Chest
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In 12 patients requiring therapy with mechanical ventilation for acute respiratory failure, total static compliance (Cst) increased from 29 +/- 4 ml/cm H2O at a tidal volume (TV) of 5 ml/kg to 42 +/- 7 ml/cm H2O at a TV of 15 ml/kg. Similarly, Cst increased from 42 +/- 7 ml/cm H2O to 52 +/- 8 ml/cm H2O between 0 and 6 cm H2O of positive end-expiratory pressure (PEEP). At high levels of pulmonary inflation (ie, high PEEP and large TV) compliance decreased. ⋯ Two mechanisms may be responsible for the changes in compliance. First, varying TV or PEEP will alter the position of tidal ventilation on the pressure-volume curve, resulting in an increase in compliance with increasing TV and PEEP up to a point, where overdistention occurs and compliance decreases. Secondly, the function of the surface-lowering substance may be altered in acute pulmonary parenchymal disease, thus disturbing the regulation of surface tension over the range of pulmonary inflation studied.
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The findings in a patient who developed a fatal pneumopericardium following tracheostomy are reported. This complication of tracheostomy does not appear to have been reported previously in the literature.. When recognized, pneumopericardium is a treatable lesion, and clinicians should be aware of this potential complication.
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Coronary arterial dissection is extremely rare. Such dissections have been reported to occur secondary to atherosclerosis, trauma, the postpartum state, and cystic medial necrosis and to be iatrogenically induced during catheterization. ⋯ This report describes a 31-year-old man who presented with an acute inferior myocardial infarction. Coronary arteriographic studies demonstrated a dissection of the right coronary artery.
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In this report, we present the findings in a patient who had paroxysmal supraventricular tachycardia and atrial flutter associated with the Wolff-Parkinson-White syndrome. During atrial flutter, localized atrial fibrillation was recorded in the coronary sinus (dissimilar atrial rhythms), near the accessory pathway; and during 90 minutes of observation, ventricular activation occurred solely over the normal pathway. We postulate that localized atrial fibrillation repetitively invaded the accessory pathway and rendered it refractory to conduction by flutter impulses.