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
What are the independent risk factors for stress ulcers requiring H2 blocker prophylaxis?
mechanical ventilation for \>48 h coagulopathy (plt \< 50, INR \> 1.5, PTT \> 2x control)
26
What is the most distinguishing receptor difference between norepinephrine and epinephrine?
only epinephrine is a clinically significant ß2 agonist
27
Which causes a greater increase in diastolic BP, norepinephrine or epinephrine?
norepinephrine \*ß2 agonist effects of epinephrine cause vasodilatation in some vascular beds, resulting in minimal change in diastolic BP\*
28
What receptors do the enantiomers of dobutamine agonize?
one enantiomer is a ß1 \>\>\> ß2 agonist one enantiomer is an a1 agonist
29
What is increased dromotropy?
increased conduction speed within the heart (particularly the AV node)
30
What is lusitropy?
diastolic relaxation achieved by decreasing cytosolic Ca2+ levels via SERCA-mediate Ca2+ uptake into the sarcoplasmic reticulum
31
How do alpha adrenergic receptors and beta adrenergic recpetors differ in the way they increase cytosolic calcium?
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
How does inhaled NO result is smooth muscle relaxation?
NO \> guanylate cyclase \> cGMP \> smooth muscle relaxation \*PDE-5 breaks down cGMP and is inhibited by sildenafil\*
33
What is nesiritide, and how is it useful in treating decompensated heart failure?
recombinant BNP activates guanylate cyclase \> cGMP \> vasodilatation, thus encouraging forward flow
34
How can nitroprusside affect hemoglobin?
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
How does cyanide toxicity result in acidosis?
CN- binds to cytochrome oxidase, preventing ATP production through the electron transport chain, necessitating anaerobic metabolism a resultant lactic acidosis
36
What happens to mixed venous O2 during cyanide toxicity?
increases due to inability of tissues to utilize oxygen in the electron transport chain
37
How is cyanide toxicity treated?
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
Which vasodilator is associated with improved subendocardial perfusion during periods of ischemia?
nitroglycerin
39
How is methemoglobinemia treated?
methylene blue