Respiratory System Flashcards
Lung Compliance
Elastic resistance of the lungs. Max compliance would be when you need the lease amount of airflow for min
Tidal Volume Definition and normal value
Amount of air displaced in a normal breath. 500ml
Vital Capacity def and normal value
Total lung capacity - residual volume. 5500ml
Inspiratory and Expiratory reserve volume
Amount of air left in the lung after normal breath.
Functional residual capacity
The total volume of air left in the lung after a normal expiration. 3500ml.
Total Lung Capacity def and normal value
amount of air you can have in the lungs, 7300ml.
Residual volume def and normal value
Amount of air left in the lungs after full expiration. 1800ml.
Inspiratory capacity def and normal value
Total amount of air you can inspire after normal expiration. 3800ml.
Volume of anatomic dead space
150ml
Total ventilation per minute and alveolar ventilation.
Total: 7500 ml/min Alveolar: 5250 ml/min
Pulmonary blood flow per minute.
5000 ml/min
Factors affecting airway resistance
Airway diameter Obstruction (causing turbulence) Dynamic compression of airways Smooth Muscle Contraction
Elastic and airway resistance
Elastic resistance: Resistance to the stretch of lung tissue and the air-liquid interface lining the alveoli. Airway Resistance: Resistance due to friction between layers of flowing air and between the air and the airway walls
Restrictive vs Obstructive lung disease
In restrictive, it is difficult to breath in due to difficulty to expand the lungs. In obstructive, there is a blockage in the lung or increased airway resistance.
Receptors in the Lung (4) and their role
Stretch Irritant Juxtapulmonary - detect pulmunary embolism, inflamation, oedemas Proprioreceptors - detects load in respiratory muscles.
Hering Breuer reflex and deflation reflex
Hering Breuer: inflation inhibits inspiration Deflation reflex: deflation augments inspiration
hypercapnia
excess CO2
Hypoxia
Low O2
Location of Central Chemoreceptors
Ventrolateral surface of medulla, exit of C9 and C10. In between cerebrospinal fluid and BBB.
Normal Conc of CO2 and O2 in deoxygenated blood
CO2: 46mmHg O2: 40mmHg
Normal conc of CO2 and O2 in oxygenated blood
CO2: 40mmHg O2: 100mmHg
Shunt
Blocked airway -> no ventilation to those alveoli
Dead space
Blocked vessel -> no blood going through system
Dynamic compression
In forced expiration, when intrapleural pressure is larger than alveolar pressure so lung collapses into itself
Effect of surfacant
Decreases surface tension (reduces the pressure difference needed to allow the lung to inflate. And hence increases compliance (volume change per unit of pressure) Also controls alveolar size: if the alveoli is too big, it will have less surfacant, so more surface tension and it will take more time to inflate than shorter alveoli. So it also keeps the rate of inflation constant over all alveoli.
Role of alveolar type 1 and type 2 cells
Type 1 : form the alveoli air fluid interface Type 2 : produces surfactant and maintains cells.
Inspiratory muscle obligate
Diaphragm Scalenes External intercostal Parasternal intercostal muscles
Expiratory muscles
Internal intercostal muscle External and internal oblique muscles Rectum abdominis Transversus abdominis
Components of surfactant
Phospholipids and surfactant proteins
FEV1 vs FVC
FEV1: forced expiratory volume in 1 sec FVC: Forced vital capacity (total amount of air released)
Effect of obstructive and restricitve lung disease on FEV1 and FVC
Water vapour pressure in the lungs
6.3 kPa
Difference between O2 and CO2 diffusing across air fluid interface
CO2 diffuses at 85% the rate of O2, CO2 is much more soluble than O2 so it equals out.
Factors influencing diffusion of gases across interface
Membrane thickness and area.
Max oxygen capacity of blood
300 ml/ L
Why a right to left shunt is dangerous for oxygen partial pressure
Because a right to left shunt causes a decrease in O2 content which causes a large decrease in partial pressure.
Explain why arterial PaCO2 is often normal or low with right to left shunts and VA/Q mismatching
In right to left shunt, increase in ventilation due to low O2 but this just further decreases CO2 content and does nothing about O2 because there is a shunt anyways.
Define a shunt
Blood does not get ventilated
Why is the pO2 in blood after ventilation not exactly equal to Avleolar pO2?
Because of natural left to right shunts
Explain how hypoxic vasoconstriction helps reduce VA/Qmismatch
Vessels in areas of poor ventilation constrict, increasing the blood flow to better ventilated areas.
List the causes of arterial hypoxia and explain how each is likely to affect arterial PaCO2.
Causes: Low inspired pO2 (e.g. altitude)
Hypoventilating: causes low O2 and only one that causes high CO2 (e.g. overdose)
Diffusion imparement: difficulty of gas exchange (e.g. pulmunary oedema)
Right to left shunt (in lung or heart)
Ventilation perfusion mismatch (e.g. emphysema)
ALL others can blow off that pCO2 except hypoventilation
Main CNS control of ventilation and location
Pre Botzinger complex (medulla)
Main role of pons and medulla and what information they collect
Effect of ventilation on increased CO2
Effect of pH on ventilation
Acidosis: ventilation is much higher even at low doses of PCO2
Alkalosis: Ventilation is much lower even at high doses of pCO2
Location of peripheral chemoreceptors
Aortic arch and biffurcation of common carotid artery
Role of central chemoreceptors
Monitor CSF pH
What is peripheral and central cyanosis
Peripheral cyanosis: reduced blood flow in a region leading to bleuish tint in periphery.
Central cyanosis: hypoxaemia in arteries, so low oxygen overall
3 ways carbon dioxide is transported in the blood
- dissolved in the blood
- carbamino compounds
- In RBC by becoming bicarbonate aided by enxyme carbonic anhydrase. Bicarbonate leaves RBC and enters it again for reverse reaction at the lungs.
Haldane effect
At any given pCO2, the amount of CO2 carried by blood will be higher because deox blood is more able to take CO2.
How much CO2 is added to about 100ml of blood
4ml
