Inspiratory Muscle Activity Research Articles

Assessing The Influence Of Work Of Breathing On Sex-differences In Inspiratory Muscle Activation During Exercise

Assessing The Influence Of Work Of Breathing On Sex-differences In Inspiratory Muscle Activation During Exercise

Influence of an inspiratory muscle fatigue protocol on healthy youths on respiratory muscle strength, vertical jump performance and muscle oxygen saturation: a randomized controlled trial

BackgroundInspiratory muscle fatigue has been shown to have effects on limbs blood flow and physical performance. This study aimed to evaluate the influence of an inspiratory muscle fatigue protocol on respiratory muscle strength, vertical jump performance and muscle oxygen saturation in healthy youths.MethodsA randomized and double-blinded controlled clinical trial, was conducted. Twenty-four participants aged 18–45 years, non-smokers and engaged in sports activity at least three times a week for a minimum of one year were enrolled in this investigation. Participants were randomly assigned to three groups: Inspiratory Muscle Fatigue (IMFG), Activation, and Control. Measurements of vertical jump, diaphragmatic ultrasound, muscle oxygen saturation, and maximum inspiratory pressure were taken at two stages: before the intervention (T1) and immediately after treatment (T2).ResultsThe IMFG showed lower scores in muscle oxygen saturation and cardiorespiratory variables after undergoing the diaphragmatic fatigue intervention compared to the activation and control groups (p < 0.05). For the vertical jump variables, intragroup differences were found (p < 0.01), but no differences were shown between the three groups (p > 0.05).ConclusionsInspiratory muscle fatigue appears to negatively impact vertical jump performance, muscle oxygen saturation and inspiratory muscle strength in healthy youths.Trial registrationClinicalTrials.gov ID: NCT06271876. Date of registration 02/21/2024. https://clinicaltrials.gov/study/NCT06271876.

Clinical correlates of respiratory disorders in patients with severe multiple sclerosis: A cross-sectional cohort

Background: Respiratory disorders remain incompletely described in multiple sclerosis (MS), even though they are a frequent cause of death. Methods: The objective was to describe respiratory disorders in MS patients with Expanded Disability Status Score (EDSS) ⩾ 6.5. Diaphragm dysfunction was defined by at least two of the seven criteria: clinical signs, inspiratory recruitment of neck muscles during wakefulness, reduced upright vital capacity (VC) < 80%, upright-to-supine VC ⩾ 15% of upright VC, decrease in Maximal Inspiratory Pressure < 60%, phasic activation of inspiratory neck muscles during sleep, and opposition of thoracic and abdominal movements during sleep. Cough weakness was defined by a peak cough flow < 270 L/min and/or need for cough assist. Sleep apnea syndrome was defined by an apnea–hypopnea index ⩾ 15. Results: Notably, 71 MS patients were included: median age 54 [48, 61] years; median disease duration 21.4 [16.0, 31.4] years. Of these, 52 patients had one or more respiratory disorders; diaphragm dysfunction was the most frequent (n = 34). Patients with diaphragm dysfunction and cough weakness were more disabled. The fatigue score and the cognitive evaluations did not differ between the groups. Five patients required non-invasive ventilation. Conclusion: Respiratory disorders are frequent in severe MS, mostly diaphragm dysfunction. Of interest, instrumental interventions are available to address these disorders.

Influence of an inspiratory muscle fatigue protocol on healthy youths on respiratory muscle strength and heart rate variability. A randomized controlled trial.

Introduction: Inspiratory muscle fatigue has been shown to have effects on the autonomic nervous system and physical condition. This study aimed to evaluate the influence of an inspiratory muscle fatigue protocol on respiratory muscle strength and heart rate variability in healthy youths. Materials and Methods: A randomized controlled clinical trial, employing double-blinding, was conducted with twenty-seven participants aged 18-45years, non-smokers and engaged in sports activity at least three times a week for a minimum of 1year. Participants were randomly assigned to three groups: Inspiratory Muscle Fatigue group, Activation group, and Control group. Measurements of heart rate variability, diaphragmatic ultrasound, and maximum inspiratory pressure were taken at two stages: before the intervention and immediately after treatment. Results: In our results with respect to baseline to post-treatment, the inspiratory muscle fatigue group showed lower values in the Sniff contraction velocity variable (10.96cm/s ± 1.99-8.34cm/s ± 1.23; p < 0.01) and higher values in the activation group (10.59cm/s ± 0.89-12.66cm/s ± 1.15; p < 0.01) with respect to the control group (10.27cm/s ± 1.48-9.97cm/s ± 1.42). On the other hand, the inspiratory muscle fatigue group showed higher values in the Low frequency variable (49.37 n.u. ± 13.91 to 69.48 n.u. ± 8.22; p < 0.01) and lower values in the activation group (57.92 n.u. ± 8.37 to 41.59 n.u. ± 11.21; p < 0.01) with respect to the control group (50.83 n.u. ± 17.30 to 52.10 n.u. ± 20.64). Additionally, significant correlations were found between respiratory variables and heart rate variability variables. Conclusion: Acute fatigue of the inspiratory musculature appears to negatively impact heart rate variability and inspiratory muscle strength in healthy youths. Clinical Trial Registration: https://clinicaltrials.gov/study/NCT06278714; Identifier: NCT06278714.

Effects of high-intensity inspiratory muscle warm-up on inspiratory muscle strength and accessory inspiratory muscle activity

This study aimed to determine the effects of work-matched moderate-intensity and high-intensity inspiratory muscle warm-up (IMW) on inspiratory muscle strength and accessory inspiratory muscle activity. Eleven healthy men performed three IMWs at different intensities, namely, placebo, moderate-intensity, and high-intensity, set, respectively, at 15 %, 40 %, and 80 % of maximal inspiratory mouth pressure (MIP). MIP was measured before and after IMW. Electromyography (EMG) was recorded for the sternocleidomastoid muscle (SCM) and intercostal muscles (IC) during IMW. MIP increased significantly in the moderate-intensity condition (104.2 ± 5.1 %, p < 0.05) and high-intensity condition (106.5 ± 6.2 %, p < 0.01) after IMW. The EMG amplitudes of the SCM and IC during IMW were significantly higher in the order of high-intensity, moderate-intensity, and placebo conditions. There was a significant correlation between changes in MIP and EMG amplitude of the SCM (r = 0.60, p < 0.01) and IC (r = 0.47, p < 0.01) during IMW. These findings suggest that high-intensity IMW increases neuromuscular activity in the accessory inspiratory muscles, which may improve inspiratory muscle strength.

Fentanyl induced disruption of the coordinated reciprocal activity of inspiratory and expiratory respiratory muscles

Opioid induced respiratory depression (OIRD) occurs when respiratory pump and/or airway muscle activity are reduced ostensibly due to reduced output from the brainstem respiratory control system, resulting in central (CA) and/or obstructive apnea (OA) and reduced breathing frequency. Although less commonly reported in the literature, ORID may also result from an inappropriate activation of accessory muscles leading to the “Wooden Chest Syndrome” (WCS) -when airflow is limited due to simultaneous activation of inspiratory and expiratory pump and/or airway respiratory muscles to decrease chest wall compliance and inappropriately increase airway resistance. This phenomenon is difficult to directly study in humans, but here we present data from our large animal model (adult female goats). We tested the hypothesis that IV fentanyl would lead to transient dysfunction in respiratory accessory muscles indicative of WCS. We surgically instrumented goats (n=7) with electromyographic (EMG) wires in inspiratory (diaphragm; DIA) and expiratory (Transversus Abdominus; TA) pump muscles, as well as airway dilator (Thyropharyngeus; Thy) and constrictor (Genioglossus; GG) muscles. After &gt;2 weeks of surgical recovery, responses to saline or various doses of fentanyl citrate (25-125 mcg/kg; IV) were tested for 30 min before and up to 90 min after injection. As described in an adjacent poster, particularly over the first several minutes after fentanyl injection, CA and OA were observed in some goats. However, disruption of airflow was primarily associated with increased simultaneous activation of pump and airway inspiratory and expiratory muscles resembling WCS. For most muscles, the rate of rise in muscle activity (an index of firing intensity) increased within 2 minutes following fentanyl injection and remained significantly (P&lt;0.05) elevated up to 90 minutes. During WCS periods, airflow was oscillatory or interrupted suggesting transient closure of the airway. In addition, there were time- and dose-dependent effects on frequency, duration, and total activity of the pump and airway muscles. By 60 minutes post-injection, there were periods of transient return of muscle activity and airflow to at or below baseline values. There was no significant effect of saline on muscle activity. Overall, these data suggest that following fentanyl injection in awake goats, there was an increase in firing of pump and airway muscles which ultimately disrupts the coordinated reciprocal activity of inspiratory and expiratory muscles and contributes to OIRD. Supported by NIH DA050571 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Effects of Stimulus Pattern on Inspiratory Muscle Activation during High Frequency Spinal Cord Stimulation in an Animal Model

Background: High Frequency Spinal Cord Stimulation (HF-SCS) is a unique method of inspiratory muscle activation and has the potential to restore breathing in ventilator dependent tetraplegic subjects. Objective: To evaluate the pattern of diaphragm (D), parasternal (PA) and external intercostal (EI) activation during rectangular vs ramp-shape HF-SCS, compared to spontaneous breathing. Methods: In 8 anesthetized dogs, a stimulating disc electrode was positioned on the ventral surface of the spinal cord at the T2 level. Stimulus train duration for ramp-shape and rectangular HF-SCS was set at 1.3s since this duration approximated that occurring during spontaneous breathing. Stimulus amplitude during HF-SCS was adjusted such that inspired volumes approximated that occurring during SB. The ramp-shape pattern of stimulation was linearly increased from zero to the desired stimulus amplitude. Single motor unit (SMU) EMG activity of the PA, EI and D muscles was assessed during SB and HF-SCS (following spinalization at the C2 level) with rectangular and ramp-shape stimulation patterns, in separate trials. Time of onset (To), b) time to peak discharge frequency (TTP) and c) peak firing frequency (PFF) were measured under each condition. To and TTP were determined relative to the onset of inspiratory flow and expressed as a percentage of inspiratory time (Ti). The patterns of the inspiratory muscle activation during HF-SCS were compared to that obtained during spontaneous breathing. Results: During SB, D was recruited first followed by PA and EI; mean ± SE To was 19.6±1.4, 32.1±2.4 and 40.4±2.3%Ti, respectively. During rectangular HF-SCS, To was 3.0±0.4, 5.8±1.2 and 4.3±0.9%Ti for D, PA and EI, respectively (p&lt;0.05 for each compared to SB). During ramp-shape HF-SCS, To was 23.1±3.7, 33.6±4.5 and 39.9±4.6%Ti for D, PA and EI respectively (NS for each compared to SB). During SB, TTP was 65.2±2.2, 71.0±2.0 and 74.0±2.0%Ti for D, PA and EI. During rectangular HF-SCS, TTP was 30.4±3.7, 25.4±3.3 and 35.2±2.8%Ti, for D, PA and EI (p&lt;0.05 for each compared to SB). During ramp-shape HF-SCS, TTP was 60.5±2.9, 58.2±2.7 and 62.6±6.0%Ti for Dia, PA and EI (p&lt;0.05 for PA and EI compared to SB). During SB, PFF of SMUs of the D, PA and EI were 10.3±0.5, 12.8±0.4 and 12.2±0.7Hz, respectively. However, during rectangular HF-SCS, PFF were 14.0±0.6, 14.7±0.7 and 14.5±0.5Hz for D, PA and EI, respectively (p&lt;0.05 for each compared to SB). During ramp-shape HF-SCS, PFF were 12.3±0.8, 13.8±0.9 and 12.6±1.2 for D, PA and EI, respectively (NS for each compared to SB). Conclusion: Activation of the inspiratory motoneuron pools via HF-SCS is receptive to different patterns of electrical stimulation.Ramp-shape HF-SCS compared to rectangular HF-SCS results in a more physiologic pattern of inspiratory muscle activation. National Institutes of Health grant no. R01 NS105785. Conflict of interest: Dr. A. DiMarco is a founder of and has a significant financial interest in Synapse BioMedical, a manufacturer of diaphragm pacing systems (nos. 5,678,535 and 5,911,218). Dr. A. DiMarco and Dr. K. Kowalski hold the U.S. patents for technology related to the content of this study, Respiratory Muscle Activation by Spinal Cord Stimulation (no. 8,352,036). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Neuromuscular coupling of obligatory respiratory muscles to inspiratory pressure is reduced in dystrophic (mdx) mice

Neuromuscular coupling (NMC) is a recognised clinical index of inspiratory muscle function which reflects the efficiency of conversion of neural activation to inspiratory pressure. Duchenne muscular dystrophy (DMD) is characterised by respiratory insufficiency culminating in respiratory failure. We investigated inspiratory pressure generating capacity and electrical activation of obligatory inspiratory muscles in X-linked muscular dystrophy ( mdx) mice, to evaluate NMC of diaphragm, external intercostal and parasternal intercostal to inspiratory pressure across a range of behaviours in early established to late progressive disease.In urethane anaesthetised mice (1.7 g/kg i.p.), inspiratory pressure was recorded via a pressure transducer positioned in the thoracic oesophagus. Diaphragm EMG activity was recorded using needle electrodes. Studies were performed in male wildtype (WT) and mdx mice at 4, 8, 12 and 16 months old. Recordings were made at baseline and during sustained tracheal occlusion to task failure, defined as an inability to sustain peak pressure. Peak pressure was determined from the average of five successive peak efforts at the maximum response. The corresponding peak inspiratory EMG activities were determined. Two factor (age x genotype) analysis of variance was performed.Obligatory muscle EMG activities were significantly lower in mdx mice from 4 months of age. Peak inspiratory pressure was significantly greater in mdx at 4 months of age. At 8 months, peak inspiratory pressure was equivalent between WT and mdx followed by a significant decrease in peak inspiratory pressure in 12- and 16-month-old mdx. NMC was lower in mdx mice across the ventilatory and non-ventilatory range, emerging early in dystrophic disease.Reduced NMC of obligatory muscles to inspiratory pressure in mdx mice reveals a greater reliance on accessory muscles to support respiratory performance in dystrophic disease. Remarkably, this burden is adequately accommodated in early disease with a preserved capacity to generate peak inspiratory pressure. We reason that the loss of compensation afforded by accessory muscles to peak inspiratory pressure generation underpins the emergence of respiratory compromise in advanced disease. Our results may have implications for the understanding and treatment of DMD. Funded by Science Foundation Ireland SFI/19/6628 INSPIRE DMD. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Effect of Inspiratory Muscle Training Combined with Trunk Stabilization Exercise on Inspiratory Muscle Activity and Pulmonary Function

Effect of Inspiratory Muscle Training Combined with Trunk Stabilization Exercise on Inspiratory Muscle Activity and Pulmonary Function

Phrenic-to-intercostal reflex activity in response to high frequency spinal cord stimulation (HF-SCS)

ObjectiveHF-SCS is a novel technique of inspiratory muscle activation which results in coincident activation of the diaphragm and inspiratory intercostal muscles via spinal cord pathways and has the potential to provide respiratory support in ventilator dependent persons with spinal cord injury. The purpose of the present study was to examine the phrenic-to-intercostal reflex during HF-SCS. MethodsIn 5 anesthetized and C2 spinalized dogs, electrical stimulation was applied via a stimulating electrode located on the ventral surface of the upper thoracic spinal cord at the T2 level. Fine wire recording electrodes were used to assess single motor unit (SMU) activity of the left and right external intercostal muscles (EI) in the 3rd interspace before and after sequential left and right phrenicotomy. ResultsMean control peak firing frequency of the right EI and left EI was 11.4 ± 0.3 Hz and 10.6 ± 0.3 Hz respectively. Following unilateral right phrenic nerve section, mean SMU peak firing frequency of right EI (ipsilateral to the section) was significantly greater when compared to control (15.9 ± 0.5 Hz vs 11.4 ± 0.3 Hz; p = 0.01). Mean SMU peak firing frequency of the contralateral left EI remained unchanged (10.2 ± 0.3 Hz vs 10.6 ± 0.3 Hz, p = 0.40). Subsequent, section of the left phrenic nerve resulted in significantly higher mean SMU peak firing frequency of the left EI (16.2 ± 0.5 Hz vs 10.2 ± 0.3 Hz) when compared to before section p = 0.01). Contralateral, right EI peak firing frequency was not different if compared to before left phrenic nerve section (16.9 ± 0.4 Hz vs. 15.9 ± 0.5 Hz; p = 0.14). ConclusionThis study demonstrates that during HF-SCS: 1) unilateral diaphragmatic afferents reflexly inhibit motor activity to the ipsilateral EI muscles, 2) the neural circuitry mediating the phrenic-to-intercostal reflex is preserved at a spinal level and does not require supraspinal input and 3) unilateral compensatory increases were observed in EI muscle activation following ipsilateral diaphragm paralysis.

Deglutition and the Regulation of the Swallow Motor Pattern.

Despite centuries of investigation, questions and controversies remain regarding the fundamental genesis and motor pattern of swallow. Two significant topics include inspiratory muscle activity during swallow (Schluckatmung, i.e., "swallow-breath") and anatomical boundaries of the swallow pattern generator. We discuss the long history of reports regarding the presence or absence of Schluckatmung and the possible advantages of and neural basis for such activity, leading to current theories and novel experimental directions.

Model-Based Optimization of Spinal Cord Stimulation for Inspiratory Muscle Activation

ObjectiveHigh-frequency spinal cord stimulation (HF-SCS) is a potential method to provide natural and effective inspiratory muscle pacing in patients with ventilator-dependent spinal cord injuries. Experimental data have demonstrated that HF-SCS elicits physiological activation of the diaphragm and inspiratory intercostal muscles via spinal cord pathways. However, the activation thresholds, extent of activation, and optimal electrode configurations (i.e., lead separation, contact spacing, and contact length) to activate these neural elements remain unknown. Therefore, the goal of this study was to use a computational modeling approach to investigate the direct effects of HF-SCS on the spinal cord and to optimize electrode design and stimulation parameters. Materials and MethodsWe developed a computer model of HF-SCS that consisted of two main components: 1) finite element models of the electric field generated during HF-SCS, and 2) multicompartment cable models of axons and motoneurons within the spinal cord. We systematically evaluated the neural recruitment during HF-SCS for several unique electrode designs and stimulation configurations to optimize activation of these neural elements. We then evaluated our predictions by testing two of these lead designs with in vivo canine experiments. ResultsOur model results suggested that within physiological stimulation amplitudes, HF-SCS activates both axons in the ventrolateral funiculi (VLF) and inspiratory intercostal motoneurons. We used our model to predict a lead design to maximize HF-SCS activation of these neural targets. We evaluated this lead design via in vivo experiments, and our computational model predictions demonstrated excellent agreement with our experimental testing. ConclusionsOur computational modeling and experimental results support the potential advantages of a lead design with longer contacts and larger edge-to-edge contact spacing to maximize inspiratory muscle activation during HF-SCS at the T2 spinal level. While these results need to be further validated in future studies, we believe that the results of this study will help improve the efficacy of HF-SCS technologies for inspiratory muscle pacing.

Dyspnea and the electromyographic activity of inspiratory muscles during weaning from mechanical ventilation

RationaleDyspnea, a key symptom of acute respiratory failure, is not among the criteria for spontaneous breathing trial (SBT) failure. Here, we sought (1) to determine whether dyspnea is a reliable failure criterion for SBT failure; (2) to quantify the relationship between dyspnea and the respective electromyographic activity of the diaphragm (EMGdi), the parasternal (EMGpa) and the Alae nasi (EMGan).MethodsMechanically ventilated patients undergoing an SBT were included. Dyspnea intensity was measured by the Dyspnea-Visual Analogic Scale (Dyspnea-VAS) at the initiation and end of the SBT. During the 30-min SBT or until SBT failure, the EMGdi was continuously measured with a multi-electrode nasogastric catheter and the EMGan and EMGpa with surface electrodes.ResultsThirty-one patients were included, SAPS 2 (median [interquartile range]) 53 (37‒74), mechanically ventilated for 6 (3‒10) days. Seventeen patients (45%) failed the SBT. The increase in Dyspnea-VAS along the SBT was higher in patients who failed (6 [4‒8] cm) than in those who passed (0 [0‒1] cm, p = 0.01). The area under the receiver operating characteristics curve for Dyspnea-VAS was 0.909 (0.786–1.032). The increase in Dyspnea-VAS was significantly correlated to the increase in EMGan (Rho = 0.42 [0.04‒0.70], p < 0.05), but not to the increase in EMGpa (Rho = − 0.121 [− 0.495 to − 0.290], p = 0.555) and EMGdi (Rho = − 0.26 [− 0.68 to 0.28], p = 0.289).ConclusionDyspnea is a reliable criterion of SBT failure, suggesting that Dyspnea-VAS could be used as a monitoring tool of the SBT. In addition, dyspnea seems to be more closely related to the electromyographic activity of the Alae nasi than of the diaphragm.

0807 Sleep-related hiccups: A case report of antidepressant associated hypnic jerks

Abstract Introduction A hiccup is a sudden activation of inspiratory muscles, followed by paradoxical glottic closure, producing a familiar sound [1]. Antidepressants are commonly prescribed and hypnic jerks and hiccups have been reported as a rare adverse drug reaction [2]. Few reports have described pronounced hypnic hiccups with subsequent audio/video polysomnogram confirmation. Report of Cases: A 44-year old man with a history of depression, anxiety, and alcohol use disorder presented to clinic with a long history of violent hypnic jerks associated with a loud hiccup. These episodes started 30 minutes before he fell asleep and continued throughout the night every 30 minutes with forceful hiccups that were so loud they wake others in his house. We believe that these episodes were likely induced by venlafaxine since they were noted initially 8 years ago when he started taking venlafaxine and there was complete remission after discontinuation of the medication. He was later prescribed escitalopram 20 mg daily, restarted on venlafaxine XR 150 mg daily, and later sertraline 100 mg daily due to refractory depression and anxiety recurrence. Episodes progressively became more frequent and pronounced that he avoided sleep and they impacted his ability to hold a relationship. Gabapentin and clonazepam did not previously improve symptoms. He took trazodone 50 mg every other night to aid falling asleep and reported to have less frequent hypnic jerks. Upon presentation to our clinic, subsequent PSG demonstrated severe obstructive sleep apnea (AHI 63, HI 52, CI 11) with significant sleep fragmentation (sleep efficiency 46%) with very frequent sudden axial myoclonic contractions with head and neck movements along with vocalizations likely representing hiccups. Video and audio demonstrated the loud hiccups described. These events occurred while the patient was resting awake and transitioning to sleep and was less frequent but persisted in N2. The patient was prescribed CPAP for sleep apnea and recommended to follow up with psychiatry to consider other medications. Conclusion Pronounced hypnic jerks and sleep-related hiccups can significantly impact total sleep time, sleep quality, and quality of life. Clinicians should be aware of these potential side effects in patients on antidepressants. Support (If Any) 1. Askenasy JJ. About the mechanism of hiccup. Eur Neurol. 1992;32:159-63.2. Bagheri H, Cismondo S, Montastruc JL. Hoquet d'origine médicamenteuse: enquête à partir de la Banque Nationale de Pharmacovigilance [Drug-induced hiccup: a review of the France pharmacologic vigilance database]. Therapie. 1999 Jan-Feb;54(1):35-9. French. PMID: 10216420.

0832 Nocturnal Tachypnea with Non-Invasive Ventilation; A case report

Abstract Introduction We present a case of nocturnal tachypnea secondary to suspected auto-triggering in a patient on Bilevel device. Auto-triggering is a patient-ventilator asynchrony in which a ventilator breath is triggered in the absence of inspiratory muscle activity. This phenomenon was mostly described in postcardiac surgery and in brain dead patients on mechanical ventilation. Detecting this asynchrony is important as it can lead to patient discomfort, poor compliance and hypocarbia that can lead to apneic events. Report of Cases: An 82-year-old male with history of chronic atrial fibrillation, coronary artery disease (s/p bypass surgery) and Ischemic cardiomyopathy (EF 25-30%). He had moderate obstructive sleep apnea with central apnea. He was started on AutoPAP then was upgraded to BPAP (IPAP 16/EPAP 9 cmH2O). His wife reported episodes of nocturnal tachypnea and increased daytime somnolence. This was confirmed by the compliance reports from his BPAP device, and a portable sleep study obtained while using the BPAP (respiratory rate &amp;gt; 40 breaths/minute). Conclusion Vignaux et al estimated the incidence of auto-triggering with NIV to be 13%. This phenomenon can be caused by a major circuit leak or secondary to cardiogenic oscillations. Effect of cardiogenic oscillation on the pulmonary air flow was described by West and Hugh-Jones in 1961. Our patient had dilated cardiomyopathy with hyperdynamic circulation which we believe was the major cause of his auto-triggering asynchrony. Changes in intracardiac volume and cardiac movements during systole resulted in intrapulmonary flow oscillations exceeding the set flow-trigger threshold leading to the tachypnea. In our patient, the events resolved after cardiac resynchronization procedure that improved the overall cardiac function and adjusting the trigger sensitivity. Support (If Any) [1]Kondili E, Prinianakis G, Georgopoulos D.; Patient ventilator interaction, Br J Anaesth. 2003; 91: 106-119 [2] Richard Arbour; Cardiogenic Oscillation and Ventilator Autotriggering in Brain-Dead Patients: A Case Series. Am J Crit Care 1 September 2009; 18 (5): 496–488. doi: https://doi.org/10.4037/ajcc2009690 [3] Imanaka, Hideaki MD; Nishimura, Masaji MD; Takeuchi, Muneyuki MD; Kimball, William R. MD, PhD; Yahagi, Naoki MD; Kumon, Keiji MD Auto-triggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation, Critical Care Medicine: February 2000 - Volume 28 - Issue 2 - p 402-407 [4]Vignaux L, Vargas F, Roeseler J, Tassaux D, Thille AW, Kossowsky MP, et al. Patient-ventilator asynchrony during non-invasive ventilation for acute respiratory failure: a multicenter study. Intensive Care Med 2009;35(5):840–846

Evaluation of Loaded Breathing on Inspiratory Intercostal Muscle Activation During High Frequency Spinal Cord Stimulation to Restore Breathing in Spinal Cord Injury – Animal Model

BackgroundHigh Frequency Spinal Cord Stimulation (HF‐SCS) is a unique method of inspiratory muscle activation and has the potential to restore breathing in ventilator dependent tetraplegic subjects. However, these subjects are 3‐4 times more likely to have sleep disordered breathing (SDB) and have a higher incidence of obstructive airways disease than individuals in the general population, resulting in an increased inspiratory load.ObjectiveTo examine the effects of increased inspiratory load (airway occlusion) on inspiratory intercostal muscle activation during HF‐SCS.MethodsIn 3 spinalized (C2 level) anesthetized dogs, recording electrodes were positioned in the parasternal (PA) and external (EI) intercostal muscles (2nd and 3rd interspaces respectively) to record multiunit (integrated) and single motor units (SMU) EMG activities. During HF‐SCS at functional residual capacity (FRC), respiratory muscle activity was assessed before and after single and multi‐breath airway occlusion.ResultsDuring HF‐SCS, tracheal occlusion resulted in augmentation of peak multi‐unit integrated EI, but little change in PA EMG activity. During the occluded breath, EI activity increased to 148 ± 3% of that observed during control breaths (p&lt;0.01) whereas PA activity was little changed (105 ± 5%; NS). EI instantaneous SMU peak firing frequency (PFF) was also greater during the occluded breath (15.7 ± 1.6Hz vs. 11.3 ± 0.3Hz; p&lt;0.05). whereas there was only a small increase in PA PFF (10.8 ± 0.6Hz vs. 10.0 ± 0.6Hz; NS).SummaryHF‐SCS during airway occlusion results in significant increases in activation of the EI but not PA muscles.ConclusionHF‐SCS applied to support ventilation in high tetraplegics with airway obstruction may elicit compensatory increases in EI muscle activation. These results support the concept that spinal reflex effects remain functional during HF‐SCS. The EI have a much higher density of muscle spindles compared to the PA muscles, which may mediate the differential activation of these muscles.

Timing of inspiratory muscle activity detected from airway pressure and flow during pressure support ventilation: the waveform method

BackgroundWhether respiratory efforts and their timing can be reliably detected during pressure support ventilation using standard ventilator waveforms is unclear. This would give the opportunity to assess and improve patient–ventilator interaction without the need of special equipment.MethodsIn 16 patients under invasive pressure support ventilation, flow and pressure waveforms were obtained from proximal sensors and analyzed by three trained physicians and one resident to assess patient’s spontaneous activity. A systematic method (the waveform method) based on explicit rules was adopted. Esophageal pressure tracings were analyzed independently and used as reference. Breaths were classified as assisted or auto-triggered, double-triggered or ineffective. For assisted breaths, trigger delay, early and late cycling (minor asynchronies) were diagnosed. The percentage of breaths with major asynchronies (asynchrony index) and total asynchrony time were computed.ResultsOut of 4426 analyzed breaths, 94.1% (70.4–99.4) were assisted, 0.0% (0.0–0.2) auto-triggered and 5.8% (0.4–29.6) ineffective. Asynchrony index was 5.9% (0.6–29.6). Total asynchrony time represented 22.4% (16.3–30.1) of recording time and was mainly due to minor asynchronies. Applying the waveform method resulted in an inter-operator agreement of 0.99 (0.98–0.99); 99.5% of efforts were detected on waveforms and agreement with the reference in detecting major asynchronies was 0.99 (0.98–0.99). Timing of respiratory efforts was accurately detected on waveforms: AUC for trigger delay, cycling delay and early cycling was 0.865 (0.853–0.876), 0.903 (0.892–0.914) and 0.983 (0.970–0.991), respectively.ConclusionsVentilator waveforms can be used alone to reliably assess patient’s spontaneous activity and patient–ventilator interaction provided that a systematic method is adopted.

Proportional assist ventilation relieves clinically significant dyspnea in critically ill ventilated patients

IntroductionDyspnea is common and often severe symptom in mechanically ventilated patients. Proportional assist ventilation (PAV) is an assist ventilatory mode that adjusts the level of assistance to the activity of respiratory muscles. We hypothesized that PAV reduce dyspnea compared to pressure support ventilation (PSV).Patients and methodsMechanically ventilated patients with clinically significant dyspnea were included. Dyspnea intensity was assessed by the Dyspnea—Visual Analog Scale (D-VAS) and the Intensive Care-Respiratory Distress Observation Scale (IC-RDOS) at inclusion (PSV-Baseline), after personalization of ventilator settings in order to minimize dyspnea (PSV-Personalization), and after switch to PAV. Respiratory drive was assessed by record of electromyographic activity of inspiratory muscles, the proportion of asynchrony was analyzed.ResultsThirty-four patients were included (73% males, median age of 66 [57–77] years). The D-VAS score was lower with PSV-Personalization (37 mm [20‒55]) and PAV (31 mm [14‒45]) than with PSV-Baseline (62 mm [28‒76]) (p < 0.05). The IC-RDOS score was lower with PAV (4.2 [2.4‒4.7]) and PSV-Personalization (4.4 [2.4‒4.9]) than with PSV-Baseline (4.8 [4.1‒6.5]) (p < 0.05). The electromyographic activity of parasternal intercostal muscles was lower with PAV and PSV-Personalization than with PSV-Baseline. The asynchrony index was lower with PAV (0% [0‒0.55]) than with PSV-Baseline and PSV-Personalization (0.68% [0‒2.28] and 0.60% [0.31‒1.41], respectively) (p < 0.05).ConclusionIn mechanically ventilated patients exhibiting clinically significant dyspnea with PSV, personalization of PSV settings and PAV results in not different decreased dyspnea and activity of muscles to a similar degree, even though PAV was able to reduce asynchrony more effectively.

Inspiratory muscle activation during inspiratory muscle training in patients with COPD

Background and objectivesThe main target of inspiratory muscle training (IMT) is to improve diaphragm function in patients with COPD who have inspiratory muscle weakness. Ventilatory demand is already increased during quiet breathing in patients with COPD, and whether threshold load imposed by IMT would active more accessory muscle remained to be determined. The purpose of this study was to examine diaphragm and sternocleidomastoid (SCM) activation during IMT with intensities of 30% and 50% maximal inspiratory pressure (PImax). MethodsPatients with COPD and a PImax lower than 60 cmH2O were recruited for the study. Surface electromyography (EMG) was used to measure diaphragm and SCM activation, and group-based trajectory modeling (GBTM) was used to identify activation patterns during IMT. The generalized estimating equation (GEE) was then used to detect differences of variables between various breathing tasks. Statistical significance was established at p < 0.05. ResultsA total of 30 patients with COPD participated in this study. All patients demonstrated significant increases in diaphragm and SCM activation during 30% and 50% PImax of IMT than during quiet breathing (all p < 0.001). Diaphragm demonstrated two distinct patterns in response to IMT: low activation (n = 8) and high activation (n = 22) group using GBTM analysis. ConclusionDiaphragm and SCM were substantially activated during IMT in patients with COPD who had inspiratory muscle weakness. Regardless of whether diaphragm activation was high or low, SCM was activated to a greater extent in response to IMT.

Acute intermittent hypoxia and respiratory muscle recruitment in people with amyotrophic lateral sclerosis: A preliminary study

Respiratory failure is the main cause of death in amyotrophic lateral sclerosis (ALS). Since no effective treatments to preserve independent breathing are available, there is a critical need for new therapies to preserve or restore breathing ability. Since acute intermittent hypoxia (AIH) elicits spinal respiratory motor plasticity in rodent ALS models, and may restore breathing ability in people with ALS, we performed a proof-of-principle study to investigate this possibility in ALS patients. Quiet breathing, sniff nasal inspiratory pressure (SNIP) and maximal inspiratory pressure (MIP) were tested in 13 persons with ALS and 10 age-matched controls, before and 60 min post-AIH (15, 1 min episodes of 10% O2, 2 min normoxic intervals) or sham AIH (continuous normoxia). The root mean square (RMS) of the right and left diaphragm, 2nd parasternal, scalene and sternocleidomastoid muscles were monitored. A vector analysis was used to calculate summated vector magnitude (Mag) and similarity index (SI) of collective EMG activity during quiet breathing, SNIP and MIP maneuvers. AIH facilitated tidal volume and minute ventilation (treatment main effects: p < 0.05), and Mag (ie. collective respiratory muscle activity; p < 0.001) during quiet breathing in ALS and control subjects, but there was no effect on SI during quiet breathing. SNIP SI decreased in both groups post-AIH (p < 0.005), whereas Mag was unchanged (p = 0.09). No differences were observed in SNIP or MIP post AIH in either group. Discomfort was not reported during AIH by any subject, nor were adverse events observed. Thus, AIH may be a safe way to increase collective inspiratory muscle activity during quiet breathing in ALS patients, although a single AIH presentation was not sufficient to significantly increase peak inspiratory pressure generation. These preliminary results provide evidence that AIH may improve breathing function in people with ALS, and that future studies of prolonged, repetitive AIH protocols are warranted.