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Ventilation
- getting air from the atmosphere INTO the alveoli
- aka transport of gas from the atmosphere to the alveolar surface
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Blood Samples from Different Sites
- a arterial
- c capillary
- v venous
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Variables Often Measured:
- P pressure
- V volume (gas)
- Q volume (blood)
- C content
- F fractional concentration
- S saturation
- eg. PaO2 = partial pressure of O2 in arterial blood
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Sites Where Gases are Measured
- A alveolar
- I inspired
- D dead space
- E expired
- T tidal
- eg. VA = alveolar ventilation (volume of air/gas flow per unit time)
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Dalton’s Law of Partial Pressures
- the total pressure (Ptotal) exerted by a mixture of gasses is the sum of the partial pressures (P1, P2, etc) exerted independently by each gas in
- the mixture
- Ptotal = P1 + P2 + P3 + ...
- the pressure of e/a gas contributes proportionally to its relative amount (if P1 = 25% of the total gas in a mixture, then P1 = Ptotal x 0.25)
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Atmosphere
- a mixture of gases: chiefly nitrogen, oxygen, water vapor, & carbon dioxide
- total pressure is the sum of e/a pressure contribution from the components of the mixture
- CO2 in atmosphere is actually low (doesn't take much of it to have adverse effects)
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Using that chart, how would we get the partial pressure of each of these gasses?
multiply it's percentage (eg. 20.9 for O2) by the TOTAL pressure (760 mmHg)
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DRY Atmospheric Air
- is ~79% nitrogen & 21% oxygen →
- PN2 = 597 mmHg & PO2 = 159 mmHg
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What happens as we breath air IN?
- it passes over nasal turbinate → through the sinuses
- by the time it arrives in the trachea (then called tracheal or inspired air), the air has been HUMIDIFIED, PH2O = 47 mmHg (dilutes other gases)
- do this so air sent down to alveoli doesn't dry them out
- air is also warmed to body temperature at this point
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Why do the partial pressures of the other components of air decrease when the partial pressure of water vapor (PH2O) increases at the trachea?
- b/c that increase in PH2O to 47 mmHg DILUTES the other components
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*How to calculate Tracheal PO2:
- PO2 (tracheal) = PIO2 (inspired)
- = (Ptotal - PH2O) x 0.21
- atmospheric air - water component * .21 (b/c the partial pressure of O2 = 20.9)
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Alveolar Air
- is FURTHER modified by the diffusion of O2 into the blood & CO2 from the blood into the alveoli
- O2 & CO2 numbers are CONSTANT
- PO2: 104 mmHg*
- PCO2: 40 mmHg*
- (eg. during exercise, you don't get TIRED from alveolar PO2 dropping)
- these values are only changes in disease
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Partial PO2 & PCO2 Throughout Respiratory System
- blood comes into alveolar capillary from the R side of the heart DEoxygenated: has low O2 (40) & elevated CO2 (46)
- passing through the capillaries O2 is picked up in exchange for CO2 - diffuse down their CONCENTRATION gradients
- blood leaving capillary has high O2 (100) & lower CO2 (40)
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Why is the PO2 of blood leaving alveolar capillaries slightly lower & not equal to the PO2 of air in the alveoli themselves?
- alveolar PO2: 105 mmHg
- blood exiting caps. PO2: 100 mmHg
- b/c the blood returning to the L atrium has some contribution from the venous blood of the BRONCHIOLE circulation - it has not been oxygenated in the lung
- the addition of bronchiole venous blood to this blood lowers the PO2
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Partial PO2 & PCO2 Throughout Systemic Circulatory System
- systemic artery PO2: 100 mmHg
- systemic artery PCO2: 40 mmHg
- average cell PO2 < 40 (mt PO2 < 5!)
- average cell PCO2 > 46
- these are STEADY STATE VALUES
- as blood passes through capillaries surrounding normal cells, it emerges on the other side as venous blood (PO2 40, PCO2 46)
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What type of blood is in pulmonary arteries & what type is in pulmonary veins?
- VENOUS blood flows through pulmonary arteries
- ARTERIAL blood flows through pulmonary veins
- it's the PO2/PCO2 composition that determines the TYPE of blood
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Minute Ventilation
- measured in (mL/min)
- is defined as:
- respiratory rate (breaths/min) * tidal volume (mL/breath)
- [conceptually analogous to C.O.; product of a rate * a volume]
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Tidal Volume
amount of air you breath in & out in one breath
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Minute Ventilation Typical Value
- respiratory rate * tidal volume
- respiratory rate at rest: ~12 breaths/min
- tidal volume: ~ 500 mL/breath
- = 12 bpm * 500 mLpb = 6000 mL/min (6 L/min)
- this is the typical amount of ventilation we supply our lungs w/
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How much of the air we inhale gets to the alveoli?
- NOT ALL OF IT
- about 150 mL of inspired air DOESN'T reach the alveoli - it fills the conducting airways/bronchial tree
- it fills Anatomic Dead Space, aka where NO gas exchange occurs
- of the 500 mL tidal volume, only ~350 mL reaches the alveoli
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Alveolar Ventilation (VA) Contributing to Gas Exchange
- 12 bpm * 350 mLpb = 4200 mL/min (4.2 L/min)
- (breaths per min) (mL per breath)
- as opposed to the 6000 mL/min calculated using the entire tidal volume
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Total Alveolar Ventilation
- the tidal volume & alveolar ventilation are equal, but the air entering the alveoli contains the DEAD SPACE GAS from a previous breath + newly inspired air
- the air derived from the anatomic dead space does NOT contribute to gas exchange ("wasted")
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Anatomic Dead Space
- @ end of expiration ~150 mL of used up alveolar gas sits in airways
- in next inspiration, 500 mL (tidal volume) of gas is inhaled
- sitting airways gas is returned to alveoli + ~350 mL of fresh air!
- the last 150 mL of inhaled gas sits in conducting airways & is exhaled in the NEXT breath w/o change
- 150 mL of inspired air filling conducting airways ~ filling anatomic dead space
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Fowler N2 Washout Method
- an experiment that measures the anatomic dead space
- subject breathes pure 100% oxygen, then expires into a rapid nitrogen gas analyzer (analyzes N2 in expired air)
- 1st air blown out = pure O2 (N2 content will be 0)
- N2 concentration rises as the dead space gas is washed out by alveolar gas
- pure alveolar gas is indicated by a CONSTANT level of N2
- dead space volume is determined from a vertical line drawn such that areas A & B are equal
- dotted line ~1.5 L aka 150 mL (corresponds to anatomic dead space)
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Respiratory (Alveolar) Dead Space
- results from alveoli that are ventilated but NOT perfused (gas entering such alveoli does NOT exchange w/ blood - same thing as in airways)
- healthy lungs have a very small amount of alveolar dead space
- it can be significant in pathologies such as Pulmonary Embolism
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How would one potentially calculate the Alveolar (physiological) Dead Space (VD)?
- can do so if you know alveolar CO2 (PACO2) & expired CO2 (PECO2) & use this eqn
- VD/VE = (PACO2- PECO2) / PACO2
- VE = volume of expired air
- *won't ask about on test
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VD/VE
- the proportion of dead space in each breath
- actual values:
- VD/VE = (40-28) / 40 = 0.3
- ~30% in this case
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Alveolar Ventilation (VA)
- the flow of air into alveoli taking part in gas exchange
- of the 500 mL tidal volume, only ~350 mL of fresh air reaches the alveoli per resting breath, assuming NO alveolar dead space in a healthy individual
- therefore VA = resp rate * (tidal vol - anatomic dead space vol)
- VA = 12 bpm * 350 mLpb = 4200 mL/min
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What must alveolar ventilation be adequate for?
- the removal of CO2 produced by cellular metabolism
- otherwise alveolar PCO2 & PACO2, will rise.
- therefore PACO2 at any point reflects the balance between CO2 production & removal by ventilation
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PACO2 ~ VCO2 / VA
- means alveolar PACO2 is proportional to the rate at which you produce CO2 by metabolism divided by alveolar ventilation
- VCO2: the rate at of metabolic CO2 production
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What will happen if alveolar ventilation fails (decreases)?
- alveolar CO2 (PACO2) will increase [based on the above relationship]
- this is what happens when certain disease processes negatively affect (suppress) alveolar ventilation
- high VCO2 (eg. in hyperthyroidism → elevated metabolic rate) will also result in ↑ PACO2
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What value can be used to ESTIMATE alveolar ventilation (VA)?
- PaCO2: arterial CO2 (~ 40 mmHg)
- clinically, the partial pressures of CO2 in alveoli & arterial blood are assumed to be equal
- the partial pressures of CO2 in arterial blood is easier to measure therefore is used to estimate PACO2
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What is another equation that can be used to calculate VA?
- VA = 0.863 * (VCO2 / PACO2)
- VA = 0.863 * (200 / 40) = 4.3 L/min (almost 4.2!)
- a change in PACO2 produces a compensatory change in VA
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What is 0.863 in the equation VA = 0.863 * (VCO2 / PACO2)?
a proportionality constant that corrects for differences in the conditions for measuring VA, VCO2, & PACO2
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top: decrease breathing rate increase breathing rate → ↑ alveolar CO2 (doubles! - morphine)
middle: normal PACO2 (40 mmHg)
bottom: increase breathing rate → ↓ alveolar CO2
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What is the MOST important factor affecting air flow?
- an airway's RADIUS - a decrease of only 5% in bronchial radius reduces airflow by 20% (b/c there's an ↑ in Resistance)
- remember, Flow = ΔPπr4 / 8ηL
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What is the total cross-sectional area of terminal versus initial airways?
- terminal airways have the LARGEST cross-sectional area
- this results in a DECREASE in airflow velocity
- the greatest resistance is actually in airways > 2 mm in diameter
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Types of Air Flow
- laminar in straight sections of the bronchial tree but turbulent at branch points, where eddies occur
- laminar can also become turbulent at high velocities of airflow (rapid breathing)
- Transitional Flow: alternation between laminar and turbulent flows
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What do Transitional & Turbulent flow require that Laminar DOESN'T for the same airflow?
a larger ΔP
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What might happen to unsupported airways during expiration?
- they may collapse, particularly w/ increased intrapleural pressures during FORCED expiration
- small airways have no cartilage supporting their walls (only larger bronchi & bronchioles have cartilage supporting their branching)
- they're easily distended or compressed as the lungs inflate & deflate
- the distension during inspiration REDUCES resistance
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What do parasympathetic cholinergic stimulation & sympathetic adrenergic stimulation cause?
- PSNS: bronchoconstriction
- SNS: bronchodilation
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What agents cause bronchoconstriction?
1. chemical irritants (eg. ammonia, smoke, dust) - cause a reflex constriction involving neuropeptides (substance P)
2. immediate hypersensitivity response (histamine mediated)
3. inflammatory mediators: arachidonic acid metabolites (prostaglandins & leukotrienes)
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What are the results of bronchoconstriction (& inflammation)?
- reduce radius
- increase resistance
- limit airflow
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How can we measure the volumes of air we breath in & out?
- using open-circuit Spirometry
- basically have an inverted drum in a volume of water
- person holds a tube in their mouth that passes through fluid into the air in the drum
- inspiration: drum goes down
- expiration: drum goes up
- hooked up to pulley system that draws a picture of that breathing
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Spirometer
- FRC: functional residual capacity
- RV: residual volume
- TLC: total lung capacity
- VC: vital capacity
- VT: tidal volume
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Graph of Lung Volume v. Time
- 1st part: normal resting breathing; change in vol. = 500 mL
- 1st dip: occurs when person's instructed to blow out all the air they can (~1 L); called the Expiratory Reserve Volume
- 1st peak: difference between normal inspiration & maximum inspiration = Inspiratory Reserve Volume
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What is it called when you move the maximum amount of air in & out voluntarily?
- Vital Capacity
- when you inhale maximally then exhale maximally
- in above graph, individual is moving ~5 L of air
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Functional Residual Capacity (FRC)
- amount of air left in the lung after a normal breath (inhale → exhale)
- FRC = Expiratory Reserve Volume + Residual Volume
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What is the one volume you can't measure directly using a spirometer?
- the Residual Volume (RV)
- even if you maximally expire, you can't expire the volume down to 0 [can't reduce lung volume to 0 - chest wall/thoracic cavity is too big]
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So how can Residual Volume (RV) be acquired?
- using the Helium Dilution Method
- know volume of spirometer
- can add He to it - know the amount of He in spirometer drum is drum vol * He concentration
- open spicket - person breathes in air from tube
- this is started at the end of a normal exhalation - meaning air in lung corresponds to Functional Residual Capacity
- person breathes in & out air that contains He
- this dilutes He into total volume
- total volume is not original (V1) + lung volume (V2)
- …solve for V2
- I don't know
- C1 * V1 = C2 * V2 = C2 * (V1 + FRC)
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