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This case report concerns a newborn with bilateral adrenal massive hemorrhage complicated by inferior cava vein thrombosis, hypertension and encephalopathy to elaborate diagnostic and therapeutic problem of neonatal thromboembolic events. Increasing of risk population (extreme prematurity), improvement of imaging, laboratory and neonatologist care enhanced in recent years the diagnosis of this group of diseases. Even if literature about this subject is poor, we remark the significant effort of neonatologist to revise and update neonatal guidelines and the relevance of the institution of the National Registry of Neonatal Thrombosis (RITI).

Because costal and crural diaphragm segments have different functional characteristics, ventilatory stimulation with hypoxia or hypercapnia may elicit differential segmental function. We report measurements of diaphragm segmental length, shortening, and electromyogram (EMG) activity from 11 canines that were chronically implanted with sonomicrometry transducers and EMG electrodes and then studied a mean of 18 days postimplantation while awake and breathing spontaneously during CO2 rebreathing and progressive isocapnic hypoxia. Ventilatory responses to hypercapnia and progressive hypoxia were moderate at 1.13 +/- 0.31 (SD) 1. min-1. mm-1 arterial Pco2 and -0.98 +/- 0.51 l. min-1.%arterial O2 saturation-1. When tidal values for breathing pattern and segmental function were compared at matching tidal volumes that correspond to mean CO2 of 49.4 arterial Pco2 and 77% arterial O2 saturation, there was no significant difference in resting length, tidal shortening, or tidal EMG of costal or crural segments. Intrabreath profiles of flow, shortening, and EMG activity at matched tidal volumes showed that 1) inspiratory flow during hypoxia was significantly greater during early inspiration, 2) crural EMG activity preceded costal EMG activity in early inspiration during both hypercapnia and hypoxia, 3) both segments showed increased postinspiratory inspiratory activity with stimulated ventilation, and 4) postinspiratory shortening and EMG were greatest for the crural segment during hypoxia. These results suggest that costal and crural diaphragm segments exhibit differential function during chemical stimulation, especially during postinspiration.

If costal and crural diaphragm segments can perform as separate muscles, then CO2-stimulated ventilation may elicit differential segmental function. We studied diaphragm segmental length, shortening, and electromyogram (EMG) activity in 10 awake dogs chronically implanted with sonomicrometer transducers and EMG electrodes. During CO2 rebreathing, segmental shortening and EMG activity per whole tidal breath progressively increased, but segmental responses could not be differentiated at any level of CO2. With increasing CO2, resting end-expiratory length of both diaphragm segments increased. During the complete intrabreath inspiratory-expiratory cycle, costal and crural diaphragm revealed distinctive segmental function. At rest, crural shortening exceeded costal shortening in earliest inspiration, costal and especially crural shortening persisted into early expiration, and EMG activity of the crural segment was greater than that of the costal segment in earliest inspiration and showed more end-inspiratory/early expiratory [post-inspiratory inspiratory activity (PIIA)] activity. During CO2-stimulated breathing, neither segment shortened during the inspiratory flow of earliest inspiration. During CO2 rebreathing, shortening of the crural segment exceeded that of the costal segment during early inspiration and outlasted costal shortening during expiration; for both segments, shortening persisted after termination of inspiratory airflow. With increased CO2, EMG activity of the crural segment preceded that of the costal segment in earliest inspiration and was dominant into expiration, whereas costal EMG activity terminated abruptly with inspiratory flow. Thus, costal EMG PIIA was not evident during hypercapnia, whereas crural EMG PIIA was significant.(ABSTRACT TRUNCATED AT 250 WORDS)

The intrabreath time course of phrenic artery blood perfusion (Qpha) was studied in five anesthetized dogs. The diaphragm was paced with submaximal levels of stimulation at various duty cycles (DC) to achieve tension-time index below and above the fatigue threshold (0.03–0.60). Left Qpha was measured via Doppler technique during control (inactive diaphragm) and during two submaximal levels of bilateral phrenic nerve stimulation sustained for 1 min. Measurements were done when Qpha reached steady state in each run. The frequency of pacing of each run was 10/min, and the DC ranged from 0.1 to 0.9 in 0.1 increments. Shortening of costal and crural segments was measured by sonomicrometry. It was found that Qpha during the diaphragmatic contraction phase (QphaC) was a sigmoidal function of DC and was not affected by the levels of transdiaphragmatic pressure (Pdi) explored (34–64% of maximal Pdi). Qpha during the diaphragmatic relaxation phase (QphaR) was a parabolic function of the DC, reaching an optimal value at DC of approximately 0.3 at any given Pdi. QphaR increased significantly with the preceding level of Pdi. QphaT (the sum of QphaC and QphaR) was a parabolic function of DC, reaching peak values at DC of 0.4–0.6 and then decreasing. This function was similar at two levels of Pdi. Post-pacing hyperemia was directly related to tension-time index greater than 0.20.

This study demonstrates the impact of the bipolar electrode transfer function on the canine diaphragm electromyogram (EMG) power spectrum, as evaluated with a new electrode design and implantation technique. The results show that: (a) changes in interelectrode distance transformed single-peaked power spectrums into double-peaked spectrums; (b) the mean action potential conduction velocity (APCV), and power spectrum center frequency (CF) and median frequency (MF), are related for interelectrode distances of 5 and 10 mm, but not for 15 and 20 mm; and (C) CF, MF, -3-dB, and -6-dB bandwith values depend on interelectrode distance. We conclude that bipolar electrodes, with a nonfixed interelectrode distance, cannot be used for physiological interpretations of the EMG power spectrum. Nonetheless, power spectrums obtained with fixed and appropriate interelectrode distances can be trusted, if the electrodes are positioned in the direction of the muscle fibers and in regions with low densities of motor endplates.

During natural panting for thermal regulation, the pattern of activation of the major respiratory muscles, including costal and crural diaphragm segments, is not known. We measured diaphragm segmental length, shortening, and electromyographic (EMG) activity in five chronically implanted canines awake and breathing spontaneously at rest and during a mild dry heat stress. During panting, minute ventilation increased fourfold from 5.07 l/min and respiratory rate increased from 16.9 to 192.8 breaths/min or 3.2 Hz. During panting, end-expiratory length of both costal and crural segments decreased, concurrent with significant increases in end-expiratory EMG. With the onset of panting, tidal costal shortening decreased significantly from 6.29% of end-expiratory length to 3.54%, whereas crural shortening decreased from 6.04 to 2.46%. Meanwhile, segmental EMG tended to increase during panting. During panting, intrabreath costal and crural segmental function revealed differential activation; the costal segment shortened in concert with inspiratory flow, whereas peak crural shortening occurred in expiration, almost 180 degrees out of phase with costal. The divergence in segmental shortening during panting was accompanied by a lesser shift in timing of segmental EMG. In the awake spontaneously panting canine, asynchronous costal and crural shortening may enhance gas mixing in a manner analogous to high-frequency ventilation.

Blood flow (Q) of the diaphragm was measured simultaneously with Doppler probes placed on diaphragmatic veins and an artery and by direct volumetric measurements obtained from cannulation of diaphragmatic blood vessels. The Doppler converting coefficients obtained were 6.27, 7.25, 4.21, and 41.07 ml.min-1.kHz-1 for left phrenic artery flow (Qpha), phrenic vein flow (Qphv), internal mammary vein flow (Qimv), and azygos vein flow (Qazv), respectively. The time course of Qpha, Qphv, Qimv, and Qazv after imposed patterns of diaphragmatic contraction was measured in nine anesthetized dogs. Each pattern consisted of various combinations of transdiaphragmatic pressure (Pdi), frequency of pacing (f), and duty cycle obtained by bilateral phrenic nerve stimulation. The dogs were prepared with chests open and loosely casted abdomens. Qpha, Qphv, Qimv, and Qazv were measured at rest (control, passive diaphragm, mechanical ventilation) and at two submaximal levels of stimulation (30 and 60% of Pdimax). The f was 10 or 30 cycles/min and the duty cycle was 0.25, 0.50, and 0.75. The results show 1) Qpha, Qphv, Qimv, and Qazv reached stable values (equilibration) after 30-36 s of pacing; 2) the steady Qpha, Qphv, and Qimv were linearly related to Pdi, and they were related by a parabolic function to duty cycle, whereas Qazv was not significantly affected by Pdi and increased linearly as a function of the duty cycle; 3) the diaphragmatic blood drainage was approximately 60% through the intercostal veins leading into the azygos trunk, 25% through the phrenic vein, and 15% through the internal mammary vein during pacing of the diaphragm at a duty cycle of 0.50 and 60% Pdimax; and 4) for a given pacing pattern, Qpha and Qphv increased with f, but Qimv and Qazv did not.

Dynamic pulmonary hyperinflation and intrinsic PEEP (PEEPi) are known to play an important role in causing acute respiratory failure in COPD patients. In the present study, we have explored (1) the prevalence and magnitude of PEEPi in stable COPD patients, and (2) the correlation of PEEPi with respiratory mechanics and PaCO2. In 96 stable COPD patients with varying degrees of airway obstruction, we measured pulmonary flow resistance (RL), dynamic lung compliance (CLdyn), breathing pattern, arterial blood gases, and dynamic PEEPi. Dynamic PEEPi was determined as a negative deflection in esophageal pressure from the start of inspiratory effort to the onset of inspiratory flow. A significant correlation was found between dynamic PEEPi and FEVi (% predicted; r = -0.56, p less than 0.001), between PEEPi and RL (r = 0.69, p less than 0.001), and between PaCO2 and PEEPi (r = 0.6, p less than 0.001). These results indicate that increased severity of airway obstruction promotes PEEPi and concomitant dynamic hyperinflation. This implies increased inspiratory work in the face of decreased effectiveness of the inspiratory muscles as pressure generators. The present results suggest that dynamic hyperinflation may play a role in causing chronic hypoventilation in COPD patients.

The respiratory sensations evoked by added inspiratory loads are currently thought to be largely mediated by the activity of the inspiratory muscles. Because of the differences in proprioceptors and in afferent and efferent innervations among the inspiratory muscles, we hypothesized that the sensation evoked by a given load would be different when the motor command is directed mainly to rib cage muscles or mainly to the diaphragm. To test this hypothesis, we studied six normal subjects breathing against several inspiratory resistances while emphasizing the use of rib cage muscles, or the diaphragm, or a combination of both. At the end of 10 loaded breaths the subjects rated the perceived magnitude of inspiratory effort on a Borg scale. A linear and unique relationship (r = 0.96 +/- 0.02; P less than 0.001) was found between the sensation and esophageal pressure (Pes) in the three thoracoabdominal breathing patterns. We conclude that the level of Pes, whether generated mainly by the rib cage muscles or the diaphragm, is the main variable related to the sensation of inspiratory effort under external inspiratory loads.

We measured regional lung volumes from apex to base in humans during changes in thoracoabdominal shape which we monitored with magnetometers. In erect subjects, voluntary changes of shape at FRC did not change regional volume distribution. In supine subjects, the effect of negative pressure applied to the abdomen and a similar thoracoabdominal configuration achieved by voluntary means were studied. The distribution of regional volumes in both situations was the same as that measured during relaxation at the same overall lung volumes. We concluded that neither voluntary changes in shape nor negative abdominal pressure influenced the human pleural pressure gradient. This result, which differed from findings in animals, was probably because the human chest was relatively stiff and behaved with one degree of freedom; all parts of the human rib cage changed dimensions proportionally while negative abdominal pressure distorted the rib cage of animals.

In cats anesthetized with Nembutal, electromyograms of the diaphragm (Edi) were recorded from an anchored esophageal electrode, a pair of silver hooks inserted in the paratendinous region, and a pair of silver hooks and a pair of clips of small surface inserted in the costal region of the diaphragm facing the rib cage at FRC but covered with lung tissue at FRC + 80 ml. When single supramaximal electrical stimuli were applied to an isolated phrenic nerve, changes in lung volume from RV to near TLC had a negligible effect on muscle potentials from esophageal or paratendinous hooks, but increased the amplitude of potentials recorded from peripheral hooks and clips. In addition, it was found that small displacements of the esophageal electrode caused substantial changes in the amplitude of the recorded muscle potentials. The integration of the Edi spontaneously generated during occluded inspirations, recorded from paratendinous hooks and the esophageal electrode was linearly related to transdiaphragmatic pressure up to 50 cmH2O at all lung volumes. Above that level, esophageal electrode recordings showed a curvilinear Edi/Pdi relationship, while hook recordings showed a rectilinear relationship.

Using 133Xe measured the regional distribution of FRC and of boluses administered at FRC in seated subjects during relaxation, lateral compression of the lower rib cage, and contraction of the inspiratory muscles so that mouth pressure was 50 cmH2O subatmospheric. Lateral compression increased apex-to-base differences of volume and bolus distribution, suggesting an increase of the apex-to-base gradient of pleural surface pressure. Changes in rib cage shape were measured with magnetometers and were qualitatively similar to those associated with increases in apex-to-base difference of pleural surface pressure in animals. Inspiratory effort decreased apex-to-base difference in volume and induced a similar trend in bolus distribution. Though changes in the rib cage shape were directionally similar, they were much smaller than those associated with decreased pleural surface pressure gradients in animals, and the changes in regional volume we observed were more likely due to forces generated by diaphragmatic contraction. These results were compatible with the apex-to-base gradient of pleural pressure being strongly influenced by shape adaptation between lung and chest wall.

The sections in this article are: 1 Physiological Aspects of Respiratory Muscle Coordination 2 Techniques for Evaluating Respiratory Muscle Activity and Coordination 2.1 Electromyography 2.2 Chest Wall Motion-Pressure Relationships 2.3 Elastic Pressure-Abdominal Pressure Diagram 3 Breathing at Rest 3.1 Ontogenic Aspects of Respiratory Muscle Coordination 3.2 Resting Breathing in the Awake Adult 3.3 Mechanical Analysis 3.4 Electromyographic Activity of Respiratory Muscles During Quiet Breathing 3.5 Intradiaphragmatic Coordination 3.6 Cortical (Volitional) Influences 3.7 Resting Breathing in Supine Position 4 Resting Breathing During Sleep 5 Stimulated Breathing

Sonomicrometry was used to measure end-expiratory length and tidal shortening of the costal and crural diaphragm in awake chronically instrumented dogs in the right lateral decubitus, standing, and sitting postures. End-expiratory length did not change significantly in standing but fell by 11.5% for the costal and by 14.4% for the crural segment in sitting, when compared with decubitus position. Tidal shortening of both segments did not change significantly in the three postures. From decubitus to sitting, diaphragmatic electromyogram (EMG) activity increased only in some dogs, not significantly for the group. The inspiratory swing of abdominal pressure was always positive in decubitus and negative in standing and sitting. In the latter two postures, abdominal pressure increased gradually during expiration and fell in inspiration, suggesting a phasic expiratory contraction of abdominal muscles. We conclude that diaphragmatic tidal shortening is maintained in the different postures assumed by the awake dog during resting breathing. It seems that the main compensatory mechanism for changes in diaphragmatic operational length is a phasic expiratory contraction of the abdominal muscles rather than an increase in diaphragmatic EMG activity.

Respiratory muscle length was measured with sonomicrometry to determine the relation between inspiratory flow and velocity of shortening of the external intercostal and diaphragm. Electromyographic (EMG) activity and tidal shortening of the costal and crural segments of the diaphragm and of the external intercostal were recorded during hyperoxic CO2 rebreathing in 12 anesthetized dogs. We observed a linear increase of EMG activity and peak tidal shortening of costal and crural diaphragm with alveolar CO2 partial pressure. For the external intercostal, no consistent pattern was found either in EMG activity or in tidal shortening. Mean inspiratory flow was linearly related to mean velocity of shortening of costal and crural diaphragm, with no difference between the two segments. Considerable shortening occurred in costal and crural diaphragm during inspiratory efforts against occlusion. We conclude that the relation between mean inspiratory flow and mean velocity of shortening of costal and crural diaphragm is linear and can be altered by an inspiratory load. There does not appear to be a relationship between inspiratory flow and velocity of shortening of external intercostals.

This study examines the hypothesis that respiratory muscle action alters regional pleural pressures. Seven normal volunteers were studied in the seated posture with three esophageal balloons positioned in the upper, middle, and lower esophagus. The intraesophageal pressure swings were recorded during natural breathing, enhanced rib cage, and enhanced diaphragmatic breathing. The pressures were also recorded at three frequencies ranging from 12 to 60 breaths/min. Data were processed with an ensemble average technique that largely removes cardiogenic artifact. During quiet natural breathing, the pressure swings in the lower esophagus were, on the average, 30% larger than the pressure swings in the upper esophagus but became nearly equal as the frequency increased to 60 breaths/min. Rib cage breathing nearly abolished the intraesophageal dynamic pressure differences, whereas abdominal breathing preserved the observed pressure difference even at 60 breaths/min. We concluded that muscle action can affect intrathoracic pressures in a regional way depending on the groups of muscles that are active. These results are discussed in terms of the topographical distribution of ventilation.

The volume and time components of the breathing cycle together with the mouth occlusion pressure P0.1) were measured in 12 patients with chronic diffuse lung fibrosis (DLF) breathing air and in nine normal subjects matched for age and sex. In addition, static lung elastance was measured in all patients. It was found that in DLF the frequency of breathing (f) and P0.1 were positively correlated with lung elastance, whereas tidal volume (VT) decreased significantly with increasing elastance. Minute ventilation and mean inspiratory flow were independent of lung elastance. The VT and f of DLF reported in this paper and those from other published reports were compared with the VT and f of elastically loaded normal subjects. At equivalent levels of elastance, both DLF and loaded normal subjects show qualitatively similar changes. This data suggests that in DLF patients the inspiratory neuromuscular drive is increased as a function of their elastic load, the increase being sufficient to maintain alveolar ventilation within normal limits.

We measured the volume and time components of the breathing cycle together with the P.1 in 16 sarcoidosis and 9 IPF patients. Patients in the IPF group were older, and their lung functions revealed a more restrictive pattern with small TLC, VC, and higher elastance values. We observed that in the two groups of patients there was a significant correlation between VT, f, and P.1 and lung elastance, and that the stiffer IPF patients had higher drive parameters. Hence, the main factor affecting the breathing pattern in both groups is the influence of the elastic load on the control of breathing. A significant relationship was also found between %VD/VT and elastance. We then compared the f values of the 16 sarcoidosis and 9 IPF patients with those of elastically loaded normal subjects. At equivalent levels of elastance, even though the patients and the normals showed qualitatively similar changes, the patients tended to have higher frequencies for the equivalent elastic load. In conclusion, ventilatory and drive parameters in interstitial lung diseases increased as a function of the elastic load, this load being greater in IPF than in sarcoidosis. Inflammation may stimulate the vagal receptors to increase the frequency of breathing, but this requires further study.

Seventeen eucapnic massively obese patients and eight normal subjects had their respiratory cycle parameters studied while breathing room air at rest. Despite large variations in the degree of obesity, our patients demonstrated normal mean inspiratory and expiratory flow rates, duty cycles, and minute ventilation. The maintenance of normal mean inspiratory flow rates was found to be dependent on an augmentation of neuromuscular drive (P0.1); furthermore, a strong positive correlation between percentage ideal body weight (i.e., the degree of obesity) and P0.1 was present. The obese were found to partition their tidal volume preferentially to their rib cage compartment, choosing to leave the abdominal compartment relatively immobile. Analysis of the diaphragmatic electromyogram revealed a persistence of activity into early expiration, the length of which also depended on the degree of obesity. These findings suggest that the diaphragm's volume-generating function in the obese is reduced, and furthermore the persistence of its activity in expiration serves to attenuate the rate of expiratory flow. No significant difference in any respiratory cycle parameter was found between simple obesity patients and formerly hypercapnic obese patients.

Changes in length of costal and crural segments of the canine diaphragm were measured by sonomicrometry within the first 100–300 ms of inspiration during CO2 rebreathing in anesthetized animals. Both segments showed small but significant decreases in end-expiratory length during progressive hypercapnia. Although both costal and crural segments showed electromyographic activity within the first 100 ms of inspiration, in early inspiration crural shortening predominated with minimal costal shortening. Neither segment contracted isometrically early in inspiration in the presence of airway occlusion. The amount of crural shortening during airway occlusion exceeded costal shortening; both segments showed increased shortening with prolonged occlusion and increasing CO2. Costal and crural shortening at 100 ms was not different for unoccluded and occluded states. These observations suggest that neural control patterns evoke discrete and unequal contributions from the diaphragmatic segments at the beginning of an inspiration; the crural segment may be predominately recruited in early inspiration. Despite traditional assumptions about occlusion pressure measurement (P0.1), diaphragm segments do not contract isometrically during early inspiratory effort against an occluded airway.

If sonomicrometry transducers could be implanted permanently into the diaphragm, direct measurements of costal and crural length and shortening could be made during recovery from the laparotomy and then indefinitely in an awake, non-anesthetized mammal. We report results from six canines in which we successfully implanted transducers onto the left hemidiaphragm through a midline laparotomy and measured segmental shortening and ventilation at intervals through 22 days of postoperative recovery. After laparotomy, breathing pattern, including tidal volume, respiratory rate and mean inspiratory flow, stabilized by the 4th postoperative day (POD). Tidal shortening of costal and crural segments increased from 1.82 and 1.45% of end-expiratory length (%LFRC) on the 2nd POD to 5.32 and 8.56% LFRC, respectively, after a mean of 22 POD. Segmental shortening did not stabilize until 10 POD, and the recovery process displayed a sequence of segmental motions: lengthening, biphasic inspiratory lengthening-shortening, and increasing simple shortening. Three weeks after implantation, costal and crural segments were stable and shortening 5.32 and 8.56% LFRC, respectively, and capable of shortening 49% LFRC with maximal phrenic stimulation. In a pair of recovered animals, the initial postoperative dysfunction did not recur after a subsequent, simple laparotomy. At postmortem examination, the chronically implanted sonomicrometer transducers were found to have evoked only a thin fibrotic capsule within the diaphragm.

To assess rib cage muscle fatigue and its relationship to diaphragmatic fatigue, we recorded the electromyogram (EMG) of the parasternal intercostals (PS), sternocleidomastoid (SM), and platysma with fine wire electrodes and the EMG of the diaphragm (DI) with an esophageal electrode. Six normal subjects were studied during inspiratory resistive breathing. Two different breathing patterns were imposed: mainly diaphragmatic or mainly rib cage breathing. The development of fatigue was assessed by analysis of the high-to-low (H/L) ratio of the EMG. To determine the appropriate frequency bands for the PS and SM, we established their EMG power spectrum by Fourier analysis. The mean and SD for the centroid frequency was 312 ± 16 Hz for PS and 244 ± 48 Hz for SM. When breathing with the diaphragmatic patterns, all subjects showed a fall in H/L of the DI and none had a fall in H/L of the PS or SM. During rib cage emphasis, four out of five subjects showed a fall in H/L of the PS and five out of six showed a fall in H/L of the SM. Four subjects showed no fall in H/L of the DI; the other two subjects were unable to inhibit diaphragm activity to a substantial degree and did show a fall in H/L of the DI. Activity of the platysma was minimal or absent during diaphragmatic emphasis but was usually strong during rib cage breathing. We conclude that fatigue of either the diaphragm or the parasternal and sternocleidomastoid can occur independently according to the recruitment pattern of inspiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)