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Biomedical subjects

M J Tobin

Publications and source records attributed to M J Tobin.

At least 55 records · Page 3Linked to original sources
PubMed1999

Influence of ventilator settings in determining respiratory frequency during mechanical ventilation.

During mechanical ventilation, changes in inspiratory flow and tidal volume (VT) have been shown to alter respiratory frequency (f ). However, the changes in flow and VT have been accompanied by alteration in ventilator inspiratory time (TI,(vent)), and it is not clear which variable is the primary determinant. To address this issue, we employed four protocols in 15 healthy volunteers receiving assist-control ventilation. When VT was fixed and flow was delivered at 30, 60, and 90 L/min, f increased as a function of the increase in flow and the decrease in TI,(vent). When flow was held constant and VT was changed among 0.5, 1.0, and 1.5 L, f increased as a function of the decreases in VT and TI,(vent). When flow was increased from 60 to 90 L/min and these changes were balanced with VT settings of 1.0 and 1.5 L to maintain a constant TI,(vent), f did not change. When flow and VT were held constant and TI,(vent) was varied by the application of inspiratory pauses (0 to 2 s), f decreased as a function of the increase in TI,(vent) (p < 0.001). In conclusion, the imposed ventilator inspiratory time during mechanical ventilation can determine f independently of delivered inspiratory flow and VT.

Adult↗
PubMed1999

Does inhaled albuterol improve diaphragmatic contractility in patients with chronic obstructive pulmonary disease?

We tested the hypothesis that the decrease in dyspnea in patients with COPD with inhaled albuterol is in part due to increased diaphragmatic contractility. Eleven patients with COPD inhaled albuterol or placebo in a double-blind randomized manner. Subsequently, dyspnea was measured while patients breathed through inspiratory resistors, and diaphragmatic contractility was quantified during maximal inspiratory efforts and after twitch stimulation of the phrenic nerves. Albuterol produced a decrease in dyspnea (5 +/- 2 to 4 +/- 2 [SD] Borg units, p < 0.01), and increases in maximal transdiaphragmatic pressure (92.4 +/- 37.2 to 102.8 +/- 37.2 cm H(2)O, p < 0.03) and potentiated twitch transdiaphragmatic pressures (21.6 +/- 7.1 to 25.2 +/- 7.6 cm H(2)O, p < 0.02). The decrease in dyspnea correlated with the increases in maximal and twitch transdiaphragmatic pressures: r = -0.64 (p = 0. 04) and r = -0.65 (p = 0.04), respectively. Compared with placebo, albuterol produced an increase in inspiratory capacity (1.87 +/- 0. 71 to 2.26 +/- 0.74 L, p = 0.002), which accounted for the increases in maximal and twitch transdiaphragmatic pressures. The decrease in dyspnea correlated with the increase in inspiratory capacity (r = -0. 62, p = 0.04), but not with the increase in FEV(1) (r = -0.13, p = 0. 72). In conclusion, albuterol relieves dyspnea and enhances respiratory muscle output in patients with COPD primarily by improving the length-tension relationship of the diaphragm rather than by improving its contractility.

Action Potentials↗
PubMed1998

Respiratory muscle dysfunction in mechanically-ventilated patients.

The interaction between a patient and a ventilator is the major determinant of the amount of respiratory muscle rest achieved by the machine. We are beginning to acquire a better understanding of the mechanisms that underlie this complex interaction, but this information has yet to be integrated into the routine clinical management of ventilator-supported patients. To achieve that goal, we need better techniques of detecting and monitoring patient-ventilation asynchrony, and the development of simple algorithms that can minimize its occurrence. Finally, research is needed to determine the occurrence and importance of respiratory muscle fatigue during failed weaning attempts so as to better guide the timing and pace of the weaning process in problematic patients.

Humans↗
PubMed1998

The effect of circuit compliance on delivered ventilation with use of an adult circle system for time cycled volume controlled ventilation using an infant lung model.

This in vitro study examined the effect of circuit compliance on delivered ventilation (VE) using a time-cycled, volume controlled circle system in an infant lung model. A Bio-Tek ventilator tester set to simulate normal and abnormal lung compliance measured VE delivered by the Narkomed 2B system. Circle circuits of varied compliance (2.75, 1.22 and 0.73 microliters.cm H2O-1) were tested. Tidal volume was adjusted to peak inflation pressures (PIP) of 20, 30, 40, and 50 cm H2O with three circuits, two lung compliances, and four different size tracheal tubes (TT) (2.5, 3.5, 4, 4.5 mm ID). Data were analysed using the multiple regression technique. Delivered VE was directly related to PIP and lung compliance. Delivered VE was not affected by the choice of circuit. TT size had minimal effects on VE when lung compliance was low; TT size was a more important factor when test lung compliance was normal. Extrapolating this data to the clinical setting, adequate ventilation of infants can be achieved with an adult circle system if an appropriate PIP is chosen, regardless of the compliance of the circuit used. Infants with poor lung compliance may require very high PIP for adequate ventilation.

Adult↗
PubMed1998

A comparison of three modes of ventilation with the use of an adult circle system in an infant lung model.

UNLABELLED: We examined the efficiency of an adult circle system with adult bellows to deliver minute ventilation (VE) to an infant test lung model. A Narkomed 2B system (North American Drager, Telford, PA) using three modes of ventilator setup were used: A = time-cycled, volume-controlled using bellows excursion to control delivered volume; B = time-cycled, pressure-controlled using inspiratory pressure limit adjustment to control delivered volume; C = time-cycled, pressure-controlled using the inspiratory flow adjustment to control delivered volume. VE was measured with two compliances (normal and low) and four endotracheal tube (ETT) sizes (2.5-, 3.0-, 3.5-, and 4.0-mm inner diameter). VE was measured at peak inspiratory pressures (PIP) of 20, 30, 40 or 50 cm H2O while respiratory rate (RR) was held constant at 20 breaths/min. VE was measured as RR was set at 20, 30, 40, or 50 breaths/min while target PIP was held constant at 20 cm H2O. Data were analyzed using the multiple regression technique. With the low compliance model, VE was nearly identical regardless of the ventilator setup. With the normal compliance model, minor differences in VE were observed, especially at the highest RR and PIP. VE was dependent on RR, PIP, and lung compliance. Overall, the ventilator setup resulted in minor changes in VE. Very high PIPs were required to deliver VE to the low compliance model. ETT size did not affect VE when lung compliance was low; however, smaller ETT size was a factor when test lung compliance was normal, decreasing delivered VE at higher PIP and RR. We conclude that with a Narkomed 2B adult circle system VE is dependent on PIP, RR, and lung compliance, but not on mode of ventilator setup. IMPLICATIONS: The results of this laboratory investigation indicate that when an adult circle system is used during infant anesthesia, the ventilation delivered depends primarily on the respiratory rate, peak inspiratory pressure, and the compliance of the lung being ventilated, rather than on the specific mode of ventilator setup.

Adult↗
PubMed1998

Does resistive loading decrease diaphragmatic contractility before task failure?

While sustaining a load that leads to task failure, it is unclear whether diaphragmatic fatigue develops progressively or occurs only at task failure. We hypothesized that incremental loading produces a progressive decrease in diaphragmatic contractility ever before task failure. Ten subjects generated 60% of maximal transdiaphragmatic pressure (Pdimax) for 2 min, 4 min, and until task failure. Before loading, 20 min after each period of loading, and approximately 20 h after the last period of loading, Pdimax, nonpotentiated and potentiated Pdi twitch pressure (Pditw), and the pattern of respiratory muscle recruitment during a CO2 challenge were recorded. Sensation of inspiratory effort at the 4th min of the task-failure protocol was greater than at the same time in the preceding 4-min protocol. Surprisingly, potentiated Pditw and Pdimax were reduced after 2 min of loading and decreased further after 4 min of loading and after task failure; nonpotentiated Pditw was reduced after 4 min of loading and after task failure. The gastric pressure contribution to tidal breathing during a CO2 challenge decreased progressively in relation to duration of the preceding loading period, whereas expiratory muscle recruitment progressively increased. A rest period of approximately 20 h after task failure was not sufficient to normalize these alterations in respiratory muscle recruitment or fatigue-induced changes in diaphragmatic contractility. In conclusion, while sustaining a mechanical load, the diaphragm progressively fatigued, ever before task failure, and when challenged the rib cage-to-diaphragmatic contribution to tidal breathing and recruitment of the expiratory muscles increased pari passu with duration of the preceding loading.

Adult↗
PubMed1998

Effect of lung volume reduction surgery on neuromechanical coupling of the diaphragm.

The mechanisms for symptomatic improvement following lung volume reduction surgery for emphysema are poorly understood. We hypothesized that enhanced neuromechanical coupling of the diaphragm is an important factor in this improvement. We studied seven patients with diffuse emphysema before and 3 mo after surgery. Patients showed improvements in 6-min walking distance (p = 0.002) and dyspnea (p = 0.04). The pressure output of the respiratory muscles, quantified as pressure-time product per minute (PTP/min), decreased after surgery (p = 0.03), as did PaCO2 (p = 0.02). Maximal transdiaphragmatic pressures (Pdi(max)) increased from 80.3 +/- 9.5 (SE) to 110.8 +/- 9.3 cm H2O after surgery (p = 0.03), and the twitch transdiaphragmatic pressure response to phrenic nerve stimulation (Pdi(tw)) increased from 17.2 +/- 2.4 to 25.9 +/- 3.0 cm H2O (p = 0.02); these increases were greater than could be accounted for by a decrease in lung volume. The contribution of the diaphragm to tidal breathing, assessed by relative changes in gastric and transdiaphragmatic pressures, increased after surgery (p = 0.008). Net diaphragmatic neuromechanical coupling, quantified as the quotient of tidal volume (normalized to total lung capacity) to tidal change in Pdi (normalized to Pdi(max)), improved after surgery (p = 0.03) and was related to the increase in 6-min walking distance (r = 0.86, p = 0.03) and decrease in dyspnea (r = 0.76, p = 0.08). In conclusion, lung volume reduction surgery effects an improvement in diaphragmatic function, greater than can be accounted for by a decrease in operating lung volume, and enhances diaphragmatic neuromechanical coupling.

Aged↗
PubMed1998

Effect of resistive loading on variational activity of breathing.

To examine the effect of resistive loading on variational activity of breathing, we studied 18 healthy subjects breathing at rest and with inspiratory resistive loads of 3 and 6 cm H2O/L/s, applied randomly for 1 h each. Compared with resting breathing, a resistive load of 3 cm H2O/L/s decreased the total variational activity of expiratory time (TE) and minute ventilation (V I), whereas a load of 6 cm H2O/L/s increased the total variational activity of inspiratory time (TI). Compared with the load of 3 cm H2O/L/s, the load of 6 cm H2O/L/s increased total variational activity of tidal volume (VT), TI, TE, and V I. Partitioning of the total variational activity revealed that these alterations were due to changes in the random uncorrelated fraction. Compared with rest, both the resistive loads of 3 and 6 cm H2O/L/s increased the number of breath lags displaying significant serial correlations ("short-term memory") of TI. Compared with rest, the load of 3 cm H2O/L/s increased the autocorrelation coefficient at a lag of one breath for VT and the load of 6 cm H2O/L/s increased the correlated fraction of variational activity of VT. Thus, three measures of correlated behavior-autocorrelation coefficient at a lag of 1 breath, "short-term memory," and the correlated fraction of total variational activity- increased with loading. In conclusion, resistive loading changed total variational activity according to the size of the load: the random fraction decreased with the smaller load but increased with the larger load; in contrast, correlated behavior increased with both loads. The different behaviors of random and correlated variability with loading may reflect different physiologic influences on respiratory control.

Adult↗
PubMed1998

Partitioning of lung and chest-wall mechanics before and after lung-volume-reduction surgery.

In the study reported here, we partitioned the mechanics of the respiratory system into lung and chest-wall components, using the rapid occlusion technique in seven patients with severe emphysema before lung-volume-reduction surgery and 3 mo later. Patients showed improvements in 6-min walk (p < 0.01) and dyspnea (p < 0.05). The resistances of the respiratory system and chest wall were not altered by surgery. Ohmic airway resistance did not change, but the component of lung resistance (DeltaRL) due to viscoelastic behavior (stress relaxation) and time-constant inhomogeneities (pendelluft) decreased in six patients (p < 0.03). Dynamic elastance of the lung (Edyn,L) decreased after surgery (p < 0.02), whereas dynamic elastance of the chest wall did not change. The ratio of dynamic intrinsic positive end-expiratory pressure (PEEPi) to static PEEPi, which also reflects viscoelastic properties and time-constant inhomogeneities, increased after surgery (p < 0.05). The decrease in dyspnea was related to the decrease in Edyn,L (r = 0.81, p = 0.03), and tended to be related to the decrease in DeltaRL (r = 0.71, p = 0. 07). In conclusion, lung-volume-reduction surgery decreased dynamic pressure dissipations caused by stress relaxation and time-constant inhomogeneities within lung tissue, and it had no effect on the static mechanical properties of the chest wall.

Aged↗
PubMed1998

Cycling of inspiratory and expiratory muscle groups with the ventilator in airflow limitation.

Research on patient-ventilator interactions has largely focused on inspiratory events, with little attention paid to expiration. We sought to determine the importance of the timing and magnitude of expiratory muscle activity in causing patient-ventilator dyssynchrony. Our study was done with healthy subjects receiving pressure support in whom we induced airflow limitation with a Starling resistor. The timing and magnitude of expiratory muscle activity were obtained by wire electromyographic recording of the activity of the transversus abdominis muscle, and were compared with the cycling of the ventilator and inspiratory muscle activity as determined from a flow tracing and diaphragmatic electromyogram (EMG), respectively. Induction of airflow limitation produced significant phase differences in the cycling of the subjects' expiratory muscle group and that of the machine. Some inspiratory efforts failed to trigger the ventilator, owing in part to an increase in elastic recoil consequent to the commencement of expiratory efforts before the termination of mechanical inflation. A delay in relaxation of the expiratory muscles did not interfere with the success of subsequent inspiratory efforts to trigger the ventilator. We also investigated the accuracy of two approaches for distinguishing between the contributions of expiratory muscle activity and elastic recoil to intrinsic positive end-expiratory pressure (PEEPi): the expiratory increase in gastric pressure (Pga) correlated better with transversus abdominis electromyographic activity (r = 0.7 to 0.95) than did the early inspiratory decrease in Pga (r = 0.04 to 0.53). In conclusion, the continuation of mechanical inflation into neural expiration was associated with failure of the subsequent inspiratory attempt to trigger the ventilator.

Abdominal Muscles↗
PubMed1998

Continuous recordings of mixed venous oxygen saturation during weaning from mechanical ventilation and the ramifications thereof.

To define the importance of hemodynamic performance and global tissue oxygenation in determining weaning outcome, we recorded mixed venous oxygen saturation (SvO2) continuously in eight ventilator-supported patients who failed a trial of spontaneous breathing and 11 patients who tolerated a trial and were successfully extubated. Immediately before the weaning trial, SvO2 was not statistically different in the two groups (p = 0.28). On discontinuation of the ventilator, SvO2 fell progressively in the failure group (p < 0.01), whereas it did not change in the success group. During the trial of spontaneous breathing, O2 demand was similar in the two groups, but it differed in the manner with which it was met. The success group demonstrated an increase in cardiac index (p < 0.05) and O2 transport (p < 0.02). The failure group did not increase O2 transport, partly because of elevations in right- and left-ventricular afterload, but, instead, increased O2 extraction ratio (p < 0.02) with a consequent fall in SvO2. In turn, the low SvO2 combined with greater venous admixture (p < 0.0006) led to rapid arterial desaturation (p < 0.006) and a relative decrease in O2 being supplied to the tissues. In conclusion, ventilator-supported patients who failed a trial of spontaneous breathing developed a progressive decrease in SvO2 caused by the combination of a relative decrease in convective O2 transport and an increase in O2 extraction by the tissues.

Aged↗
PubMed1997

Twenty-four-hour pharmacokinetics of rectal acetaminophen in children: an old drug with new recommendations.

BACKGROUND: Rectal acetaminophen is often administered during operation to provide supplemental analgesia or antipyresis in children. Recent studies examining current dose guidelines are limited by short sampling times. The authors extended the drug sampling period to more clearly define acetaminophen pharmacokinetics in children having surgery. METHODS: Children (n = 28) were randomized to receive a single dose of 10, 20, or 30 mg/kg rectal acetaminophen after induction of anesthesia. Venous blood samples were taken every 30 min for 4 h, every 60 min for 4 h, and every 4 h for 16 h. Data were analyzed using a mixed-effects modeling technique (using NONMEM software) to determine the volume of distribution and clearance normalized for bioavailability. Additional models accounted for suppository dissolution followed by acetaminophen absorption. RESULTS: Age, weight, estimated blood loss, volume of intravenous fluid administered, and anesthesia time were similar in the three groups. Most patients did not achieve peak or sustained serum values in the 10-20 microg/ml serum concentration range associated with antipyresis. The volume of distribution was 385 ml/kg, and clearance normalized for bioavailability, F, was 5.46 ml x kg(-1) x min(-1). Pharmacokinetic models suggest that absorption of acetaminophen is a function of zero-order dissolution of suppositories and first-order absorption from the rectum. Suppository dose size also may affect absorption characteristics. CONCLUSIONS: The current recommended rectal acetaminophen dose of 10-15 mg/kg yields peak serum concentrations less than the antipyretic serum concentration of 10-20 microg/ml. Based on the observed kinetics, the authors recommend that the initial dose should be approximately 40 mg/kg.

Acetaminophen↗
PubMed1997

Effects of prolonged controlled mechanical ventilation on diaphragmatic function in healthy adult baboons.

OBJECTIVE: To study diaphragmatic strength and endurance after a prolonged period of mechanical ventilation. DESIGN: Prospective animal study. SETTING: Animal research laboratory. SUBJECTS: Seven uninjured adult baboons (Papio cynocephalus) were anesthetized with ketamine, sedated, paralyzed, and mechanically ventilated. Animals were monitored with pulmonary arterial and peripheral arterial catheters. INTERVENTIONS: Mechanical ventilation was provided for 11 days with an FIO2 of 0.21 and tidal volume of 15 mL/kg. Pulmonary function tests, including lung volumes, arterial blood gases, and chest radiographs were also monitored. Nursing care procedures included frequent turning, chest physiotherapy, and endotracheal suction. Antacids and prophylactic antibiotics (intravenous penicillin, topical polymyxin B, and gentamicin sulfate) were administered. In three animals, fishhook electrodes were surgically placed around both phrenic nerves on both day 0 and after 11 days of mechanical ventilation for diaphragmatic stimulation. On day 0, the electrodes were removed after phrenic nerve stimulation studies were performed. After 11 days of mechanical ventilation, animals were electively killed and full autopsy performed. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and pulmonary function parameters were measured at baseline and every day during the 11 days of mechanical ventilation. Diaphragmatic strength and endurance were measured on days 0 and 11. Diaphragmatic endurance was determined by an inspiratory resistive loading protocol. There were no significant changes in hemodynamics, lung volumes, or gas exchange during the period of mechanical ventilation. On day 7, the chest radiographs showed patchy lobar atelectasis in six animals, which cleared by day 11 in all but two of the animals. Lung pathology showed mild, focal pneumonitis. By day 11, maximum transdiaphragmatic pressure had decreased by 25% from day 0 and diaphragmatic endurance had decreased by 36%. CONCLUSIONS: Eleven days of mechanical ventilation and neuromuscular blockade in healthy baboons resulted in nonsignificant changes in hemodynamics, oxygenation, and/or lung function. However, significant impairment in diaphragmatic endurance and strength were seen. Based on these results, it is likely that prolonged mechanical ventilation by itself impairs diaphragmatic function independent of underlying lung disease.

Animals↗
PubMed1997

Pathophysiologic basis of acute respiratory distress in patients who fail a trial of weaning from mechanical ventilation.

To determine the mechanisms of acute respiratory distress and failure in patients with chronic obstructive pulmonary disease (COPD), we studied 17 ventilator-supported patients who failed a trial of spontaneous breathing and 14 patients who tolerated such a trial and were successfully extubated. Immediately before the weaning trials, maximal inspiratory pressure was not statistically different between the two groups (p = 0.48). On discontinuation of the ventilator, the failure group immediately developed rapid shallow breathing, and higher values of dynamic lung elastance (EdynL) (p < 0.01) and intrinsic positive end-expiratory pressure (PEEPi, p < 0.03) than did the success group. Between the onset and end of the trial, the failure group developed further increases in EdynL (p < 0.0001) and PEEPi (p < 0.0001), and increases in inspiratory resistance (p < 0.009) and inspiratory pressure-time product (PTP) (p < 0.0001). Partitioning of PTP at the end of the trial revealed a 111% increase in the PEEPi component, a 33% increase in the non-PEEPi elastic component, and a 42% increase in the resistive component (all p < 0.0001). Despite the increase in PTP, 13 of the failure patients developed an increase in PaCO2. The product of PTP and PaCO2, an index of inefficient CO2 clearance, was more than twice as high in the failure group than in the success group at the end of the trial (p < 0.0005). Thus, development of acute respiratory distress during a failed weaning attempt was due to worsening of pulmonary mechanics, which in conjunction with rapid shallow breathing led to inefficient clearance of CO2.

Aged↗
PubMed1997

Passive mechanics of lung and chest wall in patients who failed or succeeded in trials of weaning.

In an accompanying article (Jubran, et al., Am. J. Respir. Crit. Care Med. 155:906-915), we report that patients with chronic obstructive pulmonary disease (COPD) who failed a trial of weaning from mechanical ventilation developed worsening of pulmonary mechanics compared with patients who tolerated the trial and were extubated. We wondered whether the greater derangements in pulmonary mechanics in the weaning failure patients are evident ever before undertaking the weaning trial. We measured mechanics of the respiratory system, lung, and chest wall during passive ventilation at usual ventilator settings in 12 patients who went on to fail a weaning trial and in 12 patients who were successfully weaned. No differences in the resistances of the respiratory system, lung, and chest wall were observed between the two groups or when the resistances were separated into the components derived from ohmic resistance and viscoelastic behavior/time-constant inhomogeneities. Likewise, the groups did not differ in terms of static elastance and dynamic intrinsic positive end-expiratory pressure (PEEPi) of the respiratory system and the respective lung and chest wall components or in terms of dynamic elastances of the respiratory system and chest wall. The failure group had a higher dynamic elastance of the lung than the success group (p < 0.01), but the individual values showed considerable overlap among the patients in the two groups so limiting its usefulness in signaling a patient's ability to sustain spontaneous ventilation. Thus, mechanics of the respiratory system and its lung and chest wall components during passive ventilation did not satisfactorily discriminate between patients who failed a weaning trial and those successfully weaned, and, thus, are unlikely to be useful in signaling a patient's ability to tolerate the discontinuation of mechanical ventilation.

Elasticity↗