Effets ventilatoires d’une hypothermic modérée (36° C–28° C) chez le chien anesthésie à l’halothane

Changes in systemic haemodynamic variables (mean arterial pressure, MAP; heart rate, HR; cardiac output, Qc), in oxygen consumption, VO2, and in ventilation (minute ventilation, V; respiratory frequency, f; tidal volume, VT; and arterial blood gases) with particular attention to respiratory times (duration of inspiration, TI; duration of expiration, TE; duration of the breathing cycle, TTOT), to respiratory timing (TI/TTOT) and respiratory drive (VT/TI) were studied during moderate progressive hypothermia (36 degrees C to 28 degrees C) during stable halothane anaesthesia (MAC = 1.5) in six dogs. MAP, HR and Qc decreased; V and f decreased, the decrease in f being correlated with that in temperature (r = 0.66; P < 0.01). Tidal volume did not change. The PaO2 and pHa decreased while PaCO2 increased slightly. The decrease in ventilation was related to changes in respiratory times (TI and TE) which increased (TE more than TI) and in respiratory drive (VT/TI which decreased due to the increase in TI). The relation between VT/TI and TI/TTOT changes was not constant during cooling. Changes in respiratory times and drive could be due to the effect of cold on medullar respiratory control.     

Comparison of patient-ventilator synchronization during pressure support ventilation versus amplified spontaneous pattern in postoperative patients

INTRODUCTION: Patient-ventilator desynchronization can develop during weaning from proportional-assist ventilation. Poor adaptation between ventilator assistance and the patient's ventilatory demand is termed asynchrony. OBJECTIVES: Comparative analysis of types and incidence of asynchrony in patients receiving pressure support (PS) ventilation or amplified spontaneous pattern (ASP) ventilation, to determine whether the presence of asynchrony is related to a patient's level of dyspnea or anxiety. PATIENTS AND METHODS: Eighteen patients were studied prospectively after undergoing coronary revascularization. Baseline anxiety was assessed before surgery. A pleural catheter was inserted during surgery. After surgery patients were randomly assigned to ventilation with PS mode or ASP. Flow curves, flow volume, airway pressure and pleural pressure were recorded by a BioCore CP100 monitor once the patient's work of breathing held steady between 0.3 and 0.5 J/l. The curves were recorded for 10 m on a computer for later analysis. After each recording dyspnea and anxiety were assessed. Fifty consecutive cycles per patient were analyzed, signalling in each case the start of inspiration and expiration. RESULTS: Nine hundred ventilatory cycles were analyzed to identify five types of patient-ventilator asynchrony: 1) self-cycled (SC: inspiratory assistance from the ventilator without demand by patient); 2) no effort detected (NED: patient inspiratory effort but no flow response from the ventilator); 3) interrupted support (IS: interruption of ventilatory support during patient inspiration); 4) prolonged mechanical inspiration (PMI: maintenance of ventilatory support during patient expiration), and 5) double-breath, single cycle (DBSC: sequence of inspiration-expiration-inspiration of the patient within a single assisted inspiration). Asynchronic cycles were found in all PS-ventilated patients (84 of 450; 18.7%): 9.1% SC, 4% NED, 2.2% IS, 1.5% PMI and 1.8% DBSC. Asynchronic cycles were seen in only two ASP patients (16 of 450; 3.5%); both cases were NED asynchrony. Levels of anxiety and dyspnea were slightly higher with the PS mode than with ASP but the differences were not significant (p = 0.05). CONCLUSIONS: The incidence of asynchrony during assisted ventilation is very high with the PS mode and is substantially less with ASP. Asynchrony is difficult to detect clinically and is revealed only by advanced cycle-to-cycle monitoring.     

Comparative effects of plasma exchange and pyridostigmine on respiratory muscle strength and breathing pattern in patients with myasthenia gravis.

BACKGROUND--Pyridostigmine, an acetylcholinesterase antagonist, is useful in improving respiratory function in patients with myasthenia gravis. More recently, plasma exchange has been employed in myasthenia gravis because it acts presumably by removal of circulating antibodies against acetylcholine receptors. Surprisingly, comparative data on the effects of pyridostigmine and plasma exchange on lung volumes, respiratory muscle strength, and ventilatory control system in patients with myasthenia gravis are lacking. METHODS--Nine consecutive patients with grade IIb myasthenia gravis were studied under control conditions and after a therapeutic dose of pyridostigmine. In a second study the patients were re-evaluated a few days after a cycle of plasma exchange, before taking pyridostigmine. In each subject pulmonary volumes, inspiratory (MIP) and expiratory (MEP) muscle force, and respiratory muscle strength, calculated as average MIP and MEP as percentages of their predicted values, were measured. The ventilatory control system was evaluated in terms of volume (tidal volume, VT) and time (inspiratory time, TI, and total time, TTOT) components of the respiratory cycle. Mean inspiratory flow (VT/TI)--that is, the "driving"--and TI/TTOT--that is, the "timing"--components of ventilation were also measured. RESULTS--In each patient treatment relieved weakness and tiredness, and dyspnoea grade was reduced with plasma exchange. Following treatment, vital capacity (VC) increased on average by 9.7% with pyridostigmine and by 14% with plasma exchange, and MIP increased by 18% and 26%, respectively. In addition, with plasma exchange but not with pyridostigmine forced expiratory volume in one second (FEV1) increased by 16% and MEP increased by 24.5%, while functional residual capacity (FRC) decreased a little (6.8%). The change in respiratory muscle strength was related to change in VC (r2 = 0.48). With plasma exchange, VT increased by 18.6% and VT/TI increased by 13.5%, while neither TI nor TI/TTOT changed. CONCLUSIONS--Plasma exchange can be used in patients with myasthenia gravis when symptoms are not adequately controlled by anticholinesterase agents. Plasma exchange increases respiratory muscle force and tidal volume due to changes in "driving" but not "timing" of the respiratory cycle.     

Neonatal pattern of breathing following cesarean section: epidural versus general anesthesia

We tested the hypothesis that different anesthetic techniques for elective cesarean section would be reflected in the pattern of breathing and its control after birth. The pattern of breathing, including tidal volume, total breath duration (TTOT), minute ventilation, inspiratory (TI) and expiratory times, TI/TTOT ratio, and mouth occlusion pressure, was measured in 27 infants delivered by elective cesarean section during maternal epidural (lidocaine-carbon dioxide-epinephrine, n = 19) or general anesthesia (66% oxygen in N2O and 0.5% halothane, n = 8) at 10, 60, and 90 min and 3-5 days of age. Neonatal acid-base values and Apgar scores were within normal limits in both groups of infants. In general, at any given age the values of the respiratory parameters measured and their variability were similar between the two groups of infants. These findings indicate that the pattern of breathing after birth is not different following epidural or general anesthesia, and on the basis of our measurements, both epidural or general anesthesia appeared equally suitable for elective cesarean section.     

The effect of breath termination criterion on breathing patterns and the work of breathing during pressure support ventilation

With pressure support ventilation (PSV), each PSV breath is flow-cycled, and the breath termination criterion (TC) is usually nonadjustable. When TC does not match the interaction between the patient's inspiratory-expiratory efforts to the opening and closing of the inspiratory and expiratory valves, patient-ventilator asynchrony may occur, and the work of breathing (WOB) may increase. Therefore, we studied the effect of TC on breathing patterns and WOB during PSV in eight patients with acute respiratory distress syndrome or acute lung injury. We studied five levels of TC during PSV-1%, 5%, 20%, 35%, and 45% of the peak inspiratory flow. With increasing levels of TC, the tidal volume decreased and respiratory frequency increased, along with a decrease in duty cycle. WOB markedly increased with increasing levels of TC from 0.31 +/- 0.12 J/L with TC 1% to 0.51 +/- 0.11 J/L with TC 45%. Premature termination with double breathing occurred in one patient with TC 35% and four patients with TC 45%. Delayed termination with a duty cycle of >0.5 occurred in two patients with TC 1%. In conclusion, the proper adjustment of TC improves patient-ventilator synchrony and decreases WOB during PSV. Implications: Although termination criterion (TC) is usually nonadjustable, it influences the effectiveness of pressure support ventilation for mechanical ventilation. The proper adjustment of TC is crucial to improve patient-ventilator synchrony and decrease work of breathing. TC 5% of the peak inspiratory flow may be the optimal value for patients with acute respiratory distress syndrome or acute lung injury.     

Ventilatory changes during nitrous oxide isoflurane anaesthesia in children

The changes in ventilatory variables under nitrous oxide isoflurane anaesthesia were studied in 10 children (mean age 46 +/- 13.4 months, mean weight 16.2 +/- 2.1 kg). Measurements of flow and volume were performed by pneumotachography. PE'CO2 was measured by capnography. The following variables (VE, VT, TI/TTOT, VI, PE'CO2) were measured or calculated under three increasing inspired isoflurane concentrations (0.75%, 1.5%, 2.25%). At each level of anaesthesia, ventilatory changes during exposure to an inspired CO2 fraction of 2% were studied. The increase in the inspired concentration of isoflurane was associated with a decrease in alveolar ventilation. PE'CO2 increased significantly with increasing depth of anaesthesia. The respiratory rate was slightly increased under light nitrous oxide isoflurane anaesthesia, but no further changes were observed with increasing depth of anaesthesia, although the children were breathing a mixture of nitrous oxide and oxygen. The ventilatory response to a raised inspired CO2 is markedly decreased under light nitrous oxide isoflurane anaesthesia, and decreases significantly with increasing depth of anaesthesia. In response to a raised CO2, VE, VT and VI increase, but respiratory rate decreases or remains constant and TI/TTOT is unchanged.     

Breathing pattern and carbon dioxide retention in severe chronic obstructive pulmonary disease.

BACKGROUND: The factors leading to chronic hypercapnia and rapid shallow breathing in patients with severe chronic obstructive pulmonary disease (COPD) are not completely understood. In this study the interrelations between chronic carbon dioxide retention, breathing pattern, dyspnoea, and the pressure required for breathing relative to inspiratory muscle strength in stable COPD patients with severe airflow obstruction were studied. METHODS: Thirty patients with COPD in a clinically stable condition with forced expiratory volume in one second (FEV1) of < 1 litre were studied. In each patient the following parameters were assessed: (1) dyspnoea scale rating, (2) inspiratory muscle strength by measuring minimal pleural pressure (PPLmin), and (3) tidal volume (VT), flow, pleural pressure swing (PPLsw), total lung resistance (RL), dynamic lung elastance (ELdyn), and positive end expiratory alveolar pressure (PEEPi) during resting breathing. RESULTS: Arterial carbon dioxide tension (PaCO2) related directly to RL/PPLmin, and ELdyn/PPLmin, and inversely to VT and PPLmin. There was no relationship between PaCO2 and functional residual capacity (FRC), total lung capacity (TLC), or minute ventilation. PEEPi was similar in eucapnic and hypercapnic patients. Expressing PaCO2 as a combined function of VT and PPLmin (stepwise multiple regression analysis) explained 71% of the variance in PaCO2. Tidal volume was directly related to inspiratory time (TI), and TI was inversely related to the pressure required for breathing relative to inspiratory muscle strength (PPLsw, %PPLmin). There was an association between the severity of dyspnoea and both the increase in PPLsw (%PPLmin) and the shortening in TI. CONCLUSIONS: The results indicate that, in stable patients with COPD with severe airflow obstruction, hypercapnia is associated with shallow breathing and inspiratory muscle weakness, and rapid and shallow breathing appears to be linked to both a marked increase in the pressure required for breathing relative to inspiratory muscle strength and to the severity of the breathlessness.     

Changes in occlusion pressure (P0.1) and breathing pattern during pressure support ventilation

BACKGROUND: The purpose of this study was to investigate changes in breathing pattern, neuromuscular drive (P0.1), and activity of the sternocleidomastoid muscles (SCM) during a gradual reduction in pressure support ventilation (PSV) in patients being weaned off controlled mechanical ventilation. METHODS: Eight non-COPD patients recovering from acute respiratory failure were included in this prospective interventional study. All patients were unable to tolerate discontinuation from mechanical ventilation. Each patient was evaluated during a period of spontaneous breathing and during PSV. Four successive levels of PSV were assessed in the following order: 20 cm H2O (PS20), 15 cm H2O (PS15), 10 cm H2O (PS10), and 5 cm H2O (PS5). RESULTS: When pressure support was reduced from PS20 to PS10 the respiratory rate (f) and the rapid shallow breathing index (f/VT) significantly increased and tidal volume (VT) significantly decreased. These parameters did not vary when pressure support was reduced from PS10 to PS5. Conversely, P0.1 varied negligibly between PS20 and PS15 but increased significantly at low PSV levels. P0.1 values were always greater than 2.9 cm H2O (4.1 (1.1) cm H2O) when SCM activity was present. When contraction of the SCM muscles reappeared the P0.1 was the only parameter that changed significantly. CONCLUSIONS: In postoperative septic patients the value of P0.1 seems to be more useful than breathing pattern parameters for setting the optimal level of pressure assistance during PSV.     

Effect of halothane on diaphragmatic muscle function in pentobarbital-anesthetized dogs

The mechanism underlying the decrease in minute ventilation (VE) observed under halothane anesthesia was investigated in nine spontaneously breathing dogs. Anesthesia was induced with pentobarbital sodium and was maintained with halothane. Inspired fraction of halothane (FIhal) was increased every 30 min, from 0.005 to 0.02. VE decreased from 8.1 +/- 0.9 to 4.8 +/- 0.4 l . min-1 (P less than 0.001), as FIhal increased from 0 to 0.02. This resulted from a decrease in both mean inspiratory flow (VT/TI) and the duty ratio (TI/TTOT). Transdiaphragmatic pressure (Pdi) and the integrated electrical activity of both hemidiaphragms (Edi) were measured during normal breathing, and during breathing against closed airways (P0di, E0di), in order to obtain an index of the inspiratory neuromuscular output of the diaphragm. With increasing FIhal, there was a significant decrease in Pdi, P0di, Edi, and E0di. The authors measured Pdi and Edi generated during supramaximal stimulation of the two phrenic nerves (PSdi, Esdi) at frequencies of 10, 20, 50, and 100 Hz, in order to eliminate in this decrease the role played by a decrease in the neural drive to breathing. PSdi and ESdi decreased significantly with increasing FIhal, and had not returned to the control values 30 min after discontinuation of halothane administration. The authors conclude that, in pentobarbital-anesthetized dogs, halothane is responsible for a diaphragmatic dysfunction, which may be located either at the neuromuscular junction, on the contractile processes of the muscle, or on both, and for a decrease in the activation time of the inspiratory muscles. Both of these effects contribute to the decrease in VE observed under halothane anesthesia.     

Cardiopulmonary effects of pressure support ventilation

Pressure support ventilation (PSV) is a newer mode of ventilatory support that augments the patient's spontaneous inspirations to a preselected peak inspiratory pressure. We studied the effects of adding low levels of PSV (5 to 10 cm H2O) in conjunction with intermittent mandatory ventilation (IMV) on 15 patients who required mechanical ventilation for flail chest and pulmonary contusion. Patients were selected for the study if, during weaning from IMV, the following criteria were met: (1) a PaCO2 level greater than 45 mm Hg, (2) a spontaneous respiratory rate (RR) greater than 30 breaths per minute, (3) a minute ventilation (VE) greater than 9.0 L/min, and (4) spontaneous tidal volumes (VT) of less than 2 mL/kg. The PSV was added to the IMV at a level that augmented spontaneous VT to greater than 4 mL/kg. An average of 9 +/- 3 cm H2O of pressure support resulted in a fall in the level of PaCO2 (50 +/- 4 to 43 +/- 5 mm Hg), spontaneous RR (36 +/- 5 to 16 +/- 3 breaths per minute), VE (12 +/- 2 to 8.4 +/- 1.5 L/min), and dead space-tidal volume ratio from (0.68 +/- 0.1 to 0.47 +/- 0.05). Mean airway pressure and PaO2 both increased, but these changes were not statistically significant. Oxygen consumption was also unchanged. These results suggest that in patients who are difficult to wean due to respiratory muscle fatigue (characterized by increasing RR and decreasing VT), PSV normalizes lung volumes, improves ventilation, and may expedite the weaning process.     

Effect of domperidone on the ventilatory response to transient hyperoxia in patients anaesthetized with isoflurane

We have studied the ventilatory responses to transient hyperoxia in two groups of patients (n = 10) anaesthetized with isoflurane (0.3 MAC); patients were allocated randomly to receive either domperidone or placebo orally before anaesthesia. In each patient, five two-breath oxygen tests were averaged and minute ventilation (VEinst) or mean inspiratory flow rate (VT/TI) for each post-test breath was compared with the mean values for these variables during baseline ventilation. A decrease to less than the 95% confidence limits of mean baseline values was considered a definite response. According to this definition, transient hyperoxia decreased VEinst in nine of 10 patients in the placebo group and in all patients in the domperidone group. Similar changes occurred in VT/TI, with eight of 10 definite responses in the placebo group and 10 of 10 in the domperidone group. Compared with placebo, in the domperidone group there were larger changes in VEinst (0.30 vs 0.55 litre min-1 (P = 0.05) and VT/TI (8.5 vs 26.6 ml s-1 (P = 0.02)) from respective baselines. Peripheral chemoreceptors appeared to be active during isoflurane anaesthesia and domperidone pretreatment enhanced this activity by increasing respiratory drive.      

Atelectasis is inversely proportional to transpulmonary pressure during weaning from ventilator support in a large animal model

Background

In mechanically ventilated, lung injured, patients without spontaneous breathing effort, atelectasis with shunt and desaturation may appear suddenly when ventilator pressures are decreased. It is not known how such a formation of atelectasis is related to transpulmonary pressure (P_L) during weaning from mechanical ventilation when the spontaneous breathing effort is increased. If the relation between P_L and atelectasis were known, monitoring of P_L might help to avoid formation of atelectasis and cyclic collapse during weaning. The main purpose of this study was to determine the relation between P_L and atelectasis in an experimental model representing weaning from mechanical ventilation.

Methods

Dynamic transverse computed tomography scans were acquired in ten anaesthetized, surfactant‐depleted pigs with preserved spontaneous breathing, as ventilator support was lowered by sequentially reducing inspiratory pressure and positive end expiratory pressure in steps. The volumes of gas and atelectasis in the lungs were correlated with P_L obtained using oesophageal pressure recordings. Work of breathing (WOB) was assessed from Campbell diagrams.

Results

Gradual decrease in P_L in both end‐expiration and end‐inspiration caused a proportional increase in atelectasis and decrease in the gas content (linear mixed model with an autoregressive correlation matrix; P < 0.001) as the WOB increased. However, cyclic alveolar collapse during tidal ventilation did not increase significantly.

Conclusion

We found a proportional correlation between atelectasis and P_L during the ‘weaning process’ in experimental mild lung injury. If confirmed in the clinical setting, a gradual tapering of ventilator support can be recommended for weaning without risk of sudden formation of atelectasis.     

Control of breathing in patients with limb girdle dystrophy: a controlled study.

BACKGROUND--In patients with limb girdle dystrophy the relative contribution of peripheral factors (respiratory muscle weakness, and lung and/or airway involvement) and central factors (blunted and/or inadequate chemoresponsiveness) in respiratory insufficiency has not yet been established. To resolve this, lung volumes, arterial blood gas tensions, respiratory muscle strength, breathing pattern and neural respiratory drive were investigated in a group of 15 patients with limb girdle dystrophy. An age-matched normal group was studied as a control. METHODS--Respiratory muscle strength was assessed as an arithmetic mean of maximal inspiratory (MIP) and expiratory (MEP) pressures. Breathing pattern was evaluated in terms of volume (ventilation VE, tidal volume VT) and time (respiratory frequency Rf, inspiratory time TI, expiratory time TE) components of the respiratory cycle. Neural respiratory drive was assessed as the mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1) and electromyographic activity (EMG) of the diaphragm (EMGd) and the intercostal parasternal (EMGp) muscles. In 10 of the 15 patients the responses to carbon dioxide (PCO2) stimulation were also evaluated. RESULTS--Most patients exhibited a moderate decrease in vital capacity (VC) (range 37-87% of predicted), MIP (range 23-84% of predicted), and/or MEP (range 13-41% of predicted). The arterial carbon dioxide tension (PaCO2) was increased in three patients breathing room air, while PaO2 was normal in all. Compared with the control group Rf was higher, and VT, TI and TE were lower in the patients. EMGd and EMGp were higher whilst VT/TI and P0.1 were normal in the patients. Respiratory muscle strength was inversely related to EMGd and EMGp. PaCO2 was found to relate primarily to VC and duration of illness, but not to respiratory muscle strength. During hypercapnic rebreathing delta VE/delta PCO2, delta VT/delta PCO2, and delta P0.1/delta PCO2 were lower than normal, whilst delta EMGd/delta PCO2 and delta EMGp/delta PCO2 were normal in most patients. A direct relation between respiratory muscle strength and delta VT/delta PCO2 was found. CONCLUSIONS--The respiratory muscles, especially expiratory ones, are weak in patients with limb girdle dystrophy. Reductions in respiratory muscle strength are associated with increased neural drive and decreased ventilatory output (delta VT/delta PCO2). The decrease in VC, together with the duration of disease, influence PaCO2. VC is a more useful test than respiratory muscle strength for following the course of limb girdle dystrophy.     

Effect of Patient-triggered Ventilation on Respiratory Workload in Infants after Cardiac Surgery

Background: Patient-triggered ventilation (PTV) is commonly used in adults to avoid dyssynchrony between patient and ventilator. However, few investigations have examined the effects of PTV in infants. Our objective was to determine if pressure-control PTV reduces infants' respiratory workloads in proportion to the level of pressure control. We also explored which level of pressure control provided respiratory workloads similar to those after the extubation of the trachea.

Methods: When seven post-cardiac surgery infants, aged 1 to 11 months, were to be weaned with the pressure-control PTV, we randomly applied five levels of pressure control: 0, 4, 8, 12, and 16 cm H2O. All patients were ventilated with assist-control mode, triggering sensitivity of 1 l/min, and positive end-expiratory pressure of 3 cm H2O. After establishing steady state conditions at each level of pressure control, arterial blood gases were analyzed and esophageal pressure (Pes), airway pressure, and airflow were measured. Inspiratory work of breathing (WOB) was calculated using a Campbell diagram. A modified pressure-time product (PTPmod) and the negative deflection of Pes were calculated from the Pes tracing below the baseline. The measurement was repeated after extubation.

Results: Pressure-control PTV supported every spontaneous breath. By decreasing the level of pressure control, respiratory rate increased, tidal volume decreased, and as a result, minute ventilation and arterial carbon dioxide partial pressure were maintained stable. The WOB, PTPmod, and negative deflection of Pes increased as pressure control level was decreased. The WOB and PTPmod at 4 cm H2O pressure control and 0 cm H2O pressure control and after extubation were significantly greater than those at the pressure control of 16, 12, and 8 cm H2O (P < 0.05). The WOB and PTPmod were almost equivalent after extubation and at 4 cm H2O pressure control.     

Quantal ventilatory variability during spontaneous breathing anaesthesia

Background. Cardioventilatory coupling is the triggering ofinspiratory onset by preceding cardiac activity. We have observedtwo forms of coupling with a bimodal (‘quantal’)variation of respiratory period. Methods. We investigated the variables of inspiratory duration(TI), expiratory duration (TE), and tidal volume (VT) whererespiratory period variation was bimodal. In 25 anaesthetizedspontaneously breathing subjects we took 11 samples of recordingwhere the variation of respiratory period was quantal. Results. In eight of these epochs the variation in respiratoryperiod was associated with fluctuations in the number of heartbeats per breath (entrainment ratio) with a constant time intervalbetween inspiration and the immediately preceding heart beat(coupling interval), which we define as pattern II coupling.During pattern II coupling, the quantal variations in respiratoryperiod were entirely caused by variation in TE, with no associatedchanges in either TI or VT. The other three epochs with quantalvariations in respiratory period were observed in pattern IIIcoupling, where an alternating fluctuation in both entrainmentratio and coupling interval occurs. During pattern III coupling,quantal fluctuations were observed in TE, TI, and VT. Implications. Cross correlation analysis suggested that whenpattern III was present, TI was dependent upon the precedingTE, which differs markedly from traditional views on the interactionbetween inspiratory and expiratory duration. VT was linearlyrelated to TI, and so could also be determined by the precedingTE during this type of coupling. Br J Anaesth 2003; 91: 184–9     

Effects of diaphragm plication for phrenic nerve paralysis on respiratory mechanics and diaphragm function

The purpose of this study is to examine the effects of unilateral diaphragm plication for phrenic nerve paralysis on the respiratory mechanics and diaphragm function. Study 1: We performed thoracotomy (BASELINE), left phrenicotomy (INJURY) and left diaphragm plication (PLICATION) in ten dogs. After chest was closed in each condition, measured were the tidal volume (TV), respiratory rate (f), esophageal and gastric pressure swing (delta Pes, delta Pga), dynamic compliance (Cdyn) the ratio of gastric to esophageal pressure swing (delta Pga/delta Pes) and the work of breathing per liter (WOB/L) under stable spontaneous breathing. Study 2: In eight other left-phrenicotomized dogs, Pdi and fractional shortening of the costal diaphragm during contralateral electrophrenic stimulation were measured before and after plication. After plication TV, delta Pga/delta Pes, Cdyn, Pdi and fractional shortening during stimulation increased significantly, whereas Pes and WOB/L decreased significantly compared with INJURY condition. In conclusion unilateral diaphragm plication after paralysis improves the intact hemidiaphragm contractility and diaphragmatic contribution to breathing.     

Inspiratory pressure support compensates for the additional work of breathing caused by the endotracheal tube

Breathing through an endotracheal tube and a demand valve may increase the work performed by the respiratory muscles. Inspiratory pressure support (PS) is known to reduce this work and might therefore compensate for this increased requirement. To test this hypothesis, we measured the work of breathing (WOB) in 11 patients whose tracheas were intubated. Five had no intrinsic lung disease, but six had chronic obstructive lung disease. We compared WOB measurements taken under several sets of conditions: during assisted breathing at four levels of PS, during unassisted breathing and connection to a T-piece, and after extubation of the trachea. During unassisted breathing via the ventilator circuit (PS set at 0 cmH20), the WOB per minute was greater than that after extubation, with a mean increase (+/- standard deviation) of 68 +/- 38% (10.3 +/- 5.1 vs. 6.5 +/- 3.7 J.min-1, P less than 0.01). While breathing through the T-piece, the WOB was 27 +/- 18% greater than after tracheal extubation (8.2 +/- 5.1 vs. 6.5 +/- 3.7 J.min-1, P less than 0.05). The principal reason why inspiratory work decreased after extubation was that the ventilatory requirement decreased. For each patient, we determined retrospectively, after extubation, the level of PS that had reduced WOB to its postextubation value and obtained levels ranging from 3.4 to 14.4 cmH2O. The PS level at which additional WOB was compensated for, was greater in patients with chronic lung disease than in those free of lung disease (12.0 +/- 1.9 vs. 5.7 +/- 1.5 cm H2O, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of patient-triggered ventilation on respiratory workload in infants after cardiac surgery

BACKGROUND: Patient-triggered ventilation (PTV) is commonly used in adults to avoid dyssynchrony between patient and ventilator. However, few investigations have examined the effects of PTV in infants. Our objective was to determine if pressure-control PTV reduces infants' respiratory workloads in proportion to the level of pressure control. We also explored which level of pressure control provided respiratory workloads similar to those after the extubation of the trachea. METHODS: When seven post-cardiac surgery infants, aged 1 to 11 months, were to be weaned with the pressure-control PTV, we randomly applied five levels of pressure control: 0, 4, 8, 12, and 16 cm H2O. All patients were ventilated with assist-control mode, triggering sensitivity of 1 l/min, and positive end-expiratory pressure of 3 cm H2O. After establishing steady state conditions at each level of pressure control, arterial blood gases were analyzed and esophageal pressure (Pes), airway pressure, and airflow were measured. Inspiratory work of breathing (WOB) was calculated using a Campbell diagram. A modified pressure-time product (PTPmod) and the negative deflection of Pes were calculated from the Pes tracing below the baseline. The measurement was repeated after extubation. RESULTS: Pressure-control PTV supported every spontaneous breath. By decreasing the level of pressure control, respiratory rate increased, tidal volume decreased, and as a result, minute ventilation and arterial carbon dioxide partial pressure were maintained stable. The WOB, PTPmod, and negative deflection of Pes increased as pressure control level was decreased. The WOB and PTPmod at 4 cm H2O pressure control and 0 cm H2O pressure control and after extubation were significantly greater than those at the pressure control of 16, 12, and 8 cm H2O (P < 0.05). The WOB and PTPmod were almost equivalent after extubation and at 4 cm H2O pressure control. CONCLUSIONS: Work of breathing and PTPmod were changed according to the pressure control level in post-cardiac surgery infants. PTV may be feasible in infants as well as in adults.     

Ventilatory compensation for inspiratory resistive loads during anaesthesia with halothane or isoflurane

We have analysed the ventilatory response to sustained inspiratory resistive loads in 14 patients, while awake and during halothane (n = 7) or isoflurane (n = 7) anaesthesia. Patients breathed halothane or isoflurane in oxygen at 1.2 minimum alveolar concentration (MAC). Inspiratory resistances of 0, 12 and 37 cm H2O litre-1 s were applied. Tidal volume (VT) was maintained with the greater loads. At the greatest resistance, a significant reduction in minute ventilation occurred in both awake (-18.9%) and anaesthetized states, with both halothane (-10.4%) and isoflurane (-14.5%). Ventilatory frequency decreased significantly from mean 14.6 (SD 4.7) to 12.5 (4.3) bpm in the awake state and during anaesthesia, with increasing inspiratory resistance (29.5 (3.6) to 23.7 (7.2) bpm and 25.8 (3.3) to 23.4 (4.0) bpm, respectively, for halothane and isoflurane) because inspiratory time (TI) was significantly longer (P < 0.01). End-tidal PCO2 increased by 0.3 kPa, on average, from baseline to the highest level of resistance (P < 0.01). Inspiratory occlusion pressure at 100 ms increased significantly with increased loading in all situations (P < 0.001). We found a similar pattern of ventilatory adaptation to sustained inspiratory flow resistive loads both in awake and anaesthetized states. VT was maintained at increased loads because of an increase in inspiratory neuromuscular output and inspiratory duration.      

The effects of the pause at the end of inspiration on gas exchange and hemodynamics during artificial ventilation]

We have studied the effects of an inspiratory pause (PI) during artificial ventilation in 13 patients in acute respiratory insufficiency. The effects on gas exchange, haemodynamics and distribution of ventilation were observed. During the period of study the total volume, the inspiration/expiration ratio and the inspired oxygen concentration were all maintained constant. With the inspiratory pause arterial oxygenation has not changed significantly, whereas it did change favourably with PEEP. The physiological dead space (VD/VT) was reduced in proportion to the duration of the inspiratory pause. These results suggest that the inspiratory pause triggers regional modification of the ventilation/perfusion ratio, favouring a reduction of the VD/VT ratio. However, this improvement of the VD/VT ratio does not seem to influence the oxygenation or the total distribution of ventilation in this type of patient.