Week 14 Physiology - Resp Phys I Flashcards
What is anatomical dead space?
Anatomical dead space = volume of conducting airways (i.e. not participating in gas exchange) usually 150mL
What is physiological dead space?
Physiological dead space = volume of lung which doesn’t eliminate CO2.
**In healthy patients, very closely mirrors anatomical dead space, but in underlying lung disease, VQ mismatch can significantly increase areas of lung not participating in gas exchange
What does Bohr’s method state regarding physiological dead space?
All measured CO2 must come from respiratory zone, therefore:
Volume of physiological dead space / tidal volume = (alveolar CO2 - expired CO2) / Alveolar CO2
i.e. dead space in non-conducting areas (or gas exchange participating areas of the lung) where exchange isn’t happening.
**PAO2 = alveolar O2, PaO2 = arterial O2
What is an acinus?
The gas exchanging unit of the lungs, comprising portion of the lung distal to the terminal bronchiole (i.e., the last purely conducting airway), which is composed of the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli
Define tidal volume:
Amount of air moving into the lungs with each inspiration/expiration - 500mL
Define inspiratory reserve:
Air inspired with with maximal inspiratory effort in excess of tidal volume - 3000mL
Define inspiratory capacity:
Maximum amount of volume that can be inhaled after a normal tidal expiration (TV + IRV)
Define expiratory reserve:
Volume expelled by active expiratory effort after passive expiration - 1200mL
Define residual volume:
Volume remaining in lungs after maximal expiratory effort -1200mL
Define forced vital capacity:
Largest amount of air that can be expired after maximal inspiratory effort - 4700mL
Define FEV1:
Fraction of vital capacity expired during the first second of forced expiration
What is Fick’s law for diffusion?
**Think, one proptional, one inversely proportional
Rate of transfer of gas across a membrane is proportional to tissue surface area and difference in gas partial pressure between the two sides.
Inversely proportional to the tissue thickness
(0.03 micrometres = usual thickness of alveolar membrane)
What is the diffusion constant of a gas mean regarding gas exchange?
Gas exchange proportional to solubility of gas and inversely proptional to molecular weight
i.e. CO2 diffuses 20x more rapidly than O2 as it is much more soluble, despite similar molecular weight
Give an example of a lung condition that affects Fick’s law gas diffusion for surface area and membrane thickness?
Emphysema = decreased tissue surface area
ILD = increased membrane thickness
What does ‘diffusion limited’ mean regarding gas exchange, and what gas is the prototypical example?
Carbon monoxide.
CO rapidly crosses blood gas barrier from alveoli to blood stream, and then tightly binds to Hb –> meaning it doesn’t really increase the partial pressure of CO in the blood, and so maintains a concentration gradient that favours movement from alveoli to blood.
Therefore, the gas transfer is limited by rate of gas crossing membrane, rather than amount of blood passing at a given time.
What does ‘perfusion limited’ mean regarding gas exchange, and what gas(es) are prototypical examples?
NO2, CO2.
Gases not bound by Hb cause increased partial pressure in the blood, which then influences diffusion down concentration gradient. It requires blood to be constantly moving to maintain a concentration gradient that is favourable to gas exchange. (i.e so that alveolar gas conc > arterial)
How is O2 a combination of both diffusion and perfusion limited?
Capillary PO2 reaches equivalent of alveolar gas when RBC is 1/3 of way along capillary. This is when gas exchange is perfusion limited (i.e. concentration gradient reaches equilibrium )
Because of Hb, that allows partial pressure of O2 to remain lower than alveolar O2, facilitating diffusion down concentration gradient.
In cases of increased membrane thickness, the Pa02 value doesn’t reach the alveolar value by the endow the capillary, and instead is more diffusion limited.
What impact does exercise have on oxygen exchange at the alveolar membrane?
Becomes diffusion limited because HR increases and blood is travelling much faster through capillary, therefore doesn’t have enough time for diffusion to equalise the alveolar and arterial O2
Where is most resistance in the airways?
Major site of airway resistance is medium sized bronchi
**Airway resistance progressively increases up to 7th airway generation, then drops –> very small bronchioles contribute very little to resistance
What are factors determining airway resistance?
Lung volume
Bronchial calibre/bronchial smooth muscle activity
Gas density
Dynamic compression of airways during forced expiration (intrapleural pressure > alveolar pressure)
**Airway resistance increases with nasal breathing (i.e. halving size of the tube)
Summarise Poiseuille’s Law:
Resistance is proportional to length and viscosity, and inversely proportional to to radius
What is a formulaic definition of compliance?
Compliance = volume change / pressure change
With a balloon analogy, the bigger the change in volume for the same pressure generated by blowing in, the greater the compliance of the balloon
What 3 elements regulate breathing?
- Sensors (i.e. chemoreceptors)
- Central controller (Midbrain)
- Effectors (respiratory muscles)
What are the 3 main groups of neurons responsible for respiration?
Medullary respiration centre
Apneustic centre
Pneumotaxic centre
**Cortex, which can override function of brainstem (within certain limits)
What is the role of the medullary respiratory centre?
Located in ventrolateral region of medulla:
1. Dorsal respiratory group: associated with inspiration
2. Ventral respiratory group: associated with expiration
Pacemaker neurons for intrinsic rate of periodic firing, responsible for generation of respiratory rhythm
Describe the “ramp” process of a breath?
After latent period between breaths, action potentials being to appear, increasing in crescendo over the next few seconds to cause a coordinated contraction of respiratory muscles to generate negative intra-thoracic pressure –> drawing air into lungs. Followed by cessation of action potentials –> relaxation and passive recoil of lungs and expiration
When is the expiratory area of respiratory centre quiescent?
During normal quiet breathing, there is no need for forced expiration
With cortical override, what parameters limit hypo and hyperventilation?
Hypoventilation limited by PCO2 and PO2
Hyperventilation limited by respiratory muscle fatigue
Where are central chemoreceptors located?
Near ventral surface of medulla (near exit of 9th and 10th cranial nerves)
What is the ion that dictates activity of central chemoreceptors?
H+
Increased = increased ventilation
Decreased = decreased ventilation
Explain how increased CO2 leads to increased H+ in CSF:
Central chemoreceptors are bathed in CSF, which is impermeable to H+ ions from plasma.
However, CO2 is freely permeable, and in CSF forms carbonic acid –> H+ and HCO3-
Increasing levels of CO2 diffusion will increase H+ content of CSF and cause increased activity of central chemoreceptors
Where are peripheral chemoreceptors located?
Located in Carotid bodies - between bifurcation of the common carotid arteries (CN IX) and aortic bodies - above and below aortic arch (CN X)
What factors influence activity of peripheral chemoreceptors?
Decreases in arterial PO2
Increases in arterial PCO2
Decreases in pH (in carotid bodies only)
What are pulmonary stretch receptors?
Located in airway smooth muscle, discharge in response to lung distension (via vagus nerve) which acts to inhibit activation of other respiratory muscles. Largely inactive in adults except for exercise.
What are irritant receptors?
Located between airway epithelial cells, stimulated by noxious gases, inhaled dust/smoke/cold air
Impulses transmitted via vagus nerve, causing reflex bronchoconstriction and hyperpnoea
What are juxtacapillary receptors?
Non-myelinated C fibres located in alveolar walls close to capillaries, send impulses via vagus nerve in response to engorgement of capillaries/increased interstitial fluid, causing rapid, shallow breathing
What physiological changes occur at altitude?
Hyperventilation (due to decreased FiO2) –> driven by hypoxic stimulation of peripheral chemoreceptors
Polycythaemia (increased EPO)
Hypoxic vasoconstriction
What does pulmonary vasoconstriction occur in response to?
Hypoxia in alveoli –> results ins increased pulmonary arterial pressure and R) sided heart strain (which can be exacerbated by polycythaemia)
What occurs to the O2 dissociation curve at altitude?
Initially a RIGHT shift (decreased Hb affinity for O2) due to increased 2-3 DPG (a metabolic breakdown product in RBCs).
At extreme elevation, extreme alkalosis can shift curve to the LEFT. (Due to decreased CO2 levels in the setting of hyperventilation)
What is the syndrome of acute mountain sickness?
Headache, fatigue, palpitations, insomnia, High Altitude Pulmonary Oedema (secondary to pulmonary hypertension)
