Ventilation–perfusion inequality and carbon dioxide sensitivity in hypoxaemic chronic obstructive pulmonary disease (COPD) and effects of 6 months of long‐term oxygen treatment (LTOT)

The aim of our study was to find out how blood gas disturbances in stable, eucapnic, severe chronic obstructive pulmonary disease (COPD) patients with an arterial oxygen tension (PaO₂) value of 7·7 (6·1–8·4) kPa are affected by ventilation–perfusion (V_A/Q) relationships and carbon dioxide (CO₂) sensitivity and how these parameters are influenced by 6 months of long‐term oxygen treatment (LTOT). V_A/Q ratios were measured using the multiple inert gas elimination technique (MIGET). Mouth occlusion pressure 0·1 s after onset of inspiration (Pi0·1) and minute ventilation (V_E) were measured to assess respiratory drive response (ΔPi0·1/ΔPCO₂) and hypercapnic ventilatory response (HCVR) to CO₂ rebreathing. At the start of LTOT, a normal median respiratory drive response level of 1·2 (0·2–2·3) cm H₂O/kPa and a low median HCVR as compared with healthy individuals (P<0·001) were found. However, 7·9 (0–29·8)% of the V_E, was directed towards hypoperfused lung areas. The dispersion of ventilation (log SDV; 0·47–1·76), and the dispersion of perfusion (log SDQ; 0·66–1·07) were wider than normal. The PaO₂ level correlated inversely with mean V_A/Q ratio for ventilation (V mean) and shunt. The PaCO₂ level correlated inversely with HCVR and vital capacity. After 6 months of LTOT, no significant changes in daytime blood gas levels, CO₂‐sensitivity or V_A/Q ratios were found. V_E tended to be reduced by 1·0 l min^–1. Conclusions: An elevated V mean and probably shunting are important contributing factors for the reduced PaO₂ and hypercapnic ventilatory response is a major determinant of PaCO₂ in eucapnic stable hypoxaemic COPD. Six months of LTOT does not affect blood gases, CO₂ sensitivity or ventilation–perfusion relationships.     

Relying on pulse oximetry to avoid hypoxaemia and hyperoxia: A multicentre prospective cohort study in patients with circulatory failure

PurposeThe purpose of this study was to assess the predictive performance of pulse oximetry (SpO₂) to rule out hypoxaemia and hyperoxia in critically ill patients.MethodsSpO₂, arterial oxygenation (SaO₂), and arterial partial pressure of oxygen (PaO₂) were prospectively and simultaneously measured every 6 h during the first 24 h of intensive care unit admission in a multicentre cohort of critically ill patients suffering acute circulatory failure. Likelihood ratios associated with different cutoff values of SpO₂ to rule out hypoxaemia (SaO₂ < 90% or PaO₂ < 60 mmHg) or hyperoxia (SaO₂ > 95% or PaO₂ > 100 mmHg) and post-test probabilities were calculated. Mean bias between SpO₂ and SaO₂ and agreement interval were calculated. Area under the receiver operating characteristics associated with SpO₂ to predict different threshold values of SaO₂ and PaO₂ were calculated.ResultsFive hundred seventy-one patients (mean [standard deviation] Simplified Acute Physiology Score II: 58.7 [20.1]; mechanically ventilated 75.6%) with 2643 available SaO₂ and PaO₂ samples and corresponding 2643 SpO₂ values were analysed. Mean bias between SpO₂ and SaO₂ was 1.1%, and its agreement interval ranged from −8.2 to +11.1%. SpO₂ cutoff values of 88%, 90%, and 92% left the possibility that 8%–13% of patients had hypoxaemia. SpO₂ < 95% left the possibility that 31% of patients had hyperoxia. All calculated areas under the receiver operating characteristics showed a lower limit of their 95% confidence interval below 0.85ConclusionIn this cohort of patients with circulatory failure, SpO₂ had poor discriminative ability to rule out hypoxaemia and hyperoxia. Overconfidence upon SpO₂ monitoring may be dangerous.     

Acute effects of continuous rotational therapy on ventilation-perfusion inequality in lung injury

Objective: To investigate ventilation-perfusion (V_A/Q) relationships, during continuous axial rotation and in the supine position, in patients with acute lung injury (ALI) using the multiple inert gas elimination technique. Design: Prospective investigation. Setting: Eighteen-bed intensive care unit in a university hospital. Patients and interventions: Ten patients with ALI (PaO₂/FIO₂ ratio < 300 mm Hg) were mechanically ventilated in a pressure controlled mode and placed on a kinetic treatment table. Measurements and results: Distributions of V_A/Q were determined 1) during rotation (after a period of 20 min) and 2) after a resting period of 20 min in the supine position. During axial rotation, intrapulmonary shunt (19.1 ± 15 % of cardiac output) was significantly reduced in comparison with when in the supine position (23 ± 14 %, p < 0.05), areas with “low” V_A/Q were not affected by the positioning maneuver. General V_A/Q mismatch (logarithmic distribution of pulmonary blood flow) was decreased during rotation (0.87 ± 0.37) in comparison with when the patient was in the supine position (0.93 ± 0.37, p < 0.05). Arterial oxygenation was significantly improved during continuous rotation (PaO₂/FIO₂ = 217 ± 137 mm Hg) as compared with in the supine position (PaO₂/FIO₂ = 174 ± 82 mm Hg, p < 0.05). The positive response of the continuous rotation on arterial oxygenation was only demonstrated in patients with a Murray Score of 2.5 or less, indicating a “mild to moderate” lung injury, while in patients presenting with progressive ARDS (Murray Score > 2.5), the acute positive response was limited. Conclusions: Continuous axial rotation might be a method for an acute reduction of V_A/Q mismatch in patients with mild to moderate ALI, but this technique is not effective in late or progressive ARDS. Further studies including a large data collection are needed. Received: 19 June 1997 Accepted: 6 November 1997     

Histamine-induced asthma in children: effects on the ventilation-perfusion relationship

Summary. . Asthma was provoked by histamine inhalation in five children in order to study the hypoxaemia that might ensue and the underlying ventilation-perfusion (V?_A/Q?) mismatching. The distribution of the V?_A/Q? ratios was measured by a multiple inert gas technique before the provocation, during the asthmatic attack and after salbutamol inhalation. All children displayed a unimodal distribution of ventilation and perfusion under baseline conditions. During asthma they all developed a bimodal distribution, one mode lying within normal V?_A/Q?regions but with increased perfusion to regions with V?_A/Q? ratios of OT-1, which correlated with the observed hypoxaemia; the other mode was centred on a V?_A/Q? ratio of approximately 10 and the magnitude of this mode correlated with FEV₁ in per cent of the predicted value. Salbutamol improved the V?_A/Q? distribution and restored the blood gases to normal. We hypothesize that histamine-induced asthma causes a state of hyperinflation which compromises regional ventilation and blood flow, resulting in a V?_A/Q? mismatching with one normal and one high V?_A/Q? mode, and hypoxaemia.     

Discriminating between the effect of shunt and reduced VA/Q on arterial oxygen saturation is particularly useful in clinical practice

There is an extensive literature on methods for discriminating between an increased shunt and a reduced ratio of ventilation to perfusion. In this review we prefer the terms “VA/Q” and “reduced or low VA/Q” rather than “V/Q inequality” to refer to the effects on arterial oxygenation of reducing V/Q below 0.8 to about 0.1. Almost without exception the conventional methods for measuring shunt and reduced VA/Q are invasive as well as technically complex. For most clinicians who are dealing with a hypoxemic patient the relevance of these entities is not so obvious as to justify the time and difficulty in either understanding or measuring them. However this review shows that, while an increased shunt and a decreased VA/Q both reduce arterial oxygen saturation (SaO₂) at a particular inspired oxygen concentration (PIO₂), the effect of shunt and reduced VA/Q have important clinical differences on the relationship between PIO₂ and SaO₂. The review also outlines a simple non-invasive method for measuring shunt and reduced VA/Q which illustrates the value of discriminating between them in clinical practice. This revised version was published online in July 2006 with corrections to the Cover Date.     

Ventilation/perfusion ratio and right to left shunt in healthy newborn infants

Oxygenation impairment can be assessed non-invasively by determining the degree of right-to-left shunt and ventilation/perfusion (V_A/Q) inequality. These indices have been used in sick newborn infants, but normative values have not been reported which are essential to determine the magnitude of the abnormality. We, therefore, aimed to measure the shunt and V_A/Q in infants with no history of respiratory conditions and determine if there was any effect of supine or prone position and the reproducibility of the data. Data were analysed from infants who had undergone a hypoxic challenge and in a subset who had been assessed in the supine or prone position. Transcutaneous oxygen saturations (SpO₂) were recorded at fractions of inspired oxygen (F_IO₂) of 0.21 and 0.15. Two independent raters used a computer software algorithm which analysed and fitted paired data for F_IO₂ and SpO₂ and derived a curve which represented the best fit for each infant’s data and calculated the shunt and V_A/Q. The raters ability to interpret the SpO₂ value which corresponded to a given F_IO₂ was compared. The downwards displacement of the F_IO₂ versus SpO₂ curve was used to estimate the degree of right-to-left shunt and the rightwards shift of the curve was used to calculate the V_A/Q ratio. The mean (SD) gestational age of the 145 infants was 39 (1.6) weeks, their birth weight was 2990 (578) gms and median (range) postnatal age at measurement 3 (1–8) days. The mean (SD) V_A/Q ratio was 0.95 (0.21). None of the infants had a right-to-left shunt. No significant differences were found in V_A/Q in the supine compared to the prone position. The intraclass correlation coefficient of V_A/Q between two independent raters was 0.968 (95% CI 0.947–0.980), p?<?0.001. Right-to-left shunt and V_A/Q ratio in healthy newborn infants were similar in the prone compared to the supine position.     

Deposition of terbutaline in the large or small airways: A single-center pilot study of ventilation-perfusion distributions and airway tone

Background: Beta₂-receptor agonists are used as bronchodilators and may influence gas exchange, leading to transient hypoxemia via hypoxic vasoconstriction.Objectives: This single-center pilot study assessed whether responses of gas-exchanging elements or airway tone would vary depending on where terbutaline sulfate, as an aerosol, a beta₂-receptor agonist commonly used by patients with asthma, is deposited in the airways. We also questioned whether identical doses of nebulized terbutaline would elicit different responses in airway tone after differential deposition.Methods: Terbutaline mixed with a solution of technetium 99m diethylenetriamine pentaacetic acid was nebulized and inhaled in different modes on 2 study days by patients with stable asthma. The aerosol was directed to either the large or small airway. To confirm that different deposition patterns were obtained while identical doses were given on the 2 study days, the deposition pattern and total count over the lungs were recorded by a gamma camera. Arterial oxygen tension (PaO₂), ventilation-perfusion (V_A/Q) distributions (by multiple inert-gas-elimination technique), and specific airway conductance (by body plethysmography) were studied before and after the inhalations.Results: Five patients (3 women, 2 men) aged 27 to 71 years (mean age, 39 years) were enrolled. An 8-fold difference in penetration index indicated major differences in the deposition pattern on the 2 study days. Despite the low statistical power of the study (45%) due to the low number of participating asthmatic patients, we found that (V_A/Q) inequality increased significantly (P < 0.05) after large-airway deposition but not after small-airway deposition. Preservation of normal or near-normal PaO₂ was noted in both series of experiments, even though increased (V_A/Q) mismatch occurred after terbutaline was deposited in the large airways. We also confirmed significant responses in airway tone after both sets of terbutaline administration (P < 0.05 for both), and no differences in bronchodilation due to deposition site were found, showing that the changes in airway tone after the 2 modes of administration occurred independently of changes in (V_A/Q) matching.Conclusions: Our results suggest that the deposition of terbutaline in the large airways tends to increase (V_A/Q) inequality and that bronchodilation occurs regardless of the deposition pattern.     

Sleep-related breathing disorders following discharge from intensive care

Objectives: To determine the incidence of sleep-related breathing disorders and nocturnal hypoxaemia in patients discharged from ICU following prolonged mechanical ventilation.¶Design: Prospective, consecutive patient observational study.¶Setting: The medical and surgical wards of a University Hospital.¶Patients and participants: Fifteen consecutive, adult patients discharged from the ICU who had received more than 48 h of mechanical ventilation were studied. Ten healthy volunteers acted as controls.¶Measurements and results: Overnight, multi-channel pneumographic studies were performed on all patients and controls. Chest and abdominal wall movement, air flow, oxygen saturation and snoring were continuously recorded. Data was analysed by both visual inspection of the traces and by computer-based algorithms. An apnoea/hypopnoea index was calculated for each patient and volunteer. Volunteers had an apnoea/hypopnoea index of less than 5 and had no episodes of nocturnal oxygen desaturation (SaO₂ < 90 %). Despite oxygen therapy 13/15 patients had episodes of desaturation and 9/15 spent more than 2 h with an SaO₂ < 90 %. Eleven patients had an abnormal apnoea/hypopnoea index (range 5–34 events/h). Four patients had predominantly obstructive events while 7 primarily had hypopnoeas.¶Conclusions: Significant overnight oxygen desaturation is common in patients discharged from ICU who have received prolonged mechanical ventilation. This group also has a significant incidence of sleep-related breathing disorders and this mechanism is likely to be important in the pathogenesis of the hypoxaemia.     

Increased pulmonary artery systolic storage associated with improved ventilation-to-perfusion ratios in acute respiratory distress syndrome

Purpose

The possibility that the increased pulmonary artery systolic storage (PASS) correlates with an improved distribution of ventilation/perfusion (V_A/Q) and hence benefits gas exchange in acute respiratory distress syndrome (ARDS) was examined. Pulmonary artery systolic storage is the fraction of stroke volume stored in PA during systole and then discharged to the capillaries. The increased PASS can augment the diastolic pulmonary capillary blood flow (PCBF), which can then increase capillary blood volume participating in gas diffusion. We examined this by assessing the correlation between PASS and physiologic dead space to tidal volume (VD/VT) ratio.

Materials and Methods

Included were 17 patients with ARDS. By using nitrous oxide-airway-pneumotachographic method, we measured the instantaneous PCBF, from which PASS was determined. Because PASS is the same as the flow volume of PCBF during diastole, PASS was determined from the flow volume of PCBF during diastole divided by the flow volume of PCBF during a whole cardiac cycle. The VD/VT ratio, used as an index of V_A/Q, was measured by using the Bohr equation.

Results

There was a good inverse correlation between PASS and VD/VT (r² = 0.785, P < .0001).

Conclusions

Our data indicate that the increased PASS correlates with an improved distribution of V_A/Q and hence benefits gas exchange in ARDS.     

Regional V˙A/Q˙ ratios in man using 133Xe and single photon emission computed tomography (SPECT) corrected for attenuation

We describe a technique to obtain non-invasively regional pulmonary ventilation–perfusion ratios (V˙_A/Q˙) using single photon emission computed tomography (SPECT) and continuous infusion of ¹³³Xe. Single photon transmission tomography was used for attenuation correction, for delineation of the lungs and for V˙_A/Q˙ calculations. Data are presented for six normal subjects and compared to those for two patients with moderate chronic obstructive pulmonary disease (COPD). The mean V˙_A/Q˙ for the whole lung of the normal subjects ranged from 0·49 to 0·65, group mean 0·56 ± 0·07 (1 SD), and there was no significant difference between the right and left lung. The consistently too low V˙_A/Q˙ values are related to the inability to measure regional blood volume and the low resolution of the scintillation camera, giving an under-estimation of tracer input. For the normal subjects, the dispersion of V˙_A/Q˙, as defined by the standard deviation of the individual distribution functions, ranged from 0·12 to 0·19. One of the patients was characterized by a low mean V˙_A/Q˙ of 0·35, and the other patient had a wide dispersion (SD) of V˙_A/Q˙ of 0·37. In the normal subjects, a consistent V˙_A/Q˙ gradient was found only in the ventrodorsal direction. ¹³³Xe and SPECT can be used to obtain meaningful biological information regarding ventilation/perfusion relationships of potential clinical value.     

High-frequency percussive ventilation attenuates lung injury in a rabbit model of gastric juice aspiration

Objective To test the effects of high-frequency percussive ventilation (HFPV) compared with high-frequency oscillatory ventilation (HFOV) and low-volume conventional mechanical ventilation (LVCMV), on lung injury course in a gastric juice aspiration model. Design Prospective, randomized, controlled, in-vivo animal study. Setting University animal research laboratory. Subjects Forty-three New Zealand rabbits. Interventions Lung injury was induced by intratracheal instillation of human gastric juice in order to achieve profound hypoxaemia (PaO₂/F_IO₂ ≤ 50). Animals were ventilated for 4 h after randomization in one of the following four groups: HFPV (median pressure 15 cmH₂O); LVCMV (V_T 6 ml kg^–1 and PEEP set to reach 15 cmH₂O plateau pressure); HFOV (mean pressure 15 cmH₂O); and a high-volume control group HVCMV (V_T 12 ml kg^–1 and ZEEP). Measurements and results Static respiratory compliance increased after the ventilation period in the HFPV, LVMCV and HFOV groups, in contrast with the HVCMV group. PaO₂/F_IO₂ improved similarly in the HFPV, LVCMV and HFOV groups, and remained lower in the HVCMV group than in the three others. Lung oedema, myeloperoxidase and histological lung injury score were higher in the HVCMV group, but not different among all others. Arterial lactate markedly increased after 4 h of ventilation in the HVCMV group, while lower but similar levels were observed in the three other groups. Conclusion HFPV, like HFOV and protective CMV, improves respiratory mechanics and oxygenation, and attenuates lung damage. The HFPV provides attractive lung protection, but further studies should confirm these results before introducing HFPV into the clinical arena.     

Gas-exchange impairment: its correlation to lung mechanics in acute airway obstruction (studies on a rabbit asthma model)

Summary. A rabbit model was developed for the studies of ventilation/perfusion relationships (V?/Q?) and thorax mechanics during bronchial provocation tests. Baseline data from 14 anaesthetized rabbits show a V?_A/Q? distribution that is broader (less efficientV?_A/Q?match) than that of lung-healthy humans, dogs and horses. Airway provocation was created by inhalation of ammonia, prostaglandin (PGE₁) and methacholine bromide. Methacholine bromide was the only substance that triggered measurable V?_A/Q? changes. Measurements 5 min after methacholine provocation showed markedly increased thorax resistance, widened V?_A/Q? distribution and in some rabbits an increased shunt. Fifteen minutes after provocation that was still a broad V?_A/Q? distribution and in several rabbits a further increase of shunt. Both thorax resistance and perfusion of regions with low V?_A/Q? were reduced. Our results suggest a correlation between thorax resistance and perfusion of regions with low V?_A/Q?. However, the slower normalization in V?_A/Q? disturbance and the remaining or increased shunt suggests that factors other than airway resistance contribute to the gas-exchange impairment. These factors might be alveolar oedema, or mucus and oedema in the smallest airways.     

The changes in leg blood flow during and after mild or severe acute hypoxaemia in healthy humans

The present study examines the leg blood flow changes in resting healthy humans during and after a 10‐min period of mild (PaO₂=5·60 kPa) or severe hypoxaemia (PaO₂=4·53 kPa) induced by breathing hypoxic gas mixtures. A Colour Duplex Scan system allowed to measure the cross‐sectional area (CSA) and mean blood flow (Qdot;) in a femoral artery (FA) and a femoral vein (FV) and also in an artery supplying leg muscles (medial gastrocnemius artery, MGA). During the mild as well as the severe hypoxaemia and their recovery periods, no significant variations of Qdot; and CSA occurred in FA and FV. During the mild hypoxaemia and the first 10 min of the recovery period, Qdot; and CSA of MGA increased (maximal changes: +84 and +20%, respectively). By contrast, a marked Qdot; decrease and a reduced CSA were measured in MGA during the severe hypoxaemia (?67 and ?60%, respectively). This reduced muscle blood flow was followed by a vasodilatation (CSA increase = +30%), which began 10 min after the hypoxaemia ended and persisted for a further 10‐min period. This study shows that the time course of muscle blood flow changes in response to acute hypoxaemia depends on the PaO₂ level. Reverse effects were measured during the mild or the severe hypoxaemia, whereas a post‐hypoxaemic vasodilatation occurred in all circumstances.     

Characteristics and outcomes of patients treated with airway pressure release ventilation for acute respiratory distress syndrome: A retrospective observational study

BackgroundThe optimal mode of ventilation in acute respiratory distress syndrome (ARDS) remains uncertain. Airway pressure release ventilation (APRV) is a recognized treatment for mechanically-ventilated patients with severe hypoxaemia. However, contemporary data on its role as a rescue modality in ARDS is lacking. The goal of this study was to describe the clinical and physiological effects of APRV in patients with established ARDS.MethodsThis retrospective observational study was performed in a 23-bed adult intensive care unit in a tertiary extracorporeal membrane oxygenation (ECMO) referral centre. Patients with ARDS based on Berlin criteria were included through a prospectively-collected APRV database. Patients receiving APRV for less than six hours were excluded.ResultsFifty patients fulfilled the eligibility criteria. Prior to APRV initiation, median Murray Lung Injury Score was 3.5 (interquartile range (IQR) 2.5–3.9) and PaO₂/FiO₂ was 99 mmHg (IQR 73–137). PaO₂/FiO₂ significantly improved within twenty-four hours post-APRV initiation (ANOVA F(1, 27) = 24.34, P < .005). Two patients (4%) required intercostal catheter insertion for barotrauma. Only one patient (2%) required ECMO after APRV initiation, despite a majority (68%) fulfilling previously established criteria for ECMO at baseline. Hospital mortality rate was 38%.ConclusionsIn patients with ARDS-related refractory hypoxaemia treated with APRV, an early and sustained improvement in oxygenation, low incidence of clinically significant barotrauma and progression to ECMO was observed. The safety and efficacy of APRV requires further consideration.     

Prognosis value of partial arterial oxygen pressure in patients with septic shock subjected to pre-hospital invasive ventilation

Objective

Mechanical ventilation can help improve the prognosis of septic shock. While adequate delivery of oxygen to the tissue is crucial, hyperoxemia may be deleterious. Invasive out-of-hospital ventilation is often promptly performed in life-threatening emergencies. We propose to determine whether the arterial oxygen pressure (PaO₂) at the intensive care unit (ICU) admission is associated with mortality in patients with septic shock subjected to pre-hospital mechanical ventilation.

Pressure-limited ventilation with permissive hypercapnia and minimum PEEP in salinelavaged rabbits allows progressive improvement in oxygenation,but does not avoid ventilator-induced lung injury

Objective To determine whether pressure-limited intermittent mandatory ventilation with permissive hypercapnia and positive end-expiratory pressure (PEEP) titrated to arterial oxygen tension (PaO₂) prevents or reduces acute lung injury, compared to conventional ventilation, in salinelavaged rabbits.Design Prospective randomised trial.Setting University animal laboratory.Subjects 18 New Zealand White rabbits.Interventions Following five sequential saline lung lavages, anaesthetised rabbits were randomly allocated in pairs to receive either of two ventilation protocols using intermittent mandatory ventilation. The study group had peak inspiratory pressure limited to 15 cm H₂O and arterial partial pressure of carbon dioxide (PaCO₂) was allowed to rise. The control group received 12 ml/kg tidal volume with rate adjusted for normocarbia. PEEP and fractional inspired oxygen (FIO₂) were adjusted to maintain PaO₂ between 8 and 13.3 kPa (60 and 100 mm Hg) using a predetermined protocol. At 10 h or following death, lung lavage was repeated and lung histology evaluated.Measurements and main results The mean increase in lavage cell counts and protein concentration and hyaline membrane scores were not significantly different between the groups. Oxygenation progressively improved more in the study group (p=0.01 vs control for PaO₂/FIO₂ ratio and alveolar-arterial oxygen tension gradient (AaDO₂)). PEEP was similar and the mean airway pressure higher in the control group, suggesting that this probably resulted from less ventilatorinduced injury in the study group. Four deaths occurred in the control group (three due to pneumothorax and one to hypoxaemia) and none in the study group (p=0.08).Conclusions This ventilatory protocol may have failed to prevent lung overdistension or it may have provided insufficient PEEP to prevent injury in this model; PEEP greater than the lower inflection point of the pressure-volume curve has been shown to prevent injury almost entirely.Funded by New Zealand Lottery Grants Board and Allen and Hanburys (NZ) Ltd.     

Preliminary Report of a Mathematical Model of Ventilation and Intrathoracic Pressure Applied to Prehospital Patients with Severe Traumatic Brain Injury

Abstract

Background: Inadvertent hyperventilation is associated with poor outcomes from traumatic brain injury (TBI). Hypocapnic cerebral vasoconstriction is well described and causes an immediate and profound decrease in cerebral perfusion. The hemodynamic effects of positive-pressure ventilation (PPV) remain incompletely understood but may be equally important, particularly in the hypovolemic patient with TBI. Objective: Preliminary report on the application of a previously described mathematical model of perfusion and ventilation to prehospital data to predict intrathoracic pressure. Methods: Ventilation data from 108 TBI patients (76 ground transported, 32 helicopter transported) were used for this analysis. Ventilation rate (VR) and end-tidal carbon dioxide (PetCO₂) values were used to estimate tidal volume (V_T). The values for VR and estimated V_T were then applied to a previously described mathematical model of perfusion and ventilation. This model allows input of various lung parameters to define a pressure–volume relationship, then derives mean intrathoracic pressure (MITP) for various V_T and VR values. For this analysis, normal lung parameters were utilized. Separate analyses were performed assuming either fixed or variable PaCO₂–PetCO₂ differences. Ground and air medical patients were compared with regard to VR, PetCO₂, estimated V_T, and predicted MITP. Results: A total of 10,647 measurements were included from the 108 TBI patients, representing about 13 minutes of ventilation per patient. Mean VR values were higher for ground patients versus air patients (21.6 vs. 19.7 breaths/min; p < 0.01). Estimated V_T values were similar for ground and air patients (399 mL vs. 392 mL; p = NS) in the fixed model but not the variable (636 vs. 688 mL, respectively; p < 0.01). Mean PetCO₂ values were lower for ground versus air patients (30.6 vs. 33.8 mmHg; p < 0.01). Predicted MITP values were higher for ground versus air patients, assuming either fixed (9.0 vs. 8.1 mmHg; p < 0.01) or variable (10.9 vs. 9.7 mmHg; p < 0.01) PaCO₂–PetCO₂ differences. Conclusions: Predicted MITP values increased with ventilation rates. Future studies to externally validate this model are warranted.     

About mechanisms of prostaglandin E1 induced deterioration of pulmonary gas exchange in COPD patients

Summary. Prostaglandin E₁ (PGE₁) has been reported to attenuate COPD-related pulmonary hypertension and to slightly lower the arterial oxygen tension (PaO₂). In order to infer the involved mechanisms, the effects of intravenous infusion of PGE₁ on pulmonary haemodynamics, diffusing lung capacity for CO (DLCO), membrane diffusing capacity (Dm), pulmonary capillary blood volume (Vc), physiological shunt (Q_ps/Q_t), arterial blood gases and other lung functional indices were evaluated in 20 COPD patients with pulmonary hypertension and, excluding right catheterization, in 14 control subjects. The examines were studied at baseline and during infusion of 20–30 ng kg^-1min PGE₁ or placebo. In control subjects PGE₁ only caused systemic arterial pressure decrease (-17.8%). In COPD patients, as expected, PGE₁ increased cardiac index (16-2%), but decreased systemic arterial pressure (-21.2%), pulmonary arterial pressure (-27.9%), pulmonary vascular resistance (-45.4%) and PaO₂ (-10.4%), worsening their hypoxaemia. However, the effect of PGE₁ on DLCO was an increase (11.9%), due to an increase in Vc (15.2%) and less markedly in Dm (4.9%). Physiological and anatomical shunts were increased with PGE₁ (20.2% and 14.8%) and the overall ventilation/perfusion ratio decreased from 0.89 to 0.79. Decrements in PaO₂ correlated with increments in Q_ps/Q_t (r= 0.86). In conclusion, in COPD patients studied, PGE₁ increased DLCO, which compensated for the deleterious effect of increased cardiac output on alveolar-capillary gas equilibration. Therefore, worsening of hypoxaemia during PGE₁ infusion was related with increased right-to-left shunt and deterioration of ventilation-perfusion relationship.,     

Non-invasive mechanical ventilation in severe chronic obstructive lung disease and acute respiratory failure: short-and long-term prognosis

Objective To evaluate the short-and long-term prognosis of patients with chronic obstructive lung disease (COLD) who had noninvasive mechanical ventilation (NMV) for acute respiratory failure (ARF).Design Retrospective study.Setting Two respiratory intermediate intensive care units.Patients Two groups of patients suffering from COLD and an ARF episode requiring mechanical ventilation. Group 1 (30 patients) was given NMV using face masks (aged 64±9 years; pH=7.28±0.05; PaCO₂=83±18 mmHg; PaO₂/FIO₂=141±61). Group 2 (27 patients) was composed of control patients (aged=65±8 years; pH=7.26±0.05; PaCO₂=75±17 mmHg; PaO₂/FIO₂=167±41) given MV using endotracheal intubation (EI) when clinical and functional conditions had further deteriorated because the medical therapy failed and NMV was not available at the time. Causes of ARF were in group 1 and 2 respectively: pneumonia in 8(27%) and 11(41%), acute exacerbation of COLD in 19 (63%) and 14 (52%) and pulmonary embolism in 3 (10%) and 2 (7%) patients.Measurements and results Success rate, mortality during stay in ICU (at 3 months and at 1 year), and the need for rehospitalization during the year following ARF were measured in this study. Group 1 showed a success rate of 74%, only 8/30 patients needing EI and conventional MV. In group 2, the weaning success was 74% (20/27 patients). The mortality for group 1 was 20% in IICU, 23% at 3 months and 30% at 1 year; and 26% for group 2 in ICU, 48% at 3 months and 63% at 1 year. Within each group 1-year mortality was greater (p<0.01) in patients with pneumonia. The number of new ICU admissions during the follow-up at 1 year was 0.12 versus 0.30 in groups 1 and 2 respectivelyp<0.05).Conclusion For patients suffering from COLD who have undergone ARF, avoiding EI by early treatment with NMV is associated with better survival in comparison to patients bound to invasive MV. Pneumonia as a cause of ARF may worsen the prognosis in both groups of patients.     

Influence of posture on gas exchange in artificially ventilated patients with focal lung disease

Six patients were artificially ventilated for a focal lung disease localized to one lung in four cases and to both lower lobes in two. Despite an inspired oxygen concentration of 100% the mean PaO₂ was 115 mmHg. The addition of PEEP slightly improved PaO₂ in two patients but led to deterioration in four. We therefore studied the effects of posture. Patients with unilateral disease were placed in the lateral position with the healthy lung dependent. The two patients with both lower lobes involved were tilted into the Trendelenburg position. The mean PaO₂ rose from 98.4 to 199.5 mmHg. Posture was maintained as long as a beneficial effect was demonstrable. The disappearance of this effect was associated either with recovery (three patients) or with the extension of the pneumonia (three patients). The improvement of gas exchange can be accounted for by the rearrangement of ventilation/perfusion relationships. This management could avoid the need for differential lung ventilation.