Respiratory Failure & Intubation (Wk1) Flashcards

1
Q

What 2 things does the respiratory system consist of?

A
  1. a ventilatory pump
  2. a gas exchanging organ
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2
Q

what are the 2 main things of the ventilatory pump?

A

respiratory muscles and thorax

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3
Q

what organ is the ‘gas exchanging organ’ of the respiratory system?

A

the lungs

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4
Q

what happens when the ventilatory pump/ gas exchanging organ fail?

A

respiratory failure

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5
Q

does the pump failing indicate a CO2 movement problem or O2?

A

CO2

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6
Q

does the lungs failing indicate a CO2 or O2 movement problem?

A

O2

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7
Q

define respiratory failure

A

syndrome in which the respiratory system fails in one/ both of its gas exchange functions

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8
Q

what are the gas exchange functions of the respiratory system?

A

oxygenation & carbon dioxide elimination

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9
Q

4 types of respiratory failure

A
  1. hypoxemic
  2. hypercapnic
  3. acute
  4. chronic
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10
Q

Hypoxemia?

A

less oxygen in the body/ O2 movement problem

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11
Q

What are the PaO2 values in hypoxemic respiratory failure?

A

<60 mmHg on room air
—-> normal = >80mmHg

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12
Q

PaCO2 levels in hypoxemic RF?

A

normal/ low

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13
Q

why are the PaCo2 levels normal / low in hypoxemic RF?

A

if there is less O2 in the body being diffused to tissues and cells, there is less gas exchange occurring and l…

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14
Q

what does hypoxemia mean? (4)

A
  1. lung failure
  2. O2 gas movement issue
  3. reduced regional ventilation
  4. lung disease which is severe enough to interfere with O2 exchange e.g. ILD
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15
Q

Signs and symptoms of Acute Hypoxaemia

A
  • dyspnoea
  • changes in pattern of breathing (e.g. increase RR)
  • agitation followed by drowsiness
  • decreased mental acuity (PaO2 <40-50 mmHg)
  • organ failure e.g. renal failure, brain injury
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16
Q

What is PaO2?

A

the partial pressure of oxygen in the arterial blood

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17
Q

is the PaO2 high or low in hypercapnic RF?

A

low

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18
Q

Is the PaCo2 high or low in hypercapnic RF?

A

high - > 50 mmHg
(normal = 35-45mmHg)

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19
Q

Hypercapnic RF means…

A
  • pump failure
  • primarily a CO2 gas movement issue
  • reduced alveolar ventilation (can’t blow off CO2 to get in O2)
  • pump = inadequate and cannot maintain ventilation to eliminate the CO2 produced by metabolism
  • PaO2 will be low as well, since inadequate fresh gas enters the lungs (CO2 cant be blown off so O2 cant be inspired)
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20
Q

Signs and symptoms of Acute Hypercapnia

A
  • dyspnoea
  • Increased RR / change in POB
  • agitation, tremor
  • confusion –> coma
  • increased ICP (CO2 does that), headache
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21
Q

what do the symptoms of hypercapnia depend on?

A
  1. rate of rise of CO2
  2. extent of metabolic compensation
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22
Q

Acute RF

A
  • rapid onset, short course
  • pronounced symptoms & can be life threatening
23
Q

Chronic RF

A
  • long duration of poor ABG values (days –> months)
  • will be (metabolic) compensation, therefore pH can be normal
24
Q

acute on chronic

A

e.g. acute exacerbation of COPD

25
Q

Minute Ventilation abbreviation

26
Q

VE formula

A

VE = Vt x RR

27
Q

VE definition

A

total volume of air moved in / out of the lungs in a minute

28
Q

Dead space abbreviation

29
Q

Dead space types

A

anatomical dead space, physiologic dead space

30
Q

Anatomical dead space definition

A

non gas exchange areas i.e. conducting airways (trachea, bronchi)

31
Q

Physiologic dead space definition

A

non gas exchange areas i.e. alveoli which are ventilated but not perfused (collapsed???)

32
Q

dead space ventilation Abbn

33
Q

dead space ventilation formula

A

VD = Vd x RR

34
Q

dead space ventilation definition

A

dead space volume over a minute

35
Q

alveolar ventilation Abbn

36
Q

alveolar ventilation formula

A

VA = (Vt-Vd) x RR
OR
VA = VE - VD

37
Q

alveolar ventilation definition

A

amount of gas which reaches the alveoli (for exchange) /minute

38
Q

how does alveolar ventilation (VA) affect the PaCO2 levels?

39
Q

how does alveolar ventilation (VA) affect the PaCO2 levels (theory)?

A
  • low VA = high PaCO2 –> less gas exchange across the alveolar membrane so less CO2 blown off
40
Q

Mechanisms and Causes of Hypoxaemic RF

A
  • reduced gas going to areas with perfusion e.g. low lung volume due to disease
  • no gas going to areas with perfusion (acute lobar collapse)
  • diffusion impairment of O2 across interstitium into circulation (pulmonary fibrosis)
    SOMETHING WRONG WITHIN LUNGS THAT STOPS O2 MOVING ACROSS THE ALV CAP WALL
41
Q

mechanisms and causes of hypercapnic RF

A
  • depressed drive to breathe (opiate overdose)
  • impaired NM function e.g. GBS, cervical spinal cord injury, respiratory muscle dysfunction
  • increased respiratory load –> issue with compliance / resistance
42
Q

what causes increased respiratory load?

A
  • increased airway resistance, e.g. asthma, COPD
  • decreased chest wall compliance e.g. kyphoscoliosis, barrel chest
  • decreased lung compliance e.g. lung collapse, consolidation
43
Q

implications of RF for physiotherapy

A
  • watch signs and Sx
  • review medical assessment & management
  • determine the type of RF
  • determine the cause of RF
  • choose appropriate interventions
44
Q

medical management of hypoxaemic RF

A
  • oxygen therapy
  • high flow nasal prongs (AIRVO)
  • CPAP delivered (non invasive)
  • intubation (invasive) & mechanical ventilation
45
Q

medical management of hypercapnic respiratory failure

A

requires ventilatory/ pump support (+ oxygenation support/ FiO2)
- non invasive ventilation (external face mask)
OR
- intubation & mech ventilation

46
Q

intubation process

A

inserting an endotracheal tube (ET), through the mouth (oro) or nose (naso) into the trachea

47
Q

what can happen after intubation

A

patient can be placed on a ventilator to assist with breathing during anesthesia, sedation/ severe illness

48
Q

reasons for intubation?

A
  1. maintain patent upper a/w
  2. protect lower respiratory tract
  3. allow (invasive) ventillatory support/ mechanical ventilation
  4. facilitate airway clearance (suctioning
49
Q

tracheostomy

A

artificial a/w inserted surgically / percutaneously through the neck into the trachea (between 2nd & 3rd tracheal rings)

50
Q

advantage of trach

A
  • bypasses upper a/w so can use mouth to eat etc
  • shorter than ETT (decreases dead space and decreases load –> easier to breathe)
  • allows reduction in the level of sedation as it is more comfortable
  • easier for the patient to communicate
51
Q

reasons for trach

A

same as ETI but
- when intubation & ventilation required for a longer period (>10-14 days)
- to facilitate weaning from mechanical ventilation
- tracheomalacia, tracheal stenosis

52
Q

physio role in a trach?

A
  • education of ward staff on trache management –> suction procedure, humidification
  • checking tube patency (open/ unobstructed)
  • tube changes
  • decannulation (remocal of trach tube)
  • decision making re ability to cough and clear secretions before tube removed