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Resp Block > Airway Physiology > Flashcards

Airway Physiology Flashcards

1
Q

Describe the mechanics of inspiration:

A
  • Active process
  • Diaphragm is stimulated by phrenic nerves and external intercostal muscles stimulated by IC nerves
  • Contraction of these muscles leads to an increase in the dimensions of the thorax
  • Lungs are pulled open and pressure within them falls
  • Air moves in to fill lungs following pressure gradient
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2
Q

What are the accessory muscles of breathing?

A
  • Sternocleidomastoid
  • Scalenes
  • Pectoralis minor
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3
Q

What factors affect the efficiency of diffusion rate across the blood-gas barrier?

A
  • Surface area
  • Diffusion constant (CO2 much higher than O2)
  • Partial pressures across membrane
  • Thickness of the membrane
  • Ventilation and perfusion matching (too little ventilation per perfusion = hypoxia)
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4
Q

What are the muscles used in active exhalation?

A
  • Abdominal muscles

- Internal intercostals

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5
Q

What factors can increase the work of breathing?

A
  1. Increased load
    - Stiff lungs
    - Narrow airways (airway obstruction)
    - Chest wall
    - Diaphragm
  2. Increased drive
    - Higher centres
    - Mechanoreceptors
    - Irritiant receptors
    - Chemoreceptors
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6
Q

What are the hallmarks of a person with increased work of breathing due to airflow obstruction?

A
  1. Reduced FEV1
  2. Recruitment of accessory muscles of inspiration (scalenes and sternocleidomastoid)
  3. Increased oxygen consumption by resp. muscles
  4. Risk of respiratory muscle fatigue (ventilatory failure)
  5. Increased work of breathing (breathlessness) due increased resistive WOB
  6. Prolonged expiratory and inspiratory time
  7. Gas trapping
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7
Q

How can airway obstruction reduce gas exchange efficiency?

A
  • Airway obstruction can lead to V/Q ratio of <1 as ventilation is insufficient
  • This includes shunts where the V/Q = 0, as there is no ventilation into the alveoli
  • Blood perfusing low V/Q units or shunts will not be sufficiently oxygenated and lead to lower PaO2
  • Compensation results in vasoconstriction in areas of low ventilation to reduce the hypoxic effect of the shunts and low V/Q regions -> but this can elevate pulmonary arterial pressure if it is occurring throughout the lungs
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8
Q

Describe type 1 vs type 2 respiratory failure:

A

Type 1:

  • Low O2 and low/normal CO2
  • PaO2 <60mmHg
  • Due a severe abnormality in gas exchange
  • PaCO2 <40mmHg due to hyperventilation as a compensatory mechanism
  • Normally accompanied with respiratory alkalosis
    e. g. an acute asthma attack

Type 2:

  • Low O2 and high CO2
  • PaO2 <60mmHg
  • PaCO2 >50mmHg
  • Due to progressive type 1 failure -> respiratory muscles have fatigued and failed or diseases outside lung e.g. MND/polio
  • Low pH (often mixed acidosis, high CO2 + lactic acid from respiratory muscles)
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9
Q

What diseases are the most likely to disrupt the alveolar capillary membrane?

A
  1. Inflammation
  2. Infection
  3. Fibrosis e.g. IPF
  4. Emphysema
  5. Fluid build-up
  6. Cancer
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10
Q

Why is diffusion impairment more likely to cause hypoxia during exercise?

A
  • Diffusion impairment reduces the rate of diffusion at the A-C membrane
  • This is especially an issue for oxygen which has a lower diffusion constant
  • During exercise cardiac output is increased which results in the blood spending less time in the capillary (.25 secs vs .75 secs)
  • In healthy lungs this will not effect oxygenation, but if the diffusion rate is impaired it will lead to hypoxia during exercise
  • In very severe disease this hypoxia will also occur at rest
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11
Q

What are the mechanical effects of restrictive lung diseases?

A
  1. Increased WOB (due to increased elastic WOB due to reduced lung compliance) experienced as breathlessness
  2. Reduced lung volume (lower FVC)
  3. Altered pattern of breathing
  4. Reduced maximum ventilation
  5. Abnormal gas exchange which worsens with exercise
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12
Q

What are the main mechanisms by which the compliance of lungs is reduced (elastic WOB increased)

A
  1. Change in tissue composition
    - Pulmonary fibrosis = inflammation and fibrosis
  2. Loss of surfactant
    - Premature neonates
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13
Q

What is respiratory acidosis?

A
  • High PaCO2, low pH
  • Due to failure to excrete CO2 in the lungs e.g. ventilatory failure
  • Compensation (if chronic) - slow: renal excretion of H+ and retention of HCO3- (base excess increased)
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14
Q

What is respiratory alkalosis?

A
  • Low PaCO2, high pH
  • Due to blowing off excess CO2 in the lungs e.g. hyperventilation during asthma attack
  • Compensation (if chronic- slow): reduced renal excretion of H+ and increased excretion of HCO3 (base excess increased)
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15
Q

What is metabolic acidosis?

A
  • Low HCO3, low pH
  • Due to loss of HCO3 e.g. diarrhoea (normal anion gap), or consumption of it by buffering acid e.g. lactic acid (larger anion gap)
  • Compensation (immediate): hyperventilation - decreased CO2
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16
Q

What is metabolic alkalosis?

A
  • High HCO3, high pH
  • Due to loss of H+ or retention of HCO3 e.g. prolonged vomiting
  • No compensation
17
Q

Describe the features of pulmonary circulation:

A
  • Low pressure, low resistance circuit
  • Receives all output of RV
  • During exercise vessels are dilated to prevent increase in pressure
  • Fluid may leak across the pulmonary capillaries if pulmonary capillary pressure is increased e.g. LH failure, oncotic pressure is decreased and permeability of the capillaries is increased (ARDS)
18
Q

What are the changes to lung function and mechanics with pulmonary oedema

A
  1. Reduced lung compliance (increased elastic WOB)
  2. Reduced lung volume (reduced FVC)
  3. Increased airway resistance (increased resistive WOB)
  4. Impaired gas exchange- diffusion impairment, low V/Q units
    - Leads to low PaO2, low CO2 and high pH
19
Q

What are the causes of pulmonary hypertension?

A
  1. Increases pulmonary vascular resistance:
    - Vasoconstriction (low alveolar O2)
    - Obstruction - embolism, primary PAH
    - Obliteration - emphysema, pulmonary fibrosis
  2. Increases LA pressure
  3. Increases pulmonary blood flow
20
Q

How is the overall effectiveness of O2 gas exchange measured?

A
  • Using an A-a gradient
  • P-alveolar O2 (-) P-arterial O2
  • P-alveolar O2 = PiO2 - P arterial CO2 /0.8
  • A-a gradient should be <15 in young people and <30 in elderly people
  • Causes of high A-a gradient = low V/Q units + shunts + diffusion impairment
21
Q

What are the main mechanism of hypoxaemia?

A
  1. Reduced PiO2 (very high altitude)
  2. Reduced ventilation e.g. hypoventilation
  3. Low V/Q units
  4. Shunts
  5. Diffusion impairment
22
Q

What is the main controller of respiratory drive?

A

Brainstem:

  • Medullary and pontine respiratory centres
  • generate an automatic rhythmic inspiratory stimuli
  • In-put is from sensors
  • Can be over-ridden by cortex (to an extent)

Cortex:
- Can lead to voluntary hyperventilation and hypoventilation (to a point)

23
Q

What are the sensors of respiratory function?

A

Central chemoreceptors:

  • Situated on ventral surface of medulla- surrounded by CSF
  • Respond to increased CSF [H+]

Peripheral chemoreceptors:

  • Situated in carotid bodies and aortic bodies
  • Respond to low O2, low pH and high CO2

Lung and other receptors:
- Pulmonary stretch, irritant and J receptors

24
Q

Which gas is the most important for ventilatory drive?

A
  • Carbon dioxide (and decreased pH) is the most important mechanism for increasing ventilation
  • A small increase in PaCO2 = rapid increase in ventilation
  • There must be a large decrease in PaO2 before there is an increase in ventilation (but this is the trigger for ventilation in people with COPD who have desensitized CO2 receptors)
25
Q

What are the 3 types of sleep disordered breathing?

A
  1. Obstructive sleep apnoea
    - Transient obstruction of throat during sleep
    - Occurs in some snorers
    - Due to 50% obesity, 50% structural abnormalities
    - Occurs in deep sleep due to relaxation of muscles
    - Obstruction -> hypercapnea -> brain wakes to lighter sleep -> muscle tone increases -> breathing recommences
    - Very fragmented sleeping
    - Can reset respiratory centre leading to day-time hypoventilation
  2. Central sleep apnoea
    - Less common than OSA
    - Can be due to heart failure
    Can reset respiratory centre leading to day-time hypoventilation
  3. Obesity hypoventilation syndrome
    - Usually presents as ventilatory failure +/- right heart failure
    - Can reset respiratory centre leading to day-time hypoventilation
26
Q

What are the respiratory causes of dyspnoea?

A
  1. Airways disease
  2. Alveolar disease
  3. Pulmonary vascular disease
  4. Pleural and chest wall disease
  5. Respiratory muscle disease
  • All result in an increased load or drive for breathing
27
Q

What are the different types of causes for dyspnoea?

A
  1. Respiratory
  2. Cardiac
  3. Muscle weakness
  4. Metabolic acidosis
  5. Anaemia
28
Q

What are the main causes of breathlessness in young adults?

A
  1. Atopic asthma
  2. Exercise induced bronchoconstriction
  3. Vocal cord dysfunction
29
Q

Where are the most common sites of DVT formation?

A
  1. Anterior tibial, common fibular and posterior tibial veins in calf
  2. Femoral vein (needs treatment immediately)
30
Q

What is Virchow’s triad?

A
  1. Blood flow stasis or turbulence:
    - Post-operative
    - Prolonged immobility
    - Prolonged plane flight
  2. Hypercoagulability:
    - OPC
    - Pregnancy
    - Cancer (pancreatic)
    - Genetic
  3. Vessel wall injury:
    - Intravenous cannula
    - Trauma
31
Q

What factors mediate DVT formation?

A
  • Clotting factors (platelets do not play as much of a role)
32
Q

How are DVTs diagnosed?

A
  1. Wells score (can indicate type of testing to be done)
  2. Compression ultrasonography of vein
  3. D-dimer (high sensitivity, low specificity): used to rule out DVT
33
Q

How are DVTs prevented?

A
  1. Prevention of blood stasis
    - Compression stockings
    - Getting people moving after surgery
    - Sequential calf compression
  2. Prevention of hypercoagulability:
    - Anti-coagulation (heparin, warfarin)
    - Treatment of underlying cause

Resp Block (5 decks)

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