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Using a 50‐compartment Python‐coded mathematical lung model, we compared mixed venous blood flow (Q) distributions and arterial oxygen tension/inspired oxygen fraction (PaO2/FiO2) relationships in lungs modeled with log normal distributions (LND) of inspired (VI) versus expired (VA) alveolar gas volumes. In lungs with normal V/Q heterogeneity, Q versus VA/Q and Q versus VI/Q distributions were similar with either approach, and PaO2/FiO2 sequences remained indistinguishable. In V/Q heterogeneous lungs at high FiO2, VILND generated low Q versus VA/Q shoulders and some negative VA units, while VALND preserved Q versus VA/Q log normality by blood flow diversion from low VI/Q units. We managed VILND‐induced negative VA units either by shunt conversion (VI decreased to 0) or VI redistribution simulating collateral ventilation (VI increased till VA = 0). Comparing oxygen transfer: VALND > VILND (redistribution) > VILND (shunt). In V/Q heterogeneous lungs VALND and VILND (redistribution) regained near optimal oxygen transfer on 100% oxygen, while impairment persisted with VILND (shunt). Unlike VALND, VILND (redistribution) produced Q versus VA/Q distributions in V/Q heterogeneity compatible with multiple inert gas (MIGET) reports. VILND (redistribution) is a physiologically–based MIGET–compatible alternative to West's original VALND lung modeling approach. [ABSTRACT FROM AUTHOR]

Abstract Using a 50‐compartment Python‐coded mathematical lung model, we compared mixed venous blood flow (Q) distributions and arterial oxygen tension/inspired oxygen fraction (PaO2/FiO2) relationships in lungs modeled with log normal distributions (LND) of inspired (VI) versus expired (VA) alveolar gas volumes. In lungs with normal V/Q heterogeneity, Q versus VA/Q and Q versus VI/Q distributions were similar with either approach, and PaO2/FiO2 sequences remained indistinguishable. In V/Q heterogeneous lungs at high FiO2, VILND generated low Q versus VA/Q shoulders and some negative VA units, while VALND preserved Q versus VA/Q log normality by blood flow diversion from low VI/Q units. We managed VILND‐induced negative VA units either by shunt conversion (VI decreased to 0) or VI redistribution simulating collateral ventilation (VI increased till VA = 0). Comparing oxygen transfer: VALND > VILND (redistribution) > VILND (shunt). In V/Q heterogeneous lungs VALND and VILND (redistribution) regained near optimal oxygen transfer on 100% oxygen, while impairment persisted with VILND (shunt). Unlike VALND, VILND (redistribution) produced Q versus VA/Q distributions in V/Q heterogeneity compatible with multiple inert gas (MIGET) reports. VILND (redistribution) is a physiologically–based MIGET–compatible alternative to West's original VALND lung modeling approach.

Abstract Objective This study aimed to determine whether ultra-low tidal volume ventilation (ULTVV) applied during cardiopulmonary resuscitation (CPR) compared with standard ventilation (intermittent positive pressure ventilation, IPPV) can reduce pulmonary end-organ damage in the post-resuscitation period. Methods A prospective, randomized trial was conducted using a porcine model (n = 45). The animals were divided into three groups: IPPV, ULTVV, and a sham control group. Juvenile male pigs underwent CPR after inducing ventricular fibrillation and received the designated ventilation intervention [IPPV: tidal volume 6–8 ml per kilogram body weight (ml/kg BW), respiratory rate 10/min, FiO2 1.0; ULTVV: tidal volume 2–3 ml/kg BW, respiratory rate 50/min, FiO2 1.0]. A 20-h observation period followed if return of spontaneous circulation was achieved. Histopathological examination using the diffuse alveolar damage scoring system was performed on postmortem lung tissue samples. Arterial and venous blood gas analyses and ventilation/perfusion measurements via multiple inert gas elimination technique (MIGET) were repeatedly recorded during the experiment. Results Out of the 45 experiments conducted, 28 animals were excluded based on predefined criteria. Histopathological analysis showed no significant differences in lung damage between the ULTVV and IPPV groups. ULTVV demonstrated adequate oxygenation and decarboxylation. MIGET measurements during and after resuscitation revealed no significant differences between the intervention groups. Conclusion In the short-term follow-up phase, ULTVV demonstrated similar histopathological changes and functional pulmonary parameters compared to standard ventilation. Further research is needed to investigate the long-term effects and clinical implications of ULTVV in resuscitation settings.

Objective: This study aimed to determine whether ultra-low tidal volume ventilation (ULTVV) applied during cardiopulmonary resuscitation (CPR) compared with standard ventilation (intermittent positive pressure ventilation, IPPV) can reduce pulmonary end-organ damage in the post-resuscitation period. Methods: A prospective, randomized trial was conducted using a porcine model (n = 45). The animals were divided into three groups: IPPV, ULTVV, and a sham control group. Juvenile male pigs underwent CPR after inducing ventricular fibrillation and received the designated ventilation intervention [IPPV: tidal volume 6–8 ml per kilogram body weight (ml/kg BW), respiratory rate 10/min, FiO2 1.0; ULTVV: tidal volume 2–3 ml/kg BW, respiratory rate 50/min, FiO2 1.0]. A 20-h observation period followed if return of spontaneous circulation was achieved. Histopathological examination using the diffuse alveolar damage scoring system was performed on postmortem lung tissue samples. Arterial and venous blood gas analyses and ventilation/perfusion measurements via multiple inert gas elimination technique (MIGET) were repeatedly recorded during the experiment. Results: Out of the 45 experiments conducted, 28 animals were excluded based on predefined criteria. Histopathological analysis showed no significant differences in lung damage between the ULTVV and IPPV groups. ULTVV demonstrated adequate oxygenation and decarboxylation. MIGET measurements during and after resuscitation revealed no significant differences between the intervention groups. Conclusion: In the short-term follow-up phase, ULTVV demonstrated similar histopathological changes and functional pulmonary parameters compared to standard ventilation. Further research is needed to investigate the long-term effects and clinical implications of ULTVV in resuscitation settings. Keypoints: The current state of research regarding the optimal ventilation strategy during cardiopulmonary resuscitation is incomplete. This study investigated the impact of ultra-low tidal volume ventilation during resuscitation compared to standard ventilation on lung end-organ damage. Histopathologically and functionally, no statistically significant differences were observed in the short-term follow-up. [ABSTRACT FROM AUTHOR]

We investigated whether machine learning (ML) analysis of ICU monitoring data incorporating volumetric capnography measurements of mean alveolar PCO2 can partition venous admixture (VenAd) into its shunt and low V/Q components without manipulating the inspired oxygen fraction (FiO2). From a 21-compartment ventilation / perfusion (V/Q) model of pulmonary blood flow we generated blood gas and mean alveolar PCO2 data in simulated scenarios with shunt values from 7.3% to 36.5% and a range of FiO2 settings, indirect calorimetry and cardiac output measurements and acid- base and hemoglobin oxygen affinity conditions. A 'deep learning' ML application, trained and validated solely on single FiO2 bedside monitoring data from 14,736 scenarios, then recovered shunt values in 500 test scenarios with true shunt values 'held back'. ML shunt estimates versus true values (n = 500) produced a linear regression model with slope = 0.987, intercept = -0.001 and R2 = 0.999. Kernel density estimate and error plots confirmed close agreement. With corresponding VenAd values calculated from the same bedside data, low V/Q flow can be reported as VenAd—shunt. ML analysis of blood gas, indirect calorimetry, volumetric capnography and cardiac output measurements can quantify pulmonary oxygenation deficits as percentage shunt flow (V/Q = 0) versus percentage low V/Q flow (V/Q > 0). High fidelity reports are possible from analysis of data collected solely at the operating FiO2. [ABSTRACT FROM AUTHOR]

Background: Invasive ventilation during cardiopulmonary resuscitation (CPR) is very complex due to unique thoracic pressure conditions. Current guidelines do not provide specific recommendations for ventilation during ongoing chest compressions regarding positive end-expiratory pressure (PEEP). This trial examines the cardiopulmonary effects of PEEP application during CPR. Methods: Forty-two German landrace pigs were anaesthetised, instrumented, and randomised into six intervention groups. Three PEEP levels (0, 8, and 16 mbar) were compared in high standard and ultralow tidal volume ventilation. After the induction of ventricular fibrillation, mechanical chest compressions and ventilation were initiated and maintained for thirty minutes. Blood gases, ventilation/perfusion ratio, and electrical impedance tomography loops were taken repeatedly. Ventilation pressures and haemodynamic parameters were measured continuously. Postmortem lung tissue damage was assessed using the diffuse alveolar damage (DAD) score. Statistical analyses were performed using SPSS, and p values <0.05 were considered significant. Results: The driving pressure (Pdrive) showed significantly lower values when using PEEP 16 mbar than when using PEEP 8 mbar (p = 0.045) or PEEP 0 mbar (p < 0.001) when adjusted for the ventilation mode. Substantially increased overall lung damage was detected in the PEEP 0 mbar group (vs. PEEP 8 mbar, p = 0.038; vs. PEEP 16 mbar, p = 0.009). No significant differences in mean arterial pressure could be detected. Conclusion: The use of PEEP during CPR seems beneficial because it optimises ventilation pressures and reduces lung damage without significantly compromising blood pressure. Further studies are needed to examine long-term effects in resuscitated animals. [ABSTRACT FROM AUTHOR]

Abstract Background Mechanical chest compression devices are accepted alternatives for cardiopulmonary resuscitation (CPR) under specific circumstances. Current devices lack prospective and comparative data on their specific cardiovascular effects and potential for severe thoracic injuries. Objectives To compare CPR effectiveness and thoracic injuries of two mechanical chest compression devices in pigs. Study design Prospective randomised trial. Animals Eighteen male German landrace pigs. Methods Ventricular fibrillation was induced in anaesthetised and instrumented pigs and the animals were randomised into two intervention groups. Mechanical CPR was initiated by means of LUCAS™ 2 (mCCD1) or Corpuls™ cpr (mCCD2) device. Advanced life support was applied for a maximum of 10 cycles and animals achieving ROSC were monitored for 8 h. Ventilation/perfusion measurements were performed and blood gas analyses were taken. Thoracic injuries were assessed via a standardised damage score. Results Five animals of the mCCD1 group and one animal of the mCCD2 group achieved ROSC (p = 0.048). Only the mCCD1 animals survived until the end of the monitoring period (p

Background: Mechanical chest compression devices are accepted alternatives for cardiopulmonary resuscitation (CPR) under specific circumstances. Current devices lack prospective and comparative data on their specific cardiovascular effects and potential for severe thoracic injuries. Objectives: To compare CPR effectiveness and thoracic injuries of two mechanical chest compression devices in pigs. Study design: Prospective randomised trial. Animals: Eighteen male German landrace pigs. Methods: Ventricular fibrillation was induced in anaesthetised and instrumented pigs and the animals were randomised into two intervention groups. Mechanical CPR was initiated by means of LUCAS™ 2 (mCCD1) or Corpuls™ cpr (mCCD2) device. Advanced life support was applied for a maximum of 10 cycles and animals achieving ROSC were monitored for 8 h. Ventilation/perfusion measurements were performed and blood gas analyses were taken. Thoracic injuries were assessed via a standardised damage score. Results: Five animals of the mCCD1 group and one animal of the mCCD2 group achieved ROSC (p = 0.048). Only the mCCD1 animals survived until the end of the monitoring period (p < 0.01). MCCD1 animals showed less pulmonary shunt (p = 0.025) and higher normal V/Q (p = 0.017) during CPR. MCCD2 animals showed significantly more severe thoracic injuries (p = 0.046). Conclusion: The LUCAS 2 device shows superior resuscitation outcomes and less thoracic injuries compared to Corpuls cpr when used for experimental CPR in juvenile pigs. Researchers should be aware that different mCCDs for experimental studies may significantly influence the respective outcome of resuscitation studies and affect comparability of different trials. Controlled human and animal CPR studies and a standardised post-resuscitation injury evaluation could help to confirm potential hazards. Trial registration: Trial approval number: G16–1-042-E4. [ABSTRACT FROM AUTHOR]

Background Optimal ventilation strategies during cardiopulmonary resuscitation are still heavily debated and poorly understood. So far, no convincing evidence could be presented in favour of outcome relevance and necessity of specific ventilation patterns. In recent years, alternative models to the guideline-based intermittent positive pressure ventilation (IPPV) have been proposed. In this randomized controlled trial, we evaluated a bi-level ventilation approach in a porcine model to assess possible physiological advantages for the pulmonary system as well as resulting changes in neuroinflammation compared to standard measures. Methods Sixteen male German landrace pigs were anesthetized and instrumented with arterial and venous catheters. Ventricular fibrillation was induced and the animals were left untreated and without ventilation for 4 minutes. After randomization, the animals were assigned to either the guideline-based group (IPPV, tidal volume 8–10 ml/kg, respiratory rate 10/min, FiO21.0) or the bi-level group (inspiratory pressure levels 15–17 cmH2O/5cmH2O, respiratory rate 10/min, FiO21.0). Mechanical chest compressions and interventional ventilation were initiated and after 5 minutes, blood samples, including ventilation/perfusion measurements via multiple inert gas elimination technique, were taken. After 8 minutes, advanced life support including adrenaline administration and defibrillations were started for up to 4 cycles. Animals achieving ROSC were monitored for 6 hours and lungs and brain tissue were harvested for further analyses. Results Five of the IPPV and four of the bi-level animals achieved ROSC. While there were no significant differences in gas exchange or hemodynamic values, bi-level treated animals showed less pulmonary shunt directly after ROSC and a tendency to lower inspiratory pressures during CPR. Additionally, cytokine expression of tumour necrosis factor alpha was significantly reduced in hippocampal tissue compared to IPPV animals. Conclusion Bi-level ventilation with a constant positive end expiratory pressure and pressure-controlled ventilation is not inferior in terms of oxygenation and decarboxylation when compared to guideline-based IPPV ventilation. Additionally, bi-level ventilation showed signs for a potentially ameliorated neurological outcome as well as less pulmonary shunt following experimental resuscitation. Given the restrictions of the animal model, these advantages should be further examined.

Background. Optimal ventilation strategies during cardiopulmonary resuscitation are still heavily debated and poorly understood. So far, no convincing evidence could be presented in favour of outcome relevance and necessity of specific ventilation patterns. In recent years, alternative models to the guideline-based intermittent positive pressure ventilation (IPPV) have been proposed. In this randomized controlled trial, we evaluated a bi-level ventilation approach in a porcine model to assess possible physiological advantages for the pulmonary system as well as resulting changes in neuroinflammation compared to standard measures. Methods. Sixteen male German landrace pigs were anesthetized and instrumented with arterial and venous catheters. Ventricular fibrillation was induced and the animals were left untreated and without ventilation for 4 minutes. After randomization, the animals were assigned to either the guideline-based group (IPPV, tidal volume 8-10 ml/kg, respiratory rate 10/min, FiO21.0) or the bi-level group (inspiratory pressure levels 15-17 cmH2O/5cmH2O, respiratory rate 10/min, FiO2 1.0). Mechanical chest compressions and interventional ventilation were initiated and after 5 minutes, blood samples, including ventilation/perfusion measurements via multiple inert gas elimination technique, were taken. After 8 minutes, advanced life support including adrenaline administration and defibrillations were started for up to 4 cycles. Animals achieving ROSC were monitored for 6 hours and lungs and brain tissue were harvested for further analyses. Results. Five of the IPPV and four of the bi-level animals achieved ROSC. While there were no significant differences in gas exchange or hemodynamic values, bi-level treated animals showed less pulmonary shunt directly after ROSC and a tendency to lower inspiratory pressures during CPR. Additionally, cytokine expression of tumour necrosis factor alpha was significantly reduced in hippocampal tissue compared to IPPV animals. Conclusion. Bi-level ventilation with a constant positive end expiratory pressure and pressure-controlled ventilation is not inferior in terms of oxygenation and decarboxylation when compared to guideline-based IPPV ventilation. Additionally, bilevel ventilation showed signs for a potentially ameliorated neurological outcome as well as less pulmonary shunt following experimental resuscitation. Given the restrictions of the animal model, these advantages should be further examined. [ABSTRACT FROM AUTHOR]

The availability of computed tomography (CT) allowed Hedenstierna to clarify the relationship between lung morphology and physiology (Brismar et al., 1985). He was the first to use this "new" method, which enabled research into the correlation between lung atelectasis and blood oxygenation (Hedenstierna et al., 1986). Keywords: atelectasis; clinical physiology; computed tomography; MIGET; obituary EN atelectasis clinical physiology computed tomography MIGET obituary 146 147 2 02/16/22 20220301 NES 220301 GRAPH Göran Hedenstierna, Professor of Clinical Physiology, died on 13 July 2021, aged 79 years. [Extracted from the article]

Objectives Anaesthetized horses commonly become hypoxaemic due to ventilation/perfusion ( [ABSTRACT FROM AUTHOR]

The mismatching of alveolar ventilation and perfusion (VA/Q) is the major determinant of impaired gas exchange. The gold standard for measuring VA/Q distributions is based on measurements of the elimination and retention of infused inert gases. Conventional multiple inert gas elimination technique (MIGET) uses gas chromatography (GC) to measure the inert gas partial pressures, which requires tonometry of blood samples with a gas that can then be injected into the chromatograph. The method is laborious and requires meticulous care. A new technique based on micropore membrane inlet mass spectrometry (MMIMS) facilitates the handling of blood and gas samples and provides nearly real-time analysis. In this study we compared MIGET by GC and MMIMS in 10 piglets: 1) 3 with healthy lungs; 2) 4 with oleic acid injury; and 3) 3 with isolated left lower lobe ventilation. The different protocols ensured a large range of normal and abnormal VA/Q distributions. Eight inert gases (SF6, krypton, ethane, cyclopropane, desflurane, enflurane, diethyl ether, and acetone) were infused; six of these gases were measured with MMIMS, and six were measured with GC. We found close agreement of retention and excretion of the gases and the constructed VA/Q distributions between GC and MMIMS, and predicted PaO2 from both methods compared well with measured PaO2. VA/Q by GC produced more widely dispersed modes than MMIMS, explained in part by differences in the algorithms used to calculate VA/Q distributions. In conclusion, MMIMS enables faster measurement of VA/Q, is less demanding than GC, and produces comparable results. [ABSTRACT FROM AUTHOR]

Rapid infusion of intravenous saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized that infusion would disrupt pulmonary gas exchange by increasing ventilation/perfusion (VA/Q) inequality as opposed to a diffusive impairment in O2 exchange. Seven males (26 ± 3 yr; FEVI: 110 ± 16% predicted.) performed spirometry and had VA/Q mismatch measured using the multiple inert gas elimination technique, before and after 20 ml/kg iv of normal saline delivered in ∼30 mm. Infusion increased thoracic fluid content from transthoracic impedance by 12% (P < 0.0001) and left FVC unchanged but reduced expiratory flows (FEF25-75 falling from 5.1 ± 0.4 to 4.2 ± 0.4 l/s, P < 0.05). However, VA/Q mismatch as measured by the log standard deviation of the ventilation (LogSDV) and perfusion (LogSDQ) distributions remained unchanged; LogSDV: 0.40 ± 0.03 pre, 0.38 ± 0.04 post, NS; LogSDQ: 0.38 ± 0.03 pre, 0.37 ± 0.03 post, NS. There was no significant change in arterial Po2 (99 ± 2 pre, 99 ± 3 mmHg post, NS) but arterial PCO2 was decreased (38.7 ± 0.6 pre, 36.8 ± 1.2 mmHg post, P < 0.05). Thus, infusion compressed small airways and caused a mild degree of hyperventilation. There was no evidence for a diffusive limitation to O2 exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at FiO2 = 0.125 (4.3 ± 1.0 pre, 5.2 ± 1.0 post, NS). After infusion, the fraction of perfusion going to areas with VA/Q < 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 ± 0.06 (FiO2 = 0.21), 0.80 ± 0.06 (FiO2 = 0.30), P <0.05] with similar effects on ventilation in the face of unchanged VA and Q. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences. [ABSTRACT FROM AUTHOR]

Abstract: Background: Studies using the multiple inert gas elimination technique (MIGET) to characterise the mechanisms of impaired gas exchange in CF, provide conflicting results on the importance of ventilation–perfusion (V A/Q) inequality over shunt. We hypothesise that the mechanisms of gas exchange abnormality have changed with changing CF management over the last two decades. Methods: Detailed gas exchange was evaluated by MIGET with venous sampling in stable patients, age>20 years, FEV1% predicted ≤50. Results: Fifteen (14 male) subjects were studied with a mean±SD age 28.1±8.4 years, FEV1% 32.6±10.3, TLC% 111.5±12.9, PaO2 9.3±1.3 kPa, (69.5±9.6 mm Hg), and PaCO2 6.2±0.7 kPa, (45.9±5.3 mm Hg). The predominant gas exchange abnormality was V A/Q inequality with a log SD of the distributions of perfusion 0.91±0.30 and of ventilation 0.60±0.14. Unimodal distributions were seen in nine subjects, a low V A/Q mode in five and one subject had a bimodal distribution, mean intrapulmonary shunt was negligible. Conclusions: Subjects had a lower FEV1% by comparison with previously published studies and demonstrated severe V A/Q inequality and negligible shunt. This suggests a low degree of complete obstruction of airways in adults with CF and severe stable pulmonary disease. The primary mechanism of hypoxaemia in CF subjects reaching adulthood today appears to have changed with modern management over the last two decades. [Copyright &y& Elsevier]

Objective: To explore the consequences of helium/oxygen (He/O(2)) inhalation on respiratory mechanics, gas exchange, and ventilation-perfusion (VA/Q) relationships in an animal model of severe induced bronchospasm during mechanical ventilation.Design: Prospective, interventional study.Setting: Experimental animal laboratory, university hospital.Interventions: Seven piglets were anesthetized, paralyzed, and mechanically ventilated, with all ventilator settings remaining constant throughout the protocol. Acute stable bronchospasm was obtained through continuous aerosolization of methacholine. Once steady-state was achieved, the animals successively breathed air/O(2) and He/O(2) (FIO(2) 0.3), or inversely, in random order. Measurements were taken at baseline, during bronchospasm, and after 30 min of He/O(2) inhalation.Results: Bronchospasm increased lung peak inspiratory pressure (49+/-6.9 vs 18+/-1 cm H(2)O, P<0.001), lung resistance (22.7+/-1.5 vs 6.8+/-1.5 cm H(2)O x l(-1).s, P<0.001), dynamic elastance (76+/-11.2 vs 22.8+/-4.1 cm H(2)O x l(-1), P<0.001), and work of breathing (1.51+/-0.26 vs 0.47+/-0.08, P<0.001). Arterial pH decreased (7.47+/-0.06 vs 7.32+/-0.06, P<0.001), PaCO(2) increased, and PaO(2) decreased. Multiple inert gas elimination showed an absence of shunt, substantial increases in perfusion to low VA/Q regions, and dispersion of VA/Q distribution. He/O(2) reduced lung resistance and work of breathing, and worsened hypercapnia and respiratory acidosis.Conclusions: In this model, while He/O(2) improved respiratory mechanics and reduced work of breathing, hypercapnia and respiratory acidosis increased. Close attention should be paid to monitoring arterial blood gases when He/O(2) is used in mechanically ventilated acute severe asthma. [ABSTRACT FROM AUTHOR]

SUMMARY 1. The use of the multiple inert gas elimination technique (MIGET) in quantifying ventilation/perfusion distributions (V•A/Q•) in small animals, such as the rat, may cause results to be biased due to haemodilution produced by the large volume of liquid infused intravenously. 2. We tested two methods of administering inert gases in rats using the MIGET: (i) standard continuous intravenous administration of inert gases (method A); and (ii) a new method based on the physicochemical properties of each inert gas (method B). This method included acute simultaneous inert gas administration using three pathways: inhalation, intravenous infusion and rectal infusion. Both MIGET methods were applied to obtain data while breathing three different inspiratory fractions of oxygen (FIO2): normoxia, hypoxia and hyperoxia. 3. Inert gas levels obtained from blood or expired air samples were sufficient for chromatographic measurement, at least during a 2 h period. The V•A/Q• distributions reported using both methods were acceptable for all the physiological conditions studied; therefore, the alternative method used here may be useful in further MIGET studies in rats because haemodilution resulting from continuous intravenous infusion of less-soluble gases can be avoided. 4. Normoxic rats showed lower mean values of the V•A/Q• ratio of ventilation distribution and higher mean values of the V•A/Q• ratio of perfusion distribution with the usual method of inert gas administration (method A). These non-significant differences were observed under almost all physiological conditions studied and they could be caused by haemodilution. Nevertheless, the effect of interindividual differences cannot be discarded. An additional effect of the low haematocrit on cardiovascular changes due to low FIO2, such as pulmonary vasoconstriction or increased cardiac output, may explain the lower dispersion of perfusion distributions found in group A during hypoxia. [ABSTRACT FROM AUTHOR]

Pulmonary gas exchange is the primary function of the lung, and during my lifetime, its measurement has passed through many stages. When I was born, many physiologists still believed that the lung secreted oxygen. When I was a medical student, the only way we had to recognize defective gas exchange was whether the patient was cyanosed. The advent of the oximeter soon showed that this sign could be very misleading. A breakthrough was the introduction of blood gas electrodes that could measure the PO2, PCO2, and pH of a small sample of arterial blood. It was soon recognized that the commonest cause of hypoxemia was ventilation‐perfusion inequality, and that this could also be responsible for CO2 retention. In the early days, the understanding of the mechanisms of pulmonary gas exchange relied on graphical analysis because the oxygen and carbon dioxide dissociation curves are nonlinear and interdependent which precluded algebraic methods. However, with the introduction of digital computing, problems that had hitherto been impossible to tackle became amenable to study. A key advance was the development of the Multiple Inert Gas Elimination Technique. Now, noninvasive methods for measuring gas exchange show promise, and the whole subject continues to develop. I have devoted much of my life thinking about pulmonary gas exchange. The topic has changed enormously from the erroneous view that the lung actively secretes oxygen, to very sophisticated computer analyses of the distribution of ventilation and blood flow in the lung. Exciting advances continue to occur. [ABSTRACT FROM AUTHOR]