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At least 1,315 records · Page 73Linked to original sources
PubMed1995

Considerations when testing and training the respiratory muscles.

The purpose of this review is to describe the muscles of respiration, mechanisms that lead to their dysfunction, and unique features of the respiratory muscles that should be considered when designing testing and training protocols for patients with respiratory compromise. The diaphragm's unique shape is an important determinant of its function. Respiratory pathophysiology combined with systemic abnormalities may result in inspiratory muscle weakness, fatigue, and injury. The specificity of training principle, as it applies to respiratory muscle training in patients with respiratory compromise, will be described. Precautions related to this type of training will also be outlined. In conclusion, a better understanding of the mechanisms contributing to inspiratory muscle dysfunction will assist physical therapists in designing the most appropriate training programs. This article, along with the other articles in this focus on respiratory muscle training, will provide therapists with scientifically based guidelines for rehabilitation of patients with impaired respiratory muscle function.

Breathing Exercises↗
PubMedDate not supplied

[Physiological mechanisms limiting external respiratory resistance].

A study was performed on 8 healthy male subjects to investigate the effect of nonelastic resistance 6-40 GPa (the air flow velocity being 90 l/min) on the duration of proprioceptive reflexes of respiratory muscles, volume and velocity parameters of forced exhalation. Resistances of 15 and 25 GPa combined with a workload of 100-150 W increased the duration of proprioceptive reflexes from 0.18 +/- 0.015 to 0.29 +/- 0.012 sec and to 0.38 +/- 0.06 sec, respectively, which indicates fatigue of respiratory muscles. Resistance of 25 GPa reduced significantly (by 55%) the maximum volume velocity of forced exhalation and increased its duration by 31%, the exhalation volume decreasing insignificantly (by 6%). The major factor limiting man's tolerance to external respiration resistance is functional deficiency of proprioceptive regulation of respiration and strength and velocity of respiratory muscles.

Adolescent↗
PubMed1976

Some characteristics of neuromuscular block in the respiratory musculature in anaesthetized man.

The ability to breathe against a mild expiratory obstruction was examined in 64 adult patients under halothane-nitrous oxide-oxygen anaesthesia. The trachea of all patients were incubated. It was found that d-tubocurarine 0.11 mg/kg blocked the respiratory musculature by 50 per cent. The onset of block was immediate, with the peak effect reached within one minute. The duration of block was either very short (1 to 2 minutes) or long (paralleling the blockade in the thumb twitch), depending upon the dose of d-tubocurarine. Following injection of a small dose (up to 0.1 mg/kg) the respiratory musculature might be blocked by 30 per cent but for only one minute, disproportionately short as compared with the thumb twitch. Following injection of a large dose (0.1-0.3 mg/kg) the duration was long, but the recovery was only slightly ahead of the thumb. Following an intermediate dose, a biaphasic pattern was observed. An initial partial recovery was observed during the first 1 to 2 minutes. Comparison of the respiratory musculature and the thumb twitch revealed that the respiratory musculature was highly sensitive to block and has a different time course. Succinylcholine 0.08 mg/kg blocked the respiratory force by 50 per cent with a time course similar to the block in the thumb twitch. The clinical significance of these observations are discussed.

Abdominal Muscles↗
PubMed1985

Respiratory muscle fatigue: a cause of ventilatory failure in septic shock.

The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Escherichia coli endotoxin (Difco Laboratories, 10 mg/kg). Diaphragmatic (Edi) and parasternal intercostal (Eic) electromyograms were recorded using fishhook electrodes. The recorded signals were then rectified and electrically integrated. Pleural, abdominal, and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system. After a short control period, the endotoxin was administered slowly intravenously (within 5 min). Death was secondary to respiratory arrest in all animals. All animals died within 150-270 min after the onset of endotoxic shock. Within 45-80 min of the endotoxin administration, mean blood pressure and cardiac output dropped to 42.1 +/- 4.1 and 40.1 +/- 6.0% (mean +/- SE) of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased from control values of 0.27 +/- 0.03 l X s-1 and 5.75 +/- 0.7 cmH2O to mean values of 0.44 +/- 0.3 l X s-1 and 8.70 +/- 1.05 cmH2O and then decreased to 0.17 +/- 0.03 l X s-1 and 3.90 +/- 0.30 cmH2O before the death of the animals. There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 360 +/- 21 and 263 +/- 22% of control, respectively, before the death of the animals. None of the dogs were hypoxic. Arterial PCO2 decreased from a control value of 42.9 +/- 1.7 Torr to a mean value of 29.9 +/- 2.8 Torr and then increased to 51 +/- 4.3 Torr before the death of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Respiratory muscle dynamics and control during exercise with externally imposed expiratory flow limitation.

To determine how decreasing velocity of shortening (U) of expiratory muscles affects breathing during exercise, six normal men performed incremental exercise with externally imposed expiratory flow limitation (EFLe) at approximately 1 l/s. We measured volumes of chest wall, lung- and diaphragm-apposed rib cage (Vrc,p and Vrc,a, respectively), and abdomen (Vab) by optoelectronic plethysmography; esophageal, gastric, and transdiaphragmatic pressures (Pdi); and end-tidal CO2 concentration. From these, we calculated velocity of shortening and power (W) of diaphragm, rib cage, and abdominal muscles (di, rcm, ab, respectively). EFLe forced a decrease in Uab, which increased Pab and which lasted well into inspiration. This imposed a load, overcome by preinspiratory diaphragm contraction. Udi and inspiratory Urcm increased, reducing their ability to generate pressure. Pdi, Prcm, and Wab increased, indicating an increased central drive to all muscle groups secondary to hypercapnia, which developed in all subjects. These results suggest a vicious cycle in which EFLe decreases Uab, increasing Pab and exacerbating the hypercapnia, which increases central drive increasing Pab even more, leading to further CO2 retention, and so forth.

Abdominal Muscles↗
PubMed1983

Mechanical load and inspiratory muscle action during induced asthma.

To examine the relationship between inspiratory mechanical load in asthma and the pattern of respiratory muscle recruitment, we studied lung and chest wall mechanics in 7 asymptomatic asthmatics in whom progressive bronchoconstriction was induced with inhaled aerosolized histamine. A fall in the FEV1 to 49.5 +/- 3.9% of the control value (mean +/- 1 SE) was associated with a 10.7-fold increase in the inspiratory work rate of the inspiratory muscles from 6.7 +/- 1.6 to 71.4 +/- 11.4 Joules/min. Elastic work accounted for 69% of the total work during the control period and 57% at the maximal level of bronchoconstriction studied. The net pressure-time product for the inspiratory muscles, measured over 1 min, rose fivefold from 245 +/- 33 cmH2O.s to a maximum of 1,211 +/- 107 cmH2O.s, indicating a relatively greater increase in the recruitment of the intercostal/accessory muscles of inspiration. The abdominal muscles, which were recruited during bronchoconstriction, relaxed during inspiration, and permitted outward movement of the abdominal wall with progressively smaller net increases in Pga. We concluded that during induced asthma (1) the increase in inspiratory muscle work was largely the result of hyperinflation, (2) the recruitment of the intercostal/accessory muscles exceeded that of the diaphragm, and (3) the combined action of the intercostal/accessory and abdominal muscles favored the diaphragm.

Abdominal Muscles↗