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Resp > Hypoxaemia And Respiratory Failure > Flashcards

Hypoxaemia And Respiratory Failure Flashcards

1
Q

Define hypoxia and hypoxaemia

A

• Hypoxaemia - low pO2 in blood
• Hypoxia - O2 deficiency at tissue level
Tissues can be hypoxic without hypoxaemia (eg anaemia, poor circulation
However, generally, the term hypoxia is used to include hypoxaemia as well

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2
Q

What are teh Normal range for O2 saturation and pO2, and what are the levels used to diagnose respiratory failure

A

Normal ranges
• O2 saturation 94 -98%
• pO2 9.3 – 13.3 kPa (UHL)
Anything below LLN is hypoxaemia

Tissue damage most likely when
•O2 saturation < 90%
• pO2 < 8 kPa
• These levels used to diagnose Respiratory failure

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3
Q

What is respiratory failure and what is type 1 and 2

A

Impairment in gas exchange causing hypoxia with or without hypercapnia
• Type 1 Respiratory failure
• low pO2 < 8 kPa or O2 saturation <90% breathing room air at sea level
• pCO2 Normal or low

  • Type 2 respiratory failure
  • low pO2 + high pCO2
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4
Q

What can hypoxia be caused by

A
  1. Low inspired pO2
  2. Hypoventilation – (respiratory pump failure)
  3. Ventilation/Perfusion mismatch
  4. Diffusion defect – problems of the alveolar capillary membrane
  5. Right to left shunt (eg. Cyanotic heart disease)
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5
Q

Give an overview of V/Q of the whole lung

A

Tidal volume. 500ml
150ML Left in anatomical dead space
Therefore 350ml involeved in gas exchange
350ml * 15 (respiratory rate) = 5250ml/min

Pulmonary blood flor from RV - about 70ml stroke volume. Is heart rate is 70 then 70*70 = 4900 ml/min

Therefore v/q ratio ~1

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6
Q

Decsribe hypovntilation

A
  • When the entire lung is poorly ventilated
  • Alveolar ventilation (minute volume) is reduced.
  • Amount of O2 entering blood and CO2 entering alveolus per minute remains unchanged (since metabolic rate is the same)
  • Alveolar pO2 falls -> arterial pO2 falls - hypoxaemia
  • Alveolar pCO2 rises -> arterial pCO2 increases -> hypercapnia
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7
Q

How does hypoventilation affect CO2 levels

A

Hypoventilation - Important
• Hypoventilation ALWAYS causes hypercapnia -
Blood test, see high CO2, tells you they are hypoventilating - does their ventilation need to be supported ?
• Therefore causes Type 2 respiratory failure with both hypoxia + hypercapnia

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8
Q

Describe acute hypoventiallion

A 
Acute Hypoventilation 
• Need urgent treatment 
• +/- artificial ventilation
E.g. 
• Opiate overdose 
• Head injury 
• Very severe acute asthma
All very serious and need itu care
Body does not have time to compensate
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9
Q

Describe chronic hypoventilation

A
  • Chronic hypoxia and Chronic hypercapnia
  • Slow onset and progression
  • Time for compensation
  • Therefore better tolerated

e.g. Severe COPD
• most common cause of chronic type2
respiratory failure
• Acute exacerbations may occur due to LRT infection - this could tip them into acute deocmpensation - acute and chronic - urgent treatment - support

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10
Q

What are causes of hypoventilation

A

1) neuromuscular
2) chest wall abnormality
3) lung abnormality

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11
Q

Descrbe neuromuscular causes o hypoventilaton

A

Respiratory centr in brain stem
Pulses originate here then travel down spinal cord
Then leave (in various peripheral nerves) and synapse on cell body of next nerve.
Message then travels down second nerve to muscles etc
Think abt what can happen at each location

Neuromuscular causes (lung healthy, pumpproblem)

B stem
— opiates
— head injury
— stroke

Spinal cord
— cervical spine trauma - c 3 4 5 phrenic nerve - innervated diaphragm - injury can cause hypoventilation

Phrenic and intercostal nerve
— Guillain-Barre syndrome - acute polyneuropathy - particularly motor nerves - start feeling weakness in legs, passing upwards, then cant cough, then arms feel weak, then can move up to neck ,affect phrenic nerve. Usually self resolving. Usually make a full recovery

NMJ
— antibodies against ACh attach to Ach receptor(myasthenia gravis)

Muscle
— Myopathies

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12
Q

What are chest wall causes of hypoventilation

A

Chest wall abnormalities - need normal thoracic cavity
— obesity
— curves spine (KYPHOSCOLIOSIS)

Pleural cavity
— pneumothorax
— large pleural effusions

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13
Q

What are lung problems that can lead to hypoventilation

A 
Lungs 
— very stiff (restrictive eg fibrosis)
— narrow air ways (obstructive eg COPD)
Cant inflate
— Upper airway obstruction Laryngeal oedema, foreign body
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14
Q

What are effects of hypoxaemia

A
  • Impaired CNS function, confusion, irritability
  • Cyanosis (bluish discolouration of the skin and mucous membranes due to presence of >50gm/litre of unsaturated Hb)
  • Cardiac arrhythmias
  • Hypoxic vasoconstriction of pulmonary vessels
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15
Q

When is cyanosis occur and what is central/peripheral cyanosis

A

Cyanosis
Present when >50gm/L of de-saturated Hb in blood

Central cyanosis Seen in oral mucosa, tongue, lips Indicates hypoxaemia
If central cyanosis is present, peripheral cyanosis will also be present

Peripheral cyanosis In fingers, toes Poor local circulation

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16
Q

Describe the compensation to chronic hypoxaemia and what are the consequences

A
  • Compensatory mechanisms to increase oxygen delivery
  • increased EPO secreted by kidney -> raised Hb (Polycythemia)
  • Increased 2,3, DPG (which shifts curve to right)
  • Chronic hypoxic vasoconstriction of pulmonary vessels results in
  • Pulmonary hypertension
  • Right heart failure
  • Cor pulmonale (Right heart failure secondary to lung problem)
17
Q

What are the effects of hypercapnia

A

• Respiratory acidosis
• Impaired CNS function: drowsiness, confusion, coma, flapping
tremors
• Peripheral vasodilatation –warm hands, bounding pulse
• Cerebral vasodilation – headache
Chronic hypercapnia
• Respiratory acidosis compensated by retention of HCO3- by kidney

18
Q

What si the effect of chronic CO2 retention of central chemoreceptors

A

CO diffuses in to CSF -> CSF pH drops -> stimulates central chemoreceptors
• Persistently CSF acidity harmful to neurons
• low CSF pH corrected by choroid plexus cells which secrete [HCO3-] into CSF
• The CSF pH returns to normal; central chemoreceptors no longer stimulated
• pCO in the blood is still high but central chemoreceptors now unresponsive to this pCO
• i.e. Central chemoreceptors have ‘reset’ to a new higher CO level
• The persistent hypoxia stimulates peripheral chemoreceptors
• Respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)

19
Q

Why may treatment of hypoxia worsen hypercapnia

A
  1. O2 removes stimulus for the hypoxic respiratory drive
    Alveolar Ventilation drops -> causes worsening hypercapnia
  2. Correction of hypoxia removes pulmonary hypoxic vasoconstriction leads to increased perfusion of poorly ventilated alveoli,
    diverting blood away from better ventilated alveoli.
    • Oxygen is life saving – it must be given, but pCO2 needs to be monitored
    • Controlled oxygen therapy with a target Saturation of 88 -92%
    • If oxygen therapy causes rise in pCO2 - need ventilatory support
20
Q

Outline V/Q mismatch

A

• Ventilation - Perfusion Ratio
• optimal gas exchange when V/Q ratio is 1
— V/Q matching must happen at alveolar level
• When V/Q ratio is <1 the
Alveolar pO2 falls and pCO2 rises
• When V/Q ratio is > 1 the (e.g. hyperventilation due to anxiety)
pO2 rises and pCO2 falls

21
Q

What happens in disorders when some alveoli are poorly ventilated

A

Occurs in disorders where some alveoli are being poorly ventilated
E.g. Asthma (variable airway narrowing )
Pneumonia (exudate in affected alveoli)
• V/Q ratio is < 1 in these alveoli
• Alveolar pO2 falls and pCO2 rises
• hypoxic vasoconstriction occurs -> this diverts some (but not all) blood to better ventilated areas
• If V/Q ratio is still <1 -> Alveolar pO2 will be low and pCO2 high
• Blood from these alveoli have a low arterial pO2 and high arterial pCO2
• therefore blood in left atrium = will have a low arterial pO2 and high arterial pCO2
• Central and peripheral chemoreceptors are stimulated –> causing hyperventilation

22
Q

What happens to V/Q miss,arch in hyperventilation

A

Hyperventilation occurs due to stimulation of chemoreceptors
• Affected alveoli still poorly ventilated due to pathology ( asthma etc.) V/Q <1
• Unaffected segments have increased ventilation. V/Q > 1
• pO2 rises and pCO2 falls
• Rise in pO2 increases dissolved oxygen (very small amount)
• But Hb is fully saturated above 10 kPa • Further increases in pO2 has no effect on Hb
•O2 content not significantly increased (oly small amount extra dissolved o2)
• Insufficient to compensate for low pO
from segments with V/Q <1
• Drop in pCO2 accompanied by reduction in total CO2 content in blood
Sufficient to compensate for CO2 retention from segments with V/Q <1
Final result: low pO2 with normal (or low) pCO2
- Type 1 respiratory failure

23
Q

What are some causes of V/Q mismatch

A

Occurs in disorders where some alveoli are being poorly ventilated
Example:
• Asthma (variable airway narrowing )
- COpD early stages
• Pneumonia (exudate in affected alveoli)
• RDS in newborn (some alveoli not expanded)
• Pulmonary oedema ( fluid in alveoli)
• Pulmonary embolism
Cause hypoxia but no hypercapnia - bc enough normal lung to get rid of co2, so type 1 resp failure

24
Q

What show does PE affect V/Q ratio

A
  • The embolus results in redistribution of pulmonary blood flow
  • The blood is diverted to unaffected areas of the pulmonary circulation -hyperventilation then needs to occur to meet needs of increased blood supply
  • Leads to V/Q ratio < 1 if hyperventilation cannot match the increased perfusion
  • causes hypoxaemia.
  • Hyperventilation sufficient to get rid of CO2
25
Q

What are conditions that cause poor diffusion and how does that lad to resp failure

A

Fibrotic lung disease: thickened alveolar embrace slows gas exchange
Pulmonary oedema: fluid in interstitial space increases diffusion distance

Co2 is more soluble, so co2 difficusion is less affected than O2
PO2 low and pCO2 normal or low

Type1 resp failur e

26
Q

What are causes of diffuse ling fibrosis

A
  • Most alveoli affected
  • Causes
  • Idiopathic Fibrosing alveolitis
  • Asbestosis
  • Extrinsic allergic alveolitis
  • Pneumoconiosis
27
Q

How can multiple mechanisms be responsible for resp failure

A

• More than 1 mechanism may be responsible for respiratory failure
seen in disease states
Lung fibrosis -> diffusion defect, but if severe hypoventilation will also be present
pulmonary oedema -> diffusion defect, and V/Q mismatch
• Type 1 respiratory failure can progress to Type 2
as disease involves more areas of the lung are involved
e.g. asthma

Resp (19 decks)

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