Physiological Consequences of Airway Obstruction Flashcards
What factors determine the work of breathing?
Load & Drive
What factors affect the load of breathing?
- Stiff lungs
- Narrow airways
- Chest wall
- Diaphragm
What factors influence the drive to breathe?
- higher centres (limbic system)
- mechanoreceptors
- irritant receptors
- chemoreceptors
- baroreceptors
- temperature
In airflow obstruction, the increased sensation of breathing is due to
- Increased load due to increased friction in the tubes - an increase in the resistive work of breathing
- expiration becomes active
What are the consequences of increased WOB?
- 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
In normal people, the work done to ventilate is a combination of
- small amount of friction
- small amount of expanding the lungs via elastic tissue
What is type I respiratory failure?
- decreased PaO2 (< 60mmHg)
- decreased PaCO2
i.e. hyperventilation is clearing CO2
What is type II respiratory/ventilatory failure?
caused by inadequate ventilation, it is not necessarily a gas exchange problem
- decreased PaO2
- increased PaCO2
i.e. hypoventilation; occurs when respiratory muscles fatigue
What is the management for type II respiratory/ventilatory failure?
- 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
The elastic work of breathing of someone with asthma or COPD is
relatively low
Active exhalation occurs by
contraction of the abdominal and internal ICMs
normal during exercise and in abnormal situations such as significant airway obstruction
During inspiration,
intra-alveolar P ___ Patm
less than
during expiration,
intra-alveolar pressure ___ Patm
greater than
at the end of inspiration and expiration,
intra-alveolar pressure ____ P atm
equals
intra-pleural pressure is always ___ intra-alveolar pressure because
intrapleural pressure is always less than intra-alveolar pressure
due to elastic recoil of the lungs and the chest wall
Why is systolic BP normally lower on inspiration than expiration at rest?
- inspiration generates negative intrapleural pressure
- becomes negative transpleural pressure
- lowers BP by reducing pulmonary return to the left side of the heart
What is pulsus paradoxus?
- 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)
Spirometry measures
- 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)
What is a normal FEV1 and FEV1 ratio?
- > 70% FVC (younger >80%)
- FEV1 decreases with increasing severity of obstruction
- FEV1/FVC > 70% (>80%)
- if
- if
What does a flow-volume loop measure?
- 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)
What is the general altered breathing pattern of airflow obstruction?
deep, slow breaths (lower frequency)
to minimize resistive work of breathing
What is the general altered pattern of breathing when the lungs are stiff (i.e. increased elastic WOB)?
e.g. pulmonary fiborosis, oedema
small, rapid breaths to minimize elastic WOB
What is maximum minute ventilation, and what are the consequences in chronic obstructive disease?
- 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.)
In normal individuals, exercise is limited by
- HR (220 - age)
- CO
- O2 metabolism by peripheral muscles
- at maximal exercise, 30% maximum ventilation (MV) is unused
What limits exercise in chronic airflow obstruction?
- maximum ventilation (MV) is markedly reduced
- tf MV is achieved before max HR, decreasing exercise capacity
What is gas trapping?
*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)
What are the mechanical effects of airflow obstruction?
- 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)
How does airflow obstruction result in gas exchange problems?
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
- pathological changes vary throughout the airways
What is the adverse outcome of pre-capillary constriction to compensate for low V/Q units?
- 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
What are high V/Q units?
- more V to units than needed for O2’n of blood
- results in wasted V –> increased physiological dead space
- does not effect PaO2
What is the A-a gradient?
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
How does asthma affect the A-a gradient?
- 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
How is PAO2 estimated?
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
What does the A-a gradient tell us?
if hypoxia (low PaO2) is due to pure hypoventilation or +/- gas-exchange problem
Patient:
- pH = 7.2
- PaCO2 = 60mmHg
- PaO2 = 50mmHg
What is the diagnosis?
- 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.
Patient:
- pH = 7.5
- PaO2 = 50mmHg
- PaCO2 = 30mmHg
What is the diagnosis?
- 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)
What are the most common common conditions causing airflow obstruction?
Asthma & COPD
