Neuromuscular Respiratory Failure

Author(s):  
Maximiliano A. Hawkes ◽  
Eelco F. M. Wijdicks

Breathing is a continuous, rhythmic, to-and-fro movement that requires a close interplay between arterial PCO2, oxygen, and respiratory centers. Certain thresholds exist for respiratory drive, and these thresholds change with acute neurologic disease. Primary structural lesions to the brainstem are most common, but decreased levels of consciousness frequently trigger episodic breathing. This chapter discusses the essentials of the respiratory pacemaker and neurologic breathing patterns.

2020 ◽  
Vol 202 (8) ◽  
pp. 1173-1178 ◽  
Author(s):  
Pierre Esnault ◽  
Michael Cardinale ◽  
Sami Hraiech ◽  
Philippe Goutorbe ◽  
Karine Baumstrack ◽  
...  

2017 ◽  
Vol 18 (4) ◽  
pp. 349-355
Author(s):  
Anita Ivosevic ◽  
Natasa Miletic ◽  
Maja Vulovic ◽  
Zoran Vujkovic ◽  
Snjezana Novakovic Bursac ◽  
...  

AbstractRespiratory failure is the predominant cause of death in humans and animals poisoned with anticholinesterases. Organophosphorus and carbamate anticholinesterases inhibit acetylcholinesterase irreversibly and reversibly, respectively. Some of them contain a quaternary atom that makes them lipophobic, limiting their action at the periphery, i.e. outside the central nervous system. They impair respiratory function primarily by inducing a desensitization block of nicotinic receptors in the neuromuscular synapse. Lipophilic anticholinesterases inhibit the acetylcholinesterase both in the brain and in other tissues, including respiratory muscles. Their doses needed for cessation of central respiratory drive are significantly less than doses needed for paralysis of the neuromuscular transmission. Antagonist of muscarinic receptors atropine blocks both the central and peripheral muscarinic receptors and effectively antagonizes the central respiratory depression produced by anticholinesterases. To manage the peripheral nicotinic receptor hyperstimulation phenomena, oximes as acetylcholinesterase reactivators are used. Addition of diazepam is useful for treatment of seizures, since they are cholinergic only in their initial phase and can contribute to the occurrence of central respiratory depression. Possible involvement of central nicotinic receptors as well as the other neurotransmitter systems – glutamatergic, opioidergic – necessitates further research of additional antidotes.


1984 ◽  
Vol 113 (1) ◽  
pp. 203-214 ◽  
Author(s):  
WILLIAM K. MILSOM

The normal breathing pattern of the Tokay gecko (Gekko gecko) consists of single breaths or bursts of a few breaths separated by periods of breath holding. Increases in pulmonary ventilation that accompany rises in body temperature are caused by increases in respiratory frequency due to shortening of the periods of breath holding. Tidal volume and breath duration remain relatively constant. Measurements of the mechanical work associated with spontaneous breathing yielded values that were similar to those calculated for breaths of the same size and duration based on work curves generated during pump ventilation of anaesthetized animals. In this species, the pattern of periodic breathing and the ventilatory responses to changes in respiratory drive correspond with predictions of optimal breathing patterns based on calculations of the mechanical cost of ventilation. Bilateral vagotomy drastically alters the breathing pattern producing an elevation in tidal volume, a slowing of breathing frequency, and a prolongation of the breath duration. These alterations greatly increase the mechanical cost of ventilation. These data suggest that periodic breathing in this species may represent an adaptive strategy which is under vagal afferent control and which serves to minimize the cost of breathing.


2021 ◽  
Vol 8 ◽  
Author(s):  
Ling Liu ◽  
Yue Yu ◽  
Xiaoting Xu ◽  
Qin Sun ◽  
Haibo Qiu ◽  
...  

Background: Patient-ventilator asynchrony is common during pressure support ventilation (PSV) because of the constant cycling-off criteria and variation of respiratory system mechanical properties in individual patients. Automatic adjustment of inspiratory triggers and cycling-off criteria based on waveforms might be a useful tool to improve patient-ventilator asynchrony during PSV.Method: Twenty-four patients were enrolled and were ventilated using PSV with different cycling-off criteria of 10% (PS10), 30% (PS30), 50% (PS50), and automatic adjustment PSV (PSAUTO). Patient-ventilator interactions were measured.Results: The total asynchrony index (AI) and NeuroSync index were consistently lower in PSAUTO when compared with PS10, PS30, and PS50, (P < 0.05). The benefit of PSAUTO in reducing the total AI was mainly because of the reduction of the micro-AI but not the macro-AI. PSAUTO significantly improved the relative cycling-off error when compared with prefixed controlled PSV (P < 0.05). PSAUTO significantly reduced the trigger error and inspiratory effort for the trigger when compared with a prefixed trigger. However, total inspiratory effort, breathing patterns, and respiratory drive were not different among modes.Conclusions: When compared with fixed cycling-off criteria, an automatic adjustment system improved patient-ventilator asynchrony without changes in breathing patterns during PSV. The automatic adjustment system could be a useful tool to titrate more personalized mechanical ventilation.


2003 ◽  
Vol 95 (1) ◽  
pp. 241-249 ◽  
Author(s):  
G. Soukhova ◽  
Y. Wang ◽  
M. Ahmed ◽  
J. F. Walker ◽  
J. Yu

We recently identified a vagally mediated excitatory lung reflex by injecting hypertonic saline into the lung parenchyma (Yu J, Zhang JF, and Fletcher EC. J Appl Physiol 85: 1485–1492, 1998). This reflex increased amplitude and burst rate of phrenic (inspiratory) nerve activity and suppressed external oblique abdominal (expiratory) muscle activity. In the present study, we tested the hypothesis that bradykinin may activate extravagal pathways to stimulate breathing by assessing its reflex effects on respiratory drive. Bradykinin (1 μg/kg in 0.1 ml) was injected into the lung parenchyma of anesthetized, open-chest and artificially ventilated rabbits. In most cases, bradykinin increased phrenic amplitude, phrenic burst rate, and expiratory muscle activity. However, a variety of breathing patterns resulted, ranging from hyperpnea and tachypnea to rapid shallow breathing and apnea. Bradykinin acts like hypertonic saline in producing hyperpnea and tachypnea, yet the two agents clearly differ. Bradykinin produced a higher ratio of phrenic amplitude to inspiratory time and had longer latency than hypertonic saline. Although attenuated, bradykinin-induced respiratory responses persisted after vagotomy. We conclude that bradykinin activates multiple afferent pathways in the lung; portions of its respiratory reflexes are extravagal and arise from sympathetic afferents.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liam Weaver ◽  
Anup Das ◽  
Sina Saffaran ◽  
Nadir Yehya ◽  
Timothy E. Scott ◽  
...  

Abstract Background There is on-going controversy regarding the potential for increased respiratory effort to generate patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients with COVID-19 acute hypoxaemic respiratory failure. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. We adapted a computational simulator of cardiopulmonary pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. In accordance with recent data, the simulator parameters were manually adjusted to generate a population of 10 patients that recapitulate clinical features exhibited by certain COVID-19 patients, i.e., severe hypoxaemia combined with relatively well-preserved lung mechanics, being treated with supplemental oxygen. Results Simulations were conducted at tidal volumes (VT) and respiratory rates (RR) of 7 ml/kg and 14 breaths/min (representing normal respiratory effort) and at VT/RR of 7/20, 7/30, 10/14, 10/20 and 10/30 ml/kg / breaths/min. While oxygenation improved with higher respiratory efforts, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. Pleural pressure swing increased from 12.0 ± 0.3 cmH2O at baseline to 33.8 ± 0.4 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH2O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH2O at baseline to 17.9 ± 0.3 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Total lung strain increased from 0.29 ± 0.006 at baseline to 0.65 ± 0.016 at 10 ml/kg/30 breaths/min. Mechanical power increased from 1.6 ± 0.1 J/min at baseline to 12.9 ± 0.2 J/min at VT/RR of 7 ml/kg/30 breaths/min, and to 24.9 ± 0.3 J/min at 10 ml/kg/30 breaths/min. Driving pressure increased from 7.7 ± 0.2 cmH2O at baseline to 19.6 ± 0.2 cmH2O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Conclusions Our results suggest that the forces generated by increased inspiratory effort commonly seen in COVID-19 acute hypoxaemic respiratory failure are comparable with those that have been associated with ventilator-induced lung injury during mechanical ventilation. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury.


1997 ◽  
Vol 272 (2) ◽  
pp. R497-R508 ◽  
Author(s):  
R. Kinkead ◽  
W. K. Milsom

This study compared the "fictive" breathing patterns of decerebrate, paralyzed, unidirectionally ventilated bullfrogs in which pulmonary stretch receptor (PSR) feedback was either absent bilateral vagotomy), maintained constant at different levels (tonic) or oscillated with each fictive breath (phasic) under different levels of hypoxic or CO2-related respiratory drive. Tonic and phasic PSR feedback had identical effects on the fictive breathing pattern; decreasing PSR feedback increased the peak integrated trigeminal electroneurogram recordings and decreased breathing frequency. The effects of bilateral vagotomy and lung deflation to 0 cmH2O on breathing pattern were identical. Although hypoxia (fractional concentration of O2 in air = 0.06) had no significant effect on fictive breathing, ventilating frogs with increasing CO2 levels (fractional CO2 concentration in inspired air range: 0.00-0.03) increased the number of breaths in each fictive breathing episode, and this effect was potentiated by PSR feedback. Whenever respiratory drive was increased, regardless of the method (increase in PSR feedback or chemoreceptor drive), occasional single breaths were replaced by breathing episodes, indicating that the mechanisms responsible for the clustering of the breaths and the onset/termination of breathing episodes are not dependent on either input alone.


1990 ◽  
Vol 259 (5) ◽  
pp. R887-R897 ◽  
Author(s):  
N. J. Smatresk

The relative contributions of O2- and CO2-sensitive chemoreceptor information to centrally generated respiratory patterns have changed dramatically during vertebrate evolution. Chemoafferent input from branchial O2 chemoreceptors modulates centrally generated respiratory patterns but is not critical for respiratory rhythmogenesis in fishes. In air-breathing fishes, branchial O2 chemoreceptors monitoring internal and external stimuli control the relative contributions of the gills and air-breathing organ to net ventilation, and chemoafferent input is necessary for initiating air breathing. In the transition from water to air breathing by amphibious vertebrates, rhythmic patterns of branchial ventilation are completely replaced by arrhythmic and intermittent patterns of air breathing, and there is progressive dependence on CO2 as a source of respiratory drive. Periodic initiation of air breathing in resting animals appears to depend on attaining a threshold level of afferent activity from O2- and CO2/pH-sensitive chemoreceptors, since hyperoxia and/or hypocapnia can abolish air breathing in all air-breathing vertebrates. Conversely, chemoreceptor stimulation in amphibians and reptiles converts intermittent to more continuous air breathing patterns, suggesting that adequate biasing input from chemoreceptors activates a central rhythm generator. Chemoafferent input in homeotherms serves as one of several sources of drive for rhythmic breathing and supplies feedback for blood gas homeostasis in the face of metabolic or environmental change.


2018 ◽  
Author(s):  
Nathan R. Manley ◽  
Martin A Croce

Acute respiratory failure (ARF) is fundamentally a dysfunction of gas exchange and can be due to either inadequate carbon dioxide elimination causing hypercapnia or poor oxygen exchange and delivery causing hypoxemia. A variety of etiologies exist that cause ARF in the surgical patient, including previous lung disease, such as chronic obstructive pulmonary disease or asthma, neurologic compromise of respiratory drive, nutritional and metabolic derangements that can alter respiratory metabolism and mechanics, direct lung injury, and infection. The type of surgery and the time since surgery are other key factors that influence medical decision making and that will influence priorities in the assessment and management of ARF. This review explores the full spectrum of ARF in the surgical patient, focusing particularly on its assessment and initial management. Figures illustrate algorithms in the approach to the surgical patient with ARF and show example radiographic images of acute respiratory distress syndrome (ARDS), a common complication. Tables summarize indications for emergent intubation, key etiologies of ARF, and the evolving definitions of acute lung injury and ARDS. Key words: acute respiratory distress syndrome, acute respiratory failure, hypercapnia, hypoxemia, mechanical ventilation 


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