To determine the mechanisms of pulsus paradoxus during asthma, six subjects known to have cold air bronchial hyperreactivity were studied while in a quiescent phase of their disease. All were free of significant airway obstruction at the time of study. After placement of an esophageal balloon to estimate intrathoracic pressure, the subjects were assessed during quiet breathing, resistive airway loading and then during a stable period of airway obstruction induced by cold air. Steady state left ventricular volume and performance were measured using radionuclide ventriculography; right ventricular volume was calculated from the stroke volume ratio and right ventricular ejection fraction. Cardiac cycles were segregated according to their occurrence in inspiration or expiration using a flow signal from a pneumotachograph. Combined inspiratory and expiratory resistance produced pulsus paradoxus and changes in esophageal pressure that were similar to those during asthma and significantly greater than those during quiet breathing. These changes were accompanied by decreases in left ventricular diastolic volume and stroke volume during inspiration, and increases in these variables during expiration; right ventricular volume and stroke volume demonstrated changes reciprocal to those seen in the left ventricle. These data indicate that during periods of increase in airway resistance, abnormal pulsus paradoxus results from an exaggeration in the normal inspiratory-expiratory difference in stroke volume mediated primarily by the effects of intrathoracic pressure on ventricular preload.
In this report, we describe two pacemaker dependent patients with outer-coil fractures in their bipolar ventricular leads who averted potentially catastrophic consequences because of a new safety feature incorporated into their pulse generators (Intermedics Cosmos II, model 284-05). Both patients were asymptomatic; the malfunctions were discovered at routine pacemaker evaluation. Magnet application resulted in symptomatic loss of ventricular capture. In each instance, the pulse generator detected an outer-coil fracture and reprogrammed itself from bipolar DDD to unipolar DOO pacing to prevent loss of capture. Subsequent lead replacement resulted in resumption of normal function. We suggest that this feature be incorporated into all devices with programmable polarity.
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