Respiratory Failure Flashcards

1
Q

What is respiratory failure?

A
  • inability to maintain gas exchange
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2
Q

In respiratory failure type 1, what happens to PaO2 and PaCO2?

A
  • hypoxaemia (low O2 in blood)
  • <8.0kPA or <60mmHg
  • normal CO2
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3
Q

What is hypoxaemia?

A
  • blood oxygen is low
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4
Q

What is hypoxia?

A
  • low O2 supply to tissue
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5
Q

What is hypocapnia?

A
  • low CO2 - <4.5kPA or <33.8mmHg
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6
Q

What is hypercapnia?

A
  • high CO2
  • >6.0kPA or >45mmHg
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7
Q

Why does CO2 remain normal in type 1 respiratory failre?

A
  • damaged lungs are sufficient to expire CO2
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8
Q

What is the main problem with the lungs in type 1 respiratory failure?

A
  • damage to lung tissue
  • lungs unable to facilitate gas exchange
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9
Q

What is ventilation/perfusion in the lungs?

A
  • ratio between ventilation and perfusion across alveoli and capillaries
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10
Q

In type 1 respiratory failure, why is there ventilation/perfusion mismatch?

A
  • ventilation is sufficient
  • perfusion is low causing ⬇️ O2
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11
Q

Is blood flow to the lungs affected in type 1 respiratory failure?

A
  • generally no
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12
Q

In respiratory failure type 2 what happens to PaO2 and PaCO2?

A

1 - hypoxaemia

  • PaO2 = <8.0kPA or <60mmHg

2 - hypercapnia

  • PaCO2 = >6.0kPA or 45mmHg
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13
Q

What is the main problem in the lungs causing type 2 respiratory failure?

A
  • ⬇️ ventilation, generally affects whole lung
  • inability to overcome ⬆️ resistance to ventilation
  • generally caused by ⬇️ compliance and/or ⬆️ elasticity
  • CO2 cannot be removed from blood
  • O2 cannot reach the blood for gas exchange
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14
Q

What happens to patients breathing in type 2 respiratory failure?

A
  • hypoventilation with short shallow breathes
  • insufficient for normal function
  • low O2 enters and CO2 not removed effectively
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15
Q

In acute type 2 respiratory failure, is renal function able to maintain homeostasis?

A
  • no
  • kidneys are slow to react
  • retention of HCO3- is too slow to buffer ⬆️ CO2
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16
Q

What generally happens to pH in acute and chronic 2 respiratory failure?

A
  • pH ⬇️
  • ⬆️ CO2 = ⬆️ carbonic acid and ⬆️ H+
  • HCO3- is insufficient to ⬆️ pH
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17
Q

How quickly can acute type 2 respiratory failure commence?

A
  • minutes to hours
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18
Q

In chronic type 2 respiratory failure, is renal function able to maintain homeostasis?

A
  • partially
  • kidneys excrete carbonic acid H2CO3
  • kidneys retain HCO3-
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19
Q

What generally happens to pH in chronic type 2 respiratory failure?

A
  • HCO3- retention ⬆️ pH slightly
  • not to normal pH though
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20
Q

What is a restrictive lung disease?

A
  • compliance is ⬇️
  • elasticity is ⬆️
  • lungs struggle to inflate and ventilation is ⬇️
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21
Q

What is a obstructive lung disease?

A
  • compliance is ⬆️
  • elasticity is ⬇️
  • lungs are able to inflate but not recoil
  • CO2 is ⬆️ and O2 is ⬇️
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22
Q

What is stagnant hypoxia?

A
  • blood flow is slow
  • ⬇️ blood supply to tissues
  • O2 levels in the blood are normal
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23
Q

What is histotoxic/cytotoxic hypoxia?

A
  • ⬇️ or no O2 absorbed from blood
  • caused by tissue poisoning
  • ⬇️ blood supply to tissues
  • O2 levels in the blood are normal
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24
Q

What is anaemic hypoxia?

A
  • ⬇️ haemoglobulin binding to blood
  • ⬇️ O2 delivered to tissue
  • CO could cause this, inhibiting O2 binding
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25
Q

What is hypoxaemia?

A
  • low level of O2 in arterial blood
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26
Q

What are the 5 mechanisms that can hypoxaemia?

A

1 - hypoventilation

2 - ⬇️ fraction of O2 (FiO2) in the air

3 - diffusion impairment

4 - shunt

5 - V/Q mismatch

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27
Q

What is hypoventilation?

A
  • slow and shallow breathing
  • ⬇️ ventilation and perfusion = low O2
  • insufficient O2 arterial blood
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28
Q

Following hypoventilation, what happens to oxyhemoglobin saturation, measured by pulse oximetry?

A
  • ⬇️ oxyhemoglobin or ⬇️ SaO2
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29
Q

During hypoventilation what happens to CO2 levels?

A
  • CO2 can ⬆️
  • CO2 cannot be removed from lungs sufficiently
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30
Q

What is the Alveolar/arterial gradient (A-a)?

A
  • measure of arterial (A) and alveolar blood concentration of O2
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31
Q

What does the big and little a mean in Alveolar/arterial gradient?

A
  • A = alveolar 2 concentration - a = arterial concentration
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32
Q

In the Alveolar/arterial gradient (A-a), what should the difference be between O2 in the alveolar and arterial blood flow?

A
  • ideally the same same as O2 defuses from alveolar to arteries
  • normal difference is 5-15mmHg
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33
Q

What does FiO2 mean?

A
  • fraction of O2 in inspired air
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34
Q

What is normal partial pressure of atmospheric air at sea level?

A
  • 760mmHg - written as Patm
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35
Q

What does Ph2O mean in the Alveolar/arterial gradient (A-a) formula?

A
  • partial pressure lost to water in upper respiratory tract - water dilutes gases
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36
Q

At normally body temperature, what is the partial pressure of air lost to water vapour in the upper respiratory tract?

A
  • 47mmHg
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37
Q

What does R mean in the Alveolar/arterial gradient (A-a) formula?

A
  • respiratory quotient - respiratory exchange ratio - ratio between O2 and CO2 of expired air
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38
Q

The R in the Alveolar/arterial gradient (A-a) relates to the ratio between O2 and CO2 in expired air, why is this useful?

A
  • provides information about metabolism - <1 = carbohydrates - 0.9 = proteins - 0.7 = fats
39
Q

What is the normal value in the western world used for R in the Alveolar/arterial gradient (A-a) formula?

A
  • 0.8
40
Q

What is the Alveolar/arterial gradient (A-a) formula?

A
  • PAO2 = FiO2 x (Patm-Ph20) - (PaCO2/R) - PaO2 - PAO2
  • standard values = 0.21 x (760-47) - (PaCO2/0.8) - PaO2
  • standard values can be affected by disease, altitude etc…
41
Q

How do you acquire PaO2 for the Alveolar/arterial gradient (A-a)?

A
  • value is taken from arterial blood gas
42
Q

Why does partial pressure of gas decrease at altitude?

A
  • gas molecules spread out
  • Boyles law = ⬆️ volume = ⬇️ pressure
  • Boyles law = ⬇️ volume = ⬆️ pressure
43
Q

If at high altitude where pressure is lower, what can happen to the Alveolar/arterial gradient (A-a)?

A
  • it will not balance
44
Q

If at high altitude where pressure is lower, and the Alveolar/arterial gradient (A-a) is offset, patients suffer with altitude sickness, such as nausea, headaches, tiredness, loss of appetite etc…, how would you treat this immediately?

A
  • give patients 80% gas
45
Q

What is impaired diffusion?

A
  • inability to facilitate gas exchange at alveolar/capillaries
46
Q

What is the most common cause of impaired diffusion?

A
  • blockage of interstitial space (0.5um)
  • space between alveolar and capillaries
47
Q

Why could exercise cause impaired diffusion?

A
  • speed of blood is ⬆️ due to increased cardiac output
  • ⬇️ time allowed for diffusion
48
Q

Why could pulmonary fibrosis cause impaired diffusion?

A
  • fibrosis causes thickening of alveoli
  • thickening of alveoli ⬇️ surface area ⬇️ perfusion
  • fibrosis may block the alveoli all together due a ⬇️ in parenchyme tissue
49
Q

In patients with impaired diffusion, is high flowing O2 (80-90%) able to help?

A
  • yes
  • forces O2 in alveoli and ⬆️ perfusion
50
Q

What is a continuous positive airway pressure (CPAP) machine?

A
  • machine that applies continuous pressure with ⬆️ O2
  • ensures respiratory tract remains open
  • ⬆️ diffusion
51
Q

What is shunting?

A
  • blood may not reach alveoli and be oxygenated
  • capillaries may reach alveoli but and low O2 perfusion occurs
  • capillaries do not reach alveoli and no O2 saturation
  • essentially O2 and CO2 rich blood can mix, causing a reduction in SaO2
52
Q

What happens to O2 saturation where shunting has occured?

A
  • SaO2 ⬇️
  • oxygenated blood mixes with non oxygenated blood
53
Q

What is airspace shunting?

A
  • pressure in part of lung is high meaning O2 will not move down the partial pressure gradient
  • can occur in pneumothorax
54
Q

What is an example of airspace shunting?

A
  • pneumothorax
  • increased pressure on part of the lung
55
Q

What is vasculature shunting?

A
  • blood vessels do not reach the alveoli
  • blood is not oxygenated
56
Q

What is heart shunting?

A
  • blood crosses from right to left side of the heart
  • oxygenation of blood is ⬇️
57
Q

Can shunting be treated with ⬆️ O2 gases?

A
  • generally no
  • helps confirm diagnosis as a form of shunting
58
Q

What is ventilation/perfusion (V/Q) mismatch?

A
  • mismatch between ventilation (V) and perfusion (Q)
  • most common cause of hypoxia
59
Q

Is ventilation/perfusion equal throughout the lungs?

A
  • no
  • gravity contributes
60
Q

Where is ventilation highest in the lungs?

A
  • at the apex
  • lowest at the base
61
Q

Where is perfusion highest in the lungs?

A
  • base of the lungs - lowest at apex
62
Q

What is dead space in the respiratory tract?

A
  • air in lungs that does not take part in perfusion
63
Q

What are some common diseases that can cause ventilation/perfusion (V/Q) mismatch?

A
  • pulmonary embolism - COPD - pneumonia
64
Q

Will air help patients with a high ventilation/perfusion (V/Q) mismatch?

A
  • yes
  • ⬆️ in perfusion
65
Q

How do we quantify ventilation?

A
  • amount of air inhaled that reaches the alveoli during 1 minute
  • measured in L/min
66
Q

How do we calculate ventilation?

A
  • alveolar ventilation rate (AVR) x respiratory rate (RR)
  • AVR = tidal volume - alveolar dead space
  • ventilation = (AVR - dead space) x RR
67
Q

What are the normal values for tidal volume, respiratory rate and dead space at rest?

A
  • tidal volume = 500ml
  • deadspace = 150ml
  • respiratory rate = 12 breaths/minute
68
Q

Using the values below, what would ventilation be at rest? - tidal volume = 500ml - deadspace = 150ml - respiratory rate = 12 breaths/minute

A
  • ventilation (V) = (AVR - dead space) x RR - V = (500-150) x 12 = 4200ml/min
  • this can ⬆️ significantly during exercise
69
Q

What is perfusion and what can we use to calculate it?

A
  • perfusion is the amount of blood reaching the capillaries at a given time
  • cardiac output is used to determine this
70
Q

What is a normal cardiac output at rest?

A
  • 5000ml/min or 5L - 5000 ml of blood reaches the capillaries/minute
71
Q

If we know a ventilation at rest is approx 4200ml and a cardiac output is 5000ml, what is the ventilation/perfusion?

A
  • ventilation/perfusion - 4200 / 5000 = 0.84 - normal V/Q is 0.8
72
Q

What are the 3 things that drive ventilation and perfusion of the lungs?

A

1 - gravity 2 - pleural pressure 3 - compliance and elasticity

73
Q

Clinically what does ventilation/perfusion mismatch lead to in the blood?

A
  • ⬇️ O2 saturation
74
Q

Generally, pneumonia (an infection) will reduce surface area of alveoli and destroy the alveoli altogether. Will this mainly affect ventilation or perfusion?

A
  • pneumonia infection causes damage throughout the lungs
  • this can reduce ventilation
  • ⬇️ surface area due to damaged alveoli
  • pus can block alveoli altogether
75
Q

A pulmonary embolism (blood clot) can block blood flow to part of the lungs, is this likely to affect ventilation of perfusion?

A
  • perfusion as no blood is available to perfuse with
  • ventilation continues as normal
76
Q

Where is the largest proportion of dead space in the respiratory tract?

A
  • upper respiratory tract
  • conducting zone
  • mouth, pharynx, larynx and bronchi
77
Q

In dead space there is high ventilation, but is any perfusion able to occur?

A
  • no
  • wasted air
78
Q

In type 1 respiratory failure, is the cause generally due to damaged lung tissue or V/Q mismatch?

A
  • damage to lung tissue
  • damage to alveoli means air arrives but cannot perfuse
  • which can lead to V/Q mismatch
79
Q

What is the definition, according to O2 levels of type 1 respiratory failure?

A
  • O2 <8kPA or 60mmHg
  • hypoxaemia
80
Q

In type 1 respiratory failure, what are the 2 things that can happen to CO2 levels?

A
  • CO2 can ⬆️ - CO2 can remain normal
81
Q

In type 2 respiratory failure, is the cause generally due to damaged lung tissue or V/Q mismatch?

A
  • V/Q mismatch - ⬇️ removal of CO2 from blood
82
Q

In type 2 respiratory failure, why can CO2 not diffuse across the capillary/alveoli efficiently?

A
  • ⬇️ ventilation effort - ⬆️ resistance to ventilation so CO2 cannot leave lungs due to partial pressure gradients
83
Q

What is the definition, according to CO2 and O2 levels of type 2 respiratory failure?

A
  • CO2 >6.5kPA or 50mmHg = hypercapnia
  • O2 <8kPA or 60mmHg (can be normal as well) = hypoxaemia
84
Q

Asthma is a form of type 1 respiratory failure, what is an effective way to treat this?

A
  • provide a bronchodilator - ⬆️ ventilation
85
Q

Asthma is a form of type 1 respiratory failure, what is the aim when treating this?

A
  • return SaO2 to normal levels - normal SaO2 = 94 - 98%
86
Q

COPD is a form of type 2 respiratory failure, what is the aim when treating this?

A
  • return SaO2 to good levels - CANNOT CURE
  • normal SaO2 = 88 - 92%
  • these SaO2 levels are likely to be normal for them
87
Q

What is an example of non-invasive ventilation?

A
  • nasal cannula or simple mask - both provide ⬆️ O2
88
Q

In patients who are extremely hypoxic, will basic masks or nasal cannulas be sufficient to treat these patients?

A
  • generally no - use continuous positive airway pressure (CPAP)
89
Q

If masks and CPAP are insufficient in patients with type 2 respiratory failure, what else can be used in really hypoxic patients?

A
  • intubation and ventilation
90
Q

What is intubation?

A
  • tube is inserted into patients throat
  • acts as patients respiratory tract
  • commonly called tracheal intubation
91
Q

What is assisted ventilation?

A
  • patients are attached to a respiratory machine
  • essentially breathes for the patient
92
Q

What is physiological and pathological dead space in the lungs?

A
  • physiological = normal parts of lungs where gas exchange does not take place
  • pathological = part of lung normally involved in gas exchange is damaged and unable to be involved in gas exchange
93
Q

What is a portal blood system?

A
  • blood flows from one capillary bed into another
  • blood flows between veins and not straight back to heart
  • characteristic of blood is de-oxygenated