[Diaphragmatic eventration which is neither hernia nor rupture].
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Biomedical subjects
Publications and source records attributed to Thomas Similowski.
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INTRODUCTION: Chronic obstructive pulmonary disease (COPD) has become a real public health problem throughout the world. In spite of its association with high rates of morbidity and mortality, it is not accorded sufficient attention. In this paper, we present the results of the French part of the international survey "Confronting COPD in North America and Europe" concerning the impact of COPD from the perspective patients'. METHODS: Subjects were randomly recruited by means of telephone questionnaires. Patients included in the survey were to be aged > or =45 years with a cumulative cigarette consumption of > or =10 packets-yrs, and having been diagnosed with COPD, emphysema or chronic bronchitis, or whose symptoms fulfilled a definition of chronic bronchitis. RESULTS: According to this survey, the prevalence of COPD among smokers (mean number of packets per year: 38.2 +/- 26.1) was 3.2%. COPD was undiagnosed in 17% of patients in spite of the presence of characteristic symptoms. Respiratory difficulties had a marked adverse effect on the quality of life although patients tended to play down the severity of their problems. DISCUSSION: This survey reveals that COPD appears to be under-diagnosed and under-treated in France, as shown by the results of the same survey in the other 7 countries taking part. Considerable efforts are thus required to improve the speed and precision of diagnosis and to improve management of these patients.
It is unknown whether changes in corticomotor excitability follow exercise in healthy humans. We hypothesized that a fall in the diaphragm and quadriceps motor-evoked potential (MEP) amplitude elicited by transcranial magnetic stimulation of the motor cortex would occur after an incremental exercise task. In 11 healthy subjects, we measured transdiaphragmatic pressure and isometric quadriceps tension in response to supramaximal peripheral magnetic nerve stimulation. MEPs were recorded from these muscles in response to transcranial magnetic stimulation. After baseline measurements, subjects performed a period of submaximal exercise (gentle walking). Measurements were repeated 5 and 20 min after this. The subjects then exercised on a treadmill with an incremental protocol to exhaustion. Transcranial magnetic stimulation was performed at baseline and at 5, 20, 40, and 60 min after exhaustive exercise, and force measurements were obtained at baseline, 20 min, and 60 min. Mean exercise duration was 18 +/- 4 min, and mean maximum heart rate was 172 +/- 10 beats/min. Twitch transdiaphragmatic pressure and twitch isometric quadriceps tension were not different from baseline after exercise, but a significant decrease was observed in diaphragm MEP amplitude 5 and 20 min after exercise (60 +/- 38 and 45 +/- 24%, respectively, of baseline, P = 0.0001). At the same times, the mean quadriceps MEPs were 59 +/- 39 and 74 +/- 32% of baseline (P < 0.0001 and P < 0.01, respectively). Studies using paired stimuli confirmed a likely intracortical mechanism for this depression. Our data confirm significant depression of both diaphragm and quadriceps MEPs after incremental treadmill exercise.
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We assessed recruitment curves of the surface diaphragm motor-evoked potential (MEP) after transcranial magnetic stimulation during relaxation and at three different levels of facilitation (20, 40, and 60% of maximal inspiratory esophageal pressure) in 10 healthy subjects (six young and four elderly). MEP amplitude recruitment curves varied between individuals during relaxation and at each level of facilitation. Amplitude recruitment curves during relaxation were reproducible in individual subjects. Inspiratory maneuvers caused a decrease in motor threshold and latency and an increase in MEP amplitude, positively correlated to the intensity of facilitation. These changes were similar in young and elderly subjects. The best fit for MEP amplitude recruitment curves for each condition was obtained with a Boltzmann model. The performance of repeated submaximal inspiratory maneuvers did not affect the amplitude recruitment curves of the relaxed diaphragm. We conclude that the recruitment curve of the diaphragm with transcranial magnetic stimulation is repeatable and changes consistently with facilitation and will, therefore, be a robust experimental tool for the investigation of supraspinal pathways to the diaphragm.
BACKGROUND: Medullary infarcts can be associated with breathing disorders that usually consist in central hypoventilation. PATIENT: We describe the case of a 54-year-old man, fully conscious, presenting with an uncontrollable high frequency and shallow tachypnea (95/min) at the onset of a unilateral medial medullary infarct. This disorder disappeared under inspiratory pressure support mechanical ventilation. MEASUREMENTS AND RESULTS: Respiratory drive (respiratory rate, occlusion pressure, and mean inspiratory flow), efferent pathway (transcranial and cervical magnetic stimulation), and afferent pathway (response to CO(2) and to lung inflation) were investigated. The respiratory drive was increased. The phrenic nerve conduction time was normal. The sensitivity of the central pattern generator to lung inflation and to CO(2) was preserved. The territory of the infarct was supplied by the spinal anterior artery. CONCLUSIONS: An extremely rapid and shallow tachypnea due to the increase in respiratory drive can be associated with unilateral medullary infarction.
In a patient with C3 quadriplegia causing complete diaphragm paralysis who developed inspiratory neck muscles (INM) hypertrophy to sustain ventilation, spontaneous breathing deeply altered sleep architecture, relegating sleep to the expiratory phase of the ventilatory cycle. A polysomnographic recording performed during mechanical ventilation (without INM activity), showed that sleep was abnormal but unaffected by the respiratory cycle. During spontaneous breathing, the polygraphic recordings showed expiratory microsleep episodes, with inspiratory arousals synchronous to bursts of INM activity. This case report illustrates the powerful adaptability of the respiratory and sleep control systems to maintain each vital function.
Respiratory muscles respond to a subcortical automatic command and to a neocortical voluntary command. In diseases such as stroke or motor neurone disease, an abnormal diaphragmatic response to single transcranial magnetic stimuli can identify a central source for respiratory disorders, but this is not likely to be the case in disorders affecting intracortical inhibitory and facilitatory mechanisms. This study describes the response of the diaphragm to paired transcranial magnetic stimulation. Thirteen normal subjects were studied (age range, 22 to 43 years; 7 men; phrenic conduction, <6.8 msec; latency of diaphragmatic motor evoked potential, <20.5 msec). Motor evoked potentials in response to paired stimulation were obtained in eight subjects only, with the motor threshold in the remaining five subjects too high to absorb the loss of power inherent in the double-stimulation montage. Interstimulus intervals less than 5 msec resulted in a statistically significant inhibition (p < 0.01 for interstimulus intervals of 1 and 3 ms), whereas intervals longer than 6 msec were facilitatory (maximal, 15 msec). The diaphragmatic pattern matched that of the biceps brachii. The authors conclude that it is possible to study intracortical inhibition and facilitation of diaphragmatic control, although not in all subjects. Technical improvement should alleviate current limitations and make paired transcranial magnetic stimulation a tool to study respiratory muscle abnormalities in settings in which intracortical interactions are important, such as movement disorders.
STUDY OBJECTIVES: Measuring respiratory-related changes in arterial pulse pressure is useful to guide fluid expansion in hemodynamically compromised patients. In the absence of automation, this can be uneasy in clinical practice. The objective of this study was to test an alternative approach (expiratory pause) that should be easier to apply. DESIGN: Prospective observational study comparing two measurement methods of a biological variable. PATIENTS: Seventeen patients receiving mechanical ventilation without spontaneous respiratory activity, with an arterial indwelling catheter, exhibiting respiratory-related fluctuations in arterial pressure. SETTING: Ten-bed respiratory ICU in a 2,000-bed university hospital. INTERVENTION: Analysis of clinically gathered data without specific experimental intervention. MEASUREMENTS: Determinations of the change in arterial pulse pressure observed during ventilatory cycling (Delta Pp,dyn) ["dynamic"] and change in arterial pulse pressure observed during expiratory pauses (Delta Pp,stat) ["static"] were performed to assess respiratory mechanics, and comparison of the two sets of data (correlation, Bland and Altman, Passing and Bablok regression). RESULTS: Delta Pp,dyn and Delta Pp,stat were strongly correlated (R = 0.964; 95% confidence interval, 0.917 to 0.987; p < 0.0001), with a good level of agreement (mean difference, 0.016; lower limit of agreement, - 0.087; upper limit, 0.120) and no systematic difference. CONCLUSION: Measuring respiratory-related Delta Pp,stat provides data that seem interchangeable with Delta Pp,dyn, providing an easy means to routinely obtain this information.
INTRODUCTION: Bedside cardiac output determination is a common preoccupation in the critically ill. All available methods have drawbacks. We wished to re-examine the agreement between cardiac output determined using the thermodilution method (QTTHERM) and cardiac output determined using the metabolic (Fick) method (QTFICK) in patients with extremely severe states, all the more so in the context of changing practices in the management of patients. Indeed, the interchangeability of the methods is a clinically relevant question; for instance, in view of the debate about the risk-benefit balance of right heart catheterization. PATIENTS AND METHODS: Eighteen mechanically ventilated passive patients with a right heart catheter in place were studied (six women, 12 men; age, 39-84 years; simplified acute physiology scoreII, 39-111). QTTHERM was obtained using a standard procedure. QTFICK was measured from oxygen consumption, carbon dioxide production, and arterial and mixed venous oxygen contents. Forty-nine steady-state pairs of measurements were performed. The data were normalized for repeated measurements, and were tested for correlation and agreement. RESULTS: The QTFICK value was 5.2 +/- 2.0 l/min whereas that of QTTHERM was 5.8 +/- 1.9 l/min (R = 0.840, P < 0.0001; mean difference, -0.7 l/min; lower limit of agreement, -2.8 l/min; upper limit of agreement, 1.5 l/min). The agreement was excellent between the two techniques at QTTHERM values <5 l/min but became too loose for clinical interchangeability above this value. Tricuspid regurgitation did not influence the results. DISCUSSION AND CONCLUSIONS: No gold standard is established to measure cardiac output in critically ill patients. The thermodilution method has known limitations that can lead to inaccuracies. The metabolic method also has potential pitfalls in this context, particularly if there is increased oxygen consumption within the lungs. The concordance between the two methods for low cardiac output values suggests that they can both be relied upon for clinical decision making in this context. Conversely, a high cardiac output value is more difficult to rely on in absolute terms.
The integrity of the central efferent motor pathways to the diaphragm can be assessed by using transcranial magnetic stimulation to measure the latency of the corresponding motor evoked potentials with surface electrodes. Because transcranial magnetic stimulation does not activate the diaphragm alone, signal contamination is a potential problem. To evaluate this issue, surface diaphragmatic motor-evoked potential latencies were compared with latencies recorded from diaphragm needle in 9 healthy volunteers. Surface latencies of muscles likely to contaminate the diaphragm signals (serratus anterior, pectoralis major, and tranversus abdominis) were also recorded. The latencies in response to nonfocal transcranial stimulation from surface electrodes were not significantly different from the needle ones (17 +/- 1.3 vs. 17.2 +/- 1.1 ms, respectively) but were significantly different from the latencies of the other muscles. In two cases, signal contamination appeared likely (serratus anterior in 1 case, abdominal muscles in 1 case). It is possible to reliably measure the latency of the diaphragm response to transcranial magnetic stimulation with adequately positioned surface electrodes.
The diagnosis of the obstructive sleep apnea syndrome relies on polysomnography. Bilateral anterior magnetic phrenic stimulation (BAMPS) mimics the dissociation between upper airway (UA) muscles and diaphragm commands that leads to UA closure during sleep. We evaluated BAMPS as a mean to identify obstructive sleep apnea syndrome patients through the characterization of the UA dynamics in 28 consecutive awake patients (18 apneic and 10 nonapneic). Driving pressure (Pd) and instantaneous flow (V) were recorded in response to BAMPS to determine the point of flow limitation (Vimax) and of minimal flow (Vimin) and the flow-pressure relationship [Vi = (k(1) x Pd) + (k(2) x Pd(2))]. Vimax, Vimin, UA resistance at Vi(min), and the coefficient of the flow-pressure relationship (k(1)) were correlated with apnea-hypopnea index (respectively, R = -0.735, P < 0.0001; R = -0.584, P = 0.001; R = 0.474, P = 0.01; and R = -0.567, P < 0.01). Body mass index was also correlated with apnea-hypopnea index (R = 0.500, P < 0.01). Apneic patients had a lower Vimax (Vimax = 678 +/- 386 vs. 1,247 +/- 271 ml/s; P < 0.001), a lower Vimin (Vimin = 460 +/- 313 vs. 822 +/- 393 ml/s; P < 0.05) and a lower k(1) (k(1) = 162 +/- 67 vs. 272 +/- 112 ml x cmH(2)O x s(-1); P < 0.01) than nonapneic ones. Using a classification and regression tree approach, we found that a Vimax of <803 ml/s (n = 12) selected only apneic patients. When Vimax of >803 ml/s (n = 16), a k(1) of >266.7 ml. cmH(2)O x s(-1) identified only nonapneic patients (n = 5). In 11 cases, Vimax > 803 ml/s and k(1) < 266.7 ml. cmH(2)O x s(-1). These included five nonapneic and six apneic patients. We conclude that UA dynamic properties studied with BAMPS during wakefulness significantly differ between nonapneic and apneic patients.
Recently, it has been suggested that peak expiratory flow (PEF) may be determined by the wave speed flow-limiting mechanism. In six normal male subjects (age = 33 +/- 8 years) performing expiratory forced vital capacity (FVC) maneuvers, a negative expiratory pressure (NEP) of -10 cm H2O was randomly applied at the beginning of maximal expiration to assess changes in PEF as compared with baseline. During FVC maneuvers, the expiratory effort was measured by changes in esophageal pressure (Pes), as either peak expiratory Pes-Pes at end expiratory lung volume (DeltaPes(peak)) or maximal rate of rise of Pes (dPes/dt(max)). In each experimental condition, at least three FVC maneuvers with comparable expiratory effort were selected for analysis for each subject. With similar DeltaPes(peak) (107.2 +/- 34.9 versus 111.7 +/- 40.5 cm H2O) and dPes/dt(max) (1181 +/- 518 versus 1177 +/- 546 cm H2O/second) PEF amounted to 10.84 +/- 1.08 L/second and to 10.82 +/- 1.03 L/second with and without NEP, respectively. These data show that PEF obtained by normal subjects to the best of their abilities (best PEF) does not increase with NEP and indicate that the best PEF is a flow-limited and effort-independent parameter, reflecting only lung and airways mechanics as the other subsequent maximal expiratory flows achieved during the FVC maneuver.
The inspiratory pump (inspiratory muscles and the rib cage) translates inspiratory commands in alveolar ventilation by applying expanding forces to the lungs. Its functioning is of paramount importance to the physiology of breathing and of many pathological situations. Major difficulties in studying its function in relationship with its structure arise from the extremely complex geometrical disposition of its active and passive elements. We herein describe a two-compartment model of the inspiratory pump, with model parameters identification derived from actual measurements obtained by magnetic resonance imaging in normal humans. The equations governing the model are presented. Numerical simulations validate the model by showing a behaviour similar to physiological observations. This opens the possibility of predicting the behaviour of the respiratory system during diseases involving changes in its mechanical or geometrical characteristics.
Of the different respiratory disorders that complicate the course of polymyositis, diaphragmatic weakness is one that is seldom described and most often suspected rather than confirmed. We report a case of severe diaphragmatic weakness as a cause of acute respiratory failure revealing a polymyositis. The diaphragmatic involvement was proven by a very low esophageal pressure in response to cervical magnetic stimulation of the phrenic nerve. Corticosteroids and intravenous gammaglobulin, combined with mechanical ventilation, achieved a progressive recovery of diaphragmatic weakness.
PURPOSE: To evaluate, with thin-section computed tomography (CT), changes in bronchial cross-sectional area and lung attenuation induced by bronchial stimulation in patients with mild intermittent asthma, at a given lung volume monitored with pneumotachography. MATERIALS AND METHODS: Twelve patients with mild intermittent asthma who were nonsmokers (National Institutes of Health staging) and six nonsmoking healthy volunteers, age and sex ratio-matched, were examined by using helical thin-collimation CT at the level of basal bronchi at 65% of total lung capacity. Three sets of acquisitions were obtained: at baseline and after inhalation of methacholine and then salbutamol. Cross-sectional areas of bronchi greater than 4 mm(2) were segmented and calculated from CT images. Lung attenuation was measured in the anterior, lateral, and posterior areas of the right lung parenchyma. Gas trapping was evaluated by using thin-section CT at residual volume in six of the patients with asthma. Statistical analysis included two factors repeated-measurement analysis of variance and Mann-Whitney and Kruskal-Wallis nonparametric tests. RESULTS: Bronchial cross-sectional areas and lung attenuation did not vary significantly compared with baseline values following bronchial challenge in healthy volunteers or patients with asthma. However, in patients with asthma, bronchial cross-sectional areas were significantly smaller than in healthy volunteers, except after inhalation of salbutamol. Lung attenuation and anteroposterior attenuation gradient were significantly higher in patients with asthma than in healthy patients (P <.001). Air-trapping scores were significantly higher after methacholine challenge. CONCLUSION: Helical thin-collimation CT at controlled lung volume and at full expiration associated with bronchial challenge may help evaluate bronchoreactivity and inflammation in mild intermittent asthma.
Phrenic nerve stimulation (PNS) can assess airflow dynamics of the upper airway (UA) during wakefulness in man. Using PNS, we aimed to assess the impact of neck flexion and mouth opening in promoting UA unstability. Measurements were made during nasal breathing in seven healthy subjects (ages = 23-39 yr; one woman). Surface diaphragm electromyogram, esophageal pressure referenced to mask pressure, and flow were recorded during diaphragm twitches with neck in neutral position and mouth closed and then with neck flexion and/or mouth opening. Twitches always exhibited a flow-limited pattern. Flow-limiting driving pressure (Pd) and peak Pd were increased by neck flexion (P < 0.01) without significant change in the corresponding flows. UA resistances at these flow values were higher with the neck flexed (P < 0.05). Mouth opening alone did not exert any significant influence. We conclude that the position of the neck has a discernible impact on the flow behavior through the nonphasically active UA faced with a negative Pd.
Phrenic nerve stimulation, electrical (ES) or from cervical magnetic stimulation (CMS), allows one to assess the diaphragm contractile properties and the conduction time of the phrenic nerve (PNCT) through recording of an electromyographic response, traditionally by using surface electrodes. Because of the coactivation of extradiaphragmatic muscles, signal contamination can jeopardize the determination of surface PNCTs. To address this, we compared PNCTs with ES and CMS from surface and needle diaphragm electrodes in five subjects (10 phrenic nerves). At a modified recording site, lower and more anterior than usual (lowest accessible intercostal space, costochondral junction) with electrodes 2 cm apart, surface and needle PNCTs were similar (CMS: 6.0 +/- 0.25 ms surface vs. 6.2 +/- 0.13 ms needle, not significant). Electrodes recording the activity of the most likely sources of signal contamination, i.e., the serratus anterior and pectoralis major, showed distinct responses from that of the diaphragm, their earlier occurrence strongly arguing against contamination. With ES and CMS, apparently uncontaminated signals could be consistently recorded from surface electrodes.