Resp Physiology Flashcards
Surfactant
Phosopholipid-rich detergant
Produced by type II alveolar cells
Coats luminal surface of alveoli
Reduces surface tension of water which is opposing expansion
Water molecules are attracted more to each other than they are to gas molecules.
When any liquid surrounds a gas, i.e. in the alveolus, this produces an inward pressure.
Functions of surfactant
Lowers surface tension
- -> increases compliance of lungs
- -> reduces work of breathing
Prevents fluid accumulating in the alveoli
Reduces the tendency of alveoli to collapse (alveolar instability).
Conditions that decrease lung compliance
Fibrosis
Pulmonary oedema
Deficiency of surfactant e.g. premature babies
Decreased lung expansion e.g. respiratory muscle paralysis
Supine position
Breathing 100 O2
Mechanical ventilation due to reduced pulmonary blood flow
Age
Conditions that increase compliance
COPD
due to destruction of elastic parenchyma
Components of work of breathing
Two major compenents:
Work required to over-come elastic recoil of lungs
Non-elastic forces:
- Air resistance (most significant)
- Frictional forces
- Inertia of air and tissues
One-third of airway resistance occurs in the upper
airways – nose, pharynx and larynx. This can be
greatly reduced by breathing through the mouth
Ventilation of upper vs lower zones
Lower zones better ventilated because:
-the weight of the lungs
-the compliance curve is sigmoid, and the upper
and lower parts of the lung lie on different parts
of this curve.
Definition of tidal volume
Volume of air inspired and expired during quiet breathing
Definition of functional residual capacity
Functional residual capacity is the volume of air in the the lungs at the end of passive expiration
FRC = Residual volume + expiratory reserve volume
At FRC, the opposing elastic recoil forces of the lungs and chest wall are in equilibrium and there is no exertion by the diaphragm or other respiratory muscles.
Measuring functional residual capacity
As it consists partly of residual volume, it cannot be measured by spirometry
Nitrogen wash-out test, helium dilution or body plethysmography
Definition of vital capacity
Volume of air that is expelled from maximal inspiration to maximal expiration
Fowler’s method
Measures anatomical deadspace using single breath of 100% O2 and a nitrogen analyser
As subject starts to expire, the nitrogen content of
alveolar air is measured.
Increasing anatomical deadspace
Increasing size of person
Standing position
Increased lung volume
Bronchodilatation
Increasing physiological deadspace
Hypotension
Hypoventilation
Emphysema
PE
Positive pressure ventilation
Nitrogen expiration curve
Phase 1
-Pure O2 = dead space
Phase 2
- Mixture of dead space and alveolar gas
- Increasing nitrogen / volume
- Mid-point here represents calculation of anatomical deadspace
Phase 3
-Plateu of nitrogen as pure alveolar air is expired
Phase 4
- Abrupt increase in nitrogen concentration as airways at the base of the lung close
- Expired air at this point is from the apex, which has received less O2, and thus the nitrogen is less dilute.
Factors affecting the closing capacity
Closing capacity is volume at which airways begin to close
–> phase 4 of single breath nitrogen test
Factors:
Age: increases with age
Posture: in a supine position in a 40-year-old
subject, the closing capacity is equal to the FRC
Anaesthesia: decrease in lung volumes results in closing capacity exceeding FRC, even in the youngest patients.
Diffusion capacity
Measured by inhaling carbon monoxide and measuring it in the blood
Diffusion capacity is decreased by:
Pulmonary oedema
Emphysema
Hypoxic pulmonary vasoconstriction (HPV)
In order to match perfusion to ventilation areas of the lung that are poorly ventilated receive less blood which is mediated by the HPV
Hypoxia –> vasoconstiction
Hypercapnoea —> Vasoconstriction
NOTE this is the opposite to the normal physiological response in other tissues which is vasodilatation
3 zones of blood supply
Zone 1: Apex
Alveolar pressure is greater than that of the pulmonary artery and hence poor blood flow
Zone 3: Base
Pulmonary artery pressure greatly exceeds the alveolar pressure and thus vessels are fully open.
Blood flow is very good.
The variations in regional blood flow are abolished on lying down.
V/Q of 3 zones
At the apex V/Q = 3, thus indicating that the alveoli
are ventilated better than they are perfused
At the base V/Q = 0.6, thus indicating that the alveoli are perfused better than they are ventilated
Ideal V/Q = 1 and is found approximately two-thirds of the way up the chest
Pathophysiological effects of pulmonary oedema
Reduces diffusion capacity
Decreased lung compliance due to the reduction
in surface tension and alveolar shrinkage
Increased airway resistance: this can occur due
to the reduction in lung volume and fluid filling
the airways.
Resistance is also due to reflex bronchoconstriction
Alveolar oedema leads to a ventilation–perfusion
mismatch as alveoli filled with fluid are still perfused
but not ventilated.
Pulmonary vascular resistance increases due to
hypoxic vasoconstriction and external compression
from interstitial oedema.
Lymphangitis carcinomatosa
Pulmonary oedema due to obstruction of lymphatics in lung from cancer
Causes of pulmonary oedema
Neurogenic: head injuries due to increased sympathetic output
Obstruction to lymphatics: lymphangitis carcinomatosa
Increased capillary permeability: ARDS, endotoxic shock, irritant gases
High altitude: likely to be due to hypoxic vasoconstriction leading to elevated pulmonary artery pressure
Raised pulmonary hydrostatic pressure, the
commonest cause, occurs with left ventricular
failure – left atrial pressure rises and this is
transmitted into the pulmonary circulation,
resulting in increased pulmonary capillary
pressure, and thus capillary hydrostatic pressure
Criteria for diagnosing ARDS
Known cause
Refractory hypoxia
New fluffy changes on CXR
Not cardiac: Pulmonary artery wedge pressure <18mmHg
Right-shift of haemoglobin
A shift of the curve to the right will result in:
- Decreased oxygen affinity
Factors causing right-shift
- Increased Temperature
- Increased 2,3 DPG
- Increased H, i.e. lower pH / acidosis
These are the factors present in metabolically active tissues so it causes off-loading of O2
Right shift –> Rid of O2
Molecules with far left-curve
Fetal haemoglobin is left-shifted
Allows for it to take up PaO2 from maternal circulation and not release it until it reachesthe tissues
Myoglobin
-Acts as oxygen store in muscles and released in profound anaerobic conditions
Haldane effect
As PO2 falls
Haemoglobin uptake of CO2 increases
Hence in hypoxic tissues red cells off-load O2 and uptake more PCO2
Medulla control of respiration
Inspiratory neurons
-Rhythmic firing
Expiratory neurons
-Inactive during normal respiration
Pons control of respiration
Pons modulates the medulla inspiratory neurons
Two centres
Apneustic centre:
- Lower pons
- Prolong inspiratory phase
- Shorten expiratory phase
Pneumotaxic centre
- Upper pons
- Inhibits inspiratory neurons and shortens inspiration
Chemoreceptors for respiration
Modulate the output from medulla
Central and Peripheral
Central
- Sensitive to changes in PCO2
- Situated in medulla close to respiration centre
- CO2 diffuses from the blood into the brain and reacts with water to produce H+ and causes the pH to fall, thus directly stimulating the chemoreceptors
- -> increase in ventilation
Peripheral
-Carotid bodies close to bifurcation of the common carotid
-AND in aortic bodies that lie in aortic arch
-Respond to changes in arterial pH and to low
levels of PO2;
Hering-Breuer reflex
Inhibits ventilation due to excessive stretch of the lungs
Stretch receptors pass signal via the vagus nerve
J receptors
Lie adjacent to capillaries in alveoli
Stimulation causes increased breathing rate
Vasomotor centre and respiration
vasomotor centre: low blood pressure detected
by baroreceptors results in an increase in the ventillation
