Capnography Flashcards

1
Q

PACO2

A

concentration of CO2 in the alveoli

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2
Q

PaCO2

A

concentration of CO2 in the arteries

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3
Q

EtCO2

A

concentration of CO2 in expired gas

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4
Q

how much higher is PaCO2 than EtCO2 normally?

A

3-5mmHg

dilutes as it travels to the capnograph

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5
Q

Do PaCO2 and EtCO2 normally correlate?

A

yes if PaCO2 increases so does EtCO2

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6
Q

When is the exception to PaCO2 and EtCO2 correlation?

A

pulmonary embolism
PaCO2 increase
EtCO2 decrease

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7
Q

what are the effects of hypercarbia? (6)

A
  1. repiratory acidosis
  2. central (pulmonary) vasoconstriction
  3. peripheral and cerebral vasodilation
  4. sympathetic response/catecholamine release
  5. CO2 narcosis
  6. possible death
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8
Q

respiratory acidosis

A

pH decrease b/c H increases

catecholamines (vaspressors) don’t work as well

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9
Q

central (pulmonary) vasoconstriction

A

increased PVR

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10
Q

when should hypercarbia be avoided specifically?

A

neurosurgery

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11
Q

CO2 narcosis

A

CO2 acts as a sedative if it reaches 70mmHg

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12
Q

What PaCO2 is equal to 1 MAC?

A

200mmHg

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13
Q

What PaCO2 could cause death?

A

> 120mmHg

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14
Q

What are the effects of hypocarbia (3)

A
  1. respiratory alkalosis
  2. central (pulmonary) vasodilation
  3. peripheral and cerebral vasoconstriction
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15
Q

what is the gold standard for confirmation of ETT placement?

A

etCO2

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16
Q

how fast does PaCO2 rise during apnea?

A

first min= 6mmHg

each min after 3-4mmHg

17
Q

Phase 0

A

inspiration

CO2 = 0

18
Q

Phase I

A

beginning expiration
CO2 = 0
represents anatomic deadspace

19
Q

Phase II

A

portion of expiration where CO2 is first seen

20
Q

Phase III

A

CO2 plateau

21
Q

Phase IV

A

end of plateau

22
Q

curare cleft

A

when there is a dip in the plateau

pt is trying to breath over the ventilator

23
Q

what else can cause a curare cleft?

A

surgeon is pushing on the chest

24
Q

what are the two options to treat a curare cleft

A
  1. suppress their drive to breath

2. turn off the vent and let the patient breathe

25
Q

how do you suppress a patients drive to breathe?

A

propofol
narcotic/ paralytic
increase minute ventilation (lower etCO2)

26
Q

what is the first thing you do when the patient is “bucking” on the vent

A

TURN THE VENT OFF

27
Q

COPD/Emphysema etCO2 waveform

A

upsloping waveform

prolonged exhalation times

28
Q

esophageal intubation etCO2 waveform

A

small waves then nothing after a few breaths

29
Q

hypocapnea waveform causes (3)

A

hyperventilation
hypotension/low Q
loose circuit connection

30
Q

cardiogenic oscillations

A

heart contractions that displace air from alveoli

31
Q

when do you normally see cardiogenic oscillations? (2)

A

low RR

end of expiration

32
Q

what are the three things the capnograph measures?

A

etCO2
etvolatile agent
RR

33
Q

what if the EtCO2 wave never reaches 0?

A

the CO2 absorbent is exhausted

34
Q

at what flow is the CO2 absorber not necessary?

A

5L/min

35
Q

when does the etCO2 wave look like a chair?

A

loose connection or circuit leak

36
Q

At what stage to patients usually go through irregular breathing?

A

Stage II

37
Q

when could exhaling during inspiration happen?

A

mapleson circuit or faulty expiratory valve

38
Q

When would you see decreased CO2 at the end of the plateau phase?

A

emergence

39
Q

What is the value of capnography during sedation?

A
RR
detect apnea (before hypoxic)