Diaphragm pacing failure secondary to deteriorated chest wall mechanics: When a good diaphragm does not suffice to take a good breath in

AbstractDiaphragm pacing allows certain quadriplegic patients to be weaned from mechanical ventilation. Pacing failure can result from device dysfunction, neurotransmission failure, or degraded lung mechanics (such as atelectasis). We report two cases where progressive pacing failure was attributed to deteriorated chest wall mechanics. The first patient suffered from cervical spinal cord injury at age 45, was implanted with a phrenic stimulator (intrathoracic), successfully weaned from ventilation, and permanently paced for 7 years. Pacing effectiveness then slowly declined, finally attributed to rib cage stiffening due to ankylosing spondylitis. The second patient became quadriplegic after meningitis at age 15, was implanted with a phrenic stimulator (intradiaphragmatic) and weaned. After a year hypoventilation developed without obvious cause. In relationship with complex endocrine disorders, the patient had gained 31 kg. Pacing failure was attributed to excessive mechanical inspiratory load. Rib cage mechanics abnormalities should be listed among causes of diaphragm pacing failure and it should be kept in mind that a “good diaphragm” is not sufficient to produce a “good inspiration”

Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans

BACKGROUND: Breathing in humans is dually controlled for metabolic (brainstem commands) and behavioral purposes (suprapontine commands) with reciprocal modulation through spinal integration. Whereas the ventilatory response to chemical stimuli arises from the brainstem, the compensation of mechanical loads in awake humans is thought to involve suprapontine mechanisms. The aim of this study was to test this hypothesis by examining the effects of inspiratory resistive loading on the response of the diaphragm to transcranial magnetic stimulation. RESULTS: Six healthy volunteers breathed room air without load (R0) and then against inspiratory resistances (5 and 20 cmH(2)O/L/s, R5 and R20). Ventilatory variables were recorded. Transcranial magnetic stimulation (TMS) was performed during early inspiration (I) or late expiration (E), giving rise to motor evoked potentials (MEPs) in the diaphragm (Di) and abductor pollicis brevis (APB). Breathing frequency significantly decreased during R20 without any other change. Resistive breathing had no effect on the amplitude of Di MEPs, but shortened their latency (R20: -0.903 ms, p = 0.03) when TMS was superimposed on inspiration. There was no change in APB MEPs. CONCLUSION: Inspiratory resistive breathing facilitates the diaphragm response to TMS while it does not increase the automatic drive to breathe. We interpret these findings as a neurophysiological substratum of the suprapontine nature of inspiratory load compensation in awake humans

Respiratory‐related cortical activity in patients with COPD and aged normal individuals: towards a different vision of dyspnoea?

International audienceNo abstract availabl

Fooling the brain to alleviate dyspnoea

International audienceThe application of a stream of air onto the face by a hand-held fan has a real place in the treatment of dyspnoea http://ow.ly/tKJk30dJ5P

Noninvasive ventilation reduces energy expenditure in amyotrophic lateral sclerosis

International audienceBackgroundAmyotrophic lateral sclerosis (ALS) leads to chronic respiratory failure. Diaphragmatic dysfunction, a major driver of dyspnea and mortality, is associated with a shift of the burden of ventilation to extradiaphragmatic inspiratory muscles, including neck muscles. Besides, energy expenditure is often abnormally high in ALS, and this is associated with a negative prognostic value. We hypothesized that noninvasive ventilation (NIV) would relieve inspiratory neck muscles and reduce resting energy expenditure (REE).MethodsUsing indirect calorimetry, we measured REE during spontaneous breathing (REESB) and NIV (REENIV) in 16 ALS patients with diaphragmatic dysfunction, during the first 3 months of NIV. Measured values were compared with predicted REE (REEpred)(Harris-Benedict equation).ResultsNIV abolished inspiratory neck muscle activity. Even though our patients were not hypermetabolic, on the contrary, with a REESB that was lower than REEpred (average 11%), NIV did reduce energy expenditure. Indeed, median REENIV, in this population with a mean body mass index of 21.4 kg.m-2, was 1149 kcal/24 h [interquartile 970-1309], lower than REESB (1197 kcal/24 h, 1054-1402; mean difference 7%; p = 0.03, Wilcoxon). REESB and REENIV were correlated with forced vital capacity and maximal inspiratory pressure.ConclusionsNIV can reduce energy expenditure in ALS patients probably by alleviating the ventilatory burden imposed on inspiratory neck muscles to compensate diaphragm weakness. It remains to be elucidated whether or not, in which population, and to what extent, NIV can be beneficial in ALS through the corresponding reduction in energy expenditure

Aerosol furosemide for dyspnea: Controlled delivery does not improve effectiveness

International audienceAerosolized furosemide has been shown to relieve dyspnea; nevertheless, all published studies have shown great variability in response. This dyspnea relief is thought to result from the stimulation of slowly adapting pulmonary stretch receptors simulating larger tidal volume. We hypothesized that better control over aerosol administration would produce more consistent dyspnea relief; we used a clinical ventilator to control inspiratory flow and tidal volume. Twelve healthy volunteers inhaled furosemide (40mg) or placebo in a double blind, randomized, crossover study. Breathing Discomfort was induced by hypercapnia during constrained ventilation before and after treatment. Both treatments reduced breathing discomfort by 20% full scale. Effectiveness of aerosol furosemide treatment was weakly correlated with larger tidal volume. Response to inhaled furosemide was inversely correlated to furosemide blood level, suggesting that variation among subjects in the fate of deposited drug may determine effectiveness. We conclude that control of aerosol delivery conditions does not improve consistency of treatment effect; we cannot, however, rule out placebo effect

Observation scales to suspect dyspnea in non-communicative intensive care unit patients

International audienceDyspnea, like pain, is a major cause of physical suffering and emotional distress. In the intensive care unit, mechanically ventilated patients are at high risk of dyspnea [1], and increasing attention is being given to this symptom [1, 2]. Because its evaluation relies on self-report and self-assessment [3], dyspnea carries the risk of being underestimated or even unrecognized and therefore unattended in many intensive care unit patients. This is particularly so in patients unable to communicate with their caregivers (sedation, delirium, etc.). We have recently developed and validated a specific intensive care unit version of the respiratory distress observation scale (IC-RDOS, http://www.ic-rdos.com) [4]. IC-RDOS, based on respiratory and behavioral signs, correlates strongly with ratings of dyspnea on a visual analogic scale in “communicative” patients, but this is by definition not the most pertinent target population. The present secondary analysis describes IC-RDOS in “non-communicative” intensive care unit patients, as the first step of its clinical and prognostic evaluation in this setting

Analgesic effects of dyspnoea: “Air hunger” does not inhibit the spinal nociception reflex in humans

International audienceDyspnoea has distinct sensory modalities, including air hunger and the sensation of excessive breathing "work/effort". Both have analgesic properties. In the case of work/effort, spinal mechanisms have been documented (inhibitory effect on the spinal nociceptive flexor reflex, RIII). This mechanism involves C-fibres. As C-fibres are unlikely to play a major role in air hunger, we hypothesised that inducing this type of dyspnoea would not result in RIII inhibition. Eight healthy volunteers were exposed to a hypercapnic hyperoxic gas mixture (5% CO2 and 95% O2) and asked to voluntarily fight the corresponding ventilatory reflex response by reducing tidal volume below its spontaneous level. Ventilatory variables and dyspnoea intensity (ordinal scale) were measured. Electromyography of the biceps femoris was used to record the amplitude of RIII in response to painful electrical sural nerve stimulation. Air hunger failed to inhibit the RIII reflex. We conclude that the mechanisms of air hunger induced analgesia do not include a spinal contribution and are therefore mostly central