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Block 2 > Pathophysiology Of Respiratory Failure > Flashcards

Pathophysiology Of Respiratory Failure Flashcards

1
Q

Define acute respiratory failure.

A

A state in which the pulmonary system is no longer able to meet the metabolic demands of the body

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2
Q

What are the 2 types of respiratory failure? How can they be defined?

A
  1. Hypoxaemic: PaO2 < 8 kPa when breathing room air - hyperventilation
  2. Hypercapnic: PaCO2 > 6.7 kPa (may also be hypoxaemic depending on FiO2)- hypoventilation
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3
Q

What are the pathophysiological causes of hypoxaemia respiratory failure?

A

Reduced diffusion or diffusion capacity via:

  • Low pressure of inspired O2 (altitude)
  • Hypoventilation
  • Ventilation-perfusion (V-Q) mismatch (shunting = 0 or mismatch <1 or diffusion abnormality)
  • Low CO
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4
Q

What causes hypercapnic respiratory failure?

A

Reduced alveolar ventilation

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5
Q

What is the end tidal gas? Why is it different to alveolar gas composition?

A

At the mouth at the end of exhalation

Also includes dead space from conducting airways

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6
Q

What is the respiratory quotient (RQ)?

A

CO2 eliminated/O2 consumed

On a mixed diet R = 0.8 so for every 10L of O2 consumed, 8L CO2 are produced

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7
Q

Define the oxygen cascade.

A

The process of declining oxygen tension/pressure from atmosphere to mitochondria allowing O2 to diffuse from the atmosphere to the tissue mitochondria due to established gradients

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8
Q

How can alveolar partial pressure of oxygen (pAO2) be calculated?

A

Alveolar gas equation

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9
Q

What are the 3 factors that influence arterial partial pressure of oxygen (paO2)?

A
  1. Diffusing capacity
  2. Lung perfusion
  3. Ventilation-perfusion matching
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10
Q

What determines arterial oxygen saturation (SpO2)?

A

paO2 determines SpO2 read from the oxyhaemoglobin dissociation curve

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11
Q

What is the alveolar-arterial (A-aO2) gradient?

A

Measure of difference between alveolar concentration (A) of O2 + arterial concentration of O2 - can be used to diagnose the extent of hypoxaemia

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12
Q

How can the A-aO2 be calculated?

A
  1. Calculate pAO2 = pIO2 - paCO2 (from ABG)/R
  2. Use result to calculate A-aO2 = pAO2 - paO2 (from ABG)

pIO2 = inspiratory O2

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13
Q

What happens to the A-aO2 with age i.e. deteriorating lung function?

A

Should be a small gap between AO2 + aO2 but as you get older + lung function deteriorates i.e. due to weaker muscles, the gap increases so the A-aO2 (kPa) number will increase with age

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14
Q

What is the alveolar gas equation?

A

pAO2 = pIO2 - paCO2/R

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15
Q

How can alveolar pressure be worked out? What does this mean?

A

Alveolar pressure = sum of partial pressures of gases within alveolus e.g. O2, CO2, H2O + N2

So increase in alveolar pressure will cause a proportionate increase in the partial pressure of all of the gases

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16
Q

What will happen to the alveolar gas composition in reduced ventilation?

A

O2 decrease
CO2 increased

Failure to remove CO2 increases pCO2 = proportional decrease in pp of other gases e.g. O2

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17
Q

What happens to the alveolar gas composition if PiO2 is increased by O2 supplementation?

A

O2 increased
CO2 unchanged

As there is no change in ventilation but pO2 will increase at mouth due to supplementation

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18
Q

Define ventilation (V).

A

Amount of gas that is exchanged through the lungs in one minute

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19
Q

Define perfusion (Q).

A

Amount of blood which passes through the lungs in one minute

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20
Q

What is the ideal V/Q relationship i.e. V/Q relationship in normal lungs?

A

V and Q would be matched i.e. V/Q = 1 so that all of the O2 inhaled is utilised + all of the CO2 returned is breathed out into the air (normal distribution curve)

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21
Q

What will happen to the V/Q ratio when there is a shunt?

A

V/Q = 0

Alveoli are not ventilated (V) but remain perfused (Q) so blood remains poorly oxygenated = blood leaving lungs is not fully saturated - alveolar O2 = venous O2 + blood leaving lungs is same as blood breathed out

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22
Q

What will happen to the V/Q ratio when there is dead space?

A

V/Q = infinity

Alveoli not perfused (Q)but ventilated (V) so ventilation will keep increasing (in reality this wont happen) e.g. in trachea where there is no blood contact

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23
Q

What does the oxyhaemoglobin dissociation curve show?

A

Relationship between paO2 + SpO2 -> sigmoid shaped because of +ve co-operativity

24
Q

What makes up the SaO2?

A

Pulmonary vein + arterial blood = 99%

25
Q

What makes up the SvO2?

A

Right ventricle + pulmonary artery = 75%

26
Q

At a constant metabolic rate, what is paCO2 largely dependent on?

A

Alveolar ventilation = RR X (VT - VD)

RR = respiratory rate
VT = tidal volume
VD = dead space
27
Q

What are the 2 components that make up the dead space (VD)?

A
  1. Anatomical dead space constant

2. Physiological dead space which depends on ventilation-perfusion (V-Q) matching (pathological)

28
Q

How do you calculate PiO2? What should it be at sea level and then at high altitude?

A

PiO2 = FiO2 (PB-PH2O)

Sea level = 19.9 kPa
High altitude = 5.8 KpA (CO2 will also decrease due to acclimatization)

29
Q

What happens at the alveoli during normal circumstances?

A

Alveoli are both ventilated (V) and perfused (Q) so blood leaves the alveoli fully saturated with O2

30
Q

What happens at the alveoli during hypoventilation?

A

O2 in alveoli not replenished fully + CO2 not fully removed -> increase in alveolar + arterial pCO2 but small fall in alveolar pO2 is easily compensated for by small increase in inspired O2

31
Q

What sites can disease cause hypoventilation?

A

Brainstem (e.g. stroke)

Spinal cord (e.g. intercostal nerves damaged)

Nerve root

Nerve

NMJ (e.g. myasthenia gravis)

Respiratory muscle (e.g. atrophy/inflammation)

Airway (e.g. obstruction)

Lung (e.g. tumor impacting upon phrenic nerve + diaphragm/reduced in size)

Pleura

Chest wall

32
Q

What problems can cause hypoventilation through respiratory drive?

A

Head injury

Drug overdose

33
Q

What problems can cause hypoventilation through neuromuscular transmission?

A

Spinal cord injury
Anterior horn of spinal cord (motor neurone disease)
Demyelination of nerve axon (guillane barre syndrome)
NMJ (myasthenia gravis)

34
Q

What problems can cause hypoventilation through muscle disease i.e. myopathy?

A

Muscular dystrophy

35
Q

What problems can cause hypoventilation through obstructive lung diseases?

A

Asthma
COPD
Cystic fibrosis
Bronchiolitis

36
Q

Why does O2 therapy only have a little effect on hypoxia?

A

Due to shunting

Increasing FiO2 cannot further increase blood saturation leaving normally ventilated alveoli as its already 100% saturated + higher [O2] does not reach non-ventilated alveoli = O2 blood saturation < 100%

37
Q

What is alveolar hypoxia a stimulus for? Why?

A

Hypoxic pulmonary vasoconstriction

Matches ventilation (V) + perfusion (Q) because reduction of perfusion to abnormal area means proportion of shunted blood is reduced in that area increasing arterial O2 saturation

38
Q

What effect will O2 supplementation have on shunting and low V/Q?

A

Shunting: no improvement

Low V/Q: Some improvement

39
Q

What will the V/Q curve show in acute respiratory failure?

A

An increased spread in the V/Q ratio as opposed to the normal distribution where ratios closely clustered around 1

40
Q

What are the intra-pulmonary causes of shunting?

A 
Pneumonia
Pulmonary oedema (heart failure)
Atelectasis
Lung collapse
Pulmonary haemorrhage or contusion
41
Q

What are the intra-cardiac causes of shunting?

A

Any cause of right to left shunt e.g. congenital heart disease (unusual cause of hypoxaemia in ICU)

42
Q

What is a diffusion abnormality?

A

Abnormality of alveolar membrane or reduction in no. of capillaries resulting in reduction in alveolar SA (less common)

Hallmark = desaturation on exercise

43
Q

What can cause a diffusion abnormality?

A
  • Acute respiratory distress syndrome (ARDS)
  • Alveolitis i.e. inflammatory problems
  • Surfactant deficiency
44
Q

What is the equation for O2 delivery (ml/min)?

A

CO X SaO2 x [Hb] x mls O2 at 100% saturation

45
Q

What effect will a low cardiac output have on O2 delivery?

A

Less O2 delivery per unit time so tissues have to extract a higher O2% to meet demand + blood returning to heart is more de-saturated than normal

More time in pulmonary capillaries for O2 uptake so blood arriving at tissues is usually fully saturated

46
Q

What are the clinical features of respiratory failure?

A
  • Respiratory compensation
  • Sympathetic stimulation
  • Tissue hypoxia
  • Hb desaturation
  • Hypercapnia
47
Q

What does respiratory compensation in respiratory failure look like?

A
  • Tachypnoea (high RR)
  • Use of accessory muscles
  • Intercostal recession (in infants)
  • Nasal flaring
  • Splinting of accessory muscles
48
Q

What does sympathetic stimulation in respiratory failure look like?

A
  • Increased HR
  • Increased BP
  • Sweating
49
Q

What does tissue hypoxia in respiratory failure look like?

A
  • Altered mental state
  • Lactic acidosis (anaerobic metabolism)
  • Decreased HR + BP (late)
50
Q

What does haemoglobin desaturation in respiratory failure look like?

A
  • Cyanosis (central/peripheral)

- Pulse oximetry result low

51
Q

What does hypercapnoea in respiratory failure look like?

A
  • Flapping tremor (CO2 retention flap) - slow
  • Confusion - coma
  • Sympathetic stimulation
  • Respiratory acidosis
52
Q

What is a pulse oximetry?

A

Measures O2 saturation of blood via a transducer on your finger

53
Q

What are the sources of error from a pulse oximetry?

A

Most commonly:

  • Poor peripheral perfusion (if cold)
  • Poorly adherent/positioned probe

But also:

  • False nails/nail varnish
  • Lipaemia
  • Bright ambient light
  • Excessive motion
  • Carboxyhaemoglobin or methaemoglobin
  • At SpO2 < 85% most are les accurate
54
Q

What are the main signs/symptoms of severe respiratory failure?

A
  • RR > 30/min or < 8/min
  • Difficulty completing sentences
  • Agitated, confused or comatose
  • Cyanosed or SpO2 < 90%
  • Deteriorating despite therapy
55
Q

If someone has a normal peripheral capillary O2 saturation (SpO2), can they still have severe ventilatory problems?

A

Yes, it does not mean severe ventilatory problems i.e. hypercapnoea are not present

56
Q

What is desaturation on exercise?

A

Alveolar membranes thickened so when demand increases, pulmonary system cannot meet demands -> time for Hb to become saturated gets longer due to increased blood flow -> Hb wont get fully saturated + CO2 will increase as more is produced in exercise, it’ll spend less time in capillary so less will be breathed out

Block 2 (45 decks)

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