Respiratory muscles function

Suxamethonium sensitivity," prolonged paralysis of respiratory muscle function caused by failure to cleave the short-acting muscle relaxant succinylcholine widely used in anesthesia, was made testable with a simple bedside assay in 1968 (Motulsky and Morrow). However, that test was not incorporated widely into practice. Most anesthesiologists felt they could simply monitor all patients and "bag" those not resuming respiratory action, without testing for a trait that would be found in only one of 2000 patients. 

Function begins to return as soon as nutritional support is introduced, even before any tissue gain, suggesting an immediate and direct effect on cellular function. Skeletal and respiratory muscle function deteriorates steeply after a loss of 20% of body protein stores (equivalent to 15% total body weight loss) and improves by 10-20% within the first few days of nutritional support. 

Established indications for somatropin (growth hormone) include growth hormone deficiency in children, Turner s syndrome, Noonan s syndrome, and renal insufficiency in children. Other well-studied indications include idiopathic short stature, adult growth hormone deficiency, osteoporosis, and catabolic states associated with acute and chronic illness and injury. Body composition, respiratory muscle function, physical strength, and height improved in a 12-month trial of somatropin in 54 children with Prader-Willi syndrome (1). 

Injection of botulinum toxin is a rather innovative way to control localized muscle hyperexcitability. Botulinum toxin is a purified version of the toxin that causes botulism. Systemic doses of this toxin can be extremely dangerous or fatal because botulinum toxin inhibits the release of acetylcholine from presynaptic terminals at the skeletal neuromuscular junction. Loss of presynaptic acetylcholine release results in paralysis of the muscle fiber supplied by that terminal. Systemic dissemination of botulinum toxin can therefore cause widespread paralysis, including loss of respiratory muscle function. Injection into specific muscles, however, can sequester the toxin within these muscles, thus producing localized effects that are beneficial in certain forms of muscle hyperexcitability. 

Al Jarad N, Carroll MP, Laroche C, et al. 1994. Respiratory muscle function in patients with asbestos-related pleural disease. Resp Med 88 115-120. 

Mechanical restriction caused by chest bellows malfunction may result from chest wall or skeletal deformity, loss of neuromuscular function, fibrosis of the pleural space, and abdominal overdistension causing upward displacement of the diaphragm, as well as decreased diaphragm movement. The most common pulmonary function pattern seen in these patients is a decrease in TLC and VC with only a slight decrease in RV. The RV is maintained in these diseases because lung compliance remains normal. The Dlco is normal or only minimally reduced, and the Dlco a (corrected for alveolar volume) is normal. The RV/TLC ratio is often increased in patients with restrictive chest bellows disease. Patients with neuromuscular disease also have reduced respiratory muscle function with a reduction in their MIP. 

Sodium also plays an important role in nerve impulse generation and transmission. As a part of the sodium-potassium pump, the difference between the potassium and sodium concentrations is maintained through active transport across the cell membrane as needed with the help of adenosine triphosphate (ATP) as an energy source. The flow of sodium and potassium across the cell membrane of electrically charged cells results in depolarization. Thus sodium is important for nerve and muscle function. As such, sodium imbalances can affect cardiac and respiratory muscle function as well as mobility. 

De Troyer A. Respiratory muscle function in chronic obstructive pulmonary disease. In Casaburi R, Petty YL, eds. Principles and Practice of Pulmonary Rehabilitation. Philadephia WB Saunders Company, 1993 33-49. 

Hypothyroidism, hyperthyroidism, and acromegaly can adversely affect respiratory muscle function (40). Proteolysis of myofibrillar proteins by the ubiquitin-proteasome proteolytic system is probably responsible for respiratory muscle catabolism and weakness of hyperthyroidism (40) This mechanism is implicated in the muscle wasting associated with acidosis, renal failure, cancer, diabetes, acquired immunity deficiency syndrome, trauma, and... 

Alkalosis, either metabolic or respiratory, does not affect skeletal muscle function (40). In contrast, whether acidosis, either metabolic or respiratory, impairs respiratory muscle function remains controversial. 

In healthy volunteers, acute increases of arterial carbon dioxide to 54 mmHg (corresponding to a pH of about 7.29) reduces the capacity of the unfatigued diaphragm to generate pressure by 10-30% (Fig. 12) (98). This direct inhibitory effect of respiratory acidosis on respiratory muscle function could provide a potential mechanism for the rapid clinical deterioration that can occur with severe asthma and during COPD exacerbations (98). Yet, the human data suggesting a direct deleterious effect of respiratory acidosis on respiratory muscle function... 

Respiratory muscle function may be impaired by decreased levels of phosphate, calcium, magnesium, and potassium (40). 

Tobin MJ, Laghi E. Monitoring respiratory muscle function. In Tobin MJ, ed. Principles and Practice of Intensive Care Monitoring. New York McGraw-Hill Co., 1998 497-544. 

Gibson GJ, Gilmartin JJ, Veale D, et al. Respiratory muscle function in neuromuscular disease. In Jones NL, Killian KJ, eds. Breathlessness. The Campbell Symposium. Hamilton, Ontario Boehringer-Ingelheim, 1992 66-73. 

The most common causes of failure to wean include chronic obstructive pulmonary disease (COPD) exacerbations, neuromuscular diseases, h) oxic respiratory failure, post surgical complications (2), and heart failure. Weaning from the tracheostomy must consider the balance of respiratory muscle function and work of breathing. The work of breathing is determined by ventilatory demand, compliance of the lungs and chest wall, airway resistance, and intrinsic positive end-expiratory pressure (PEEPi). Adequacy of ventilatory drive and neuromechanical output can be assessed from the respiratory rate, airway occlusion pressure at 100 milliseconds (Po.i), maximum inspiratory pressure (MIP), and maximum voluntary ventilation (MW). 

There is an important distinction between dependence on an artificial airway and mechanical ventilation, which can be provided noninvasively (9). The requirement for an artificial airway may reflect bulbar impairment as, in those with adequate bulbar function, noninvasive ventilation will sustain adequate ventilation even with veiy limited respiratory muscle function. Therefore, tracheostomized patients with preserved bulbar control can undergo decannulation. Airway secretions are important determinants of dependence on mechanical ventilation through an artificial airway, and aspiration pneumonia may result from an impaired level of consciousness, poor bulbar function, or inability to cough effectively. Such issues must be addressed by airway clearance techniques, prior to decannulation. 

Figure 2 Lung volume recruitment. Flow volume loops. The MIC is maintained (higher expired flow) in a patient with ALS over a period of one year despite complete loss of measurable, spontaneous (lower flow) respiratory muscle function. Abbreviations MIC, maximum insufflation capacity ALS, amyotrophic lateral sclerosis.

In conclusion, although several theories exist, there are currently no studies on negative predictive value (NPV) or NIPPV that have provided definitive evidence that the benefits in gas exchange were related to improvements in respiratory muscle function or in sleep efficiency. The relationship between improved gas exchange and hyperinflation needs further investigation. The restoration of the central drive to breathe is the most consistent finding. It is therefore important in any evaluation of NIPPV to be confident that nocturnal hypoventilation has been reduced. 

Cropp A, DiMarco AF. Effects of intermittent negative pressure ventilation on respiratory muscle function in patients with severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1987 135(5) 1056-1061. 

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