72 - Physiological Consequences of Airway Obstruction Flashcards
Sensation of airflow obstruction 1) 2) 3) 4)
1) Increased sensation of breathing
2) Increased respiratory muscle effort
3) Active exhalation
4) Longer time to inspire and expire
Things that can increase load on breathing 1 2 3 4
Stiff lungs
Narrow airways
Chest wall
Diaphragm
Things that can increase the drive to breathe 1 2 3 4 5 6
Higher centres (limbic system) Mechanoreceptors Irritant receptors Chemoreceptors Baroreceptors Temperature
Factors contributing to the work required to breathe
1)
2)
1) Load on lungs.
2) Drive to breathe
When is difficulty breathing a sensation?
When appropriate
When is difficulty breathing a symptom?
When inappropriate
Nerve stimuli leading to inspiration
Stimulation of the diaphragm by phrenic nerves.
External intercostal stimulation by intercostal nerves.
Contraction of the diaphragm does what to thoracic dimensions?
Increases the longitudinal and lateral dimensions of the thorax
Amount of breathed oxygen that goes to respiratory muscles at rest
~3%
When does the intra-alveolar pressure equal atmospheric pressure?
At the end of inspiration and expiration
Intra-pleural pressure relative to intra-alveolar pressure
Intra-pleural is always lower than intra-alveolar, because of elastic recoil of lungs and chest wall (pleura held together by fluid tension, upon inspiration negative pressure within lungs pulls inwards on pleura. Fluid pressure resists this, leading to decreased pressure in pleural space).
Intrapleural pressure during inspiration
Decreases pressure in pleural cavity
Pleural cavity pressure during one inspiration/expiration cycle.
Decreases until change from inspiring to expiring, then increases in pressure again. Frequency is ~1/2 that of inspiration/expiration pressure.
Why is work of breathing increased when there is an airway obstruction
Inspiratory muscles need to generate higher pressures to overcome obstruction to airflow
Consequences of obstruction
1
2
3
1) Recruitment of accessory muscles of inspiration
2) Increased oxygen consumption by respiratory muscles
3) Risk of respiratory muscle fatigue (if obstruction is severe)
Effect of respiratory muscle fatigue
Too little O2 dissolved in blood
Ventilatory failure
When rate of O2 entry into body is below rate of CO2 expiration.
Arterial partial pressures considered to be ventilatory failure
PaO2 under 60mmHg, PaCO2 over 50mmHg
How is exhalation normally passive?
Elastic recoil of lungs generates positive intrapulmonary pressure, pushing air out.
Muscles involved in active exhalation
Abdominals, internal intercostals
TLC
Total lung capacity.
Greatest possible breath.
Amount of time for a normal FVC
2-3 seconds
Spirometric measurement of total lung capacity
FVC
% of vital capacity in FEV1
~80%
FEV1 percentage of FVC considered normal
Over 70% (if older)
~80% in a young person
Appearance of a FVC graph for someone with airway obstruction
Flatter, increases less quickly than that of a healthy person (person able to expire less quickly)
Flow-volume loop
Measurement of flow rate vs volume during a FVC, followed by a forced inspiratory manoeuvre.
FVC is on the upper part of y-axis, inspiratory pressure is on the lower part of y-axis
WOB
Work of breathing
Effect of obstruction leading to uneven ventilation
Leads to impaired gas exchange
Examples of obstructions that can lead to uneven ventilation
COPD, asthma
Ventilation/perfusion matching
Gas exchange is most efficient when ventilation and perfusion are matched (V/P=1) in all alveolar-capillary units.
How can you image whether ventilation and perfusion match?
Ventilation and perfusion scans.
Ventilation - inhale radioactive particles, which are non-absorbable.
Perfusion - Inject radioactive particles into systemic vein which lodge in small pulmonary arterioles.
Appearance of COPD on ventilation/perfusion scan
Non-homogenous ventilation and perfusion in lungs
Effect of V/Q mismatch
O2 binding sites on Hb not filled.
Some blood returning to left atrium not fully oxygenated.
Most clinically important cause of reduced PaO2
Low V/Q units
Shunt
A unit of blood that goes through a non-ventilated area of lungs, so isn’t oxygenated.
An extreme form of low V/Q unit.
Compensatory mechanism for regions of reduced ventilation (causing low V/Q)
Vasoconstriction occurs in areas of low ventiation to reduce the hypoxaemic effects of low V/Q units.
This is effective in reducing altered gas exchange, but not usually fully successful
Potential downstream effect of compensatory mechanism for low V/Q units
Increased pulmonary arterial pressure
Things that airflow obstruction can be due to
1)
2)
1) Spasm of bronchial smooth muscle
2) Airway inflammation
Things that can be used to treat spasm of bronchial smooth muscle
1)
2)
3)
1) Beta agonists
2) Anti-cholinergics
3) Methyl-xanthines
COPD
Smoking related disease
Causes inflammation of bronchial mucosa.
Inflammation is not steroid-responsive
Causes destruction of lung parenchyma
Differences between asthma and COPD
COPD inflammation is not steroid responsive
COPD leads to destruction of airway parenchyma
Asthma is steroid responsive and doesn’t destroy airway parenchyma
Effects of COPD
1)
2)
3)
1) Collapse of small airways (destruction of elastic tissue in airways), particularly in inspiration
2) Impaired gas exchange from V/Q mismatch, loss of alveolar-capillary membrane
3) Reduced capillary bed, from pulmonary hypertension
What are asthma inflamed airways responsive to?
Corticosteroids
Leukotriene antagonists
Alveolar-arterial gradient for oxygen
Measure of the overall efficiency of gas exchange across all alveolar-capillary units
How is alveolar pressure calculated for A-a gradient of O2?
Estimated using the ideal gas equation:
PAO2 = PiO2 - PACO2/RQ
R=~0.8
PiO2 = Partial pressure of inspired oxygen
PACO2 = Alveolar CO2
Effect of hypoventilation on O2 and CO2
Decrease O2, increase CO2
How to tell if someone is hypoxic from hypoventilation, so something more.
Calculate the amount of hypoxia from alveolar-arterial gradient for O2, see if there is more in a patient than is expected.
RQ
0.8
PiO2 at sea level
150
Normal A-a gradient
15-30
How can cellular O2 consumption be calculated?
Fick equation
QO2 (cellular use of O2) = Cardiac output x (arterial O2 content - venous O2 content)
