Respiratory #5-7 Flashcards
What is efficiency of ventilation dependent on?
Depends on the ratio of tidal volume to dead space
Usual ratio ~ 3:1 (Vt/Vd)
At low ratios, big changes in Ve and needed to change Va because a big portion goes to the alveolar dead space
How does posture affect lung volumes?
What are the % of TLC for FRC and RV?
Standing:
FRC ~ 55% of standing TLC
RV ~ 20% of standing TLC
Sitting:
FRC goes down a bit
4 pattes:
a little higher standing FRC (maximal value)
Supine (lying):
The abdomen pushed up and compresses the lungs
FRC ~ 32% of standing TLC → when diaphragm is relaxed at the end of quiet breath, organs in abdomen move upwards
RV goes dow 2% compared to standing (because of increase in blood volume and abdominal cavity, but minimal
TLC ~ 90% of standing TLC → net volume of the heart changes so less space for lungs (shift in blood volume from periphery to heart)
*Can still recruit you muscles maximally
How do lung volumes change from seated to suping in obese and non-obese subjects?
*Disadvantegous for work of breathing, also as all ariways availablity of all airways to be open to receive air (shunts)
In obese subjects:
TLC goes down a lot more from seated to supine, is also ~90% of capacity (normal ~ 100%)
ERV (between FRC and RV) doesn’t changes (normally goes to for non-obese subjects) → because obese subjects are already breathing close to RV ~ 45% of TLC instead of ~60% when standing
RV doesn’t change but is greater ~ 30% (non-obese ~ 22%)
How does the transpulmonary pressures and volumes differ from apex to base of the lungs at different lung volumes?
- The absolute gradient of pressure it the same from apex to bas of lungs at all stages and volume*
(volumes in % of TLC)
(pressure top lower → bottom higher)
At TLC → not much difference between apex and base, both at ~ 100% of lung volume (-40 → -33 cm H2O)
At FRC → Apex ~ 70%, Base ~ 25% (biggest gradient in volume because steep part of the curve) (-7.5 → -0.5 cm H2O)
At RV → Apex ~ 40%, Base ~ 20% (plateau) (-2.2 → + 4.8 cm H2O)
How does regional lung expansion differ?
At TLC → homogenous inflation of alveoli
At FRC → top more inflated than bottom
At RV → In upper half, same as FRC (top more inflated than bottoms), in lower half → homogeneously inflated ~ 20% of TLC because significant number airways are closed which fixes volumes of that regions
Explain the results of the single breath nitrogen washout.
- Single breath of pure O2 from RV → TLC (~5L)
- Measure concentration of N2 during slow expiration
*Last gas in = 1st gas out
Start of expiration → concentration of N2 increases rapidly as air from the dead space comes out first (low N2) than air from respiratory zones starts to come out
Form 4L to 1L → constant concentration of N2 with little waves (heart beating causes changes in gas exchange?)
From 1L to RV → Gradual closing of the airways in lower zones first → more contributions of nitrogen from upper zones (upper zones have more N concentration because they didn’t get 100% new O2 as they started a bit more inflated)
What happens to subjects with chronic obstructive lung disease when they take the single breath nitrogen washout test?
- Increased slope in phase that is constant for normaly subjects (phase III) → heterogeneity of lung subunit emptying (and filling)
- Also plateau phase starts at higher N2 point as lungs are not as well oxygenated (higher RV)
*With bronchodilator → slight decrease in phase 3 slope, but not to normal
What is Starling’s equation for fluid flux?
Fluid flux = filtration coeff X * (vascular pressure - oncotic pressure)
*Flux between alveolar compartement and pulmonary capillaries for diffusion
What are the mechanical determinants of pulmonary vascular resistance (equation for PVR)?
PVR = (Pa - Pv)/Q
- Varies depending on pressure in vessels
- On lung volume
Passive way to reduce PVR → Recruitement and Distention
Important to maintain low PVR to prevent pulmonary EDEMA
- What is the effect of lung volume on pulmonary vascular resistance?
- What is the effect of vascular pressure on PVR?
PVR = (Pa - Pv)/Q
1. At RV → extra-alveolar vessels reponsible for high PVR (corner vessels are squeezed)
At FRC → lowest PVR
At TLC → alveolar vessels responsible for high PVR (alveoli being stretched → increased resistance in capillary bed)
- PVR depends on pressure within vessels
- Increase in arterial pressure → very significant decline in PVR
- Increase in venous pressure (blood returning to the heart for greater preload) → much smaller decrease in PVR than Pa
Passive influences on PVR → recruitement and distention of vessels
What are the differences in capillary density and inflation between upper and lower zones of the lungs?
Upper zones → more inflated, less capillaries
Lower zones → more deflated at every expiration, more capillaries
What determines the flow through the alveolar capillary?
How does perfusion change in different lung zones?
Gradient of pressure through Arterial and venous capillaries has to be greater than alveolar pressure
At apex of the lungs → collapse of capillaries (Palv»_space; Part → not blood flow)
Line between zone1 and zone2 → Part = Palv
Zone 2 → waterfall → intermittant flow
Line between zone2 and zone3 → Pven = Palv
Zone 3 → distension of capillaries → max perfusion
line between zone3 and zone4 = max blood flow
Zone 4 → interstitial pressure (high hydrostatic pressure within the vessels)
How can regional blood flow (1) and regional ventilation (2) in the lungs be measured?
- By 133Xe injections in the blood → assess concentration in the lungs:
More in lower lung zones because more blood flow - Inspire 133Xe → assess concentration in the lungs:
More in lower zones are the ventilation in greater in lower zones
Measure by imaging of the lungs?
Where in the lungs is the V/Q ratio greatest?
At the top of the lungs → V/Q ratio greatest meaning more ventilation for the flow that comes by (even top is less ventilated than bottom)
*V/Q ratio is not just because of gravity as it is seen in mice and dogs
What are the time constants for filling and emptying of different lung units?
τ = RC (resistance * compliance)
τ = ~ 67% of the volume is expired (exponential curve)
V(t) = V0e^(-t/τ)
How does ventilation ratio (upper/lower) vary by flow rate?
Time constants for filling of different regions determine the dynamic distribution of ventilation
Always follows regional compliance but more or less depending on flow rate
At low flow rates (breathing slowly) → smaller ratio ~ 0.7 = upper/lower (more relative ventilation in lower part) (0 - 1.5 L/sec)
At higher flow rate (breathing fast) → ratio closer to 0.9 (upper/lower)
*The curve plateaus a bit from 1.5 → 5 L/sec
What is the pendelluft phenomenon
Unequal distribution of air in lung compartements
Movement between compartements during respiration cycle in heterogenous lungs (different time constants)
Contributes to uneven ventilation
At 0 flow (transition from inspiration to expiration) → Non-homogeneous inflation and deflation of different regions of the lung → pressure differences → gas moves from one region to the other → if bronco-constriction is present also, some lung regions may be exposed to high inflation pressure at end-inspiration → may rupture
*If one airway fill much faster than another one and forces air into the other one
What is the V/Q ratio in ideal situation, in physiological shunt or in physiological dead space?
Ideal situation → V/Q just over 1
Physiological shunt → there is flow, but the blood is not oxygenated → V/Q ~ 0
Physiological dead space → alveoli are ventilated, but not perfused → V/Q ~ infinite
At sea level, how does PO2 changes between inspired dry air, alveolar, arterial, venous?
Inspired dry air → 159 mm Hg (out of 760 mm Hg, rest is N2)
Alveolar → 104 mm Hg (water vapour is added, PCO2 ~ 40)
Arterial → 100 mm Hg
Venous → 40 mm Hg
*Always for a total of 760 mm Hg, N2 takes up the biggest portion
What are partial pressure of O2 and CO2 in the blood (arteries and veins) and in the alveoli?
Pulmonary artery: PO2 = 40, PCO2 = 45
Alveoli: PO2 = 100, PCO2 = 40
Pulmonary vein: PO2 = 100, PCO2 = 40
How do PO2 and PCO2 vary with changes in V/Q?
As V/Q increases → Alveolar PO2 increases
- V/Q ~ 0 → PO2 = mixed venous PO2
- V/Q ~ 100 → PO2 = inspired PO2
As V/Q increases → Alveolar PCO2 decreases
- V/Q < 1 → PCO2 = mixed venous PCO2
What are the normal values for the parameters of gas exchange (ventilation, perfusion, V/Q ratio) ?
Ventilation ~ 2.6 L/min
Perfusion ~ 3.0 L/min
V/Q ratio ~ 0.9
How can the diffusion capacity of O2 be measured across the lungs?
Replace O2 by CO → diffuse in similar manner and there is no appreciable build up of CO in the blood (because bound with very high affinity to Hb partial pressure never builds up in the blood) → no background noise, alv CO is the gradient
1. Breathe in (CO)
2. Hold breathe for x seconds
3. Breathe out → measure concentration
Done when suspect obstructive lung disease
*Hard to use find diffusion for O2 because of continuous change in partial pressure
Diffusion ~ A/T * K * (P1 - P2)
A = area, T = thickness, K = diffusion constant = solubility/sqrt(MW) , ∆P = gradient of partial pressures across the tissue
