Justin's Critical Care Flashcards

1
Q

Postop pt VSS and afib: metoprolol, anticoagulation, or digoxin?

A

Metoprolol, not anti-coagulation since immediately post op (but if lasting longer than a few days need to consider long term AC)

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2
Q

Stable Afib in setting of heart failure in postop pt, how to treat acutely

A metoprolol
B verapamil
C diltiazem
D cardioversion
E adenosine

A

Metoprolol (this one if they are stable; multiple RCTs show decreased mortality with BB), verapamil, diltiazem (ca ch blockers have negative inotropic), cardioversion (if unstable) –>
based on uptodate amio or dogoxin maybe not choices
NOT adenosine

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3
Q

What is pulsus paradoxus and associated with what?

A

Inspiratory fall in SBP >10 mmHg. results from alterations in the mechanical forces imposed on the chambers of the heart and pulmonary vasculature often due to pericardial disease, particularly cardiac tamponade

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4
Q

What is the Goldman cardiac risk index?

A

For patients undergoing non-cardiac surgery cardiac risk factors to predict perioperative M&M

*per up to date - the revised Goldman is now used. Pic is attached

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5
Q

Most predictive of postoperative cardiac performance?

A

Dobutamine stress test

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6
Q

What electrolyte abnormalities from massive transfusion?

A

HyperK, HypoCalcemia

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7
Q

Treat hypermagnesemia with slow infusion of one of the following
a)Lasix
b)calcium
c) other choices

A

calcium gluconate (reverse neuromuscular and cardiac effects of magnesium); used for SEVERE cases

UTD:
- normal renal function: loop (or even thiazide) diuretics can be used to increase renal excretion of magnesium.
- pts on dialysis: patients with symptomatic hypermagnesemia should be given intravenous calcium as a magnesium antagonist to reverse the neuromuscular and cardiac effects of hypermagnesemia while awaiting dialysis

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8
Q

Signs/ Sx of hypokalemia

A

Weakness, decreased DTR, mental status change, ileus, cardiac issues

flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression in more severe hypokalemia.

Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.

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9
Q

Sx of hypercalcemia

A

Stones, bones, groans, psych overtones

mnemonic, “painful bones, renal stones, abdominal groans, and psychic moans,” can be used to recall the typical symptoms of hypercalcemia. Painful bones are the result of abnormal bone remodeling due to overproduction of PTH. Nephrolithiasis occurs secondary to hyperparathyroid disease–induced hypercalcemia and resultant hypercalciuria. Abdominal groans refers to hypercalcemia-induced ileus. Psychic moans or depression may occur

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10
Q

Most common cause of hypercalcemia

A

Hyper PTH

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11
Q

What drugs cause hypocalcemia

A

cisplatin, aminoglycosides, bisphosphonates, cimetidine, heparin, anti-epileptics, PPIs

(FYI- aminoglycosides:gentamicin, tobramycin, amikacin, plazomicin, streptomycin, neomycin, and paromomycin)

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12
Q

Adverse effects from transfusion massive

A

HYPOcalcemia and alkalosis due to citrate tox
[FYI: Citrate intoxication is a frequent complication after massive blood transfusions and often presents itself as metabolic alkalosis. The reason this term comes about is due to the conversion of citrate, which is applied as an anticoagulant in blood bags, to bicarbonate, and this conversion happens, predominantly in the liver. Stored blood is anticoagulated using citrate (3 g/unit of RBC), which chelates calcium. In a healthy adult, the liver metabolizes 3 g of citrate in 5 min. Infusion rates greater than 1 unit of RBC/5 min, or liver dysfunction, drive citrate elevation and lower plasma ionized calcium ]

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13
Q

Hypercalcemia EKG changes

A

Shortened QT
ST segment elevation

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14
Q

Hypocalcemia EKG changes

A

Prolonged QT

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15
Q

What is the least likely metabolic abnormality in tumor lysis syndrome
a) hyponatremia
b) hyperkalemia
c) hyperphosphatemia
d) hyperuricemia
e) hypocalcemia

A

a) hyponatremia

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16
Q

What is NOT associated with hypOcalcemia?
a) seizures
b) tetany
c) Short ST
d) cramps
e ) Trousseau sign

A

c) Short ST

FYI EKG findings include prolongation of the QT interval as a result of lengthening of the ST segment.

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17
Q

Tumor lysis syndrome - Part 1
-electrolyte abnormalities
-renal effect
-occurs in which tumors

A
  • hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia due to catabolism of nucleic acids; LDH (biomarker of rapid cell turnover)
    -Acute kidney injury
    -Occur in tumors with high proliferative rates, large tumor burdern, high sensitivity to cytotoxic therapy
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18
Q

Tumor lysis syndrome - Part 2
-other symptoms
-treatment

A

-symptoms: n/v, diarrhea, anorexia, lethargy, hematuria, HF, cardiac arrhythmia, seizures, cramps, tetany, syncope, sudden death
-supportive care, electrolyte optimization, allopurinol ( for intermediate risk patients) (MOA prevents uric acid formation) or rasburicase (for high risk patients or those with impaired renal function)(MOA: breaks down uric acid) to lower serum uric acid

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19
Q

Hypocalcemia symptoms/signs

A

Prolonged QT, hyperreflexia, tetany,

Chvostek sign (twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear), Trousseau’s sign (latent tetany - carpopedal spasm induced by ischemia secondary to the inflation of a sphygmomanometer cuff)

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20
Q

What is major reason to heat blood when transfusing during major intraop blood loss

A

Avoid hypothermia and hypothermic coagulopathy

Hypothermia: Impact on platelets, reduced function. impaired enzymes of the coagulation cascade

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21
Q

which antibiotic is not renally metabolized/cleared?

A

Flagyl

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22
Q

Tx for initial recurrence of cdiff

A

Fidaxomicin) [Up to date says favor fidaxomicin] or Vanco - pulsed and tapered
Both with bezlotoxumab

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23
Q

Treatment options for cdff

A

PO vanc or Fidaxiomicn. Can use po flagyl but less effective

24
Q

Treatment for HCAP

A

Cefepime (4TH GEN), Zosyn, OR levofloxacin IV (reserve imipenem for ESBL) if LOW risk.

Add AG if high risk for pseudomonas (for double coverage)

Add vanc/linezolid if high risk MRSA.
Low risk mort (i.e., no vent or sepsis) and no MRSA factors: IV zosyn, IV cefepime (4th gen), IV levaquin, IV imipenem/meropenem

High risk mort and no MRSA factors: dual therapy with above + add IV fluoroquinolone or aminoglycoside (these add Pseudomonas coverage)

If MRSA (tx’ed IV abx last 90 days or >20% in unit), add IV vanco or IV linezolid to above

If high risk mortality or IV abx last 90d: need 2 abx but now can consider gent or tobra (both AGs) or aztreonam (avoid beta-lactams) from above PLUS vanco

25
Q

Torsades de pointes is associated with #1 and total 3 electrolyte abnormalities

A

1) hypomag - then hypok (often result of hypomag) - then hypoCa. associated with QT prolongation. Can resolve spontaneously

26
Q

SVR 300 dyne and increased CO - what type of shock?

A

Sepsis. Distributive shock- low SVR (<900 dynes per second/cm^5) and normal or high CO. Cardiogenic shock- high SVR (>1400 dynes/second/cm^5) and low CO ; high PCWP geater than 15 mmHg (right atrial pressure)

27
Q

What is the difference between cardiogenic and hypovolemic shock (PCWP = LA pressure)

A

cardiogenic (high PCWP), hypovolemic (low PCWP)

28
Q

Which pressor not use in sepsis

A

Dobutamine - not a pressor but an inotrope, b/c associated with hypotension, usually used for cardiogenic failure. Most commonly used - norepi, epi

29
Q

Sepsis is associated with increased venous _______

A

Capacitance

Lit review: Sepsis increases venous capacitance and decreases systemic vascular resistance (SVR), leading to cardiovascular compromise and tissue hypoperfusion. In septic shock, the TBV status is unchanged, but the progressive vasodilation shifts a portion of the Vs to Vu, which decreases mean circulatory filling pressure (Pmcf) and venous return [6].

Sepsis —> vasodilation [increased venous capacitance (venodilation) AND decreased SVR (arterial dilation)] due to overproduction of NO

30
Q

Predictor of mortality in sepsis

A

sustained tachycardia

31
Q

Cytokine pro-inflammatory in sepsis

A

TNF-alpha

32
Q

Leading cause neutropenic sepsis

A

Gram negative aerobics: ie Pseudomonas, Klebsiella, E coli

33
Q

What is the 10 year and lifetime risk of sepsis in a patient who has undergone splenectomy?

A

These episodes occur in patients who have had splenectomy at a rate of 0.2%–0.5% per year, with a lifetime risk of about 5%.

I found this on NIH - jv

34
Q

Why is PEEP important for tx of ARDS

A

Improve oxygenation and prevent alveolar collapse

35
Q

What to do if on vent and low PaO2?

A

Increase FiO2 and Increase PEEP

36
Q

What to do if on vent and hypercapnea?

A

Increase tidal volume and respiratory rate

37
Q

What med to give someone with normal wedge pressure and hypotension

A

Since wedge pressure is OK, need to increase SVR: use Phenylephrine

38
Q

What does more PEEP due to cardiac output

A

Decreases cardiac output (reduces right heart filling, decreases stroke volume)

39
Q

Effect of PEEP use in ARDS

A

For ARDS patients who responded to increased PEEP by improved oxygenation, high PEEP could reduce hospital mortality, ICU mortality and 28-d mortality. High PEEP does not increase the risk of clinically objectified barotrauma.

40
Q

Which has the least ionotropy?
a) dobutamine
b) dopamine
c) phenylephrine
d) epinephrine

A

Phenylephrine (Phenylephrine is a synthetic alpha-adrenergic receptor agonist with virtually no affinity for beta receptors. Therefore, it is a potent vasoconstrictor with essentially no chronotropic or inotropic effects.)

41
Q

Which opioid has the longest half-life

A

Methadone (12-24 hrs)

42
Q

Fulminant C diff disease* is supported by the following clinical data: Hypotension or shock, ileus, megacolon. What treatment is indicated?

A

IV flagyl + po vancomycin

*I added this question

43
Q

most abundant electrolyte in the body

A

Calcium

44
Q

most abundant extracellular cation?

A

Sodium

45
Q

most abundant intracellular cation

A

Potassium

46
Q

Which electrolyte issues can be treated with loop diuretics (lasix)

A

hyperK and HyperMg

47
Q

Electrolyte abnormalities associated with hypoaldosteronism

A

HypoNa, HyperK
Metabolic acidosis

H goes with K as single letters

48
Q

Electrolyte abnormalities associated with HYPERaldosteronism

A

HyperNa, HypoK, HypoMg
Metabolic Alkalosis

H (H for acid) goes with K as single letters

49
Q

Treatment of HYPERaldosteronism

A

spironolactone

50
Q

Treatment of hypoaldosteronism

A

steroids

51
Q

Hyponatremia correction rate to avoid what complication

A

4-6 mEq/L in 24 hrs (UTD) to avoid osmotic demyelination syndrome (formerly called central pontine myelinolysis)

52
Q

What is a measure of preload

A

CVP
Card used to read PCWP but incorrect

53
Q

What is the measure of afterload?

A

SVR

54
Q

What is the enzyme associated with COPD

A

alpha -1- antitrypsin

55
Q

How long can you store RBCs

A

42 days