Changes In Pleural Pressure Research Articles

Influence of breathing pattern and lung inflation on impulse oscillometry measurements in horses

The objective of this paper was to determine if changes in ventilation patterns could influence the outcome of respiratory function measurements performed with our impulse oscillometry system (IOS) in horses. In a first study, IOS tests were performed in vitro on six isolated equine lungs. Lung inflation levels were controlled by modifying depressurisation inside an artificial thorax and different ventilation patterns were imposed. In a second in vivo study, transient variations in breathing pattern were evaluated both with the IOS and a current reference technique (CRT) in five healthy mature horses after an intravenous (i.v.) injection of lobeline hydrochloride. In both studies, respiratory rate (RR, range: 7–42 breaths/min.) and tidal volume ( V T, range: 0.4–25 L) had minor or no influence on IOS parameters. The influence of lung inflation, most marked for resistance at 5 Hz ( R 5 Hz), was limited for the considered physiological range. In vivo, statistical models indicated that maximal changes in pleural pressure (MaxΔ Ppl) and peak flows were the main determinants of the variability of the resistance ( R rs) and the reactance ( X rs) of the respiratory system. The fourfold increase in baseline MaxΔ Ppl and peak flows obtained during hyperpnoea caused a significant increase in R rs at 5 and 10 Hz and a decrease in X rs at all frequencies. We conclude that IOS parameters are not influenced by tachypnoea, but will reflect alterations in respiratory mechanics caused by hyperpnoeic breathing.

Determinants of diaphragm motion in unilateral diaphragmatic paralysis.

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (DeltaPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate DeltaPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to DeltaPpl and the force generated by the intact hemidiaphragm.

Efficacy of montelukast in the treatment of chronic obstructive pulmonary disease in five horses

Five horses with moderate to severe chronic obstructive pulmonary disease (COPD) were treated with 0.11 (0.01) mg/kg bodyweight of montelukast, a cysteinyl leukotriene receptor antagonist, once a day for 26...

Determinants of the Y Descent and its Usefulness as a Predictor of Ventricular Filling

Our objective was to determine if the magnitude of the Y descent in the central venous pressure tracing could be used to determine which patients have restrictive hemodynamics. To better understand the determinants of the Y descent, we also examined the effects of changes in blood volume, changes in pleural pressure, and respiratory maneuvers on its magnitude. Studies were performed in both humans and dogs. In six anesthetized dogs, we examined the effect on the Y descent in central venous pressure (CVP) of an infusion of normal saline, a decrease in pleural pressure produced by having animals perform a Mueller maneuver, and the combination of a Mueller maneuver and volume loading. Observations were made with the chest closed, chest open, and chest and pericardium open. The state of the chest did not effect the Y descent. The Y descent was only significantly increased when a Mueller maneuver was combined with volume loading. There was a significant inverse relationship between the magnitude of the decrease in esophageal pressure and the Y descent. There was also a linear relationship between the CVP and Y descent. For the human studies, we examined patients undergoing routine cardiac surgery. They were examined during spontaneous breathing before intubation, with positive pressure breathing and closed chest, with positive pressure breathing and open chest, with an open pericardium, with a closed chest and positive pressure breathing postsurgery, and with spontaneous breathing after extubation following surgery. The Y descent was greater in spontaneous breaths postsurgery compared to before surgery, and this was associated with an increase in CVP. However, the magnitude of CVP did not correlate with the magnitude of the Y descent. A restrictive pattern in cardiac filling was identified by a lack of respiratory variation in right atrial pressure during spontaneous breaths. All patients with large Y descents had a restrictive pattern, but many patients with restrictive filling patterns did not have a large Y descent. The magnitude of the Y descent is affected by the volume status, the magnitude and direction of the changes in pleural pressure, and the compliance of the pericardial compartment. A large Y descent indicates a restrictive cardiac state, but a small Y descent does not rule out a restrictive condition because of the many interacting variables.

Determinants of the Y Descent and its Usefulness as a Predictor of Ventricular Filling

Our objective was to determine if the magnitude of the Y descent in the central venous pressure tracing could be used to determine which patients have restrictive hemodynamics. To better understand the determinants of the Y descent, we also examined the effects of changes in blood volume, changes in pleural pressure, and respiratory maneuvers on its magnitude. Studies were performed in both humans and dogs. In six anesthetized dogs, we examined the effect on the Y descent in central venous pressure (CVP) of an infusion of normal saline, a decrease in pleural pressure produced by having animals perform a Mueller maneuver, and the combination of a Mueller maneuver and volume loading. Observations were made with the chest closed, chest open, and chest and pericardium open. The state of the chest did not effect the Y descent. The Y descent was only significantly increased when a Mueller maneuver was combined with volume loading. There was a significant inverse relationship between the magnitude of the decrease in esophageal pressure and the Y descent. There was also a linear relationship between the CVP and Y descent. For the human studies, we examined patients undergoing routine cardiac surgery. They were examined during spontaneous breathing before intubation, with positive pressure breathing and closed chest, with positive pressure breathing and open chest, with an open pericardium, with a closed chest and positive pressure breathing postsurgery, and with spontaneous breathing after extubation following surgery. The Y descent was greater in spontaneous breaths postsurgery compared to before surgery, and this was associated with an increase in CVP. However, the magnitude of CVP did not correlate with the magnitude of the Y descent. A restrictive pattern in cardiac filling was identified by a lack of respiratory variation in right atrial pressure during spontaneous breaths. All patients with large Y descents had a restrictive pattern, but many patients with restrictive filling patterns did not have a large Y descent. The magnitude of the Y descent is affected by the volume status, the magnitude and direction of the changes in pleural pressure, and the compliance of the pericardial compartment. A large Y descent indicates a restrictive cardiac state, but a small Y descent does not rule out a restrictive condition because of the many interacting variables.

Relationship between clinical signs and lung function in horses with recurrent airway obstruction (heaves) during a bronchodilator trial.

During a trial to determine the dose response to the beta2-adrenergic agonist pirbuterol, we judged the severity of airway obstruction by use of a clinical scoring system and compared this to objective data obtained by quantitative measures of lung function. Six horses affected by recurrent airway obstruction were used in this trial. Four hundred and sixty-eight measurements of lung function and clinical scores were obtained from 13 measurement periods when horses received each of 6 doses of pirbuterol. Scores of 1-4 were assigned to degree of nasal flaring and abdominal effort and summed for a total score. The veterinarian scoring the signs did not know the dose of pirbuterol received by the horse and was unaware of the lung function data. Nasal, abdominal and total scores were significantly related to changes in lung function and changes in breathing pattern. There were significant differences between total scores greater than 5 in indices that reflected changes in breathing strategy (peak inspiratory and expiratory flow), peripheral airway obstruction (dynamic elastance), and effort of breathing (maximal change in pleural pressure). Below a total score of 5, there were fewer significant differences in lung function even though measurements of pulmonary resistance and dynamic elastance indicated considerable airway obstruction. Failure of clinical score to reflect this low-grade airway obstruction suggests that airway disease is underdiagnosed and its detection would be helped by the availability of a convenient lung function test.

Pulmonary capillary pressure in horses undergoing alteration of pleural pressure by imposition of various upper airway resistive loads.

We hypothesized that changes in pleural pressure induced by resistive breathing would affect transmural pulmonary artery, pulmonary capillary, and pulmonary wedge pressures. Seven horses were assigned to exercise with each of 4 upper respiratory resistive loads in random order at intervals of at least 2 days: 1) control--no added resistive loads; 2) inspiratory resistive load (Iobst)--left laryngeal hemiplegia; 3) expiratory resistive load (Eobst)--one-way valve in the right nostril; and 4) combined inspiratory and expiratory resistive loads (CIEobst)--left nostril occlusion. On each occasion, the horses performed an incremental exercise protocol consisting of exercise episodes of 3 min duration at 75, 90, and 100% of maximal heart rate (HRmax). Pulmonary artery and oesophageal pressures were recorded continuously. Subsequent analysis was carried out on the pulmonary arterial pressure signal with the oesophageal pressure signal subtracted, hence the pulmonary vascular pressures in this paper approximate transmural pressures. Pulmonary vascular pressures, heart rate, and arterial blood gas tensions were measured at each level of exercise. Pulmonary capillary and pulmonary wedge pressures were determined from the pulmonary artery waveform after dynamic occlusion of a branch of the pulmonary artery. During exercise, peak expiratory oesophageal pressure was more positive in horses with Eobst and CIEobst (adjusted means = 43, and 39 mmHg, respectively) compared with control (adjusted mean = 23 mmHg) (P = 0.0001). Peak inspiratory oesophageal pressure was more negative in horses at exercise with Iobst and CIEobst (adjusted means = -42 and -39 mmHg, respectively) compared with control (adjusted mean = -26 mmHg) (P = 0.0012). Eobst was associated with an increase in mean oesophageal pressure while Iobst was associated with a decrease in mean oesophageal pressure. There were significant increases in mean pulmonary artery pressure in horses with CIEobst (adjusted means = 82 mmHg) and in pulmonary wedge pressure in horses with CIEobst and Iobst (adjusted means = 51, and 55 mmHg, respectively) when compared to control (73 and 42 mmHg, respectively) (P = 0.0001). Pulmonary capillary pressure was significantly increased in horses with CIEobst or Iobst (adjusted means = 61 mmHg, 63 mmHg, respectively) when compared to control (adjusted mean = 50 mmHg)(P = 0.0001). At maximal exercise intensity with inspiratory obstruction, the mean oesophageal (pleural) pressure was -17 mmHg while the mean pulmonary capillary pressure was 77 mmHg. The latter exceeds the reported 75 mmHg threshold for capillary failure in horses. We conclude that inspiratory resistive breathing can lead to a significant increase in transmural pulmonary capillary pressure which may contribute to loss of capillary integrity and rupture.

Pulmonary distribution of aerosolized technetium Tc 99m pentetate after administration of a single dose of aerosolized albuterol sulfate in horses with recurrent airway obstruction

Abstract Objective To determine whether pulmonary distribution of aerosolized technetium Tc 99m pentetate is improved after inhalation of a single dose of albuterol sulfate in horses susceptible to recurrent airway obstruction (heaves). Animals 6 horses with heaves and 4 horses with normal respiratory tract function. Procedure Images were obtained during ventilation of horses at baseline (maximal change in pleural pressure during tidal breathing [ΔPplmax] > 15 cm H2O) and after aerosolized albuterol sulfate (360 µg) administration, with a 24-hour washout period between experiments. The ΔPplmax was determined prior to the baseline scan, prior to albuterol sulfate administration, and 5 minutes after albuterol sulfate administration. Images were assessed by visual inspection (semiquantitative scoring system) and histogram analysis. Results Images obtained from horses with heaves had nonuniform pulmonary distribution of radionuclide characterized by poor penetration in peripheral lung fields and excess deposition in large airways. Histogram analysis of images of the caudal portions of the lungs revealed nonuniform radionuclide deposition in horses with heaves and uniform radionuclide deposition in control horses. Conclusion Administration of a single dose of aerosolized albuterol sulfate improved pulmonary distribution of aerosolized radiolabeled pentetate suspension in horses with heaves but did not alter pulmonary distribution in clinically normal horses. Clinical Relevance Precedent bronchodilator administration may improve pulmonary distribution of aerosolized, surface-active anti-inflammatory preparations. (Am J Vet Res 1999;60:764–769)

Determinants of the Maximal Change in Pleural Pressure during Tidal Breathing in COPD-Affected Horses

In six COPD-affected horses, we analysed the factors responsible for the changes in pleural pressure (ΔPplmax) that occur during tidal breathing. Four-hundred-and-sixty-eight measurements of each parameter: pulmonary resistance (RL), dynamic elastance (Edyn), air flow rates, and the timing of breathing, were gathered during a trial of the bronchodilator pirbuterol. Data were placed into seven ranks, based on the magnitude of ΔPplmax; rank 1: 5–15; rank 2: 15–25; rank 3: 25–35; rank 4: 35–45; rank 5: 45–55; rank 6: 55–65; and rank 7 > 65 cm H2O. Up to rank 4 (45 cm H2O), the increase in ΔPplmaxwas due to increases in RL, Edyn, and inspiratory and expiratory air flow rates. Further increases in ΔPplmaxwere due to continuing increases in Edynand flow rates with little change in resistance. The increase in inspiratory flow rates was the result of a decrease in inspiratory time. The large increase in peak expiratory flow could not be explained by the small decrease in expiratory time and must therefore be due to a change in breathing strategy as ΔPplmaxincreased. Changes in air flow rates as well as changes in RLand Edynmust be considered as reasons for a change in ΔPplmaxwhen evaluating horses with COPD.

Pulmonary function in horses with recurrent airway obstruction after aerosol and parenteral administration of beclomethasone dipropionate and dexamethasone, respectively

Abstract Objective To determine changes in clinical signs of disease and response to pulmonary function testing in horses with recurrent airway obstruction (heaves) after aerosol and parenteral administration of beclomethasone dipropionate and dexamethasone, respectively. Animals 6 horses with inducible and reversible heaves. Procedure Episodes of heaves were induced by exposure (challenge) to moldy hay and straw for 7 days. Horses were assigned to treatment groups (aerosolized beclomethasone dipropionate, parenterally administered dexamethasone, aerosolized propellant [control]), and respiratory frequency and subjective assessment of respiratory effort were determined twice daily. Maximal change in pleural pressure (ΔPplmax), pulmonary resistance (RL), and dynamic compliance (Cdyn) was determined on days 0, 7, 10, 14, and 21. Results The RL and ΔPplmax were increased, and Cdyn was decreased in all horses in response to natural challenge. Beclomethasone reduced RL on day 10, reduced ΔPplmax on days 14 and 21 and increased Cdyn on day 14. Dexamethasone reduced RL and ΔPplmax on days 10, 14, and 21 and increased Cdyn on days 10 and 14. Respiratory effort (subjective assessment) improved after 2 and 3 days of beclomethasone and dexamethasone administration but rebounded to pretreatment values 1 and 3 days after discontinuation of drugs. Conclusions Pulmonary function testing responses and clinical signs of airway obstruction were improved by administration of beclomethasone. The magnitude of response to aerosolized beclomethasone generally was less marked than the response to parenterally administered dexamethasone. Higher or more frequent dosing of aerosolized beclomethasone may be necessary to achieve the anti-inflammatory response to parenterally administered dexamethasone. (Am J Vet Res 1998;59:1039–1043)

Effect of the 5‐lipoxygenase inhibitor, fenleuton, on antigen‐induced neutrophil accumulation and lung function changes in horses with chronic obstructive pulmonary disease

The leukotrienes (LT) LTD4 and LTB4 have been shown to cause bronchoconstriction and neutrophil accumulation, respectively, in horse lungs. Such changes are characteristic of the equine allergic respiratory disease, chronic obstructive pulmonary disease (COPD). To further investigate the role of these putative mediators in the pathogenesis of equine COPD the effect of a 5-lipoxygenase inhibitor, fenleuton, on antigen-induced changes in horses with this condition has been examined. Six horses with COPD underwent a series of four antigen challenges, one month apart, with placebo pre-treatment on three occasions and fenleuton (4 days oral dosing 5 mg/kg) pre-treatment on one occasion. Three horses received fenleuton prior to the second challenge and three horses received the drug prior to the fourth antigen challenge. Changes in radiolabelled neutrophil distribution, lung function and peripheral leucocyte counts were monitored on each occasion for 7 h following the start of antigen challenge. Antigen challenge caused an increase in radioactive counts over the lungs and a decrease in peripheral leucocyte count. Neither response was affected by fenleuton pre-treatment. Mean maximal changes in pleural pressure (delta Pplmax) and respiratory rate were also unaffected by fenleuton pre-treatment. However, in the two horses which responded to antigen-challenge with a particularly marked increase in delta Pplmax (> 15 cm H2O), prior administration of fenleuton reduced the response by 64 and 63%. These results suggest that 5-lipoxygenase inhibitors warrant further investigation as bronchodilators in equine COPD.

A novel method for chronic measurement of pleural pressure in conscious rats

Pleural pressures are used to evaluate lung function and are generally measured acutely in anesthetized animals. Previous attempts to measure pleural pressure chronically in conscious animals have involved surgical implantation of pressure-sensitive catheters directly into the pleural cavity. The success of these techniques has been limited by lung damage and/or tissue growth and encapsulation of the pressure-sensitive catheter with damping or loss of the signal. These problems have been eliminated by developing a novel surgical procedure for placement of a pressure-sensitive catheter beneath the pleural surface. The catheter (attached to a radiotelemetry transmitter) is surgically implanted beneath the serosal layer of the esophagus within the thoracic cavity. This is accomplished by making a small incision in the serosal layer of the esophagus caudal to the diaphragm and advancing the catheter cranially into the thoracic cavity until pressure changes are maximal. The accuracy of these measurements was verified by comparison with direct pleural pressure measurements over the range of −3 to −34 cm H 2O. The pleural pressure changes remained constant for at least 14 weeks following surgery, and there was no evidence of tissue damage or growth around the catheter. This novel method for measuring pleural pressure chronically in conscious rats will facilitate evaluation of the effects of drugs, environmental agents, or disease on respiratory function by allowing repeated and simultaneous measurements of both ventilatory (breathing) patterns and lung function in conscious animals.

Does an acute COPD crisis modify the cardiorespiratory and ventilatory adjustments to exercise in horses?

The present study was conducted to understand better the mechanisms leading to the decrease in exercise capacity observed in horses suffering from chronic obstructive pulmonary disease (COPD). Five COPD horses were submitted to a standardized submaximal treadmill exercise test while they were in clinical remission or in acute crisis. Respiratory airflow, O2 and CO2 fractions in the respired gas, pleural pressure changes and heart rate were recorded, and arterial and mixed venous blood were analyzed for gas tensions, hemoglobin, and plasma lactate concentrations. O2 consumption, CO2 production, expired minute ventilation, tidal volume, alveolar ventilation, cardiac output, total pulmonary resistance, and mechanical work of breathing were calculated. The results showed that, when submaximally exercised, COPD horses in crisis were significantly more hypoxemic and hypercapnic and that their total pulmonary resistance and mechanical work of breathing were significantly higher and their expired minute ventilation significantly lower than when they were in remission. However, their O2 consumption remained unchanged, which was probably due to the occurrence of compensatory mechanisms, i.e., higher heart rate, cardiac output, and hemoglobin concentration. Last, their net anaerobic metabolism seemed to be more important.

Intraventricular Pressure Dynamics in Patients with Ventriculopleural Shunts: A Telemetric Study

Extracranial CSF shunting to the pleural absorptive surface is sometimes used as an alternative to ventriculoperitoneal shunting. The pressure dynamics of this type of shunt would be expected to differ from peritoneal shunting due to active changes in pleural pressures caused by the ventilatory cycle. We have had opportunity to examine the in vivo intraventricular pressure (IVP) dynamics of ventriculopleural shunts utilizing a commercially available implantable telemonitor (Telesensor; Radionics, Burlington, Mass.). Four patients with ventriculopleural shunts were monitored telemetrically while supine and at increments of head elevation to 90°. Two patients with ‘medium’ grade differential pressure valves exhibited IVPs which were never greater than zero. One patient with an in-line antisiphoning device in the shunt system appeared to have IVPs closely resembling those seen in shunting to the peritoneal space. Another patient with valve opening pressure set at 19 cm of water consistently had supine intraventricular pressures less than 10 cm of water that readily fell to zero with minimal head elevation. We conclude that the negative intrapleural pressures generated by the ventilatory cycle tend to cause IVPs in ventriculopleural shunts to be lower than those expected in peritoneal shunting. This observation suggests that ventriculopleural shunts may be appropriate for patients requiring very low intraventricular pressures in order to resolve their hydrocephalic symptoms.

The effect of doxapram-induced hyperventilation on respiratory mechanics in horses

To investigate the influence of increased respiratory frequency on respiratory mechanics in the horse, measurements were made in two groups of seven tracheostomised horses before and after the administration of doxapram. The horses in group I had normal base line values for respiratory mechanics, whereas the horses in group II had significantly lower values of dynamic compliance (Cdyn), higher respiratory resistance (R), and a higher total change in pleural pressure (ΔP). The administration of 0·3 mg kg −1 doxapram intravenously resulted in a significant increase in respiratory frequency (f R), R, ΔP, tidal volume (V T), and peak to peak respiratory flow (V̇), and a decrease in Cdyn in both groups of horses. The group II horses had significantly greater increases in R and ΔP than the horses in group I.

Dysfunctional muscarinic M 2 autoreceptors in vagally induced bronchoconstriction of conscious guinea pigs after the early allergic reaction

We studied the function of autoinhibitory muscarinic M 2 receptors on vagal nerve endings in the airways of conscious, unrestrained, ovalbumin-sensitized guinea pigs after the early and late allergic reaction. For this purpose, the effects of the selective muscarinic M 2 receptor antagonist gallamine were examined on unilateral vagus nerve stimulation-induced bronchoconstriction, which was determined as an increase in basal respiration amplitude, measured as changes in pleural pressure. Under control conditions, i.e., before antigen challenge, a significant increase in the pleural pressure was found after inhalation of 0.1 mM and, even more pronounced, 1.0 mM gallamine, at medium stimulation frequencies (2–16 Hz), leading to a leftward shift of the frequency-response curve. After inhalation of 10 mM of gallamine, a complete reversal of the left-shift was observed and the frequency-response curve was depressed. However, 6 h after challenge with ovalbumin (i.e., after the early allergic reaction) no increase in nerve stimulation-induced bronchoconstriction by gallamine was found; a decrease in this bronchoconstriction was again observed with the highest concentration. At this moment, bronchial responsiveness to histamine was enhanced 4.5-fold compared to control, i.e., prior to antigen provocation. Both after the late allergic response (24 h after challenge; 1.6-fold histamine hyperresponsiveness) and 4 days after allergen challenge (normal histamine responsiveness) the gallamine-induced potentiation of the bronchoconstriction was restored, similar to the responses under control conditions. The results clearly demonstrate that prejunctional muscarinic M 2 receptors control bronchoconstriction in conscious, unrestrained guinea pigs in vivo. Furthermore, these autoinhibitory receptors appear to be completely dysfunctional after the early allergic phase, but their function is largely restored after the late phase. The results indicate that dysfunction of autoinhibitory muscarinic M 2 receptors might contribute to the strongly enhanced responsiveness to histamine after the early allergic response.

Respiratory muscle and cardiopulmonary function during exercise in very severe COPD.

Chronic obstructive pulmonary disease (COPD) is thought to limit exercise capacity through a decreased ventilatory reserve, with cardiovascular factors playing a minimal role. We assessed respiratory muscle (RM) and cardiopulmonary function during exercise in very severe COPD (FEV1 0.79 +/- 0.17 L). We determined minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), heart rate (HR), respiratory rate (RR), and O2 pulse with a metabolic cart. RM function was assessed from esophageal and gastric pressures. Dyspnea was assessed with a visual analog scale (VAS). Exercise capacity (peak VO2 = 36 +/- 31%), ventilatory reserve (VE/maximum voluntary ventilation [MW] = 89 +/- 31%), HR = 76 +/- 15%, and O2 pulse (O2Pmax = 45 +/- 15%) were abnormal. Peak VO2 correlated with O2Pmax(r = 0.82), the change in end-inspiratory pleural pressure (deltaPpli) (r = -0.74), maximal transdiaphragmatic pressure (Pdimax) (r = 0.68), and VEmax (r = 0.58). There were similar correlations with exercise endurance time. Multiple regression analysis revealed O2Pmax to be the best predictor of peak VO2. Thereafter, only VEmax and deltaPpli remained significant (r2 = 0.87). O2Pmax correlated with inspiratory muscle function (Pplimax, r = -0.58; Pdimax, r = 0.53; deltaPpli, r = -0.47; and PImax, r = -0.47). By multiple regression analysis, the predictors of O2Pmax were Pplimax and deltaPpli (r2 = 0.47). In very severe COPD, the impressive swings in intrathoracic pressure resulting from deranged ventilatory mechanics are the most likely cause of exercise limitation and reduced O2 pulse. The contributions of factors such as deconditioning, hypoxemia, and concurrent heart disease remain unknown.

Respiratory mechanics after abdominal surgery measured with continuous analysis of pressure, flow and volume signals

We studied 10 patients during the first night after upper abdominal surgery to assess the effect of airway obstruction on chest wall mechanics, by recording nasal gas flow and carbon dioxide concentration, rib cage and abdominal dimensions, abdominal muscle activity, and oesophageal and gastric pressures. The mean duration of study of each subject was 5.8 h, and 5.2 h were analysed. The median proportion of time spent breathing with normal mechanics was 29% (interquartile values 0-57%). Abnormal abdominal mechanical events were common and associated with airway obstruction (P < 0.001). Two common patterns of abnormal pressure and movement were found. In the first, abdominal pressure decreased at the onset of inspiration and there was a phase lag in abdominal movement. The incidence was 33 (14-50)%. In the second pattern, abdominal pressure decreased and in addition the abdominal wall moved inwards at the onset of inspiration. This occurred for 34 (0-52)% of the time. Both patterns were associated with evidence of increased activation of the abdominal muscles during expiration, changing the relationship of abdominal and pleural pressure changes and chest wall movements. Such changes have been interpreted previously as evidence of diaphragm dysfunction.

Pleural pressure changes during exercise do not affect measurement of mean pulmonary vascular pressures

SummaryThis study was designed to evaluate the influence of pleural pressure on mean pulmonary vascular pressures in exercising horses. Pulmonary artery (Pa), pulmonary wedge (Pw) and oesophageal pressures (Pes) were measured with transducer tip catheters in 6 Standardbred horses at rest and during treadmill exercise at 75, 90 and 100% of maximal heart rate. Oesophageal pressure (Pes) measurements were used to estimate pleural pressure. Vascular pressures were determined in 4 ways: 1) mean transmural vascular pressure (Ptm) at Pesequal to resting end expiratory pressure; 2) mean Ptmat Pesequal to mean Pesfor the data collection period; 3) mean Ptmwithout selection of specific data points and 4) mean pulmonary vascular pressure relative to atmospheric pressure (conventional method). Despite large fluctuations associated with breathing, mean Pesduring exercise remained close to zero, suggesting that pleural pressure fluctuates equally about zero. The swings in Peswere associated with approximately equal swings in vascular pressure so that, despite the marked fluctuations, mean Paand Pwdetermined with the 4 methods were not significantly different. The results indicate that during exercise it is valid to report mean pulmonary vascular pressures without accounting for the fluctuations in pleural pressure.

Pathophysiological response of bovine pulmonary function to gastric distension.

The purpose was to determine whether gastric overdistension leads to life-threatening perturbations of pulmonary gas exchange in healthy calves. Six animals were studied with normal (0 kPa) and increased (1, 2, 3, 4 and 5 kPa) intragastric pressure (IGP). Changes in pleural pressures and peak expiratory flow paralleled those of IGP. Inspiratory pressure-time index remained stable throughout the insufflation process. Pulmonary function values were characterized by abrupt changes with increasing IGP. Tidal volume declined as IGP increased and, along with inspiratory flow, decreased abruptly with the highest pressure (5 kPa). Respiratory rate progressively increased up to an IGP of 4 kPa, then decreased by 30%, due to breath-holding at the end of inspiration. Minute volume increased with IGP up to 4 kPa, but dramatically declined at 5 kPa. Total pulmonary resistance remained stable throughout the insufflation process, whereas lung dynamic compliance fell abruptly to one-half of its baseline value at IGPs of 1 kPa and above. Arterial oxygen tension was maintained at an IGP of 1 kPa, slightly diminished at 2-3 kPa, and markedly decreased at 4-5 kPa. Hypercapnia and respiratory acidosis developed progressively with increasing IGP. Changes in arterial gases were probably due to a combination of (1) alveolar hypoventilation, caused by altered tidal to dead space volume ratio, inadequate central nervous system "drive", altered effectiveness of inspiratory muscle action, or end-inspiratory breath-holding, and (2) ventilation to perfusion mismatch, caused by perfusion of collapsed lung units. In the range of IGPs used, standardized arterial pH did not decline below the control value, which suggests that perfusion of peripheral tissues remained sufficient, and that respiratory failure rather than cardiovascular failure may be the principal physiopathological effect of increased gastric pressure.