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Respiratory failure Flashcards

1
Q

Define respiratory failure?

A
  • Impairment in gas exchange causing hypoxaemia with or without hypercapnia
  • May be acute or acute on chronic condition
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2
Q

Outline type 1 respiratory failure

A
  • Low PaO2 <8kPa
  • Or O2 saturation <90%
  • Breathing room air at sea level
  • pCO2 normal or low
  • Gas exchange is impaired at level of alveolar-capillary membrane
  • Type 1 RF can progress to type 2
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3
Q

Outline type 2 respiratory failure

A
  • Low PaO1 and high PaCO2 >6.5 kPa
  • Breathing room air at sea level
  • Reduced ventilatory effort (pump failure) or inability to overcome increased resistance to ventilate entore lung
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4
Q

Define hypoxaemia

A
  • Low pO2 in arterial blood
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5
Q

Define hypoxia

A
  • O2 deficiency at tissue level
  • Tissues can be hypoxic without hypoxaemia
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6
Q

What are the normal ranges of O2 saturation and PaO2?

A
  • O2 saturation should be 94-98%
  • PaO2 should be 10.6-13.3 kPa
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7
Q

When is tissue damage most likely?

A
  • O2 saturation <90%
  • pO2 < 8kPa
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8
Q

Where is central cyanosis seen?

A
  • Oral mucosa
  • Tongue
  • Lips
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9
Q

What does central cyanosis indicate?

A
  • Hypoxaemia with oxygen saturation below 85%
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10
Q

Where is peripheral cyanosis seen?

A
  • Fingers
  • Toes
  • If central cyanosis is present, peripheral cyanosis will also be present
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11
Q

What are the effects of hypoxaemia?

A
  • Impaired CNS function
  • Confusion
  • Irritability
  • Agitation
  • Cardiac arrhythmias
  • Cardiac ischaemia
  • Hypoxic vasoconstriction of pulmonary vessels
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12
Q

What are the signs of hypoxaemia?

A
  • Central cyanosis
  • Tachypnoea/tachycardia
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13
Q

Why does central cyanosis occur?

A
  • Bluish discolouration of skin and mucous membranes due to presence of 4-6 gm/dl of deoxyhaemoglobin (unsaturated Hb)
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14
Q

What happens in chronic hypoxaemia?

A
  • Compensatory mechanisms increase oxygen delivery and therefore decrease hypoxia
  • Chronic hypoxic vasoconstriction of pulmonary vessels
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15
Q

Which compensatory mechanisms increase oxygen delivery and decrease hypoxia during chronic hypoxaemia?

A
  • Increased EPO secreted by kidney to raise Hb (polycythaemia)
  • Increased 2,3 DPG to shift Hb/O2 saturation curve to right so oxygen is released more freely
  • Increased capillary density
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16
Q

What does chronic hypoxic vasoconstriction of pulmonary vessels result in?

A
  • Pulmonary hypertension
  • Right heart failure
  • Cor pulmonale
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17
Q

What are some causes of hypoxaemia?

A
  • Low inspired pO2 - e.g. high altitude
  • V:Q mismatch
  • Diffusion defect - problems of alveolar capillary membrane
  • Intra-lung shunt - ARDS
  • Hypoventilation
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18
Q

How does low inspired pO2 result in hypoxaemia?

A
  • Can occur due to high altitude
  • pO2 = FiO2 x total atmospheric pressure
  • Therefore partial pressure oxygen falls in alveoli at higher altitude
  • Partial pressure oxygen in arterial blood is low - hypoxaemia
  • Fully improves with O2
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19
Q

What are some causes of V:Q mismatches?

A
  • Asthma (variable airway narrowing)
  • COPD (variable airway narrowing/collapse, loss of some alveoli)
  • Pneumonia (exudate in affected alveoli)
  • RDS in newborn (some alveoli not expanded)
  • Pulmonary oedema (fluid in alveoli)
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20
Q

How do we treat hypoxaemia caused by V:Q mismatch?

A
  • Improves with O2 administration
  • O2 will not completely correct hypoxaemia until underlying pathology is corrected
21
Q

What happens if an alveolar unit is inadequately ventilated?

A
  • Perfusion is still unchanged
  • PaO2 falls
  • PaCO2 rises
  • Blood equilibrates to new alveolar paO2 and paCO2 i.e. plasma ends up with poor paO2 and high paCO2
22
Q

What is the body’s response to hypoxaemia due to V:Q mismatch?

A
  • Hyperventilation is induced by peripheral chemoreceptor firing
  • Chemoreceptors in carotids detect that blood mixture is hypoxaemic and hypercapnic
  • If lung disease is severe, hyperventilation may not be able to compensate for mismatch and CO2 remains elevated
  • Pulmonary arteriole hypoxic vasoconstriction occurs to divert blood to better oxygenated areas of lung
23
Q

Why does V:Q mismatch trigger hyperventilation?

A
  • Output from poorly ventilated alveoli is mixed with output of healthy alveoli in blood
  • Blood mixture is hypoxaemic and hypercapnic
24
Q

How does pulmonary embolism lead to V:Q mismatch?

A
  • Blood can’t get past blockage
  • V/Q mismatch created - V>Q
  • Backwards pressure is applied
  • Blood redistributes to over-supply unaffected alveoli
  • Hyperventilation occurs to try and increase V so that it matches Q
  • Hyperventilation sufficient to get rid of CO2
25
What do diffusion defects lead to?
- Low pO2 - Normal or low pCO2 - Because CO2 is more soluble - So CO2 diffusion is less affected in lung disease than diffusion of O2 - Initially leads to type 1 respiratory failure - As disease progresses, leads to hypoventilation - Results in hypercapnia
26
What problems with the alveolar capillary membrane can result in diffusion defects?
- Fibrotic lung disease: thickened alveolar membrane slows down gas exchange - Pulmonary oedema: fluid in interstitial space increases diffusion distance
27
What are some causes of diffuse lung fibrosis?
- Idiopathic pulmonary fibrosis - Asbestosis - Extrinsic allergic alveolitis - Pneumoconiosis
28
How do we improve diffuse lung fibrosis?
- Oxygen administration
29
What is an intra-pulmonary shunt?
- Shunting where some of blood flow through lungs is not properly oxygenated
30
What can cause intra-pulmonary shunting?
- ARDs
31
Outline ARDS
- ARDS can result in widespread acute alveolar injury - Many types of injuries which lead to common pathway: damage to alveolar capillary unit - Injury produces increased vascular permeability, oedema, fibrin-exudation - Heavy, red lungs showing congestion and oedema - alveoli contain contain fluid and lined by hyaline membranes
32
How does ARDS affect the lungs?
- Diffuse loss of surfactant resulting in alveolar atelectasis - Lung becomes stiff/less compliant - Lung volumes decrease - Loss of hypoxic pulmonary vasoconstriction mechanism - Tremendous intrapulmonary shunt - no ventilation with respect to perfusion
33
How is ARDS managed?
- Hard to manage on a ventilator - Even 100% O2 might not correct hypoxaemia - Need to add positive pressure ventilation to open alveoli
34
Outline hypoventilation
- When entire lung is poorly ventilated due to inadequate respiratory rate or volume of alveolar ventilation - Alveolar ventilation is reduced - Alveolar pO2 falls so arterial pO2 falls, resulting in hypoxaemia - Alveolar pCO2 rises so arterial pCO2 increases, resulting in hypercapnia - Leads to type 2 respiratory respiratory failure
35
What does hypoventilation always lead to?
- Hypercapnia - Therefore causes type 2 respiratory failure with both hypercapnia and hypoxaemia - Hypoxaemia secondary to hypoventilation will correct with added oxygen - Does not solve hypercapnia problem though as ventilation is impaired
36
Outline acute hypoventilation
- Need urgent treatment - +/- artificial ventilation - Commonly caused by opiate overdose, head injury, and very severe acute asthma
37
Outline chronic hypoventilation
- Chronic hypoxaemia and chronic hypercapnia - Slow onset and progression - Time for compensation - Therefore is better tolerated than acute hypoventilation - Common causes include severe COPD and LRT infection
38
What are some hypoventilation disorders?
- Central control due to opioid OD - Motor neuron due to motor neuron disease - Peripheral neuropathy due to Guillain Barre disease - Muscle weakness due to Duchenne's MD - Chest wall disorders e.g. Kyphoscoliosis - End stage COPD due to emphysema - Severe asthma exacerbation
39
Which central disorders can cause hypoventilation?
- Central sleep apnoea - Obesity hypoventilation syndrome - Narcotic overdose - Sedatives - Hypothyroidism
40
Which motor disorders can cause hypoventilation/respiratory failure?
- Tetanus - Amyotrophic lateral sclerosis - Motor neurone disease - Spinal cord injury at C3 level
41
Which disorders of the neuromuscular junction can result in hypoventilation/respiratory failure?
- Myasthenia gravis - Organophosphate toxicity - Botulism toxin
42
Which diseases/conditions can result in muscle fatigue or weakness and then hypoventilation?
- COPD - Asthma - Malnutrition - Diaphragmic dysfunction - Muscular dystrophy
43
What is scoliosis?
- Sideways curvature of the spine
44
What is kyphosis?
- Spinal disorder - Excessive outward curve of spine results in abnormal rounding of upper back
45
What does kyphoscoliosis cause?
- Causes disordered movement of chest wall - Respiratory system compliance reduced - Due to reduction in chest wall compliance and a reduction in lung compliance due to microatelectasis
46
What are the effects of acute hypercapnia?
- Respiratory acidosis - Impaired CNS function: drowsiness, confusion, coma etc. - Peripheral vasodilation - warm hands, bounding pulse - Cerebral vasodilation - headache
47
What are the effects of chronic hypercapnia?
- Respiratory acidosis compensated by retention of HCO3- by kidney - Acclimation to CNS effects - CSF pH normalised - Vasodilation mild but may still be present
48
Why might treatment of hypoxaemia worsen hypercapnia?
- Correction of hypoxia removes pulmonary arteriole hypoxic vasoconstriction - Leads to increased perfusion of poorly ventilated alveoli - Diverts blood away from better ventilated alveoli - worsens V/Q mismatch - Haldane mechanism: oxygenated haemoglobin has low affinity for CO2 so CO2 dissociates from haemoglobin into blood
49
Should we give O2 to patients with respiratory failure?
- Giving O2 can resolve hypoxaemia but also worsen hypercapnia - Must give O2 (it is life-saving) but need to monitor pCO2 - Give controlled O2 therapy with a target saturation of 88-92% - If O2 therapy causes rise in pCO2, patient will need ventilatory support (assisted or mechanical ventilation)

Respiratory (21 decks)

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