Resp Physiology Flashcards
Conductive vs respiratory zone?
Conductive is site if respiratory passage (warms and humidifies air) carrying air to site of exchange
Respiratory zone is site of gas exchange with increased cross sectional area from resp bronchioles to alveolar ducts
3 functions of the pleura?
- Reduce friction
- create suction
- compartmentalization preventing spread of infection
What is boyles law?
Increase volume = decreased pressure and gas flows from high to low pressure so by increasing chest volume, you decrease pressure allowing for air to enter alveoli
What muscles are used for inspiration and expiration?
Inspiration - diaphragm, scalene, external intercostal muscles, SCM
Expiration - internal intercostals, int/ext oblique, transverse abdominus
What is the atmospheric and intrapleural pressures?
Atmospheric - 760mmHg
Intrapleural - 756mmHg
How does alveolar pressure change with inspiration and expiration?
Inspiration - increase thoracic cavity increases lung volume which decreases alveolar pressure to 758mmHg causing air to flow in
Expiration - decrease thoracic cavity and decrease lung volume so alveolar pressure increases to 763mmHg causing air to flow out
Outline the different volumes for a spirometry chart? M/F?
TV - 500mL
IRV - 3100/1900 inspiratory reserve volume
ERV - 1200/700
RV - 1200/1100
TLC - 6000/4200
VC - 4800/3100
IC - 3600/2400
FRC - 2400/1800
Normal minute ventilation and alveolar ventilation values?
Minute - 7.5L/min
Alveolar - 5.25L/min
What two factors create resistance to breathing?
Elastic recoil of lungs and chest wall (65%)
Non-elastic resistance to airflow (35%)
What is elastance?
Tendency to recoil after inflation with the first kick to get air out of the body and back to initial size. Must overcome
Chest - at greater than 80% total lung capacity, recoil directed inwards, at less than 50% TLC, elastance directed outwards
Lungs - at high volume, elastin fibres will overstrech and loose elasticity and at low volumes, lung wants to collapse to 0mmHg but surfactants stops it
What does surfactant do?
Lowers surface tension by reducing attractive forces of H binding to open alveoli from 0mmHg. A lack of surfactant created huge surface tension which requires high pressures to overcome it.
Produced by type 2 pneumocytes around week 34
What is compliance and what happens if its low or high?
Compliance is the ability to increase volume or the stretchability of pulmonary or thoracic tissue.
Low compliance = stiff lung which is hard to inflate to high volumes and extra work required eventually leading to fibrosis and decrease in pulmonary compliance
High compliance = floppy lung which is hard to deflate from high volumes due to elastic tissue damage seen in COPD/emphysema
Which size bronchi display most resistance due to turbulence?
Medium bronchi
What is mucosal resistance and 3 examples of causes?
Mucosal oedema from histamine release with increased permeability leading to transduction of fluid through intracellular gaps
1. Histamine from mast cells increased mucous secretions and viscocity
2. Chronic bronchitis increased mucous production by lungs clogging bronchioles
3. CF with CFTR mutation meaning Cl transporters cannot remove Cl, disrupting osmotic gradient leading to increased mucous and difficulty for mucocillary elevator
What controls bronchodilation and bronchoconstriction?
Bronchodilation - parasympathetic b2 aadrenergic receports with endocrine (adrenaline) major control. Has no sympathetic nerves so adrenaline in blood acts as endocrine with longer lasting effects
Bronchoconstriction - muscarinic cholinergic receptor activation and histamine H1 receptor action
Outline control of the bronchial reflex system?
Bronchial epithelium responds to noxious stimuli - reflex - Ach - muscarinic R - sm
1.Constriction when increase of Ach - inhalation smoke, dust, chemicals, low CO2, cold, PE
2. Dilation when decreased Ach - during inspiration, arterial HT (carotid sinus reflex)
How is a flow-volume plot changed due to restrictive lung disease and what are the causes?
Decreased lung capacity due to reduced compliance and increasing stiffness which limits expansion. Change in lung volume is major problem so same shape as original but less volume to right shift
Causes
-lobectomy
-abnormalities in surrounding tissue
-weak inspiratory muscles
How is a flow-volume plot changed due to obstructive lung disease and what are the causes?
increased resistance due to airway obstruction so reduced peak flow and larger volume as air can become trapped in lungs due to incomplete emptying
Causes - increased resistance to airflow
-abnormality within airway lumen (tumour, mucus)
- changes in wall (sm contraction, oedema)
-Decreased elastic recoil
What is henrys law?
When a mixture of gases comes in contact with a liquid, each gas will dissolve in proportion to its partial pressure (concentration)
What are the values of O2 and CO2 in atmosphere, in alveoli and in blood coming back from the body
- Atmosphere
O2 - 160mmHg
CO2 - 0mmgh - Alveoli
O2 - 100mmHg
CO2 - 40mmHg - Blood from body
O2 - 40mmHg
CO2 - 45mmHg
What does diffusion rate depend on? (4)
- SA
- Concentration gradient
- thickness of membrane
- Diffusion constant (CO2 22x more soluble than O2)
How long do RBC spend in pulmonary capillaries at rest?
0.8s so during exercise, blood rate is sped up and there is less time available tor each equilibrium
What is V/Q and what does it mean when its impaired?
V/Q is ratio of air reaching alveoli to the blood reaching alveoli
V = alveolar ventilation (air)
Q = perfusion (blood)
normal ratio is 4.2L air to 5L blood so 0.84
1. Decreased V/Q = impaired ventilation - shunt so blood flowing but no air reaching alveoli
Increased V/Q = impaired perfusion - dead space as normal air but no blood flowing
What are the regional differences of V/Q?
Hydrostatic pressure greater (Q) is greater lower in lungs so stringer flow at base of lungs
1. Apex of lung = higher V/Q = impaired perfusion so underperfused (3.3)
2. Base of lung = lower V/Q = impaired ventilation so underventilated (0.6)
Causes of high and low V/Q and how to adjust them?
High V/Q = impaired perfusion eg. PE, which is adjusted by O2 as high O2 causes vasodilation allowing more blood to lungs
Low V/Q = impaired ventilation eg. Bronchitis, asthma, pulmonary oedema, which is adjusted byCO2 and high CO2 causes bronchodilation allowing more CO2 to be flushed out
3 ways to transport CO2?
- Dissolved CO2 (7%) - in plasma, quick exchange
- Carbamino (20%) - CO2 combines with terminal amino groups on proteins
- Bicarbonate (70%) - slower exchange in plasma, faster in RBC
What is the Haldane effect?
Deoxygenated blood holds more CO2 so O2 loading causes CO2 unloading
What is the Bohr effect?
CO2 loading causes O2 unloading
What area of the brain controls the rhythm of ventilation and is mediated by what? (4)
Medullary respiration center
1. Chemoreceptor - central (medulla), peripheral (carotid, aortic)
2. Proprioceptors (resp muscles have spindles and GTO)
3. Upper and lower airway receptors
4. Higher centers (limbic and hypothalamus
What are the 5 respiratory centers and where are they?
Pons - pneumotaxis and apneustic centers
Medulla - Pre-botzinger, ventral and dorsal groups
What sets up tidal breathing and how is it controlled?
Rhythm set by pre-botzinger group which spontaneously discharges neurons initiating next cycle
DRG controls phrenic nerve by emitting repetitive bursts of APs
Where does DRG receive input from?
- Higher centers
- Pneumotaxic/apneustic determining stop point
- CNS and peripheral chemoreceptors
- Respiratory muscles
What controls forced inspiration?
Pre-botzinger inspiratory activates DRG (diaphragm) and VRG (external IC, SCM, pectoralis, scalene)
What controls forced expiration?
Pre-botzinger activated expiratory area only - VRG only (internal IC, int/ext obliques, abdominal
What does the apneustic center do?
Inhibits inspiratory switch off therefore prolonging inspiration meaning breathing in deeper/longer and reducing RR
What does pneumotaxic center do?
Inhibits apneustic therefore limiting inspiration to reduce inspirational breathing and increasing RR
2 areas of chemoreceptors regulating input to respiratory centers?
- Central - medullary CSF measuring CO2 and O2 as acids cannot cross BBB. Increase in CO2 in cerebral capillary - crosses BBB - dissociates to H in CSF - response in medulla as lowered pH reflects CO2 retention therefore ventilation is increased
- Peripheral - carotid and aortic measuring arterial blood O2. Glomus cells sensing hypoxaemia in ARTERIAL blood and when excited, cause resp centers to increase ventilation but must be a drop uder 60mmHg as normal control by CO2 sensors.
Pathway - low O2 in blood - K channel close in glomus cell - cell depolarize - Ca voltage gated channel opens - Ca entry - exocytosis of NT - AP - ventilation
What CN is sensory for carotid and aortic chemoreceptors?
Carotid - CN.IX glossopharyngeal
Aortic - CN.X vagus
How do higher brain centers control respiration?
Hypothalamic/limbic modifying rate/depth. Cortical controls directly from cerebral motor cortex that bypass medullary control causing voluntary breath holding (anger) or grasping with pain
How to upper airway receptors control respiration?
Vagal afferents sense flow, temp, pressure, muscle contraction and obstruction with pharyngeal/laryngeal receptors
How to lower airway receptors control respiration? (2)
- Myelinated pulm. receptors - slow adapting stretch, rapidly adapting or irritant in upper lobe. Mechanoirritant by tough or noxious substance causing cough, gasp or constriction
- Unmyelinated pulm. receptors - bronchial C fibres, juxtacapillary receptors in lower lobe. Stimulated by chemicals (capsaicin) with an airway defense of bronchoconstriction, tachypnoea and mucus. No cough as cough increases pressure and pushes id down further
What is the Hering-Breuer reflex?
Inflating reflex with stretch receptors in pleura and airway stimulated by lung inflation. This sends inhibitory signals to medullary resp centers to end inspiration and start expiration. More protective than normal responce
Outline the cough reflex?
Larynx, carina, trachea and bronchi sensitive to light tough so mechanoreceptors to sensory neuron to vagus to medulla to cough.
1. Inspire 2.5L air
2. Close epiglottis and shut vocal cords to trap air
3. Contract abdominal muscles/internal intercostals to create pressure
4. Open epiglottis and vocal cords
5. Air explodes out around 120-160km/h carrying out foreign material
