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13. THE ROLE OF LOSS O F LUNG RECOIL I N
CHRONIC AIRFLOW OBSTRUCTION
D. G. LEAVER,
ANNETATTERSFIELD
and N. B. PFUDE
Department of Medicine, Royal Postgraduate Medical
School, London, W.12
Airflow obstruction in chronic pulmonary disease is
usually attributed to ‘intrinsic’ disease of the airways.
In emphysema, however, there is severe loss of lung
recoil pressure which could directly cause considerable airflow obstruction, since recoil pressure has
been shown to be an important determinant of airways conductance (Butler et al., 1960, Journal of
Clinical Investigation, 39, 524) and of maximum
expiratory flow rates (Mead et al., 1967, Journal of
Applied Physiology, 22, 95; Pride et al., 1967, Journal
of Applied Physiology, 23, 646).
In twenty patients with chronic bronchitis and
reduction of the 1 s forced expiratory volume we have
measured total airways conductance (at an inspiratory
flow of 0-5 l/s), lung recoil pressure and maximum
expiratory flow rates over a wide range of lung
volumes.
In seven of the twenty patients the observed reduction in conductance could be accounted for entirely
by the loss of lung recoil pressure; in all twenty
patients, however, maximum expiratory flow was
reduced more than could be accounted for by the
changes in lung recoil pressure.
In contrast, in five patients whose disability was
mainly due to ‘intrinsic’ disease of the airways,
conductance at functional residual capacity was
greatly reduced and changed very little as lung recoil
pressure increased. In these patients the reduction
in maximum expiratory flow rates was not as marked
as would be anticipated from the severe reduction in
conductance at low flows.
The relation of these two functional patterns to
the ‘emphysematous’ and ‘bronchial‘ types of airways obstruction (Burrows et al., 1966, Lancet, I,
830) was discussed.
1 3 ~
preferential distribution of the bolus to the lower
lobes if inspired slowly because the lower lobes are
more compliant than the upper as a result of the
gradient of pleural pressure. With increasing inspiratory flow rate more of the inspired bolus is distributed
to the upper lobes. ‘Cross-over’, where ventilation
per alveolus in the upper and lower lobes is equal
after a given inspired volume, occurs at approximately
2 l/s when the inspired volume is 400 ml. Above this
flow rate there is a preferential distribution of gas
to the upper lobes. This cross-over is a direct result
of the volume-dependence of resistance, the more
expanded upper airways having a lower resistance.
The computations are made for a wide range of
physiological and anatomical parameters, so that the
influence of various factors, such as overall lung
volumes, airway resistance, and pressure-volume
relations, on the distribution of inspired gas, can be
explored. The flow rate at which ‘cross-over’ occurs is
influenced to some extent by all parameters but is
most sensitive to change in the lung volume at which
the bolus of gas is injected. The results are in good
agreement with recent experiments on the distribution
s f gas using boluses of radioactive xenon and external
counters at the chest wall. It is stressed that the theory
can readily be extended to calculate the distribution of
ventilation in situations other than uniform inspiration, for example during cyclic breathing at high
frequency (for example during exercise), if the appropriate anatomical and physiological variables for
expiration can be determined.
15. THE EFFECT O F HALOTHANE ON VENTILATORY RESPONSES MEDIATED BY THE
PERIPHERAL CHEMORECEPTORS
J. G. WHITWAM,J. DUFFIN
and A. TRISCOTT
Department of Anaesthetics, The Royal Postgraduate
Medical School, London, W .12
(Introduced by C. M. Oakley)
The peripheral chemoreceptors provide a continuing
drive to normal respiration which can be detected by
14. A NON-LINEAR THEORY OF THE
observing a transient fall in ventilation following two
DISTRlBUTION OF PULMONARY
breaths of 100% oxygen (Dejours, 1963, Annals of the
VENTILATION
New York Academy of Sciences, 109, 682). In addiT. J. PEDLEY,
M. F. SUDLOW
and J. MILIC-EMILI
tion, the peripheral chemoreceptors contribute a fast
The Physiological Flow Studies Unit, Imperial College, component to the ventilatory response to carbon
London, S. W.7
dioxide during normoxia, but it is eliminated by
The theory for the distribution of ventilation in a hyperoxia (Bernards et al., 1966, Respiratory Phytwo-compartment model of the lung is developed, siology, 1, 390; Cunningham et al., 1965, Journal of
neglecting inertial forces but allowing resistance and Physiology, 179,68~.)This component can be detected
compliance to vary with lung volume and resistance by observing a difference in the timing of the ventilato vary with flow rate, all in a non-linear manner. tory response to Pa,co2, raised by a rapid intravenous
Numerical solutions to the basic equation are found injection of sodium bicarbonate, between air and
for the distribution of inspired gas between the upper oxygen breathing.
Twelve female patients premedicated with atropine
and lower lobes of erect human lungs.
Results are presented to show how a bolus of (0.6 mg) and pethidine (75-100 mg), were anaesthelabelled gas inspired at various volumes and flow tized with thiopentone (3-4 mg/kg), intubated using
rates would be distributed. The theory predicts the suxamethonium chloride (50-75 mg) after spraying