Expiratory and inspiratory action of transversus abdominis during eupnea and hypercapnic ventilation.

BACKGROUND: Recently, there is interest in the clinical importance of monitoring abdominal muscles during respiratory failure. The clinical interpretation relies on the assumption that expiration is a passive physiologic process and, since diaphragm and abdomen are arranged in series, any inward motion of the abdominal wall represents a sign of diaphragm dysfunction. However, previous studies suggest transversus abdominis might be active even during eupnea and is preferentially recruited over the other abdominal muscles. OBJECTIVE: 1) Is transversus abdominis normally recruited during eupnea? 2) What is the degree of activation of transversus abdominis during hypercapnia? 3) Does the end-inspiratory length of transversus abdominis change during hypercapnia, while diaphragm function is normal? METHODS: In 30 spontaneously breathing canines, awake without confounding anesthetic, we measured directly both electrical activity and corresponding mechanical length and shortening of transversus abdominis during eupnea and hypercapnia. RESULTS: Transversus abdominis is consistently recruited during eupnea. During hypercapnia, transversus abdominis recruitment is progressive and significant. Throughout hypercapnia, transversus abdominis baseline end-inspiratory length is not constant: baseline length decreases progressively throughout hypercapnia. After expiration, into early inspiration, transversus abdominis shows a consistent neural mechanical post -expiratory expiratory activity (PEEA) at rest, which progressively increases during hypercapnia. CONCLUSION: Transversus abdominis is an obligatory expiratory muscle, reinforcing the fundamental principle expiration is not a passive process. Beyond expiration, during hypercapnic ventilation, transversus abdominis contributes as an "accessory inspiratory muscle" into the early phase of inspiration. Clinical monitoring of abdominal wall motion during respiratory failure may be confounded by action of transversus abdominis.

Parasternal intercostal, costal, and crural diaphragm neural activation during hypercapnia.

The parasternal intercostal is an obligatory inspiratory muscle working in coordination with the diaphragm, apparently sharing a common pathway of neural response. This similarity has attracted clinical interest, promoting the parasternal as a noninvasive alternative to the diaphragm, to monitor central neural respiratory output. However, this role may be confounded by the distinct and different functions of the costal and crural diaphragm. Given the anatomic location, parasternal activation may significantly impact the chest wall via both mechanical shortening or as a "fixator" for the chest wall. Either mechanical function of the parasternal may also impact differential function of the costal and crural. The objectives of the present study were, during eupnea and hypercapnia, 1) to compare the intensity of neural activation of the parasternal with the costal and crural diaphragm and 2) to examine parasternal recruitment and changes in mechanical action during progressive hypercapnia, including muscle baseline length and shortening. In 30 spontaneously breathing canines, awake without confounding anesthetic, we directly measured the electrical activity of the parasternal, costal, and crural diaphragm, and the corresponding mechanical shortening of the parasternal, during eupnea and hypercapnia. During eupnea and hypercapnia, the parasternal and costal diaphragm share a similar intensity of neural activation, whereas both differ significantly from crural diaphragm activity. The shortening of the parasternal increases significantly with hypercapnia, without a change in baseline end-expiratory length. In conclusion, the parasternal shares an equivalent intensity of neural activation with the costal, but not crural, diaphragm. The parasternal maintains and increases its active inspiratory shortening during augmented ventilation, despite high levels of diaphragm recruitment. Throughout hypercapnic ventilation, the parasternal contributes mechanically; it is not relegated to chest wall fixation.NEW & NOTEWORTHY This investigation directly compares neural activation of the parasternal intercostal muscle with the two distinct segments of the diaphragm, costal and crural, during room air and hypercapnic ventilation. During eupnea and hypercapnia, the parasternal intercostal muscle and costal diaphragm share a similar neural activation, whereas they both differ significantly from the crural diaphragm. The parasternal intercostal muscle maintains and increases active inspiratory mechanical action with shortening during ventilation, even with high levels of diaphragm recruitment.

Limitations of surface EMG estimate of parasternal intercostal to infer neural respiratory drive.

BACKGROUND: Recently, surface EMG of parasternal intercostal muscle has been incorporated in the "ERS Statement of Respiratory Muscle Testing" as a clinical technique to monitor the neural respiratory drive (NRD). However, the anatomy of the parasternal muscle risks confounding EMG "crosstalk" activity from neighboring muscles. OBJECTIVES: To determine if surface "parasternal" EMG: 1) reliably estimates parasternal intercostal EMG activity, 2) is a valid surrogate expressing neural respiratory drive (NRD). METHODS: Fine wire electrodes were implanted into parasternal intercostal muscle in 20 severe COPD patients along with a pair of surface EMG electrodes at the same intercostal level. We recorded both direct fine wire parasternal EMG (EMGPARA) and surface estimated "parasternal" EMG (SurfEMGpara) simultaneously during resting breathing, volitional inspiratory maneuvers, apnoea with extraneous movement of upper extremity, and hypercapnic ventilation. RESULTS: Surface estimated "parasternal" EMG showed spurious "pseudobreathing" activity without any airflow while real parasternal EMG was silent, during apnoea with body extremity movement. Surface estimated "parasternal" EMG did not faithfully represent real measured parasternal EMG. Surface estimated "parasternal" EMG was significantly less active than directly measured parasternal EMG during all conditions including baseline, inspiratory capacity and hypercapnic ventilation. Bland-Altman analysis showed consistent bias between direct parasternal EMG recording and surface estimated EMG during stimulated breathing. CONCLUSION: Surface "parasternal" EMG does not consistently or reliably express EMG activity of parasternal intercostal as recorded directly by implanted fine wires. A chest wall surface estimate of parasternal intercostal EMG may not faithfully express NRD and is of limited utility as a biomarker in clinical applications.

Distinct neural-mechanical efficiency of costal and crural diaphragm during hypercapnia.

Classic physiology suggests that the two distinct diaphragm segments, costal and crural, are functionally different. It is not known if the two diaphragm muscles share a common neural mechanical activation. We hypothesized that costal and crural diaphragm are recruited differently during hypercapnic stimulated ventilation, and the EMG recordings of the esophageal crural diaphragm segment does not translate to the same level of mechanical shortening for costal and crural segments In 30 spontaneously breathing canines, without confounding anesthetic, we measured directly electrical activity and corresponding mechanical shortening of both the costal and crural diaphragm, at room air and during increasing hypercapnia. During hypercapnic ventilation, the costal diaphragm showed a predominant recruitment over the crural diaphragm. The distinct mechanical contribution of the costal segment was not due to a different level of neural activation between the two muscles as measured by segmental EMG activity. Thus, the two diaphragm segments exhibited a significantly different neural-mechanical relationship.

Aminophylline increases parasternal muscle action in awake canines.

The traditional theophylline bronchodilator, aminophylline, is still widely used, especially in the treatment of COPD. The effects of aminophylline on ventilation and action of the costal diaphragm have been previously defined, but other respiratory muscles - notably the chest wall, are not well determined. Therefore, we investigated the effects of aminophylline on the Parasternal intercostal, a key obligatory inspiratory muscle, examining muscle length, shortening and EMG. We studied 11 awake canines, chronically implanted with sonomicrometer crystals and fine-wire EMG electrodes in the parasternal muscle. Ventilatory parameters, muscle length (shortening), and moving average muscle EMG activity, were measured at baseline and with aminophylline, during resting and hypercapnic stimulated breathing. Experiments were carried out prior to administration of aminophylline (baseline), and 1.5 h after loading and ongoing infusion. Minute ventilation, tidal volume and respiratory frequency all increased significantly with aminophylline, both during resting breathing and at equivalent levels of hypercapnic stimulated breathing. Parasternal baseline muscle length was entirely unchanged with aminophylline. Parasternal shortening increased significantly with aminophylline while corresponding parasternal EMG activity remained constant, consistent with increased contractility. Thus, in awake, intact mammals, aminophylline, in the usual therapeutic range, elicits increased ventilation and increased contractility of all primary inspiratory respiratory muscles, including both chest wall and diaphragm.

Costal and crural diaphragm function during sustained hypoxia in awake canines.

In humans and other mammals, isocapnic hypoxia sustained for 20-60 min exhibits a biphasic ventilation pattern: initial increase followed by a significant ventilatory decline ("roll-off") to a lesser intermediate plateau. During sustained hypoxia, the mechanical action and activity of the diaphragm have not been studied; thus we assessed diaphragm function in response to hypoxic breathing. Thirteen spontaneously breathing awake canines were exposed to moderate levels of sustained isocapnic hypoxia lasting 20-25 min (80 ± 2% pulse oximeter oxygen saturation). Breathing pattern and changes in muscle length and electromyogram (EMG) activity of the costal and crural diaphragm were continuously recorded. Mean tidal shortening and EMG activity of the costal and crural diaphragm exhibited an overall biphasic pattern, with initial brisk increase followed by a significant decline (P < 0.01). Although costal and crural shortening did not differ significantly with sustained hypoxia, this equivalence in segmental shortening occurred despite distinct and differing EMG activities of the costal and crural segments. Specifically, initial hypoxia elicited a greater costal EMG activity compared with crural (P < 0.05), whereas sustained hypoxia resulted in a lesser crural EMG decline/attenuation than costal (P < 0.05). We conclude that sustained isocapnic hypoxia elicits a biphasic response in both ventilation and diaphragmatic function and there is clear differential activation and contribution of the two diaphragmatic segments. This different diaphragm segmental action is consistent with greater neural activation of costal diaphragm during initial hypoxia, then preferential sparing of crural activation as hypoxia is sustained. NEW & NOTEWORTHY In humans and other mammals, during isocapnic hypoxia sustained for 20-60 min ventilation exhibits a biphasic pattern: initial increase followed by significant ventilatory decline ("roll-off"). During sustained hypoxia, the function of the diaphragm is unknown. This study demonstrates that the diaphragm reveals a biphasic action during the time-dependent hypoxic "roll-off" in ventilation. These results also highlight that the two diaphragm segments, costal and crural, show differing, distinctive contributions to diaphragm function during sustained hypoxia.