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We demonstrated a constant and significant increase in inspiratory systolic, diastolic and pulse arterial pressures during MAST inflation while expiratory pressures remained unchanged. In consequence, delta systolic (paradoxic pulse), delta diastolic and delta pulse pressures all decreased. All pressures returned to baseline values in inspiration after MAST deflation.

Respiratory and heart rates were unchanged during the whole MAST procedure, suggesting that there had been no change in airway obstruction during the limited duration of the protocol.

Criticsm of Methodology

The choice of MAST inflation for realizing a rapid filling test seems most appropriate in such patients. Indeed, this method has two advantages: (1) reversi­bility of volume loading in a situation in which vigorous fluid therapy may promote pulmonary edema, and (2) the possibility for a patient to be his own control: the short duration of the protocol and the reversibility allowed us to check for the absence of other causes (such as airway obstruction improvement) to explain the variations of arterial pressures.

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We included ten procedures for nine patients. A single patient was admitted twice in the same week for two distinct severe bronchial asthma episodes. All patients had evidence of respiratory and circulatory failure with alveolar hypoventilation, hypoxia, tachy­cardia and metabolic acidosis with hyperlactacidemia (Tables 1 and 2). No patient had hypotension (Fig 1) but during the inspiratory phase, five had systolic pressure below 100 mm Hg and diastolic pressure less than 70 mm Hg. For these five patients the pulse pressure was below 30 mm Hg (Fig 2). We observed no difference in respiratory and heart rates during MAST inflation (Table 2). Radial systolic, diastolic and pulse pressures were not significantly changed by MAST inflation during the expiratory phase (Fig 1 and 2) but all three parameters significantly increased during the inspiratory phase (Fig 1 and 2) for each individual patient. Pressure variations between inspi­ration and expiration (delta pressures) were markedly decreased by MAST inflation (Fig 3); delta systolic (ie, paradoxic pulse): 44.3 ±20.3 vs 27.5 ±13.0 mm Hg; delta diastolic: 26.2 ±9.4 vs 19.5 ±7.4 mm Hg. Delta pulse pressure was also significantly decreased by MAST inflation (18.5±11.8 vs 8.0±6.5 mm Hg). After MAST deflation, all patients returned to baseline values.

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Patients

We prospectively studied all patients admitted to the hospital for asthma between August 1986 and January 1988. The following protocol was accepted by the ethical committee of our institution. To be included in the study, patients met the following criteria: (1) age between 15 and 65 years old; (2) no evidence of previous cardiac or renal disease; (3) a clear past history of reversible airway obstruction of allergic or idiopathic etiology; (4) evidence for actual episode of asthma; (5) no chest x-ray evidence of emphysema, chronic bronchopathy, interstitial or other restrictive pathology; (6) paradoxic pulse greater than 20 mm Hg using sphygmomanometry; (7) informed consent from patient or family for children. All patients were examined by a senior intensivist before entry in the protocol and admitted immediately to the intensive care unit. Standard therapy for asthma was initiated: nasal administration of humidified oxygen; intravenous hydrocortisone, 600 mg/24 h; and continuous salbutamol intravenous infusion at an initial dose of 0.25 mg/h and increased if no clinical improvement occurred. The protocol was started without delay. The total time for completing the protocol was less than 10 min. In all patients the standard therapy was effective and all recovered. One patient with a previous history of epilepsy needed transient mechanical ventilation because of an episode of grand mal seizure, 15 min after the MAST procedure.

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Paradoxic pulse is frequently associated with acute asthma and is considered an index of the severity of both airway obstruction and its cardiovascular consequences. Paradoxic pulse reflects a decreased arterial systolic pressure in inspiration and an increase during expiration and is defined as the maximum difference of systolic arterial pressure within a respi­ratory cycle.

Prior studies implied that the inspiratory fall is the major factor, and that it is caused by inspiratory decrease in LVSV due to three main mechanisms: (1) decreased pulmonary venous return, (2) enhanced ventricular interdependence and (3) increased left ventricle afterload.

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Almost all of the roentgenographically occult, spu­tum cytology positive lung cancers are squamous cell carcinomas. Detection and localization of these occult lung cancers have long presented a diagnostic chal­lenge. Even for experienced endoscopists, carcinoma in situ is bronchoscopically visible in less than 30 percent of cases and microinvasive tumors are visible in only about two thirds of cases. The earliest recognizable changes are subtle consisting of increase in granularity or a slight thickening of the bronchial mucosa. These changes were observed in half of the tumor sites in this study. When no abnormality is visible, localization of these tumors is time consuming and can be difficult. Multiple examinations may be necessary. For this reason, the use of fluorescent “tumor markers” has been developed to facilitate detection and localization of these early lung cancers. Hematoporphyrin derivative or Photofrin II have been the most extensively studied for the detection and localization of small as well as large bronchial can­cers. Fluorescence diagnosis of tumors is based on the principles that HpD and Photofrin II emit red fluorescence (with peaks at 630 nm and 690 nm when excited by a violet light near 405 nm) that can be detected by special imaging devices; and HpD and Photofrin II are preferentially retained by tumor tissues compared to most nonmalignant tissues from hours to days after intravenous injection. The tumor can consequently be imaged or detected because it can be differentiated from the surrounding normal tissue by its more intense fluorescence. If a different fluorescent tumor marker is used, the principles remain the same although a different excitation wave­length, filtering, and detection system may be re­quired.

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The findings on white light bronchoscopic exami-nation and fluorescence imaging are shown in Table

I. Subtle mucosal changes were observed at five of the ten tumor sites. Positive fluorescence was observed in all ten sites. Elevated red-green ratios in the tumor area vs the control area were also observed at all ten sites. In areas of the bronchial tree that were not involved by tumor, the red-green ratios varied be¬tween 0.9 to 1.8. The ratios were less than 1.6 in all except one area. The one nontumor area with a red- green ratio of 1.8 in patient 3 showed moderate atypia on biopsy.
Following localization of the tumor area(s), the patients received an additional 1.75 mg/kg Photofrin

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