(1/1644) Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction.
BACKGROUND: Impaired alveolar-capillary membrane conductance is the major cause for the reduction in pulmonary diffusing capacity for carbon monoxide (DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmonary microvascular damage, or is variable is unknown. The aim of this study was to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects of volume loading on airflow rates. METHODS AND RESULTS: Ten patients with left ventricular dysfunction (LVD) and 8 healthy volunteers were studied. DM and Vc were determined by the Roughton and Forster method. The forced expiratory volume in 1 second (FEV1), vital capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL. kg-1 body wt of 0.9% saline acutely reduced DM (12.0+/-3.3 versus 10.4+/-3.5 mmol. min-1. kPa-1, P<0.005), FEV1 (2.3+/-0.4 versus 2.1+/-0.4 L, P<0.0005), and PEFR (446+/-55 versus 414+/-56 L. min-1, P<0.005). All pulmonary function tests had returned to baseline values 24 hours later. In normal subjects, saline infusion had no measurable effect on lung function. CONCLUSIONS: Acute intravascular volume expansion impairs alveolar-capillary membrane function and increases airflow obstruction in patients with LVD but not in normal subjects. Thus, the abnormalities of pulmonary diffusion in heart failure, which were believed to be fixed, also have a variable component that could be amenable to therapeutic intervention. (+info)
(2/1644) Peripheral muscle ergoreceptors and ventilatory response during exercise recovery in heart failure.
Recent studies have suggested that the increased ventilatory response during exercise in patients with chronic heart failure was related to the activation of muscle metaboreceptors. To address this issue, 23 patients with heart failure and 7 normal subjects performed arm and leg bicycle exercises with and without cuff inflation around the arms or the thighs during recovery. Obstruction slightly reduced ventilation and gas exchange variables at recovery but did not change the kinetics of recovery of these parameters compared with nonobstructed recovery: half-time of ventilation recovery was 175 +/- 54 to 176 +/- 40 s in patients and 155 +/- 66 to 127 +/- 13 s in controls (P < 0.05, patients vs. controls, not significant within each group from baseline to obstructed recovery). We conclude that muscle metaboreceptor activation does not seem to play a role in the exertion hyperventilation of patients with heart failure. (+info)
(3/1644) Continuous arterial P(O2) and P(CO2) measurements in swine during nitrous oxide and xenon elimination: prevention of diffusion hypoxia.
BACKGROUND: During nitrous oxide (N2O) elimination, arterial oxygen tension (PaO2) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination. METHODS: Nineteen anesthetized and paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO2 and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor. RESULTS: The PaO2 decreased from 119+/-10 mm Hg to 102+/-12 mm Hg (mean+/-SD) during N2O washout (P<0.01) and from 116+/-9 mm Hg to 110+/-8 mm Hg during xenon elimination (P<0.01), with a significant difference (P<0.01) between baseline and minimum PaO2 values (deltaPaO2, 17+/-6 mm Hg during N2O washout and 6+/-3 mm Hg during xenon washout). The PaCO2 value also decreased (from 39.3+/-6.3 mm Hg to 37.6+/-5.8 mm Hg) during N2O washout (P<0.01) and during xenon elimination (from 35.4+/-1.6 mm Hg to 34.9+/-1.6 mm Hg; P< 0.01). The deltaPaCO2 was 1.7+/-0.9 mm Hg in the N2O group and 0.5+/-0.3 mm Hg in the xenon group (P<0.01). CONCLUSION: Diffusive hypoxia is unlikely to occur during recovery from xenon anesthesia, probably because of the low blood solubility of this gas. (+info)
(4/1644) Breathing patterns during slow and fast ramp exercise in man.
Breathing frequency (fb), tidal volume (VT), and respiratory timing during slow (SR, 8 W min-1) and fast (FR, 65 W min-1) ramp exercise to exhaustion on a cycle ergometer was examined in seven healthy male subjects. Expiratory ventilation (VE), pulmonary gas exchange (VO2 and VCO2) and end-tidal gas tensions (PET,O2 and PET,CO2) were determined using breath-by-breath techniques. Arterialized venous blood was sampled from a dorsal hand vein at 2 min intervals during SR and 30 s intervals during FR and analysed for arterial plasma PCO2 (PaCO2). PET,CO2 increased with increasing work rates (WRs) below the ventilatory threshold (VT); at WRs > or = 90% VO2,max, PET,CO2 was reduced (P < 0.05) below 0 W values in SR but not in FR.fb and VT were similar for SR and FR at all submaximal WRs, resulting in a similar VE. At exhaustion VE was similar but fb was higher (P < 0.05) and VT was lower (P < 0.05) in SR (fb, 51 +/- 10 breaths min-1; VT, 2590 +/- 590 ml) than in FR (fb, 42 +/- 8 breaths min-1; VT, 3050 +/- 470 ml). The time of expiration (TE) decreased with increasing WR, but there was no difference between SR and FR. The time of inspiration (TI) decreased at exercise intensities > or = VT; at exhaustion, TI was shorter (P < 0.05) during SR (0.512 +/- 0.097 s) than during FR (0.753 +/- 0.100 s). The TI to total breath duration (TI/TTot) and the inspiratory flow (VT/TI) were similar during SR and FR at all submaximal exercise intensities; at VO2,max, TI/TTot was lower (P < 0.05) and VT/TI was higher (P < 0.05) during SR (TI/TTot, 0.473 +/- 0.030; VT/TI, 5.092 +/- 0.377 l s-1) than during FR (TI/TTot, 0.567 +/- 0.050; VT/TI, 4.117 +/- 0.635 l s-1). These results suggest that during progressive exercise, breathing pattern and respiratory timing may be determined, at least at submaximal work rates, independently of alveolar and arterial PCO2. (+info)
(5/1644) Airway closure, atelectasis and gas exchange during general anaesthesia.
Airway closure and the formation of atelectasis have been proposed as important contributors to impairment of gas exchange during general anaesthesia. We have elucidated the relationships between each of these two mechanisms and gas exchange. We studied 35 adults with healthy lungs, undergoing elective surgery. Airway closure was measured using the foreign gas bolus technique, atelectasis was estimated by analysis of computed x-ray tomography, and ventilation-perfusion distribution (VA/Q) was assessed by the multiple inert gas elimination technique. The difference between closing volume and expiratory reserve volume (CV-ERV) increased from the awake to the anaesthetized state. Linear correlations were found between atelectasis and shunt (r = 0.68, P < 0.001), and between CV-ERV and the amount of perfusion to poorly ventilated lung units ("low Va/Q", r = 0.57, P = 0.001). Taken together, the amount of atelectasis and airway closure may explain 75% of the deterioration in PaO2. There was no significant correlation between CV-ERV and atelectasis. We conclude that in anaesthetized adults with healthy lungs, undergoing mechanical ventilation, both airway closure and atelectasis contributed to impairment of gas exchange. Atelectasis and airway closure do not seem to be closely related. (+info)
(6/1644) Cardiopulmonary resuscitation: effect of CPAP on gas exchange during chest compressions.
BACKGROUND: Conventional cardiopulmonary resuscitation (CPR) includes 80-100/min precordial compressions with intermittent positive pressure ventilation (IPPV) after every fifth compression. To prevent gastric insufflation, chest compressions are held during IPPV if the patient is not intubated. Elimination of IPPV would simplify CPR and might offer physiologic advantages, but compression-induced ventilation without IPPV has been shown to result in hypercapnia. The authors hypothesized that application of continuous positive airway pressure (CPAP) might increase CO2 elimination during chest compressions. METHODS: After appropriate instrumentation and measurement of baseline data, ventricular fibrillation was induced in 18 pigs. Conventional CPR was performed as a control (CPR(C)) for 5 min. Pauses were then discontinued, and animals were assigned randomly to receive alternate trials of uninterrupted chest compressions at a rate of 80/min without IPPV, either at atmospheric airway pressure (CPR(ATM)) or with CPAP (CPR(CPAP)). CPAP was adjusted to produce a minute ventilation of 75% of the animal's baseline ventilation. Data were summarized as mean +/- SD and compared with Student t test for paired observations. RESULTS: During CPR without IPPV, CPAP decreased PaCO2 (55+/-28 vs. 100+/-16 mmHg) and increased SaO2 (0.86+/-0.19 vs. 0.50+/-0.18%; P < 0.001). CPAP also increased arteriovenous oxygen content difference (10.7+/-3.1 vs. 5.5+/-2.3 ml/dl blood) and CO2 elimination (120+/-20 vs. 12+/-20 ml/min; P < 0.01). Differences between CPR(CPAP) and CPR(ATM) in aortic blood pressure, cardiac output, and stroke volume were not significant. CONCLUSIONS: Mechanical ventilation may not be necessary during CPR as long as CPAP is applied. Discontinuation of IPPV will simplify CPR and may offer physiologic advantage. (+info)
(7/1644) Hemodynamic effects of bilevel nasal positive airway pressure ventilation in patients with heart failure.
AIMS: Benefits of nasal continuous positive airway pressure (CPAP) in patients presenting with chronic heart failure (CHF) are controversial. The purpose of this study was to compare the hemodynamic effects of CPAP and bilevel positive airway pressure (BiPAP) in patients with or without CHF. METHODS AND RESULTS: Twenty patients with CHF and 7 with normal left ventricular function underwent cardiac catheterization. Measurements were made before and after three 20-min periods of BiPAP: expiratory positive airway pressure (EPAP) = 8 cm H2O and inspiratory positive airway pressure (IPAP) = 12 cm H2O, EPAP = 10 cm H2O and IPAP = 15 cm H2O, and CPAP = EPAP = IPAP = 10 cm H2O administered in random order. Positive pressure ventilation decreased cardiac output (CO) and stroke volume. No change was observed in either pulmonary or systemic arterial pressure. There was no difference in the hemodynamic effects of the three ventilation settings. Only mean pulmonary wedge pressure (MPWP) and heart rate were lower with CPAP than with BiPAP. CO decreased only in patients with low MPWP (=12 mm Hg). BiPAP ventilation increased PaO2 and decreased PaCO2 more than CPAP. CONCLUSIONS: In patients with cardiac failure, a decrease in CO occurs both during CPAP and BiPAP, when pulmonary wedge pressure is low (=12 mm Hg). (+info)
(8/1644) A chest wall restrictor to study effects on pulmonary function and exercise. 2. The energetics of restrictive breathing.
Chest wall restriction, whether caused by disease or mechanical constraints such as protective outerwear, can cause decrements in pulmonary function and exercise capacity. However, the study of the oxygen cost associated with mechanical chest restriction has so far been purely qualitative. The previous paper in this series described a device to impose external chest wall restriction, its effects on forced spirometric volumes, and its test-retest reliability. The purpose of this experiment was to measure the oxygen cost associated with varied levels of external chest wall restriction. Oxygen uptake and electromyogram (EMG) of the external intercostals were recorded during chest restriction in 10 healthy males. Subjects rested for 9 min before undergoing volitional isocapnic hyperpnea for 6 min. Subjects breathed at minute ventilations (V.I) of 30, 60, and 90 liters/min with chest wall loads of 0, 25, 50 and 75 mm Hg applied. Frequency of breathing was set at 15, 30, and 45 breaths per minute with a constant tidal volume (VT) of 2 liters. Oxygen uptake was measured continuously at rest and throughout the hyperventilation bouts, while controlling V.I and VT. Integrated EMG (IEMG) from the 3rd intercostal space was recorded during each minute of rest and hyperventilation. Two-way ANOVA with repeated measures revealed that chest wall loading and hyperpnea significantly increased V.O2 values (p < 0.01). External intercostal IEMG levels were significantly increased (p < 0.05) at higher restrictive load (50 and 75 mm Hg) and at the highest minute ventilation (90 liters/min). These data suggest that there is a significant and quantifiable increase in the oxygen cost associated with external chest wall restriction which is directly related to the level of chest wall restriction. (+info)