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Health Assessment > Ventilator Modes (restrictive lung disease) > Flashcards

Ventilator Modes (restrictive lung disease) Flashcards

1
Q

volume cycled ventilation (VCV) is

A

fixed VT with inflation pressure as dependent variable

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2
Q

on VCV a pressure limit can be set which

A

when inflation pressure exceeds this value the pressure relief valve prevents durther gas flow, preventing high airway pressures

this valve warns a change in pulmonary compliance has occured

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3
Q

increases in peak airway pressure may reflect

A

worsening pulmonary edema
pneumothorax
kinked ETT
mucous plug

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4
Q

in VCV mode - VT is maintained despite

A

small changes in peak airway pressures

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5
Q

disadvantage of VCV is the

A

inability to compensate for leaks in delivery system

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6
Q

primary modes of VCV are

hint: youre familiar with these

A

Assisted/Controlled (A/C)
Synchronized Intermittent Mandatory Ventilation (SIMV)

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7
Q

A/C ventillation

A

set RR, VT
if sponatenous effort sensed - set VT will be delivered

set rate ensures the # of breaths be delivered even with no effort

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8
Q

SIMV allows synchornized ventilation while providining a

A

predefined minute ventilation

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9
Q

SIMV and spontanueous patient effort

A

the circuit provides sufficient gas flow and periodic mandatory breaths that are syncrhonous with pt inspiratory efforts

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10
Q

advantage of SIMV over AC

A

SIMV allows for continued use of respiratory muscles, lower mean airway and mean intrathroacic pressures, prevention of respiraotry alkalosis, and improved pt/ventilator coordination

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11
Q

pressure cycled ventilation

A

provides gas flow the lugns until a present airway pressure is reached. VT is the dependent variable and varies wirth changes in compliance and airway resistance

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12
Q

what is the most important predisoposing factor for developing nonsocimal pneumonai (VAP)

A

mechanically ventilated patietns with acute repsiratory failure

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13
Q

what is the primary cause of VAP in mechanically ventilated patients

A

micro-apsiration of contaminated secretions around ETT cuff

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14
Q

nosocomial sinusitus is related to

A

presence of nasotracheal tube

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15
Q

treatment of noscomial sinusitis includes

A

antibiotics, replace NT tube wtih oral tubes, decongestants, and HOB elevation to facilitate drainage

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16
Q

barotrauma may present as

A

SQ emphysema,
pneumomediastinum/peritoneum/percardium
pulmonary intersitial emphysema
arterial gas embolism
tension pneumo

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17
Q

barotrauma reflects

A

dissection or passage of air from overdistended and ruptured alveoli

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18
Q

infection increases the risk of

A

barotrauma - by weakening the pulmonary tissue

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19
Q

what is the common of hypoxemia with MV

A

atelactasis

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20
Q

T/F hypoxemia due to atelectasis is not responsive to incrase in FiO2

A

true

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21
Q

in actute hypo-oxygenation states check for

A

ETT migration
kinks
mucous plugs

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22
Q

other causes of sudden hypoxemia in MV patients include

A

tension pneumo and PE which are accompanied by hypotension

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23
Q

what may be necessary to remove mucous plugs

A

bronchoscopy

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24
Q
A
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25
Q

bedside lung US shows atelactasis as

A

presence of static air bronchograms

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26
Q

PaO2 reflects the adequacy of

A

O2 exchange across alveolar capillary membranes

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27
Q

the efficacy of gas exchange is measured by the difference of

A

calculated PAO2 (alveolar) - measured PaO2 (arterial)

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28
Q

of following arterial hypoxic conditions which is not responsive to supplemental O2
a. low inspired O2 concentrations (high altitude)
b. hypoventilation (drug overdose)
c. VQ mismatch (COPD, PNE)
d. right to left intrapulmonary shunt (pulm edema)
e. diffusion impairment (pulmonary fibrosis)

A

D. Pulmonary edema

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29
Q

of following arterial hypoxic conditions which has a increased PAO2- PaO2 (SATA)
a. low inspired O2 concentrations (high altitude)
b. hypoventilation (drug overdose)
c. VQ mismatch (COPD, PNE)
d. right to left intrapulmonary shunt (pulm edema)
e. diffusion impairment (pulmonary fibrosis)

A

C.D.E

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30
Q

of the following which of these arterial hypoxemic conditions have low PaO2 (SATA)
a. low inspired O2 concentrations (high altitude)
b. hypoventilation (drug overdose)
c. VQ mismatch (COPD, PNE)
d. right to left intrapulmonary shunt (pulm edema)
e. diffusion impairment (pulmonary fibrosis)

A

all of them!

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31
Q

when does significant desaturation occur

A

when PaO2 < 60 mmHg

32
Q

3 main causes of arterial hypoxemia

A

VQ mismatch
right to left pulmonary shunting
hypoventilation

33
Q

increasing inspired O2 concentration improves PaO2 in which causes of arterial hypoxemia (SATA)
VQ mismatch
right to left pulmonary shunting
hypoventilation

A

VQ mismatch
hypoventilation

34
Q

compensatory responses when PaO2 < 60mmHg

same responses present in chronic hypoxemia (PaO2< 50)

A

carotid body - induces increase alveolar ventilation
HPV - divert pulmonary blood flow away from hypoxic alveoli
incrreased SNS activity to increase COP and enhance O2 delivery

35
Q

chronic hypoxemia leads to

A

increased RBCs to improve O2 carrying capacity

36
Q

PaCO2 reflects the adequacy of

A

alveolar ventilation to relative CO2 production

37
Q

dead space: VT ratio refelcts the efficcay of

A

CO2 transfer across alevolar membranes

38
Q

wht is normal VD:VT ratio

A

less than 0.3

39
Q

in increased deadspace ventilation what can the VD:VT ratio increase to

A

greater equal to 0.6

40
Q

what causes an increased VD:VT ratio

A

acute respiratory failure
decreased cardiac ouput
and PE

41
Q

VD:VT ratio indicates

A

areas in the lung that recieve adequate ventilation but inadequate or no pulmonary blood flow

42
Q

hypercarbia is defined as

A

PaCO2>45 mmHg

43
Q

permissive hypercarbia can be used to

A

to avoid or delay the need intubation and ventilation

44
Q

acute increases in PaCO2 are associated with

A

increased CBF and ICP

45
Q

extreme istances in PaCO2 > 80 mmHg results in

A

CNS depression

46
Q

mixed venous partial O2 is the difference between

A

PaO2 - PvO2 reflecting the overal adequacy of cardiac output relative to tissue oxygen extraction

47
Q

a PvO2 < 30 mmHg or AV O2 content > 6 mL/dL indicates the need to

A

increase CO to facilitate oxygenation

48
Q

what invasive montioring tool can be used to measure PvO2 and calculate CvO2

A

pulmonary artery catheter

49
Q

in regards to pH what accompanies arterial hypoxemia

A

metabolic acidosis

50
Q

acidemia caused by metbaolic/respiratory derangements is assocaited with

A

dysrhtymias and pulmonary HTN

51
Q

alkalemia is assoaited with

A

mechanical hyperventilation and diuretic use
leading to loss of chloride and K+ ion

52
Q

T/F dysrhtymias may be increased with respiratory alkalosis

A

true

53
Q

alkalemia in patients recovering from acute respiratory failure may exhibit

A

compensatory hypoventilation which may delay weaning from the ventilator

54
Q

what is an intrapulmonary shunt

A

right to left shunt
perfusing nonventialted alveoli

55
Q

what is the net effect with intrapulmonary shunting

A

decrease in PaO2 reflecting the dilution of oxygenated blood with hypo-oxygenated blood from underventilated alveoli

56
Q

a physiologic shunt accounts for

A

2-5% cardiac output

57
Q

what does the physiologic shunt of 2-5% of cardiac output reflect

A

passage of arterial blood directly to the left side of the circualtion through the bronchial and thebesian veins

58
Q

determing the shunt fraction in patients breathing < 100% O2 reflects contributions of

A

VQ mismatching as well as right to left intrapulmonary shunting

59
Q

to calculate shunt fraction - the patient needs to breathe

A

100% O2 which eliminates the contribution of VQ mismatching

60
Q

guidelines for discontinuing mechanical ventilation

A

VC of >15mL/kg
alveolar-arterial O2 difference <350 cmH2O while breathing 100% O2
PaO2 > 60 mmHg with an FiO2 < 50%
normal pH
RR < 20
VD:VT <0.6

61
Q

what other criteria is needed to determine if patients can safely be weaned from ventialtion and tolerate extubation

A

pt is alert and cooperative and can tolerate a spotaneous breathing trial without excessive tachypnea, tachycardia, or respiratory distress

62
Q

t/f breathing at rapid rates with low volumes signifies inability to tolerate extubation

A

true

but remember ur restrictive lung disease pt breathes like this baseline

63
Q

3 options for ventilatory weaning

A

SIMV, allows progressive fewer mandatory breaths until. breathing on their own
intermittent trails of total support removal and breathing through a T piece
use of decreasing elvels of pressure support

64
Q

if you notice a deteroriation in oxygenation after vent withdrawal reflecting alveolar collapse what are your’e options
a. re-intubate
b. CPAP/NIPPV

A

CPAP/Non-invasive Positive pressure ventilation

65
Q

what can interfere with sucessful extubation

A

excessive workload on the respiratory muscles due to hyperinflation, copious secretions, bronchospasm, increased lung water, increased CO2 production

66
Q

what can be used as a bridge between intubation and extubation

A

noninvasive ventilation immediately after early extubation
decreases incidence of VAP, shortens ICU syay, and reduce mortality

66
Q

drawback of NIV post extubation

A

impairs the ability to clear secretions and may have inadequate minute ventilation

67
Q

extubation should be considered when

A

patients tolerate 30 min of SV with CPAP 5 cmH2O without deteroration in ABG, mental status, or cardiac functions

68
Q

PaO2 during vent weaning needs to be above with an FiO2 less than

A

PaO2 > 60 mmhg
FiO2 < 50 %

69
Q

where should the PaCO2 be during vent weaning, and where should the pH be

A

PaCO2< 50 mmhg
pH > 7.3

70
Q

additional criteria for vent weaning

A

PEEP < 5 cmH2O
RR < 20
VC > 15 mL/kg

71
Q

patients during vent weaning should be

A

Alert, with active laryngeal reflexes, and the ability to generate an effective cough and clear secretions

72
Q

why is O2 supplementation needed immediately after extubatiom

A

VQ mismatchign

73
Q

O2 is weaned by decreasing the FiO2 and is guided by

A

PaO2 and SpO2

74
Q
A

Health Assessment (16 decks)

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