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Respiratory Physiology > Physiological Consequences of Airway Obstruction > Flashcards

Physiological Consequences of Airway Obstruction Flashcards

1
Q

What factors determine the work of breathing?

A

Load & Drive

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2
Q

What factors affect the load of breathing?

A
  • Stiff lungs
  • Narrow airways
  • Chest wall
  • Diaphragm
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3
Q

What factors influence the drive to breathe?

A
  • higher centres (limbic system)
  • mechanoreceptors
  • irritant receptors
  • chemoreceptors
  • baroreceptors
  • temperature
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4
Q

In airflow obstruction, the increased sensation of breathing is due to

A
  • Increased load due to increased friction in the tubes - an increase in the resistive work of breathing
  • expiration becomes active
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5
Q

What are the consequences of increased WOB?

A
  • recruitment of accessory muscles (scalene, sternomastoids)
  • increased O2 consumption by respiratory muscles (40-50%, compared to 2% in normal)
  • risk of respiratory muscle fatigue (severe obstruction)
    • can lead to type II respiratory (ventilatory) failure
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6
Q

In normal people, the work done to ventilate is a combination of

A
  • small amount of friction
  • small amount of expanding the lungs via elastic tissue
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7
Q

What is type I respiratory failure?

A
  • decreased PaO2 (< 60mmHg)
  • decreased PaCO2

i.e. hyperventilation is clearing CO2

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8
Q

What is type II respiratory/ventilatory failure?

A

caused by inadequate ventilation, it is not necessarily a gas exchange problem

  • decreased PaO2
  • increased PaCO2

i.e. hypoventilation; occurs when respiratory muscles fatigue

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9
Q

What is the management for type II respiratory/ventilatory failure?

A
  • O2 administration if breathing (will not impact CO2)
  • bronchodilators to manage obstruction
  • ventilatory support if above are not working or immediate urgent tx required (will lower CO2)
    • will automatically +O2 if no gas exchange problem occuring simultaneously
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10
Q

The elastic work of breathing of someone with asthma or COPD is

A

relatively low

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11
Q

Active exhalation occurs by

A

contraction of the abdominal and internal ICMs

normal during exercise and in abnormal situations such as significant airway obstruction

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12
Q

During inspiration,

intra-alveolar P ___ Patm

A

less than

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13
Q

during expiration,

intra-alveolar pressure ___ Patm

A

greater than

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14
Q

at the end of inspiration and expiration,

intra-alveolar pressure ____ P atm

A

equals

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15
Q

intra-pleural pressure is always ___ intra-alveolar pressure because

A

intrapleural pressure is always less than intra-alveolar pressure

due to elastic recoil of the lungs and the chest wall

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16
Q

Why is systolic BP normally lower on inspiration than expiration at rest?

A
  • inspiration generates negative intrapleural pressure
  • becomes negative transpleural pressure
  • lowers BP by reducing pulmonary return to the left side of the heart
17
Q

What is pulsus paradoxus?

A
  • in severe airflow obstruction
  • contraction of inspiratory muscles to generate more negative intrapleural (tf transpleural) pressure to suck air in
  • much greater drop in systolic BP on inspiration relative to expiration
  • disappears on respiratory muscle fatigue (type II resp/vent failure)
18
Q

Spirometry measures

A
  • mechanical lung function
  • FEV1 (~80% of FVC comes out in the first second, total within 1-3s)
  • produces volume vs. time curve (rate of flow)
19
Q

What is a normal FEV1 and FEV1 ratio?

A
  • > 70% FVC (younger >80%)
    • FEV1 decreases with increasing severity of obstruction
  • FEV1/FVC > 70% (>80%)
    • if
    • if
20
Q

What does a flow-volume loop measure?

A
  • flow rate vs. volume during a forced expiration (upper loop) followed by a forced inspiration (lower loop)
  • can distinguish lower bronchial obstruction (asthma, COPD) from higher tracheal obstruction (tumour, stenosis)
21
Q

What is the general altered breathing pattern of airflow obstruction?

A

deep, slow breaths (lower frequency)

to minimize resistive work of breathing

22
Q

What is the general altered pattern of breathing when the lungs are stiff (i.e. increased elastic WOB)?

A

e.g. pulmonary fiborosis, oedema

small, rapid breaths to minimize elastic WOB

23
Q

What is maximum minute ventilation, and what are the consequences in chronic obstructive disease?

A
  • same term as maximum ventilation (MV), ~100L/min (minute ventilation)
  • 35x FEV1
    • FEV1 ~ 4-5L tf MV 100-200L/min
    • in severe chronic obstruction, FEV1 < 1 tf MV ~ 20-30L/min
      • rest: requires 8-10L/min
      • exercise: requires 15-20L/min
        • tf limiting factor in severe airflow obstruction; cannot increase ventilation to supply O2 or clear CO2
  • in COPD, emphysema, MV is significantly reduced (50, 30, 20 etc.)
24
Q

In normal individuals, exercise is limited by

A
  • HR (220 - age)
  • CO
  • O2 metabolism by peripheral muscles
  • at maximal exercise, 30% maximum ventilation (MV) is unused
25
Q

What limits exercise in chronic airflow obstruction?

A
  • maximum ventilation (MV) is markedly reduced
  • tf MV is achieved before max HR, decreasing exercise capacity
26
Q

What is gas trapping?

A

*common in COPD, less common in asthma*

  • air can get into alveoli but due to proximal airway obstruction it cannot get out
    • gas becomes ‘trapped’ and inaccessible
    • causes hyperinflation of lungs
  • results in:
    • decreased VC - air cannot move out of lungs
    • increased TLC, RV, and RV/TLC - RV takes up more of TLC (tf VC decreases, trapped air increases)
27
Q

What are the mechanical effects of airflow obstruction?

A
  • increased sensation of breathing
  • increased respiratory muscle effort
  • active exhalation
  • prolonged inspiration and expiration
  • altered pattern of breathing
  • reduced maximum ventilation
  • (gas trapping in some cases)
28
Q

How does airflow obstruction result in gas exchange problems?

A

e.g. asthma, bronchiolitis, COPD

  • airflow obstruction is non-uniform
    • ​pathological changes vary throughout the airways
      • e.g. bronchiole narrowing, mucous plugging some airways, bronchial inflammation
    • reduces homogeneity of ventilation that is required for efficient gas exchange
      • i.e. there are low V/Q units
      • compensatory mechanism in precapillaries supplying these units is to constrict to reduce perfusion to underventilated/non-ventilated alveoli
29
Q

What is the adverse outcome of pre-capillary constriction to compensate for low V/Q units?

A
  • mechanism works well in focal disease e.g. pneumonia
  • in general obstructive disease like asthma, cuts off alveoli and reduces gas exchange
  • this increases pulmonary arterial pressure
    • impedes right heart’s ability to pump blood to the lungs
30
Q

What are high V/Q units?

A
  • more V to units than needed for O2’n of blood
  • results in wasted V –> increased physiological dead space
    • does not effect PaO2
31
Q

What is the A-a gradient?

A

normal: PAO2 - PaO2 < 15mmHg

  • Alveolar-arterial gradient
  • measure of overall efficiency of gas exchange across all A-C units
  • difference between the average Alveolar O2 partial pressure and the average arterial O2 partial pressure
  • normal <15mmHg
32
Q

How does asthma affect the A-a gradient?

A
  • widens it due to low V/Q units
    • i.e. larger disparity between PAO2 and PaO2
  • asthma does not affect the A-C membrane, it alters gas exchange due to non-homogeneous ventilation
33
Q

How is PAO2 estimated?

A

Ideal gas equation: PAO2 = PiO2 - PACO2/RQ

i.e. mean alveolar O2 = mean inspired O2 - PACO2/respiratory ratio

  • mean inspired O2 ~150mmHg
  • RQ at rest ~ 0.8
  • use PaCO2 for PAO2 (~same)

normal < 15mmHg

34
Q

What does the A-a gradient tell us?

A

if hypoxia (low PaO2) is due to pure hypoventilation or +/- gas-exchange problem

35
Q

Patient:

  • pH = 7.2
  • PaCO2 = 60mmHg
  • PaO2 = 50mmHg

What is the diagnosis?

A
  • pH = 7.2 - abnormally low, acidosis
  • PaCO2 = 60mmHg - high –> tf respiratory acidosis
  • PaO2 = 50mmHg - low, hypoxic
  • PAO2 = 150mmHg - 60mmHg/0.8 = 75mmHg
  • A-a = 75mmHg - PaO2 = 75mmHg - 50mmHg = 25mmHg

Patient is hypoventilating (low PaO2), causing hypoxia. A-a is wider than normal (>15mmHg), therefore there may also be a gas exchange problem.

36
Q

Patient:

  • pH = 7.5
  • PaO2 = 50mmHg
  • PaCO2 = 30mmHg

What is the diagnosis?

A
  • pH = 7.5 - **abnormally **high, alkalosis
  • PaO2 = 50mmHg - low, hypoxic
  • PaCO2 = 30mmHg - low –> respiratory alkalosis

Patient is hypoxic (low PaO2) and hyperventilating (low PaCO2), therefore there must be a gas exchange problem (don’t need to look at A-a because hypoxic & hyperventilating @ sea level = GE problem)

37
Q

What are the most common common conditions causing airflow obstruction?

A

Asthma & COPD

Respiratory Physiology (8 decks)

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