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Respiratory Unit > 11.1 Respiratory Failure > Flashcards

11.1 Respiratory Failure Flashcards

1
Q

What is respiratory failure?

A

Impairment in gas exchange causing hypoxaemia with or without hypercapnia

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2
Q

What is type 1 respiratory failure?

A

– low PaO2 < 8 kPa or O2 saturation <90% breathing room air at sea level (Hypoxaemia)
– pCO2 normal or low
– Gas exchange is impaired at the level of aveolar-capillary membrane
– Type 1 RF can progress to Type 2

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3
Q

What is type 2 respiratory failure?

A

– Low PaO2 AND high PaCO2 > 6.5 kPa breathing room air at sea level
– Reduced ventilatory effort (pump failure) or inability to overcome increased resistance to ventilation entire lung

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4
Q

What is hypoxaemia?

A

Low arterial pO2 in arterial blood

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5
Q

What is hypoxia?

A

O2 deficiency at tissue level (anaemia)

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6
Q

When might tissues be hypoxia without hypoxaemia?

A

Anaemia

Poor circulation

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7
Q

What are the normal ranges for PaO2 and oxygen saturation?

A
  • O2 saturation 94 -98%

* PaO2 10.6 – 13.3 kPa

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8
Q

What is the difference between being hypoxaemic and RF?

A

Hypoxaemia is when levels of O2 saturation and PaO2 fall below normal levels.
RF occurs when tissue damage begins due to lack of oxygen

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9
Q

Below what oxygen saturation’s and PaO2 is tissue damage most likely?

A

– O2 saturation < 90%

– pO2 < 8 kPa

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10
Q

What is the clinical presentation of hypoxaemia?

A
  • Impaired CNS function, confusion, irritability, agitation
  • Tachypnaea
  • Tachycardia
  • Cardiac arrhythmias & cardiac ischaemia
  • Hypoxic vasoconstriction of pulmonary vessels
  • Cyanosis (bluish discolouration of the skin and mucous membranes due to presence of 4 to 6 gm/dl of deoxyhaemoglobin (i.e. unsaturated Hb)
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11
Q

what is central cyanosis?

A

Blueish discolouration seen in oral mucosa, tongue, lips. Indicates hypoxaemia - occurs when the level of deoxygenated haemoglobin in the arteries is below 5 g/dL with oxygen saturation below 85%.

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12
Q

What is peripheral cyanosis?

A

Bluish discolouration of the fingers, toes.

Poor local circulation. More oxygen extracted by the peripheral tissues. Always present if central cyanosis present.

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13
Q

What are causes of hypoxaemia?

A
  1. Low inspired pO2 - e.g. high altitude
  2. Ventilation:Perfusion mismatch
  3. Diffusion defect – problems of the alveolar capillary membrane
  4. Intra-lung shunt – Acute Respiratory Distress Syndrome
    (ARDS)
  5. Hypoventilation – (respiratory pump failure)
  6. Extra (outside of)- lung shunt- congenital heart defects – will not be discussed (covered in CVS)
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14
Q

In chronic hypoxaemia, compensatory mechanisms can establish to decrease hypoxia. What are the compensatory mechanisms?

A

– increased EPO secreted by kidney raised Hb (Polycythemia)
– Increased 2,3, DPG – shifts haemoglobin saturation curve so oxygen released more freely
– Increased capillary density

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15
Q

What are pathological consequences of chronic hypoxaemia?

A

Results in chronic hypoxia vasoconstriction that causes:
Pulmonary hypertension
Right heart failure
Cor pulmonale

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16
Q

What is cor pulmonale?

A

enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance

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17
Q

What is the most common cause of chronic hypoxaemia?

A

Ventilation:perfusion mismatch

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18
Q

How does high altitude affect oxygen saturation of blood?

A

Causes hypoxaemia. Partial pressure of oxygen falls
the further up we are from sea level. Therefore partial pressure oxygen falls in alveoli. Therefore partial pressure oxygen in arterial blood is low. Fully improves with O2

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19
Q

What is the optimal ventilation:perfusion ratio?

A

optimal gas exchange when V/Q ratio is 1. V/Q matching must happen at alveolar level

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20
Q

What happens if V:Q ratio is less than 1?

A

Inadequate ventilation.
PaO2 is low. Hypoxaemia.
Initially PaCO2 rises (hypercapnia) UNTIL/UNLESS there is compensatory hyperventilation – then PaCO2 will be either normal or low
Hyperventilation induced by peripheral chemoreceptor firing secondary to hypoxaemia – If lung disease severe hyperventilation may not be able to compensate for V:Q <1 and CO2 remains elevated

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21
Q

What happens if V:Q ratio is greater than 1?

A 
PaO2 rises (slightly)  and PaCO2 falls
If lungs not healthy the “extra” air going to these parts of the lung is “wasted” – increased dead space (alveoli ventilated but not perfused)
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22
Q

What commonly causes V: Q mismatch?

A

Alveoli being poorly ventilated but still adequately perfused (V:Q ratio of less than 1)
• Asthma (variable airway narrowing )
• COPD
• Pneumonia (exudate in affected alveoli)

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23
Q

In V:Q mismatch where ratio is less than 1, what is the initial compensatory mechanism?

A

Pulmonary arteriole hypoxic vasoconstriction. Some blood is diverted from poorly ventilated areas to better ventilated areas.

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24
Q

If initial compensatory mechanism doesn’t work to increase V:Q mismatch where ratio is less than 1, how will the respiratory system be affected?

A

Blood from hypoventilated alveoli mixes with blood in left atrium. Hypoxaemia stimulates peripheral chemoreceptors causing hyperventilation – if there is enough functioning lung tissue CO2 levels will normalise or fall leading to final arterial blood with low PaO2 and normal or low PaCO2

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25
Q

How does V:Q mismatch explain hypoxaemia in pulmonary embolism?

A

Sections of lung not adequately perfused. Embolus results in redistribution of pulmonary flow. Blood is diverted to unaffected areas.
• Leads to V/Q ratio < 1 if hyperventilation cannot match the
increased perfusion -Causes hypoxaemia
• Very small minority PEs PaO2 normal – small infarct area

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26
Q

Why can arterial blood gas tests not be used to diagnose PE?

A

As can compensate for hypoperfusion in lungs with hyperventilation. Arterial blood gases may appear normal.
Will almost always have a low CO2 level due to tachypnoeia (95%)

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27
Q

What is the typical arterial BG in a patient with PE?

A
  • Low PaO2
  • Low PaCO2
  • High pH – i.e alkalotic
28
Q

What are common causes of V:Q mismatch?

A

– Asthma (variable airway narrowing )
– Pneumonia (exudate in affected alveoli)
– RDS in newborn (some alveoli not expanded)
– Pulmonary oedema ( fluid in alveoli)
– Pulmonary embolism

29
Q

How are V:Q mismatches treated?

A

Oxygen administration

Treat underlying condition

30
Q

What sort of respiratory failure is seen in a patient with a diffusion defect?

A

Type 1 respiratory failure
CO2 is more soluble than O2, diffusion isnt as effected so levels will be normal/low
PO2 is low as oxygen is less soluble

31
Q

What causes diffusion defects in the alveoli?

A

Problems with alveolar capillary membrane:
Fibrotic Lung disease/ diffuse pulmonary fibrosis = thickened alveolar membrane slows gas exchange
Pulmonary oedema = fluid in interstitial space increases diffusion distance.

32
Q

How does diffuse lung fibrosis affect the alveolar membrane?

A

Interstitium of alveolar membrane thickened by collagen fibres. Most alveoli are affected.

33
Q

What causes diffuse lung fibrosis?

A
  • Idiopathic pulmonary Fibrosis
  • Asbestosis
  • Extrinsic allergic alveolitis
  • Pneumoconiosis
34
Q

How will diffuse lung fibrosis appear on Spirometry?

A

Restrictive pattern on spirometry (restrictive lung disease)

35
Q

What is meant by shunt in the respiratory system?

A

Alveoli with no ventilation still being perfused. No gas exchange at that alveoli. Cannot be corrected by oxygen administration

36
Q

Give an example of a condition with diffuse intra-pulmonary shunting?

A

Acute respiratory distress syndrome

37
Q

What is acute respiratory distress syndrome?

A

ARDS is the end result of acute alveolar injury caused by different insults and probably initiated by different mechanisms. There are many types of injuries which lead to the ultimate, common pathway, i.e., damage to the alveolar capillary unit. Heavy, red lungs showing congestion and
oedema - alveoli contain fluid & lined by hyaline membranes.

38
Q

What might cause ARDS?

A

Toxic chemical inhalation
Sepsis
Pneumonia

39
Q

What are complications of acute respiratory distress syndrome?

A
  1. Diffuse loss of surfactant resulting in alveolar atelectasis.
  2. Loss of hypoxic pulmonary vasoconstriction mechanism - alveoli with no ventilation are still being completely perfused.
40
Q

What is alveolar atelectasis?

A

A complete or partial collapse of the entire lung or lobe of the lung. It occurs when the alveoli become deflated. Lung becomes stiff and less compliant. Lung volumes decrease.

41
Q

How is a patient with ARDS treated?

A

Mechanical ventilation

PEEP - positive pressure ventilation to try and open alveoli

42
Q

Where are we currently seeing ARDS happening?

A

Patients with COVID19 pneumonia

43
Q

What is hypoventilation?

A

When the entire lung is poorly ventilated. Alveolar ventilation (minute volume) is reduced. Alveolar pO2 falls,arterial pO2 falls resulting in hypoxaemia. Hypercapnia.

44
Q

What sort of respiratory failure is cause by hypoventilation?

A

Type 2 RF due to hypoxaemia and hypercapnia.

45
Q

How is hypoxaemia secondary to hypoventilation corrected?

A

Oxygen administration

46
Q

How is acute hypoventilation treated?

A

Urgent treatment

Artificial ventilation

47
Q

What causes acute hypoventilation?

A

– Opiate overdose
– Head injury
– Very severe acute asthma

48
Q

What are the causes of chronic hypoventilation?

A

– Severe COPD

Most common cause of chronic type 2 respiratory failure. Acute exacerbations may occur due to LRT infection

49
Q

What are the different causes of hypoventilation?

A

Disorders of ventilation ( neuropathy/chest wall disorders/COPD/severe asthma exacerbation)
Central disorders
Motor disorders

50
Q

What is meant by disorders of ventilation?

A 
Conditions that reduce ventilation: 
• Central control 
• Motor neurons 
• Peripheral neuropathy 
• Neuromuscular junction 
• Muscle weakness 
• Muscle fatigue 
• Chest wall disorders 
• End stage COPD 
• End Stage Restrictive Lung Disease 
• Severe Asthma exacerbation
51
Q

What central disorders cause hypoventilation?

A
  • Central sleep apnea
  • Narcotic overdose
  • Sedatives
  • Medullary disorders
  • Hypothyroidism
  • S/p CNS trauma/brainstem herniation
52
Q

What motor disorders can lead to hypoventilation?

A

Tetanus
ALS - amyotrophic lateral sclerosis
Spinal cord injury at the C3 level

53
Q

What are common disorders of the neuromuscular junction

A

Myasthenia Gravis
Organophosphate toxicity
Botulism

54
Q

What conditions cause muscle weakness or fatigue resulting in hypoventilation?

A
  • COPD
  • Asthma
  • Malnutrition
  • Diaphragmatic dysfunction
  • Muscular dystrophy
  • Severe restrictive lung disease - muscles arent strong enough to expand stiff lungs
55
Q

What is scoliosis?

A

sideways curvature of the spine

56
Q

What is kyphosis?

A

spinal disorder in which an excessive outward curve of the spine results in an abnormal rounding of the upper back

57
Q

What is kyphoscoliosis?

A

Scoliosis and kyphosis

58
Q

What chest wall disorders can cause hypoventilation?

A

Scoliosis/kyphosis/kyphoscoliosis

disordered movement of the chest wall - respiratory system compliance reduced
Will have restrictive lung disease pattern on spirometry

59
Q

What are the systemic affects of acute hypercapnia?

A
  • Respiratory acidosis
  • Impaired CNS function: drowsiness, confusion, coma, flapping tremors, patients may become obtunded - carbon dioxide narcosis
  • Peripheral vasodilatation –warm hands, bounding pulse
  • Cerebral vasodilation – headache
60
Q

What are the systemic results in chronic hypercapnia?

A
  • Respiratory acidosis compensated by retention of HCO3- by kidney
  • Acclimation to CNS effects – CSF pH normalised (central chemos reset)
  • Vasodilation mild but may still be present – “pink” puffers
61
Q

How does chronic CO2 retention effect the central chemoreceptors?

A

CO2 diffuses into Brain ECF, Brain ECF pH drops which stimulates central chemoreceptors
Persistently acidic CSF (brain ECF mixes with CSF) harmful to neurons – low CSF pH corrected by choroid plexus cells which secrete bicarbonate in to CSF. This lowers the pH.
(HCO3:CO2 ratio returned to 20:1, pH normalised)
The CSF pH returns to normal; central chemoreceptors no longer stimulated. CO2 is still high but central chemoreceptors now unresponsive to this .

62
Q

Why might treatment of hypoxaemia worsen hypercapnia?

A

Giving O2 may result in:

1) Worsened V:Q mismatch
Correction of hypoxia removes pulmonary arteriole hypoxic vasoconstriction. This leads to increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli – i.e worsens V:Q mismatch (V

63
Q

How is a patient with type 2 respiratory failure managed?

A

oxygen administration - monitor CO2 as might cause hypercapnia.
• Give controlled oxygen therapy with a target Saturation of 88 -92%
• If oxygen therapy causes rise in pCO2 - need ventilatory support

64
Q

How does lung fibrosis cause RF?

A

diffusion defect

but if severe hypoventilation will also be present (V:Q mismatch)

65
Q

When might type 1 RF progress to type 2 RF?

A

Asthma exacerbation

End stage COPD

66
Q

Why is V:Q mismatch might the arterial blood gases have low PaO2 and low PaCO2?

A

Hyperventilation occurs due to stimulation of chemoreceptors by hypoxaemia (peripheral) and/or hypercapnia (peripheral, and central depending on chronicity) – Affected alveoli still poorly ventilated due to pathology ( asthma etc.) V/Q <1
– Unaffected segments have increased ventilation, pO2 rises and pCO2 falls. Slight increase in dissolved O2 but Hb soon becomes fully saturated. Drop in pCO2 reduces hypercapnia.

Respiratory Unit (12 decks)

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