Biomedical subjects

C S Sassoon

Publications and source records attributed to C S Sassoon.

48 records · Page 3Linked to original sources

PubMed1989

Effect of radiation therapy on bronchial obstruction due to bronchogenic carcinoma.

We evaluated the effect of radiation therapy in 57 patients with obstruction of a large bronchus with NSCC. Response with aeration of the atelectatic lung was seen in 12 patients (21 percent). Three patients (5 percent) showed partial response with persistent partial atelectasis, and nine patients (16 percent) showed good response with complete aeration of the atelectatic lung. In these patients the response appeared to be related to the dose of radiation. All of the patients who responded received more than 50 Gy. The difference in the response rate related to the dose of radiation was statistically significant (p less than 0.05). The rates were similar with all histologic types of NSCC. Regardless of the clinical response observed, bronchoscopy performed two to four months after completion of radiation therapy in 14 patients revealed persistent endobronchial tumor. There was no significant relationship between the persistence of endobronchial tumor, the dose of radiation therapy, and the tumor's histologic type. Of the 12 patients with radiographic improvement in atelectasis, fibrotic changes developed in four (33 percent) patients and pneumonitis in two (17 percent). Progression of disease with distant metastases occurred in 58 percent (seven) of the 12 patients who showed a clinical response of their bronchial obstruction. The median time to survival was nearly identical in responders and nonresponders.

Aged↗

PubMed1988

Work of breathing and airway occlusion pressure during assist-mode mechanical ventilation.

We determined the effect of varying ventilator tidal volume (VT) and inspiratory flow (V) on the inspiratory muscle work (WI) during assist-mode mechanical ventilation (AMV) in four healthy subjects. In another four subjects, under constant chemoreceptor input, we determined the responses of neuromuscular output as assessed by the mouth occlusion pressure (P0.1) to alteration in WI. During AMV, the inspiratory external work of breathing is partitioned between WI and ventilator work. With a constant ventilator trigger sensitivity, we calculated WI (joules/L of volume) as the difference between the area subtended by the airway pressure-inspiratory volume curves and the ordinate of the assisted breaths subtracted from that of the controlled breaths at ventilator V of 40, 60 and 80 L/min and ventilator VT of 100, 125 and 150 percent spontaneous breathing VT. At all ventilator settings, WI was less than inspiratory muscle work of spontaneous breathing (SB) and was a function of both ventilator VT and V (p less than 0.05), but ventilator V has more effect on WI. Under isocapnia and hyperoxia, we measured P0.1 and WI during AMV at ventilator VT of 125 percent of spontaneous breathing VT and ventilator V of 60, 80 and 100 L/min. End-expiratory lung volume remained constant. P0.1 during AMV was similar to that of the SB. Although WI decreased with increasing ventilator V, P0.1 did not decrease significantly. We conclude that during AMV, both ventilator V and to a less extent ventilator VT determine W. In healthy subjects changes in WI do not affect P0.1.

Airway Resistance↗

PubMed1987

Validation of esophageal balloon technique at different lung volumes and postures.

The esophageal balloon technique for measuring pleural surface pressure (Ppl) has recently been shown to be valid in recumbent positions. Questions remain regarding its validity at lung volumes higher and lower than normally observed in upright and horizontal postures, respectively. We therefore evaluated it further in 10 normal subjects, seated and supine, by measuring the ratio of esophageal to mouth pressure changes (delta Pes/delta Pm) during Mueller, Valsalva, and occlusion test maneuvers at FRC, 20, 40, 60, and 80% VC with the balloon placed 5, 10, and 15 cm above the cardia. In general, delta Pes/delta Pm was highest at the 5-cm level, during Mueller maneuvers and occlusion tests, regardless of posture or lung volume (mean range 1.00-1.08). At 10 and 15 cm, there was a progressive increase in delta Pes/delta Pm with volume (from 0.85 to 1.14). During Valsalva maneuvers, delta Pes/delta Pm also tended to increase with volume while supine (range 0.91-1.04), but was not volume-dependent while seated. Qualitatively, observed delta Pes/delta Pm fit predicted corresponding values (based on lung and upper airway compliances). Quantitatively there were discrepancies probably due to lack of measurement of esophageal elastance and to inhomogeneities in delta Ppl. At every lung volume in both postures, there was at least one esophageal site where delta Pes/delta Pm was within 10% of unity.

Adult↗

PubMed1987

Massive pulmonary embolism complicating streptokinase treatment for deep vein thrombosis.

A fatal massive pulmonary embolus developed in a patient treated with streptokinase for acute deep vein thrombosis. This fatal complication occurred despite a careful selection of the patient and the presence of a lytic state. Embolization of a fragmented thrombus or/and attenuation of the lytic state leading to fresh embolization is/are the possible mechanism(s). Although rare, massive pulmonary embolus must be considered to be a major risk of thrombolytic therapy for deep venous thrombosis.

Humans↗

PubMed1987

Airway occlusion pressure. An important indicator for successful weaning in patients with chronic obstructive pulmonary disease.

The objective of this study was to determine whether airway occlusion pressure (P0.1) is a useful predictor for successful weaning during discontinuation of assisted ventilation (AV) in patients with chronic obstructive pulmonary disease (COPD). We studied 12 patients with COPD receiving AV with maximal inspiratory pressure (MIP) less than or equal to -20 cm H2O and FVC greater than or equal to 10 ml/kg. The P0.1, VT, frequency, mean inspiratory flow rate (VT/TI), inspiratory time to total breath cycle duration (TI/Ttot), and arterial blood gases were determined just prior to weaning, within 5 min after discontinuing AV (Time 0), and at 30, 60, 90, 120, 180, and 240 min. Five of the 12 patients failed to wean, defined as requiring AV within 24 h after discontinuing AV. At Time 0, all patients who subsequently failed to wean had a P0.1 of greater than 6 cm H2O, and those who were successfully weaned had a P0.1 of less than 6 cm H2O (p less than 0.001), although the arterial blood gas determinations were comparable in both groups. Throughout the study period, P0.1 in the patients who failed to wean was persistently higher than in the successfully weaned patients. Despite the high P0.1, VT and VT/TI decreased significantly at the termination of the study compared with those at Time 0 in 3 of the patients who failed to wean. Tachypnea was not useful in predicting failure to wean. The TI/Ttot in the patients who failed to wean was persistently lower than in the successfully weaned patients. We conclude that P0.1 is an important indicator for successful weaning.

Aged↗

PubMed1987

Partitioning of respiratory mechanics in young adults. Effects of duration of anesthesia.

General anesthesia increases total respiratory elastance and flow resistance within minutes after induction. We determined if respiratory mechanics changed progressively during anesthesia by measuring total respiratory elastance and resistance and their respective lung and chest wall components in 10 young adults free of cardiorespiratory disease at the start and end of premedicated anesthesia administered for orthopedic surgery (isoflurane, enflurane, or halothane, minimal alveolar concentration approximately 1.5 in 60% N2O-40% O2; interval between measurements was 0.42 to 5.0 h, mean +/- SD = 2.08 +/- 1.56 h). Static lung recoil pressure, static total respiratory and lung elastance, dynamic lung elastance, chest wall elastance, and total respiratory and lung and chest wall resistances were measured during steady-state breathing (greater than 10 min after induction). Resistance of the endotracheal tube, pneumotachygraph and connectors were subtracted from the total flow resistance to obtain total intrinsic resistance. Average values of static lung recoil pressure and all elastances and chest wall resistance did not change significantly from start to end of the study, regardless of the elapsed time. Total respiratory and lung resistance increased by 49% (p less than 0.05) and 45% (p less than 0.02), respectively, but were not time-dependent. We conclude that lung static recoil and total respiratory and lung elastances did not change beyond the first 10 min after induction, regardless of duration of anesthesia. The increases in total respiratory and lung resistance were small, independent of duration of anesthesia, and may have been due to accumulated airway secretions.

Adult↗

PubMed1987

Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease.

We investigated the mechanism of hyperoxic-induced hypercapnia in 17 stable patients with moderate to severe chronic obstructive pulmonary disease (mean FEV1 = 0.95 L and FVC = 2.43 L). Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia were measured with standard rebreathing techniques. In a randomized, single-blind fashion, we studied the effect of 15 min of hyperoxia or air on transcutaneous carbon dioxide (PtcCO2), CO2 production (VCO2), total minute ventilation (VE), and calculated dead space to tidal volume ratio (VD/VT). With O2, the PtcCO2 (p less than 0.01) and VD/VT (p less than 0.02) increased. The change in PtcCO2 with O2 was not significantly related to the indices of respiratory drive, nor to the baseline PtcCO2 or SaO2, but was related to the FEV1 (p less than 0.05). The O2 caused a slight decrease in mean VE and mean VCO2, but the effects in individual patients were variable. Both substantial increases or decreases in VE (delta VE) occurred, but these were accompanied by changes in VCO2 (delta VCO2) in the same direction. The effect of changes in VE on PaCO2 is shown to be almost completely cancelled by the concomitant changes in VCO2. Thus, the major portion of the change in PaCO2 was due to changes in VD/VT. We conclude that hyperoxic-induced hypercapnia is primarily due to impairment in gas exchange rather than to depression of ventilation. A reduced FEV1 appears to be a significant risk factor, whereas indices of respiratory drive are not likely to play a major role.

Aged↗

PubMed1986

Mechanisms of respiratory elastic load compensation in anesthetized humans.

In anesthetized humans the nature of tidal volume (VT) compensation during elastic loading (as reflected in the difference between passive and effective respiratory elastances (Ers) and (E*rs), respectively) has not been fully elucidated. We assessed the relative contribution of various mechanisms contributing to VT compensation during linear elastic loading in 10 young anesthetized adults free of cardiorespiratory disease. Ers averaged 22.0 cmH2O X 1(-1), representing 64% of E*rs. Most of E*rs (84%) was comprised of the active elastance (E'rs), reflecting the major role played by the addition of force-length properties of inspiratory muscles to the internal impedance, and chest wall distortion played in the defense of VT. Of the remaining 16% of E*rs, the difference between E*rs and isotime E*rs, representing the contribution of prolongation of inspiratory time (TI) via the Hering-Breuer reflex, amounted to only 9%. Finally, the remainder of E*rs, which reflects the difference between E*rs and E'rs in the absence of vagal modulation, and attributed to several factors [shape of driving pressure wave, duration of control TI, and magnitude of E'rs and intrinsic flow resistance plus external resistances (Zin, Rossi, Zocchi, and Milic-Emili. J. Appl. Physiol. 57: 271-277, 1984)], amounted to less than 7%.

Adult↗

PubMed1986

Respiratory drive and timing during assisted ventilation in dogs.

In 8 anesthetized dogs, during isocapnic hyperoxia we studied the effect of assisted ventilation (AV) on ventilatory drive, inspiratory off-switch volume (Voff) and duration of inspiratory diaphragmatic activity (Tdi). Tidal volumes (Vt) during AV were double spontaneous Vt. Two electrodes were inserted in the diaphragm to obtain the electromyogram (EMG). The index of ventilatory drive was the EMG 0.3--i.e., the amplitude of the moving average EMG 300 ms after the onset of inspiratory activity. AV decreased EMG 0.3 but had no effect on Voff and Tdi. Vagotomy not only abolished the reduction in drive, but may have increased drive during AV.

Animals↗

PubMed1986

Active inspiratory impedance and load compensation: effects of duration of anesthesia.

General anesthesia results in increases in respiratory elastance and flow resistance within 10-15 min after induction. Stabilization (compensation) of the respiratory system in the face of this added load is related to the addition of active (contractile) force-length and force-velocity properties to its internal impedance during inspiration. The difference between active (inspiratory) and passive (relaxation-exhalation) values of elastance and resistance can be used as an index of load compensation. We therefore evaluated the effects of duration of anesthesia on respiratory impedance and stabilization by comparing active elastance (E'rs) and flow resistance (R'rs) to their corresponding passive values (Ers, Rrs) at the beginning and end of steady-state breathing in ten young, healthy anesthetized adults undergoing orthopedic surgery (anesthesia approximately 1.5 MAC of a halogenated anesthetic in 60% N2O-40% O2). Occlusion pressure (P0.1) and components of ventilation also were measured. Duration of anesthesia did not correlate with changes in active or passive mechanics or with control of ventilation. Mean Rrs increased by 76% (P less than 0.025), probably due to a decline of atropine effect; however, R'rs increased by only 17%, indicating near-maximum stabilization of flow-resistive properties at the end. Passive elastance increased 6%, whereas E'rs increased 3.8%, indicating essentially constant volume-elastic stabilization throughout. Occlusion pressure increased 20% and VT/TI 22%, probably due to a decline in effects of sedation and neuromuscular blockade. We conclude that after induction of anesthesia, the reserve available to overcome flow resistance (intrinsic plus equipment) diminishes but is not related to duration of anesthesia. The reserve available to overcome elastic properties remains essentially constant throughout anesthesia.

Adult↗

PubMed1985

Chylothorax and pseudochylothorax.

Both chylothorax and pseudochylothorax are characterized by milky or turbid pleural effusions. The importance of distinguishing these two conditions cannot be overemphasized because the prognosis and management are different.

Adult↗

PubMed1984

Small airways function in nonsmokers with rheumatoid arthritis.

To evaluate the possible relationship between rheumatoid arthritis (RA) and airways dysfunction independent of cigarette smoking, we studied 19 lifetime nonsmokers with RA and 47 healthy nonsmokers. Ten tests of small airways function were administered to the subjects. In addition, diffusing capacity and static lung compliance were measured, and upstream airway conductance at mid-to-low lung volumes was calculated. Mean values were not significantly lower in the RA group than in the control group in any of the tests of small airways function. Three of the 19 (16%) patients with RA versus 15 of the 47 (32%) control subjects had abnormal findings on greater than 2 tests of small airways function (P greater than 0.1). Although mean diffusing capacity and static lung compliance were both within normal limits in each group, the former tended to be lower, while the latter was significantly lower, in the RA subjects. We conclude that airways dysfunction in RA, if present, is probably related to factors other than the underlying disease; if an association between RA and small airways abnormality is present in some patients, its prevalence is too small to have been detected in our sample.

Adult↗