Respiratory Insufficiency Flashcards

1
Q

main types of classification for pneumonia

A
  • site of acquisition (HAP, CAP, HCAP)
  • causal agent (bacterial, viral, fungal)
  • severity (low, medium, high risk)
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2
Q

inspiration

A

active process requiring contraction of resp muscles to move gases from high pressure to low pressure area

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3
Q

what does the diaphragm do during inspiration?

A

contracts, moves downwards, increases vertical dimension of thoracic cavity creating negative pressure and air goes into the lungs

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4
Q

what does the external intercostal muscles do during inspiration?

A

contract to lift ribcage up and out, expanding thoracic cavity in ant-post-lat dimensions

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5
Q

what pressure changes occur with inspiration?

A

reduces intrapulmonary pressure to below atmospheric pressure, allowing air to come into the lungs

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6
Q

expiration

A

passive process during quiet breathing; relies on elastic recoil of lungs and chest wall

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7
Q

what happens with the diaphragm and external intercostal muscles during expiration?

A

relax, reduce thoracic cavity volume; ribcage moves down and in

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8
Q

what occurs with elastic recoil during expiration?

A

lungs elastic tissue recoils, increasing intrapleural and alveolar pressure. air flows out of the lungs as intrapulmonary pressures exceed atmospheric pressures

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9
Q

active expiration

A

during forceful breathing, abdo muscles and internal intercostal muscles contract to further compress thoracic cavity, expelling more air forcefully

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10
Q

what generates positive pressure and what generates negative pressure?

A

INSPIRATION = NEGATIVE, ACTIVE
EXPIRATION = POSITIVE, PASSIVE

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11
Q

what is the difference between spontaneous breathing and breathing with NIV?

A

intrapulmonary pressures

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12
Q

what does CPAP and BIPAP utilize to support the entire resp cycle?

A

positive pressure

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13
Q

2 major functions of resp system

A
  • ventilation
  • gas exchange
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14
Q

when does resp insufficiency exist?

A

where there is an inability to perform one or both functions between gas exchange and ventilation

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15
Q

how is RI diagnosed?

A
  • early recognition is critical
  • clinical findings like dyspnea, abnormal ABGs, need for supplemental O2
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16
Q

continuum of resp function

A

normal > RI > resp failure

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17
Q

what are some examples and effects on ventilation and gas exchange for CNS disorders?

A

ex = brainstem stroke, MS, brain tumors, spinal cord injury
effects = ventilation, increased PACO2

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18
Q

what are some examples and effects on ventilation and gas exchange for extra pulmonary disorder?

A

ex = scoliosis, pleural effusions, obesity, rib fractures, ascites
effects = ventilation, increased PACO2

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19
Q

what are some examples and effects on ventilation and gas exchange for intrapulmonary disorders?

A

ex = asthma, COPD, pulm fibrosis, pneumonia, PE, lung CA
effects = impact gas exchange diffusion

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20
Q

what are some examples and effects on ventilation and gas exchange for neuromuscular disorders?

A

ex = ALS, muscular dystrophy, myasthenia gravis, GBS
effects = ventilation

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21
Q

dyspnea

A
  • subjective, self-reported, multidimensional
  • can only be known from pt’s perspective
  • smothered, suffocating, breathlessness, difficulty speaking in full sentences, SOB
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22
Q

how can dyspnea present?

A

1) acute: sudden onset (PE, pneumothorax, infection)
2) chronic: persistent (COPD, interstitial lung disease)
3) exertional or resting: only during physical activity or even at rest in severe cases
4) orthopnea: dyspnea while lying flat (HF)

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23
Q

pneumonia

A

acute infection of the lung parenchyma caused by bacterial, viral or fungal pathogens leading to alveolar inflmtn and consolidation

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24
Q

what can pneumonia range from?

A

mild resp symptoms manageable as outpt to severe resp failure requiring ICU, mechanical ventilation, and ECMO

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25
Q

pneumonia is the ____ leading cause of death from infectious diseases globally

A

3rd

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26
Q

in canada, pneumonia causes ~______ deaths annually

A

8000

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27
Q

hospital acquired pneumonia (HAP)

A
  • lasts 48hrs or more after hospital admit, not present on admit
  • only gram negative bacteria
  • usually thick, yellow/greene
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28
Q

examples of gram neg bacteria

A

staphylococcus, e coli, klebsiella helicobacter, pseudomonas

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29
Q

HCAP (healthcare associated) risk factors

A
  • recent hospitalization for 2 or more days in the past 3 months
  • outpt dialysis
  • residing in LTC
  • family member MRDO infection
  • immunocompromised
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30
Q

CAP

A
  • acquired in community
  • hospitalized <48hrs, present on admit
  • commonly gram positive bacteria
  • watery sputum, dry cough, fatigue
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31
Q

examples of gram positive bacteria

A

streptococcus pneumonia, H. influenzae, legionella

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32
Q

causative agent for bacterial pneumonia examples

A

streptococcus pneumoniae, h. influenzae, mycoplasma pneumoniae

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33
Q

causative agent for viral pneumonia examples

A

flu, RSV, COVID, adenovirus

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34
Q

causative agent for fungal pneumonia examples

A

histoplasma capsulatum, cryptococcus neoformans, coccidioides immitis (common in immunocompromised or endemic regions)

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35
Q

typical pneumonia: what is it caused by? where does inflmtn occur? what does it show on CXR?

A
  • bacterial pathogens that multiply extracellularly in the alveoli
  • causes inflmtn and fluid accumulation in air filled spaces
  • lobar consolidation or CXR (dense opacities in one or more lobes of the lung)
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36
Q

atypical pneumonia: what is it caused by? where does inflmtn occur? what does it show on CXR?

A
  • viruses, fungus, mycoplasma
  • inflmtn occurs in alveolar septum and interstitium of the lung
  • CXR shows patchy or diffuse interstitial infiltrates, often bilateral
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37
Q

what four mechanisms can pathogens cause pneumonia by?

A
  • inhalation (direct into resp tract)
  • aspiration (oropharyngeal/gastric contents aspirate into resp tract)
  • translocation (pathogens travel from gut to lungs d/t damaged gut barrier)
  • bloodborne spread (via bloodstream from distant infection)
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38
Q

what does pneumonia infection result in?

A
  • pulm infltmn with/without exudate, impaired lung compliance
  • increased capillary permeability
  • increased interstitial and alveolar fluid
  • V/Q mismatching, intrapulmonary shunting
  • hypoxia
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39
Q

signs and symptoms of pneumonia

A
  • dyspnea, fever, cough (productive vs non-productive), coarse crackles
  • severe = confusion, disorientation, tachypnea, tachycardia, hypoxemia, uremia, and hypotension
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40
Q

how do you diagnose pneumonia?

A

CXR, sputum C&S, CBC, CP7, blood cultures, ABGs

41
Q

is the causative agent always identified?

A

not in 50% of cases

42
Q

gram stain: what is it? what does it identify?

A
  • sample is smeared onto a culture plate then stained with dye
  • identify bacterial morphology, size and shape of bacterial walls (cocci vs rods), grouping or chains of cells, presence or lack of structures of organelles
  • whether pathogen is positive or negative
43
Q

gram positive bacteria - how does the stain look?

A

retain the dye in their walls so it appears deep blue or violet

44
Q

gram negative bacteria - how does the gram stain look?

A

thinner walls are dissolved by alcohol in dye, and washes out of cell body so its pink or red

45
Q

how long do gram stain results take? how long do cultures take?

A

gram stain = 24hrs
cultures = 48-72hrs

46
Q

management of pneumonia involves?

A
  • primary care: treating infection and correcting cause of RI
  • supportive care: supporting ventilation, gas exchange, maintaining hemodynamic stability, minimizing increased O2 and metabolic demand
47
Q

what is abx selection guided by?

A

site of acquisition, what causative organisms is prevalent at this time; start with broad spectrum, then narrow to morphology of gram stain, then narrow to organism and sensitivity when sputum C&S results come back

48
Q

what is the nurse’s role in abx therapy?

A
  • communicate results of gram stain and C&S, know when last cultures were drawn
  • be aware of abx stop dates
  • monitor pt response closely - if not getting better as demo’d by labs, continuing s&s of pneumonia, maybe there’s a new source of infection
49
Q

what are supportive care things the nurse can do?

A
  • optimize oxygenation and ventilation
    -prevent spread of infection
    -provide comfort and emotional support
    -chest physio, mobilizing, oral hygiene, deep breathing and coughing
  • observe for complications
    -communication ax findings/C&S findings
  • initiate O2 therapy!
50
Q

O2 therapy - what is it required for?

A
  • hypoxemia (SaO2 < 90%, PaO2 < 60)
  • O2 is a med
  • try to use lowest possible level of O2
  • dose response method to evaluate effectiveness
51
Q

how can O2 be delivered?

A
  • low flow (nasal cannula)
  • reservoir (simple face mask, face mask with reservoir bag)
  • high flow
52
Q

oxygen toxicity

A
  • when FiO2 >50% for 24-48hrs
  • O2 free radicals are a toxic byproduct of O2 metabolism; enzymes that are supposed to clear the metabolites can’t keep up with high dose of O2
  • damages lung parenchyma and vasculature leading to ARDS/fibrosis
  • early symptoms can be reversed
53
Q

oxygen toxicity: what don’t we want to rely on? what can we improve/optimize?

A
  • don’t rely on supplemental O2 alone
  • optimize VQ matching through positioning, secretion clearance etc.
  • improve diffusion with use of diuretics for interstitial edema etc.
54
Q

NIV:
1. what is the role of non invasive ventilation?
2. what does it involve the use of?
3. how is it delivered?
4. what are common modes of NIV?

A
  1. provides ventilatory support without the use of an ET or trach
  2. a machine to deliver pre-set oxygen and air
  3. via tight fitting mask
  4. CPAP and biPAP
55
Q

what functions of the resp system does NIV support?

A

oxygenation and ventilation

56
Q

what is NIV used for?

A

RI; chronic conditions (sleep apnea, stable COPD, CHF, neuromuscular disorders); bridge therapy to facilitate weaning from invasive mechanical ventilation

57
Q

indications for NIV

A
  • moderate to severe dyspnea
  • tachypnea >24/min if hypercapneic, >30/min if hypoxemic
  • accessory muscle use
  • paradoxical breathing
  • pH less than 7.35
  • PaCO2 >45mmHg
  • PaO2/FiO2 ratio <200
58
Q

absolute exclusion criteria for NIV

A
  • resp arrest
  • hemodynamic instability
  • uncontrolled ACS
  • dysrhythmias
  • uncontrolled GI bleeding, hematemesis
59
Q

relative exclusion criteria for NIV

A
  • unable to protect airway
  • high risk aspiration
  • excessive secretions
  • agitated, uncooperative
  • facial trauma, burns, recent upper airway or GI surgery
  • mask fit
60
Q

can a mechanical ventilator be used when set on CPAP or BIPAP modes for NIV?

61
Q

what does a simple CPAP machine control?

A

pressure only

62
Q

functions of NIV machine

A
  • oxygen delivery
  • control settings (how breath is initiated, how quickly air/O2 is delivered, how inhalation is ended, degree of exhalation)
  • patient data (parameters, RR, TV, minute ventilation)
  • alarm parameters (airway pressure, volume, resp rate)
63
Q

modes of NIV

A
  • CPAP and BIPAP, mode is based on patient’s needs
  • need to determine if its an issue with gas exchange and oxygenation? or ventilation? or both? and what the underlying patho of RI is
64
Q

what is required of the pt with CPAP?

A

spontaneous breathing
so that continuous positive
airway pressure is
maintained throughout
the entire respiratory
cycle

65
Q

T or F: Although pressure
becomes more negative
during inhalation, it
remains above zero
(positive) throughout the
entire respiratory cycle.

66
Q

what does CPAP prevent the patient from doing?

A

fully exhaling which means baseline pressure for whole resp cycle is raised

67
Q

the pressure maintained at the end of expiration can also be called?

A

EPAP (expiratory positive airway pressure) or PEEP (positive end expiratory pressure)

68
Q

the patient can only exhale until when with the CPAP?

A

until the set end expiratory pressure is reached

69
Q

what does the pressure setting commonly begin at for CPAP?

70
Q

what are the benefits of CPAP on oxygenation (PaO2)?

A
  • keeps alveoli open at end of exhalation = more time for gas exchange
  • recruits and opens under ventilated alveoli
  • increases SA and thins AC membrane
  • improve VQ matching and diffusion
71
Q

benefits of CPAP on ventilation

A
  • improves lung compliance
  • increases FRC
  • decreases WOB
72
Q

what does CPAP primarily improve?

A

gas exchange and oxygenation

73
Q

BIPAP

A
  • form of positive pressure ventilation
  • 2 pressure settings (one for inspiration, one for expiration; IPAP and EPAP)
74
Q

IPAP

A

Inspiratory Positive Airway
Pressure: high flow of
gas delivered to a pre-set
pressure level that is
maintained t/o inspiratory
phase.

75
Q

EPAP

A

Expiratory Positive Airway
Pressure – Pre-set
pressure level maintained t/o
expiratory phase. Can also set back up RR

75
Q

when does inspiratory support begin?

A

when the BIPAP machine senses the pt’s inspiratory effort or if a set time interval elapses

76
Q

what is IPAP usually set at?

A
  • 10-20cm H2O, which boosts inspiration and provides tidal volume
77
Q

what happens when the machine senses the end of inspiration for BIPAP?

A

the flow of gas stops and the pt breathes out

78
Q

EPAP is the same as _______?

A

CPAP/PEEP because they both apply positive pressure at the end of expiration. can only breathe out until set pressure is reached (preventing them from fully exhaling and emptying alveoli)

79
Q

what is EPAP usually set at?

80
Q

benefits of BIPAP on oxygenation (PaO2)

A

same as benefits of CPAP on oxygenation

81
Q

benefits of BIPAP on ventilation (PaCO2)

A
  • reduces work of beginning a breath, allowing a pt to have more energy for the remainder of the inspiratory phase
  • gas being delivered to create IPAP provides some tidal volume
  • this improves pt’s ventilation by decreasing WOB and improving tidal volumes. will also improve VQ matching by bringing O2 to ac membrane
82
Q

what is the difference between IPAP and EPAP?

A

the amount of inspiratory support a patient receives

83
Q

IPAP supports _____ while EPAP supports ____

A

IPAP = ventilation
EPAP = oxygenation

84
Q

if its a ventilation issue, what will you do? what do you need to ensure about the pressure difference? how do you determine whether to use CPAP or BIPAP?

A
  • optimize IPAP
  • pressure difference is 10 or greater
  • is it oxygenation/gas exchange or ventilation issue?
85
Q

if you increase IPAP and leave EPAP…

A

you increase tidal volume which decreases CO2 level

86
Q

if you decrease IPAP and leave EPAP…

A

you decrease tidal volume and increase CO2 level

87
Q

what happens when you have positive pressure in the chest?

A

you have increased intrathoracic pressure - venous return decreases - preload decreases

88
Q

how do you minimize impact of PPV?

A

make sure pt is hemo stable

89
Q

what pts would benefit from a physiological response from PPV?

A

pts with CHF bc they have too much preload so IPAP will shunt the preload away

90
Q

if someone is on BIPAP and you take it off, what should you be mindful of?

A

increasing preload and venous return - at risk of increased contractility and flash pulm edema

91
Q

nurse’s role in establishing NIV

A
  • assist, collab with RT, start low and adjust PRN based on tolerance and response, should have good mask seal, ok to have small air leak as long as its not directed at eyes
  • ensure pt is comfortable, give direction and reassurance as it can be anxiety provoking wearing a mask
92
Q

assessment of NIV

A
  • Patient’s initial response to NIV is the best indicator for success or failure
  • Ventilation: Improved TV, RR, decreased WOB, wheezes and improved air entry to bases.
  • Gold standard measurement:
    PaCO2
  • Oxygenation: Improved SpO2, SaO2, PaO2, improved crackles or air entry to bases. Improved RR and effort (if driven by hypoxemia).
  • Gold standard
    measurement: PaO2
93
Q

monitoring of NIV

A
  • Monitor hemodynamic parameters (preload status)
  • Monitor for signs of adequate EOP
  • Expected to show improvement in ventilation and gas exchange
    parameters within 1 hr of initiation of NIV
  • This includes: Improved patient comfort, decreased RR, decreased
    accessory muscle use, synchronization with BIPAP machine,
    normalizing ABG’s. SaO2> 90%.
  • Check ABG within 1 hr of starting NIV, if no improvement within 2
    hrs, consider intubation
94
Q

what to assess on monitor

A
  • Review settings on BIPAP or ventilator ( IPAP, EPAP, Fio2, RR)
  • Assess patient data displayed on machine, noting RR, tidal volume, and minute volume
  • Assess safety of alarm settings on machine, high/low pressure, high/low resp rate, high/low minute ventilation
  • Depending on unit policy, you will also be documenting these parameters and your patient’s data.
95
Q

complications with NIV

A
  • Mask fitting issues,
  • Discomfort, nasal or oral dryness
  • Skin breakdown
  • Air leaks, (more common with higher IPAP). Small leak (<6L/min) is good.
  • Airway is not secured, stomach can inflate increasing risk of vomiting and aspirating.
96
Q

when can weaning be considered?

A
  • when cause of RI is corrected and pt is hemodynamic stable.
  • NIV is short term intervention
  • ABG is better
  • accessory muscle use gone
  • CXR may or may not be improving
  • primary reason for initiating BIPAP should be resolved or improved
97
Q

approaches to weaning

A

It can be uncomfortable for the patient, having them do more work
will look like they are doing more work! Provide reassurance and time to adapt. Can trial periods off BiPAP. Gradually reduce inspiratory support by weaning IPAP; Or can stop all at once if tolerated

98
Q

O2 therapy decision making flowchart

A
  • NP
  • FM/high flow, simple face mask 5-12L/min, FiO2 35-50%, high flow O2 up to 100% FIO2
  • BiPAP = FiO2 100%, ventilation support
  • mechanical ventilation = FiO2 up to 100%, significant vent support