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RESP > Lecture 19: Respiratory failure > Flashcards

Lecture 19: 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 are the different types of respiratory failure?

A 
Type 1:
-low PaO2 < 8kPa, or O2 sat is <90%
-pCO2 is normal/low
-gas exchange impaired at level of alveolar-capillary membrane 
(type 1 can progress to type 2)
Type 2:
-low PaO2 and high PaCO2 >6.5kPa
-reduced ventilatory effort or inability to overcome increased resistance to ventilation (in whole lung)
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3
Q

What is the difference between hypoxia and hypoxaemia?

A

Hypoxaemia: low pO2 in arterial blood
Hypoxia: oxygen deficiency at tissue level
(tissues can be hypoxic without hypoxaemia e.g. poor circulation/anaemia)

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4
Q

What is the normal oxygen range?

A

O2 sat: 94-98%

PaO2: 10.6-13.3 kPa

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5
Q

When is tissue damage most likely to occur in relation to oxygen levels?

A

O2 sat <90%
pO2 <8 kPa
On oxygen dissociation curve these oxygen ranges are in the steep section, so small drop in pO2 leads to a markedly increased desaturation of Hb
= Resp failure, clinical presentation will vary depending on whether it is acute or chronic resp failure

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6
Q

What are the effects of hypoxaemia?

A
  • impaired CNS function, confusion, irritability, agitation
  • tachypnaea
  • tachycardia
  • cardiac arrythmias and cardiac ischaemia (as heart is working harder)
  • hypoxic vasocontriction of pulmonary vessels to match perfusion to ventilation
  • cyanosis (central: mucous membranes, peripheral: n fingers/toes, if you have central cyanosis you always have peripheral too)
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7
Q

What are the causes of hypoxaemia?

A
  1. low inspired pO2 (high altitudes)
  2. ventilation:perfusion mismatch
  3. diffusion defect: problems of the alveolar capillary membrane
  4. intra-lung shunt: acute respiratory distress syndrome
  5. hypoventilation
    - Extra (outside of) lung shunt: congenital heart defects where the blood bypasses the lungs
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8
Q

What happens during chronic hypoxaemia?

A

Compensatory mechanisms to increase oxygen delivery and decrease hypoxia (seen in people who live in high altitudes)

  • increased EPO secreted by kidney
  • increased 2,3,DPG which shifts the curve so oxygen can be released freely
  • increased capillary density

Chronic hypoxic vasoconstriction of pulmonary vessels causes: pulmonary hypertension which leads to right heart failure and cor pulmonale (pulmonary heart disease)

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9
Q

What is the most common cause of hypoxaemia?

A

Ventilation-perfusion mismatch
V:Q<1
-ventilation is less than perfusion, so PaO2 is low
-initially pCO2 is high until compensatory hyperventilaton occurs and pCO2 becomes normal/low
-hyperventilation may not be able to compensate for V:Q<1 on some occassions and pCO2 remains elevated

V:Q>1 e.g. lung apices

  • PaO2 rises slightly, and PaCO2 falls
  • if lungs not healthy, extra air going to these areas are wasted
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10
Q

In what disorders do we get V/Q<1?

A

Alveoli are poorly ventilated but still perfused

  • asthma (variable airway narrowing)
  • COPD
  • RDS in newborn (some alveoli not expanded)
  • pneumonia (exudate in affected alveoli)
  • pulmonary oedema
  • pulmonary embolism

These will improve with oxygen administration but will only partially correct hypoxaemia until underlying pathology is corrected

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11
Q

How does a pulmonary embolism lead to hypoxaemia?

A
  • embolus results in redistribution of pulmonary blood flow to unaffected areas
  • leads to V/Q<1 if hyperventilation can’t match the increased perfusion

(pO2 may be normal-rare, if they can hyperventilate enough, but pCO2 will be low)

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12
Q

What is a typical ABG in a patient with a PE?

A

Low PaO2
Low PaCO2
High pH (H+ combine with HCO3- to replenish CO2)

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13
Q

How does a diffusion defect affect oxygen and carbon dioxide?

A

-CO2 is more soluable so CO2 diffusion is less affected than diffusion of O2
= pO2 low
=pCO2 normal

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14
Q

In what disorders do we have diffusion impairment?

A
  • fibrotic lung disease

- pulmonary oedema

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15
Q

What is a shunt in the respiratory system?

A

When an alveoli has no ventilation but is still being perfused= no gas exchange

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16
Q

What is acute respiratory distress syndrome?

A

ARDS
-end result of acute alveolar injury
-injury produces increased vascular permeability, oedema, fibrin-exudation/hyaline membranes through which no gas exchange can take place
-diffuse loss of surfactant resulting in alveolar atelectasis
-lungs become stiff and less compliant, lung volumes decrease and minute ventilation increases
-in ARDS we lose hypoxic pulmonary vasoconstriction mechanism
=tremendous intrapulmonary shunt develops
(hard to manage even on a ventilator- used PEEP (positive pressure) at 100% saturation to try and expand the alveoli, but this can lead to oxygen toxicity)

17
Q

What is pulmonary atelectasis?

A

Lung collapse

18
Q

What is oxygen toxicity?

A

High concentrations of oxygen over a long time can cause an overproduction of free radicals in the lungs which can damage/kill lung tissue

19
Q

What does hypoventilation lead to?

A

Entire lung is poorly ventilated
-alveolar pO2 falls so PaO2 falls = hypoxaemia
-alveolar pCO2 rises, PaCO2 rises = hypercapnia
= Type 2 respiratory failure
(hypoxaemia secondary to hypoventilation will correct with added oxygen fully or partially as long as airways are open and air is moving in and out,this doesn’t solve the hypercapnia though)

20
Q

What are the different types of hypoventilation?

A

Acute hypoventilation

  • need urgent treatment (artificial ventilation)
    e. g. opiate overdose, head injury, very severe acute asthma

Chronic hyperventilation

  • allows for compensation so better tolerated
  • e.g. severe COPD
21
Q

How does end stage COPD lead to disordered ventilation?

A

Lost lots of normal lung, nearly the entire lung is diseased. Very few healthy alveoli

22
Q

What are some central disorders leading to disordered ventilation?

A
  • central sleep apnea
  • narcotic overdose
  • sedatives
  • medullary disorders
  • hypothyroidism
  • CNS trauma/brainstem herniation
23
Q

What are some neuromuscular junction disorders leading to disordered ventilation?

A
  • myasthenia gravis
  • organophosphate toxicity
  • botulism (caused by Clostridium botulinum)
24
Q

What are some motor disorders leading to disordered ventilation?

A
  • tetanus (painful muscle contractions, particularly of jaw and neck)
  • ALS (amyothrophic lateral sclerosis- progressive nervous system disease)
  • spinal cord injury at C3 level or above
25
Q

What are some conditions causing muscle weakness/fatigue which lead to disordered ventilation?

A
  • COPD (weak muscles and tired muscles as hard to breath)
  • asthma (in a severe acute asthma attack hyperventilation tires muscles)
  • malnutrition
  • diaphragmatic dysfunction
  • muscular dystrophy
  • severe restrictive lung disease (lung so stiff that the muscles aren’t strong enough to expand the lungs)
26
Q

Give some examples of chest wall disorders:

A

Scoliosis: sideways curvature of spine
Kyphosis: excessive outward curve of spine resulting in abnormal rounding of upper back
Kyphoscoliosis: both of above

=causes disordered movement of the chest wall, due to reduced chest wall compliance and decreases lung compliance due to micro-atelectasis

27
Q

What are the effects of hypercapnia?

A

Acute

  • respiratory acidosis
  • impaired CNS function: drowsiness, confusion, coma, flapping tremors, carbon dioxide narcosis
  • peripheral vasodilation: warm, red hands
  • cerebral dilatation: headache

Chronic

  • respiratory acidosis is compensated by the retention of HCO3- by the kidney
  • CSF pH normalised
  • vasodilation mild but may still be present
28
Q

Why does hypercapnia cause vasodilation?

A

Hypercapnia acts on vascular smooth muscle where it causes vasodilation

29
Q

How does chronic CO2 retention effect central chemoreceptors?

A
  • CO2 diffuses into the brain ECF, the brain ECF pH drops which stimulates central chemoreceptors
  • persistently acidic CSF (brain ECF mixes with CSF) is harmful to neurones
  • low CSF corrected by choroid plexus which secrete HCO3- into CSF
  • CSF pH returns to normal and central chemoreceptors are no longer stimulated
  • PaCO2 is still high but central chemoreceptors are now unresponsive, if the PaCO2 goes higher than the reset value, central chemoreceptors will fire
30
Q

Why can treatment of hypoxaemia worsen hypercapnia?

A
  1. Correction of hypoxia removes pulmonary arteriole hypoxic vasoconstriction. This leads to increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli= CO2 rises as can’t be ventilated
  2. Haldane mechanism: oxygenated blood can’t carry as much CO2, so CO2 dissociates from Hb into the blood, so CO2 levels go up
31
Q

Can more than one mechanism be responsible for respiratory failure?

A

Yes

e. g. lung fibrosis is a diffusion defect but if severe, hypoventilation will also be present
e. g. pulmonary oedema: diffusion defect and V/Q mismatch

32
Q

Give some examples where type 1 resp failure can progress to type 2:

A
  • asthma exacerbation

- end stage COPD

RESP (18 decks)

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