Oxygen uptake during weaning from mechanical ventilation

Total body oxygen uptake (VO2) increases during the transition from machine-assisted ventilation to spontaneous breathing. Since the volume of oxygen consumed by the respiratory muscles must contribute to the increase in VO2 (delta VO2), we explored whether delta VO2 and/or measurements of respiratory power output (Wresp) provide clinically useful information in the evaluation of disease state and weaning decisions in patients with respiratory failure. We determined the metabolic, ventilatory, and hemodynamic responses of ten patients during weaning from controlled mechanical ventilation, and compared delta VO2 and Wresp of patients without overt heart-lung disease (group 1) to that of patients with significant cardiopulmonary dysfunction and ventilator-dependent respiratory failure (group 2). We reasoned that for delta VO2 to be clinically useful, individual values must either clearly differ between groups, must be higher in patients with heart-lung disease, and/or correlate with weaning outcome and independent measurements of respiratory work. The VO2 increased in nine of ten patients. The differences between the groups in the values of delta VO2 (27 ml/min and 49 ml/min) and respiratory power (9.38 J/min and 11.99 J/min) were not significant. delta VO2 and Wresp were not correlated (r = 0.2), and neither predicted weaning outcome. We conclude that the sensitivity and specificity of delta VO2 and Wresp appear insufficient for evaluation of disease state and weaning decisions in individual patients.     

Oxygen cost of breathing. Changes dependent upon mode of mechanical ventilation

We describe a patient with respiratory failure who demonstrated marked increases in O2 consumption (VO2) when breathing with synchronized intermittent mandatory mechanical ventilation (SIMV). When the mode of ventilation was changed to facilitate inspiratory gas flow (pressure-support) during spontaneous breathing, O2 consumption decreased 27 percent. Several important factors contributing to the increased O2 cost of breathing in patients requiring mechanical ventilation are reviewed, including the high internal resistance of demand-flow SIMV systems.     

Rate-modulated cardiac pacing based on transthoracic impedance measurements of minute ventilation: correlation with exercise gas exchange

The relation of pacing rate to physiologic variables of metabolic demand was examined in 10 consecutive patients with a minute ventilation-sensing, rate-modulating ventricular pacemaker implanted for complete heart block. All patients had paroxysmal (seven patients) or chronic (three patients) atrial fibrillation and were referred for catheter ablation of the atrioventricular junction. Treadmill exercise testing with measurement of expired gas exchange and respiratory flow was performed before ablation and 4 weeks after pacemaker implantation, with the pacemaker programmed to both the fixed-rate VVI and rate-modulating minute ventilation VVIR pacing modes in random sequence. The relation of pacing rate to oxygen consumption (VO2), expired carbon dioxide concentration (VCO2), respiratory quotient, tidal volume, respiratory rate and minute ventilation was determined during exercise in the rate-modulating minute ventilation pacing mode. Pacing rate was highly correlated with minute ventilation (r = 0.89), respiratory quotient (r = 0.89), VCO2 (r = 0.87), tidal volume (r = 0.87), VO2 (r = 0.84) and respiratory rate (r = 0.84). The mean exercise duration increased from 8.3 +/- 2.8 min in the fixed rate pacing mode to 10.2 +/- 3.4 min in the rate-modulating, minute ventilation mode (p = 0.0001). The maximal VO2 increased from 13.4 +/- 3.4 to 16.3 +/- 4.1 cc/kg per min (p = 0.0004). The maximal heart rate achieved in the minute ventilation pacing mode was 136 +/- 9.7 beats/min, similar to that observed in the patient's intrinsic cardiac rhythm before ablation (134.9 +/- 30.1 beats/min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Oxygen consumption and ventilation during normal labor.

Oxygen consumption (VO2) and minute ventilation (VE) were measured breath-by-breath for 10 min periods in the third trimester of pregnancy in 16 healthy women. These measurements were repeated during the first stage of labor in eight of the women. The 10-min mean VO2 was 3.56 ml/kg/min (+/- 0.82 SD) at term and 4.28 ml/kg/min (+/- 0.93) during labor, for an average increase of 23 percent (+/- 28 percent, p = 0.04) from third trimester to labor. The mean VE was 0.15 L/kg/min (+/- 0.03) at term and increased significantly (p = 0.05) to 0.24 L/kg/min (+/- 0.11) during labor for an average increase in VE of 65 percent (+/- 78 percent). Peak VO2 and VE occurred during contractions with five-breath average peak VO2 being 86 percent (+/- 53%) above the 10-min mean value at term and VE increasing 167 percent (+/- 154 percent) from third trimester to peak values during labor. These data may be useful in identifying patients at risk for developing respiratory insufficiency during labor. We propose an algorithm for approaching the obstetric patient with respiratory disease.     

Lung mechanics and oxygen consumption during spontaneous ventilation and severe heart failure.

The effects of acute heart failure on lung mechanics and oxygen consumption (VO2) during normocarbic spontaneous ventilation were studied in 21 anesthetized pigs. Heart failure severe enough to double oxygen extraction (O2ex) was induced with intravenous esmolol boluses and infusion. Compared to normal, the inspiratory elastic work of breathing (Wel) increased from 335 +/- 371 (mean +/- SD) to 559 +/- 48 mm Hg.ml (p less than 0.003) during heart failure, lung compliance (CL) fell from 121 +/- 144 to 22 +/- 15 ml/mm Hg (p less than 0.05), and respiratory power climbed from 140 +/- 200 to 245 +/- 214 mm Hg.ml.min-1 (p less than 0.002). These mechanical changes were accompanied by a decrease in both VO2 (221 +/- 61 to 191 +/- 50 mlO2/min, p less than 0.05) and oxygen delivery (DO2) (680 +/- 240 to 260 +/- 90 mlO2/min, p less than 0.004). The VO2/DO2 ratio doubled (p less than 0.0002), confirming increased O2ex. In conclusion, severe acute heart failure decreased CL, and increased Wel and respiratory power significantly. The depressed cardiac output limits both DO2, and to some extent, VO2. However, a greater proportion of the delivered O2 is consumed, supplying indirect evidence which suggests that the respiratory muscles' VO2 increases as a consequence of increased power expenditure.     

Computer analysis of oxygen consumption and minute ventilation for the detection of the lactate threshold

A group of 15 normal subjects performed a maximal-exercise test on a treadmill. Arterial lactate measurements were related to oxygen consumption (VO2) in an exponential fashion (individual correlation coefficients ranged from 0.9 to 0.99). In the same subjects, minute ventilation (VE) was related to VO2 in an exponential fashion (individual correlation coefficients ranged from 0.98 to 1). There was a close correlation (r = 0.97, p less than 0.001) between the slope of the log of lactate versus VO2 and the slope of the log of VE versus VO2. A computer program for predicting the VO2 corresponding to the accumulation of arterial lactate above the resting normal value (1.3 mM), defined as the lactate threshold, is described. The program is based on the slopes of the exponential relationship between lactate and VO2 and between VE and VO2 derived in the normal subjects. The program analyses 30-second values of VO2 and VE. In 28 subjects, the reproducibility of the lactate threshold prediction was evaluated during two exercise tests 1-7 days apart. The mean predicted VO2 at the lactate threshold was 18.6 +/- 7 ml/(kg.min) during test 1 and during test 2 it was 17.9 +/- 7.3 ml/(kg.min); r = 0.91, p less than 0.001. The corresponding values for maximal VO2 were 30.4 +/- 13 ml/(kg.min) and 31 +/- 13 ml/(kg.min); r = 0.99, p less than 0.001. It is concluded that this program offers a reproducible method of determining the lactate threshold during exercise testing employing a frequently used clinical protocol.     

Diaphragm function after pulmonary resection. Relationship to postoperative respiratory failure

We studied the lung mechanics and respiratory muscle function in 20 patients undergoing pulmonary resection. Transdiaphragmatic pressure (delta Pdi) during quiet breathing did not show any remarkable change after the operation (9.5 +/- 1.1 to 10.9 +/- 1.0 cm H2O), while the ratio of abdominal to transdiaphragmatic pressure changes (delta Pab/delta Pdi) revealed a significant difference between the preoperative and the early postoperative periods (0.32 +/- 0.06 to 0.00 +/- 0.11, p less than 0.05). The postoperative delta Pab/delta Pdi correlated significantly with the work of breathing (r = -0.60, p less than 0.01). The maximal transdiaphragmatic pressure (Pdimax) decreased significantly after operation (75.0 +/- 15.8 to 32.8 +/- 12.4 cm H2O, p less than 0.05), with no significant change in the maximal inspiratory mouth pressure (MIP) (74.2 +/- 16.8 to 39.5 +/- 11.6 cm H2O). Four of 20 patients developed respiratory failure postoperatively and required mechanical ventilation. delta Pab/delta Pdi in these patients was significantly lower than in the other patients (-0.62 +/- 0.24 versus 0.16 +/- 0.09, p less than 0.005). Our results suggested that during quiet breathing diaphragmatic function was preserved and intercostal/accessory muscles recruitment increased, but maximal strength of the diaphragm might be reduced in patients undergoing pulmonary resection.     

Spontaneous breathing and total body oxygen consumption in children recovering from open-heart surgery.

The effects of withdrawal of ventilatory support on cardiopulmonary function, oxygen consumption and carbon dioxide production were assessed in 25 infants and children within seven days (2.9 +/- 2.5 days; mean +/- SD) of an open heart operation, during weaning from ventilatory support. The average age of the patients was 3.4 +/- 3.5 years and weight 12.4 +/- 8.3 kg. Heart rate, blood pressure, arterial and central venous blood gas values, and oxyhemoglobin saturations were measured during controlled mechanical ventilation and during spontaneous breathing with continuous positive airway pressure. Simultaneously, VO2 and VCO2 were measured using indirect calorimetry. Withdrawal of ventilatory support effected an expected, significant decrease in arterial pH (7.42 +/- 0.10 to 7.37 +/- 0.06; p less than 0.001) and an increase in PaCO2 (34 +/- 6 to 40 +/- 5 mm Hg; p less than 0.0001), while arterial blood oxyhemoglobin saturation, heart rate, and blood pressure remained unchanged. A significant increase in central venous oxyhemoglobin saturation (67.9 +/- 11.9 to 74.8 +/- 8.3 percent; p less than 0.001) indicated improvement in systemic blood flow during spontaneous breathing. Average VO2 and VCO2 did not change significantly. A decrease in VO2 by more than 5 percent was seen in seven patients, an increase by more than 5 percent in nine, and a change within +/- 5 percent in nine patients. The change in VO2 was inversely related to the difference between measured and expected VO2 during mechanical ventilation (r = -0.73) and to body temperature (r = -0.69). The results indicate that factors other than the oxygen uptake by the respiratory muscles may have significant effects on total body VO2 in infants and children after open-heart surgery. Therefore, monitoring of VO2 during withdrawal of ventilatory support may not be an accurate indicator of respiratory work and oxygen cost of breathing in these patients.     

Beta-blockade and exercise capacity in patients with mitral stenosis in sinus rhythm

BACKGROUND AND AIM OF THE STUDY: The study aim was to determine whether beta-blocker treatment (atenolol) improves cardiopulmonary exercise performance and ventilatory response in patients with mitral stenosis in sinus rhythm. METHODS: A prospective study comparing the results of cardiopulmonary exercise tests (CPETs) was performed before and after atenolol therapy in 17 patients in NYHA classes I and II with mitral stenosis in sinus rhythm. Transthoracic echocardiography was performed pre-study, and left ventricular diameters, ejection fraction and mitral valve area monitored. CPETs (Naughton protocol) were performed by two different investigators before and after one-week atenolol therapy (50 mg/day). The second investigator was blinded to the result of the baseline test. O2 consumption, CO2 production, ventilatory parameters and respiratory exchange ratios were measured on line. RESULTS: Maximal O2 uptake (VO2max) did not differ significantly before and after beta-blockade (median 16.8 and 15.0 ml/kg/min, respectively. Median heart rate at rest (72 versus 55 beats/min; p = 0.0003) and during peak exercise (153 versus 105 beats/min; p = 0.0003), and anaerobic threshold (10 versus 8.9 ml/kg/min; p = 0.02) were lower with beta-blockade compared with the baseline state. Minute ventilation at maximum exercise (41 versus 40 l/min) and ventilatory equivalent for CO2 (34 versus 35) were unchanged with atenolol therapy, indicating no improvement in ventilatory performance. When patients were grouped into those in whom VO2max was improved with atenolol therapy (n = 7) and those in whom it was impaired (n = 10), there were no inter-group differences with respect to age, left ventricular function, severity of mitral stenosis, NYHA class and grade of beta-blockade reached. Four patients felt symptomatically worse during atenolol treatment (lower NYHA functional class). CONCLUSION: Beta-blockade does not improve exercise tolerance in patients with mitral stenosis in sinus rhythm. In addition, ventilatory performance does not change with treatment.     

Serotonergic modulation of ventilation and upper airway stability in obese Zucker rats

To elucidate the role of serotonin in the maintenance of normal breathing and upper airway (UA) patency in obesity, we studied the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antagonist, on ventilation (V E) during room air breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake young (6-8 wk) and older (7-8 mo) obese and lean Zucker (Z) rats. Older obese Z rats adopted a more rapid shallow breathing pattern compared with older lean rats. The administration of ritanserin (1 mg/kg intraperitoneally) to older obese rats resulted in a reduction in V E (439 +/- 35 [SD] to 386 +/- 41 ml/kg/min, p < 0.01), a decrease in respiratory rate, a prolongation of inspiratory time, and an increase in V O2 (16.4 +/- 1.7 to 18.2 +/- 1.9 ml/kg(0.75)/min, p < 0.05) during room air breathing. By comparison, it had little effect on ventilation in young lean and obese Z or older lean Z rats. Ritanserin also had no effect on ventilatory responses to either hypoxia or hypercapnia in young or older lean and obese Z rats. The collapsibility of the isolated UA was examined in older Z rats. The pharyngeal critical pressure (Pcrit) of older obese rats was significantly greater than that of lean rats (p < 0.05), indicating that obese rats have more collapsible UA than lean rats. The administration of ritanserin significantly increased Pcrit in older obese rats (-1.6 +/- 0.3 to -0.8 +/- 0.2 cm H2O, p < 0.01) and in lean rats (-3.1 +/- 1.0 to -2.4 +/- 0.6 cm H2O, p < 0.05). We suggest that the 5-HT(2A/2C) receptor subtype plays an important role in the maintenance of UA stability and normal breathing in obesity, and we speculate that older obese Z rats may have augmented serotonergic control of UA dilator muscles as a mechanism to prevent pharyngeal collapse.     

Respiratory response and ventilatory muscle recruitment during arm elevation in normal subjects.

Despite the fact that the arms are used extensively in daily life and that some of the muscles of the shoulder girdle share both a respiratory and a positional function for the arms, surprisingly little is known about the respiratory response to unsupported upper extremity activity. To determine the respiratory consequences of simple arm elevation during tidal breathing, we measured minute ventilation (VE), tidal volume (VT), respiratory rate (f), heart rate (HR), oxygen uptake (VO2), and carbon dioxide production (VCO2) in 22 normal subjects seated with arms elevated in front of them to shoulder level (AE) for 2 min and down at the sides (AD) for the same time period. The sequence was randomized. Compared with AD, during AE there were significant increases in VO2 (336 +/- 18 vs 289 +/- 14 ml/min, p less than 0.001), VCO2 (315 +/- 23 vs 245 +/- 16 ml/min, p less than 0.001), HR (84 +/- 6 vs 73 +/- 4 beats/min, p less than 0.05), VE (11.5 +/- 0.9 vs 9.3 +/- 0.6 L/min, p less than 0.001), and VT (868 +/- 66 vs 721 +/- 48 ml, p less than 0.001). In 11 subjects, breath-by-breath metabolic and ventilatory parameters were studied with AD for 2 min, AE for 2 min, and with AD for 3 min while also recording gastric (Pg), pleural (Ppl), and transdiaphragmatic pressures (Pdi). With AE, there was a significant increase in Pg at end inspiration (PgI, 15.4 +/- 3.2 vs 11.9 +/- 2.7 cm H2O, p less than 0.01) and in Pdi (26.5 +/- 3.4 vs 21.4 +/- 2.4 cm H2O, p less than 0.01) with no change in Pg at end expiration (PgE) or in Ppl. The increases in VO2, VCO2, VE, and VT during arm elevation persisted for 2 min after arm lowering, whereas Pgi and Pdi abruptly dropped as the arms were lowered. We conclude that simple arm elevation during tidal breathing results in significant increases in metabolic and ventilatory requirements. These increased demands are associated with higher PgI and Pdi suggesting an increased diaphragmatic contribution to the generation of ventilatory pressures. The sudden drop in Pg with arm lowering indicate a change in ventilatory muscle and or torso recruitment independent of the metabolic drive and ventilatory needs. These findings may help explain the limitation that has been reported in some normal subjects and in many patients with lung disease during unsupported upper extremity activity.     

The pattern of breathing during successful and unsuccessful trials of weaning from mechanical ventilation

We prospectively examined the pattern of breathing in patients being weaned from mechanical ventilation: one group (n = 10) underwent a successful weaning trial and were extubated, whereas another group (n = 7) developed respiratory failure and required the reinstitution of mechanical ventilation. During the period of ventilator support, minute ventilation (VI), tidal volume (VT), and respiratory frequency (f) were similar in the 2 groups. After discontinuation of the ventilator, VI remained similar in the 2 groups, but VT was lower and f was higher in the patients who failed the trial compared with those who were successful, 194 +/- 23 and 398 +/- 56 ml (p less than 0.001), respectively, and 32.3 +/- 2.3 and 20.9 +/- 2.8 breaths/min (p less than 0.001), respectively. The failure group displayed a significant increase in PaCO2 (p less than 0.005) during spontaneous breathing, without a concomitant increase in the alveolar-arterial PO2 difference. Eighty-one percent of the variance in PaCO2 was accounted for by the pattern of rapid, shallow breathing. During weaning, resting respiratory drive (reflected by mean inspiratory flow, VT/TI) and fractional inspiratory time (TI/Ttot) were similar in the 2 groups. The patients in the failure group showed significant increases in VT/TI, 265 +/- 27 to 328 +/- 32 ml/s (p less than 0.01), and VI, 5.82 +/- 0.53 to 7.32 +/- 0.52 L/min (p less than 0.01), from the beginning to the end of the weaning trial; VT and f showed no further change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Peak oxygen consumption and the minute ventilation/carbon dioxide production relation slope in morbidly obese men and women: influence of subject effort and body mass index

The authors evaluated the minute ventilation/carbon dioxide production relation (VE/VCO2 slope) as a complementary measure to peak oxygen consumption (peak VO2) in 76 patients (mean +/- SD age = 44.3+/-10.8 years, 69.7% female) with morbid obesity (mean +/- SD body mass index [BMI] = 49.4+/-7.0 kg/m(2)), as it is not limited by effort. Nearly one-half (43%) of the patients achieved a peak respiratory exchange ratio <1.10. Mean peak VO2 and VE/VCO2 slope were 17.0+/-3.7 mL/kg/min and 27.8+/-4.0, respectively. Peak VO2 correlated with BMI (r=-0.45, P<.0001), while VE/VCO2 slope did not (r=-0.04, P=.73). There was a linear trend for declining mean peak VO2 (P=.001) but not for VE /VCO2 slope (P=.59) with increasing BMI quintiles. The VE/VCO2 slope is an effort-independent measure that is also independent of BMI and may serve as an adjunctive cardiorespiratory variable when evaluating morbidly obese men and women.     

Rate of oxyhemoglobin desaturation in obstructive versus nonobstructive apnea

Preapneic thoracic gas volume (Vtg), arterial saturation (SaO2), and mixed venous oxygen saturation (SvO2), have been shown to influence the rate of SaO2 fall (dSaO2/dt) during apnea. We asked the following question: does tissue oxygen consumption (tVO2) affect the dSaO2/dt during apnea? We attempted to answer this question by comparing dSaO2/dt during obstructive apneas (high tVO2) with dSaO2/dt during nonobstructive apneas (low tVO2) in six adult baboons. Fiberoptic central venous and arterial catheters were used for continuous monitoring of SvO2, SaO2, and cardiac output. A sapphire-bearing turbine monitored minute ventilation and airflow cessation. A Respitrace and esophageal pressures were used to assess relative differences in Vtg. Obstructive apneas (30, 45, and 60-s) were created by clamping an indwelling cuffed endotracheal tube at end-expiration. Nonobstructive apneas were created by paralyzing the animals with atracurium and interrupting ventilation for periods equivalent to those of the obstructed apneas. The ventilator was adjusted to duplicate the respiratory rate, tidal volume, and relative Vtg of the spontaneously breathing animal. Mean tVO2 during spontaneous breathing was 110 ml/min (Fick method) and decreased to 90 ml/min during paralysis (p less than 0.05). The dSaO2/dt for the three apnea durations (mean, all animals), obstructive versus nonobstructed were: 0.85 and 0.74%/s (n = 6), 0.87 and 0.75%/s (n = 6), and 0.60 and 0.48%/s (n = 4), respectively. The dSaO2/dt was significantly lower during the nonobstructive apneas. We conclude that differences in VO2 during apnea may affect the dSaO2/dt and that for the same duration apnea, central apneas may show less desaturation than obstructive apneas where vigorous muscular efforts at overcoming obstruction are common.     

Relationship between O2 delivery and O2 consumption in the adult respiratory distress syndrome

We evaluated the relationship between O2 delivery and oxygen consumption (VO2) in ten patients with the adult respiratory distress syndrome (ARDS) over the course of their illness (mean 7 +/- 5 days) while they were receiving positive mechanical ventilation with varying levels of positive end-expiratory pressure (PEEP). Mean values and standard deviations for O2 delivery and VO2 were 15.2 +/- 4.8 ml/min/kg and 4.1 +/- 1.2 ml/min/kg, respectively. In our ten patients, below an O2 delivery of 21 ml/min/kg, VO2 was linearly related to O2 delivery (VO2 = 0.32 X O2 delivery--0.53, n = 83, r = 0.76). However, at an O2 delivery rate higher than 21 ml/min/kg, there was no correlation between VO2 and O2 delivery. Mixed venous O2 content (CvO2) and arteriovenous oxygen content difference (C(a-v)O2) did not correlate with O2 delivery, nor was there a significant correlation between cardiac output (Qt) and mixed venous O2 tension (PvO2) or saturation (SvO2). We conclude that in patients with ARDS on mechanical ventilation with PEEP, VO2 and O2 delivery are linearly related except at high levels of O2 delivery. PvO2 and (C(a-v)O2) do not correlate with O2 delivery and are not sensitive indicators of tissue oxygenation in ARDS.     

Chest wall kinematics in patients with hemiplegia

Owing to difficulties in measuring ventilation symmetry, good evidence of different right/left respiratory movements has not yet been provided. We investigated VT differences between paretic and healthy sides during quiet breathing, voluntary hyperventilation, and hypercapnic stimulation in patients with hemiparesis. We studied eight patients with hemiparesis and nine normal sex- and age-matched subjects. Right- and left-sided VT was reconstructed using optoelectronic plethysmography. In control subjects, no asymmetry was found in the study conditions. VTs of paretic and healthy sides were similar during quiet breathing, but paretic VT was lower during voluntary hyperventilation in six patients and higher during hypercapnic stimulation in eight patients (p = 0.02). The ventilatory response to hypercapnic stimulation was higher on the paretic than on the healthy side (p = 0.012). In conclusion, hemiparetic stroke produces asymmetric ventilation with an increase in carbon dioxide sensitivity and a decrease in voluntary ventilation on the paretic side.     

Dependence of enhanced maximal exercise performance on increased peak skeletal muscle perfusion during long-term captopril therapy in heart failure

Maximal oxygen uptake (VO2), skeletal muscle blood flow by xenon-133 washout technique and femoral vein arteriovenous oxygen difference and lactate were measured at rest and during maximal bicycle exercise in eight patients with severe congestive heart failure before and after 8 weeks of therapy with captopril. During therapy, skeletal muscle blood flow at rest increased significantly from 1.5 +/- 0.6 to 2.6 +/- 1.0 ml/100 g per min (p less than 0.05), with a concomitant decrease in the femoral arteriovenous oxygen difference from 10.0 +/- 1.7 to 8.3 +/- 1.9 ml/100 ml (p less than 0.05). Maximal VO2 increased significantly from 13.4 +/- 3.0 to 15.5 +/- 4.1 ml/kg per min (p less than 0.05). In four patients, the increase in maximal VO2 averaged 3.7 ml/kg per min (range 2.7 to 4.9), whereas in the remaining four patients, it was less than 1 ml/kg per min. Overall, peak skeletal muscle blood flow attained during exercise did not change significantly during long-term therapy with captopril (19.6 +/- 6.2 versus 27.6 +/- 14.3 ml/100 g per min, p = NS). However, the four patients with a significant increase in maximal VO2 experienced substantial increases in peak skeletal muscle blood flow and the latter changes were linearly correlated with changes in maximal VO2 (r = 0.95, p less than 0.001). Femoral arteriovenous oxygen difference at peak exercise was unchanged (12.6 +/- 2.6 versus 12.6 +/- 2.4 ml/100 ml). Thus, improvement in maximal VO2 produced by long-term therapy with captopril is associated with an increased peripheral vasodilatory response to exercise, and this improvement only occurs when the peak blood flow is augmented.(ABSTRACT TRUNCATED AT 250 WORDS)     

Managing acute respiratory decompensation in the morbidly obese

Morbid obesity adversely affects respiratory physiology, leading to reduced lung volumes, decreased lung compliance, ventilation perfusion mismatch, sleep-disordered breathing and the impairment of ventilatory control, and neurohormonal and neuromodulators of breathing. Therefore, morbidly obese subjects are at increased risk of various pulmonary complications that can present either acutely or chronically. Respiratory failure is one of the most common pulmonary complications related to morbid obesity. Both acute hypoxaemic and hypercapnic respiratory failure are more common among obese patients. The management pathway of respiratory failure depends, to a large extent, on the underlying cause, primarily due to the diversity of the underlying triggering diseases, the pathophysiology and the prognosis associated with each disease. Morbidly obese patients with hypoventilation have an increased risk of acute hypercapnic respiratory failure. Early diagnosis of this disorder and the application of non-invasive ventilation in this group of patients have been shown to improve respiratory parameters, decrease the need for invasive mechanical ventilation and improve survival. Invasive ventilation remains the last life-saving procedure in patients with respiratory failure who do not respond to non-invasive measures. However, due to the abnormal respiratory physiology in obese patients, special precautions are required during intubation, mechanical ventilation and weaning.     

Morbid obesity in the medical ICU.

Study objective: To describe the clinical course, complications, and prognostic factors of morbidly obese patients admitted to the ICU compared to a control group of nonobese patients. DESIGN: A retrospective study. SETTING: Two university-affiliated hospitals. METHODS: We reviewed the medical records of 117 morbidly obese patients (body mass index >/= 40 kg/m(2)) admitted to the medical ICU between January 1994 and June 2000. Data collected included demographic information, comorbid condition, APACHE (acute physiology and chronic health evaluation) II score, invasive procedures, organ failure, and in-hospital mortality. RESULTS: Obstructive airway disease, pneumonia, and sepsis were the main reasons for admission to the ICU in the morbidly obese group. Sixty-one percent of the morbidly obese patients and 46% of the nonobese group required mechanical ventilation (p = 0.02). The mean lengths of mechanical ventilation and ICU stay were significantly longer for the morbidly obese group (7.7 +/- 9.6 days and 9.3 +/- 10.5 days vs 4.6 +/- 7.1 days and 5.8 +/- 8.2 days, respectively; p < 0.001). APACHE II scores were not significantly different in the two groups (19.1 +/- 7.6 and 20.6 +/- 12.2; p = 0.6). Overall mortality was 30% for the morbidly obese patients and 17% for the nonobese group (p = 0.019). By multivariate analysis, multiorgan failure (odds ratio [OR], 4.6; 95% confidence interval [CI], 2.1 to 16.6), PaO(2)/fraction of inspired oxygen < 200 for > 48 h (OR, 2.3; 95% CI, 1.2 to 7.8), and depressed left ventricular ejection fraction < 40% (OR, 1.4; 95% CI, 1.03 to 13.8) were independently associated with ICU mortality in the morbidly obese group. CONCLUSION: We conclude that critically ill morbidly obese patients are at increased risk of morbidity and mortality compared to the nonobese patients.     

Physiological response to pressure support ventilation delivered before and after extubation in patients not capable of totally spontaneous autonomous breathing

We designed a prospective, physiological study in 12 patients affected by chronic respiratory disorders. The study was aimed at assessing the diaphragm energy expenditure (PTPdi), lung resistance (RL) and elastance (EL), arterial blood gases (ABG), breathing pattern, and dyspnea measured by a visual analog scale during invasive pressure support ventilation (i-PSV) and noninvasive PSV (n-PSV). The ventilator settings were kept the same. Both i-PSV and n-PSV significantly reduced the PTPdi per minute, compared with that during a T-piece trial (204.4 +/- 93.8 cm H(2)O x s/min [i-PSV]; 197.5 +/- 119.8 [n-PSV]; 393.8 +/- 129.0 [T-piece]). Expired tidal volume (VTe) was significantly higher (p < 0.05) during n-PSV (615 +/- 166 ml) than during i-PSV (519 +/- 140 ml). The respiratory pump (PTPdi/VTe) was more effective (p < 0.05) with noninvasive ventilation (22.3 +/- 2.3 cm H(2)O x s/L for i-PSV versus 17.2 +/- 3.3 for n-PSV). RL and EL were similar with the two modes of ventilation. Overall dyspnea was significantly (p < 0.05) better during n-PSV than i-PSV, whereas ABG were similar. We have shown, in patients affected by stable chronic respiratory disorders not ready to sustain totally spontaneous breathing, that i-PSV and n-PSV are equally effective in reducing the PTPdi and in improving ABG, but that n-PSV seems to be better tolerated.