Respiratory Physiology Flashcards
Internal respiration
Intracellular mechanisms which consume O2 and produce CO2
External respiration
sequence of events leading to the exchange of O2 and CO2 between the external environment and the body cells
4 steps of external respiration
- Ventilation between atmosphere and alveoli
- Exchange of O2 and CO2 between air in alveoli and the blood
- Transport in blood of O2 and CO2 between lungs and tissues
- Exchange of O2 and CO2 between the blood and tissues
Process of ventilation
For air to flow into lungs, intra-alveolar pressure must be less than atmospheric pressure (Boyle’s Law). During inspiration, thorax and lungs expand (result of contraction of inspiratory muscles). This increase in volume causes the intra-alveolar pressure to drop and air to flow in
Boyle’s Law
As the volume of a gas increases the pressure exerted by the gas decreases
In what two ways are the thoracic wall and the lungs linked?
- Intrapleural fluid cohesiveness (pleural membranes stick together)
- Negative intrapleural pressure creates a transmural pressure gradient
pneumothorax
air in the pleural cavity, causing lung to collapse. Can be spontaneous or due to trauma
inspiration is ____ process and expiration is _____ process (normally)
active, passive
inspiratory muscles used during normal resting breathing
external intercostal muscles, diaphragm
how do the lungs recoil?
elastic tissue in the lungs, and (more importantly) alveolar surface tension
role of pulmonary surfactant
It’s a complex mixture of lipids and proteins (secreted by type II alveoli). Lowers alveolar surface tension by interspersing between water molecules lining the alveoli, preventing the smaller alveoli from collapsing and emptying their contents into larger alveoli
forces keeping the alveoli open
transmural pressure gradient, alveolar interdependence, pulmonary surfactant
forces causing the alveoli to close
alveolar surface tension, elasticity of stretched pulmonary connective tissue fibres
significance of transmural pressure gradient across lung wall
intra-alveolar pressure pushes outwards and intra-pleural pressure pushes inwards. The 4mmHg difference pushes out on the lungs so they fill the thoracic cavity
significance of transmural pressure gradient across chest wall
atmospheric pressure pushes inwards, while intra-pleural pressure pushes outwards. The 4mmHg difference pushes inwards to compress the thoracic wall
alveolar surface tension
attraction between water molecules at liquid air interface. (In alveoli this produces a force which resists stretching of the lungs).
Law of LaPlace
the smaller the alveoli (radius), the higher the tendency to collapse
Accessory muscles of forceful inspiration)
sternocleidomastoid, scalenus, (pectoralis major)
factors influencing airway resistance
- radius of conducting airway
- parasympathetic and sympathetic stimulation
- disease states (COPD, asthma)
significance of airway resistance in patients with airway obstruction
Normally resistance to flow is very low and air moves with a small pressure gradient. In patients with increased airway resistance, expiration is more difficult than inspiration.
pulmonary compliance
measure of effort that has to go into stretching or distending the lungs. The less compliant the lungs, the more work required to produce a given degree of inflation
work of breathing
normally requires 3% of total energy expenditure for quiet breathing.
factors which increase work of breathing
- decreased pulmonary compliance
- decreased elastic recoil
- increased need for ventilation
- increased airway resistance
Residual Volume
Minimum volume of air remaining in lungs even after maximal expiration
Functional Residual Capacity
Volume of air in lungs at end of normal passive expiration
Vital Capacity
Maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TV + ERV)
Total Lung Capacity
Maximum volume of air that the lungs can hold (VC + RV). TLC cannot be measured by spirometry.
Forced Vital Capacity
Maximum volume that can be forcibly expelled from lungs after maximum inspiration
Forced Vital Capacity (FVC)
Maximum volume that can be forcibly expelled from lungs after maximum inspiration
Forced Expiratory Volume in one second (FEV1)
Volume of air that can be expired during first second of expiration
spirometry
a test that helps diagnose obstructive and restrictive lung disease
Decreased FEV1/ FVC ratio (less than 70%) indicates ____ lung disease
obstructive lung disease (they may be able to bring out normal FVC, but take longer to do so)
Low FVC but normal FEV1/ FVC (or often high), indicates ______ lung disease
Restrictive lung disease (lungs cannot fully expand so FVC is low)
Restrictive lung disease, and examples
Restricts lung expansion
Examples: pulmonary fibrosis
Obstructive lung disease, and examples
Airways are obstructed (e.g. by narrowed alveoli and bronchioles
Examples: COPD, emphysema
Obstructive lung disease, and examples
Airways are obstructed (e.g. by narrowed alveoli and bronchioles
Examples: COPD, emphysema
Dynamic airway compression
This is active expiration and is not a problem for normal people, but makes expiration difficult for patients with airway obstruction. Rising pleural pressure during active expiration compresses alveoli and airway. The airway tends to compress and causes increased pressure upstream (in alveoli). This helps open airways by driving pressure between alveolus and airway. However, in patients with obstruction, the driving pressure is lost over the obstructed segment so there is a fall in airway pressure downstream, leading to airway compression by the rising pleural pressure during active expiration
Dynamic airway compression
This is active expiration and is not a problem for normal people, but makes expiration difficult for patients with airway obstruction. Rising pleural pressure during active expiration compresses alveoli and airway. The airway tends to compress and causes increased pressure upstream (in alveoli). This helps open airways by driving pressure between alveolus and airway. However, in patients with obstruction, the driving pressure is lost over the obstructed segment so there is a fall in airway pressure downstream, leading to airway compression by the rising pleural pressure during active expiration. (In patients with obstructed airways caused by COPD, it’s even harder to breathe out due to loss of elastic properties of lungs
Dynamic airway compression
This is active expiration and is not a problem for normal people, but makes expiration difficult for patients with airway obstruction. Rising pleural pressure during active expiration compresses alveoli and airway. The airway tends to compress and causes increased pressure upstream (in alveoli). This helps open airways by driving pressure between alveolus and airway. However, in patients with obstruction, the driving pressure is lost over the obstructed segment so there is a fall in airway pressure downstream, leading to airway compression by the rising pleural pressure during active expiration. (In patients with obstructed airways caused by COPD, it’s even harder to breathe out due to loss of elastic properties of lungs
Peak flow meter
gives an estimate of peak flow rate. Patient gives short sharp blow into it. Peak flow rate varies with age and height
Peak flow meter
gives an estimate of peak flow rate. Patient gives short sharp blow into it. Peak flow rate varies with age and height
Factors decreasing pulmonary compliance (this causes shortness of breath and a restrictive pattern in spirometry)
- pulmonary fibrosis
- pulmonary oedema
- lung collapse
- pneumonia
- absence of surfactant
Factors increasing pulmonary compliance
- Elastic recoil of lungs being lost
- Ageing
This occurs in emphysema (causes hyperinflation of lungs and patient has to work harder to expire)
Pulmonary ventilation
This is the volume of air breathed in and out per minute. It is the tidal volume x respiratory rate (6L/min under resting conditions)
Alveolar ventilation
This is the volume of air exchanged between atmosphere and alveoli per minute. It is less than pulmonary ventilation due to anatomical dead space: (tidal volume - dead space) x respiratory rate
(4.2L/min under resting conditions)
Ventilation-perfusion matching
Transfer of gases between body and atmosphere depends on rate at which gas passes through lungs, and also the rate at which blood passes through lungs. Ideally these are matched.
Alveolar dead space
This is alveoli which are ventilated but poorly (or not at all) perfused and so do not take part in gas exchange. This dead space increases a lot in disease, but normally very small.
Physiological dead space
Anatomical dead space + alveolar dead space
when alveolar O2 increases, the airways ____ and the arterioles ____
constrict, dilate
when alveolar CO2 increases, the airways ____ and the arterioles ____
dilate, constrict
4 factors influencing gas transfer across alveolar membranes (Fick’s Law)
- partial pressure gradient of O2 and CO2
- diffusion coefficient for O2 and CO2
- Surface area of alveolar membrane
- thickness of alveolar membrane
Dalton’s Law of partial pressures
The total pressure exerted by a gaseous mixture = the sum of the partial pressures of each individual component in the gas mixture
Alveolar gas equation (works out an average value for partial pressure of oxygen in alveolar air)
PAO2 = PiO2 - (PaCO2/ 0.8)
PAO2 = partial pressure of oxygen in alveolar air
PiO2 = partial pressure of O2 in inspired air
PaCO2
Alveolar gas equation (works out an average value for partial pressure of oxygen in alveolar air)
PAO2 = PiO2 - (PaCO2/ 0.8)
PAO2 = partial pressure of oxygen in alveolar air
PiO2 = partial pressure of O2 in inspired air
PaCO2 = partial pressure of CO2 in arterial blood
0.8 = respiratory exchange ratio (CO2/ O2)
The PAO2 is approx. 100mmHg
Non-respiratory functions of respiratory system
- water and heat loss
- enhances venous return
- speech
- maintains normal acid-base balance
- defends against inhaled foreign matter
- smell (nose)
- removes, modifies, inactivates materials passing through pulmonary circulation
Henry’s Law
If the partial pressure in gas phase increases, the concentration of the gas in the liquid phase increases proportionally
Ways O2 is carried in blood
Most bound to Hb (98.5%)
the rest is in dissolved form
Shape of O2-Hb dissociation curve and why
sigmoid, due to cooperativity
O2 Delivery Index
DO2I = CaO2 x CI
oxygen delivery to tissues is a function of oxygen content of arterial blood and the cardiac output
Bohr Effect
tissue conditions increase the release of oxygen by Hb (these could be increased PCO2, increased H+, increased temperature, increased 2,3-biphosphoglycerate)
Foetal Hb
has two alpha and two gamma subunits. Interacts less with 2,3-biphosphpglycerate in RBCs, and so has higher affinity for O2 than adult Hb. Allows O2 transfer from mother to foetus.
O2-Myoglobin dissociation curve
present in skeletal and cardiac muscle. One haem per molecule so curve is hyperbolic. Releases O2 at very low PO2. Provides short-term storage for anaerobic conditions. Presence of myoglobin in blood = muscle damage
oxygen content of arterial blood
CaO2 = 1.34 x (Hb) x SaO2
O2 content of arterial blood is determined by the Hb concentration and the saturation of Hb with O2
(one gram of Hb carries 1.34ml)
Things which cause oxygen delivery to tissues to be decreased
- decreased partial pressure of inspired O2
- anaemia (decreases Hb concentration)
- respiratory disease (decreases arterial PO2 and so decreases Hb sats with O2 and O2 content of blood)
- heart failure (decreases cardiac output)
How CO2 is carried in blood
solution (10%)
as bicarbonate H2CO3 (60%)
as carbamino compounds (30%) (formed by combination of CO2 with terminal amine group)
Formation of bicarbonate ion
Formed in RBCs, where there is carbonic anhydrase to dissociate H2CO3:
CO2 + H2O H2CO3 H+ + HCO3-
Chloride shift
Bicarbonate diffuses out of RBC into the plasma, Chloride moves in by means of the same passive carrier down the electrical gradient created by the outward diffusion of bicarbonate. (This is reversed at pulmonary level).
CO2 dissociation curve
almost linear,
oxygen shifts curve to the right ( Haldane effect)
Haldane Effect
Removing O2 from Hb increases Hb’s ability to pick up CO2 and CO2 generated H+
(works with Bohr effect to facilitate O2 liberation and uptake of CO2 and CO2 generated H+)
Location of peripheral chemoreceptors
- Aortic Body
- Carotid Body
Location of central chemoreceptors
Near the medulla oblongata
A fall in arterial PO2 causes ventilation to increase. How?
Peripheral chemoreceptors are only stimulated at extreme low PO2 levels.
Central chemoreceptors are depressed themselves when PO2 is less than 60mmHg
A rise in arterial PCO2 causes ventilation to increase. How?
Peripheral chemoreceptors are weakly stimulated.
Central chemoreceptors are strongly stimulated.
A rise in arterial H+ concentration causes ventilation to increase. How?
(NB: Question says ARTERIAL, so referring to H+ concentration in the blood. Remember that H+ cannot cross BBB).
H+ doesn’t readily cross BBB, but CO2 does.
Peripheral chemoreceptors play a major role in adjusting for acidosis caused by addition of non-carbonic acid H+ to the blood (e.g. lactic acid, diabetic ketoacidosis).
Their stimulation causes hyperventilation to increase CO2 elimination (therefore reducing H+ load in body).
Acute adaptations to hypoxia?
hyperventilation and increased cardiac output
Chronic adaptations to high altitude hypoxia?
NB: these changes will go back to normal if person moves back to sea level
- increased RBC production
- increased 2,3 BPG production within RBCs
- increased number of capillaries
- increased number of mitochondria
- kidneys conserve acid
Respiratory centres are influenced by stimuli received from:
- medulla
- pons
- higher brain centres (cerebral cortex, limbic system, hypothalamus)
- stretch receptors in walls of bronchi and bronchioles
- J receptors (sensory nerve endings in alveolar walls, in juxtaposition to the pulmonary capillaries, innervated by the vagus nerve)
- joint receptors
- baroreceptors
- central chemoreceptors
- peripheral chemoreceptors
Juxtapulmonary Receptors (J receptors) What stimulates them? What effect do they have?
They are stimulated by events which cause a decrease in oxygenation (pulmonary capillary congestion and pulmonary oedema - caused by e.g. LV failure, also pulmonary emboli).
The effect is rapid, shallow breathing, increasing ventilation.
Pulmonary Stretch Receptors
What activates them?
What effect do they have?
Only activated during large (<1L tidal volume) inspiration: they respond to excessive stretching of the lung.
The effect is inhibition of inspiration (Hering-Breur reflex).
Joint Receptors
What stimulates them?
What effect do they have?
Stimulated by moving limbs.
The effect is increased breathing, contributing to increased ventilation during exercise.
Factors which increase ventilation during exercise
- Reflexes from body movement (joint receptors)
- adrenaline release
- impulses from the cerebral cortex
- increase in body temperature
- LATER: accumulation of CO2 and H+ generated by active muscles
Cough Reflex can be activated by irritation of airways, or tight airways (e.g. asthma). Sequence of cough reflex?
Afferent discharge stimulates:
- Short intake of breath
- Closure of larynx
- Contraction of abdominal muscles (increases intra-alveolar pressure)
- Opening of the larynx and expulsion of air at a high speed
Chemoreceptors
These sense the values of the gas tensions. There are two categories: peripheral chemoreceptors, and central chemoreceptors
Peripheral Chemoreceptors
Function and location
These sense the tension of O2 and CO2, and H+ concentration in the blood. They are on aorta (aortic bodies) and carotid arteries (carotid bodies).
Aortic bodies detect changes in blood O2 and CO2, but not pH.
Carotid bodies detect changes in blood O2 and CO2 and also pH.
(The effect of peripheral chemoreceptors is less than that of central chemoreceptors).
Central Chemoreceptors
Function and location
Responds to the H+ concentration of the CSF.
(CSF is separated from blood by BBB - which is impermeable to H+ and HCO3-, but CO2 readily diffuses through it. CSF has no Hb (so less buffers than blood) and so is less buffered than blood, and is very responsive to H+ concentration changes).
Situated near the surface of the medulla.
Hypercapnia
High CO2 in blood
As PCO2 increases, ventilation increases very steeply and rapidly. Why is the system so responsive to rises in PCO2?
When PCO2 increases, CO2 accumulates in blood, goes to CSF (and generates H+), central chemoreceptors are therefore stimulated and this stimulates the respiratory centre.
PCO2 is the main driver to keep you alive by breathing.
Effect of hypoxia on ventilation
When PO2 drops to about 8kPa, ventilation is not really affect much. Beyond this, peripheral chemoreceptors are stimulated and ventilation increases, up until PO2 falls to very low levels, at which point the ventilation rate falls. This is because at these extremely low PO2 levels, there is not enough O2 for the respiratory centre to function. PO2 is not important in everyday life, as it’s rare for O2 to drop so low.
Hypoxic Drive of Respiration
The effect is completely via the peripheral chemoreceptors. This is stimulated when PO2 falls below 8kPa. It is not important in normal respiration, but may be important in patients with chronic CO2 retention (e.g. COPD). Also important at high altitudes.
