Respiratory muscles resistive

Figure 5 Respiratory muscle resistive training with threshold loading in a patient weaning from mechanical ventilation.

In severe cases, or those refractory to treatment, truncal and limb weakness may be accompanied by involvement of masticatory, bulbar, and respiratory muscles. However the most life-threatening clinical manifestations are those affecting the gastrointestinal tract, since stomach ulceration can occur and death from perforation and peritonitis are not unknown. Medication with steroidal antiinflammatory agents is necessary but weakens the childrens resistance to infection, so that systemic spread of usually self-limiting disorders, such as candidiasis, may occasionally occur. 

Normal expiration is a passive process, and when the inspiratory muscles end their contraction, the elastic recoil of the lung pulls the lung back to its original size and shape. This process makes the alveolar pressure positive relative to the pressure at the mouth, and air flows out of the lung. During inspiration, the respiratory muscles must overcome the elastic properties of the lung (elastic recoil) and the resistance to airflow by the airways. During expiration, the flow of air is determined primarily by the elastic recoil and airway resistance. 

The work of breathing can be calculated with a suitable model of the respiratory system. Resistance, compliance, and inertance are all present. Thus, the pressure that must be developed by the respiratory muscles is (Johnson, 1993)... 

The mechanical efficiency of the respiratory muscles is limited by the force-velocity and force-length relationships which may be modeled as linear active resistance and elastance, respectively [Mihc-Emih and Zin, 1986]. Neuromechanical efficiency may be impaired in respiratory muscle fatigue or muscle weakness, resulting in diminished Pmus for any given neural drive. 

Fernandez AB, Perez M, Soto L. Sudden respiratory muscle paralysis and apnea in a patient infected with multidrug-resistant Pseudomonas aeruginosa treated with intravenous colistin. Int J Infect Dis 2013 17(5) e357. 

FIGURE 11.4 (a) Optimal waveforms for respiratory muscle driving pressure, P(t) respiratory airflow, V and respired volume, R, during normal breathing (NL) or under various types of ventilatory loads IRL and ERL, inspiratory and expiratory resistive load lEL and CEL, inspiratory and continuous elastic load, (b) Optimal waveforms for P(t) under increasing respiratory muscle fatigue (amplitude limited upper panel) and muscle weakness (rate limited lower panel). (From Poon and coworkers [1992]. With permission.)... 

Exercise limitation and functional disability in COPD have a complex, multifactorial basis. Ventilatory limitation is caused by increased airways resistance, static and dynamic hyperinflation, increased elastic load to breathing, gas exchange disturbances, and mechanical disadvantage and/or weakness of the respiratory muscles (4-6). Car-diocirculatory disturbances (7,8), nutritional factors (9), and psychological factors, such as anxiety and fear, also contribute commonly to exercise intolerance. Skeletal muscle dysfunction is characterized by reductions in muscle mass (10,11), atrophy of type I (slow twitch, oxidative, endurance) (12,13) and type Ila (fast twitch) muscle fibers (14), altered myosin heavy chain expression (15), as well as reductions in fiber capillarization (16) and oxidative enzyme capacity (17,18). Such a dysfunction is another key factor that contributes... 

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). 

NO activates soluble guanylyl cyclase to elevate cGMP levels in vascular smooth muscle Vasodilator relaxes other smooth muscle inhalation of NO leads to increased blood flow to parts of the lung exposed to NO and decreased pulmonary vascular resistance Hypoxic respiratory failure and pulmonary hypertension Inhaled gas Toxicity Methemoglobinemia... 

On contact with moist membranes, S02 forms sulfurous acid, which is responsible for its severe irritant effects on the eyes, mucous membranes, and skin. Approximately 90% of inhaled S02 is absorbed in the upper respiratory tract, the site of its principal effect. The inhalation of S02 causes bronchial constriction parasympathetic reflexes and altered smooth muscle tone appear to be involved. Exposure to 5 ppm S02 for 10 minutes leads to increased resistance to airflow in most humans. Exposures of 5-10 ppm are reported to cause severe bronchospasm 10-20% of the healthy young adult population is estimated to be reactive to even lower concentrations. The phenomenon of adaptation to irritating concentrations has been reported in workers. However, current studies have not confirmed this phenomenon. Asthmatic individuals are especially sensitive to S02. 

When nonselective beta blockers are used, some antagonism of beta-2 receptors also occurs.2,31 The antagonism of beta-2 receptors on bronchiole smooth muscle often leads to some degree of bronchoconstric-tion and an increase in airway resistance. Although this event is usually not a problem in individuals with normal pulmonary function, patients with respiratory problems such as asthma, bronchitis, and emphysema may be adversely affected by nonselective beta antagonists. In these patients, one of the beta-1-selective drugs should be administered. 

Nitric oxide also produces vasodilation in vascular smooth muscle. As indicated earlier, hypertension may be perpetuated by a defect in the production of nitric oxide by the vascular endothelium. In follows that providing nitric oxide directly or administering precursors for nitric oxide production may help reduce vascular resistance and decrease arterial pressure in specific hypertensive syndromes.6 To date, inhaled nitric oxide has been used to treat acute pulmonary hypertension associated with respiratory distress syndrome in new-... 

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