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Biomedical subjects

C Roussos

Publications and source records attributed to C Roussos.

At least 181 records · Page 10Linked to original sources
PubMed1981

The pathophysiology of inspiratory muscle fatigue.

The critical value of the rate of energy consumption of the inspiratory muscles above which fatigue occurs appears in some instances to be predictable from the relationship between energy demands and energy supplies rather than from the percentage of fatigue-resistant fibres in the inspiratory muscles. When this is the case the critical value of the external power produced by the inspiratory muscles is given by the product of muscular efficiency and the rate at which energy is supplied. Efficiency is reduced by hyperinflation and recruitment of the intercostal and accessory muscles of inspiration. The rate at which energy is supplied is decreased in states characterized by low cardiac output. The condition of low cardiac output, combined with the high oxygen cost of breathing against fatiguing loads, may be lethal in cardiogenic shock. Although the immediate cause of fatigue may not be related to reduced energy supplies, clinically useful predictions of conditions predisposing to fatigue result from an understanding of factors determining the balance between the energy demands and supplies of the inspiratory muscles. These predictions aid in the diagnosis of inspiratory muscle fatigue and have important therapeutic implications.

Animals↗
PubMed1981

Detection of diaphragmatic fatigue in man by phrenic stimulation.

Transdiaphragmatic pressure (Pdi) was measured at functional residual capacity (FRC) in four normal seated subjects during supramaximal, supraclavicular transcutaneous stimulation of one phrenic nerve (10, 20, 50, and 100 Hz--0.1 ms duration) before and after diaphragmatic fatigue, produced by breathing through a high alinear inspiratory resistance. Constancy of chest wall configuration was achieved by placing a cast around the abdomen and the lower one-fourth of the rib cage. Pdi increased with frequency of stimulation, so that at 10, 20, and 50 Hz, the Pdi generated was 32 +/- 4 (SE), 70 +/- 3, and 98 +/- 2% of Pdi at 100 Hz, respectively. After diaphragmatic fatigue, Pdi was less than control at all frequencies of stimulation. Recovery for high stimulation frequencies was complete at 10 min, but at low stimulation frequencies recovery was slow: after 30 min of recovery, Pdi at 20 Hz was 31 +/- 7% of the control value. It is concluded that diaphragmatic fatigue can be detected in man by transcutaneous stimulation of the phrenic nerve and that diaphragmatic strength after fatigue recovers faster at high than at low frequencies of stimulation. Furthermore, it is suggested that this long-lasting element of fatigue might occur in patients with chronic obstructive lung disease, predisposing them to respiratory failure.

Adult↗
PubMed1981

Respiratory muscle fatigue during cardiogenic shock.

The effect of cardiogenic shock (tamponade) on respiratory muscles performance was studied in 13 dogs breathing spontaneously. These 13 dogs were compared with 7 dogs artificially ventilated and paralyzed. Cardiac output amounted in both groups to 25-35% of the control value and was maintained constant. None of the dogs were hypoxic. All the spontaneously breathing dogs died on the average 140 +/- 15 min after the onset of cardiogenic shock, whereas the seven dogs artificially ventilated were all alive after 3 h and then killed. Death in the spontaneously breathing dogs was secondary to respiratory failure. Transdiaphragmatic pressure increased during the 1st h by 152 +/- 25% of control and then decreased by 286 +/- 18% in relation to the peak value before the death of the animals. No major changes in the mechanical properties of the respiratory system occurred. The decrease in transdiaphragmatic pressure occurred despite a marked increase per breath in the amplitude of the integrated electrical activity of the diaphragm and of the phrenic nerve. It is concluded that the ventilatory failure of cardiogenic shock is due to an impairment of the contractile process of the respiratory muscles. Artificial ventilation avoids respiratory failure and prolongs survival, which may bear important therapeutic implications.

Animals↗
PubMed1981

The failing inspiratory muscles under normoxic and hypoxic conditions.

The effects of hypoxemia on inspiratory muscle fatigue were assessed in 4 normal subjects. They breathed to exhaustion through high inspiratory resistances producing an inspiratory mouth pressure (Pm) of about 80% of maximal mouth pressure. The endurance time (tlim) during hypoxia (13% O2) was found to be shorter than that while breathing room air at equal inspiratory mouth pressures. Endurance time during hypoxia was also compared with that while breathing room air at equal rates of energy consumption (C), assuming that C is proportional to: Formula: (See Text). At these equal rates, endurance time during hypoxia still remained shorter than that during normoxia. Fatigue was also assessed by measuring the electromyographic power spectrum of the diaphragm and the parasternal intercostals. The power spectrum shifted towards low frequencies during fatigue and a greater rate of shift was observed under hypoxic conditions. The rate of lactate production during hypoxemia was greater than that during normoxia; however, blood lactate concentrations at the end of the tests were similar under both conditions. It was concluded that respiratory muscles, working against high inspiratory resistances, fall as pressure generators sooner during low oxygen breathing. The effect of low oxygen breathing on inspiratory muscle fatigue resulted in a shorter endurance time, a faster rate in the shift of the electromyographic power spectrum, and a greater rate of increase in blood lactate concentrations.

Diaphragm↗
PubMed1979

The interaction between the diaphragm, intercostal/accessory muscles of inspiration and the rib cage.

During Mueller maneuvers (MM), the volume change of rib cage, delta Vrc, and abdomen, delta Vab, are equal and opposite. Thus delta Vrc = -delta Vab. Substituting delta Prc.Crc for delta Vrc and delta Pab.Cab for delta Vab yields: delta Prc = - delta Pab.Cab/Crc, where delta Prc, delta Pab, Crc and Cab are applied pressures and compliances of rib cage and abdomen respectively. MM performed solely with the diaphragm permits calculations of Prc in terms of observed changes in Pab and pleural pressure, Ppl. Three trained subjects performed MM with no evidence of inspiratory intercostal or abdominal muscle contraction. During the diaphragmatic MM delta Pab was positive and delta Prc negative. The magnitude of delta Prc/delta Pab was 2-6 times greater than that of delta Ppl/delta Pab. We conclude that neither Pab nor Ppl by themselves displace the relaxed rib cage during Mueller maneuvers. A model in which the diaphragm acts both in parallel and in series with the rib cage, and in which Prc is the sum of Pab and a pressure lying between Pab and Ppl explains these results as well as the hypothesis that Pab displaces the relaxed rib cage during quiet breathing.

Diaphragm↗
PubMed1979

Influence of immersion to the neck in water on airway closure and distribution of perfusion in man.

We measured closing volume (CV), expiratory reserve volume (ERV) regional distribution of lung volume (Vr) and perfusion in 7 normal subjects in air and during immersion to the neck in water. In four subjects immersion resulted in a CV greater than ERV and the normal perfusion distribution became inverted. In the other subjects, ERV remained larger than CV and perfusion distribution during immersion was uniform, not inverted. In 5 subjects closing volume increased and in 3 of them, the ratio of apical/basal Vr increased significantly during immersion. One subject had nomeasurable CV and in the other it was not measured. The data suggest: (1) that when CV is greater than ERV during immersion there is an inversion of the normal perfusion distribution, caused by hypoxia and/or an increase in mean alveolar pressure in the alveoli beyond the closed airways, and (2) that an increase in pleural pressure gradient during immersion may contribute to the increase in C.V.

Adolescent↗
PubMed1979

Fatigue of inspiratory muscles and their synergic behavior.

The time (tlim) required to produce inspiratory muscle fatigue was measured in five normal subjects breathing at functional residual capacity (FRC) against a variety of high inspiratory resistive loads. In every breathing test the subjects generated with each inspiration a mouth pressure (Pm) that was a predetermined fraction of maximum Pm (Pmmax). They continued breathing until they were unable to generate this Pm. The Pm/Pmmax that could be generated indefinitely (Pmcrit) was around 60%. The inspiratory power output at that level of breathing was 6.6 kg.m/min (Wcrit). In three of those subjects the same experiment was conducted at an end-expiratory volume of FRC + one-half inspiratory capacity (1/2IC). The higher lung volume was actively maintained by the subjects watching end-expiratory transpulmonary pressure on an oscilloscope. For any fraction of the maximum mouth pressure at FRC + 1/2IC (Pm'max), tlim was shorter than FRC. Pmcrit decreased to 30% Pm'max and Wcrit to 2.6 kg.m/min. Monitoring the abdominal pressure revealed that the contribution of the diaphragm and intercostal accessory muscles alternated in time, possibly postponing the onset of fatigue.

Diaphragm↗
PubMed1978

Partitioning of inspiratory pressure swings between diaphragm and intercostal/accessory muscles.

We tested the hypothesis that the inspiratory pressure swings across the rib-cage pathway are the sum of transdiaphragmatic pressure (Pdi) and the pressures developed by the intercostal/accessory muscles (Pic). If correct, Pic can only contribute to lowering pleural pressure (Ppl), to the extent that it lowers abdominal pressure (Pab). To test this we measured Pab and Ppl during during Mueller maneuvers in which deltaPab = 0. Because there was no outward displacement of the rib cage, Pic must have contributed to deltaPpl, as did Pdi. Under these conditions the total pressure developed by the inspiratory muscles across the rib-cage pathway was less than Pdi + Pic. Therefore, we rejected the hypothesis. A plot of Pab vs. Ppl during relaxation allows partitioning of the diaphragmatic and intercostal/accessory muscle contributions to inspiratory pressure swings. The analysis indicates that the diaphragm can act both as a fixator, preventing transmission of Ppl to the abdomen and as an agonist. When abdominal muscles remain relaxed it only assumes the latter role to the extent that Pab increases.

Diaphragm↗