Lectures 1-4.txt

• Anatomic structures
• Dynamics
• Epidemiology

• Pulmonary functions, arterial blood gas measurements
• Partial CO2 pressure should be around 40

• Diaphragm moves the chest wall and separates the thoracic and abdominal cavities
• High cervical fractures can affect the phrenic nerve. Whenever put needle into chest, need to go right above the rib, NOT right under rib.

• The diaphragm - sharply marginated domes
• Peripheral margins of the diaphragm define the

• “digital x-ray”
• Differentiation is much clearer, can clearly see ribs, spine, the canals, the xcapula, different muscle groups, etc.
• A lot better resolution and have a rapid way to scan

• Long volumes – static properties
• And flow volumes
• Performed with pulmonary function instruments, can also use a “body box”.
• Also look at how fast the air comes out of the lungs, with the most important test being FEV1

• 


• Lecture 2

• Lungs can’t collapse completely
• Breathe deeper
• Interaction btw the lungs and “chest wall” (intercostals, diaphragm, etc. ) determine the volumes

• Tidal volume: normal breathing
• Inspiratory Reserve Volume (IRV): What you can inspire past the tidal volume
• Expiratory reserve volume (ERV): Maximum you can breathe out past tidal end expiration
• Residual Volume: still have an amount of air remaining after breathing out down to ERV.

IRV+TV+ERV+RV

• Amount at the maximum inspiration which you can blow out.
• IRV+TV+ERV

• Amount of air in lungs at the end of the normal tidal breath
• ERV+RV

• What you can breathe in at the end of a normal breath
• TV+IRV

• Pulmonary fibrosis
• Muscle weakness
• Chest wall deformity
• Lung surgery – pneumonectomy

Negative pressure is generated

Muscles relax, the balloon of the lung recoils

• Moving air from mouth, to the alveolus, etc. with no effort
• Need to work efficiently
• Airways are a branching system
• The active cross sectional area of the lung effectively increases as you go from trachea to the alveoli
• So effective resistance is a lot lower because have many more numbers of smaller ducts, but with a lot of a greater area (cross sectional area of alveoli size of a tennis court)

• Flow = Driving pressure/airway resistance
• P/R

• Try to get maximum driving pressure
• Flow inversely related to resistance
• If flow id decreased over time, infer that resistance is increased

• Maximum inspiration
• Maximum effort forced expiration
• The total expired volume is FVC

• Expressed as absolute value and as percent of predicted value
• Expressed as percent of the FVC: FEV1/FVC %

• Normal: >/= 75% most; >/= 70 in pts >50 y.o.
• Abnormal: < 70% - Obstructive pattern – increased airway resistance
• Lower the value, greater the resistance

• Average flow over midrange of FVC
• Divide FVC into 4 parts
• Draw line 25% exhaled to 75% exhaled
• Slope of line (chord is average flow over midrange of FVC

• Obstruction
• Declines linearly as disease worsens
• Mortality increases as value worsens
• Useful in predicting response to therapy
• Predicts likelihood of surgical complications

Flow-volume loops, etc.

• Correlates well with FEV1 so can use it as surrogate
• And in disease it can be measured at home and be used for management of disease at home as well.
• Peak flow, is measured during expiration

• Measure rate of transfer of gas from lungs to blood
• Use carbon monoxide (small amount – 0.3%)
• Avidly taken up and bound by hemoglobin
• So in the alveolus gets quickly across the membrane

• Measure amnt of CO taken up during breath – hold
• Estimate pressure of CO in the alveolus across the membrane
• Diffusing capacity (DLco) is amount of CO taken up by blood divided by the driving pressure

• 1)Delivery of CO to alveolar-capillary membrane: need normal capillaries and need normal SA for diffusion
• 2)Ability of CO to cross the alveolar-capillary membrane: diffusion depends in part on thickness.
• 3)Reaction rate: depending on the concentration/function of Hb

• Interstitial lung diseases: loss of SA / ? thickness of membrane
• Emphysema:
• Etc.

• Reproducibility
• Testing standards
• Predicted values – what compared to?
• Factors make PFTs unique

• Vital capacity, FEV1: 2-5% variation on repeated testing
• Diurnal variation: Lowest in early morning (3-6am)
• Response to bronchodilators: At least twice expected variations; at least a 12% of dilation in response to be sure that it’s not just part of normal variation

• Americal Thoracic Society Guidelines
• No real quality controls
• “Hope that PFTs are done correctly”

• Mexican-Americans – lower VC & FEV1 than age-matched Caucasians BUT same if compare height
• African-Americans – lower VC & FEV1 than age-matched Caucasians: Smaller trunk:leg ratio than Caucasians

Because don’t have good normals for certain different populations, the normal range

• Quantitative PFTs in those known to have disease
• Predict morbidity and mortality
• Follow course of disease and response
• BUT have limited function because of low reproducibility and because of the predicted values based on limited populations

Breathe into an air space where some is filled with water the level of which is allowed to lower when you breathe into the air space

• TLC = IRV + TV + ERV + RV
• VC = IRV + TV + ERV
• FRC = ERV + RV
• IC = TV + IRV air in lungs at end of normal breath

• TV - Tidal volume
• IRC – Inspiratory residual capacity
• ERC – Expiratory residual capacity
• VC – Vital Capacity

• Those capacities that contain residual volume:
• RV
• Functional residual capacity (FRC)
• Vital Capacity

• A patient has a certain amnt of air in his/her lungs
• Helium distributed in the spirometer volume and tubing, remove the block, and let person breathe back and forth and let them equilibrate the helium
• Now the concentration of He is lower, and Volume has increased
• So since mass = concentration * volume, by conservation of mass, can calculate the change in the volume of helium
• Helium mixed throughout spiromoter V1. And lungs V2
• Helium has lower concentration now
• Mass of helium = C2*(V1+V2)
• C1*V1 = C2*(V1+V2)
• So V2 = [(C1-C2)*V]/C2

• Measure lung volume V1 at FRC ( at the end of a normal breath and let rebreathe)
• So with helum dilution measurement really measure FRC
• And measure the ERV and can then calculate the RV: RV=FRC-ERV

• Valsalva maneuver: expire against a closed glottis
• Muller maneuver: inspire against a closed glottis

• Inspire against a closed glottis
• Pressure in lungs lowered
• Volume of lungs expand

• Mass of gas in lungs hasn’t changed
• Initial pressure times initial volume = P1*V1=P2*(V1+deltaV)
• Can measure P1 and P2: Mouthpiece with closed shutter; measure pressure between mouth and closed shutter
• If we can measure change in volume, can calculate V1

RV=FRC-ERV

• As inspire against closed shutter, pressure in lungs decreases
• Small volume increase in thorax -- > compresses gas in box
• Box pressure rises
• Box calibrated so know change in volume from rise in box pressure

• Breathe in and out against a closed shutter at FRC
• Measure changes in pressure at mouth
• Measure pressure (volume) changes in box
• Calculate RV: RV=FRC-ERV

FRC in box – Thoracic Gas Volume (TGV)

• More accurate: Body Box is a lot faster, and can make many measurements in a short time and average
• Body Box measures “true volume of gas in thorax at FRC”
• In severe obstructive disease may not reach true equilibrium with He dilution – the blocked areas may not equilibrate with the rest of He in lungs
• In Body Box can also measure flow and get the volume by integrating the flow over time

• Lung volumes determined by mechanical properties of respiratory tract as well as the chest wall
• It’s their elastic properties that directly determine the volume and breathing

• Size of lung
• Distending pressure: pressure inside lung minus pressure outside of lung
• To distend: P in lung(alveoli) > P outside of lung (pressure of pleural space)
• Plung = Palveoli – Ppleura
• Plung = Pa-Ppl
• Lung Pressure volume curve – increases from minimum volume and goes flattening out to a maximum volume
• Lungs act as a balloon

Lung collapses to 5-10% of maximum volume

• Compliance: = Change in volume / change in pressure
• C = delta V / delta P

• The volume at any given pressure is larger on deflation than inflation
• At any given volume, pressure larger on inflation than deflation
• Surfactant gives lungs this property, surface tension at the interface

• Lowers surface tension
• Surface tension changes as a function of area (volume of alveolus): greater effect at lower volume
• Surface tension lower with deflation than inflation

• When inspire all the way, molecules are spread out
• When expire, all surfactant molecules move closer together, and they lower surface tension
• Some of the molecules will form micelles because in expiration they com so very close together and will no longer be at the air-alveolar interface, and therefore as you inspire, they won’t be available to lower the surface tension as much as in expiration. But as inspire, you recruit more and more surfactant from micells and then get back to a regular surfactant spreading over alveolar surface

• Start at maximum inflation
• Molecules compressed on deflation
• Molecules form micelles and leave surface as deflation ends
• On inflation, new surfactant spread on surface
• Near maximum inflation molecules spread out and lose some effect

• Allows small and large alveoli to co-exist at same pressure
• Without surfactant, small alveoli would have higher pressure and empty into large alveoli, and would end up with less surface area for exchange of gases
• In smaller alveoli, surfactant will have a greater surface tension lowering effect
• Lecture 4: Ventilation
• Variables
• Volume V
• Concentration C
• Gas Fraction F
• Pressure P
• Remember wheras pressures can be different and can have pressure gradient, with no partial pressure gradient. For diffusion, need a gradient of partial pressure!

• Inspired – I
• Expired E
• Alveolar A
• Tidal T
• Dead space D – where there is no functioning gas exchange
• a = arterial
• v = venous

The sum of all partial pressures will equal the total pressure

P N2 is effectively zero in inspired air

• Under normal conditions you waste about 1/3 of your breath
• Doesn’t change much – it does expand during exercise, but not by much

The tidal volume increases tremendously, so wasted volume is only about 1/10 th of inspired gas

Dead space at normal conditions = ~ 1ml/lb ideal body weight

• Anatomic + Alveolar
• Alveolar dead space doesn’t occur much
• BUT can supply ventilation in excess of what can be accommodated by the blood supply, then, effectively have increased volume that is wasted, because of effective dead space in the alveolus: this can lead to as much as 2/3 of Vt to be wasted

With greater area, almost no resistance to air flow, so in alveoli with VERY SMALL area, the air velocity is very very low, so the diffusion will happen faster than convective air flow. So when auscultate – can’t hear the air in alveoli

• Put out the same CO2 as take in O2
• Means that the Inspired oxygen will be equal to the Partial oxygen in alveoli + Partial pressure of alveolar CO2

• R is slightly less than 1
• So the Alveolar oxygen is = inspired oxygen – alveolar CO2/ R

• P AO2 = 148 – 1.2(P ACO2)
• P AO2 = P iO2 – 1.2(P ACO2)

Look at P co2

O2 terribly insoluble in aqueous solution, so need Hb! Which provides the vast amount of O2 transport

• Because it’s a tetramer, and as you bind each oxygen, O2 affinity changes
• The vast amount of O2 is bound to Hb, and reach maximum at about 100 mmHg of PO2, so don’t really need to go higher than that because the only thing that will increase is the dissolved oxygen at that point

• The heart – takes out the most O2, about 1/3 total
• But, heart can’t use up all, because need to leave some for the muscle as well.
• Can take out a lot of O2 with not a huge change in PO2 because the curve is pretty steep

Curve can shift to the right or to the left depending on Hb affinity to O2

Oxygen content x 100 / Maximum Oxygen content

• Increased PO2 required to reach P50
• Increased H+ (decreased pH)
• Increased CO2
• Increased 2,3-DPG
• Increased Temperature – though not a very important factor normally

• Decreased H+
• Decreased CO2
• Decreased 2,3-DPG
• Decreased temp – worry about only in severe hypothermia

So will take a higher concentration of O2 to change the conformation of Hb

• so will have less affinity for O2
• And will need a higher O2 concentration

• Major effect of Bohr effect: Prevents shift in pH as we go from arterial to venous blood
• This change called Oxylabile change
• So Hb will have some buffering ability for H+, can accommodate a change of about 8% in pH

• If different alveoli oxygenate blood to their respective PO2, will later mix blood, and can’t get any more O2 into blood.
• This means that you switch from PO2 being the independent variable, to another independent variable

• 1.Diffusion of O2 from alveoli into plasma: Barrier thickness, Alveolar-capillary surface area, Partial pressure difference, Solubility of O2 in membrane ….diffusion will also be time-limited – the time that the air stays in the alveoli
• 2.Simultaneous combination of O2 with Hb and diffusion inside the RBC

• 1.Dissolved CO2
• 2.Bicarbonate
• 3.Carbamate
• 4.Haldane effect

• 1.Oxylabile carbamate formation
• 2.Oxylabile buffering of H+ by Hb
• About 40% of the O2 is excreted in the lungs because you shift from one curve to the other.

• BUT the carbonic anhydrase that converts H2CO3 into CO2 and H2O and allows diffusion to occure (over msecs)
• Also have transmembrane exchange of bicarbonate and chloride (carbonate is pumped into cell, where carbonic anhydrace converts it to O2 and H2O

• Oxylabile release of CO2 bound as carbamates
• Oxylabile buffering of hemoglobin:
• H+ used in HCO3- reaction
• H+ used in carbamate reaction