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3 - Respiratory > Hypoxaemia and Respiratory Failure > Flashcards

Hypoxaemia and Respiratory Failure Flashcards

1
Q

Define hypoxia

A

Oxygen deficiency at tissue level

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2
Q

Define type 1 respiratory failure

A

Low pO2 with normal or low pCO2 (hypoxia)

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3
Q

Define type 2 respiratory failure

A

Low pO2 and high pCO2 (hypoxaemia and hypercapnia)

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4
Q

What is normal ventilation and perfusion ratio determined by

A
  • Alveolar ventilation per minute = 5250 ml/min = ~5 L/min

- Stroke volume x heart rate = 70ml x 70bpm = 4900 ml/min = ~5 L/min

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5
Q

Explain how ventilation/perfusion mismatch causes type 1 respiratory failure

A
  • Some alveoli may be poorly ventilated, leading to V/Q < 1
    - Causes pO2 to fall and pCO2 to rise
  • Hyperventilation occurs to compensate for this by causing unaffected alveoli to have increased ventilation - V/Q > 1
    - This causes pO2 to rise and pCO2 to fall in these segments
  • However haemoglobin is well saturated and further increases in pO2 have no effect and do not significantly increase pO2 in the body
  • pCO2 drops due to increased ventilation, thus the final result is hypoxaemia with normal or low pCO2
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6
Q

List some causes of V/Q mismatch

A
  • Occurs in disorders where some alveoli are being poorly ventilated
  • Asthma - variable airway narrowing
  • Pneumonia - exudate in affected alveoli
  • Respiratory distress in newborn - some alveoli not expanded due to lack of surfactant
  • Pulmonary oedema - fluid in alveoli
  • Pulmonary embolism
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7
Q

Outline how pulmonary embolism causes type 1 respiratory failure

A
  • Embolus results in redistribution of pulmonary blood flow
    § Blood is diverted to unaffected areas of the pulmonary circulation
    • Causes V/Q < 1 in unaffected alveoli and V/Q > 1 in affected
  • Leads to V/Q < 1 if hyperventilation cannot match the increased perfusion
    • Hyperventilation sufficient to get rid of CO2, therefore type 1 respiratory failure
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8
Q

Explain how diffusion defects result in type 1 respiratory failure

A
  • CO2 is more soluble than oxygen and therefore more readily diffuses between the lung and blood
  • Diffusion defects cause low pO2 and normal (or low) pCO2
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9
Q

Explain some causes of diffusion defects

A
  • Fibrotic lung disease - thickened alveolar membrane slows gas exchange
    • CO2 able to cross but oxygen has trouble
  • Pulmonary oedema - fluid in interstitial space increases diffusion distance
    - CO2 more soluble and more readily diffuses across
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10
Q

Explain how hypoventilation causes type 2 respiratory failure

A
  • When the entire lung is poorly ventilated
  • Hypoxaemia - alveolar pO2 falls leading to fall in arterial pO2
  • Hypercapnia - alveolar pCO2 rises leading to rise in arterial pCO2
  • Hypoventilation always causes hypercapnia, therefore type 2 respiratory failure
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11
Q

Explain if acute or chronic hypoventilation is more severe

A
  • Acute hypoventilation
    • Need urgent treatment
    • Artificial ventilation may be needed
  • Chronic hypoventilation
    • Chronic hypoxia and chronic hypercapnia
    • Slow onset and progression therefore time for compensation
    • Can be better tolerated
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12
Q

List some causes of acute and chronic hypoventilation

A

Acute - opiate overdose, head injury, very severe acute asthma
Chronic - severe COPD, lung fibrosis, kyphoscoliosis, Guillain Barre syndrome, myasthenia gravis

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13
Q

Explain how type 1 respiratory failure can progress to type 2

A
  • Type 1 respiratory failure can progress to type 2 as more areas of the lungs are involved in disease
  • Asthma/COPD- when CO2 unable to leave lungs and reduces CO2 diffusion, trouble sustaining hyperventilation
  • Lung fibrosis - very thick barrier that CO2 has trouble diffusing across, trouble sustaining hyperventilation
  • Respiratory disease of the newborn - loss of hyperventilation as baby cannot maintain so alveoli without sufficient surfactant lose ventilation
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14
Q

Explain what cyanosis is

A

Cyanosis - bluish discoloration of the skin and mucous membranes due to presence of > 50 g/L of unsaturated haemoglobin

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15
Q

Distinguish between central and peripheral cyanosis

A
  • Central cyanosis - serious problem
    • Seen in oral mucosa, tongue, lips
      • Tongue normally warm and well perfused - severe if cyanosis seen
    • Indicates hypoxaemia
    • Congenital heart defect - right to left shunt allowing deoxygenated blood to leave the aorta
  • Peripheral cyanosis
    • Seen in fingers and toes
      • Poor local circulation
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16
Q

Explain the effects of acute hypoxia

A
  • Impaired CNS function - confusion, irritability
  • Cyanosis
  • Cardiac arrhythmias
  • Hypoxic vasoconstriction of pulmonary vessels - redistribution of blood to well-ventilated alveoli
17
Q

Explain the chronic effects of hypoxia

A
  • Compensatory mechanisms to increase oxygen delivery
    • Increased EPO secreted by kidney - raised haemoglobin
    • Increased 2,3 DPG
  • Chronic hypoxic vasoconstriction of pulmonary vessels results in:
    • Pulmonary hypertension
    • Right heart failure
    • Cor pulmonale - heart failure secondary to pulmonary hypertension
18
Q

Explain the acute effects of hypercapnia

A
  • Respiratory acidosis
  • Impaired CNS function - drowsiness, confusion, coma, flapping tremors
  • Peripheral vasodilation - warm hands, bounding pulse
  • Cerebral vasodilation - headache
19
Q

Explain the chronic effects of hypercapnia

A

Respiratory acidosis compensated by retention of HCO3 by kidney

20
Q

Explain the effect of chronic hypercapnia on the central chemoreceptors

A
  • CO2 diffuses into CSF -> CSF pH drops -> stimulates central chemoreceptors
  • Persistent CSF acidity harmful to neurons
  • Low CSF pH corrected by choroid plexus cells which secrete HCO3 into CSF
  • CSF pH returns to normal, central chemoreceptors no longer stimulated
  • pCO2 in the blood is still high but central chemoreceptors now unresponsive to this pCO2
    • Central chemoreceptors have reset to a new higher CO2 level
  • Persistent hypoxia stimulates peripheral chemoreceptors
    - Respiratory drive now driven by low oxygen
21
Q

How can treatment of chronic type 2 respiratory failure with oxygen be a problem

A
  • Treatment of hypoxia may worsen hypercapnia
  • Increasing oxygen removes the stimulus for hypoxic respiratory drive
    • Alveolar ventilation drops as person breathes less, leading to worsening hypercapnia
  • Correction of hypoxia removes pulmonary hypoxic vasoconstriction
    • Leads to increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli
  • When giving oxygen, pCO2 levels need to be monitored
    • Controlled oxygen therapy with a target saturation of 88-92%
    • If oxygen therapy causes rise in pCO2, need ventilation support

3 - Respiratory (16 decks)

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