Alveolar Dead Space Ventilation Research Articles

Apneustic anesthesia ventilation improves pulmonary function in anesthetized bottlenose dolphins (Tursiops truncatus).

Use of mechanical ventilation during general anesthesia is a necessary practice in the anesthetization of small cetaceans as spontaneous ventilation fails to provide adequate gas exchange. Currently available methods of ventilation do not account for the intermittent breathing strategy of representative species within this infraorder of fully aquatic mammals and may have a significant effect on cardiac and respiratory physiology. To understand the impact of mechanical ventilation on cardiopulmonary function in one small species of cetacean, the bottlenose dolphin (Tursiops truncatus), we compared controlled mechanical ventilation (CMV) to a novel ventilation method known as apneustic anesthesia ventilation (AAV). AAV simulates the normal inspiratory breath-hold pattern of dolphins. Ten anesthetic procedures (dental procedure, n = 9; bronchoscopy, n = 2) were performed on nine dolphins (age range: 10-42 years; mean = 32 years; median = 37 years; female = 3, 40%; male = 6, 60%). In a cross-over study design, dolphins were instrumented and randomly assigned to AAV or CMV as the initial mode of ventilation, then switched to the alternate mode. Baseline cardiopulmonary data were collected and again after 30 min on each mode of ventilation. Cardiac index, stroke volume index, systemic vascular resistance, alveolar dead space, alveolar-arterial oxygen tension gradient, arterial oxygen content, oxygen delivery index, and dynamic respiratory system compliance index were calculated at each of the four time points. During AAV, dolphins had higher arterial oxygen tension, higher mean airway pressure, reduced alveolar dead space ventilation and lower alveolar-arterial oxygen difference. Cardiovascular performance was not statistically different between the two modes. Our study suggests AAV, which more closely resembles the conscious intermittent respiratory pattern phenotype of dolphins, improves ventilation and pulmonary function in the anesthetized dolphin. Future studies should evaluate the cardiopulmonary effects of neutral buoyancy and cardiopulmonary sparing drug protocols to reduce the need for hemodynamic support of current protocols.

Correlation of Respiratory Physiologic Parameters in Mechanically Ventilated Coronavirus Disease 2019 Patients.

Acute respiratory distress syndrome secondary to severe acute respiratory syndrome coronavirus-2 pneumonia or coronavirus disease 2019-related acute respiratory distress syndrome is the primary cause of mortality in coronavirus disease 2019. Some studies have described the concept of “high and low” elastance coronavirus disease 2019-related acute respiratory distress syndrome and proposed individualized management for the acute respiratory distress syndrome, deviating from low tidal volume ventilation. We report simultaneously measured respiratory parameters (static lung compliance, alveolar dead space ventilation, and shunt fraction) in 14 patients with advanced coronavirus disease 2019-related acute respiratory distress syndrome. The results were consistent with typical acute respiratory distress syndrome and did not support the concept of high-type coronavirus disease 2019-related acute respiratory distress syndrome and low-type coronavirus disease 2019-related acute respiratory distress syndrome.

Pathophysiology of dyspnoea in acute pulmonary embolism: A cross-sectional evaluation.

Dyspnoea in pulmonary embolism (PE) remains poorly characterized. Little is known about how to measure intensity or about the underlying mechanisms that may be related to ventilatory abnormalities, alveolar dead space ventilation or modulating factors such as psychological modulate. We hypothesized that dyspnoea would mainly be associated with pulmonary vascular obstruction and its pathophysiological consequences, while the sensory-affective domain of dyspnoea would be influenced by other factors. We undertook a prospective study of 90 consecutive non-obese patients (mean ± SD age: 49 ± 16 years, 41 women) without cardiorespiratory disease. All patients were hospitalized with symptoms for <15 days and a confirmed PE (multi-detector computed tomography (MDCT) scan, n = 87 and high-probability ventilation/perfusion scan, n = 3). Patients underwent assessment of dyspnoea using the Borg score, modified Medical Research Council (mMRC) scale, assessment of psychological trait, state of anxiety and depression and chest pain via the Visual Analogical Scale at the time of maximum dyspnoea. Functional evaluations such as the quantitative ventilation-perfusion lung scan, echocardiography, alveolar dead space fraction and tidal ventilation measurements were completed within 48 h of admission. Multivariate analyses demonstrated that dyspnoea was mainly linked to pulmonary vascular obstruction and/or its consequences such as raised pulmonary arterial pressure and chest pain. The sensory-affective domain of dyspnoea showed additional determinants such as age, depression and breathing variability. Dyspnoea is mainly related to vascular consequences of PE such as increased pulmonary arterial pressure or chest pain. The sensory-affective domain of dyspnoea also correlates with age, depression and breathing variability.

Comparison of pressure and volume-controlled ventilation in laparoscopic cholecystectomy operations.

Laparoscopic cholecystectomy has many advantages such as shorter hospital stay of patients, minimal postoperative pain, rapid recovery after the operation; however, systemic disadvantages because intra-abdominal pressure, position and general anaesthesia may also appear. In this study, pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV) modes during laparoscopic cholecystectomy operations were compared in terms of their effects on haemodynamic, respiratory and blood gas parameters. Patients were randomly assigned to two groups according to the modes of mechanical ventilation, either to the PCV group, group P (35 patients) or to the VCV group, group V (35 patients). A standard electrocardiogram, pulse oximetry, non-invasive blood pressure, end-tidal CO2 , BIS and TOF monitoring were performed. Anaesthesia was induced with propofol, fentanyl and rocuronium. Anaesthesia was maintained with 50% O2 + 50% N2 O, propofol infusion and fentanyl. Haemodynamic data, respiratory parameters, arterial blood gases of the patients were measured. Dynamic compliance of the respiratory system, oxygenation index, alveolar-arterial oxygen gradient and dead space ventilation to tidal volume ratio were calculated. No difference was detected between the groups in terms of descriptive data, operation, anaesthesia, pneumoperitoneum and recovery period (P > 0.05). Haemodynamic data and blood gas values were compared between the two groups, and no significant difference was found (P < 0.05). After pneumoperitoneum, lung compliance decreased in both groups, more importantly in the Group P (P > 0.05). Tidal volume increased 10 min and 20 min after insufflation in the Group V (P < 0.05). Alveolar dead space ventilation to tidal volume ratio before pneumoperitoneum and alveolar-arterial oxygen gradient after pneumoperitoneum were significantly higher in the Group P compared to the Group V (P < 0.05). Dynamic compliance of the respiratory system was similar in both groups. In this study, with volume-controlled ventilation anaesthesia in laparoscopic cholecystectomy, higher tidal volume and lower alveolar-arterial oxygen gradient were achieved after pneumoperitoneum. These findings indicated that VCV mode can provide a better alveolar ventilation than PCV mode in laparoscopic cholecystectomy operations.

Importance of alveolar recruitment strategy revisited.

Low tidal volume, rather than high tidal volume, ventilation is often used for mechanical ventilation during surgery to avoid lung injury due to alveolar overdistention. Under general anesthesia with a muscle relaxant, there is a risk of compressing the lungs by diaphragmatic displacement, which can be aggravated in patients placed in the supine position. Such a risk becomes even higher during reduced tidal volume ventilation, causing alveolar atelectasis and hypoxemia. Therefore, positive end expiratory pressure (PEEP) is applied to prevent spontaneous closure of alveoli. In this volume, Jung et al. [1] reports on the importance of the alveolar recruitment strategy (ARS). The authors applied ARS before the start of one-lung ventilation (OLV), and compared the oxygenation score between high- and low-tidal volume groups. Repetitive open and closure of collapsed alveoli by positive pressure ventilation could cause damage to the capillary endothelium and alveolar epithelium. Excessive expansion and risk of alveolar injury may even occur during low tidal volume ventilation due to an uneven distribution of ventilated volume to already open alveoli. However, Jung et al. [1] showed that preemptive ARS commonly increases PaO2 without causing hemodynamic instability in groups with or without PEEP during OLV. The improvement in oxygenation was better in the group where ARS was combined with PEEP. Their study design and intriguing results will draw the attention of general readers of the journal. The ARS helps to open collapsed alveoli, which is effectively maintained by PEEP. Therefore, both ARS and PEEP maneuvers are compulsory to improve oxygenation and lung mechanics during general anesthesia [2]. Diverse ARS methods have been reported in recent clinical studies. The recommended ARS is peak inspiratory pressure up to 40 cmH2O at 10 respiratory cycles with 15-20 cmH2O PEEP. Adequate PEEP level following ARS is reportedly 5-20 cmH2O depending on the condition of the patient (i.e., pulmonary function and physical condition) and also the type of operation. The time to apply ARS is typically (1) immediately after intubation before confirming lung sounds, (2) after suctioning, or (3) just before extubation. Functional residual capacity is reduced in 50% of patients after tracheal suctioning, in which case combined ARS and PEEP effectively restores PaO2 [3]. Along with increased PaO2, several reports have indicated that ARS with PEEP during OLV decreases AaDO2, and decreases the alveolar dead space ventilation ratio [4,5,6]. In addition to OLV anesthesia, ARS with appropriate PEEP is required to improve PaO2 in patients with minimal lung injury during other surgeries with a high risk of atelectasis such as laparoscopic surgery [7,8,9], pediatric patients [10], and obese patients [9]. This preemptive ARS effect during low tidal volume OLV has been described previously [11]. Preemptive ARS can also be applied before pneumoperitoneum during laparoscopic surgery [8] with the purpose of improving oxygenation. However, high intrathoracic pressure during ARS may cause hemodynamic instability. Therefore, adjustment of the pressure and application duration should consider a patient's hemodynamic status and the potential risks [5]. In obese patients, higher pressures are required for adequate ARS and PEEP [9]. The risk of hemodynamic derangement by such high pressures can be prevented by intravascular volume replacement [12]. Interestingly, one study reported that applying ARS with PEEP to the donor lung in situ as well as after transplantation lowers the risk of primary graft dysfunction [13]. Several reports have suggested the beneficial effects of ARS with PEEP during general abdominal surgery to reduce post-operational complications [14]. In conclusion, applying ARS and PEEP during surgery or in patients vulnerable to atelectasis is helpful for improving oxygenation and lowering postoperative pulmonary complications. PEEP must be sustained to keep alveoli in their open state and optimize patient oxygenation. In addition, adequate ARS before applying PEEP is essential to maximize the benefits of PEEP.

Effect of 50% and maximal inspired oxygen concentrations on respiratory variables in isoflurane-anesthetized horses

BackgroundThe purpose of this study was to compare the effects of 0.5 fraction of inspired oxygen (FiO2) and >0.95 FiO2 on pulmonary gas exchange, shunt fraction and oxygen delivery (DO2) in dorsally recumbent horses during inhalant anesthesia. The use of 0.5 FiO2 has the potential to reduce absorption atelectasis (compared to maximal FiO2) and augment alveolar oxygen (O2) tensions (compared to ambient air) thereby improving gas exchange and DO2. Our hypothesis was that 0.5 FiO2 would reduce ventilation-perfusion mismatching and increase the fraction of pulmonary blood flow that is oxygenated, thus improving arterial oxygen content and DO2.ResultsArterial partial pressures of O2 were significantly higher than preanesthetic levels at all times during anesthesia in the >0.95 FiO2 group. Arterial partial pressures of O2 did not change from preanesthetic levels in the 0.5 FiO2 group but were significantly lower than in the >0.95 FiO2 group from 15 to 90 min of anesthesia. Alveolar to arterial O2 tension difference was increased significantly in both groups during anesthesia compared to preanesthetic values. The alveolar to arterial O2 tension difference was significantly higher at all times in the >0.95 FiO2 group compared to the 0.5 FiO2 group. Oxygen delivery did not change from preanesthetic values in either group during anesthesia but was significantly lower than preanesthetic values 10 min after anesthesia in the 0.5 FiO2 group. Shunt fraction increased in both groups during anesthesia attaining statistical significance at varying times. Shunt fraction was significantly increased in both groups 10 min after anesthesia but was not different between groups. Alveolar dead space ventilation increased after 3 hr of anesthesia in both groups.ConclusionsReducing FiO2 did not change alveolar dead space ventilation or shunt fraction in dorsally recumbent, mechanically ventilated horses during 3 hr of isoflurane anesthesia. Reducing FiO2 in dorsally recumbent isoflurane anesthetized horses does not improve oxygenation or oxygen delivery.

End-tidal CO2for exclusion of suspected pulmonary embolism: a new partner for Wells?

Pulmonary embolism (PE) has been labelled as one of the leading causes of cardiovascular death in the Western World 1 and, still today, more than 40,000 patients in Germany and 200,000 in the USA die of acute PE each year. However, hospital mortality rates can fall from as high as 30% to 8% 2 when diagnosis and treatment are properly provided. The diagnosis of PE remains a challenge because of highly variable clinical symptoms. Consequently, the diagnosis of PE has been finally confirmed in <35% of patients with a clinical suspicion of PE 3. A simple bedside test with the ability to exclude PE in patients who do not have it, while not overlooking true-positive cases, is desired and will prevent unnecessary exposure to contrast agents and radiation. The assessment of alveolar dead space ventilation and the expired tracer gas CO2 as surrogates for pulmonary vascular obstruction have been proposed as valuable tools for excluding PE. The underlying pathophysiological principle is based on the three-compartment model of the …

Effects of changing body position on oxygenation and arterial blood pressures in foals anesthetized with guaifenesin, ketamine, and xylazine

ObjectiveTo investigate the impact of a change in body position on blood gases and arterial blood pressures in foals anesthetized with guaifenesin, ketamine, and xylazine. Study designProspective, randomized experimental study. AnimalsTwelve Quarter Horse foals, age of 5.4 ±0.9 months and weighing 222 ± 48 kg. MethodsFoals were anesthetized with guaifenesin, ketamine, and xylazine for 40 minutes in lateral recumbency and then assigned to a change in lateral recumbency after hoisting (Group 1, n = 6), or no change (Group 2, n = 6). Oxygen 15 L minute−1 was insufflated into the endotracheal tube throughout anesthesia. Arterial blood pressure, heart rate, respiratory rate (fR), inspired fraction of oxygen (FiO2), and end-tidal carbon dioxide (Pe’CO2) were measured every 5 minutes. Arterial pH and blood gases [arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2)] were measured at 10, 30, and 40 minutes after induction, and 5 minutes after hoisting. Alveolar dead space ventilation and PaO2/FiO2 were calculated. Two repeated measures models were used. All hypothesis tests were two-sided and significance level was α = 0.05. All values are presented as least square means ± SE. ResultsValues at time-matched points from the two groups were not significantly different so they were combined. Arterial partial pressure of oxygen decreased significantly from 149 ± 14.4 mmHg before hoisting to 92 ± 11.6 mmHg after hoisting (p=0.0013). The PaO2/FiO2 ratio decreased from 275 ± 30 to 175 ± 24 (p=0.0055). End-tidal carbon dioxide decreased significantly from 48.7 ± 1.6 to 44.5 ± 1.2 mmHg (p=0.021). Arterial partial pressure of carbon dioxide, blood pressures and heart rates measured 5 minutes after hoisting were not different from measurements obtained before hoisting. Conclusion and clinical relevanceHoisting decreased PaO2 in anesthetized healthy foals. Administration of supplemental oxygen is recommended to counter the decrease in oxygenation and PaO2 measurement is necessary to detect early changes.

Arterial minus end-tidal CO 2 as a prognostic factor of hospital survival in patients resuscitated from cardiac arrest

The purpose of this study was to determine the clinical value of arterial minus end-tidal CO(2) [P(a-et)CO(2)] and alveolar dead space ventilation ratio (V(dA)/V(t)) as indicators of hospital mortality in patients that have been resuscitated from cardiac arrest at emergency department. Forty-four patients with a return of spontaneous circulation (ROSC) after cardiac arrest were studied in the emergency department of a university teaching hospital from March 2004 to February 2006. Mean arterial pressure (MAP), serum lactate, arterial blood gas studies, end-tidal CO(2) (EtCO(2)), P(a-et)CO(2), and V(dA)/V(t) were evaluated at 1 h after ROSC. We compared these variables between hospital survivors and non-survivors. The rates of ventricular fibrillation and pulseless ventricular tachycardia in hospital survivors were higher than those of non-survivors (53.0 and 9.7%, respectively, p=0.002). Hospital survivors had significantly higher MAP, lower serum lactate, lower P(a-et)CO(2), and lower V(dA)/V(t) value than non-survivors. Receiver operator characteristic (ROC) curves of serum lactate, P(a-et)CO(2), and V(dA)/V(t) showed significant sensitivity and specificity for hospital mortality. Specifically, lactate > or = 10.0 mmol/L, P(a-et)CO(2) > or = 12.5 mmHg, and V(dA)/V(t) > or = 0.348 were all associated with high hospital mortality (p=0.000, 0.001 and 0.000, respectively). This study showed that high serum lactate, high P(a-et)CO(2) and high V(dA)/V(t) during early ROSC in cardiac arrest patients suggest high hospital mortality. If future studies validate this model, the P(a-et)CO(2) and V(dA)/V(t) may provide useful guidelines for the early post-resuscitation care of cardiac arrest patients in emergency departments.

Diagnostic Studies in Patients With Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) is a clinical-radiological diagnosis. Clinical diagnosis comprises severe hypoxemia assessed by arterial oxygen tension/fraction of inspired oxygen ratio of less than 200 and bilateral infiltrate on a chest radiograph in the absence of left atrial hypertension. The sensitivity and specificity of the clinical diagnosis vary based on the underlying etiology for ARDS. Except for presence of bilateral infiltrate on chest radiograph and severe hypoxemia on arterial blood gas, most diagnostic studies are used to exclude mimics of ARDS and potentially modify treatment. Computerized tomography of the chest is helpful in understanding the extent of the disease and is more sensitive in identifying pneumomediastinum and pneumothoraces seen frequently in patients with ARDS, which can be missed on a chest radiograph, especially if they are small in size. Measurements of alveolar dead space ventilation fraction can be helpful in determining the prognosis in individuals with ARDS. Bronchoalveolar lavage, transbronchial lung biopsy, and open lung biopsies can be safely performed in patients with ARDS. Bronchoalveolar lavage fluid in patients with ARDS shows neutrophil predominance with increased edema fluid to serum protein ratio. Diffuse alveolar damage, a pathognomic of ARDS, is seen on histopathology on transbronchial lung biopsy or open lung biopsy. Most common complications of these procedures include transient hypoxemia, respiratory acidosis, and pneumothorax with occasional persistent air leak. The potential risk of diagnostic studies should be balanced against the possible foreseeable benefits of the diagnostic studies.

Luxury lung perfusion in end-stage liver disease during liver transplantation.

End-stage liver disease is accompanied by a hyperkinetic circulation sometimes combined with hypoxaemia. Nitric oxide overproduction has been described as a possible cause by dilating the vasculature and decreasing cardiac afterload. The aim of this study was to evaluate haemodynamics, ventilation/perfusion matching, alveolar and alveolar dead space ventilation and resistance of systemic and pulmonary vasculature during liver transplantation. Ten liver transplantation patients were studied. Cardiac output, CO, was measured with thermodilution technique. Pulmonary shuntflow was calculated from standard formulas. Effective cardiac output, COeff, was defined as the CO in contact with alveolar ventilation, VA. Effective alveolar ventilation, VAeff, was defined as VA in contact with pulmonary circulation. Measurements were performed during dissection, anhepatic and reperfusion phases. During the dissection phase the shunt was 23 +/- 3%, COeff was 7.9 +/- 0.6 l/min, SVR was 620 +/- 67 dyn.s/cm5, VAeff was 3.4 +/- 0.5 l/min, SaO2 was 98 +/- 1% and SvO2 was 86 +/- 2%. Corresponding values during the anhepatic phase were 16 +/- 2%, 5.6 +/- 0.4 l/min, 931 +/- 78 dyn.s/cm5, 3.1 +/- 0.2 l/min, 99 +/- 1% and 88 +/- 1%. During the reperfusion phase the values returned to levels close to that of the dissection phase. The reduction of COeff between the dissection and the anhepatic phase was significant (P < 0.01). The low vascular resistance is accompanied by a high cardiac output. In spite of the high shunt fraction, these patients were not hypoxaemic. This is explained by the fact that the increased cardiac output leads to a decrease in arterio-mixed venous oxygen content difference and an increase in mixed venous oxygenation level, SvO2 86-88%, normal value approximately 70%. The VAeff/COeff in this study was approximately 0.5, i.e. the effective cardiac output, COeff is 235, 180 and 197% of the effective alveolar ventilation, VAeff during the three phases. Thus, about twice the amount blood is oxygenated as compared to a normodynamic situation, which compensates for the effect of the shunt flow on oxygenation.

Invited commentary:H. Jellinek et al.: “Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference” — (Acta Chir. Austriaca 1994; 26:47–51)

Invited commentary:H. Jellinek et al.: “Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference” — (Acta Chir. Austriaca 1994; 26:47–51)

Invited commentary: Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference

Invited commentary: Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference

Invited commentary: Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference

Invited commentary: Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference

Alveolar dead space ventilation during bilateral lung transplantation determined by the arterial to end-tidal CO2 tension difference

Background: Transplanted lungs transiently may present with underperfused lung compartments (alveolar dead space). In order to evaluate intraoperative changes of alveolar dead space in transplanted lungs the difference between the arterial and the end-tidal CO2 tension (P[a-et]CO2) was determined.Methods: In 5 patients undergoing bilateral lung transplantation without using cardiopulmonary bypass arterial CO2 and end-tidal CO2 (infrared absorption capnography) were determined simultaneously. P(a-et)CO2 was calculated.Results: Intraoperatively, during 1-lung ventilation of the first transplanted lung (with the contralateral pulmonary artery crossclamped for sequential replacement of the second lung) increased P(a-et)CO2 values of 11±4 mm Hg were observed. During ventilation of both transplanted lungs the P(a-et)CO2 difference showed a further increase to a mean of 17±4 mm Hg (p<0.01), indicating that up to 50% of the alveoli were unperfused. 24 hours post transplant P(a-et)CO2 had normalized to 4±2 mm Hg (p<0.05 and p<0.005 vs. intraoperative 1-lung- and 2-lung ventilation, respectively).Conclusions: Intraoperative determination of P(a-et)CO2 during bilateral lung transplantation revealed an abnormally increased alveolar dead space in transplanted lungs during early reperfusion that was reversible after 24 hours. The second lung seemed to be more affected by this mismatch between ventilation and perfusion, even if ischemic time was not excessive.

Alveolar dead space does not affect indirect Fick cardiac output determinations

We examined the influence of three variables (different breathing circuits, breath selected for analysis, and alveolar dead space ventilation) on the accuracy of noninvasive cardiac output determinations with the Fick CO2 (indirect) equation. We compared noninvasive determinations with invasive thermodilution measurements over a wide range of cardiac outputs in 17 2-mo-old pigs anesthetized with halothane and nitrous oxide and paralyzed with either pancuronium or d-tubocurare. We found that rebreathing and nonrebreathing circuits provide accurate cardiac output determinations and that the optimal breath for analysis with either the rebreathing or nonrebreathing technique appears to depend on the cardiac output. When alveolar dead space was increased by using positional changes and the intracardiac administration of glass beads, there was still a good correlation between noninvasive and invasive cardiac output determinations. We conclude that both rebreathing and nonrebreathing techniques of indirect Fick cardiac output determinations correlate well with thermodilution measures over a wide range of cardiac outputs and alveolar dead space/tidal volume fractions.

The controversy about blood-gas CO2 equilibrium in lungs: reinvestigation by prolonged CO2 rebreathing in awake dogs during rest and exercise.

When pulmonary diffusing capacity for O2 is to be determined in lungs with unequal distribution of alveolar ventilation to pulmonary perfusion it is common practice to correct arterial PO2 for the shunt effect and the end-tidal PO2 for alveolar dead space ventilation. The latter correction is based on the assumption that PCO2 in end-capillary blood is in equilibrium with alveolar gas (Riley and Cournand, 1949). It appears to follow from this assumption that in conditions of no gas exchange, such as rebreathing, PCO2 in alveolar gas should be equal to that in arterial blood. Thus the finding of negative blood-to-gas PCO2 differences during rebreathing in dogs (Gurtner et al., 1969) and in man (Jones et al., 1969, 1972; Denison et al., 1971) has challenged the fundamental concepts of pulmonary gas exchange. However, these results could not be reproduced by others (Scheid et al., 1972).KeywordsPulmonary Diffuse CapacityRespiratory MassArterial PC02Rebreathing PeriodBlood PC02These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Measurement of dead space ventilation using a pHa servo-controlled ventilator.

A control system for the systemic arterial pH (pHa) servo control of mechanical ventilation has recently been developed. If pHa is maintained constant by the change, separation of minute volume into alveolar ventilation and physiological dead space ventilation (VE = fVA VDp) can be manipulated to show that VDp = (VE1 - VE 2)/(f1 - fe) where f1 and f2 are different ventilator frequencies and VE1 and VE2 are expired minute volumes at these frequencies. Also, added dead space can be measured. VDadded = (VE2 - VE1)/f where VE1 and VE2 are the minute volumes before and after the dead space was added. The validity of these equations was tested in the anesthetized dog. The measured added dead space was in close agreement with the volume of dead space which was added and with that measured by another independent method. The measurement of VDp, probably as a result of tidal volume-related changes in VDp, did not agree as well with VDp measured by an independent method.

Inert gas elimination from lungs with stratified inhomogeneity: Theory

The effects of diffusion limitation in alveolar space (stratified inhomogeneity) on steady state inert gas elimination by the lung from blood are studied in theory. The lung models used for the calculations are characterized by a diffusion barrier in the alveolar space, which is quantified by a diffusive conductance (diffusing capacity), D′. In both homogeneous and inhomogeneous lung models (with log-normal distribution of V̇ a, Q̇ and D′) increasing stratified inhomogeneity (decreasing D′) is shown to diminish inerg gas elimination. The effect, which depends on the solubility of the gases, is similar to the effect of alveolar dead space ventilation.

Static and dynamic lung volumes and ventilation-perfusion abnormality in adult asthma.

Dynamic lung volumes (forced vital capacity, forced expiratory volume in 0·5 second and in 1·0 second), static lung volumes (total lung capacity, functional residual capacity, residual volume), and ventilation-perfusion relationships (alveolar-arterial oxygen tension difference, alveolar dead space ventilation to tidal volume ratio, arterial oxygen and carbon dioxide tension, and the fractional ventilation and perfusion relationship by the three-compartment lung model) were measured in adult asthmatics during the acute, recovery, and stable or asymptomatic phases of an asthmatic attack. Eighteen patients were studied during 20 separate asthmatic attacks. The patients behaved in one of three ways with regard to total lung capacity (TLC): group I had an elevated TLC during the acute asthmatic attack which returned to normal, group II had a normal TLC throughout the attack, and group III had an elevated TLC that did not return to normal on recovery from the asthmatic attack. With the patients separated into the three groups, the other pulmonary function measurements, especially the measurements of ventilation-perfusion abnormality, were compared. There were no statistically significant differences of ventilation-perfusion abnormality between groups I, II, or III. There was a tendency for perfusion abnormality to be less during the acute phase of the asthmatic attack in patients with an elevated TLC (group I). The three-compartment lung model revealed the major abnormality in all groups to be an increased fraction of unventilated but perfused lung.