Phrenic nerve injury.
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Biomedical subjects
Publications and source records attributed to N M Braun.
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Of 1225 patients undergoing open heart surgery over an 18-month period, 13 had diaphragmatic dysfunction due to phrenic nerve injury; 11 of these had internal mammary artery grafting. Nine had diaphragmatic dysfunction on the same side as the internal mammary artery graft side (7 bilateral and 2 unilateral) as determined by fluoroscopy during phrenic nerve stimulation. Although topical cardiac hypothermia has been the prevailing mechanism for diaphragmatic dysfunction due to phrenic nerve injury after open-heart surgery, dissection of the internal mammary artery with electrocautery, traction, or vascular compromise to the phrenic nerve, or a combination, could be additional factors. Rocking bed ventilation was instituted to facilitate passive diaphragmatic movement and airway decannulation and was continued at home until the phrenic nerve or nerves recovered. These patients were followed up clinically and with serial measurements of vital capacity, respiratory muscle strength, phrenic nerve latency, and fluoroscopy to determine recovery rate. Phrenic nerve recovery occurred from 4 to 27 months after surgery. This recovery was heralded by the patients' ability to assume the supine position without dyspnea when use of the rocking bed was discontinued. Unilateral diaphragmatic recovery was sufficient for the restoration of symptom-free supine posture.
A 19-year-old man with SCI at C5 suffered recurrent life-threatening bradycardia and asystole. We detail his course, which included continual movement in a motion bed and propantheline-bromide (Pro-Banthine) therapy, over 3 1/2 months. Possible causes of bradycardia and autonomic dysfunction in this setting are discussed.
More than 150 years have passed since the birth of the idea of intermittent mechanical ventilation. Many types of ventilatory disorders can result in excessive loading of the respiratory muscles, thus causing them to fail. We now have several types of ventilatory assist devices to choose from so that we can select a system that fulfills the physical, physiologic, and psychological needs of patients and return them to a more satisfactory level of living in the home. This is successful when the care team and the patient and family set realistic goals and maintain close clinical supervision. Much more study is needed to determine the optimal times for respiratory muscle rest. Future technologic designs for ventilatory systems should aim to decrease cost and increase efficiency, ease of use, and durability.
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Inspiratory muscle strength in COPD could be reduced either because of mechanical disadvantage consequent to increased lung volume or because respiratory muscles share in generalized muscle weakness. To assess the relative contributions of these factors, we measured maximal inspiratory and expiratory pressures (Pimax, Pemax, cmH2O) at RV and TLC, respectively, in 32 patients with COPD. The TLC, RV, and diaphragm length index at RV (DLI, cm/cm height) were determined roentgenographically and compared with values from 22 normal subjects studied at comparable lung volume. Half the patients with COPD had normal and half had low values of Pemax, but both groups had similar values of TLC, RV, and DLI. In patients with COPD, Pimax correlated (p less than 0.001) with Pemax (r = 0.73) and DLI (r = 0.64). The slope of the Pimax-DLI relationship was essentially the same in both groups of patients with COPD as it was in the normal subjects. However, at any value of DLI, Pimax was in the normal range in patients with normal Pemax, but significantly lower in patients with low Pemax (p less than 0.001). Expressing Pimax as a combined function of Pemax and DLI yielded the highest correlation (r = 0.84, p less than 0.001), with Pemax explaining 46% and DLI explaining 35% of the variance in Plmax not explained by the other variable alone (p less than 0.001). The PaCO2 was elevated in 13 of 18 patients whose Pimax was less than 55 cm H2O, and inversely correlated with Pimax (r = -0.66, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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A 58-year-old woman with high fever, dyspnea, rapidly progressive hypoxemia and opacification of the lung fields presented the clinical picture of catastrophic respiratory failure. Extracorporeal support of oxygenation using a membrane oxygenator and a new ventricle pump was initially successful. At autopsy, miliary tuberculosis was found to be the cause of this "shock lung like" syndrome.
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