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ABSITE > Critical Care > Flashcards

Critical Care Flashcards

1
Q

Arterial O2 content equation

A

CaO2 = Hgb x 1.34 x O2 saturation + PO2 x 0.003

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2
Q

O2 delivery equation

A

O2 delivery = cardiac output x arterial O2 content x 10

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3
Q

MAP equation

A

MAP = cardiac output x systemic vascular resistance

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4
Q

cardiac index equation

A

cardiac index = cardiac output / BSA

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5
Q

stroke volume equation

A

stroke volume = LVEDV - LVESV

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6
Q

ejection fraction equation

A

ejection fraction = stroke volume / LDEDV

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7
Q

O2 consumption equation

A

VO2 = cardiac output x (arterial O2 content - venous O2 content)

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8
Q

mechanism of action milrinone

A

phosphodiesterase inhibitor (leads to increased cAMP), results in increased Ca flux and myocardial contractility, pulmonary vasodilation

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9
Q

mechanism of action of vasopressin

A

V1 receptor - vasoconstriction of vascular smooth muscles, V2 receptor (intrarenal) - water reabsorption at collecting ducts V3 receptors (extrarenal) mediate release of factor VIII and vWF

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10
Q

mechanism of action of dobutamine

A

beta1 (increases contractility mostly, tachycardia with higher doses)

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11
Q

mechanism of action of dopamine

A

low dose - dopamine receptor (renal), med dose beta / contractility, high dose alpha adrenergic vasoconstriction and increased BP

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12
Q

mechanism of action of phenylephrine

A

alpha1 (vasoconstriction)

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13
Q

mechanism of action of norepinephrine

A

beta1 (increased contractility) and alpha1/alpha 2 (splanchnic vasoconstriction)

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14
Q

mechanism of action of isoproterenol

A

beta1/beta2 increases HR and contractility, vasodilates; extremely arrythmogenic, can lead to hypotension

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15
Q

mechanism of action of nipride

A

arterial vasodilator, can lead to cyanide toxicity which you tx w/ amyl nitrite/sodium nitrite

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16
Q

mechanism of action of nitroglycerin

A

predominately venodilation with decreased myocardial wall tension from decreased preload, moderate coronary vasodilator

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17
Q

total lung capacity equation

A

TLC = forced vital capacity + residual volume

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18
Q

functional residual capacity equation

A

FRC = expiratory reserve volume + residual volume

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19
Q

Berlin definition of ARDS

A

1) within 1 week of insult or worsening symptoms 2) bilateral opacities not otherwise explained (effusion, ATX, mass), 3) resp failure not explained by HF/volume overload 4)PaO2/FiO2 <=300 – mild 200-300, moderate 100-200, severe <100

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20
Q

most common site of aspiration?

A

super seg of RLL

21
Q

definition of SIRS

A

temp >38 or <36, HR > 90, RR >20 or PCO2 <32, WBC >12 or <4

22
Q

methemoglobinemia O2 sat? treatment?

A

O2 sat reads 85%, tx w/ methylene blue

23
Q

carbon manoxide - O2 sat? tx?

A

falsely increases O2 sat on pulse ox, binds to Hgb directly, tx w/ 100% O2 on ventilator, rarely need hyperbaric O2

24
Q

mechanism of action of dexmedetomidine?

A

similar to clonidine - selective alpha 2 antagonist

25
Q

mechanism of action of ketamine? limitations?

A

blocks glutamate NMDA receptors, limited by psychoactive effects

26
Q

what is the benefit of CRRT in septic shock?

A

earlier use = filter inflammatory mediators, defined as within 8 hours of AKI onset, duration of RRT and LOS were shorter in early vs later, no difference in long term RRT needs, pt w/ increased IL8 increased risk of RRT dependence after hospital discharge (ELAIN trial in 2016)

27
Q

free water deficit equation

A

( serum sodium - 140 ) / 140 x total body water – total body water is 50% of lean body mass in men, 40% in women – 50% is to be given over 24 hours

28
Q

issue with treating hypernatremia too quickly?

A

cerebral edema – give 50% of deficient free water over 24 hrs (free water equation = serum sodium - 140 / 140 x total body water (weight * .5 men, .4 women)

29
Q

normal cardiac output? cardiac index?

A

4-8 L/min, 2.5-4 L/min

30
Q

normal SVR?

A

800-1400

31
Q

normal pulmonary capillary wedge pressure? central venous pressure? pulmonary artery pressure?

A

PCWP 11+/-4, CVP 7+/-2, PAP 25/10 +/-5

32
Q

Normal mixed venous O2 sat?

A

75+/-5

33
Q

causes of increased SvO2?

A

increased SvO2 occurs with shunting or decreased O2 extraction (sepsis, cirrhosis, cyanide toxicitiy, hyperbaric O2, hypothermia, paralysis, coma, sedation)

34
Q

causes of decreased SvO2?

A

decreased SvO2 occurs with increased O2 extraction or decreased O2 delivery – anything that decreases O2 saturation, cardiac output, malignant hyperthermia

35
Q

symptoms of hypomagnesia?

A

similar to hypocalcemia = HYPERactive reflexes, muscle tremors, tetany, +Chvostek sign, severe deficiency can lead to delirium and seizures – also see prolonged QT

36
Q

symptoms of hypermagnesia?

A

loss of tendon reflexes; respiratory/cardiac arrest

37
Q

how to determine cause of metabolic alkalosis?

A

measure urine chloride, if low, means chloride responsive, is much more common in surgical patients and results from vomiting (GI loss of hydrogen ions), diuretics (GU loss of chloride), volume depletion (aldosterone stimulated hydrogen ion loss in urine); chloride resistant types (urine chloride >25), result form mineralcorticoid excess or potassium depletion

38
Q

definition of hemorrhagic shock / classes

A

class 1 = up to 750 ml or <15% total blood volume, class 2 = 1500 ml or 30%, can have tachycardia, decreased pulse pressure; class 3 = 2000 ml or 40% decreased BP, class 4 = >2L or >40%, significantly decreased BP

39
Q

general Swan-Ganz findings in sepsis – CVP? SVR? cardiac index? PCWP? SVO2?

A

CVP low (from loss of intravascular volume due to increased capillary permeability), SVR is low (due to toxins that produce vasodilation), cardiac index (usually elevated initially), PCWP (usually unaffected), SVO2 (usually high because tissues unable to extract O2 from blood for consumption)

40
Q

acute treatment for hypermagnesia?

A

calcium chloride (cardiac protection), then dialysis if still elevated/persistent symptoms

41
Q

effects of increased PEEP on - cardiac output, arterial oxygen content, pCO2

A

can decrease cardiac output due to increased intrathoracic pressure, can increased O2 content due to recruitment of collapsed/atelectatic lung, does not affect PCO2

42
Q

most common organism involved with transfusion transmitted bacterial infection?

A

gram negatives (yersinia, pseudomonas – can grow at 4C

43
Q

definition of intra-abdominal hypertension? abdominal compartment syndrome?

A

hypertension >= 12mm Hg; ACS is sustained pressures >20 w/ new end organ dysfunction

44
Q

treatment of new VT (stable / unstable)?

A

stable - amiodarone, procainamide, sotalol; unstable defibrillation

45
Q

characteristic findings in hepatorenal syndrome

A

relative hypovolemia, splanchnic and peripheral arterial vasodilation, intense vasoconstriction of the renal circulation – leads to azotemia, oliguria, very low urinary sodium, high urine osmolarity; type 1 is worse than type 2, associated with acute liver failure or EtOH cirrhosis

46
Q

what is the pulmonary artery wedge pressure an indirect estimation of?

A

left atrial and left ventricular diastolic pressure

47
Q

features of argatroban

A

direct thrombin inhibitor, used for HIT, monitored with aPTT, short half life (40-50 minutes), cleared by liver – drug of choice for pt w/ HIT and renal problems

48
Q

features of lepirudin?

A

direct thrombin inhibitor, used for HIT, monitored with aPTT, 60-90 minute half life, cleared by renal metabolism, drug of choice for pt w/ HIT and liver problems

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