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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxia and hypercapnic acidosis have been shown to have a negative inotropic effect on diaphragmatic contractility. The effect of combined hypercapnia and hypoxia was studied in vitro using hamster diaphragm strips. A 12% CO2, 21% O2, and 67% N2 gas mixture was used to produce hypoxic, hypercapnic acidosis. Force-frequency curves were generated using twitches and maximal tetanic contractions produced by stimulating with 0.2-ms pulses at 10 to 120 Hz for 300 to 500 ms. Moderate fatigue was then induced by repeated submaximal contractions (25 Hz, 160 ms, at the rate of 1/s for 45 contractions). Muscle strips exposed to hypoxic, hypercapnic acidosis had a decreased force response at all frequencies. The decrease in force was not different from that seen with hypoxia alone but was significantly worse than with hypercapnia alone. In the combined hypercapnic, hypoxia solution, tension produced by stimulating at 25 Hz for 160 ms was decreased to 52 +/- 11% of control (p less than 0.001). For these submaximal contractions, hypercapnic acidosis had a greater negative inotropic effect than did hypoxia alone. With repeated contractions, tension declined at a faster rate than in control, hypoxia alone, or hypercapnia alone. In the combined hypoxic, hypercapnic solution, the time constant of relaxation (tau) was increased prior to the start of the fatigue run compared to the control (tau = 35 +/- 6 versus 45 +/- 5 ms; p less than 0.001), and the tau increased at a faster rate than in control. These studies suggest that hypoxic, hypercapnic acidosis has a greater detrimental effect on the muscle than either abnormality alone and makes the muscle more susceptible to fatigue.
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PMID:Hypoxic, hypercapnic acidosis decreases tension and increases fatigue in hamster diaphragm muscle in vitro. 265 1

New technologies for the noninvasive assessment of oxygen and carbon dioxide are transforming clinical practice. Transcutaneous monitoring of PO2 (PtcO2) and PCO2 (PtCO2) provides an approximation of PaO2 and PaCO2 values in hemodynamically normal individuals, but both PtcO2 and PtcCO2 diverge from the corresponding arterial values when cardiac output is reduced, even in the absence of hypotension. Transcutaneous monitors also have relatively slow equilibration and response times. Pulse oximeters rapidly assess arterial O2 saturation, but give spurious results when dyshemoglobins (for example, carboxyhemoglobin, methemoglobin) are present in significant quantity. End-tidal CO2 (PetCO2) monitoring tracks breath-by-breath changes in ventilation, and PetCO2 approximates PaCO2 when significant physiologic dead-space is not present. Respiratory inductive plethysmography provides a semiquantitative assessment of tidal volume and the relative contribution of the thorax and abdomen to ventilation; among other uses, this technology may allow for the early detection of respiratory muscle fatigue prior to the onset of respiratory failure.
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PMID:Noninvasive monitoring of oxygen and carbon dioxide. 266 Nov 21

Normal human subjects (n = 7) breathing 21% O2 (normoxia), 13% O2 (hypoxia), or 100% O2 (hyperoxia) performed repeated maximal inspiratory maneuvers (inspiratory duration = 1.5 s, total breath duration = 3.5 s) on an "isoflow" system, which delivered a constant mouth flow (1.25 or 1 l/s) while maintaining normocapnia (5.5% end-tidal CO2). Respective mean arterial O2 saturation values (ear lobe oximetry) were 98 +/- 1, 91 +/- 4 (P less than or equal to 0.01), and 99 +/- 1% (NS). Maximal mouth pressure (Pm) was measured during inspirations at rest and during a 10-min fatigue trial, and the Pm measurements obtained during the fatigue trials were fit to an exponential equation. The parameters of the equation included the time constant (tau), which describes the rate of decay of Pm from the initial pressure (Pi) to the asymptote, or "sustainable" pressure (Ps). The mean fraction of Pm remaining at the end of the fatigue trials (Ps/Pi) was 63 +/- 5%. No significant differences in Pi, Ps, or tau were observed between O2 treatments. This suggests that fatigue of the inspiratory muscles in normal humans occurs by a mechanism that is insensitive to changes in blood O2 content that occur during inspiration of O2 in the range of 13-100%.
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PMID:Hyperoxia and moderate hypoxia fail to affect inspiratory muscle fatigue in humans. 270 19

Respiratory muscle fatigue is caused by excessive effort relative to the strength and endurance of the respiratory muscles. It can be manifested by reductions in respiratory drive (central fatigue), by impaired neuromuscular transmission (transmission fatigue), by decreased contractility (contractile fatigue), or by a combination of these factors. Respiratory muscle fatigue probably contributes to the difficulties some patients have with weaning from mechanical ventilation, the symptoms of exercise intolerance and dyspnea in chronic lung disease, and CO2 retention. Therapy depends on a reduction in the required level of respiratory effort and/or an improvement in respiratory muscle strength and endurance.
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PMID:Respiratory muscle fatigue. 283 16

The ferrihaemoglobin (HbFe3+) formation by amyl nitrite (AN) or sodium nitrite (NaNO2) was studied in different species including man, in vivo and in vitro. In in vivo studies AN was administered intravenously (i.v.), intramuscularly (i.m.), by inhalation, or orally. NaNO2 was injected i.v.. AN i.v. produced HbFe3+ much more rapidly than NaNO2 in dogs, cats, rabbits, and rats. In dogs, i.m. injection of AN was followed by a very slow linear increase in the HbFe3+ content. Inhalation of AN did not lead to HbFe3+ formation in dogs unless it was rebreathed in a closed (bag) or not completely open (gas mask) system. HbFe3+ was produced by oral AN in dogs, the effect being enhanced by addition of DMSO. Inhalation of AN by human volunteers in a gas mask and from ampoules crushed close to the nose did not induce haemoglobin oxidation to a practically significant extent, but it was associated with headache, tiredness, dizziness, and a fall in blood pressure. In in vitro studies, in contrast to NaNO2, AN produced HbFe3+ instantaneously in erythrocytes of various species and in purified human haemoglobin. AN 1 mol yielded 2 mol Fe3+. Only 20% of the oxygen released during the oxidation of haemoglobin by AN or NaNO2 was recovered. In 0.2 M phosphate buffer, pH 7.4, 0.01 mol O2/mol AN was consumed. CO2 was released in the presence of AN, but not of NaNO2, from blood, plasma, and 0.02 M NaHCO3 solution. The ratio (lactate)/(pyruvate) decreased when HbFe3+ was formed by AN or NaNO2.
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PMID:Ferrihaemoglobin formation by amyl nitrite and sodium nitrite in different species in vivo and in vitro. 290 49

H+ ions are generated rapidly when muscles are maximally activated. This results in an intracellular proton load. Typical proton loads in active muscles reach a level of 20-25 mumol X g-1, resulting in a fall in intracellular pH of 0.3-0.5 units in mammalian muscle and 0.6-0.8 units in frog muscle. In isolated frog muscles stimulated to fatigue a proton load of this magnitude is developed, and at the same time maximum isometric force is suppressed by 70-80%. Proton loss is slowed when external pH is kept low. This is paralleled by a slow recovery of contractile tension and seems to support the idea that suppression results from intracellular acidosis. Nonfatigued muscles subjected to similar intracellular proton loads by high CO2 levels show a suppression of maximal tension by only about 30%. This indicates that only a part of the suppression during fatigue is normally due to the direct effect of intracellular acidosis. Further evidence for a component of fatigue that is not due to intracellular acidosis is provided by the fact that some muscle preparations (rat diaphragm) can be fatigued with very little lactate accumulation and very low proton loads. Even under these conditions, a low external pH (6.2) can slow recovery of tension development 10-fold compared with normal pH (7.4). We must conclude that there are at least two components to fatigue. One, due to a direct effect of intracellular acidosis, acting directly on the myofibrils, accounts for a part of the suppression of contractile force. A second, which in many cases may be the major component, is not dependent on intracellular acidosis. This component seems to be due to a change of state in one or more of the steps of the excitation-contraction coupling process. Reversal of this state is sensitive to external pH which suggests that this component is accessible from the outside of the cell.
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PMID:The effect of acid-base balance on fatigue of skeletal muscle. 299 67

The intracellular pH of frog sartorius muscles exposed to an extracellular pH 8.0 (25 mM HCO3-, 1% CO2) was 6.9-7.1. Following a fatiguing stimulation period (one tetanic contraction per second for 3 min), the intracellular pH was 6.5-6.7. When similar experiments were repeated with frog sartorius muscles exposed to pH 6.4 (2mM HCO3-, 1% CO2), the intracellular pH was 6.8-6.9 at rest and 6.3-6.4 following fatigue. So, in both experiments the intracellular pH decreased by 0.4-0.5 pH unit during fatigue. When the CO2 concentration of the bathing solution was increased from 1 to 30%, the intracellular pH of resting muscles decreased from 7.0 to 6.2-6.3. Although the effect of CO2 on the intracellular pH was greater than the fatigue effect, the decrease in tetanic force with CO2 was less than 40%, while during fatigue the tetanic force decreased by at least 70%. Therefore in frog sartorius muscle the decrease in tetanic force during fatigue exceeds the decrease that is expected from just a change in intracellular pH.
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PMID:Is the change in intracellular pH during fatigue large enough to be the main cause of fatigue? 309 36

In experiments on 10 adult anaesthetized cats (pentobarbital 30 mg.kg-1 i.p.) the effect of stimultaneous hypoxia and hypercapnia was studied on the defence respiratory reflexes of the airways. Expiratory reflex and cough were elicited by mechanical stimulation of the airways mucosa, and the obtained values were evaluated on basis of the intrapleural pressure. Inhalation of the hypoxic-hypercapnic gas mixture (11% + 7% CO2 in N2) for 15 minutes led to a significant decrease of respiratory frequency, tidal volume and PaCO2, while pHa and PaCO2 also decreased significantly together with the intensity of the expiratory reflex and that of cough. Recent studies, showed that in the course of the effect of hypoxia (11% O2) and of hypercapnia (5% CO2), cough intensity decreased, but the change was not significant. The decrease of the intensity of respiratory defence reflexes under hypoxic-hypercapnic conditions might have been due to the changes of centrally controlling structures, or to the effector part of the reflex arc, resulting from fatigue of the respiratory muscles. The possible effect of anaesthesia exerting a significant influence on the intensity and character of airways defence reflexes could not be excluded.
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PMID:Effect of hypoxia and hypercapina on the airways defence reflexes. 312

Inspired by Traditional Chinese Medicine and Qigong, we designed a new anti-G maneuver, the Q-G Maneuver, which has proved promising. This maneuver consists of volition mobilization, stepwise tensing of leg and abdominal muscles, and maintenance of a shallow thoracic respiration throughout. It was tested on 24 pilots on the ground and 3 pilots on a centrifuge. All pilots were monitored with heart level blood pressure, oximetry, ear lobe pulse, CO2 concentration in exhaled gas, EEG and ECG; in centrifuge runs, peripheral vision was also monitored. Blood pressure was maintained at 180-240 mm Hg for more than 30 s without fatigue. On the centrifuge, the pilots tolerated a G load 2.25-3.0 G higher than without the maneuver, without any visual disturbance. Oximetry readings were 96-97%, and there was no evidence of hyperventilation. The ear lobe pulse was even enhanced during G load with the maneuver. Follow-up visits to 18 out of 24 pilots with 455 inflight applications of the maneuver showed that the maneuver is feasible and can be used effectively during high-G load.
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PMID:A preliminary report on a new anti-G maneuver. 319 Jun 25

The vast majority of patients who undergo mechanical ventilation are able to discontinue ventilatory assistance within a few days. Typically, patients who require only short-term mechanical ventilation do not have severe underlying lung disease, and the problem for which they require ventilatory support is most commonly rapidly reversible. In these patients on short-term ventilatory support, parameters of spontaneous ventilatory requirements and respiratory muscle strength, including minute ventilation, maximal voluntary ventilation, vital capacity, and maximal inspiratory pressure, are useful in predicting the success of discontinuation of mechanical ventilation. Ventilatory support can generally be discontinued by a variety of techniques in these patients without the need for weaning from the ventilator per se. The smaller group of patients in whom it is not possible to discontinue mechanical ventilation within less than 7 days comprises individuals who frequently have severe acute or chronic lung disease, multisystem extrapulmonary disease, or neuromuscular disease. After a period of prolonged mechanical ventilatory support, these complicated patients require a process of progressive weaning in which they gradually become able to support spontaneous ventilation. Spontaneous ventilatory parameters do not correlate well with weaning ability in patients on long-term ventilatory support. A systematic and comprehensive approach in which attention is focused on optimizing pulmonary and nonpulmonary factors that affect the weaning process provides the best chance for successful withdrawal of ventilatory support after long-term mechanical ventilation. Inadequate ventilatory drive, respiratory muscle weakness and fatigue, increased work of breathing, excessive CO2 production, and cardiac failure are potential mechanisms that may play a role in inhibiting successful weaning. Adverse factors relevant to each of these mechanisms must be addressed and corrected to whatever extent possible. Studies have not demonstrated the superiority of either classic T-piece weaning or IMV weaning methods in difficult-to-wean patients on long-term ventilatory support. Both techniques may be used successfully as long as all patient variables that may adversely affect weaning ability are corrected or optimized and close care and attention to the details of the weaning process itself are provided.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Discontinuation of mechanical ventilation. 328 Feb 25


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