Ventilation I

ventilation

process by which air moves in and out of lungs

minute (total) ventilation

= tidal volume x frequency

tidal volume 

amount of air inhaled or exhaled in one breath during relaxed, quiet breathing

typically around 500 mL

varies by age, gender, body position, metabolic activity

eupnea

normal, quiet breathing

hyperpnea

increased respiratory rate and/or volume in response to increased metabolism (e.g. exercise)

hyperventilation

increased respiratory rate and/or volume without increase metabolism (e.g. emotional hyperventilation, blowing up a balloon)

hypoventilation

decreased alveolar ventilation (e.g. shallow breathing, asthma, restrictive lung diseases)

tachypnea

rapid breathing, usually increased respiratory rate with decreased depth (e.g. panting)

dyspnea

subjective feeling of difficulty in breathing or air hunger (e.g. various cardiopulmonary conditions)

apnea

cessation of breathing (e.g. voluntary breath-holding, depression of CNS control)

inspiratory reserve volume

amount of air in excess of tidal inspiration that can be inhaled with maximum effort

expiratory reserve volume

amount of air in excess of tidal expiration that can be exhaled with maximum effort

residual volume

amount of air remaining in lungs after maximum expiration; keeps alveoli inflated between breaths and mixes with fresh air on next inspiration

cannot be measured by spirometry

vital capacity

amount of air that can be exhaled with maximum effort after maximum inspiration 

ERV + TV + IRV

used to assess strength of thoracic muscles as well as pulmonary function

inspiratory capacity

maximum amount of air that can be inhaled after a normal tidal expiration

TV + IRV

functional residual capacity

amount of air remaining in lungs after a normal tidal expression

RV + ERV

cannot be measured with spirometry

total lung capacity

maximum amount of air the lungs can contain

RV + VC

cannot be measured with spirometry

respiratory volumes vary with

body size (all are larger in large people), age (all volumes smaller in children, in old age VC is decreased and RV increased because of degeneration of pulmonary tissue), sex (all volumes smaller in women), muscle training (increases all lung volumes and permits greater maximal ventilation during exercise), disease (changes from the normal values can be used in the diagnosis of pulmonary disease)

measurement of FRC by helium dilution

subject connected to spirometer containing a known concentration of helium, which is insoluble in blood

after several breaths, the [He] in spirometer and subject are the same

because no He lost, amount present before equilibration C1 x V1 is equal to the amount after equilibration C2 x (V1 + V2)

helium dilution equation

FRC= V1 x ((C1 - C2)/C2)

measurement of FRC by body plethysmography

subject sits in airtight box, at end of normal expiration, a shutter closes the mouthpiece and subject makes panting respiratory efforts

during expiratory effort, gas in lungs becomes compressed, lung volume decreases and pressure inside the box falls as the gas volume in the box increases

by knowing the volume of the box and measuring the change in pressure of the box, the change in the volume of the lung can be calculated

when the subject makes respiratory effort to inhale against a closed airways, they slightly increase the volume of their lungs, airway pressure decreases, and the pressure in the box is measured- lung volume obtained using boyle’s law

body plethysmography equation

P1 x V = P2 (V - delta V)

V=FRC

P1= pressure in box pre-respiratory effort

P2= pressure in box post-respiratory effort

what does body plethysmography measure?

the total volume of gas in the lung, including any trapped behind closed airways

what does helium dilution measure?

only ventilated lung volume (can be lower if person has obstructed airways)

anatomic dead space

volume of conducting airways, at FRC this is typically 100-200 mL

can be measured using Fowler’s method

physiological dead space

anatomical dead space plus ventilated, but not perfused, alveoli

volume of gas that does not eliminate CO2

can be estimated using Bohr’s method

increased in many lung diseases

alveolar ventilation

(Vt - Vd) x f

amount of fresh air getting into the alveoli and available for gas exchange

Fowler’s method

also called nitrogen washout

measures anatomic dead space

subject breathes through a valve box with a rapid nitrogen analyzer continuously sampling gas at the lips

single inspiration of 100% O2

N2 concentration is initially zero because the subkect is exhaling the dead space O2 they just breathed in

N2 concentration then rises as the dead space gas is increasingly washed out by alveolar gas

finally a uniform gas concentration is seen, called the alveolar plateau

dead space calculated by plotting N2 concentration against expired volume and drawing a vertical line so that area above the curve = area below the curve. dead space is the area expired up to the vertical line

single breath nitrogen test of uneven ventilation

four phases seen:

1. pure O2 exhaled from upper airways so N2 concentration is zero

2. N2 concentration rises rapidly as the anatomic dead space is washed out by alveolar gas

3. alveolar plateau consists of alveolar gas. flat in normal patients, but in pts with uneven ventilation, N2 conc steadily increases. slope of increase is a measure of the inequality of ventilation (expressed as % increase in [N2] per litre expired volume)

4. [N2] rises rapidly, as the most poorly ventilated airways empty, likely due to closure of small airways in the lowest part of the lung

CV= closing volume (when small airways start to collapse)

CV + RV = closing capacity

uneven ventilation

occurs in many pts with lung disease

an important factor contributing to impaired gas exchange

can be measured using the single breath N2 test

alveolar gas phase plateaus in normal subjects, but not in pts with this- here, slope rises steadily and is a measure of the inequality of this

reasons not fully understood, some regions of lung are ventilated poorly and tend to empty last

three proposed mechanisms of uneven ventilated

parallel, series, collateral

uneven ventilation- parallel mechanism

area is poorly ventilated due to partial obstruction

high resistance means area empties late

series mechanism- uneven ventilation

dilation of peripheral airspace causes differences of ventilation along the air passages of lung unit

if small airways are enlarged (emphysema), concentration of inspired gas in the most distal airways remains low

poorly ventilated areas empty last

collateral mechanism- uneven ventilation

some lung units receive inspired gas from neighbouring units rather than from large airways (COPD)

Bohr’s method

tidal volume is a mixture of gas from the anatomic dead space plus a contribution from alveolar gas

all of the expired CO2 comes from alveolar gas and none from anatomic dead space

this method allows for calculation of anatomic dead space

bohr’s equation

Vd = Vt x ((PaCO2 - PECO2)/PaCO2)

A and E refer to alveolar and mixed expired

lowercase a is arterial

what is the normal ratio between Vd and Vt?

0.2-0.35 when resting

assumptions required for calculation of physiological dead space

all of the CO2 in expired air comes from the exchange of CO2 in functioning (ventilated and perfused) alveoli

there is essentially no CO2 in inspired air

the physiological dead space (non-functioning alveoli and airways) neither exchanges nor contributes any CO2

what happens if physiological dead space is zero?

then PECO2 will be equal to PACO2 (and PaCO2)

what happens if physiological dead space is greater than zero?

then PECO2 will be diluted by dead space air and will be less than PACO2