Respiratory Muscle Injury: Evidence to Date and Potential Mechanisms

2001 ◽  
Vol 26 (4) ◽  
pp. 356-387 ◽  
Author(s):  
W. Darlene Reid ◽  
Tyler James Clarke ◽  
Alison M. Wallace

Respiratory muscle dysfunction associated with ventilatory loading may be partially attributed to respiratory muscle injury. Exertion-induced muscle injury can be defined as structural alterations of the muscle, however, a better understanding of the biochemical, morphologic, and functional correlates of injured respiratory muscles will facilitate discrimination of how injury, fatigue, and weakness contribute to respiratory muscle dysfunction. In addition to the increased loads associated with lung disease, many factors such as poor arterial blood gases, immobilization, sepsis, decreased nutrition, and corticosteroids may increase susceptibility to exertion-induced respiratory muscle injury. Respiratory muscle injury in humans is not well-described, however, more extensive evidence has been shown in animal models of increased ventilatory loading. Potential mechanisms of respiratory muscle injury are mechanical stress, metabolic stress, and inflammation. In order to optimize therapeutic interventions, a better understanding of these mechanisms and the patients that are most susceptible to respiratory muscle injury needs to be determined. Key words: resistive loading, respiratory muscles, exertion, muscle adaptation, muscle injury

1983 ◽  
Vol 54 (3) ◽  
pp. 803-808 ◽  
Author(s):  
S. Matalon ◽  
M. S. Nesarajah ◽  
J. A. Krasney ◽  
L. E. Farhi

We studied the cardiorespiratory effects of acute hypercapnia in 10 unanesthetized sheep. After a 15-min exposure to either 7.3 or 10% CO2 in air, we measured arterial blood gases, minute ventilation (VE), O2 consumption (VO2), cardiac output (Q), heart rate (HR), an index of left ventricular contractility [(dP/dt)/P], and vascular pressures. In addition, regional flows to all major organs were determined by injecting 15-microns radiolabeled microspheres into the left heart. Exposure to 7.3% CO2 (arterial CO2 partial pressure, PaCO2, 58 Torr) resulted in increased VE, (dP/dt)/P, and higher blood flows to the brain and respiratory muscles. All other variables remained unchanged. Exposure to 10% CO2 (PaCO2 75 Torr) resulted in a further augmentation of VE and a 48% increase in Q, which was associated with a tachycardia, a decrease in systemic vascular resistance, and an increase in VO2. Coronary and respiratory muscle flows increased, but all other variables remained unchanged. Thus the hemodynamic effects of hypercapnia are not related linearly to the level of PaCO2.


1997 ◽  
Vol 82 (2) ◽  
pp. 500-507 ◽  
Author(s):  
Harly E. Greenberg ◽  
Rammohan S. Rao ◽  
Anthony L. Sica ◽  
Steven M. Scharf

Greenberg, Harly E., Rammohan S. Rao, Anthony L. Sica, and Steven M. Scharf. Effect of chronic resistive loading on hypoxic ventilatory responsiveness. J. Appl. Physiol. 82(2): 500–507, 1997.—Depression of ventilation mediated by endogenous opioids has been observed acutely after resistive airway loading. We evaluated the effects of chronically increased airway resistance on hypoxic ventilatory responsiveness shortly after load imposition and 6 wk later. A circumferential tracheal band was placed in 200-g rats, tripling tracheal resistance. Sham surgery was performed in controls. Ventilation and the ventilatory response to hypoxia were measured by using barometric plethysmography at 2 days and 6 wk postsurgery in unanesthetized rats during exposure to room air and to 12% O2-5% CO2-balance N2. Trials were performed with and without naloxone (1 mg/kg ip). Room air arterial blood gases demonstrated hypercapnia with normoxia in obstructed rats at 2 days and 6 wk postsurgery. During hypoxia, a 30-Torr fall in[Formula: see text] occurred with no change in[Formula: see text]. Hypoxic ventilatory responsiveness was suppressed in obstructed rats at 2 days postloading. Naloxone partially reversed this suppression. However, hypoxic responsiveness at 6 wk was not different from control levels. Naloxone had a small effect on ventilatory pattern at this time with no overall effect on hypoxic responsiveness. This was in contrast to previously demonstrated long-term suppression of CO2 sensitivity in this model, which was partially reversible by naloxone only during the immediate period after load imposition. Endogenous opioids apparently modulate ventilatory control acutely after load imposition. Their effect wanes with time despite persistence of depressed CO2 sensitivity.


2018 ◽  
Vol 125 (3) ◽  
pp. 820-831 ◽  
Author(s):  
A. William Sheel ◽  
Robert Boushel ◽  
Jerome A. Dempsey

Sympathetically induced vasoconstrictor modulation of local vasodilation occurs in contracting skeletal muscle during exercise to ensure appropriate perfusion of a large active muscle mass and to maintain also arterial blood pressure. In this synthesis, we discuss the contribution of group III-IV muscle afferents to the sympathetic modulation of blood flow distribution to locomotor and respiratory muscles during exercise. This is followed by an examination of the conditions under which diaphragm and locomotor muscle fatigue occur. Emphasis is given to those studies in humans and animal models that experimentally changed respiratory muscle work to evaluate blood flow redistribution and its effects on locomotor muscle fatigue, and conversely, those that evaluated the influence of coincident limb muscle contraction on respiratory muscle blood flow and fatigue. We propose the concept of a “two-way street of sympathetic vasoconstrictor activity” emanating from both limb and respiratory muscle metaboreceptors during exercise, which constrains blood flow and O2 transport thereby promoting fatigue of both sets of muscles. We end with considerations of a hierarchy of blood flow distribution during exercise between respiratory versus locomotor musculatures and the clinical implications of muscle afferent feedback influences on muscle perfusion, fatigue, and exercise tolerance.


2020 ◽  
Vol 92 (3) ◽  
pp. 19-24 ◽  
Author(s):  
B. I. Geltser ◽  
A. A. Dej ◽  
I. N. Titorenko ◽  
V. N. Kotelnikov

Aim. To assess the strength of the respiratory muscles in patients with community-acquired pneumonia (CAP) with varying severity of endogenous intoxication. Materials and methods. In the hospital, 78 men aged 1826 years with CAP were examined. СAP was diagnosed in 56 (72%) patients, severe CAP in 22 (28%). The severity of endogenous intoxication was verified using intoxication indices: hematological index of intoxication (HII), leukocyte index of intoxication (LII), nuclear index of intoxication (NII) and Krebs index. Middleweight molecules (MWM) was determined by spectrophotometry in the serum and the concentration of interleukin (IL)-10 and tumor necrosis factor  (TNF-) by ELISA. The strength of the respiratory muscles was measured on the device Micro RPM (Care Fusion, Great Britain). The maximum expiratory pressure (МЕР), inspiratory pressure (MIP) in the oral cavity, the Maximal Rate of Pressure Development (MRPD) during inhalation (MRPDin) and exhalation (MRPDex), and intranasal test (SNIP) were determined. Statistical processing was performed using descriptive statistics, MannWhitney test, correlation and cluster analysis. Results. Three clusters of endogenous intoxication corresponding to mild, moderate and severe degree were identified. The first cluster was represented only by patients with mild CAP, the second-mild CAP and severe CAP, and the third severe CAP. Dysfunction of the expiratory respiratory muscles prevailed during the height of the disease in patients with the first cluster, and in the second and third inspiratory, including the diaphragm. The level of actually measured values of MIP and SNIP was 68% and 58% of those due to severe endogenous intoxication. Significant negative correlations were established LII, HII, MWM, TNF-, IL-10 с MEP, MRPDex, MIP и SNIP. Respiratory muscle dysfunction remained only expiratory respiratory muscles in convalescents of the first cluster, and expiratory and inspiratory muscles of the second and third cluster. Conclusion. The development of respiratory muscle dysfunction in CAP is associated with the influence of endogenous intoxication factors. The results can be used in personalized programs of rehabilitation.


2020 ◽  
Vol 92 (3) ◽  
pp. 36-41
Author(s):  
A. K. Suleymanova ◽  
I. A. Baranova

Chronic obstructive pulmonary disease (COPD) is a group of diseases with high levels of comorbidity. Pathological changes of peripheral skeletal and respiratory muscles in COPD patients, which are often underestimated, occupy a special place. Aim. To study the relationship between functional and quantitative parameters of the peripheral (limb muscle) and respiratory muscles in COPD patients. Materials and methods. 127 patients (98 men/29 women, mean age 67.68.2 years) were under observation without acute COPD. All COPD patients were classified according to GOLD (2019) into groups A, B, C, D. The algorithm of the European Working Group on Sarcopenia in Older People (EWGSOP2) was used to diagnose sarcopenia. The muscle mass was measured using dual energy X-ray absorptiometry (DXA) and the appendicular lean mass index (ASM) was estimated. Maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) were measured by body plethysmograph MasterScreen Body. Quantitative assessment of thoracic muscle cross-sectional areas were performed using the CT scan using Vidar Dicom Viewer software. Results. Sarcopenia was diagnosed in 43.3% of COPD patients. Respiratory muscle dysfunction was determined in 66.1% of patients with COPD, its probability increased in groups C and D in comparison with groups A and B [chance ratio 6.6 (95% confidence interval 2.915.0); p0.0001]. Correlations between the functional parameters of sarcopenia and respiratory muscle strength as well as between the mass of peripheral skeletal muscles and respiratory muscle area have been established according to the data of computerized tomography (р0.01). Sarcopenia as well as respiratory muscle dysfunction was observed more frequently in persons with severe and extremely severe airway obstruction and in patients with predominantly emphysematic COPD phenotype (p0.01). Conclusion. Sarcopenia is a frequent comorbidity in COPD and its development is connected with the severity of the course of the main disease. Correlation between parameters of peripheral (limb muscle) and respiratory muscles in patients with COPD has been determined.


2021 ◽  
Vol 99 (6) ◽  
pp. 15-21
Author(s):  
I. G. Kurpаtov ◽  
B. I. Geltser ◽  
V. N. Kotelnikov ◽  
M. F. Kinyaykin

The objective: to assess the strength of respiratory muscles (RM) in patients with chronic obstructive pulmonary disease (COPD) and determine the role of certain pathogenetic factors of COPD in the development of respiratory muscle dysfunction.Subjects and methods. In in-patient settings, the strength characteristics of respiratory muscles were studied in 85 men aged 39-78 years suffering fromCOPD exacerbation. MicroRPM (CareFusion, UK) was used to determine the levels of maximum inspiratory and expiratory pressures in the oral cavity, maximum rate of their rise during inspiration and expiration as well as the level of intranasal pressure before and after the test with salbutamol.Results. Significant variability in strength characteristics of respiratory muscles was observed depending on the stage of COPD, its phenotype, and the presence of hypoxemia or hypercapnia. In patients at early stage of COPD, only expiratory respiratory muscle dysfunction was documented; at moderate and severe stages, inspiratory and expiratory muscle dysfunction was observed, and at very severe stage – diaphragm dysfunction prevailed. The results of the salbutamol test demonstrated the maximum increase in the strength of respiratory in early and moderate COPD and the minimum increase in extremely severeCOPD indicating the role of the irreversible component of bronchial obstruction in the development of respiratory muscle dysfunction. The emphysematous phenotype of COPD was characterized by inspiratory respiratory muscle dysfunction, while the bronchitic phenotype was characterized by expiratory respiratory muscle dysfunction. In patients with hypoxemia and hypercapnia, the strength of inspiratory respiratory muscle was lower versus normoxemia.


Author(s):  
Theodore Dassios ◽  
Aggeliki Vervenioti ◽  
Gabriel Dimitriou

Abstract 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.


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Eman Sobh ◽  
Fatma Elhussieny ◽  
Taghreed Ismail

Abstract Background Nasal obstruction is a significant medical problem. This study aimed to examine the effect of nasal obstruction and nasal packing on arterial blood gases and pulmonary function indices, and the impact of the elimination of nasal obstruction on preoperative values. Results The mean age of the study population was 26.6 ± 10.1 years, males represented 50.8%. Spirometric indices showed statistically significant improvement (preoperative forced expiratory volume in 1st second 66.9 ± 13.9 vs 79.6 ± 14.9 postoperative and preoperative forced vital capacity 65.5 ± 12.7 vs 80.4 ± 13.8 postoperative). Oxygen saturation was significantly lower during nasal packing (95.6 ± 1.6 preoperative vs 94.7 ± 2.8 with nasal pack), and significant improvement (97.2 ± 1.4) was observed after removal of the nasal pack. Nasal obstruction scores significantly improved. Conclusion The results of this study indicate that either simple nasal obstruction or nasal packing may cause hypoxemia and abnormalities in lung function tests. Hypoxemia was more evident with nasal packing.


2020 ◽  
Vol 8 (S1) ◽  
Author(s):  
Chiara Robba ◽  
Dorota Siwicka-Gieroba ◽  
Andras Sikter ◽  
Denise Battaglini ◽  
Wojciech Dąbrowski ◽  
...  

AbstractPost cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. The control of gas exchange, and in particular oxygenation and carbon dioxide levels, is fundamental in mechanically ventilated patients after resuscitation, as arterial blood gases derangement might have important effects on the cerebral blood flow and systemic physiology.In particular, the pathophysiological role of carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and oxygen demand. Hypo/hypercapnia, as well as mechanical ventilation during and after resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and catecholamine levels. The developing hypocapnia can nullify the beneficial effects of the hypothermia. The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest.According to our findings, the optimal ventilator strategies in post cardiac arrest patients are not fully understood, and oxygen and carbon dioxide targets should take in consideration a complex pattern of pathophysiological factors. Further studies are warranted to define the optimal settings of mechanical ventilation in patients after cardiac arrest.


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