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עמוד בית
Thu, 21.11.24

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September 2008
I. Ben-Dov, N. Kaminski, N. Reichert, J. Rosenman and T. Shulimzon
Diaphragmatic paralysis has a predictable effect on lung function. However, the symptoms depend on the preexisting heart-lung diseases and may mimic various cardiorespiratory processes. We describe the presentation in six patients. In a fit man, unilateral diaphragmatic paralysis caused dyspnea only at strenuous exercise. In a patient with emphysema it caused dyspnea mainly when carrying light weights. In another patient with emphysema it caused life-threatening hypoxemia simulating parenchymal lung disease. A patient with mild chronic obstructive lung disease and nocturnal wheezing following the onset of ULDP[1] was believed for 15 years to have asthma. A patient with bilateral diaphragmatic weakness had severe choking sensation only in the supine position, simulating upper airway obstruction or heart failure. A female patient suffered nocturnal sweating due to ULDP. The clinical manifestations of diaphragmatic paralysis vary and can mimic a wide range of cardiorespiratory diseases. 





[1] ULDP = unilateral diaphragmatic paralysis


March 2005
R. Reuveny, I. Ben-Dov, M. Gaides and N. Reichert
Background: One mechanism that may limit training effect in chronic obstructive pulmonary disease is the ventilatory limitation and associated dyspnea. 

Objectives: To minimize ventilatory limitation during training of patients with severe COPD[1] by applying bi-level positive pressure ventilation during training in order to augment training intensity (and effect).

Methods: The study group comprised 19 patients (18 males, 1 female) with a mean age of 64 ± 9 years. Mean forced expiratory volume in 1 second was 32 ± 4% of predicted, and all were ventilatory-limited (exercise breathing reserve 3 ± 9 L/min, normal >15 L/min). The patients were randomized: 9 were assigned to training with BiPAP[2] and 10 to standard training. All were trained on a treadmill for 2 months, twice a week, 45 minutes each time, at maximal tolerated load. Incremental maximal unsupported exercise test was performed before and at the end of the training period.

Results: BiPAP resulted in an increment of 94 ± 53% in training speed during these 2 months, as compared to 41 ± 19% increment in the control group (P < 0.005). Training with BiPAP yielded an average increase in maximal oxygen uptake of 23 ± 16% (P < 0.005), anaerobic threshold of 11 ± 12% (P < 0.05) and peak O2 pulse of 20 ± 19% (P < 0.05), while peak exercise lactate concentration was not higher after training. Interestingly, in the BiPAP group, peak exercise ventilation was also 17 ± 20% higher after training (P < 0.05). Furthermore, contrary to our expectation, at any given work rate, ventilation (and tidal volume) in the BiPAP group was higher in the post-training test as compared to the pre-training test, and the end tidal partial pressure of CO2 at 55 watts was lower, 40 ± 4 and 38 ± 4 mmHg respectively (P < 0.05). No improvement in exercise capacity was observed after this short training period in the control group.

Conclusion: Pressure-supported ventilation during training is feasible in patients with severe COPD and it augments the training effect. The improved exercise tolerance was associated with higher ventilatory response and therefore lower PETCO2[3] at equal work rates after training.

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[1] COPD = chronic obstructive pulmonary disease

[2] BiPAP = bi-level positive pressure ventilation

[3] PETCO2 = end tidal partial pressure of CO2
 

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