Physiological Consequences of Airway Obstruction

Question 1

What factors determine the work of breathing?

Answer 1

Load & Drive

Question 2

What factors affect the load of breathing?

Answer 2

• Stiff lungs
• Narrow airways
• Chest wall
• Diaphragm

Question 3

What factors influence the drive to breathe?

Answer 3

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

Question 4

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

Answer 4

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

Question 5

What are the consequences of increased WOB?

Answer 5

• 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

Question 6

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

Answer 6

• small amount of friction
• small amount of expanding the lungs via elastic tissue

Question 7

What is type I respiratory failure?

Answer 7

• decreased PaO2 (< 60mmHg)
• decreased PaCO2

i.e. hyperventilation is clearing CO2

Question 8

What is type II respiratory/ventilatory failure?

Answer 8

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

• decreased PaO2
• increased PaCO2

i.e. hypoventilation; occurs when respiratory muscles fatigue

Question 9

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

Answer 9

• 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

Question 10

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

Answer 10

relatively low

Question 11

Active exhalation occurs by

Answer 11

contraction of the abdominal and internal ICMs

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

Question 12

During inspiration,

intra-alveolar P ___ Patm

Answer 12

less than

Question 13

during expiration,

intra-alveolar pressure ___ Patm

Answer 13

greater than

Question 14

at the end of inspiration and expiration,

intra-alveolar pressure ____ P atm

Answer 14

equals

Question 15

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

Answer 15

intrapleural pressure is always less than intra-alveolar pressure

due to elastic recoil of the lungs and the chest wall

Question 16

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

Answer 16

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

Question 17

What is pulsus paradoxus?

Answer 17

• 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)

Question 18

Spirometry measures

Answer 18

• 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)

Question 19

What is a normal FEV1 and FEV1 ratio?

Answer 19

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

Question 20

What does a flow-volume loop measure?

Answer 20

• 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)

Question 21

What is the general altered breathing pattern of airflow obstruction?

Answer 21

deep, slow breaths (lower frequency)

to minimize resistive work of breathing

Question 22

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

Answer 22

e.g. pulmonary fiborosis, oedema

small, rapid breaths to minimize elastic WOB

Question 23

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

Answer 23

• 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.)

Question 24

In normal individuals, exercise is limited by

Answer 24

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

Question 25

What limits exercise in chronic airflow obstruction?

Answer 25

* maximum ventilation (MV) is markedly reduced * tf MV is achieved before max HR, decreasing exercise capacity

Question 26

What is gas trapping?

Answer 26

\*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)**

Question 27

What are the mechanical effects of airflow obstruction?

Answer 27

* 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)

Question 28

How does airflow obstruction result in gas exchange problems?

Answer 28

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

Question 29

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

Answer 29

* 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

Question 30

What are high V/Q units?

Answer 30

* more V to units than needed for O2'n of blood * results in wasted V --\> increased physiological dead space * does not effect PaO2

Question 31

What is the A-a gradient?

Answer 31

**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**

Question 32

How does asthma affect the A-a gradient?

Answer 32

* 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

Question 33

How is PAO2 estimated?

Answer 33

Ideal gas equation: P_AO₂ = P_iO₂ - P_ACO₂/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**

Question 34

What does the A-a gradient tell us?

Answer 34

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

Question 35

Patient: * pH = 7.2 * PaCO2 = 60mmHg * PaO2 = 50mmHg What is the diagnosis?

Answer 35

* 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.

Question 36

Patient: * pH = 7.5 * PaO2 = 50mmHg * PaCO2 = 30mmHg What is the diagnosis?

Answer 36

* 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)

Question 37

What are the most common common conditions causing airflow obstruction?

Answer 37

Asthma & COPD