Ventilation II

alveolar ventilation

can’t simply measure but can calculated if you measure dead space volume

total ventilation - dead space ventilation

but not easy to measure anatomic dead space, so use conc of CO2 in expired gas

because no gas exchange in anatomic dead space, there is no CO2 entering from anatomic space and all expired CO2 must come from alveolar gas

alveolar ventilation equation

(VCO2/PCO2) x K

or VCO2/FCO2

FCO2= fractional concentration, %CO2/100

VCO2= rate of CO2 production

what is FCO2 proportional to?

PCO2, which equals FCO2 x K

K= 863 mmHg

alveolar gases in ventilation

do not change much with quiet breathing

but changes in ventilation can significantly affect amount of O2 that reach alveoli

as VA increases, alveolar PO2 increases and PCO2 decreases (and vice versa)

what is normal ventilation rate?

4.2L/min

alveolar (or arterial) PCO2 as a function of alveolar ventilation

for a constant level of CO2 production, there is a hyperbolic relationship between PACO2 and alveolar ventilation

increases in VA cause decrease in PACO2

decreases in VA cause increase in PACO2

if CO2 production doubles (exercise), hyperbolic relationship shifts to right

• under these conditions, only way to maintain PACO2 at its normal value of 40 mmHg is for alveolar ventilation to double

regional differences in ventilation

not uniform

lower regions of lung ventilate better than upper regions

can be demonstrated when subject inhales radioactive Xenon gas (Xe-133)

radiation from Xe-133 penetrates chest wall and can be counted so the volume of inhaled Xe going to various regions can be determined

ventilation/unit volume is greatest near bottom and decreases as move up lung

measurements of FVR and FEV1 are

simple, informative

abnormal in many pts with lung disease

valuable in assessing progress of disease

valuable in assessing efficacy of bronchodilators

FEV1 and FRC in obstructive vs normal

FEV1 much lower

FVC lower but not as much

percent much lower

FEV1 and FRC in restrictive vs normal

FEV1 lower

FVC also lower

percent can be equal or higher due to ratio of these two 

obstructive lung disease

obstruction to airflow leading to increased resistance

can be inside lumen, in airway wall, in surrounding airway

obstructive airway disease examples

asthma

COPD-emphysema/chronic bronchitis

localized airway obstruction

restrictive lung disease

expansion of lung is somehow restricted

restrictive disease examples

diffuse interstitial pulmonary fibrosis

diseases of pleura-pneumothorax

diseases of chest wall- scoliosis

neuromuscular disorders

forced expiratory flow

flow of air coming out of the lungs during the middle part of a forced expiration maneuver 

simple model of factors that may reduce ventilatory capacity

relates lungs and thorax to simple air pump

output depends on stroke volume and the resistance

vital capacity or FVR is a measure of stroke volume so any decrease in VC will affect the ventilatory capacity

forced expiratory volume is affected by airway resistance during a forced expiration

diseases that decrease stroke volume

kyphoscoliosis

interstitial lung disease

poliomyelitis

muscular dystrophy

pleural disease

diseases that increase airway reistance

asthma

bronchitis

spirogram can determine

FVC, FEV1, FEV1/FVC ratio

FEF25-75

flow volume loop gives you

FVC

PEFR

expiratory flow rates

peak expiratory flow rate

maximal flow rate achieved during expiratory maneuver

flow-volume curves

subject inhales to TLC and exhales as hard as possible

flow increases rapidly to high value

declines over most of expiration

impossible to change downward portion of curve

something limits expiratory flow, so that flow rate is independent of effort and is a result of the dynamic compression of airways by intrathoracic pressure

limited by compression of airways by intrathoracic pressure

isovolume curves

gives relationship between respiratory flow rate and lung volume

as effort increases, peak expiratory flow increases

flow rates at lower lung volumes converge- termed effort independent and flow limited because maximal flow is achieved with modest effort and no amount of additional effort can increase flow rate beyond this

first 20% is effort dependent- increasing effort will increase flow rate

preinspiration pressures

airway pressure is 0

Pip -5

+5 holding airways open, no flow

during inspiration pressures

Pip and PA fall by 2, flow begins

because pressure drops along airway inside airways in -1, so +6 holding airway open

end inspiration pressures

no flow again, with 8+ transmural pressure holding airways open

forced expiration pressures

both Pip and PA increase much more than usual, here +38

because of pressure drop along airway, there is a pressure of -11 wanting to close the airways. compression occurs

pressure limiting low is the Pip, if increased more by increased muscular effort in an attempt to expel the air, still ineffective

flow independent of effort

dynamic compression of airways

when the airways collapse during a forced expiration, the flow rate is determined by the resistance of the airways up to the point of collapse

as lung volume decreases, airways narrow and resistance increases. therefore pressure is lost more rapidly and the collapsing point moves more distally

in late forced expiration, flow is determined by the properties of small, distal, peripheral airways

flow volume curves with obstructive disease

maximal expiration begins and ends at abnormally high lung volumes and flow rates are lower

curve may be scooped out

flow volume curves with restrictive disease

lung volumes lower

if flow rate normalized to lung volume, flow is higher than normal

dyspnea

sensation of difficulty in breathing, breathing becomes laboured, uncomfortable

subjective, so difficult to measure. often look at tolerance to exercise

dyspnea- increase demand for ventilation

usually caused by changes in blood gases and pH

high ventilations on exercise seen in patients with inefficient gas exchange (large physiological dead space) who develop CO2 retention and acidosis unless there is a high rate of ventilation

role of juxtacapillary (J) receptor stimulation in dysnpea

sensory nerve endings in alveolar walls next to pulmonary capillaries of lung

innervated by vagus nerve

respond to pulmonary edema

dyspena- reduced ability to respond to ventilatory needs

usually caused by problems in lung mechanics of problems with chest wall, eg increased resistance (asthma) or stiff chest wall (kyphoscoliosis)