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NSCC 7320 - Critical Care Theory 3 > Mechanical Ventilation (MV) & ARF > Flashcards

Mechanical Ventilation (MV) & ARF Flashcards

1
Q

what is ventilation

A

movement of gases in and out of lungs

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2
Q

what is gas exchange

A

O2/CO2 across membrane

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3
Q

what is respiration

A

exchange of O2/CO2 out of cell (internal)

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4
Q

What is compliance

A

distensibility of the lung tissue

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5
Q

2 examples of when lung compliance may be decreased

A

PNA

pulmonary edema

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6
Q

what ventilation method is preferred in cases of decreased lung compliance

A

pressure support

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7
Q

what is meant by resistance in terms of ventilation and ARF

A

diameter of airways

i.e. increased airway resistance in asthma

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8
Q

what is respiratory failure

A

condition in which the respiratory system fails in one or both of its major fns - gas exchange or ventilation

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9
Q

how is respiratory failure diagnosed regarding blood gases

A

blood gases
PaO2 <60
PaCO2 >45
pH < 7.35

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10
Q

what are other diagnostic criteria for ARF aside from blood gases

A

clinical presentation, deviation from pts baseline if they have COPD, history, imaging, VQ scan

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11
Q

what is the difference between respiratory insufficiency and respiratory failure

A

insufficiency gradually needing some O2 support

failure - full O2 support with MV and O2

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12
Q

what are the 3 types of respiratory failure

A

Type 1: acute hypoxemic respiratory failure
type 2: acute hypercapnic respiratory failure
combined

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13
Q

what is the primary problem in type 1

A

gas exchange

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14
Q

what is the primary problem in type 2

A

ventilation

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15
Q

what are the two main causes of type 1 resp failure

A

diffusion

V/Q mismatch

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16
Q

what are the 4 components affecting diffusion in type 1 resp failure

A

SA of alveoli
thickness of AC membrane
diffusion coefficient CO2: O2
Driving pressure - difference between alveolar partial pressure and capilliary partial pressure

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17
Q

what are the two components of V/Q mismatch

A

intrapulmonary shunt

alveolar deadspace

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18
Q

what can cause alveolar deadspace

A

PE, decreased CO, shock

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19
Q

does respiratory acidosis or alkalosis occur in early stages of resp failure? why?

A

decreased PaO2 causes peripheral chemoreceptors to trigger resp center to increase rest rate/depth (ventilation) causes more CO2 exhaled resulting in resp alkalosis

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20
Q

what type of gas would you expect with prolonged type I resp failure

A

resp acidosis as pt fatigues and hypogentilation occurs, decreased O2 delivery to cells causes impaired tissue perfusion and lactic acidosis and MODS

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21
Q

what PaO2 triggers peripheral chemoreceptors to increase RR and depth

A

<60

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22
Q

what is the diffusion coefficeint and what does it mean

A

20:1 CO2 diffuses 20X faster than O2

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23
Q

What happens with CO2 in blood and alveoli in type 2 resp failure

A

equalize so CO2 can’t cross AC membrane

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24
Q

what is alveolar hypotension? what type of resp failure does it occur in?

A

amount of O2 to alveoli is insufficient to meet O2 demand

type 2

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25
Q

what can cause type II resp failure? (10)

A 
neuromuscular disease (GBS, myasthinis gravis)
spinal cord injury
musculoskeletal abnormalities
supression of CNS resp fxn - drug poisoning
post cardiac arrest
brain injury
upper airway obstruction
general anestehsia
bedrest
pneumo
chest trauma 
obesity
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26
Q

what 3 things does resp failure type II result from

A

decreased muslc fn - malnutrition, underlying disease, fatigue
increased airway resistance - stridor, upper airway disease, asthma
decreased lung compliance

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27
Q

what are common management strategies for type 1 resp failure (4)

A

PEEP
minimize deadspace by optimizing CO
increase driving pressure (FiO2)
repositioning

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28
Q

What are common management for Type 2 Resp failure

A

improve ventilation - WOB, RR, tidal volumes
optimize O2 demand, CO and O2 transport
bicarb
intubation and MV

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29
Q

what are 4 ways in which pneumonia can be acquired

A

aspiration
inhalation
bloodborn
translocation - changing pH of gastric content encourages growth of microbes which can travel to the lungs

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30
Q

what are the two main types of pnuemonia

A

CAP

HCAP

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31
Q

what is a subset pneumonia of HCAP

A

VAP

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32
Q

CAP dx vs HCAP

A

CAP dx <48hrs from admission

HCAP dx >48 hrs within hospital or w/in last 90 days

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33
Q

what are typical gram positive bacteria responsible for CAP

A

streptoccus pneumonia, MRSA

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34
Q

what are typical gram negative bacteria responsible for CAP

A

mycoplasma, legionella, chlamydia, psudomonmas

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35
Q

Aside from bacteria what else can cause pneumonia

A

viruses - coronavirues, adenovirus, influenza, RSV

fungi - aspergillosis, spiralis

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36
Q

is HAP typically gram positive or gram negative

A

negative

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37
Q

what is VAP typically caused by (3)

A

MRSA, pseudomonas, Enterobacter

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38
Q

4 things about ETT that increase chance of VAP

A

prevents cough - bodies natural defense
prevents upper airway filtering and humidification
inhibits ciliary transport by epithelium
direct conduit into lungs for airborne pathogens

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39
Q

how is VAP dx

A

positive cultures
new consolidation on CXR
worsening infiltrates
S&S

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40
Q

8 ways VAP can be prevented

A

semi recumbent position HOB 30-45 degrees
hand hygiene
sedation vacation
ETT with polyurethane cuff, subglottic or EVAC suction
non-invasive postive pressure ventilation/extubate ASAP
conduct SBT trial daily
early mobilization and exercise
oral care

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41
Q

how do you treat atypical pneumonias

A

antivirals - tamiflu

antifuncal - clotrimazaole, fluconazole, micafungin

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42
Q

how do atypical pneumonias present

A

inflammation in alveolar septums and interstitial of lung

appear as patchy infiltrates on CXR more diffuse

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43
Q

fungal pneumonias are most often found in what type of pts

A

immunocompromised

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44
Q

2 types of ventilation and main difference between the two

A

spontaneous - negative pressure for inspiration

mechanical - positive pressure for inspiration

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45
Q

what causes the start of inspiration in spontaneous breathing

A

increased PaCO2 stimulates resp center in medulla

46
Q

is inspiration in spontaneous breathing passive or active? exhalation?

A

inhalation - active

exhalation - passive

47
Q

Is which mode of ventilation is intrathoracic pressure increased, what can this cause

A

MV

inhibits venous return and lowers preload

48
Q

T or F exhalation is passive in both MV and spontaneous breathing

A

T

49
Q

Benefits of mech vent

A 
alveoli recruitment
reversal of atelectasis
increased FRC
decreases WOB 
improves gas exchange
50
Q

what is the best indicator for needing MV

A

PaCO2 >55 or pH < 7.20

51
Q

above what RR might we consider MV

A

35

52
Q

at what PO2 might we consider MV

A

<55

53
Q

What are the 3 types of ventilator breaths

A

controlled
assisted - delivered if they attempt to trigger breath
spontaneous - triggered by pt effort and provides some support

54
Q

in spontaneous ventilator breaths who determines the TV

A

pt

55
Q

when is pressure cycle ventilation indicated

A

for decreased compliance and pts at inc risk for barotrauma

56
Q

what is Vt

A

tidal volume

57
Q

how is Vt calculated

A

4-7mL/kg to protect lungs

calculated based on pts ideal body weight to reduce baotraumas

58
Q

what is Mv and how is it caluclated

A

minute volume
amount of air delivered to pt in one min
TV x RR

59
Q

what is goal MV

A

5-10 L/min

60
Q

how do you calculate PiP or Ppeak

A

PEEP + pressure

61
Q

what is measured to determing lung compliance; how is this done

A

plateau pressure

measured @ end of inspiration by inspiratory hold goal <30 increased values indicate poor lung compliance

62
Q

what is FRC and how do we improve it

A

functional residual capacity
opening more alveoli and preveenting collapse
PEEP and CPAP

63
Q

what is the most common mode of ventilation

A

volume control/assist control

64
Q

what is set in Assisted Volume Control

A

RR and TV, trigger

PEEP, FiO2

65
Q

what can the pt do in VC

A

breathe above set RR receive set TV

66
Q

what values should you monitor in VC (3)

A

RR
PIP
plateau pressures

67
Q

what happens if compliance deteriorates in VC how would you know and what should you do

A

will see inc PiP

change to PC

68
Q

can VC cause resp alkalosis?

A

yes if pt is breathing at inc RR for non-resp reasons such as pain, anxiety

69
Q

what type of patients is PC used for

A

pts with decreased lung compliance and severe oxygenation problems

70
Q

what do you set in PC

A

pressure, RR, Ti, trigger

PEEP, FiO2, alarms

71
Q

what can a pt do in PC

A

can breathe above set RR but receive set P

72
Q

what values should you monitor in PC

A

RR
MV
TV
EtCO2 - will vary based on MV

73
Q

what setting do you see I:E

A

PC

74
Q

in what setting do we see laminar flow

A

PC

75
Q

what are the benefits of laminar flow

A

less turbulent better at opening smaller airways

76
Q

what can affect I:E

A

RR

77
Q

why is PC better for sever oxygenation issues

A

because you can alter I:E, improves V/Q mismatch

78
Q

what does inc PiP over time indicate

A

decreased lung compliance

79
Q

what can an isolated event of inc PiP incidate

A 
ETT obstruction
secretions
pneumo
kink in system
bronchospasms
80
Q

what is the most common mode for weaning a pt from the vent

A

pressure support

81
Q

what is set for PS mode

A

level of inspiratory pressure
flow and trigger parameters
FiO2/PEEP/CPAP alaras and apena mode

82
Q

what must the pt be able to do for PS mode

A

spontaneously breath

own RR and TV

83
Q

what values should be monitored for PS

A

RR
TV and MV
EtCOT2 - will change based on MV

84
Q

What does SIMV stand for and when is it used

A

sychrnoized intermittent mandaotry ventilation SIMV

short term post anasethsia CSICU

85
Q

what is set in SIMV

A

RR and TV triggers

Peep, Fio2 and alarms

86
Q

what can the pt do in SIMV

A

breathe above rate and receive own TV

87
Q

what should be monitored in SIMV

A

RR
TV and MV - minute volume is set to gaurantee a minimum
PIP - fluctuate based on compliance

88
Q

why is SIMV synchronized

A

ventilator has the ability to sense pts inspiratory effrot and can reschedule mandatory breaths to avoid breath stacking

89
Q

when do apnea alarms occur

A

occurs if no breath is taken for 10-20s

90
Q

what would cause a high pressure alarm

A 
biting on ETT
water in tubing
secretions
kinked tube
pneumo
bronchospasm
91
Q

what would cause a low pressrure

A

leak in system
leak in cuff
disconnection

92
Q

what can cause a low exhaled volume

A

leak in system or cuff
pt tiring
pressure limit being reached - decreased lung compliance

93
Q

what can cause high RR

A

anxiety, agitation, hypoxia, hypercapnia, pain, readiness to wean?

94
Q

when can O2 toxicity occur

A

FiO2 > 50% for over 24 hours

95
Q

what happens in O2 toxicity and what can it cause

A

O2 free radiacls toxic metabolites of O2 metabolism can damage AC membrane
can cause atelectasis, localized edema, reduced compliance

96
Q

what is absorption atelectasis

A

too much O2 can wash out nitrogen in the alveoli

nitrogen helps keep alveoli open so can cause them to collaspse

97
Q

what are the 7Ps of RSI

A 
preparation
preoxygenate for 3-5 mins
pre-treatment
paralysis
positioning sniff position
placement
post intubation managment
98
Q

what type of trauma can occur with insufficient PEEP

A

atelectrauma - shearing injury d/t alveoli repeatedly opening and closing

99
Q

weaning criteria

A

able to initiate spontaneous breathing
cause has resolved
hemodynamically stable low or no pressers
able to protect airway

100
Q

does a patient have to be awake and alert to wean from ventilator

A

no

101
Q

what results in failure to wean

A 
HR >140 bpm
SBP <90 or >180
RR >35 for >5 mins, inc WOB diaphroesis
changes in mental status 
spO2 <90 or PaO2 decrease by 10 or <50
102
Q

what are 3 weaning methods

A

SBT - spontaneous breathing trials
Progressive decrease in PS in PSV
progressive decrease in ventilator initated breaths in SIMV mode

103
Q

when would a MV pt be switched from from ETT to trach

A

1-3 weeks

104
Q

why are trachs preferred to ETT (3)

A

less analgesia and sedation required
facilitates communication
facilites weaning

105
Q

hwy are post pyloric feedings preferred in MV

A

lowers risk of aspiration
fewere GI complications
higher caloric/protein intake

106
Q

what vitamin do we need to ensure is supplemented in MV and why

A

thimaine
glucose/dextrose load increases demand for thiame
thiamine deficiency can occur in <28 days
and can cause lactic acidosis, cardiac dysfxn, hypertrophy and arrhythmias

107
Q

what is gluconeogenesis

A

creating glucose from non-carb sources mainly in liver

108
Q

what is glycogenolysis

A

breakdown of glycogen to provide energy for muslce contraction

109
Q

why does hyperglycemia occur in critically ill

A

hypermetabolic state results in increased glycogenolysis and glucoenoesis results in increased glucose levels

110
Q

what can hyperglycemia do to the body

A

weakened immune system
decreased GI motility
increased cardiovascular tone
abnormal inflammatory response

111
Q

what are benefits of feeding

A 
decreased catabolic response
reduces risk of infection
improved healing
improved GI fn
improved glucose absorption
prevents bacterial translocation
decreases lenght of stay

NSCC 7320 - Critical Care Theory 3 (5 decks)

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