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ABA Advanced Exam COPY***** > Critical Care > Flashcards

Critical Care Flashcards

1
Q

What is the first step in resuscitation of a drowning victim?

A

rescue breathing

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2
Q

How should CVLs placed under emergency conditions be managed?

A

replaced within 24 hours at a new site

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3
Q

Why is propofol infusion syndrome associated with lactic acidosis?

A

propofol prevents mitochondria from using fatty acids as an energy source, so after glucose and amino acids stores are used up, lactic acidosis develops

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4
Q

What is the equation for arterial oxygen content?

A

CaO2 = (1.34 x Hgb x SaO2) + (0.003 x PaO2)

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5
Q

What is the equation for oxygen delivery?

A

DO2 = CaO2 x CO

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6
Q

What is the equation for oxygen consumption?

A

VO2 = 1.34 x (SaO2 - SmvO2) x Hgb x CO

OR

SmvO2 = SaO2 - [VO2/(1.34 x Hgb x CO)]

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7
Q

What is the oxygen extraction ratio?

A

ER = VO2/DO2

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8
Q

What is the alveolar gas equation?

A

PAO2 = FiO2(Patm - PH2O) - PaCO2/RQ

Patm = 760 mmHg

PH2O = 47 mmHg

RQ = 0.8

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9
Q

What factors affect the Hgb dissociation curve?

A
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10
Q

What is a normal value for VO2?

A

250 mL/min

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11
Q

What is dysoxia?

A

When oxygen consumption (VO2) decreases because oxygen delivery (DO2) is so low (i.e., no more oxygen can be extracted from what is delivered)

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12
Q

What is the Bohr effect?

A

Increased CO2 binding to Hgb reduces its affinity for O2 (i.e., a right shift in the hgb dissociation curve)

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13
Q

What is the Haldane effect?

A

oxygenated Hgb has a lower affinity for CO2 (facilitating CO2 unloading in the lungs)

deoxygenated Hgb has a higher affinity for CO2 and can act as a buffer

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14
Q

What is the law of LaPlace?

A

pressure = 2 x wall tension x wall thickness/radius

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15
Q

How is the majority of CO2 carried in the blood?

A

as bicarbonate in the plasma and RBCs

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16
Q

Where does carbonic anhydrase act to store CO2 as bicarbonate in the blood?

A

in endothelium and RBCs

17
Q

What is the P/F ratio in ARDS?

A

Berlin criteria for PaO2/FiO2*

200-300 = mild ARDS

100-200 = moderate ARDS

< 100 = severe ARDS

*with PEEP of at least 5

18
Q

What are the components of ARDSnet ventilation?

A

low tidal volumes: 6 mL/kg and titrated down

keep plateau pressures < 30

PEEP for oxygenation and reduced atelectrauma

permissive hypercapnea

19
Q

What is airway pressure release ventilation?

A

Two levels of CPAP with long periods spent at the high level (oxygenation) and brief periods spents at the low level (ventilation). Spontaneous respiration remains possible at both levels.

20
Q

What is an RSBI? How is it used in the ICU?

A

rapid shallow breathing index = frequency*/TV**

*frequency in breaths/min

**tidal volume in liters

RSBI < 100 is predictive of successful extubation

21
Q

What is the risk of ETTs left in place for more than 2-3 weeks?

A

subglottic stenosis

22
Q

What are the SIRS criteria?

A

hypo/hyperthermia

tachypnea

tachycardia

high or low WBCs or left shift

23
Q

What should be done if a patient aspirates on intubation?

A
  1. suction the oropharynx
  2. place the ETT
  3. suction the lungs (to prevent pushing particulate matter into smaller airways)
  4. begin ventilation
24
Q

What is negative inspiratory force? What is the minimum value necessary for extubation?

A

a test of inspiratory force

-20 to -25 cm H2O is minimum for extubation

25
Q

What are the independent risk factors for stress ulcers requiring H2 blocker prophylaxis?

A

mechanical ventilation for >48 h

coagulopathy (plt < 50, INR > 1.5, PTT > 2x control)

26
Q

What is the most distinguishing receptor difference between norepinephrine and epinephrine?

A

only epinephrine is a clinically significant ß2 agonist

27
Q

Which causes a greater increase in diastolic BP, norepinephrine or epinephrine?

A

norepinephrine

*ß2 agonist effects of epinephrine cause vasodilatation in some vascular beds, resulting in minimal change in diastolic BP*

28
Q

What receptors do the enantiomers of dobutamine agonize?

A

one enantiomer is a ß1 >>> ß2 agonist

one enantiomer is an a1 agonist

29
Q

What is increased dromotropy?

A

increased conduction speed within the heart (particularly the AV node)

30
Q

What is lusitropy?

A

diastolic relaxation achieved by decreasing cytosolic Ca2+ levels via SERCA-mediate Ca2+ uptake into the sarcoplasmic reticulum

31
Q

How do alpha adrenergic receptors and beta adrenergic recpetors differ in the way they increase cytosolic calcium?

A

alpha adrenergic receptors: activate Gaq going through PLC > DAG + IP3 > release of intracellular Ca2+ stores

beta adrenergic receptors: activate Gas going through adenylate cyclase > cAMP > PKA and increased intracellular Ca2+

32
Q

How does inhaled NO result is smooth muscle relaxation?

A

NO > guanylate cyclase > cGMP > smooth muscle relaxation

*PDE-5 breaks down cGMP and is inhibited by sildenafil*

33
Q

What is nesiritide, and how is it useful in treating decompensated heart failure?

A

recombinant BNP

activates guanylate cyclase > cGMP > vasodilatation, thus encouraging forward flow

34
Q

How can nitroprusside affect hemoglobin?

A

oxidizes the the heme iron from the 2+ to 3+ state, creating met-hemoglobin

breaks down into CN-, which can bind met-hemoglobin and create cyan-met-hemoglobin

35
Q

How does cyanide toxicity result in acidosis?

A

CN- binds to cytochrome oxidase, preventing ATP production through the electron transport chain, necessitating anaerobic metabolism a resultant lactic acidosis

36
Q

What happens to mixed venous O2 during cyanide toxicity?

A

increases due to inability of tissues to utilize oxygen in the electron transport chain

37
Q

How is cyanide toxicity treated?

A

Increasing the “sinks” for cyanide:

1) increasing methemoglobin with sodium nitrite
2) sodium thiosulfate, generating sodium thiocyanate which can be excreted by the kidneys

38
Q

Which vasodilator is associated with improved subendocardial perfusion during periods of ischemia?

A

nitroglycerin

39
Q

How is methemoglobinemia treated?

A

methylene blue

ABA Advanced Exam COPY***** (23 decks)

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