Divergent expiratory braking activity of costal and crural diaphragm.

BACKGROUND: There is increasing clinical interest in understanding the contribution of the diaphragm in early expiration, especially during mechanical ventilation. However, current experimental evidence is limited, so essential activity of the diaphragm during expiration and diaphragm segmental differences in expiratory activity, are unknown. OBJECTIVES: To determine if: 1) the diaphragm is normally active into expiration during spontaneous breathing and hypercapnic ventilation, 2) expiratory diaphragmatic activity is distributed equally among the segments of the diaphragm, costal and crural. METHODS: In 30 spontaneously breathing male and female canines, awake without confounding anesthetic, we measured directly both inspiratory and expiratory electrical activity (EMG), and corresponding mechanical shortening, of costal and crural diaphragm, during room air and hypercapnia. RESULTS: During eupnea, costal and crural diaphragm are active into expiration, showing significant and distinct expiratory activity, with crural expiratory activity greater than costal, for both magnitude and duration. This diaphragm segmental difference diverged further during progressive hypercapnic ventilation: crural expiratory activity progressively increased, while costal expiratory activity disappeared. CONCLUSION: The diaphragm is not passive during expiration. During spontaneous breathing, expiratory activity -"braking"- of the diaphragm is expressed routinely, but is not equally distributed. Crural muscle "braking" is greater than costal muscle in magnitude and duration. With increasing ventilation during hypercapnia, expiratory activity -"braking"- diverges notably. Crural expiratory activity greatly increases, while costal expiratory "braking" decreases in magnitude and duration, and disappears. Thus, diaphragm expiratory "braking" action represents an inherent, physiological function of the diaphragm, distinct for each segment, expressing differing neural activation.

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 function during sustained hypoxia.

Ventilatory response to sustained isocapnic hypoxia in adult humans and other mammals is characterized by a biphasic pattern, with attenuation of neuromotor output to the diaphragm. However, there is no a priori reason that hypoxia-mediated attenuation of respiratory drive would be a common event among other respiratory muscles. At present, little is known about the function of the chest wall muscles during sustained hypoxia. As an obligatory inspiratory muscle with potential to act as a surrogate for neural drive to the relatively inaccessible costal diaphragm, parasternal intercostal has gained interest clinically: its function during a sustained hypoxic insult, as may occur in respiratory failure, warrants investigation. Therefore, in 11 chronically instrumented awake canines, we simultaneously recorded muscle length and shortening and electromyogram (EMG) activity of the parasternal chest wall inspiratory muscle, along with breathing pattern, during moderate levels of sustained isocapnic hypoxia lasting 20-25 min (mean 80 ± 2% oximeter oxygen saturation). Phasic inspiratory shortening and EMG activity of the parasternal intercostal were observed throughout room air and hypoxic ventilation in all animals. Temporal changes in parasternal intercostal shortening tracked the biphasic changes in ventilation during sustained hypoxia. Mean shortening and EMG activity of parasternal intercostal muscle increased significantly with initial hypoxia (P < 0.01) and then markedly declined with constant hypoxia (P < 0.05). We conclude that attenuation of central neural respiratory drive extends to the primary chest wall inspiratory muscle, the parasternal intercostal, during sustained hypoxia, thus directly contributing to biphasic changes in ventilation.NEW & NOTEWORTHY With the potential to act as a surrogate for the generally inaccessible costal diaphragm, parasternal intercostal has gained great interest clinically as a muscle to monitor neural drive and function in respiratory disease. This study demonstrates for the first time the impact of sustained hypoxia on neural activation and mechanical contraction of the parasternal intercostals. Parasternal intercostals reveal a biphasic action during the time-dependent hypoxic response, with a transient increase in shortening and EMG activity with acute hypoxia followed by a progressive decline when hypoxia is sustained.

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.

Genioglossus muscle activity during sniff and reverse sniff in healthy men.

NEW FINDINGS: What is the central question of this study? Maximal sniff nasal inspiratory and reverse sniff nasal expiratory pressures are measured as inspiratory and expiratory muscle strength, respectively. Is the genioglossus muscle activated during short maximal inspiratory and expiratory efforts through the nose? What is the main finding and its importance? Genioglossus muscle activity occurred with inspiratory muscle activity during a maximal sniff and with expiratory muscle activity during a maximal reverse sniff. These results indicate that genioglossus muscle activity is closely related to the generation of maximal sniff nasal inspiratory and reverse sniff nasal expiratory pressures. ABSTRACT: Maximal sniff nasal inspiratory pressure (SNIPmax ) is widely used to assess inspiratory muscle strength. The sniff nasal inspiratory pressure (SNIP) is lower in patients with neuromuscular disease with bulbar involvement compared with those without, possibly owing to impaired upper airway muscle function. However, the degree to which the genioglossus (GG) muscle, one of the upper airway muscles, is activated during inspiratory and expiratory efforts through the nose remains unclear. Therefore, we examined GG activity during short and sharp inspiratory and expiratory efforts through the nose, i.e. sniff and reverse sniff manoeuvres. In eight normal young subjects, we inserted fine wire electrodes into the GG muscle, parasternal intercostal and scalene (inspiratory) muscles and transversus abdominis (expiratory) muscle. We assessed EMG activity of each muscle and measured SNIP and reverse sniff nasal expiratory pressure (RSNEP) during sniffs and reverse sniffs from low to high intensities in the sitting position. The highest SNIP and RSNEP were analysed as SNIPmax and maximal RSNEP (RSNEPmax ), respectively. In each subject, GG EMG activity increased linearly with increasing SNIP and RSNEP. The SNIPmax and RSNEPmax were -85.1 ± 15.9 and 83.2 ± 24.2 cmH2 O, respectively. Genioglossus EMG activity varied with EMG activity of the parasternal intercostal and scalene muscles during generation of SNIPmax and with EMG activity of the transversus abdominis muscle during RSNEPmax . Genioglossus EMG activity during generation of SNIPmax was higher than during RSNEPmax (62.9 ± 31.1% EMG of SNIPmax , P = 0.012). These results suggested that GG activity was closely related to the generation of both SNIPmax and RSNEPmax .

Assessment of sleep quality post-hospital discharge in survivors of critical illness.

BACKGROUND: Sleep quality is impaired during critical illness and may remain abnormal after discharge from hospital. Sleep dysfunction in patients after critical illness may impair recovery and health related quality of life. The purpose of this study was to use objective and subjective measures to evaluate sleep quality in critical illness survivors 3 months after hospital discharge. METHODS: This was a prospective cohort study of 55 patients admitted to a multidisciplinary intensive care unit (ICU) between April 1st, 2009 and March 31, 2010. Patients enrolled were over 17 years of age and stayed a minimum of 4 days in the ICU. Patients were assessed in an outpatient clinic 3-months after hospital discharge. Sleep quality was measured using multi-night sleep actigraphy and the Pittsburgh Sleep Quality Index (PSQI). RESULTS: A total of 62% of patients had poor sleep quality measured with the PSQI. The average (SD) sleep time, sleep efficiency and number of sleep disruptions per night was 6.15 h (3.4), 78% (18), and 11 disruptions (5) respectively. The APACHE II score was correlated with total sleep time (ß = -12.6, P = 0.019) and sleep efficiency (ß = -1.18, P = 0.042). The PSQI score was associated with anxiety (ß = 4.00, p = 0.001), reduced mobility (ß = 3.39, p = 0.002) and EuroQol-5D visual analogue scale score (ß = -0.85, p = 0.003) and low Physical Composite Scores (ß = -0.13, p = 0.004) and Mental Composite Scores (ß = -0.15, p = 0.002) of the Short-Form 36 survey. CONCLUSIONS: Reduced sleep quality following critical illness is common and associated with reduced health related quality of life. Critical illness severity is a predictor of reduced sleep duration and sleep disruption 3 months after hospital discharge. This cohort study highlights the important role sleep may contribute to the long-term recovery from critical illness.

Parasternal intercostal and diaphragm function during sleep.

Action of the uppermost medial internal intercostal muscles-the parasternals-during rapid eye movement (REM) is uncertain; no direct recordings exist of shortening of these muscles during sleep. Historically, motor inhibition of skeletal muscles during REM sleep is thought to cause global loss of chest wall muscle function, REM "atonia," with preservation of only diaphragm function. However, recent evidence during wakefulness shows parasternals as distinctive obligatory inspiratory muscles. Therefore we hypothesized that attenuation of chest wall function during sleep may spare the parasternals along with the diaphragm, as essential muscles of inspiration during REM. We studied seven canines, comparing costal and crural diaphragm and parasternal intercostal muscle function during wakefulness and non-REM (NREM) and REM sleep, during normal spontaneous sleep, continuously recording ventilation and simultaneous muscle electromyogram (EMG) and length from sonomicrometry microtransducers. Ventilation during sleep declined significantly from wakefulness. From wakefulness to NREM and REM, costal and crural tidal EMG increased, while parasternal tidal EMG was preserved unchanged. Costal and crural shortening per breath during NREM and REM did not change significantly from wakefulness. Concurrently, parasternal shortening decreased equally in both NREM and REM despite preservation of the parasternal EMG. We conclude that diaphragm and parasternals are not inhibited, and both remain active together as essential inspiratory muscles, during REM sleep. The lesser contraction of parasternal intercostals compared with diaphragm may be attributed to net changes in mechanics affecting the chest wall during sleep.

Ventilation and diaphragm activity during sustained hypoxia in awake canines.

In humans, isocapnic hypoxia sustained for 20-30 min elicits a biphasic ventilatory response with an initial increased peak followed by a roll-off to a lesser, intermediate plateau. However, it is uncertain if this hypoxic roll-off is common for all mammals, as canines have been a notable exception. We examined the effect of moderate isocapnic hypoxia (SpO2 80%) sustained for 20 min in 13 adult, awake, intact canines. The ventilatory response to sustained isocapnic hypoxia in these canines was not maintained: after an initial brisk response, ventilation declined significantly to an intermediate plateau. The hypoxic ventilatory decline occurred via a decrease in tidal volume, without change in breathing frequency. Distinct from airflow, costal diaphragm EMG showed a concurrent decline during sustained isocapnic hypoxia. However, the change in ventilation during sustained hypoxia in canines was very different from the response in humans. Although some decline in ventilation during sustained hypoxia may be common to all mammals, there are notable differences among species.

Aminophylline increases respiratory muscle activity during hypercapnia in humans.

BACKGROUND: Theophylline is an old drug traditionally used as a bronchodilator, although it was recently shown to possess anti-inflammatory properties, enhance the actions of corticosteroid actions, and stimulate the respiratory neuronal network. Theophylline has been recognized as an important drug for not only asthma but also corticosteroid-insensitive chronic obstructive pulmonary disease (COPD). To clarify the role of theophylline in hypercapnic ventilatory responses in humans, we analyzed the effects of aminophylline administered at the usual clinical therapeutic doses on ventilation and augmentation of respiratory muscle contractility in room air and under 3 conditions of hypercapnia. STUDY DESIGN: We performed electromyography (EMG) of the parasternal intercostal muscle (PARA) and transversus abdominis muscle (TA) in 7 healthy subjects and recorded both ventilatory parameters and EMG data in room air and under 3 conditions of hypercapnia before (control) and during aminophylline administration. RESULTS: Before aminophylline administration (control), hypercapnic stimulation elicited ventilatory augmentation in a hypercapnia intensity-dependent manner. Ventilatory parameters (tidal volume, frequency of respiration, and minute ventilation) showed significant increases from lower PaCO2 levels during aminophylline administration when compared with the corresponding values before aminophylline administration. EMG activity of both PARA and TA increased significantly at each level of hypercapnia, and those augmentations were shown from lower PaCO2 levels during aminophylline administration. CONCLUSION: Aminophylline administered at the usual clinical therapeutic dose increases ventilation and EMG activity of both inspiratory and expiratory muscles during hypercapnia in healthy humans.

Parasternal muscle activity decreases in severe COPD with salmeterol-fluticasone propionate.

BACKGROUND: The effect of the long acting beta(2)-agonist/corticosteroid combination salmeterol-fluticasone propionate (SFC) on respiratory muscles and ventilation in severe COPD is unknown. As COPD hyperinflation worsens, diaphragm efficiency decreases, and a compensatory increase in chest wall inspiratory muscle activity occurs. If a bronchodilator successfully alleviates hyperinflation and improves diaphragm efficiency in severe COPD, then the extraordinary activation of the chest wall may be relieved. We examined directly the effect on the parasternal intercostal respiratory chest wall muscle and ventilation of four puffs of salmeterol 25 microg and fluticasone propionate 125 microg via the metered dose combination inhaler in 12 patients with severe Global Initiative on Obstructive Lung Disease stage III-IV COPD, mean FEV(1) = 0.91 L (32% predicted). METHODS: We measured parasternal intercostal electromyogram (EMG) recorded from implanted fine-wire electrodes, ventilation, and breathing pattern, during resting and CO(2)-stimulated breathing. Full pulmonary function tests were recorded at the beginning and end of the study. RESULTS: In this patient group, severe airflow obstruction and hyperinflation were poorly reversible after SFC: FEV(1) increased 4.2%, functional residual capacity decreased 1.4%, and inspiratory capacity increased 5.9%. However, with SFC there was a significant increase in minute ventilation, tidal volume, and mean inspiratory flow. There was a very large decrease in directly recorded parasternal EMG, with parasternal EMG disappearing completely in some patients after SFC. CONCLUSIONS: In severe COPD, with minimal change in hyperinflation or pulmonary mechanics, salmeterol-fluticasone induced a significant decrease in activity of the chest wall parasternal inspiratory muscle. This may be of practical benefit to reverse the extensive use of the chest wall muscles and alleviate dyspnea in severe COPD.

Respiratory muscle electromyogram and mouth pressure during isometric contraction.

When extra-diaphragmatic muscles are activated progressively under approximately isometric conditions, we expect a corresponding increase in respiratory muscle output. Therefore, we examined relative recruitment shown as the latency to onset of EMG activity, and the relationship between mouth pressure and electromyogram activity of the neck accessory and transversus abdominis (TRANS) muscles during respiratory maneuvers against occlusion. Fine wire electrodes were inserted into the scalene (SCLN), sternocleidomastoid (STERNO), trapezius (TRAPZ) and TRANS in six awake, healthy subjects. Mouth pressure, raw and moving average EMG signals were recorded during gradual production of expiratory or inspiratory mouth pressure to maximum (MPmax) at FRC in the standing posture. Group mean linear regression lines of EMG activity versus mouth pressure were strongly significant for SCLN and TRANS, less for STERNO, and least for TRAPZ. The SCLN and STERNO showed EMG activities with low, and TRAPZ showed EMG activity only with high, mouth pressure. At 90% MPmax, TRAPZ was much less active compared with TRANS, SCLN, or STERNO. These results suggest that over a wide range of respiratory effort there is a significant difference in the relationship between mouth pressure and EMG activity in the accessory muscles, with differential recruitment of individual respiratory muscles.