Alveolar Gas Composition Research Articles

Breath holding as an example of extreme hypoventilation: experimental testing of a new model describing alveolar gas pathways.

What is the central question of this study? We modelled the alveolar pathway during breath holding on the hypothesis that it follows a hypoventilation loop on the O2 -CO2 diagram. What is the main finding and its importance? Validation of the model was possible within the range of alveolar gas compositions compatible with consciousness. Within this range, the experimental data were compatible with the proposed model. The model and its characteristics might allow predictions of alveolar gas composition whenever the alveolar ventilation goes to zero; for example, static and dynamic breath holding at the surface or during ventilation/intubation failure in anaesthesia. According to the hypothesis that alveolar partial pressures of O2 and CO2 during breath holding (BH) should vary following a hypoventilation loop, we modelled the alveolar gas pathways during BH on the O2 -CO2 diagram and tested it experimentally during ambient air and pure oxygen breathing. In air, the model was constructed using the inspired and alveolar partial pressures of O2 ( and , respectively) and CO2 ( and , respectively) and the steady-state values of the pre-BH respiratory exchange ratio (RER). In pure oxygen, the model respected the constraint of . To test this, 12 subjects performed several BHs of increasing duration and one maximal BH at rest and during exercise (30W cycling supine), while breathing air or pure oxygen. We measured gas flows, and before and at the end of all BHs. Measured data were fitted through the model. In air, =150±1mmHg and =0.3±0.0mmHg, both at rest and at 30W. Before BH, steady-state RER was 0.83±0.16 at rest and 0.77±0.14 at 30W; =107±7mmHg at rest and 102±8mmHg at 30W; and =36±4mmHg at rest and 38±3mmHg at 30W. By model fitting, we computed the RER during the early phase of BH: 0.10 [95% confidence interval (95% CI) =0.08-0.12] at rest and 0.13 (95% CI=0.11-0.15) at 30W. In oxygen, model fitting provided : 692 (95% CI=688-696) mmHg at rest and 693 (95% CI=689-698) mmHg at 30W. The experimental data are compatible with the proposed model, within its physiological range.

A New, Noninvasive Method of Measuring Pulmonary Gas Exchange: Results in Normal Subjects and Patients with Lung Disease

MethodsThe person breathes through a device that continually measures and displays the inspired and expired PO2 and PCO2. An oximeter is worn, and the arterial PO2 is calculated from the SpO2 and the oxygen dissociation curve, using the end–tidal PCO2 to account for the effect of PCO2 on the oxygen affinity of hemoglobin. The PO2 difference between the end‐tidal gas and the calculated arterial value is called the Oxygen Deficit. Since the calculation is only accurate when the arterial oxygen saturations are 94% or less, the normal subjects breathed 12.5% oxygen.ResultsStudies were made on 17 patients with a variety of pulmonary diseases who were attending an outpatient clinic. The mean oxygen deficit was 48.7 mm Hg, SE 3.1. This can be contrasted with a mean oxygen deficit of 4.0 mm Hg, SE 0.91 in a group of 30 normal subjects who were previously studied. The p value for the difference between the two groups was < 0.0001. Within the normal subjects, the mean oxygen deficit for the 19 younger participants (ages 22–31) was 2.02 mm Hg, SE 0.84 while that in the 11 older participants (ages 47–88) was 7.53 mm Hg, SE 1.55. The p value for the difference between the young and old groups was 0.0015. The mean oxygen deficit in younger normal subjects is remarkably small. This implies that there is very little difference between the calculated arterial PO2 and the alveolar PO2, consistent with little impairment of gas exchange. However, the mean oxygen deficit in older normal subjects is significantly higher consistent with the increased Alveolar‐arterial (A‐a) PO2 gradient with age, which has been well documented in the literature. Analysis of the factors determining the magnitude of the oxygen deficit showed that the end–tidal PO2 was the most important factor, followed by the end–tidal PCO2, and the calculated arterial PO2. Interestingly the SpO2 had a minor influence in spite of the fact that the oximeter reading is frequently used to guide therapy. The analysis emphasizes the value of measuring the composition of alveolar gas in determining ventilation‐perfusion ratio inequality. Remarkably, this factor is largely ignored in the classical index of impaired pulmonary gas exchange using the ideal alveolar PO2 to calculate the A‐a O2 gradient. We argue that ignoring the actual alveolar value gives an incomplete picture of gas exchange in the lungs because the traditional index is heavily biased by lung units with low ventilation‐perfusion ratios. Therefore, by using the new index of oxygen deficit, we derive a more comprehensive measurement of gas exchange in the lungs.Support or Funding InformationSupported by MediPines IncThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A New, Noninvasive Method of Measuring Impaired Pulmonary Gas Exchange in Lung Disease: An Outpatient Study

It would be valuable to have a noninvasive method of measuring impaired pulmonary gas exchange in patients with lung disease and thus reduce the need for repeated arterial punctures. This study reports the results of using a new test in a group of outpatients attending a pulmonary clinic. Inspired and expired partial pressure of oxygen (PO2) and Pco2 are continually measured by small, rapidly responding analyzers. The arterial PO2 is calculated from the oximeter blood oxygen saturation level and the oxygen dissociation curve. The PO2 difference between the end-tidal gas and the calculated arterial value is called the oxygen deficit. Studies on 17 patients with a variety of pulmonary diseases are reported. The mean ± SE oxygen deficit was 48.7 ± 3.1mmHg. This finding can be contrasted with a mean oxygen deficit of 4.0 ± 0.88mmHg in a group of 31 normal subjects who were previously studied (P< .0001). The analysis emphasizes the value of measuring the composition of alveolar gas in determining ventilation-perfusion ratio inequality. This factor is largely ignored in the classic index of impaired pulmonary gas exchange using the ideal alveolar PO2 to calculate the alveolar-arterial oxygen gradient. The results previously reported in normal subjects and the present studies suggest that this new noninvasive test will be valuable in assessing abnormal gas exchange in the clinical setting.

Alveolar gas composition during maximal and interrupted apnoeas in ambient air and pure oxygen

IntroductionWe tested the hypothesis that the alveolar gas composition at the transition between the steady phase II (φ2) and the dynamic phase III (φ3) of the cardiovascular response to apnoea may lay on the physiological breaking point curve (Lin et al., 1974). MethodsTwelve elite divers performed maximal and φ2-interrupted apnoeas, in air and pure oxygen. We recorded beat-by-beat arterial blood pressure and heart rate; we measured alveolar oxygen and carbon dioxide pressures (PAO2 and PACO2, respectively) before and after apnoeas; we calculated the PACO2 difference between the end and the beginning of apnoeas (ΔPACO2). ResultsCardiovascular responses to apnoea were similar compared to previous studies. PAO2 and PACO2 at the end of φ2-interrupted apnoeas, corresponded to those reported at the physiological breaking point. For maximal apnoeas, PACO2 was less than reported by Lin et al. (1974). ΔPACO2 was higher in oxygen than in air. ConclusionsThe transition between φ2 and φ3 corresponds indeed to the physiological breaking point. We attribute this transition to ΔPACO2, rather than the absolute PACO2 values, both in air and oxygen apnoeas.

Abstract PR532

Background & Objectives: Preoxygenation is used to maximise alveolar oxygen reserves prior to induction of anaesthesia thus allowing a longer safe apnoea time prior to securing the airway. A barrier to routine preoxygenation is the delay that such practice might incur in the time to induction of anaesthesia1. Optimal preoxygenation is defined as FeO2≥0.9. However, this may predispose to alveolar absorption atelectasis and may be unachievable within an acceptable timeframe. Therefore, a FeO2≥0.8 is a compromise target. The purpose of this study was to determine whether Non-Invasive Ventilation (NIV) would achieve a targeted Fractional Expired Oxygen (FeO2) concentration faster than standard ventilation (SV) during preoxygenation prior to induction of anaesthesia. Materials & Methods: This was a cross-over study of 20 adult patients (age range 18-80) undergoing elective surgery. The patients were recruited via the Pre-Operative Assessment Clinic to undergo a controlled comparison of two preoxygenation techniques. SV consisted of 10L/min of 100% oxygen via tight fitting facemask. NIV consisted of 10L/min of 100% oxygen via tight fitting facemask, with 5cmH20 pressure support and 5cmH20 positive end expiratory pressure. Each patient was preoxygenated using both techniques. The sequence of preoxygenation was randomised, with sufficient time interval between techniques to allow alveolar gas composition to return to baseline. Patients were placed in the supine position and initial FeO2 after the first breath was recorded. The time the patient reached a FeO2 0.8 was recorded. An additional 2 minutes were allowed for the patient to reach 0.9. If this was not achieved the maximal FeO2 was recorded. At the end of the study patients were asked for their preferred technique. Results: Of the 20 patients recruited 14 were male and 6 female. The average age was 60 years. The mean time to achieve FeO20.8 using NIV (57 seconds: range 30 - 105 sec) was faster than SV (148 seconds: range 50 - 440 sec). The mean difference was 92 seconds faster for NIV (95% confidence interval: range 43.3 -142.6; P=0.0009). In addition, when subjected to NIV, 15/20 patients (75%) achieved FeO2 0.9 in a further 2 minutes, compared to only 6/20 patients (30%) in the standard preoxygenation group. 78% of patients preferred NIV to standard technique (P=0.0184).Conclusion: This study demonstrates that NIV is a technique that achieves a FeO2 0.8 faster and is better tolerated than standard preoxygenation.

Equivalent Air Altitude and the Alveolar Gas Equation.

It is expedient to use normobaric hypoxia (NH) as a surrogate for hypobaric hypoxia (HH) for training and research. The approach matches inspired oxygen partial pressure (P(I)o₂) at the desired altitude to that at site pressure (PB) by reducing the inspired fraction of oxygen (FIo₂) to <0.21 using the equation: PIo₂= (PB - 47) × FIo₂, where 47 mmHg is the vapor pressure of water at 37°C. The investigator then has at site pressure the equivalent PIo2 as at altitude, i.e., the NH exposure is at an "equivalent air altitude." Some accepted as fact identical signs and symptoms of hypoxia for both conditions. However, those that derived the alveolar air equation showed that the coupled alveolar oxygen (PAo₂) and carbon dioxide partial pressures (PAco₂) for NH and HH are not identical when PIo₂is equivalent. They attribute the difference in alveolar gas composition under equivalent PIo₂to a nitrogen dilution effect or, more generally, to the respiratory exchange effect. Those that use NH as a convenient surrogate for HH must concede that physiological responses to NH cannot be identical to the responses to HH given only equivalent hypoxic PIo₂.

Images in Anesthesiology: Severe Unilateral Atelectasis during Induction of Anesthesia

AN 11-yr-old scoliotic female presented for posterior spine fusion. After IV induction with an Fio2 of 1.0, mask ventilation briefly failed and her oxygen saturation dropped to 60%. Intubation took multiple attempts. Severe right-sided atelectasis was noted on chest x-ray (fig.), predominantly in the middle and lower lobes. The case was cancelled and she recovered uneventfully in a pediatric intensive care unit. Elective bronchoscopy performed 2 months later revealed moderate bronchomalacia of the bronchus intermedius.Atelectasis during general anesthesia occurs in approximately 90% of individuals, usually as microatelectasis particularly in alveoli in dependent regions, affecting intra- and postoperative pulmonary function.1 Severe atelectasis after anesthesia induction, as was seen in our patient, is uncommon. Mechanisms of atelectasis include compression (morbid obesity), absorption (bronchial obstruction), and surfactant deficiency. Absorption atelectasis may result from either complete or partial airway obstruction. In a partially obstructed airway, if the ventilation/perfusion ratio decreases below a critical value with less ventilation in than alveolar gas removal by capillary blood flow, then atelectasis can occur. We hypothesize that our patient developed absorption atelectasis as a result of partial bronchial obstruction from bronchomalacia, exacerbated by brief hypoventilation during masking. Alveolar gas composition may also contribute to atelectasis formation. Induction with 30% oxygen promotes less atelectasis when compared with 100% oxygen because of nitrogen’s slower blood diffusion.2 This may, however, cause quick and severe desaturation should apnea occur. Application of positive end-expiratory pressure or continuous positive airway pressure during anesthesia induction can also prevent atelectasis formation.3 When severe atelectasis is diagnosed, bronchoscopy and selective single-lung manual ventilation with high inflating pressures should be considered.The authors declare no competing interests.

O2-CO2 diagram as a tool for comprehension of blood gas abnormalities

The O 2 -CO 2 diagram is an often neglected but very useful tool to understand the implications of arterial blood gas (ABG) analysis, which is a challenging concept not only to the undergraduate medical student but also to practicing clinicians. Here, we present a simplified description of the O2-CO2 diagram that was developed in all its elegance by Rahn and Fenn (6) and subsequently reviewed by others (2, 5). The O2-CO2 diagram plots PCO2 on the y-axis against PO2 on the x-axis. Any set of values of PO2 and PCO2, whether in atmospheric air, tracheal (inspired) air, alveolar air, mixed expired air, arterial blood, or venous blood, can be plotted on this diagram. It will be appreciated at the end of this discussion that 1) there are certain physical limits to what combinations of O2 and CO2 can exist in the alveolus and, therefore, the blood; and 2) even if arterial blood gases are the only available laboratory parameters, one can make reasonable assumptions about alveolar gas composition and assess if a patient has a pure ventilatory defect or a diffusion defect; however, it is difficult to assess mixed disorders without direct measurement of alveolar gas partial pressures. To begin, let us review the composition of atmospheric air, inspired air, and alveolar air (Fig. 1). Dry atmospheric air is composed of 21% O 2, with the rest N2 and negligible CO2. Therefore, PO2 in dry atmospheric air at sea level is 21% of the atmospheric pressure (Patm) of 760 mmHg, which is 159 mmHg. As air passes through the upper airways during inspiration, it is saturated with water vapor, the partial pressure of which at body temperature, pressure, saturated (BTPS) is 47 mmHg. The addition of water vapor dilutes inspired air, thereby reducing both the partial pressure of nitrogen and PO2 proportionally. The PO2 in inspired air is therefore 149 mmHg [21% of (760 47) mmHg] and is henceforth represented as PIO2 . While the inspired air in the conducting zone is composed of N2 ,O 2, and water vapor, a fourth gas, namely, CO2, is added to alveolar air. Since the alveoli are open to the atmosphere and during either phase of respiration alveolar pressure is only slightly different from Patm, it is safe to assume that alveolar pressure at all times is almost equal to Patm or the total pressure of inspired air (760 mmHg). The partial pressures of nitrogen (564 mmHg) and water vapor (47 mmHg) are almost the same in inspired and alveolar air. The remaining 149-mmHg pressure is due to O 2 alone in the inspired air (PI O2 ), whereas in the alveolus, the combined pressures of O 2 (PA O2 ) and CO 2 (PA CO2 ) must be close (but not necessarily equal 1 ) to 149 mmHg. Since O 2 diffuses out of the alveolus, it is obvious that removal of O2 and, therefore, reduction of its partial pressure compensates for the addition of CO2. The crude relationship is therefore as follows:

Extent to which pulmonary vascular responses to Pco2 and Po2 play a functional role within the healthy human lung

Regional blood flow in the lung is known to be influenced by the alveolar Pco2 and alveolar Po2. For the healthy lung, the extent to which this influence is of functional importance in limiting heterogeneity in alveolar gas composition by matching regional perfusion (q̇) to regional ventilation (v̇) remains unclear. To address this issue, the efficiency of regulation (E) was defined as the percent correction to an initial perturbation in regional alveolar gas composition generated by the pulmonary vascular response to the disturbance. This study develops the theory to calculate E from global measurements of vascular reactivity to CO2 and O2 in human volunteers. For O2, these data were available from the literature. For CO2, an experimental component of the present study used Doppler echocardiography to evaluate the magnitude of the global vascular response to hypercapnia and hypocapnia in 12 volunteers over a timescale of ∼0.5 h. The results suggest a value for E of ∼60% over a wide range of values for v̇-to-q̇ ratio (∼0.1–10) encompassing those found in normal lung. At low v̇/q̇ (<0.65), the vascular response to O2 forms the dominant mechanism; however, at higher v̇/q̇ (>0.65), the response to CO2 dominates. The values for E suggest that the pulmonary vascular responses to both CO2 and O2 play a significant role in ventilation-perfusion matching in the healthy human lung.

Estimation of arterial from a lung model during ramp exercise in healthy young subjects

The aim of this study is to propose a new approach to estimate non-invasively arterial carbon dioxide partial pressure (P(a)CO2) approach was based on the reconstruction of alveolar gas composition over each breath from a tidally ventilated lung model (P(M)(CO2)). Eight healthy young subjects were studied during a ramp exercise test on a cycle ergometer. Arterial samples were drawn at rest and every minute during the exercise test for determination of P(a)CO2 . P(a)CO2 was compared with indirect estimates of P(CO2) : P(M)(CO2), end-tidal P(CO2) (P(ET)(CO2)) and an empirical equation involving P(ET)(CO2) and tidal volume (P(J)(CO2)). The difference between estimated and measured P(a)CO2 on the whole ramp exercise was -0.3+/-1.9mmHg for P(M)(CO2), 1.0+/-2.2mmHg for P(ET)(CO2) and -1.7+/-1.7mmHg for P(J)(CO2) . P(ET)(CO2) and P(J)(CO2) were significantly different from actual P(a)CO2 (P<0.001). It is concluded that, on the basis of the bias, the breathing lung model gave better estimates of P(a)CO2 than the two other indirect methods during ramp exercise.

Human pulmonary vascular responses to hypoxia and hypercapnia.

The ability of alveolar gas composition to influence pulmonary vascular tone has been appreciated for over 50 years. In particular, it has been proposed that both O2 and CO2 could play a role in the matching of perfusion to ventilation within the lung, improving the overall efficiency of gas exchange. A wide variety of experimental approaches has been used to investigate pulmonary vascular effects of the respiratory gases in a range of mammalian species. In this article, we review experiments performed in healthy humans, identify particular difficulties in the interpretation of such experiments, and discuss possible approaches to future study.

Theoretical Study of Inspiratory Flow Waveforms during Mechanical Ventilation on Pulmonary Blood Flow and Gas Exchange

A lumped two-compartment mathematical model of respiratory mechanics incorporating gas exchange and pulmonary circulation is utilized to analyze the effects of square, descending and ascending inspiratory flow waveforms during mechanical ventilation. The effects on alveolar volume variation, alveolar pressure, airway pressure, gas exchange rate, and expired gas species concentration are evaluated. Advantages in ventilation employing a certain inspiratory flow profile are offset by corresponding reduction in perfusion rates, leading to marginal effects on net gas exchange rates. The descending profile provides better CO2 exchange, whereas the ascending profile is more advantageous for O2 exchange. Regional disparities in airway/lung properties create maldistribution of ventilation and a concomitant inequality in regional alveolar gas composition and gas exchange rates. When minute ventilation is maintained constant, for identical time constant disparities, inequalities in compliance yield pronounced effects on net gas exchange rates at low frequencies, whereas the adverse effects of inequalities in resistance are more pronounced at higher frequencies. Reduction in expiratory air flow (via increased airway resistance) reduces the magnitude of upstroke slope of capnogram and oxigram time courses without significantly affecting end-tidal expired gas compositions, whereas alterations in mechanical factors that result in increased gas exchanges rates yield increases in CO2 and decreases in O2 end-tidal composition values. The model provides a template for assessing the dynamics of cardiopulmonary interactions during mechanical ventilation by combining concurrent descriptions of ventilation, capillary perfusion, and gas exchange.

Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection.

To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6-8 degreesC also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.

Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model.

The purpose of this study was to evaluate algorithms for estimating O2 and CO2 transfer at the pulmonary capillaries by use of a nine-compartment tidally ventilated lung model that incorporated inhomogeneities in ventilation-to-volume and ventilation-to-perfusion ratios. Breath-to-breath O2 and CO2 exchange at the capillary level and at the mouth were simulated by using realistic cyclical breathing patterns to drive the model, derived from 40-min recordings in six resting subjects. The SD of the breath-by-breath gas exchange at the mouth around the value at the pulmonary capillaries was 59.7 +/- 25.5% for O2 and 22.3 +/- 10.4% for CO2. Algorithms including corrections for changes in alveolar volume and for changes in alveolar gas composition improved the estimates of pulmonary exchange, reducing the SD to 20.8 +/- 10.4% for O2 and 15.2 +/- 5.8% for CO2. The remaining imprecision of the estimates arose almost entirely from using end-tidal measurements to estimate the breath-to-breath changes in end-expiratory alveolar gas concentration. The results led us to suggest an alternative method that does not use changes in end-tidal partial pressures as explicit estimates of the changes in alveolar gas concentration. The proposed method yielded significant improvements in estimation for the model data of this study.

Laryngeal reflex apnea is blunted during and after hindlimb muscle contraction in sheep.

This study was carried out on seven chloralose-anesthetized sheep and was designed to investigate the role of muscular afferent fiber stimulation on the duration of reflex apnea triggered by laryngeal stimulation (LS). In six animals, injection of distilled water onto the laryngeal mucosa provoked a 15.7 +/- 1.0 s (mean +/- SE) apnea associated with a rise in systemic blood pressure (+7 +/- 0.8 Torr). Electrically induced contractions (EIC) of the hindlimb muscles doubled the metabolic rate and ventilation and reduced the duration of the apnea produced by LS to 7.4 +/- 1.0 s (P < 0.01). Apnea duration was still reduced during the first minute after the cessation of EIC (7.2 +/- 1.1 s, P < 0.01) but returned to control after a 5-min recovery period (16.7 +/- 1.6 s). The apnea triggered by LS was also reduced during EIC when the venous return was impeded by occluding the inferior vena cava (5.2 +/- 1.1 s, P < 0.01), despite a profound hypocapnia (20.7 +/- 0.3 Torr). The duration of apnea was not significantly affected (14.2 +/- 1.4 s) by breathing a 6% CO2-14% O2 in N2 gas mixture that roughly mimicked the alveolar gas composition when the apnea turned off. These results suggest that chemical drive has a negligible role in the fast reinitiation of breathing after LS during muscular stimulation. Stimulation of muscle afferent fibers does, however, appear to be a potent source of ventilatory reflexes capable of counteracting the inhibition of breathing resulting from laryngeal stimulation. Conversely, it is postulated that any reduction in somatic afferent traffic during this type of reflex apnea, including that resulting from the LS-induced systemic vasoconstriction, may delay the termination of apnea.

Oxygraphy in spontaneously breathing subjects.

Continuous monitoring of O2 and CO2 in the airways of spontaneously breathing patients can be carried out by sampling air to a gas monitor through a catheter placed in the upper airway. The graphical display of O2 (oxygraphy) is a rather new facility. To describe the photo-acoustic and magneto-acoustic technique for CO2 and O2 monitoring in the open unintubated airway, to evaluate the efficacy of oxygen therapy by oxygraphy and to determine alveolar gas tensions and alveolar-arterial partial pressure gradients. O2 and CO2 fractions in the airways were monitored in 9 healthy subjects. Blood samples were drawn from the radial artery. The Multigas Monitor 1,304 (Brüel and Kjaer, Naerum, Denmark) was used; end-expiratory measurements were considered as representative for the alveolar gas composition. Arterial blood was analysed by ABL520 (Radiometer Medical A/S, Copenhagen, Denmark). Reliable tracings of gas fractions (FCO2 and FO2) were obtained during the respiratory cycle in all subjects. When oxygen was supplied, FO2 of the airway varied considerably during the inspiratory phase whereas it remained almost constantly during the expiratory phase. The end-expiratory FO2 increased from 0.15 breathing atmospheric air to 0.41 breathing oxygen 15 L/min through a Hudson mask. Alveolar-arterial partial pressure differences were: pO2(A-a): 1.07 +/- 0.85 kPa and pCO2(A-a): -0.04 +/- 0.33 kPa during normoventilation in atmospheric air. Continuous monitoring of CO2 and O2 in the airway gives information about the pulmonary gas exchange and the efficacy of oxygen supply. Combined with arterial blood gas analysis the method allows determination of alveolar-arterial CO2 or O2 gradients.

Increased pulmonary perfusion worsens ventilation-perfusion matching.

Severe exercise and administration of vasopressors may adversely affect pulmonary gas exchange in humans. The role of increases in pulmonary perfusion in worsening ventilation-perfusion (VA/Q) relationships is unclear, however, because concomitant changes in ventilation and alveolar gas composition occur. The purpose of this study was to determine whether increasing of lobar blood flow increased VA/Q heterogeneity in the absence of changes in respiratory parameters. Six pentobarbital-anesthetized dogs underwent bilateral thoracotomies, left upper lobectomy, and placement of an electromagnetic flow probe on the left lower lobe (LLL) pulmonary artery, and catheters were inserted into the LLL pulmonary artery distal to the flow probe and confluent trunk of the LLL pulmonary vein. A bronchial divider was inserted to allow separate ventilation of the right lung and LLL. Blood flow to the LLL (QLLL) was increased in random order to two and three times baseline blood flow by opening an arteriovenous fistula and partially occluding the right pulmonary artery. Minute ventilation and alveolar PCO2 of the lobe were unchanged due to use of constant tidal volume and respiratory rate and inspiration of variable amounts of carbon dioxide. VA/Q distributions of the LLL were obtained using the multiple inert gas elimination technique. The tracer inert gas arterial-alveolar difference ([a-A]D) area was used to assess VA/Q mismatch. Increasing QLLL increased mean pulmonary artery pressure in the LLL (LLL Ppa). The PO2 of the LLL pulmonary venous blood remained unchanged, as the mixed venous oxygen tension (PvO2) was markedly increased. VA/Q inequality was increased, indicated by a 40% increase in the [a-A]D area when QLLL was increased to two times greater than baseline QLLL and a 58% increase in the [a-A]D area with three times greater than baseline QLLL. The [a-A]D area was highly correlated with the lobar blood flow (r = 0.97) and LLL Ppa (r = 0.97). Marked increases in lobar blood flow and Ppa worsened pulmonary gas exchange. The degree of impairment was correlated with the degree of increase in lobar perfusion. However, increased lobar perfusion did not affect LLL pulmonary venous blood oxygenation because the decrease in PO2, due to increased VA/Q mismatch, was opposed by an increase in PO2, due to increased PvO2.

Pulmonary blood flow and ventilation-perfusion heterogeneity

We studied the independent influence of changes in perfusion on pulmonary gas exchange in the left lower lobe (LLL) of anesthetized dogs. Blood flow to the LLL (QLLL) was raised 50% (increased QLLL) or reduced 50% (decreased QLLL) from baseline by partial occlusion of the right or left pulmonary artery, respectively. Minute ventilation and alveolar PCO2 of the LLL remained constant throughout the study. We determined ventilation-perfusion distributions of the LLL using the multiple inert gas elimination technique. Increased QLLL impaired LLL pulmonary gas exchange. All dispersion indexes and all arterial-alveolar difference areas increased (P less than 0.01). Decreased QLLL increased the log standard deviation of the perfusion distribution (P less than 0.05) and reduced the log standard deviation of the ventilation distribution (P less than 0.01) but did not affect the dispersion indexes or alveolar-arterial difference areas. We conclude that ventilation-perfusion heterogeneity is increased by independent changes in perfusion from normal baseline blood flow, even when ventilation and alveolar gas composition remain constant.

Alveolar gas composition and exchange during deep breath-hold diving and dry breath holds in elite divers

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.

A model for evaluation of gas exchange: mouth to mouth ventilation of infants by emergency medical technicians

We describe a model for evaluating techniques of infant ventilation during resuscitation. The utility of the model is illustrated by testing performance of emergency medical technicians in mouth to mouth ventilation of a model 4 kg infant. Ventilation was generally adequate with mean (+/- S.D.) frequency 22 +/- 9 breaths per minute and tidal volume 40 +/- 13 ml. Gas delivered to the model consisted of PICO2 7 +/- 6 mmHg and FIO2 0.20 +/- 0.007. Assuming normal metabolic rate and respiratory dead space, alveolar gas composition resulting from the simulated resuscitations would be PACO2 = 31 +/- 20 and PAO2 = 110 +/- 19 mmHg. Nine of ten rescuers would have achieved satisfactory PACO2 less than or equal to 50 and PAO2 greater than or equal to 100. However, the rescuers' exhaled oxygen concentration is not adequate to correct hypoxemia if associated with hypoventilation or a wide alveolar to arterial oxygen gradient.