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Respiratory > Week 5 - Control of breathing, respiratory failure, asthma > Flashcards

Week 5 - Control of breathing, respiratory failure, asthma Flashcards

1
Q

Define hypoxia

A

A fall in alveolar, thus arterial pO2

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2
Q

Define hypercapnia

A

A rise in alveolar, thus arterial pCO2

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3
Q

Define hypocapnia

A

A fall in alveolar, thus arterial pCO2

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4
Q

Define hyperventilation

A

Ventilation increases with no change in metabolism

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5
Q

Define hypoventilation

A

Ventilation decreases with no change in metabolism

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6
Q

What are the effects on plasma pH of hyperventilation?

A
  • Hypocapnia and respiratory alkalosis
  • If pH rises above 7.6 then free calcium concentration falls enough to produce fatal tetany
  • – Ca2+ is only soluble in acid, so when pH rises, Ca2+ cannot stay in the blood
  • – Nerves become hyper-excitable
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7
Q

What are the effects on plasma pH of hypoventilation?

A
  • Hypercapnia and respiratory acidosis

- If pH falls below 7 then enzymes become lethally denatured

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8
Q

Define respiratory acidosis

A

Alveolar pCO2 rises, so [dissolved CO2] rises more than [HCO3-], producing a fall in plasma pH
- pH decreased, pCO2 increased, HCO3- normal or increased

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9
Q

Define compensated respiratory acidosis

A

If respiratory acidosis persists, the kidneys respond to low pH by reducing excretion HCO3-

  • Thus restoring the ratio [dissolved CO2]/[HCO3-]
  • Hence restoring the pH
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10
Q

Define compensated respiratory alkalosis

A

If respiratory alkalosis persists, the kidneys respond by excreting HCO3-
- The ratio [dissolved CO2]/[HCO3-] returns near to normal

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11
Q

Define metabolic acidosis

A

Metabolic production of acid displaces HCO3- from plasma as the acid is buffered, so the pH of blood falls
- pH decreased, pCO2 normal or decreased, HCO3- decreased

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12
Q

Define metabolic alkalosis

A
  • Metabolic production of HCO3- –> plasma [HCO3-] rises, causing the pH of blood to rise
  • pH increased, pCO2 normal or increased, HCO3- increased
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13
Q

Define compensated metabolic acidosis

A

The ratio [dissolved CO2]/[HCO3-] may be restored near to normal by lowering pCO2 (increased ventilation)

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14
Q

Define compensated metabolic alkalosis

A

The ratio [dissolved CO2]/[HCO3-] may be restored near to normal by raising pCO2 (decreased ventilation)

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15
Q

What happens if there is a decrease in inspired O2?

A
  • Detected by peripheral chemoreceptors located in the carotid and aortic bodies
  • These are stimulated by a decrease in oxygen supply relative to their own oxygen usage, which is small
  • – So they only respond to large drops in O2
  • Stimulation of the receptors:
  • – Increases the tidal volume and rate of respiration
  • – Changes in circulation directing more blood to the brain and kidneys
  • – Increased pumping of blood by the heart
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16
Q

What happens if there is an increase in inspired CO2?

A
  • Peripheral chemoceptors detect changes in pCO2, but are insensitive
  • Central chemoreceptors in the medulla of the brain detect changes in arterial pCO2
  • Small rises in pCO2 increase ventilation
  • Small falls in pCO2 decrease ventilation
17
Q

Describe how central chemoreceptors work

A
  • Located on the ventral surface of the medulla
  • Exposed to cerebro-spinal fluid
    — Separated from the blood by the blood brain barrier, which allows free passage of CO2 but not hydrogen carbonate
    — The pH of the CSF is determined by its own hydrogen carbonate/carbonic acid buffer system
    — Contains no haemoglobin
    — CSF [HCO3-] is determined by plasma pCO2 and controlled by choroid plexus cells
    • Rapid changes in plasma pCO2 take time to influence CSF
    — CSF pCO2 determined by arterial pCO2
    • So falls in pCO2 lead to rises in CSF pH
    • Rises in pCO2 lead to falls in CSF pH
    — pH of CSF is determined by the ratio of [HCO3-] to pCo2
    — In the short term, [HCO3] is fixed (can’t cross BBB) so falls in pCO2 → increase in pH, and rises in pCO2 → decrease in pH
    — Persisting changes in pH can be compensated for via the choroid plexus cells altering CSF [HCO3-]
  • Respond to a fall in CSF pH
18
Q

What are the different types of hypoxia?

A
  • Hypoxaemic – low pO2 or low O2 saturation
  • Anaemic – normal pO2 but insufficient Hb to carry O2
  • Stagnant – reduced delivery of O2 due to poor perfusion
  • Cytotoxic – O2 delivery is adequate but tissues are unable to utilise O2
19
Q

Describe type 1 respiratory failure

A
  • Not enough oxygen enters the blood
  • CO2 removal not compromised
  • pO2 of arterial blood low
20
Q

Describe type 2 respiratory failure

A
  • Not enough oxygen enters the blood
  • Not enough CO2 leaves it
  • pO2 in arterial blood
21
Q

What are some of the causes of respiratory failure?

A
  • Low pO2 in inspired air
    — Everything is normal, the air breathed in just has low pO2
  • Hypoventilation
    — Always associated with increased pCO2 (Type 2 respiratory failure)
    — Neuromuscular problems
    • Respiratory depression due to opiate overdose
    • Head injury
    • Muscle weakness
    — Chest wall problems
    • Scoliosis/kyphosis
    • Morbid obesity
    • Trauma
    • Pneumothorax
    — Hard to ventilate lungs
    — Airway obstruction
    • COPD and asthma when the airway narrowing is severe and widespread
    — Severe fibrosis
  • Diffusion impairment
    — O2 diffuses much less readily than CO2, so is always first
    — pCO2 is hence low/normal, so type 1 respiratory failure
    — Structural changes
    • Lung fibrosis causing thickening of alveolar capillary membrane
    — Increased path length
    • Pulmonary oedema
    — Total area for diffusion reduced
    • Emphysema
    o Elastin breakdown in alveolar walls, so reduced elastic recoil, increasing compliance
  • Ventilation/perfusion mismatch
    — O2 diffuses much less readily than CO2, so is always first
    — pCO2 is hence low/normal, so type 1 respiratory failure
    — Reduced ventilation of some alveoli
    • Lobar pneumonia
    — Reduced perfusion of some alveoli
    • Pulmonary embolism
  • Abnormal right to left cardiac shunts
22
Q

Define asthma

A

A chronic disorder characterised by:

  • Variable airflow obstruction
  • – Due to airway smooth muscle
  • Airway wall inflammation and airway wall remodelling
  • – Airways have thickened smooth muscle and basement membranes
  • Increase in airway responsiveness to a variety of stimuli
  • – Reduces airway radius, increasing resistance and hence reducing airflow
  • – Triggers: muscarinic agonists, histamine, cold air, arachadonic acid metabolites
23
Q

What inflammation is there is asthma?

A
  • Mast cells:
  • – Increased in asthma
  • – Release prostaglandinds, histamine, etc
  • Eosinophils
  • – Large numbers in the bronchial wall and secretions of asthmatics
  • Dendritic cells and lymphocytes
  • – Dendritic cells have a role in the initial uptake and presentation of allergens to lymphocytes
  • – T-helper lymphocytes release cytokines that plan a key part in the activation of mast cells
  • – Th2 phenotype favour the production of antibody production by B lymphocytes to IgE
24
Q

What remodelling is there is asthma?

A
  • Epithelium
  • – Stressed and damaged with a loss of ciliated columnar cells
  • Basement membrane
  • – Deposition of collages, causing it to thicken
  • Smooth muscle
  • – Hyperplasia causing thickening of the muscle
25
Q

What are the major precipitating factors for asthmatic attacks?

A
  • May occur spontaneously
  • Most commonly caused by:
  • – Lack of treatment adherence
  • – Respiratory virus infections associated with the common cold
  • – Exposure to allergen or triggering drug
26
Q

Describe the recurrent symptoms of asthma

A
  • Wheeze
    — High pitched, expiratory, musical sound
    — Originates in airways which have been narrowed by compression or obstruction
    — Has a variable intensity and tone
  • Breathlessness
    — With exercise
    — In acute exacerbations
    — Objective assessment:
    • Tachypnoea
    • Recession
    • Tracheal tug
  • Chest tightness
  • Cough
    — Often worse at night
    — Exercise induced
    — Dry
  • Variable airway obstruction
27
Q

What tests are used for diagnosing asthma?

A
  • Spirometry
  • – Low PEFR
  • – Low FEV1/FVC ratio
  • – >12% increase in FEV1 following salbutamol
  • Allergy testing
  • – Skin prick to aero-allergens
  • – Blood IgE levels to specific aero-allergens
  • Chest x-rays
  • – Generally normal in the chronic situation
  • – Should be performed to exclude a pneumothorax during severe acute exacerbations
28
Q

What are some primary preventions for asthma?

A
  • Stop smoking
  • Wood/laminate flooring
  • Cleaning
  • Fresh air
  • Breast feeding
  • Exposure to allergens/triggers
  • Weight loss
  • Diet
29
Q

What are some pharmacological interventions for asthma?

A
  • Airway relaxants:
  • – β2 agonists
  • – Muscarinic antagonists
  • Anti-inflammatory agents
  • – Corticosteroids
  • – Leukotriene receptor antagonists

Respiratory (8 decks)

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