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Respiratory Care Feb 2011Patient-ventilator interaction has been the focus of increasing attention from both manufacturers and researchers during the last 25 years. There is now compelling...
Patient-ventilator interaction has been the focus of increasing attention from both manufacturers and researchers during the last 25 years. There is now compelling evidence that passive (controlled) mechanical ventilation leads to respiratory muscle dysfunction and atrophy, prolonging the need for ventilatory support and predisposing to a number of adverse patient outcomes. Although there is consensus that the respiratory muscles should retain some activity during acute respiratory failure, patient-ventilator asynchrony is now recognized as a cause of ineffective ventilation, impaired gas exchange, lung overdistention, increased work of breathing, and patient discomfort. Far more common than previously recognized, it also predisposes to respiratory muscle dysfunction and other complications, leads to excessive use of sedation, increases the duration of ventilatory support, and interferes with weaning. Appropriate recognition and management of patient-ventilator asynchrony require bedside assessment of ventilator graphics as well as direct patient observation. Among currently available ventilation modes and approaches, none has been shown to be clearly superior to all the others with respect to patient-ventilator interaction, and strongly held preferences among investigators have led to controversy and difficulties in carrying out appropriate studies evaluating them. As a result, marked practice variation exists among different specialties as well as in different institutions and geographical areas. The respected authorities on mechanical ventilation who participated in this conference differed in the modes they preferred but agreed that proper understanding and use according to the individual patient's needs are more important than which mode is chosen. Conference participants discussed the determinants, manifestations, and epidemiology of patient-ventilator asynchrony, and described and compared several ventilation modes aimed specifically at preventing and ameliorating it. The papers arising from these discussions represent the most thorough examination of this important aspect of respiratory care yet published.
Topics: Humans; Hypnotics and Sedatives; Monitoring, Physiologic; Observation; Pulmonary Gas Exchange; Respiration, Artificial; Respiratory Muscles; Risk Factors; Ventilator Weaning; Ventilators, Mechanical; Work of Breathing
PubMed: 21333181
DOI: 10.4187/respcare.01115 -
Infection Oct 2022Symptoms often persistent for more than 4 weeks after COVID-19-now commonly referred to as 'Long COVID'. Independent of initial disease severity or pathological...
PURPOSE
Symptoms often persistent for more than 4 weeks after COVID-19-now commonly referred to as 'Long COVID'. Independent of initial disease severity or pathological pulmonary functions tests, fatigue, exertional intolerance and dyspnea are among the most common COVID-19 sequelae. We hypothesized that respiratory muscle dysfunction might be prevalent in persistently symptomatic patients after COVID-19 with self-reported exercise intolerance.
METHODS
In a small cross-sectional pilot study (n = 67) of mild-to-moderate (nonhospitalized) and moderate-to-critical convalescent (formerly hospitalized) patients presenting to our outpatient clinic approx. 5 months after acute infection, we measured neuroventilatory activity P, inspiratory muscle strength (PI) and total respiratory muscle strain (P/PI) in addition to standard pulmonary functions tests, capillary blood gas analysis, 6 min walking tests and functional questionnaires.
RESULTS
Pathological P/PI was found in 88% of symptomatic patients. Mean PI was reduced in hospitalized patients, but reduced PI was also found in 65% of nonhospitalized patients. Mean P was pathologically increased in both groups. Increased P was associated with exercise-induced deoxygenation, impaired exercise tolerance, decreased activity and productivity and worse Post-COVID-19 functional status scale. Pathological changes in P, PI or P/PI were not associated with pre-existing conditions.
CONCLUSIONS
Our findings point towards respiratory muscle dysfunction as a novel aspect of COVID-19 sequelae. Thus, we strongly advocate for systematic respiratory muscle testing during the diagnostic workup of persistently symptomatic, convalescent COVID-19 patients.
Topics: COVID-19; Cross-Sectional Studies; Humans; Pilot Projects; Respiratory Muscles; Post-Acute COVID-19 Syndrome
PubMed: 35570238
DOI: 10.1007/s15010-022-01840-9 -
Sports Medicine (Auckland, N.Z.) Jul 2019The physiological demands of marathon and ultra-marathon running are substantial, affecting multiple body systems. There have been several reviews on the physiological... (Review)
Review
The physiological demands of marathon and ultra-marathon running are substantial, affecting multiple body systems. There have been several reviews on the physiological contraindications of participation; nevertheless, the respiratory implications have received relatively little attention. This paper provides an up-to-date review of the literature pertaining to acute pulmonary and respiratory muscle responses to marathon and ultra-marathon running. Pulmonary function was most commonly assessed using spirometry, with infrequent use of techniques including single-breath rebreathe and whole-body plethysmography. All studies observed statistically significant post-race reductions in one-or-more metrics of pulmonary function, with or without evidence of airway obstruction. Nevertheless, an independent analysis revealed that post-race values rarely fell below the lower-limit of normal and are unlikely, therefore, to be clinically significant. This highlights the virtue of healthy baseline parameters prior to competition and, although speculative, there may be more potent clinical manifestations in individuals with below-average baseline function, or those with pre-existing respiratory disorders (e.g., asthma). Respiratory muscle fatigue was most commonly assessed indirectly using maximal static mouth-pressure manoeuvres, and respiratory muscle endurance via maximum voluntary ventilation (MVV). Objective nerve-stimulation data from one study, and others documenting the time-course of recovery, implicate peripheral neuromuscular factors as the mechanism underpinning such fatigue. Evidence of respiratory muscle fatigue was more prevalent following marathon compared to ultra-marathon, and might be a factor of work rate, and thus exercise ventilation, which is tempered during longer races. Potential implications of respiratory muscle fatigue on health and marathon/ultra-marathon performance have been discussed, and include a diminished postural stability that may increase the risk of injury when running on challenging terrain, and possible respiratory muscle fatigue-induced effects on locomotor limb blood flow. This review provides novel insights that might influence marathon/ultra-marathon preparation strategies, as well as inform medical best-practice of personnel supporting such events.
Topics: Humans; Lung; Maximal Voluntary Ventilation; Muscle Fatigue; Physical Endurance; Respiratory Muscles; Running
PubMed: 31030408
DOI: 10.1007/s40279-019-01105-w -
Respiratory Medicine Jan 2018Respiratory muscle dysfunction, being a common cause of weaning failure, is strongly associated with prolonged mechanical ventilation (MV) and prolonged stay in... (Review)
Review
INTRODUCTION
Respiratory muscle dysfunction, being a common cause of weaning failure, is strongly associated with prolonged mechanical ventilation (MV) and prolonged stay in intensive care units. Inspiratory muscle training (IMT) has been described as an important contributor to the treatment of respiratory muscle dysfunction in critically ill patients. Its effectiveness is however yet controversial.
OBJECTIVE
To discuss evidence for assessment of readiness and the effectiveness of interventions for liberation from MV, with special attention to the role of IMT.
METHODS
PubMed, LILACS, PEDro and Web of Science were searched for papers of assessment and treatment of patients who failed liberation from MV after at least one attempt published in English or Portuguese until June 2016.
RESULTS
Weaning predictors are related to weaning success (86%-100% for sensitivity and 7%-69% for specificity) and work of breathing (73%-100% for sensitivity and 56%-100% for specificity). Spontaneous breathing trials (SBT), noninvasive MV and early mobilization have been reported to improve weaning outcomes. Two modalities of IMT were identified in five selected studies: 1) adjustment of ventilator trigger sensitivity 2) inspiratory threshold loading. Both IMT training modalities promoted significant increases in respiratory muscle strength. IMT with threshold loading showed positive effect on endurance compared to control.
CONCLUSION
Methods to indentify respiratory muscle weakness in critically ill patients are feasible and described as indexes that show good accuracy. Individualized and supervised rehabilitation programs including IMT, SBT, noninvasive MV and early mobilization should be encouraged in patients with inspiratory muscle weakness.
Topics: Humans; Muscle Weakness; Respiration, Artificial; Respiratory Muscles; Respiratory Therapy; Treatment Failure; Ventilator Weaning
PubMed: 29413508
DOI: 10.1016/j.rmed.2017.11.023 -
Chest Nov 2010The mechanisms and pathways of the sensation of dyspnea are incompletely understood, but recent studies have provided some clarification. Studies of patients with cord... (Review)
Review
The mechanisms and pathways of the sensation of dyspnea are incompletely understood, but recent studies have provided some clarification. Studies of patients with cord transection or polio, induced spinal anesthesia, or induced respiratory muscle paralysis indicate that activation of the respiratory muscles is not essential for the perception of dyspnea. Similarly, reflex chemostimulation by CO₂ causes dyspnea, even in the presence of respiratory muscle paralysis or cord transection, indicating that reflex chemoreceptor stimulation per se is dyspnogenic. Sensory afferents in the vagus nerves have been considered to be closely associated with dyspnea, but the data were conflicting. However, recent studies have provided evidence of pulmonary vagal C-fiber involvement in the genesis of dyspnea, and recent animal data provide a basis to reconcile differences in responses to various C-fiber stimuli, based on the ganglionic origin of the C fibers. Brain imaging studies have provided information on central pathways subserving dyspnea: Dyspnea is associated with activation of the limbic system, especially the insular area. These findings permit a clearer understanding of the mechanisms of dyspnea: Afferent information from reflex stimulation of the peripheral sensors (chemoreceptors and/or vagal C fibers) is processed centrally in the limbic system and sensorimotor cortex and results in increased neural output to the respiratory muscles. A perturbation in the ventilatory response due to weakness, paralysis, or increased mechanical load generates afferent information from vagal receptors in the lungs (and possibly mechanoreceptors in the respiratory muscles) to the sensorimotor cortex and results in the sensation of dyspnea.
Topics: Afferent Pathways; Animals; Chemoreceptor Cells; Dyspnea; Humans; Mechanoreceptors; Reflex; Respiration; Respiratory Muscles; Vagus Nerve
PubMed: 21051395
DOI: 10.1378/chest.10-0534 -
Anesthesiology Apr 2013Postoperative pulmonary complications are responsible for significant increases in hospital cost as well as patient morbidity and mortality; respiratory muscle... (Review)
Review
Postoperative pulmonary complications are responsible for significant increases in hospital cost as well as patient morbidity and mortality; respiratory muscle dysfunction represents a contributing factor. Upper airway dilator muscles functionally resist the upper airway collapsing forces created by the respiratory pump muscles. Standard perioperative medications (anesthetics, sedatives, opioids, and neuromuscular blocking agents), interventions (patient positioning, mechanical ventilation, and surgical trauma), and diseases (lung hyperinflation, obesity, and obstructive sleep apnea) have differential effects on the respiratory muscle subgroups. These effects on the upper airway dilators and respiratory pump muscles impair their coordination and function and can result in respiratory failure. Perioperative management strategies can help decrease the incidence of postoperative respiratory muscle dysfunction. Such strategies include minimally invasive procedures rather than open surgery, early and optimal mobilizing of respiratory muscles while on mechanical ventilation, judicious use of respiratory depressant anesthetics and neuromuscular blocking agents, and noninvasive ventilation when possible.
Topics: Humans; Minimally Invasive Surgical Procedures; Patient Positioning; Postoperative Complications; Posture; Respiratory Insufficiency; Respiratory Muscles; Risk Factors
PubMed: 23429163
DOI: 10.1097/ALN.0b013e318288834f -
Pediatric Research Mar 2022Our aim was to summarise the current evidence and methods used to assess respiratory muscle function in the newborn, focusing on current and future potential clinical... (Review)
Review
Our aim was to summarise the current evidence and methods used to assess respiratory muscle function in the newborn, focusing on current and future potential clinical applications. The respiratory muscles undertake the work of breathing and consist mainly of the diaphragm, which in the newborn is prone to dysfunction due to lower muscle mass, flattened shape and decreased content of fatigue-resistant muscle fibres. Premature infants are prone to diaphragmatic dysfunction due to limited reserves and limited capacity to generate force and avoid fatigue. Methods to assess the respiratory muscles in the newborn include electromyography, maximal respiratory pressures, assessment for thoraco-abdominal asynchrony and composite indices, such as the pressure-time product and the tension time index. Recently, there has been significant interest and a growing body of research in assessing respiratory muscle function using bedside ultrasonography. Neurally adjusted ventilator assist is a novel ventilation mode, where the level of the respiratory support is determined by the diaphragmatic electrical activity. Prolonged mechanical ventilation, hypercapnia and hypoxia, congenital anomalies and systemic or respiratory infection can negatively impact respiratory muscle function in the newborn, while caffeine and synchronised or volume-targeted ventilation have a positive effect on respiratory muscle function compared to conventional, non-triggered or pressure-limited ventilation, respectively. IMPACT: Respiratory muscle function is impaired in prematurely born neonates and infants with congenital anomalies, such as congenital diaphragmatic hernia. Respiratory muscle function is negatively affected by prolonged ventilation and infection and positively affected by caffeine and synchronised compared to non-synchronised ventilation modes. Point-of-care diaphragmatic ultrasound and neurally adjusted ventilator assist are recent diagnostic and therapeutic technological developments with significant clinical applicability.
Topics: Caffeine; Diaphragm; Fatigue; Humans; Infant, Newborn; Respiration, Artificial; Respiratory Muscles
PubMed: 33875805
DOI: 10.1038/s41390-021-01529-z -
Respiratory Medicine Jun 2015Respiratory dysfunction frequently occurs in patients with advanced multiple sclerosis (MS), and may manifest as acute or chronic respiratory failure, disordered control... (Review)
Review
Respiratory dysfunction frequently occurs in patients with advanced multiple sclerosis (MS), and may manifest as acute or chronic respiratory failure, disordered control of breathing, respiratory muscle weakness, sleep disordered breathing, or neurogenic pulmonary edema. The underlying pathophysiology is related to demyelinating plaques involving the brain stem or spinal cord. Respiratory complications such as aspiration, lung infections and respiratory failure are typically seen in patients with long-standing MS. Acute respiratory failure is uncommon and due to newly appearing demyelinating plaques extensively involving areas of the brain stem or spinal cord. Early recognition of MS patients at risk for respiratory complications allows for the timely implementation of care and measures to decrease disease associated morbidity and mortality.
Topics: Humans; Multiple Sclerosis; Respiratory Insufficiency; Respiratory Muscles
PubMed: 25724874
DOI: 10.1016/j.rmed.2015.01.018 -
Progress in Cardiovascular Diseases 2022Exercise limitation is a cardinal manifestation of many cardiovascular diseases (CVD) and is associated with poor prognosis. It is increasingly well understood that... (Review)
Review
Exercise limitation is a cardinal manifestation of many cardiovascular diseases (CVD) and is associated with poor prognosis. It is increasingly well understood that exercise-based cardiac rehabilitation (CR) is an intervention that portends favorable clinical outcomes, including improvements in exercise capacity. The etiology of exercise limitation in CVD is multifactorial but is typically governed by terminal sensations of pain, fatigue, and/or breathlessness. A known but perhaps underestimated complication of CVD that contributes to breathlessness and exercise intolerance in such patients is inspiratory muscle dysfunction. For example, inspiratory muscle dysfunction, which encompasses a loss in muscle mass and/or pressure generating capacity, occurs in up to ~40% of patients with chronic heart failure and is associated with breathlessness, exertional intolerance, and worse survival in this patient population. In this review, we define inspiratory muscle weakness, detail its prevalence in a range of CVDs, and discuss how inspiratory weakness impacts physiological function and clinical outcomes in patients with CVD often referred to CR. We also evaluate the available evidence addressing the effects of exercise-based CR with and without concurrent specific inspiratory muscle training (IMT) on inspiratory muscle function, general physiological function, and clinical outcomes in patients with CVD. Finally, we consider whether the assessment of global respiratory muscle function should become standard as part of the patient intake assessment for phase II CR programs, giving practical guidance on the implementation of such measures as well as IMT as part of phase II CR.
Topics: Cardiac Rehabilitation; Cardiovascular Diseases; Dyspnea; Exercise Tolerance; Humans; Muscle Strength; Muscle Weakness; Respiratory Muscles
PubMed: 34688670
DOI: 10.1016/j.pcad.2021.10.002 -
Experimental Physiology Apr 2023What is the central question of this study? Is the attenuation of the respiratory muscle metaboreflex preserved after detraining? What is the main finding and its...
NEW FINDINGS
What is the central question of this study? Is the attenuation of the respiratory muscle metaboreflex preserved after detraining? What is the main finding and its importance? Inspiratory muscle training increased respiratory muscle strength and attenuated the respiratory muscle metaboreflex as evident by lower heart rate and blood pressure. After 5 weeks of no inspiratory muscle training (detraining), respiratory muscle strength was still elevated and the metaboreflex was still attenuated. The benefits of inspiratory muscle training persist after cessation of training, and attenuation of the respiratory metaboreflex follows changes in respiratory muscle strength.
ABSTRACT
Respiratory muscle training (RMT) improves respiratory muscle (RM) strength and attenuates the RM metaboreflex. However, the time course of muscle function loss after the absence of training or 'detraining' is less known and some evidence suggest the respiratory muscles atrophy faster than other muscles. We sought to determine the RM metaboreflex in response to 5 weeks of RMT and 5 weeks of detraining. An experimental group (2F, 6M; 26 ± 4years) completed 5 weeks of RMT and tibialis anterior (TA) training (each 5 days/week at 50% of maximal inspiratory pressure (MIP) and 50% maximal isometric force, respectively) followed by 5 weeks of no training (detraining) while a control group (1F, 7M; 24 ± 1years) underwent no intervention. Prior to training (PRE), post-training (POST) and post-detraining (DETR), all participants underwent a loaded breathing task (LBT) to failure (60% MIP) while heart rate and mean arterial blood pressure (MAP) were measured. Five weeks of training increased RM (18 ± 9%, P < 0.001) and TA (+34 ± 19%, P < 0.001) strength and both remained elevated after 5 weeks of detraining (MIP-POST vs. MIP-DETR: 154 ± 31 vs. 153 ± 28 cmH2O, respectively, P = 0.853; TA-POST vs. TA-DETR: 86 ± 19 vs. 85 ± 16 N, respectively, P = 0.982). However, the rise in MAP during LBT was attenuated POST (-11 ± 17%, P = 0.003) and DETR (-9 ± 9%, P = 0.007) during the iso-time LBT. The control group had no change in MIP (P = 0.33), TA strength (P = 0.385), or iso-time MAP (P = 0.867) during LBT across all time points. In conclusion, RM and TA have similar temporal strength gains and the attenuation of the respiratory muscle metaboreflex remains after 5 weeks of detraining.
Topics: Humans; Respiration; Respiratory Muscles; Breathing Exercises; Intercostal Muscles; Muscle, Skeletal; Muscle Strength
PubMed: 36754374
DOI: 10.1113/EP090779