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Biomedical subjects

C K Mahutte

Publications and source records attributed to C K Mahutte.

At least 55 records · Page 3Linked to original sources
PubMed1990

Ventilator modes: old and new.

CPPV is an accepted standard of treatment in patients with acute respiratory failure. Because of rapid technologic advancements, new modes of ventilation have been developed. Unfortunately, this occurs at a time when there are still many controversies about the relative benefits and modes of action of CPPV. Before the proliferation of use of these newer modes in the intensive care units, documentation of the beneficial effects and safety of these modalities under controlled condition is of utmost importance. Although some of the "new" ventilatory modes (PSV, PAV) improve patient comfort and synchrony, and PAV has the potential to replace CPPV, the superiority of the "new" ventilatory modes over that of CPPV remains to be established, particularly in the area of patient survival, morbidity, and cost.

High-Frequency Ventilation↗
PubMed1989

Relationship between improvement in exercise performance with supplemental oxygen and hypoxic ventilatory drive in patients with chronic airflow obstruction.

The purpose of this study was to determine if there is a relationship between improvement in exercise capacity with supplemental oxygen and the magnitude of hypoxic ventilatory drive in patients with CAO. We hypothesized that those patients with the highest hypoxic drives would be the most likely to have increased exercise tolerance with supplemental oxygen. Seventeen patients with CAO (mean FEV1 = 0.99 +/- 0.45 L) underwent identical maximal cycle ergometry exercise tests on two occasions 45 minutes apart while breathing either air or 30 percent oxygen in a randomized single-blind fashion. With supplemental oxygen, the ventilation decreased and the PaCO2 increased significantly at rest. The patients had a significantly greater exercise tolerance on supplemental oxygen (76.7 vs 69.1 watts, p less than 0.005) but no increase in the maximal ventilation. When the nine patients who improved were compared to the eight patients who did not improve, the two groups were basically identical. Specifically, there were no significant differences in the mean ventilatory or mouth occlusion responses to hypoxia or in the blood gases. The patients who did improve tended to have a greater reduction in their ventilatory response to exercise while exercising on oxygen as compared to when they were exercising on room air. From this study, it was concluded that measurements of hypoxic ventilatory drive are not helpful in predicting which patients with CAO are likely to have improved exercise capability while breathing supplemental oxygen.

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↗
PubMed1988

Etiology of carbon dioxide retention at rest and during exercise in chronic airflow obstruction.

The purpose of this project was to better define factors that influence the resting PaCO2 and the change in the PaCO2 from rest to exercise in patients with moderate to severe chronic airflow obstruction. Pulmonary function testing, symptom-limited exercise tests using arterial catheter lines, and resting ventilatory and mouth occlusion pressure responses to hypercapnia and hypoxia were obtained in 19 patients (mean FEV1 = 1.07 +/- .50 L). The resting PaCO2 was closely related to the resting hypercapnic response. The highest correlation coefficient was between the PaCO2 and the ventilation at PCO2 = 60 obtained from the resting hypercapnic response (r = -0.74, p less than 0.001). A higher PaCO2 also tended to occur in patients with a lower FEV1 and a lower PaO2. The resting PaCO2 was not correlated significantly with the VT or the VD/VT. The change in the PaCO2 from rest to exercise was not significantly related to any measure of resting hypercapnic or hypoxic response, but rather was most dependent on the ventilatory response to exercise (delta VE/delta VCO2). Patients with a lower FEV1 or smaller decreases in the PaO2 with exercise tended to have larger increases in PaCO2 with exercise. The delta VE/delta VCO2 was higher in those with a high FEV1, a low resting PaCO2, and a low resting SaO2.

Carbon Dioxide↗
PubMed1987

Comparison of arterial blood gas with continuous intra-arterial and transcutaneous PO2 sensors in adult critically ill patients.

We compared the partial pressure of oxygen directly via a continuous intra-arterial probe (PiaO2) and indirectly using a transcutaneous device (PtcO2) with simultaneously obtained arterial blood PaO2. The PiaO2 values were measured using a bipolar oxygen sensor placed through an 18-ga arterial catheter. The PtcO2 values were measured using a transcutaneous O2-CO2 sensor placed on the abdomen. Seven critically ill, hemodynamically stable, ventilator-dependent adult patients were studied. Measurements were obtained at varying concentrations (0.25 to 1.0) of inspired oxygen after a 10-min stabilization. A total of 78 simultaneous values were obtained; by linear regression: PiaO2 = 0.91 PaO2 + 1.39 (r = .98, standard errors of the estimate [SEE] = 18.6); PtcO2 = 0.39 PaO2 + 36.2 (r = .89, SEE = 14.1). To assess these instruments as trend monitors, we compared the changes in simultaneous PaO2, PiaO2, and PtcO2 values; by linear regression: delta PiaO2 = 0.90 delta PaO2 + 3.88 (r = .96, SEE = 27.7); delta PtcO2 = 0.43 delta PaO2 + 5.6 (r = .94, SEE = 15.2). We conclude that, although these instruments correlate highly with the PaO2, the SEE was substantial and therefore may limit their clinical reliability in adults. Any acute or clinically significant change in PiaO2 or PtcO2 should be confirmed with a blood gas PaO2.

Adult↗
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

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↗
PubMed1985

Effect of desipramine on control of ventilation and depression scores in patients with severe chronic obstructive pulmonary disease.

Decreased ventilatory responses to carbon dioxide (CO2) correlate with elevated scores on tests for depression in normal subjects and with episodes of endogenous depression in psychiatric patients. Patients with severe chronic obstructive pulmonary disease (COPD) frequently develop resting hypercapnia due to impaired ventilatory mechanics or drive, and may also have elevated scores on tests for depression. Tricyclic antidepressant drugs can improve ventilatory mechanics and possibly drive. We hypothesized that antidepressant drugs might enhance ventilatory drive and improve arterial blood gases in patients with severe COPD and that these improvements might correlate with improvement in depression scores. Therefore, we studied the effects of desipramine versus placebo on spirometry, resting arterial blood gases, hypercapnic ventilatory and mouth occlusion pressure responses, and scores on the Beck and Zung self-rated depression scales. In our patients the resting arterial CO2 (PaCO2) was found to depend almost equally on ventilatory mechanics and drive. In addition, patients with higher depression scores tended to have a lower PaCO2 when the severity of airways obstruction was taken into consideration. In a 16-week, double-blind, crossover comparison of desipramine with placebo, both treatments led to significant improvement in depression scores. Desipramine had no effects on resting PaCO2, spirometry, or ventilatory control.

Aged↗
PubMed1984

Treatment of theophylline toxicity with oral activated charcoal.

Oral activated charcoal was administered to 4 patients with theophylline toxicity, who had gastrointestinal and neurologic symptoms as well as cardiac arrhythmias. Administration of oral charcoal significantly reduced the theophylline half-life in the serum of each patient. The charcoal was well tolerated and symptoms of toxicity rapidly resolved. We conclude that administration of oral charcoal rapidly reduces the serum theophylline concentration and should be used as the initial treatment in patients with theophylline toxicity.

Administration, Oral↗
PubMed1984

Evaluation of a single transcutaneous PO2-PCO2 sensor in adult patients.

We evaluated a new transcutaneous gas monitor designed to measure simultaneously transcutaneous oxygen (PtcO2) and carbon dioxide (PtcCO2) tensions. A total of 514 simultaneous transcutaneous and arterial gases were obtained in 47 adult ICU patients. Mean PtcCO2 was close (SEE less than 4 torr) to mean PaCO2, but mean PtcO2 was considerably less than mean PaO2. However, PtcO2 changes larger than 15 torr virtually always indicated respective increases or decreases in PaO2. Similarly, PtcCO2 changes larger than 5 torr almost invariably indicated a parallel change in PaCO2. From this study we conclude that monitoring of transcutaneous gases yields reliable trend information on arterial gases and that it is a valuable noninvasive adjunct in the monitoring of gas exchange in adult patients.

Aged↗
PubMed1984

Exercise performance with added dead space in chronic airflow obstruction.

Individuals with chronic airflow obstruction (CAO) are thought to have limited exercise tolerance primarily because of impaired ventilatory mechanics. We studied the effects of added external dead space (DS) on exercise capacity [maximum O2 consumption (VO2max)], maximum exercise ventilation (VEmax), and blood gases (arterial PO2, PCO2, pH) in 22 patients with CAO [forced expired volume at 1 s (FEV1) = 0.96 +/- 0.41 liter]. Maximum exercise testing (Emax) was performed by incremental cycle ergometry. Patients exercised at base line (BL) and with DS (0.25 liter if FEV1 less than 0.8, and 0.50 liter if FEV1 greater than 0.8 liter), in random-order single-blind fashion. DS resulted in a 12.2% increase in VEmax (P less than 0.001); tidal volume increased (P less than 0.025) while respiratory frequency was unchanged. The VO2max and maximum CO2 production decreased (P less than 0.001) with DS. Arterial PCO2 at rest and at exhaustion increased with DS (P less than 0.001). The pH and arterial PO2 showed small declines at rest and at Emax. Thus, at the lower maximum work load achieved with DS, the patients ventilated more and tolerated a higher arterial PCO2 and a lower arterial PO2 and pH before stopping from dyspnea as compared with the BL exercise run. In contrast, the VO2max of nine normal control subjects was unaffected by the addition of DS. Although VEmax can be increased in CAO patients with DS, this increase is not sufficient to prevent further CO2 retention or a decrease in exercise capacity. We conclude that exercise performance is limited primarily by impaired ventilatory mechanics in CAO.

Aged↗
PubMed1983

Theory of resistive load detection.

During normal breathing the brain sets the required muscle pressure to overcome resistance and elastance and presumably monitors the resultant flow (rate of change of volume). The lag in flow compared to the pressure can be described by a phase angle. When a small resistive load is added the resultant flow is delayed further and the phase angle increases. We postulate that if the change in phase angle exceeds a critical phase lag, the added load is detected. Over a wide range of basal resistances, R, the mathematical analysis predicts that detection occurs if the just noticeable added resistance, delta R, is a constant fraction of the basal resistance. Resistive load detection thus obeys the Weber psychophysical law, delta R/R = constant. This is in accord with previous experimental observations. The theory also predicts that delta R/R increases at low basal resistance in accord with recent experimental observations. Further as yet untested predictions of the theory are that breathing frequency and elastance should affect the Weber relationship.

Airway Resistance↗
PubMed1983

Effect of ethanol and naloxone on control of ventilation and load perception.

The respiratory depressant effects of ethanol and their potential reversibility by naloxone were studied in 10 normal subjects. Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia without and with an inspiratory resistive load (13 cmH2O X 1(-1) X S) were measured. The resistive load detected with 50% probability (delta R50) and the exponent (n) in Stevens' psychophysical law for magnitude estimation of resistive loads were studied using standard psychophysical techniques. Each of these studies was performed before ethanol ingestion, after ethanol ingestion (1.5 ml/kg, by mouth), and then again after naloxone (0.8 mg iv). Ethanol increased delta R50 (P less than 0.05) and decreased n (P less than 0.05). Naloxone caused no further change in these parameters. The load compensation (Lc), defined as the ratio of loaded to unloaded response slopes, was not significantly changed after ethanol and naloxone. No correlation was found between the Lc and delta R50 or n. The ventilatory and P0.1 responses to hypercapnia and hypoxia with and without inspiratory resistive loading decreased after ethanol (P less than 0.05, hypercapnia; NS, hypoxia). After naloxone the hypercapnic ventilatory responses increased (P less than 0.05). This suggests that the respiratory depressant effects of ethanol may be mediated via endorphins.

Adult↗
PubMed1983

Increased serum theophylline clearance with orally administered activated charcoal.

The purpose of this study was to determine whether the oral administration of activated charcoal would increase the clearance of theophylline. Seven normal subjects received aminophylline intravenously (8 mg/kg) on 2 separate days. On Day 1 at 2-h intervals starting immediately after the completion of the aminophylline infusion, subjects ingested 4 doses of a slurry of activated charcoal (30 g each). On Day 2 they received no charcoal. The order of the days the subjects received charcoal or no charcoal was randomized. Plasma theophylline levels were determined by an enzyme immunoassay (Syva) every 2 h after the completion of the intravenous infusion. The theophylline half-life was reduced with charcoal from 10.2 to 4.6 h (p less than 0.001), and clearance increased from 35.6 to 72.6 ml/kg/h (p less than 0.001). In a patient with an initial serum theophylline concentration of 31.0 micrograms/ml and signs of toxicity (arrhythmias and seizures), the administration of charcoal (4 doses of 30 g every 2 h) reduced the half-life from 34.4 to 5.7 h concomitant with rapid resolution of signs of toxicity. We conclude that orally administered activated charcoal significantly enhances the clearance of theophylline and offers a new therapeutic modality in the treatment of theophylline toxicity.

Administration, Oral↗
PubMed1983

Naloxone reverses ethanol-induced depression of hypercapnic drive.

Ethanol depresses the ventilatory responses to hypercapnia and hypoxia. We hypothesized that this ventilatory depression, like some other central nervous system effects of ethanol, might be mediated via endorphins. In a double-blind placebo-controlled study, we assessed the effect of the opiate antagonist naloxone on ventilatory responses during ethanol intoxication in 18 normal men. Standard rebreathing studies were done at baseline, after ethanol (1.5 ml/kg, p.o.), and after each of 2 intravenously administered injections. One of the injection sequences PP, NP, or PN (N = naloxone, 0.8 mg; P = placebo, 2 ml) was randomly assigned to each subject. The ventilatory responses were reduced after ethanol administration compared with those at baseline (p less than 0.05). In groups NP and PN, naloxone restored the hypercapnic response (p less than 0.05). Placebo injection did not significantly alter the response slopes. Hypoxic ventilatory responses showed the same trends but did not reach statistical significance. This study shows that naloxone reverses ethanol-induced depression of hypercapnic drive, suggesting that an opiate-mediated mechanism is responsible for this depression.

Adult↗