin:
- Bradykinin:
- Thromboxane A2
- Complement
- Prostaglandin: vasodilation/constriction, platelet disaggregation
- Bradykinin: inc capillary permeability
- Thromboxane A2: Vasoconstriction
- Complement: attraction of leukocyte and leukotriene release
Renin release is (Increased/Decreased) in cirrhotic pts secondary to _______ factors that are released
Increased
- Cirrhosis: hyperdynamic circulatory system (high Cardiac output, reduced systemic vascular resistance, reduced arterial pressure), secondary to vasodilating factors (NO, VIP)
In hepatopulmonary syndrome, _______is d/t an increased shunting of blood through the lungs, causing dyspnea.
platypnea (dyspnea while sitting)
the ____ wave on a central venous pressure (CVP) tracing is a result of increased venous return and systolic filling of the RA
v wave
Central venous pressure (CVP) waveforms are classically defined by 5 phasic events:
a, c , v waves (peaks)
x, y (descents)
Central Venous Pressure (CVP) is used to assess _____ and evaluate ____
R heart function
blood volume
The most prominant wave of the CVP tracing occurs during ___ which is noted by the ___ wave
atrial contraction, “atrial kick”
a wave
Central venous pressure (CVP) waveform changes in:
- a fib
loss of a wave
Central venous pressure (CVP) waveform changes in:
- AV dissociation
cannon a wave
Central venous pressure (CVP) waveform changes in:
- Tricuspid regurg
Tall C & V waves
Loss of x descent
Central venous pressure (CVP) waveform changes in:
- Tricuspid stenosis
tall a & v waves
minimal y descent
Central venous pressure (CVP) waveform changes in:
- RV ischemia
Tall a & v waves
Steep x & y descent
M or W configuration
Central venous pressure (CVP) waveform changes in:
- Pericardial constriction
Tall a & v waves
Steep x & y descent
M or W config
Central venous pressure (CVP) waveform changes in:
- Cardiac tamponade
dominant x descent
minimal y descent
Normal Central venous pressure (CVP) tracing:
____: atrial contraction
____: TV buldging into RA during RV isovol contraction
____: TV descends into RV with vent. ejection and atrial relaxation
____: venous return to and systolic filling of the RA
____: atrial emptying into RV through open TV
a wave : atrial contraction
c wave: TV buldging into RA during RV isovol contraction
x descent: TV descends into RV with vent. ejection and atrial relaxation
v wave: venous return to and systolic filling of the RA
y descent: atrial emptying into RV through open TV
First line treatment in cyanide toxicity
hydroxocobalamin
Sodium thiosulfate (older and slower)
Pts with cyanide toxicity may show normal oxygenation with metabolic ______.
acidosis
but could be masked by respiratory compensation
Hydrocortisone (promotes/inhibits) nitric oxide synthesis
inhibits
Of the 4 etiologies of hypoxemia, _____ is the only one which shows a normal a-a gradient
hypoventilation
______ is the most common cause of hypoxemia and will response to increased FiO2
V/P mismatch
- atelectasis, bronchospasm, COPD, airway obstruction, PNA
Strong Ion Difference (SID) in pts can be reduced by _______.
infusing lg volumes of fluid that has a SID of zero (ie: NS) to create dilutional acidosis
ie: cl-, lactate, HCO3-, PO34-, Albumin
Strong ion difference (SID) is normally ___ mEq/L
40
Tx for infant < 1 yr and adult botulism
Infant < 1 yr: Hu Ig
Age > 1 yr: equine derived antitoxin
onset of paralysis for botulism toxin is ____, and peaks at ____, and stabilizes at _____
6 - 72 hrs
2 weeks
10 weeks
(Hyper/Hypo)phosphatemia causes muscle weakness d/t lack of energy source. Cause difficulty weaning off mechanical ventilation.
Hypophosphatemia
Drugs common with drug fever
- amphotericin
- cephalosporins
- PCN
- phenytoin
- procainamide
- quinidine
ARDS net uses TV of ___ mL/kg of PBW and plateau pressures of ___ cm H2O
6 mL/kg
< 30 cm H2O
Use of vasopressin in pts with CAD can ppt _________ d/t ______
MI
- Vasoconstriction of coronary arteries
Vasopressin aka _____, promotes reabsorption of water in kidney tubules by increasing cell membrane permeability
ADH
Is it safe to give vaso in pts with renal dysfunction and liver failure secondary to hepatitis?
Yes
Calcium gluconate is used to treat (Hyper/Hypo) magnesemia.
Ca can raise BP quickly, easily titratable, and is readily available
Hypermag
PLasma OSM equation
2 * Na + Glucose/18 + BUN/2.8
Significant increase in angiotensin II in approximately ___ (time) after a blood pressure decrease is sensed by juxtaglomerular apparatus
20 minutes
*after anesthetic induction in nl pts, transient hypotension is offset by RAAS in ~20 min