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Query: UMLS:C0231807 (exertional dyspnea)
 3,402 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify the effect of chronotropic responsive cardiac pacing on ventilatory responses to exercise, 9 patients with chronotropic incompetence underwent paired cardiopulmonary exercise tests with fixed demand rates (AAI, VVI) and chronotropic responsive (AAIR, VVIR, DDD) pacing modes. Compared with fixed rate pacing, chronotropic responsive pacing increased peak oxygen uptake and delayed the attainment of the anaerobic threshold (AT) with a higher level of oxygen consumption (p < 0.01). Dyspnea was a major symptom that limited exercise time in 7 patients with fixed rate pacing, which was prominent with chronotropic responsive pacing. Ventilation (VE) and the ratio of ventilation to CO2 production (VE/VCO2) were consistently higher with fixed rate pacing during exercise. To compare the responses between the 2 pacing modes with the same work loads under aerobic conditions, we measured ventilatory variables one min prior to the AT as obtained with fixed rate pacing. When switching the pacing mode from fixed rate pacing to chronotropic responsive pacing, VE and VE/VCO2 decreased significantly from 22.0 +/- 7.8 to 19.8 +/- 6.8 l/min, and from 37.4 +/- 5.4 to 33.6 +/- 5.2, respectively. Tidal volume did not change, but respiratory frequency decreased more with chronotropic responsive pacing (p < 0.05). Although peak VE did not differ between the 2 pacing modes, VE/VCO2 decreased more with chronotropic responsive pacing (p < 0.01). Respiratory frequency decreased and tidal volume increased more with chronotropic responsive pacing (p < 0.05). This study suggests that chronotropic responsive cardiac pacing attenuates exertional dyspnea by improving ventilatory responses to exercise as well as increasing the cardiac output in patients with chronotropic incompetence.
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PMID:[Effects of chronotropic responsive cardiac pacing on ventilatory response to exercise in patients with bradycardia]. 133 9

To identify the effect of chronotropic responsive cardiac pacing on the ventilatory response to exercise, ten selected patients with complete atrioventricular block underwent paired cardiopulmonary exercise tests in fixed rate ventricular (VVI) and dual chamber (DDD) or rate responsive ventricular (VVIR) pacing modes. Compared to VVI pacing, DDD or VVIR pacing increased peak oxygen uptake (P < 0.005) and augmented anaerobic threshold (P < 0.001). In eight patients, dyspnea was the major symptom limiting exercise with VVI pacing and this was markedly attenuated with DDD or VVIR pacing. In all patients, ventilation (VE) and the ratio of ventilation to CO2 production (VE/VCO2) were consistently higher with VVI pacing during exercise. To compare the response of the two pacing modes at the same workloads in an aerobic condition, we measured ventilatory variables 1 minute prior to the anaerobic threshold obtained with VVI pacing. When DDD or VVIR pacing was compared with VVI pacing, VE and VE/VCO2 significantly decreased from 20.5 +/- 5.3 L/min to 18.3 +/- 5.0 L/min (P < 0.005) and from 35.9 +/- 5.8 to 31.9 +/- 5.0 (P < 0.001), respectively. Respiratory frequency rose significantly more with VVI pacing (P < 0.001) despite an unchanged tidal volume. Although peak VE did not differ between the two pacing modes, VE/VCO2 at the peak exercise increased significantly more with VVI pacing (P < 0.005). Respiratory frequency also rose more with VVI pacing (P < 0.005) and tidal volume did not change. This study suggests that chronotropic responsive cardiac pacing attenuates the exertional dyspnea by improving the ventilatory response to exercise as well as increasing the cardiac output in patients with complete atrioventricular block.
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PMID:Effects of chronotropic responsive cardiac pacing on ventilatory response to exercise in patients with complete AV block. 138 60

Two patients who presented with dyspnea on effort, persisting after insertion of a fixed rate ventricular demand pacemaker (VVI) for sick sinus syndrome, were evaluated by cardiopulmonary exercise testing. During VVI pacing a heightened ventilatory response to exercise and a fluctuation of ventilation occurred. The high ventilatory equivalent for CO2 throughout exercise with VVI pacing suggests that the patients had ventilation-perfusion mismatching due to an increase in the pulmonary capillary wedge pressure caused by 1:1 ventriculoatrial conduction. Rate responsive ventricular (VVIR) pacing associated with intact 1:1 ventriculoatrial conduction exaggerated the exertional dyspnea, while rate responsive atrial (AAIR) pacing improved the ventilatory response to exercise. We suggest that a heightened ventilatory response to exercise due to ventilation-perfusion mismatching may be an important factor causing the pacemaker syndrome, and that cardiopulmonary exercise testing is useful in identifying the exercise-induced symptoms with ventricular pacing.
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PMID:Pacemaker syndrome evaluated by cardiopulmonary exercise testing. 170 37

Pulmonary function and pulmonary gas exchange at rest, and during and after a standard exercise load of 500 kpm in 1 min on bicycle ergometer were studied in 34 women with severe, uncomplicated obesity, aged 37.8 (20-59) years, before and 1 year after gastric banding, resulting in a weight loss from 113.2 (84-156) to 81.7 (60-110) kg. Following the weight loss, TLC and VC rose from 93 and 94 per cent of expected to 98 and 101 per cent, respectively. FRC, ERV and FRC/TLC rose more markedly from 77, 64 and 83 per cent to 98, 109 and 99 per cent. IC fell from 108 to 99 per cent. RV and RV/TLV remained unchanged. FEV1.0 rose from 97 to 103 per cent, while MVV rose from 102 to 112 per cent, i.e. above normal. TLCO and PaCO2 remained unchanged, at 90 and 95 per cent, whereas PaO2 rose from 86 to 91 per cent. Resting O2 intake (VO2) decreased from 147 to 115 per cent of the expected for normal weight women, while VO2/BSA decreased from 113 to 99 per cent, the changes being greater than expected from commonly used formulas for prediction of metabolic rate. O2 cost of work (EO2) decreased from 142 to 105 per cent. Resting ventilation (V) declined from 136 to 113 per cent, while ventilatory cost of work (EV) decreased from 142 to 105 per cent. CO2 recovery time after work (CO2RT) decreased from 121 to 100 per cent, while the ratios CO2RT to EO2 and to extra CO2 output of work (ECO2) rose slightly. Thus, the loss of weight led to increased filling of the lungs, improved dynamic function, reduced ventilation/perfusion disturbances and greater than expected reduction of energy expenditure, both at rest and exercise. In the obese state there was no evidence of alveolar hypoventilation or impaired ventilatory control. The beneficial effect of weight reduction on the exertional dyspnea included a combination of marked reduction of ventilatory demands and moderate rise in ventilatory capacity.
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PMID:Pulmonary function and energy expenditure after marked weight loss in obese women: observations before and one year after gastric banding. 211 Dec 93

Elevated endorphin levels in patients with COPD may act to diminish the sensation of dyspnea. Exogenous opioids decrease exertional dyspnea and increase exercise capacity in COPD patients. The purpose of this study was to determine the effects of endogenous opioids on the exercise capacity and control of breathing in patients with COPD. We hypothesized that naloxone, an opioid antagonist, would block the endogenous endorphins and decrease the exercise capacity of our patients. Six patients (mean age, 58.8 +/- 3.2 years) with COPD (mean FEV1, 1.28 +/- 0.46 L) underwent identical incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following the IV administration of naloxone (0.4 mg/kg) (N) or placebo (P) in a randomized, double-blind fashion. Perceived dyspnea (modified Borg scale), breathing patterns, and expired gas levels were compared at rest and at maximal workload (WL). There was no significant difference after N compared with after P in the WL or the duration of work. At Emax there were no significant differences after N compared with after P in ventilation, the level of dyspnea, P0.1, VO2, or VCO2. The ventilatory response to CO2 production during exercise (delta VE/delta VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after N compared with after P. This study does not support the hypothesis that endogenous opioids play a significant role in dampening dyspnea and facilitating exercise in patients with COPD.
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PMID:Effect of naloxone on maximal exercise performance and control of ventilation in COPD. 267 90

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

We report the case of a woman, now 58 years old, with chronic respiratory failure due to spinal progressive muscular atrophy. She first noticed gradual progressive muscular weakness in her extremities in 1973. She started to complain of dyspnea on exertion in 1978. Chronic respiratory failure due to spinal progressive muscle atrophy was diagnosed in 1983. Home oxygen therapy was begun, but CO2 narcosis and exacerbation of chronic respiratory failure occurred at the end of that year. A tracheotomy was done and mechanical ventilation was begun. As her general condition improved and she could breathe without the ventilator for a few hours each day, home mechanical ventilation was begun. Seven years later, her general condition is still good and she can live without any life-threatening distress. There are few reports of patients in Japan who have survived for long periods of time with home mechanical ventilation. We believe that improvement in her respiratory care and in her social situation contributed to her long standing clinical course.
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PMID:[Chronic respiratory failure--survival for nine years with home mechanical ventilation]. 858 19

Noninvasive cardiopulmonary exercise (CPX) testing has proven useful in the assessment of heart and lung disease, including cardiac and ventilatory reserves. CPX includes the monitoring of respiratory gas exchange, O2 uptake the CO2 production, together with minute ventilation and its components--tidal volume and respiratory rate--together with surveillance of electrocardiography and blood pressure during supervised, incremental exercise. Exercise responses in anaerobic threshold and/or maximal O2 uptake are used to grade functional capacity objectively and to predict cardiac reserve (exercise cardiac output), which grades the severity of chronic cardiac or circulatory failure. CPX also serves to distinguish primary cardiac from ventilatory-based exertional dyspnea.
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PMID:What can we learn from exercise testing beyond the detection of myocardial ischemia? 925 61

Anxiety is a medical mimicker that can imitate both cardiac and neurological symptoms. Anxiety disorder research protocols regularly use hyperventilation or i.v. lactate infusion to trigger panic attacks in susceptible subjects. Susceptible patients experience panic attacks with slight decreases in CO2 or increases in lactate production seen in mild exercise such as stair climbing. To the unsuspecting physician this appears to be dyspnea on exertion. Hyperventilation during rapid eye movement (dream) sleep may trigger panic attacks in patients with panic disorder, mimicking paroxysmal nocturnal dyspnea. Syncope from panic-induced hyperventilation can mimic seizures. When panic-like anxiety is discovered in aircrew it necessitates grounding. The prognosis is frequently good after treatment with psychotherapy, with return to full flying status a strong possibility.
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PMID:You're the flight surgeon. Anxiety. 1292 69

It has been suggested that hyperventilation and the disproportionate increase in VCO2 versus VO2 above the ventilatory threshold (V(TH)) in ramp exercise are due to the production of nonmetabolic CO2 in muscle because of lactic acid buffering by plasma bicarbonate entering the cell in exchange with lactate [Wasserman, K., 1982. Dyspnea on exertion. Is it the heart or the lungs? JAMA 248, 2039-2043]. According to this model, plasma standard bicarbonate concentration decreases in a approximately 1:1 ratio with the increase in plasma lactate concentration, 1 mmol of CO2 is generated above that produced by aerobic metabolism for each mmol of lactic acid buffered, and nonmetabolic CO2 produced in the muscle is partly responsible for hyperventilation because of the resulting increase in the CO2 flow to the lungs. The present report shows that this model is not consistent with experimental data: (1) bicarbonate is not the main buffer in the muscle; (2) the decrease in standard bicarbonate concentration is not the mirror image of the increase in lactate concentration; (3) buffering by bicarbonate does not increase CO2 production in muscle (no nonmetabolic CO2 is produced in tissues); (4) the CO2 flow to the lungs, which should not be confused with VCO2 at the mouth, does not increase at a faster rate above than below V(TH). The disproportionate increase in VCO2 at the mouth above V(TH) is due to hyperventilation (not the reverse) and to the low plasma pH which both reduce the pool of bicarbonate readily available in the body.
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PMID:Lactic acid buffering, nonmetabolic CO2 and exercise hyperventilation: a critical reappraisal. 1589 May 62


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