physiology ventilation

Question 1

inspiration, expiration
(4)
(what is it against-2)
when is the most work done?

Answer 1

Inspiration = muscle contracts 
most work is done in inspiration :
-Against lung elastane (lungs naturally want to recoil but we want to breathe in and increase v) 
-Against airway resistance 
expiration =should be passive

Question 2

what movements do the lungs do to increase volume ?

4

Answer 2

1-bucket handle movement x rib = increases in transverse dimension
2-Pump handle movement x rib = increases anterior-posterio dimension

Question 3

how do we measure residual volume?
what method do we use?
(4)

Answer 3

Helium dilution method
1- 1 vital capacity of air inhaled into the alveoli with concentrated He
2-Then the residual volume = residual volume + Helium after inhalation. He is now diluted
use c=n/v to calculate the volume of RV
He = inert, not taken up by blood or lost from alveoli

Question 4

what are the following volumes :
tidal volume 
inspiratory reserve volume 
expiratory reserve volume 
vital capacity 
total lung capacity 
Ventilation rate 

(6)

Answer 4

• Tidal volume = normal in/out
• Volume left after inspiration (reserve air , possibility to breathe in more air )
• Expiratory reserve volume = volume left after expiration (still possible to blow out)
• Residual volume = cant be blown out (He dilution method) = volume of air left after max exhalation
• Vital capacity = fully in –>fully out
• Total lung capacity =max vol of air fully in
• Ventilation rate = tidal volume x respiratory freq ( breaths per min )

Question 5

What is lung compliance ?

3

Answer 5

-measure of lungs ability to stretch and expand , increase in volume with increase in pressure

increase in lung volume /increase in distending pressure measured statically

Question 6

what is lung elastic recoil? (3)

Answer 6

1-Elastic recoil refers to the lung’s intrinsic tendency to deflate the following inflation.

2-amount of pressure needed to inflate the lung
increase in pressure/increase in Volume

(reciprocal of compliance )

Question 7

To breathe in what do we need
How do we achieve this?
(6)
3 main ways

Answer 7

Negative pressure compared to atmospheric pressure

We achieve this in different ways :
1- elasticity of lung=wants to recoil- visceral pleura pulled away from parietal pleura

2-Surface tension = tension at air surfactant interface , alveoli wants to collapse = visceral layer pulled away from parietal

3-Elasticity of chest wall =wants to push chest wall out = pulling parietal away from visceral

So what does all this do ?

• Increases pleural cavity space
• increase thoracic volume
• Using boyles law = volume increases so pressure decreases
• Negative pressure draws air in for inspiration

Question 8

what Is the process of inspiration in detail

3

Answer 8

1- external intercostals and diaphragm contract ( moves down )
-bucket handle and water pump notion of external intercostals
2- Thoracic cavity volume (think of it as mainly inter pleural pressure ) increase hence pressure decreases (-4mmHg–>-6mmhg during inspiration )

3-Intrapulmonary pressure (lungs) Ppul =0 mmHg
Volume increases so pressure decreases
inhalation Ppul =-1mmhg so air is drawn in !

Question 9

what are the airways ?

5

Answer 9

trachea PSCC
Bronchus PSCC
Bronchioles-simple columnar and simple cuboidal
Alveoli- squamous

Question 10

what is laminar and turbulent flow ?(4)

Answer 10

• laminar = straight and plane sailing =silent
• Turbulent = jagged flow =narrowed airways make this sound = vibrates the walls x airways = sound = wheeze and auscultation

Question 11

what factors increase airway resistance?
(10)

1- where is it highest?
2-what factors affect AWR? think about tubes and maths
3-outline action of ACH
4-B2 Adrenaline actions

Answer 11

REMEMBER airway resistance is HIGHEST IN BRONCHUS ( radius of all bronchioles together is much larger than the radius of one bronchus!)

AWR = p/f ( flow is greater through bronchioles because the CSA is increased )
TOTAL RADIUS
LUMEN= does it have cilia or not
WALL= bronchial smooth muscle innervated by parasympathetic cholinergic Broncho CONSTRICTOR fibres:

1)Acetylcholie=muscarinic receptor = causes vasoconstriction as its G protein linked:
=G-protein is linked to inhibition x K+ current into cell = less positive celll = DEPOLARISES
=Ca2+ channels are opened by this = increases ca2+ levels inside cell as it diffuses in
=Ca2+ cause contraction = vasoconstriction
( Parasympathetic nerves =maintain the vascular tone )

Not many sympathetic receptors on the smooth muscle

2)B2 adrenergic receptor = + adrenaline = vasodilation
G-protein linked causes cAMP increases–>relaxes smooth muscle by inhibiting myosin light chain kinase enzyme

-mast cells= releases inflammatory mediators = vasoconstriction= increases AWR

3- OUTSIDE THE WALL =ELASTIC FIBERS =loss of elastic fibre = obstructive lung disease =emphysema

Question 12

explain the actions of the parasympathetic and nerves on the airways, how does the ACHe muscarinic receptor work?
(5)

Answer 12

WALL= bronchial smooth muscle innervated by parasympathetic cholinergic
Broncho CONSTRICTOR fibres:
Ache=muscarinic receptor = causes vasoconstriction as its G protein linked :
1-G-protein is linked Gq –>GTP–>activates phospholipase C (3rd letter in alphabet)–>IP3 (number 3 again ) + DAG = increase intracellular ca2+ ( from Endoplasmic reticulum ) = bronchoconstriction

2-PIP2= IP3, in this process ca2+ binds to calmodulin and produces an enzyme called Ca2+ calmodulin kinase, which causes myosin light chain kinase to be activated

3-DAG activates an enzyme called protein kinase C
both PKC + Ca2+ calmodulin kinase =phosphorylate proteins enzymes causing VASOCONSTRICTION
Parasympathetic nerves =maintain the vascular tone

Not many sympathetic receptors on the smooth muscle
B2 adrenergic receptor = + adrenaline = vasodilation

G-protein linked causes cAMP increases–>relaxes smooth muscle by inhibiting myosin light chain kinase enzyme
-mast cells= releases inflammatory mediators = vasoconstriction= increases AWR

Question 13

what is the mucocillary escalator?

2

Answer 13

• Goblet cells secrete mucous and ciliated cells waft mucous and pathogen back up trachea —> swallowed in stomach or coughed out !

Question 14

describe the defence action of alveolar macrophages ?

2

Answer 14

-ingest small inhaled particles resulting in the degradation, clearance and presentation of the antigen to adaptive immune cells=(APC)

Question 15

What is the airway resistance equation and what is it affected by -mainly?
(4)

Answer 15

1- FLOW= Pressure/ AWR
high awr= HIGHER alveolar pressure to maintain flow ! hence breathlessness
2- RADIUS = effects flow rate = link to poisieulle equation
flow = (pi x pressure x radius ^4 ) /8 x fluid viscosity x length of tube
- this means that increasing radius will increase flow dramatically (^4)
this explains why BRONCHI / BRONCHUS = highest resistance ! ie :2/5= 0.4 (awr=p/f)
Bronchioles = 2/10 = o.2 lower AWR because the CSA is much much greater !
hence we prescribe BRONCHOdilaters to overcome resistance to flow .

Question 16

treatments for breathlessness and lung disease = main three (3)

Answer 16

1) B2 agonists = increase vasodilation
2) Xanthines = inhibit phosphodiesterase so that cAMP is NOT cleared = cAMP levels remain HIGH = prolonged smooth muscle relaxation
3) Muscarinic antagonists = stop vasoconstriction

Question 17

what is pulmonary circulation and how does it differ from bronchial (systemic ) circulation
(4)

Answer 17

• Pulmonary circulation is from the RV of the heart = provides deoxygenated blood to lungs to become oxygenated and taken back to heart
• this circulation is low pressure to ensure fluids won’t move in capillary beds
• Hypoxic Pulmonary vasoconstriction =directs blood flow away from the area of low oxygen = OPPOSITE TO BRONCHIAL SYSTEMIC CIRCULATION
• systemic circulation dilates vessels + is also higher pressure

Question 18

what is bronchial circulation
(3)
systemic or pulmonary

Answer 18

-Systemic circulation to provide oxygenated blood to the airway wall = higher pressure
-Blood drains back into systemic veins BUT they drain near the pulmonary veins = venous mixture
=> venous shunt = slightly deoxygenated blood mixed with the oxygenated blood from the systemic circulation = lower o2 sat

Question 19

describe the diffusion across the alveolar -capllary membrane and what factors effect it
(3)

Answer 19

Diffusion is effected by :
1-short diffusion distance
2- good ventilation
3-good blood supply to maintain steep gradient
4-rate x diffusion = (pO2 /co2 grad x SA xSolubilty)/ Membrane thickness x root of Mr
- so it is effected by SA, solubility , gradient , thickness and Mr

Question 20

explain the effect of ventilation -perfusion mismatch

Answer 20

• for effective gas transfer the blood should flow to an area of good ventilation = v:Q ration where Q = flow
• dead space = ventilated but no GAS exchange takes place :
• wasted ventilation = increases work of breathing
• hypoxic Hypoxia with HYPOcapnia = not enough O2 or CO2
• when

Question 21

explain the effects of a physiological shunt and
-increased dead space
(2)

Answer 21

• SHUNT = mixes oxygenated blood from a pulmonary vein with deoxygenated blood from air space or bronchial systemic artery (Deox)
  the pulmonary vein has lower oxygen sat now ( giving 100% O2 will help Lung BRANCH ox sat =100% , but the SHUNT will remain low O2 sat so mean ox sat will only rise a little = not useful )

-DEAD SPACE = no gas exchange = work of breathing is increased and the air can’t get out! no blood supply in dead space! = inhaling O2 won’t help here!
SHUNT AND DEAD SPACE ARE DIFFERENT!

Question 22

Is hypoxic Hypoxia due to impaired ventilation or impaired gas transfer
explain both scenarios
is o2 therapy safe ?

Answer 22

-impaired ventilation Hypoxic Hypoxia = hypoventilation = both PO2 AND pCO2 exchange impaired =HIGHER CO2 pressure /LOWER O2

O2 therapy is unsafe

Impaired gas transfer = VERY low PCO2, as oxygenation is impaired
Low O2
O2 therapy is safe
Hypocapnia occurs when alveolar ventilation is excessive relative to carbon dioxide production and usually results from hyperventilation due to hypoxia, acidosis or lung disease.

Question 23

what are the three main steps of gas transfer?

3

Answer 23

1-diffusion
2-reaction with blood ( O2 reacts with Hb , CO2 main reacts with H2O molecules )
3-matching ventilation to perfusion