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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
Q

What do diffusion defects lead to?

A
  • 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
Q

What problems with the alveolar capillary membrane can result in diffusion defects?

A
  • Fibrotic lung disease: thickened alveolar membrane slows down gas exchange
  • Pulmonary oedema: fluid in interstitial space increases diffusion distance
27
Q

What are some causes of diffuse lung fibrosis?

A
  • Idiopathic pulmonary fibrosis
  • Asbestosis
  • Extrinsic allergic alveolitis
  • Pneumoconiosis
28
Q

How do we improve diffuse lung fibrosis?

A
  • Oxygen administration
29
Q

What is an intra-pulmonary shunt?

A
  • Shunting where some of blood flow through lungs is not properly oxygenated
30
Q

What can cause intra-pulmonary shunting?

A
  • ARDs
31
Q

Outline ARDS

A
  • 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
Q

How does ARDS affect the lungs?

A
  • 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
Q

How is ARDS managed?

A
  • Hard to manage on a ventilator
  • Even 100% O2 might not correct hypoxaemia
  • Need to add positive pressure ventilation to open alveoli
34
Q

Outline hypoventilation

A
  • 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
Q

What does hypoventilation always lead to?

A
  • 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
Q

Outline acute hypoventilation

A
  • Need urgent treatment
  • +/- artificial ventilation
  • Commonly caused by opiate overdose, head injury, and very severe acute asthma
37
Q

Outline chronic hypoventilation

A
  • 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
Q

What are some hypoventilation disorders?

A
  • 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
Q

Which central disorders can cause hypoventilation?

A
  • Central sleep apnoea
  • Obesity hypoventilation syndrome
  • Narcotic overdose
  • Sedatives
  • Hypothyroidism
40
Q

Which motor disorders can cause hypoventilation/respiratory failure?

A
  • Tetanus
  • Amyotrophic lateral sclerosis
  • Motor neurone disease
  • Spinal cord injury at C3 level
41
Q

Which disorders of the neuromuscular junction can result in hypoventilation/respiratory failure?

A
  • Myasthenia gravis
  • Organophosphate toxicity
  • Botulism toxin
42
Q

Which diseases/conditions can result in muscle fatigue or weakness and then hypoventilation?

A
  • COPD
  • Asthma
  • Malnutrition
  • Diaphragmic dysfunction
  • Muscular dystrophy
43
Q

What is scoliosis?

A
  • Sideways curvature of the spine
44
Q

What is kyphosis?

A
  • Spinal disorder
  • Excessive outward curve of spine results in abnormal rounding of upper back
45
Q

What does kyphoscoliosis cause?

A
  • 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
Q

What are the effects of acute hypercapnia?

A
  • Respiratory acidosis
  • Impaired CNS function: drowsiness, confusion, coma etc.
  • Peripheral vasodilation - warm hands, bounding pulse
  • Cerebral vasodilation - headache
47
Q

What are the effects of chronic hypercapnia?

A
  • Respiratory acidosis compensated by retention of HCO3- by kidney
  • Acclimation to CNS effects - CSF pH normalised
  • Vasodilation mild but may still be present
48
Q

Why might treatment of hypoxaemia worsen hypercapnia?

A
  • 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
Q

Should we give O2 to patients with respiratory failure?

A
  • 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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