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A new method has been developed for measuring virtually continuous distributions of ventilation-perfusion ratios (V(A)/Q) based on the steadystate elimination of six gases of different solubilities. The method is applied here to 12 normal subjects, aged 21-60. In nine, the distributions were compared breathing air and 100% oxygen, while in the remaining three, effects of changes in posture were examined. In four young semirecumbent subjects (ages 21-24) the distributions of blood flow and ventilation with respect to V(A)/Q were virtually log-normal with little dispersion (mean log standard deviations 0.43 and 0.35, respectively). The 95.5% range of both blood flow and ventilation was from V(A)/Q ratios of 0.3-2.1, and there was no intrapulmonary shunt (V(A)/Q of 0). On breathing oxygen, a shunt developed in three of these subjects, the mean value being 0.5% of the cardiac output. The five older subjects (ages 39-60) had broader distributions (mean log standard deviations, 0.76 and 0.44) containing areas with V(A)/Q ratios in the range 0.01-0.1 in three subjects. As for the young subjects, there was no shunt breathing air, but all five developed a shunt breathing oxygen (mean value 3.2%), and in one the value was 10.7%. Postural changes were generally those expected from the known effects of gravity, with more ventilation to high V(A)/Q areas when the subjects were erect than supine. Measurements of the shunt while breathing oxygen, the Bohr CO(2) dead space, and the alveolar-arterial oxygen difference were all consistent with the observed distributions. Since the method involves only a short infusion of dissolved inert gases, sampling of arterial blood and expired gas, and measurement of cardiac output and minute ventilation, we conclude that it is well suited to the investigation of pulmonary gas exchange in man.

Jastrzebski, J., Sykes, M. K., and Woods, D. G. (1974).Thorax, 29, 534-538. Cardiorespiratory effects of protamine after cardiopulmonary bypass in man. The cardiorespiratory changes following the injection of protamine sulphate (6 mg/kg) were studied in 15 patients who had undergone cardiopulmonary bypass. There was a transient fall in arterial pressure and a more prolonged increase in pulmonary artery pressure. There was a significant fall in arterial oxygen tension which was mainly due to a reduction in mixed venous oxygen tension resulting from a fall in cardiac output. Dead space/tidal volume ratio and percentage shunt did not change significantly.

Adult mongrel dogs were exposed to 95% oxygen either awake and spontaneously breathing or anesthetized and mechanically ventilated for periods of 24 to 48 hr. A marked increase in dead space ventilation indicates that pulmonary capillary area decreases early during exposure to 95% oxygen. After 48 hr of breathing 95% oxygen, the capillary bed appeared to be maximally dilated exposing a surface area which is markedly permeable to water.

Finite difference solutions of the differential diffusion equation, incorporating simultaneous longitudinal diffusion and exponentially time varying flow, served as simulations of single-breath nitrogen washout. Using Weibel's anatomic model “A” for the conducting airways and assuming a well-mixed alveolar region, an anatomic dead space 70% larger than commonly measured values was predicted. This is due in part to the Weibel parameter values which overestimate conducting airway volume when inspiration is initiated at FRC. Moreover, the existence of additional mixing processes in the real lung would lead to a smaller dead' space than predicted by longitudinal diffusion alone. To test the reasonableness of the model, simulations with varying respiratory conditions were performed. The predicted dead space decrease for an increase in inspiration time, for a decrease in inspiratory volume and for an increase in diffusion coefficient were in agreement with experimental data. Decreases in dead space by breath-holding and increased expiratory times followed the experimental trends only qualitatively. A major point of interest in this work was the effect of variations in conducting airway geometry upon the washout data. The upper airways were found to behave as pure dead space because of the small role that diffusion plays in the overall transport occurring therein. For example, a 40-ml increase in conducting airway volume brought out by increasing the length or cross-section of the first four airway generations caused an equal volume change in the anatomic dead space. However, the same airway volume increase brought about by lengthening the 4th to 17th generation airways increased dead space by only 20 ml. If brought about by increasing the summed crosssection of these airways, the dead space increased by only 5–10 ml and the washout curve was only slightly changed. Thus, the washout test is especially insensitive to cross-sectional alterations in the lower airways because of the compensating effects of diffusion.

The resolution of the technique considered is sufficient to describe smooth distributions containing blood flow to unventilated regions (shunt), ventilation to unperfused regions (dead space), and up to three additional modes over the range of finite ventilation-perfusion ratios. In particular, areas whose ventilation-perfusion ratios are low can be separated from unventilated regions and those whose ventilation-perfusion ratios are high can similarly be distinguished from unperfused areas.

The conventional method of measuring cuff pressures from endotracheal or tracheostomy tubes by injecting air from a syringe via a three-way stopcock into the cuff, then allowing equilibration with a manometer gives false low pressure measurements because of the dead space of the tube and manometer system. The correct way to measure intracuff pressures is with a four-way stopcock which fills the balloon and measures pressure simultaneously.

1. Action potentials have been recorded from single laryngeal motor fibres, with expiratory or inspiratory phases, in cats anaesthetized with pentobarbitone and breathing through a tracheal cannula. 2. Pneumothorax increased the discharge of both inspiratory and expiratory units, the inspiratory response being greatly reduced by bilateral vagotomy below the origin of the recurrent laryngeal nerves. 3. Addition of a ‘viscous’ resistance to breathing, or asphyxial rebreathing through an added dead space, increased the activity of inspiratory units and decreased that of expiratory units. 4. Induction of pulmonary oedema decreased the discharge of inspiratory units and increased that of expiratory units. After vagotomy the response of inspiratory units was reversed. 5. Intravenous injections of potassium cyanide increased the activity of both types of unit. 6. Chemical irritation of the laryngeal mucosa decreased the discharge of inspiratory units and increased that of expiratory units, whether the vagi were intact or cut. 7. It is concluded that expiratory unit discharge can be correlated with expiratory laryngeal resistance, but that inspiratory unit discharge does not correlate so well with inspiratory laryngeal resistance. 8. The relationship between laryngeal motor-fibre activity and the contractions of the inspiratory and expiratory muscles of breathing is discussed.

Lung volumes in irreversible diffuse obstructive pulmonary syndromes (DOPS(I)) have been studied by using an analog of the lung that simulates an 18-breath nitrogen washout. The functional residual capacity (FRC), the dead space volume (Vd), the distribution of ventilation, as well as the pattern of lung emptying have been measured in normal subjects and those with obstructive syndromes. The Vd increased progressively with severity of the obstructive syndrome, as did FRC. For all subjects, both normal and obstructed, the ratio of Vd/FRC remained relatively fixed with the regression line of Vd upon FRC showing a minimal value for Vd of 67 cm(3). Vd increased by an average value of 33 cm(3) per liter of lung volume above this value. The increase in FRC resulted from the increased volume of the poorly ventilated compartment for the most part. X-ray evidence of emphysema was poorly correlated with the changes in Vd or FRC. A significant increase in anatomical Vd in DOPS(I) makes up an appreciable portion of the total Vd (physiological).

A lung model that analyzes an 18-breath washout for the distribution of ventilation, the functional residual capacity, the dead-space volume and the pattern of compartmental emptying, has been used in a study of normal subjects and those with irreversible obstructive pulmonary syndromes. Lung compartments are defined in terms of their alveolar dilution ratio (ω) as determined from endtidal nitrogen concentrations. Simulating the nitrogen washout at specific volumes expired in each breath gives the contribution at that volume coming from each compartment. Dead space is treated as one of these compartments, having a dilution ratio of zero. The emptying pattern in subjects with moderate and severe obstructive syndromes is altered when compared with that of normals. Dead space is not delivered within one tidal volume and the late delivery served to distinguish normal subjects from those with an obstructive syndrome. The relative flow from compartments other than dead space progressively increases throughout expiration in severe obstructive syndromes. The nitrogen rise on the alveolar plateau with normal tidal volumes in obstructive syndromes is principally a function of the dead-space delivery. On the average, the flow from the well-ventilated compartment increased throughout expiration in those with obstructive syndromes, whereas it fell off from an early peak in normal subjects.

The determination of dead space of any kind is rarely done because it is of more interest to determine blood gases and pH which will be altered as a result of the increase in the functional dead space (anatomic and physiologic). The most frequent cause of increased dead space is an imbalance between ventilation and perfusion, and this alteration is present in any pulmonary illness

Crew, A. D., Varkonyi, P. I., Gardner, L. G., Robinson, Q. L. A., Wall, E., and Deverall, P. B. (1974). Thorax , 29 , 437-445. Continuous positive airway pressure breathing in the postoperative management of the cardiac infant. Continuous positive airway pressure with spontaneous ventilation was used in the postoperative period following palliative or corrective surgery for congenital heart defects in a group of children of less than 3 years of age. After stabilization of the cardiovascular state, continuous positive airway pressure breathing (CPAP) was shown to be a suitable alternative to continuous positive pressure ventilation (CPPV). A statistically significant increase in PaO2 was observed on changing from CPPV to CPAP. A statistically significant decrease in PaO2 and increase in pulmonary venous admixture was observed after discontinuing the positive airway pressure and allowing the patient to breathe at ambient pressure. We would recommend CPAP as an intermediate manoeuvre in the withdrawal of ventilatory support as it introduces a smoothness and stability into patient management regimes which was previously lacking. Careful selection of apparatus is necessary as the airway pressure should be truly continuous and steady. In neonates the dead space of the system should be reduced to a minimum; CPAP alternating with periods on CPPV may be necessary for some time after cardiovascular stability has been attained.

We studied gas exchange in 19 children with cystic fibrosis in whom measurement of lung volumes, flow rates and airway conductance, diffusing capacity and mixing efficiency were normal. A significant decrease in arterial oxygen tension was found together with a significant increase in alveolar-arterial difference for oxygen and physiologic dead space/tidal volume ratio. These findings are consistent with evidence that early in cystic fibrosis the site of obstruction is in the small airways. It is also suggested from these data that blood gas abnormalities occur before other parameters of lung function become abnormal.

Summary. Hyperventilation due to extra dead space did not cause any significant improvement in ventilatory efficiency as measured in nitrogen wash-out experiments during oxygen breathing. In the experiments with extra dead space a significant increase in degree of uniformity of ventilation could be demonstrated. The subject's dead space increased, and the over-all efficiency remained constant. The efficiency-improving effect of a better distribution and the efficiency-deteriorating effect of a larger dead space probably cancelled out. The better distribution is most probably explained by the effect of mixing of gas from different lung fractions in the large dead space. The experiments were performed with a nitrogen meter.

SummaryThe measurement of arterial pCO2 and expired CO2, by means of formula established by Enghoff, Rossier and co., Riley and co., allows to determine alveolar ventilation and physiological dead space, which represent very important functional data in respiratory physiology.The physiological and anatomical dead spaces in healthy subjects at rest are closely related, but they differ notably during hyperventilation, work and in pathological conditions.Variation of physiological dead space results from the fact that it is conditionned by anatomical dead space, by total ventilation, respiratory frequency, intensity of exchange of gases and alveolar ventilation.The existence of these various factors and their susceptibility to vary in opposite direction allows to explain that it is quite impossible to look upon absolute values of physiological dead space as an easy test of pulmonary function.On the other side, repeated measurements in the same subject on two occasions have shown that, despite the fact that s...

Methods approaching the ultimate in simplicity, accuracy, reproducibility, and rapidity have been described for the calibration of manometric vessel and capillary volumes with either known or unknown volumes of air, withdrawn from or added to the test manometer system by means of a precalibrated reference standard manometer system (or other equivalent precalibrated device) connected by tubing to the test manometer. Two fundamental steps of procedure are employed, in accordance with Boyle's law, to obtain measurements applicable in two simultaneous equations for two unique conditions of simplicity, the one at constant pressure, the other at constant volume. In the first step, after initial equilibration, the standardizing volume of air is transferred between standard (∗) and test manometer with releveling to constant initial pressure (Δ P = 0), yielding a determination of v , the capillary volume per specified length, from no more than simple inverse proportionality between the observed capillary fluid length changes ( v = v ∗ L ∗ L ). In the second step the manometers are closed off at their stopcocks and the confined gases brought back to their initial space volumes (Δ V = 0), yielding a determination of the vessel gas space volume v g , from no more than simple inverse proportionality between the observed capillary fluid pressure changes ( v g = v g ∗ h ∗ h ). v ∗ and v g ∗ are previously known from the standard manometer, L ∗ and h ∗ are obtained with it, and L and h with the test manometer. Our most recommended procedures for measuring manometric capillary ( v ) and vessel ( V ) values (Eqs. (1′) and (5) with known volumes of air, see Table I, and Fig 1, and Eqs. (1′ u ) and (5 u ) with unknown volumes) require no (numerical) knowledge of barometric pressure, watervap or pressure, absolute temperature, “dead space” of connecting tubes, solubility of air in water, etc., apart from assurance of maintenance of their constancy during manipulations. These factors and other second- and third-order effects (difference in draining of capillaries, changes in dissolved air with pressure changes, differences of temperature outside and inside the thermostat) that enter into applied manometry, are in principle rendered negligible by the differential methodology of our procedure of calibrating a test manometer with another (precalibrated) manometer. The accuracy and reproducibility of these air calibrations can be adjusted, depending upon the will and the skill of the investigator, either to the maximum attainable in operating manometry (say ± 0.2%), or to an accuracy as good or better than that employed in 95 % of all manometry, namely ±1 %. Methods for the minimization or actual elimination of thermobarometric (TB) changes, an important factor largely neglected in previously described methodology of air calibration, are outlined. The outer manometer arms are not left open to the external atmosphere, but are connected with a large vessel (e.g., a 20-l. carboy) whose pressure can be manipulated (as by a large connected syringe) so that any effects of pressure or temperature variations can be readily restored to precisely zero in the TB manometer, and simultaneously thereby in all other manometers connected in parallel. The uses and advantages of such a carboysyringe device in not only calibration, but even more importantly and generally, in many aspects of operative manometry, are indicated. No manometric laboratory should be without such a device (see Fig 1). The proposed methodology is recommended to all indolent mercurophobes and aerophiles, for whom the gravity of the problem of mercury calibration is herewith reduced by the levity of air, and a little air of levity.

1. Dead space (CO2-front method), lung compliance, cervical tracheal volume change and total lung resistance were measured simultaneously in anaesthetized dogs, paralysed or open-chest, and the responses to nerve section and stimulation and to ventilation of the dogs with different gas mixtures were studied. 2. Bilateral cervical vagotomy changed all four parameters in a way consistent with airway dilation, and bilateral vagal stimulation had the opposite actions. A weak airway dilator role was indicated for the sympathetic nerves. 3. Ventilation with 4% CO2, 8% CO2 or 10% O2 changed all four parameters as if the airways had constricted, and 100% O2 caused oppossite, but weaker, responses. 4. The responses to the three airway constricting gas mixtures were present, but reduced in intensity, after bilateral cervical vagotomy and some even weaker responses were present after additional bilateral sympathectomy. 5. During restoration of airway smooth muscle tone by electrical stimulation of the distal ends of the cut vagus nerves, administration of CO2-rich or hypoxic gas mixtures had no greater effect than during controls with vagi cut but without stimulation. 6. No dilator responses to hypercapnia or hypoxia were seen, either in innervated or denervated trachea and airways.

Three tests of the distribution of ventilation are performed in our laboratory during the closed circuit equilibration with oxygen of a patient who has previously breathed air. The forced equilibrating expiration (FEE) is the procedure designed to test for a new type of distribution abnormality, not previously distinguished from the others, namely, the presence of inelastic sacs or bullae open to the bronchi. Such bullae would presumably not be ventilated while held open at volumes above the end-tidal, yet would empty during forced expirations below the end-tidal volume. The Fowler single breath test examines the distribution of ventilation within a single expiration due to the differences in time constants, differences in percentage elastance and differences in the per cent dead space among the alveoli. The time to equilibrium (TTE), like other qualitative tests of the efficiency of washout during a series of breaths, examines for all of these types of unevenness and even for unevenness due to alveoli that open during forced inspiration but that close early as inspiration is reduced. By examining 115 normal subjects, standards delimiting the range of normal were found for the FEE, the TTE and for some modifications of the single breath test. Even in normal subjects, about a third of variance in the TTE may be accounted for by the variation in the other two tests, distributed about equally between them.

Minute volume, tidal volume, dead space volume (E, VT, VD), and diving lung volume were measured in adult, unrestrained Weddell seals, Leptonychotes weddelli, whose mean weight was 425 kg. The effects of oxygen ventilation on dive duration were observed in four adult seals. E ranged from 19.5 L/min while resting to 224 L/min after a dive, VT was 5.4 L to 15.2 L, the average VD for two animals was 1.6 L, and lung volumes ranged from 5 L during a dive to 21 L after inspiration. Dive durations of 66 min and probably 87 min were observed after oxygen ventilation. The results indicate that the ability to increase ventilation rate above the resting value, is less than that in terrestrial mammals. Diving lung volumes are large enough that blood and tissue inert gas tensions could increase to several atmospheres during deep dives if small airways closed at low pressures and most of the gases were trapped in the lungs. Blood oxygen tensions may play a primary role in influencing the length of the dive.

Hesser, C. M. and B. Holmgren. Effects of raised barometric pressures on respiration in man. Acta physiol. scand. 1959. 47. 28—43. – The effects of raised barometric pressures (up to 4.0 atm) on various respiratory functions, hitherto largely neglected, were studied on 8 healthy subjects at rest in a recompression chamber. The independent effects of changes in inspired oxygen and nitrogen pressures were studied by comparing data obtained on air, 100 % oxygen, and 5 % oxygen in nitrogen at various ambient pressures. Breathing air with increasing ambient pressure, respiration became progressively slower and deeper, whereas at 4.0 atm the effective alveolar ventilation was slightly increased. Other observations at 4.0 atm were: Average increase of 33 % in tidal volume; average decreases in respiratory rate of 27 %, respiratory minute volume of 10 %, and functional dead space/tidal volume ratio of 9 %; no demonstrable changes in expiratory reserve volume, functional dead space and respiratory exchange ratio. Evidence is presented that the respiratory changes were caused by the combined effects of increased oxygen tension and of increased breathing resistance due to increased gas density. Thus, nitrogen at high pressures (up to 3.8 atm) exerted little, if any, depressant action on respiration.

Subjects given oral doses of paraldehyde exhale about 7% of the administered dose within 4 hours. Paraldehyde itself is the only detectable exhaled excretion product. The excreted percentages do not depend on dose. The concentrations of paraldehyde in the exhaled air are unaffected by changes in ventilatory minute volume; the amounts excreted per time unit, however, are proportional to the volume of respiration. Dead space analyses showed that paraldehyde is excreted across alveolar membranes in a fashion similar to CO 2 . These findings lend an experimental basis to the clinical practice of hyperventilation in patients who have ingested toxic amounts of paraldehyde.

Evacuating speed of a rotary vacuum pump decreases as pressure decrease, but mathematical expression showing this tendency is unknown. Only the equation dP/dt=-So/V (P-Pmin) is introduced by experiences, but the physical meaning of Pmin (final pressure) is very chaotic.The author explains this meaning by simple calculation, as Pmin is the parameter containing dead space volume, outgassing and leakage.But unfortunately, as the above equation is not always appropriate for the actual pumps, the author proposes more adequate expression S = {1- (Pmin/P)a} So.

A method is described for making bronchial tree casts using a polystyrene resin, Bioplastic. The lung is first air dried under pressure and then filled with the resin by gravity while the plastic polymerizes. The pulmonary vessels may also be injected, yielding a double cast. The relative weights of individual lobes of the dog's lung after air drying are presented. A linear relationship is established between the dead space volume of individual lobes and their dry weight. Variations in length of the bronchial systems supplying each lobe may modify the relation between anatomical dead space and weight in that lobes supplied by short bronchial pathways seem to have smaller dead space/weight ratios than those supplied by longer bronchial pathways. Submitted on July 16, 1956

Summary Gas transport within the airways of the lung occurs by two mechanisms. Bulk flow of air dominates in the upper airways and is the method most obvious to the observer. Gas transport takes place by means of molecular diffusion in the fine structure of the lung. The architecture of the lungs appears to be adapted to facilitate gas transport by both methods. The upper airways conduct the bulk flow of air with a minimum of resistance but small dead space, and the fine alveolar regions have short pathways that are adapted to the requirements of molecular diffusion. Disturbance of the bulk flow transport system occurs in the widely encountered condition of airway obstruction. Disturbance of the diffusion system may be an important feature of the dilated airways in emphysema.

Hydrogen has been used for the determination of the pulmonary capacity by VanSlyke and Binger,1 who pointed out the danger of explosion and of poisoning with arsine. This procedure was replaced by oxygen dilution methods, particularly the Christie method,3 which has been in use in this laboratory for the last 10 years. A recent report2 has resulted in new interest in hydrogen, because of the ease and rapidity of analysis for this gas by thermal conductivity. A preliminary report is made at this time of a new method employing helium, because it has all the advantages and none of the dangers of the hydrogen method.A closed spirometer system with a blower is used. Carbon dioxide is absorbed by soda-lime. An important precaution is the addition of a water bottle to replace water vapor lost in the soda-lime. Dead space is measured by the oxygen dilution method. Part of the mixture circulating in the respiratory system is shunted through a thermal conductivity cell∗ with precautions to assure complete saturatio...

The panting mechanism is considered as resulting from the joint effort of the two systems regulating the body temperature and the blood gas tensions respectively. Equations are derived which describe the equilibrium conditions for each system. A nomogram for the evaluation of the amount of heat taken up by one liter of respiratory air is given. Combination of the equilibrium equations leads to a infinite series due to the fact that heat dissipation by the respiratory tract involves increased heat production by the respiratory muscles. The conditions of convergence for the infinite series are derived assuming a quadratic relation between heat production of the respiratory muscles and respiratory minute volume. It is shown that the system will become unstable if the series diverges. Equations for the partial washout of the dead space are given which are essential for the independent control of alveolar ventilation and dead space ventilation by proper adjustment of tidal volume and respiratory rate. Two examples demonstrate the limited value of the panting mechanism as compared with the heat dissipation by sweat production, when the animals are subjected to high environmental temperatures. Panting seems superior however for eliminating an increased heat production due to muscular exercise at very low temperatures as for instance in sled dogs.

Pulmonary hemodynamics and gas exchange were studied in four physicians during 72 hr acclimatization to 12,470 ft. Pulmonary catheters were left in three subjects for 72 hr. Resting mean pulmonary arterial pressure (PAP) rose progressively during the first 24 hr from 10.3 +/-1.0 to 21.1 +/-4.0 torr and remained at this level. During this same 24 hr period cardiac output increased from 7.1 +/-1.4 to 8.4 +/-2.0 liters/min and total pulmonary resistance rose from 122 +/-16 to 209 +/-40 dynes.sec/cm(-5). Excercise at 60 w after 24 hr of hypoxia increased PAP to 28.8 +/-5.1 torr and decreased total pulmonary resistance to 155 +/-25. Shunt fractions were 11 +/-3.8% after 24 hr at altitude and fell to 7 +/-0% after 72 hr. Alveolar to arterial O(2) difference (P(A-a)(O2)) breathing oxygen fell from 116 +/-10.8 to 92 +/-33.3 torr during the same period of acclimatization, whereas dead space to tidal volume ratio (V(D)/V(T)) rose from 33 +/-4.0% to 40 +/-5.3% and P(A-a)(O2) breathing ambient air rose from 8 +/-2.6 to 11 +/-3.0 torr. Inspiratory static lung compliance decreased significantly from a control of 176 +/-8 to 141 +/-8 ml/cm H(2)O after 72 hr of hypoxia. After 4-7 days at altitude, further deterioration in gas exchange was observed after a 5 mile, 1800 ft climb to the summit (14,255 ft) and return. P(A-a)(O2) on air rose from 2.5 +/-2.1 just before starting, to 16.3 +/-2.8 at the summit (rested), and was still 9.0 +/-2.2 several hours after returning. The O(2)-breathing values paralleled these, whereas dead space appeared to fall. We speculate that the hypoxic pulmonary hypertension which develops over 24 hr in some way may be responsible for a reduction of compliance and deterioration in oxygen exchange efficiency, possibly representing a sub-clinical form of pulmonary edema of high altitude. The increased alveolar to arterial O(2) difference induced by hypoxic exercise persists for several hours of hypoxic rest.

An equation of conservation or continuity is derived which relates the deposition of homogeneous aerosol in the human respiratory tract during steady breathing to the deposition in the alveolated regions of the lungs, the fraction of aerosol traversing the dead space airways which is deposited in them, the fraction of the aerosol entering the dead space airways during inhalation but not traversing them, which is deposited in them, and the tidal volume. This equation imposes constraints upon possible values of deposition and alveolar deposition. Further constraints arise if considerations of particle mechanics are used to fix limits for the alveolar deposition.

The distribution of tidal air and nonshunted blood flow to each lung, the elimination of CO2 from each lung, and Paco2 were measured in ten anesthetized and paralyzed dogs during intermittent positive-pressure breathing in the supine position and before and after thoracotomy in the lateral decubitus position. Ventilation via a divided tracheal airway (Wright-Lategola) at a constant rate and a constant volume (±5%) with 65% oxygen in nitrogen was provided by a Bird ventilator. Reduction of total CO2 elimination and increase of ratio of total physiologic dead space to tidal volume were observed after thoracotomy. Mean percentages of total ventilation and blood flow to, and CO2 elimination from, the right lung were about 58% in the supine position. When the right or left lung became dependent in the lateral decubitus position, its proportional ventilation and CO2 elimination decreased. After thoracotomy was made on the superior nondependent side, further reductions were noted and blood flow to the dependent lung also decreased. Proportional CO2 elimination was more dependent on alveolar ventilation than on the ratio of ventilation to perfusion.

An automatic, electronically controlled respiratory cycling valve is described. This valve was designed for use in aerosol inhalation experiments with humans or dogs and is characterized by a low dead space (27 cc) and by wide channels for air flow (minimum dimension 1.3 cm). The valve is automatically operated by respiratory pressure changes in the order of 3 mm water.

When physiological dead space (Vd(p)) is calculated for a patient who has alveolar dead space, e.g., after pulmonary vascular occlusion, less than the full volume of attached mechanical dead space (Vd(m)) appears in the measured dead space (Vd(n)). Under these conditions the traditional subtraction of Vd(m) from Vd(n) leads to underestimation of Vd(p) and can give a falsely small ratio of Vd(p) to tidal volume (Vt) when, in fact, an abnormally large Vd(p)/Vt exists. To make the proper correction for Vd(m), two equations have been derived and validated with seven subjects having Vd(p)/Vt from 0.29 to 0.87, using Vd(m)'s from 120 to 322 ml. With only a small modification, these equations are suitable for routine clinical use and give Vd(p)/Vt within 0.02 of that by the validated equations (32 of 33 comparisons). The fraction of Vd(m) subtracted from Vd(n) is the square of the ratio of effective alveolar to total alveolar ventilation and is never > 1. This fraction is (Pa(CO2)/Pa(CO2))(2), where Pa(CO2) and Pa(CO2) are the mean partial pressures of expired alveolar and of arterial CO(2); in the other equation this fraction is [Pe(CO2)/Pa(CO2) (Vt - Vd(an) - Vd(m))](2) where Pe(CO2) is mixed expired Pco(2) and Vd(an) is anatomical dead space. The second equation requires an estimated Vd(an) and is applicable when Pa(CO2) is not measured or does not plateau (as in exercise).

Alternate patients (from a group of 40) after cardiac surgery received ventilation with pure oxygen, or the minimal inspired oxygen concentration required to maintain an arterial oxygen tension between 80 and 120 mm of mercury. The latter group of 20 patients did not receive more than 42 per cent inspired oxygen, and their mean duration of exposure was 21 hours, with a maximum of 44 hours. The mean exposure of 18 patients inspiring pure oxygen was 24 hours, with a maximum of 48 hours. No difference in intrapulmonary shunt, effective compliance, ratio of dead space to tidal volume or clinical course could be detected between the two groups. Of two additional patients who inspired pure oxygen for a prolonged period, one died of massive pulmonary hemorrhage related to clotting deficit after seven days' exposure, and the other recovered after five days' exposure. Fear of pulmonary oxygen toxicity should not prevent use of elevated inspired oxygen concentrations in critically ill patients requiring ar...

Hyperventilation with its attendant alveolar distention and stimulation of coughing is an important factor in the prevention and treatment of pulmonary atelectasis. A light cardboard tube of 1,000 cc. volume with a plastic mouthpiece has been developed, which by elevating the alveolar carbon dioxide tension stimulates such hyperventilation both in normal personnel and in patients before and after operation. Studies indicate the parallel changes in alveolar carbon dioxide tension and tidal volume which reach an equilibrium after approximately three minutes of rebreathing through the dead space tube. Some decrease in alveolar oxygen tension can be prevented by delivery of oxygen into the end of the rebreathing tube if necessary. Routine use of this tube in patients postoperativly in the past year and a half has been useful in preventing and treating pulmonary complications. A regimen of three to five minutes rebreathing every two hours is recommended. Following each patient's use the cardboard tube is discarded and the plastic mouthpiece autoclaved prior to use by the next patient.

Alveolar arterial tension differences for oxygen, and ratios of physiologic dead space to tidal volume measured at rest, were significantly greater in eight patients with mild bronchitis and seven with asymptomatic asthma as compared to normal controls. Routine pulmonary-function tests, including pulmonary resistance, gave normal or only minimally abnormal results. On exercise, oxygen tension differences became normal in three patients with bronchitis and four with asthma but remained abnormal in the others. Ratios of dead space to tidal volume were normal on exercise in only one bronchitic and three asthmatic patients. Abnormalities of ventilation distribution and gas exchange occur before other abnormalities of lung function become apparent.

Two mathematical models of pulmonary single breath gas washout (one analytic, one numerical) are developed and their predictions compared with experimental data on human subjects. Weibel's 23 generation symmetric anatomical model is used as a guide to bronchial tree geometry. Experimental plots of nitrogen concentration versus volume expired, dead space versus breath holding time, and dead space versus tidal volume are compared with plots predicted by the models. Agreement is good. A plot of nitrogen concentration in the airways as predicted by the numerical model at different times during inhalation and exhalation of a single breath of oxygen is shown. Model predictions for changes in dead space with changes in washout gas and expiratory flow rate are discussed. Use of the analytic model for obtaining average values of the path length from mouth to alveoli in a given subject is discussed. To the extent of their agreement with experiment, the models provide a sound physical basis for the correlation of airway structure and function.

1. Arterial blood gas tensions have been studied in 50 cases of chest crush injuries. Hypoxia was present in most of these cases, but raised P CO 2 was present in only six cases and in no case was it grossly abnormal. In most cases the P CO 2 was below normal limits. Standard bicarbonate was normal in most cases. 2. The alveolar-arterial oxygen tension difference was increased in all nine cases studied but the ratio of dead space/tidal volume was within normal limits in four out of seven cases where this was estimated. 3. Ten patients treated with 100% oxygen for 20 min failed to show a normal rise in oxygen tension, suggesting that the hypoxia in many cases of chest injury is from a true shunt presumably due to blood perfusing atelectatic areas of lung or to pulmonary oedema. 4. These shunts persisted in many cases for a considerable time, even though there was no radiological evidence of atelectasis, and some were present for as long as 6 weeks after the injury.

Renal clearances (C IN , C CR , C PAH , C H 2 O , and C OSM ) were performed in 12 antepartal and 14 postpartal healthy, hydrated subjects during periods of 0, 20, 100, and 1,000 mU. per minute of oxytocin. The antidiuresis which resulted from oxytocin infusions was found to be due to absorption of water from the renal distal convoluted tubules and collecting ducts. Slight decreases in C IN , C CR , and C PAH were demonstrated during most of the oxytocin infusions, but these are believed to have been caused principally by the relatively large urinary "dead space" and low flow rates. We do not believe that the glomerular filtration rate or renal plasma flow is materially affected by oxytocin, even in doses as large as 1,000 mU. per minute.

The effects of increasing ventilation-perfusion inequality on overall gas exchange were studied in digital computer models of the lung. Ventilation/unit volume and perfusion/unit volume were distributed log normally with respect to lung volume. Ventilation-perfusion inequality was found to affect the transfer of carbon dioxide nearly as much as oxygen. The reasons for the misconception that inequality does not interfere with carbon dioxide transfer are discussed. The effects of changing overall ventilation, blood flow, inspired oxygen, hemoglobin concentration, and the acid-base status of the blood were investigated when oxygen uptake and carbon dioxide output were held constant at normal values. In general, mismatch of ventilation and blood flow in a lung caused the arterial oxygen tension to fall and the carbon dioxide to rise; increasing overall ventilation rapidly restored blood carbon dioxide tensions to normal but improved oxygen tensions little. Considerable improvement in oxygen tensions occurred, however, if the oxygen dissociation curve was made linear. In spite of large increases in inspired oxygen, severe hypoxemia and large alveolar-arterial oxygen differences remained when the inequality was severe. The results help to explain how the lung maintains oxygen and carbon dioxide transfer in the face of ventilation-perfusion ratio inequality and may be useful in characterizing the degree of ventilation-perfusion inequality in real situations.

In 25 cases of unexpandable lung treated with artificial pneumoperitoneum to close the pleural dead space, clinical studies on mediastinal shift and mediastinal hernia were performed and following results were obtained:1) Either mediastinal shift or mediastinal hernia was observed in 21 cases (81.0%), while only 4 cases (16.0%) were without both of them.2) The longer the pleural dead space existed, the more often mediastinal shift and hernia was found.3) In most of cases with remarkable mediastinal shift, mediastinal hernia was not or only in slight degree observed, while remarkable hernia was likely to be observed in cases without or with mediastinal shift of slight degree.4) Mediastinal shift, which was additionally increased or newly formed by artificial pneumoperitoneum, was observed in 14 of 25 cases (56.0%).In 5 cases with mediastinal hernia the degree of hernia was increased in only one case by artificial pneumoperitoneum.5) The dead space was closed more earlier in cases without mediastinal shift or hernia than in cases with them. In some patients among the latter the dead space failed to be closed.6) Function of the affected lung was not improved even after the dead space had been closed. And the dysfunction of the opposite lung, which happened to occur due to expected overexpansion, was not observed in most cases.7) The lung wss forced to be deformed and expanded in horizontal axis as the result of the collaps in apico-caudal axis due to artificial pneumoperitoneum. In this case the deformity of the lung was observed not only in the affected side with dead space, but also in the opposite side. Mediastinal shift or hernia is thought to be formed under these circumstances. These factors seems to play a great role of closing pleural dead space.