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We discuss three cases of diaphragmatic flutter in patients with extreme polypnea and symptoms of respiratory alkalosis. Initially, the diagnosis for each case was HVS. However, analysis of the respiratory pattern during attacks revealed two frequencies. A fast respiratory rhythm (230 to 250 breaths per minute) was superimposed on a slow rhythm (15 to 30 breaths per minute). The fast rhythm maintained blood gases at normal limits or hypocapnic levels. The dual respiratory rhythms, which do not occur with HVS, indicated diaphragmatic flutter. In addition, the usual treatment for HVS-breathing CO2 mixed air-did not influence the attacks. For two of the three patients, an intravenous dose of DPH suppressed the abnormal respiratory patterns immediately and completely. The third patient responded to an intramuscular injection of haloperidol. For these cases, the dual respiratory rhythms were the key to diagnosis of diaphragmatic flutter which accompanied hyperventilation.

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The patient was a 67-year-old male. A diagnosis of sarcoidosis was made both by transbronchial lung biopsy and by scalene node biopsy. The findings of his chest roentgenogram were categorized as the group II. There were no symptoms during follow-up period of one year at the out-patient clinic with no medication. The chest X-ray findings of the patient were slowly progressive. Intractable hiccup developed one year after his first visit to the hospital. With administration of prednisolone, serum angiotensin converting enzyme level decreased promptly, and the incidence of the hiccup attack decreased. As the dose of prednisolone was tapered, the hiccup recurred. All the drugs used for hiccup including quinidine sulfate and metoclopramide was not effective. A thoracic CT revealed slight enlargement of mediastinal lymph nodes. A brain CT and a brain MRI demonstrated no abnormalities. Acetazolamide, which induces acidosis in brain extra-cellular fluid, worsened the symptoms. As prednisolone was given again, infiltrates on the chest roentgenogram began to resolve and the incidence of hiccup decreased. We concluded that the long-standing hiccup observed in this patient may be brought by the lesion in central nervous system due to sarcoidosis.

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Cardiovascular deconditioning (CD) has been reported to occur in weightlessness, bed rest, and head-out water immersion. An expanded intrathoracic blood volume results, at least initially, in all these diverse conditions. Subjects in hyperbaric environments exhibit cephalad redistribution of blood volume, which also occurs in weightlessness, bed rest, and head-out water immersion. This physiologic similarity led us to suspect that CD may also occur as a consequence of hyperbaric exposure. We examined this possibility in 3 young male subjects during a 7-d dry saturation dive at 31 ATA. Changes in blood pressure, heart rate, and stroke volume were measured before and during 15 min of the 90 degree body tilt. These changes, expressed either singly or in combination, provided indications of CD during and immediately after hyperbaric exposure. One of the principal indicators of CD was the inability to exert adequate vasoconstriction. In addition, 1 subject fainted during hyperbaric exposure, whereas no such episode occurred before or after the exposure. These findings suggest that inappropriate orthostatic reflexes may be evoked by hyperbaria and reduced physical activity over the period of confinement. It should be noted, however, that CD was already evident within 24 h of hyperbaric exposure, suggesting that the initial phase of CD was unrelated to physical confinement. We postulate that CD occurs during hyperbaric exposure as an expression of cardiovascular and neurohumoral adaptation to an expanded central blood volume with a reduced total blood volume.

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The effects of two different combination chemotherapies, i.e. cyclophosphamide (CPM) + vincristine (VCR) + methotrexate (MTX) and ACNU + VCR, with or without radiotherapy, were studied in twenty patients with untreated small cell carcinoma of the lung. Respective response rates were 66.7% for CVM and 50% for AV. Median survival time was 51 weeks for CVM and 27 weeks for AV. There was no statistically significant difference between the survival probability curves of CVM and AV. Concerning toxicity, two hazardous side effects, myelosuppression and interstitial pneumonitis, were observed although the incidences were low. We concluded that both regimens are useful as chemotherapy of small cell carcinoma.

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A case of diaphragmatic flutter following status asthmaticus is presented. The initial symptom was tachypnea resembling hyperventilation syndrome. When spontaneous ventilation was completely suppressed for 15 minutes with intravenous administration of pethidine, levels of arterial blood gases were not much deviated from normal limits, because of possible high frequency ventilation. Although the medical therapeutics previously reported in literatures, including diphenylhydantoin, were ineffective in this case, butylophenones provided favourable results despite of some complications. The etiology and management of diaphragmatic flutter are discussed.

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A 22-year-old female patient presenting complete atrioventricular block and giant P waves in electrocardiogram had anomalous pulmonary venous drainage from the entire left lung. There was normal drainage from the right lung and no associated atrial septal defect or other intracardiac abnormalities. After a permanent pacemaker was implanted, she manifested signs and symptoms of heart failure. Although the anomalous pulmonary vein was anastomosed to the left atrium, intractable heart failure continued. She died six months later after surgical intervention. Postmortem examination revealed diffuse interstitial fibrosis throughout the myocardium.

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