Breathing patterns in infants and children under halothane anesthesia: effect of dose and CO2

We studied the amplitude, timing, and shape of the airflow waveform at the mouth of spontaneously breathing children under two sets of conditions: 1) in 30 children aged 9 wk-4.5 yr at 2, 1, and 0% inspired halothane concentration and 2) in 22 children aged 5 mo-7 yr during hyperoxic CO2 rebreathing while recovering from anesthesia. Compared with control values, the relative changes in breath parameters at 1 and 2% halothane were, respectively, as follows: total cycle time -19 and -31%, tidal volume (VT) -30 and -44%, minute ventilation -11 and -17%, and VT/inspiratory time (TI) -16 and -20%. Parameters of timing and breath shape did not change except for the significant but small increase in TI/total cycle time (by 6 and 8%, respectively). With CO2 rebreathing, parameters reflecting inspiratory drive increased significantly in all patients as shown by the slopes of the regressions of these parameters against end-tidal PCO2. Mean slopes expressed in %control value per millimeter of mercury CO2 were 12.1 for minute ventilation, 8.3 for VT, and 10.67 for VT/TI. Parameters reflecting the timing and breath shape remained essentially unchanged. Our results suggest that, in children under halothane anesthesia, the amplitude, timing, and shape of the breathing pattern are controlled independently. In particular, the amplitude and timing of the breath may vary widely without any significant change in the shape.     

Effects of negative pressure assisted ventilation on dyspnoeic sensation and breathing pattern

Although negative pressure assisted ventilation with an assist-control mode may have a potential therapeutic role in the treatment of severe dyspnoea, the effects of negative pressure assisted ventilation with the assist-control mode on dyspnoea and breathing patterns have not been examined. We examined the effects of negative pressure assisted ventilation with the assist-control mode on dyspnoea and breathing patterns produced by a combination of resistive loading and hypercapnia in nine healthy subjects breathing spontaneously. Subjects were asked to rate their sensation of respiratory discomfort using a visual analogue scale. Negative pressure assisted ventilation caused a significant reduction in sensation of respiratory discomfort from a visual analogue scale score of 74 (55-91) (median (range)) before negative pressure assisted ventilation to 34 (15-53) during negative pressure assisted ventilation (p<0.01). During negative pressure assisted ventilation, there were significant changes in breathing patterns characterized by an increase in tidal volume and a decrease in respiratory frequency, while neither minute ventilation nor end-tidal carbon dioxide tension changed. Our results indicate that negative pressure assisted ventilation with the assist-control mode is effective in relief of dyspnoea and that negative pressure assisted ventilation influences the control of breathing to minimize respiratory discomfort.     

Tumor necrosis factor-alpha in serum of macaques during SIVmac251 acute infection

Peripheral chemoreceptors may be immature in neonatal animals, exhibiting maturational changes in the perinatal period. Even though methylxanthines are respiratory stimulants, many premature neonates do not respond to them. Thus, we hypothesized that carotid body activity is necessary for aminophylline to reverse hypoxia-induced respiratory depression. We exposed 16 anesthetized newborn piglets (age 2-7 days) to hypoxia (inhalation of 12% oxygen) for 5 min. Aminophylline (15 mg/kg iv) was administered either prior to (11 piglets) or following (5 piglets) carotid body denervation (CBD). Before CBD, hypoxia elicited transient initial increases in tidal volume (from 79 +/- 4 to 99 +/- 1% of maximum, mean +/- SE), minute ventilation (from 64 +/- 5 to 93 +/- 4%), and peak phrenic electroneurogram (from 63 +/- 8 to 91 +/- 6%, all P < 0.05). This was followed by a decrease in tidal volume, minute ventilation and phrenic electroneurogram (all P < 0.05). Prior to CBD, aminophylline pretreatment prevented the decrease in all the measures of respiratory output during late hypoxia. After CBD, hypoxia induced an initial and sustained depression of ventilation (tidal volume from 100 to 33 +/- 14%; frequency from 94 +/- 4 to 42 +/- 17%; minute ventilation from 100 to 32 +/- 14%, all P < 0.05) and phrenic electroneurogram (peak phrenic from 100 to 47 +/- 18%; minute phrenic from 85 +/- 6 to 55 +/- 21%, both P < 0.05). Administration of aminophylline after CBD did not prevent the profound respiratory depression elicited by hypoxia in the chemodenervated piglets.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea

We hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.     

Suicidal behavior in bipolar and unipolar affective disorders: a meta-analysis

Manual ventilation (MAV) or handbagging is a frequent and often life-saving procedure for neonates; however, few studies allow for an objective evaluation of techniques or possible risks. We compared parameters of ventilation and pulmonary mechanics obtained during routine pressure-limited MAV to those obtained during spontaneous breathing (SPB) in the same infant at approximately the same time. We selected 20 preterm neonates in the recovery phase of respiratory distress syndrome who received periodic MAV and were capable of optimum spontaneous minute ventilation (> 300 mL/kg/min). During MAV compared to SPB we measured higher tidal volume (8.1 +/- 0.5 SE vs. 5.4 +/- 0.4 SE mL/kg, P < 0.001), lower total pulmonary compliance (0.65 +/- 0.05 vs. 1.16 +/- 0.11 SE mL/cmH2O, P < 0.001), end-inspiratory compliance, higher pulmonary resistance (121 +/- 11 vs. 61 +/- 7 SE cmH2O/L/s, P < 0.001) and higher peak inspiratory airflow (2.8 +/- 0.2 vs. 1.6 +/- 0.1 L/s, P < 0.001). Inspiratory time (Ti) was consistently longer during MAV (0.49 +/- 0.02 vs. 0.36 +/- 0.02 SE, P < 0.001) such that during MAV the difference between actual Ti and minimal effective Ti (fivefold inspiratory time constant) was larger (0.29 +/- 0.03 vs. 0.13 +/- 0.03 s, P < 0.05). Our study suggests that operator-dependent ventilatory variables such as tidal volume, inspiratory time, frequency, and airflow need to be further evaluated in order to develop standardized guidelines for the safe administration of MAV. Until then the ventilator used for brief or augmented ventilatory support is a reasonable alternative to administering MAV by inconsistent standards.     

Physiological dead space/tidal volume ratio during face mask, laryngeal mask, and cuffed oropharyngeal airway spontaneous ventilation

OBJECTIVE: To compare the physiological dead space/tidal volume ratio and arterial to end-tidal carbon dioxide tension (ETCO2) difference during spontaneous ventilation through a face mask, a laryngeal mask (LMA), or a cuffed oropharyngeal airway. DESIGN: Prospective, randomized, cross-over study. SETTING: Inpatient anesthesia at a university department of orthopedic surgery. PATIENTS: 20 ASA physical status I and II patients, without respiratory disease, who underwent ankle and foot surgery. INTERVENTIONS: After a peripheral nerve block was performed, propofol anesthesia was induced and then maintained with a continuous intravenous (i.v.) infusion (4 to 6 mg/kg/h). A face mask, a cuffed oropharyngeal airway, or an LMA were placed in each patient in a random sequence. After 15 minutes of spontaneous breathing through each of the airways, ventilatory variables, as well as arterial, end-tidal, and mixed expired CO2 partial pressure, were measured, and physiological dead space/tidal volume ratio was calculated. MEASUREMENTS AND MAIN RESULTS: Expired minute volume and respiratory rate (RR) were lower with LMA (5.6 +/- 1.2 L/min and 18 +/- 3 breaths/min) and the cuffed oropharyngeal airway (5.7 +/- 1 L/min and 18 +/- 3 breaths/min) than the face mask (7.1 +/- 0.9 L/min and 21 +/- 3 breaths/min) (p = 0.0002 and p = 0.013, respectively). Physiological dead space/tidal volume ratio and arterial to end tidal CO2 tension difference were similar with the cuffed oropharyngeal airway (3 +/- 0.4 mmHg and 4.4 +/- 1.4 mmHg) and LMA (3 +/- 0.6 mmHg and 3.7 +/- 1 mmHg) and lower than with the face mask (4 +/- 0.5 mmHg and 6.7 +/- 2 mmHg) (p = 0.0001 and p = 0.001, respectively). CONCLUSION: Because of the increased dead space/tidal volume ratio, breathing through a face mask required higher RR and expired minute volume than either the cuffed oropharyngeal airway or LMA, which, in contrast, showed similar effects on the quality of ventilation in spontaneously breathing anesthetized patients.     

The content of electrolytes (Na, K, Ca, Mg) in vertebrate otoliths and otoconia

IVOX (intravenous oxygenator and CO2 removal device) augments venous gas exchange in patients with severe respiratory failure. Controlled hypoventilation with permissive hypercapnia reduces airway pressures during mechanical ventilation and augments CO2 exchange through the IVOX. To quantify the additive effects of gradual permissive hypercapnia and IVOX on gas exchange and reduction of airway pressures, 13 adult sheep underwent tracheostomy and severe smoke inhalation injury. Seven were mechanically ventilated alone (control), and six had mechanical ventilation, systemic anticoagulation, and implantation of IVOX (size 7 with 0.21-m2 surface area) (IVOX group). Both groups were anesthetized and paralyzed for 24 hr. In the IVOX group, minute ventilation was decreased in a stepwise fashion to produce a gradual increase in PaCO2, from 30 to 95 mm Hg, over 12 hr, and then sustained for an additional 12 hr. Sodium bicarbonate was given intravenously as necessary to keep arterial pH above 7.25. There were no significant differences in mean arterial pressure, cardiac output, or pulmonary artery pressure between the two groups. In the IVOX/permissive hypercapnia group, IVOX CO2 removal increased as a linear function of PaCO2 (y = 0.87x + 8.99, R2 = 0.80). IVOX CO2 removal was only 40 ml/min at normocapnia (40 mm Hg) but increased to 91 ml/min when PaCO2 was 95 mm Hg. Both peak inspiratory pressure and minute ventilation of the IVOX/permissive hypercapnia group were significantly lower than the control group, 30 +/- 4 mm Hg vs 51 +/- 3 mm Hg and 3.9 +/- 0.3 liters vs 8.4 +/- 0.5 liters (P < 0.05) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of drive and timing mechanisms on breathing pattern and ventilation during mental task performance

Assessment of multiple respiratory measures may provide insight into how behavioral demands affect the breathing pattern. This is illustrated by data from a study among 44 subjects, in which tidal volume, respiration rate, minute ventilation and indices of central drive and timing mechanisms were assessed via inductive plethysmography, in addition to end-tidal PCO2. After a baseline, three conditions of a memory comparison task were presented. The first two conditions differed only with regard to the presence or absence of feedback of performance (NFB and FB). In the third 'all-or-nothing' (AON) condition, subjects only received a monetary bonus, if their performance exceeded that of the previous two conditions. Minute ventilation increased from baseline to all task conditions, and from NFB and FB to AON. Respiration rate increased in all task conditions, but there were no differences between task conditions. Tidal volume decreased during NFB, but was equal to baseline during FB and AON. Of the respiratory control indices, inspiratory flow rate covaried much more closely with minute ventilation than duty cycle. The task performance induced a minor degree of hyperventilation. The discussion focusses on how behavioral demands affect respiratory control processes to produce alterations in breathing pattern and ventilation.     

Theophylline improves measurements of respiratory muscle efficiency

To determine the effect of theophylline on respiratory muscle efficiency (RME), 12 normal subjects were given theophylline vs placebo in a double-blind, randomized crossover protocol. Spirometry, resting energy expenditure, minute ventilation, RME and oxygen cost of breathing were measured at baseline, after taking theophylline, and after placebo. RME was calculated by dividing the added work required to breathe through a threshold load by the added energy consumed during loaded breathing. Oxygen cost of breathing was calculated by dividing the increase in oxygen consumption induced by breathing an air/carbon dioxide mixture by the associated increase in minute ventilation. RME increased from 3.3 +/- 1.6% at baseline to 7.9 +/- 3.2% after theophylline (p < 0.01) but did not change significantly after placebo (4.8 +/- 2.4%). Oxygen cost of breathing decreased from 3.9 +/- 2.4 mL O2 per liter at baseline to 1.7 +/- 0.7 mL O2 per liter after theophylline (p < 0.05) but did not change significantly after placebo (2.8 +/- 1.3 mL O2 per liter). Theophylline use was also associated with an 18% increase in minute ventilation (p < 0.01) and a 15.7% increase in resting energy expenditure (p < 0.01). Theophylline improves measured RME and reduces oxygen cost of breathing in normal subjects. These effects are offset by increases in resting energy expenditure and minute ventilation.     

Precise measurement of individual rapid eye movements in REM sleep of humans

An automated analyzer for individual eye movements (EMs) has been developed that enables precise analyses of their incidence. Three new parameters for each EM are obtained: EM magnitude, the angle and speed of eyeball rotation, and the energy of each EM. All rapid eye movement (REM) sleep EMs from 40 nights of polysomnography for 20 healthy young men were analyzed. The mean frequency of eye movement (EM frequency) was 15.9 per minute. Compared to conventionally analyzed rapid eye movement (REM) density, EM frequency was more sensitive to differences among sleep cycles, nights, and individuals. The mean EM rotation was 6.27 +/- 0.021 degrees, the mean speed of rotation was 58.73 +/- 0.18 degrees/second, and mean energy was 525.85 +/- 3.82 degrees2/second. The distribution of changes in these new parameters differed from conventional measures across REM episodes. The conventional measures, REM episode duration, and REM density increased progressively in successive REM episodes in an ascent-to-right pattern. However, the new parameters peaked in the second, followed by relatively low values, producing an inverted V pattern. This discrepancy could indicate physiological mechanisms of EM that are not revealed in conventional measures of REM sleep intensity.     

Estimation of arterial PCO2 in the elderly

Arterial PCO2 (PaCO2), determined directly in the radial artery, was compared with indirect estimates of PCO2 in six elderly men (mean age 73.8 yr). Estimates of PaCO2 included arterialized venous PCO2 (PavCO2); end-tidal PCO2; mean alveolar PCO2, calculated by using a reconstruction of the alveolar oscillation in PCO2 and accounting for the presence of dead space (time-weighted mean for PCO2 throughout the respiratory cycle); and values calculated by using the empirical formula developed by Jones et al. (N. L. Jones, D. G. Robertson, and J. W. Kane. J. Appl. Physiol. 47: 954-960, 1979), which incorporates end-tidal PCO2 and tidal volume (PaCO2 derived from end-tidal PCO2 and VT). Measurements were made at rest and during cycle ergometry at 25 and 50 W while the subjects breathed various gas mixtures (euoxic-eucapnic, hypoxic-eucapnic, hyperoxic-eucapnic, and hyperoxic-hypercapnic). The mean differences between the estimates and the actual PaCO2 at rest and in 25- and 50-W exercise were as follows: PavCO2, 0.3 +/- 0.7 (SD), -0.1 +/- 0.7, and 1.8 +/- 1.2 Torr; end-tidal PCO2, 2.9 +/- 1.7, 4.0 +/- 3.1, and 3.7 +/- 3.2 Torr; time-weighted mean of alveolar PCO2, 2.6 +/- 1.9, 3.3 +/- 3.1, and 3.6 +/- 3.8 Torr; and PaCO2 derived from end-tidal PCO2 and VT, 2.4 +/- 1.3, 1.3 +/- 3.0, and 0.6 +/- 2.9 Torr. It is concluded that mean PavCO2 agreed most closely with mean PaCO2 both at rest and in exercise. All methods of deriving PaCO2 using measurements from the respired gases overestimated arterial values at rest. Of the noninvasive techniques, mean estimates calculated using the regression equation developed by Jones et al. corresponded most closely with PaCO2 in exercise.     

Oxyhemoglobin desaturation and aberrant carbon dioxide homeostasis during electrically stimulated exercise in a ventilator-dependent tetraplegic patient

This single-subject case examined oxyhemoglobin saturation and alveolar end-tidal carbon dioxide levels in a ventilator-dependent tetraplegic patient undergoing electrical stimulation cycle ergometry. When exercising with a closed tracheostomy cuff under resting ventilator settings (resting intermittent mandatory ventilation; frequency = 6breaths/min, tidal volume = 83.3mL, minute ventilation =5L/min), his oxyhemoglobin saturation decreased from 100% to 92%, while alveolar endtidal carbon dioxide increased linearly to 47mmHg. These undesirable changes were corrected under adjusted intermittent mandatory ventilation conditions (frequency = 12breaths/min, tidal volume = 83.3mL, minute ventilation = 10L/min), during which oxyhemoglobin saturation remained above 98% and the alveolar end-tidal carbon dioxide trend resembled that of ventilator-independent tetraplegic individuals undergoing the same exercise. Because the subject's heart rate was higher under adjusted ventilation conditions, these responses may have been caused by augmented venous return resulting from greater abdominothoracic pumping at the higher breathing frequency. These findings support the need to modify ventilator settings in ventilator-dependent tetraplegic persons while undergoing exercise to maintain oxyhemoglobin saturation and carbon dioxide homeostasis.     

Skeletal muscle chemoreflex and pHi in exercise ventilatory control

To determine whether skeletal muscle hydrogen ion mediates ventilatory drive in humans during exercise, 12 healthy subjects performed three bouts of isotonic submaximal quadriceps exercise on each of 2 days in a 1.5-T magnet for 31P-magnetic resonance spectroscopy (31P-MRS). Bilateral lower extremity positive pressure cuffs were inflated to 45 Torr during exercise (BLPPex) or recovery (BLPPrec) in a randomized order to accentuate a muscle chemoreflex. Simultaneous measurements were made of breath-by-breath expired gases and minute ventilation, arterialized venous blood, and by 31P-MRS of the vastus medialis, acquired from the average of 12 radio-frequency pulses at a repetition time of 2.5 s. With BLPPex, end-exercise minute ventilation was higher (53.3 +/- 3.8 vs. 37.3 +/- 2.2 l/min; P < 0.0001), arterialized PCO2 lower (33 +/- 1 vs. 36 +/- 1 Torr; P = 0.0009), and quadriceps intracellular pH (pHi) more acid (6.44 +/- 0.07 vs. 6.62 +/- 0.07; P = 0.004), compared with BLPPrec. Blood lactate was modestly increased with BLPPex but without a change in arterialized pH. For each subject, pHi was linearly related to minute ventilation during exercise but not to arterialized pH. These data suggest that skeletal muscle hydrogen ion contributes to the exercise ventilatory response.     

N-Glycosylation affects endoplasmic reticulum degradation of a mutated derivative of carboxypeptidase yscY in yeast

BACKGROUND: Reports of short- and medium-term evolution of Lung Function Tests (LFT) in infants with bronchopulmonary dysplasia (BPD) are still scarce. POPULATION AND METHODS: The results of the first (before 3 months of corrected age) and the second (between 3 and 9 months of corrected age) LFT in 22 premature infants with BPD (gestational age 31 +/- 2.5 weeks; birth weight: 1570 +/- 440 g; duration of mechanical ventilation: 46 +/- 24 days, total duration of oxygen therapy: 88 +/- 47 days) were compared to those obtained in 27 normal infants for the first LEF and 10 normal infants for the second LFT, similar to the patients for birth weight and corporeal index (CI). RESULTS: In the first LFT, major abnormalities were an increased thoracic gaz volume (TGV) (16.5 +/- 42 vs 122 +/- 24 mL; P < 0.001) and TGV CI ratio (1.25 +/- 0.31 vs 0.89 +/- 0.17 ml/kg/m2; P < 0.0001) a decreased pulmonary compliance (2.49 +/- 1.46 vs 11.60 +/- 4.50 mL/cmH2O; P < 0.0001) and specific pulmonary compliance (0.015 +/- 0.10 vs 0.100 +/- 0.042 mL/cmH2O/mL de TGV; P < 0.0001), an increased total pulmonary resistance (20.4 +/- 12.1 vs 10.5 +/- 5.3 cmH2O/L/s; P < 0.001). In the second LFT, an increased TGV (235 +/- 62 vs 166 +/- 28 mL; P < 0.01) and TGV CI ratio (1.64 +/- 0.65 vs 0.98 +/- 0.11 ml/kg/m2; P < 0.05), a decreased pulmonary compliance (2.68 +/- 2.0 vs 15.2 +/- 5.7 mL/cmH2O; P < 0.0001) and specific pulmonary compliance (0.013 +/- 0.010 vs 0.106 +/- 0.050 mL/cmH2O/mL de TGV; P < 0.0001), an increased total pulmonary resistance (17.1 +/- 9.6 vs 8.6 +/- 4.9 cmH2O/L/s; P < 0.05) were noted when compared with the control group results. Major abnormalities of the blood gases were hypoxemia (63 +/- 10 vs 85 +/- 20 mmHg; P < 0.05), hypercapnia (38.5 vs 31 +/- 4 mmHg; P < 0.0001) during the first LFT. Hypoxemia (77 +/- 14 vs 90 +/- 14 mmHg and hypercapnia (37 +/- 4 vs 29 +/- 5 mmHg) continued in the second LFT. Thoracic distention and total pulmonary resistances in infants with BPD did not improve but their pulmonary compliance (P < 0.0001) and PaO2 (P < 0.01) between the first and second LFT did it. Infants who had been ventilated for a hyaline membrane disease (HMD) were more hypoxic on the second LFT (P < 0.05) than those who had been ventilated for other causes. Statistically significant relationships were found between thoracic distention and duration of positive inspiratory pressure (P < 0.05; r = 0.43), duration of positive expiratory pressure (P < 0.05, r = 0.45) total oxygen therapy duration; between total pulmonary resistance and duration of mechanical ventilation with high frequency (P < 0.05; r = 0.52); between hypoxemia and duration of oxygen therapy with FiO2 > or = 60% (P < 0.05; r = 0.54). CONCLUSIONS: This study shows prolonged clinical and functional abnormalities of the respiratory functions requiring longer follow-up.     

Effects of changes in pH and CO2 on pulmonary arterial wall tension are not endothelium dependent

We examined the changes in isolated pulmonary artery (PA) wall tension on switching from control conditions (pH 7.38 +/- 0.01, PCO2 32.9 +/- 0.4 Torr) to isohydric hypercapnia (pH change 0.00 +/- 0.01, PCO2 change 24.9 +/- 1.1 Torr) or normocapnic acidosis (pH change -0.28 +/- 0.01, PCO2 change -0.3 +/- 0.04 Torr) and the role of the endothelium in these responses. In rat PA, submaximally contracted with phenylephrine, isohydric hypercapnia did not cause a significant change in mean (+/- SE) tension [3.0 +/- 1.8% maximal phenylephrine-induced tension (Po)]. Endothelial removal did not alter this response. In aortic preparations, isohydric hypercapnia caused significant (P < 0.01) relaxation (-27.4 +/- 3.2% Po), which was largely endothelium dependent. Normocapnic acidosis caused relaxation of PA (-20.2 +/- 2.6% Po), which was less (P < 0.01) than that observed in aortic preparations (-35.7 +/- 3.4% Po). Endothelial removal left the pulmonary response unchanged while increasing (P < 0.01) the aortic relaxation (-53.1 +/- 4.4% Po). These data show that isohydric hypercapnia does not alter PA tone. Reduction of PA tone in normocapnic acidosis is endothelium independent and substantially less than that of systemic vessels.     

Effect of sleep on changes in breathing pattern accompanying sigh breaths

We studied the effect of sleep on the characteristics of sigh breaths and the associated changes in breathing pattern in breaths following spontaneous sighs in 4 unrestrained dogs with an intact upper airway. The sigh breath was characterized by its large tidal volume (VT), long TI and TE in comparison with the control breath. The volume of the sigh breath was larger in awake sighs than in those recorded during non-REM (NREM) and REM sleep. The strength of Hering-Breuer reflex as determined by duration of the post-sigh apnea was similar in NREM and REM sleep. Sighs occurring during wakefulness, NREM and REM sleep were associated with augmented activity of the parasternal muscles during inspiration, and a persistent tonic abdominal muscle activity during the expiratory period. Breathing pattern in the post-sigh period was characterized by a smaller VT and longer TE in the first post-sigh breath in all sleep states (compared with the control breath), but the pattern returned to control level within the second or third post-sigh breath in both NREM and REM sleep. Sighs did not precipitate periodic breathing or other forms of abnormal breathing patterns in either wakefulness or sleep. We conclude that the respiratory control mechanisms stabilizing breathing after a sigh in the awake dog are intact in NREM and REM sleep.     

Cortical blood flow response to hypercapnia during anaesthesia in Moyamoya disease

Cortical blood flow (CoBF) was measured continuously by the laser-Doppler method to evaluate the effect of hypercapnia on cortical blood flow during ten surgical procedures in ten young patients (mean +/- SD 9.3 +/- 6.4 yr) with Moyamoya disease. The CoBF was 42.8 +/- 13.4 (ml.100 g-1.min-1) during normocapnia (PaCO2 = 39.0 +/- 2.4 mmHg), and 38.7 +/- 14.4 during hypercapnia (PaCO2 = 47.1 +/- 2.5 mmHg). There was a decrease in CoBF with hypercapnia (P < 0.05) so that the normal CoBF response to hypercapnia was impaired during surgery in the patients with Moyamoya disease. He concluded that patients with Moyamoya disease have a precarious cerebral circulation and hypercapnia may be detrimental to the cortical circulation. This suggests that normocapnia is preferable to hypercapnia in patients with Moyamoya disease during anaesthesia.     

Ventilation is stimulated by small reductions in arterial pressure in the awake dog

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 +/- 2, 10 +/- 3, and 16 +/- 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 +/- 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 +/- 75%) and step reductions in arterial PCO2 (PaCO2; maximum reduction -4.8 +/- 0.8 Torr). Although eupneic PaCO2 threshold was lowered during MAP reduction, ventilatory sensitivity to CO2 remained unchanged. Despite the lowered PaCO2, arterial [H+] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 +/- 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.     

The development of hyperventilation in patients with chronic heart failure and Cheyne-Strokes respiration: a possible role of chronic hypoxia

AIM: To analyze the relationship between daytime respiratory and cardiac function in patients with compensated chronic heart failure (CHF) with and without periodic breathing (PB) or Cheyne-Stokes respiration (CSR). PATIENTS: We studied 132 patients (female, 13%; mean age, 53+/-8 years; body mass index, 25.9+/-3.5 kg/m2; left ventricular ejection fraction <40%; 23% in New York Heart Association class I, 43% in class II, and 34% in class III-IV). METHODS: Measurement of pulmonary function and blood gases, hemodynamic evaluation, analysis of breathing profile, echocardiography, recording of ECG, beat-to-beat arterial oxygen saturation, and respiration during spontaneous breathing. RESULTS: Fifty-eight percent of patients showed PB or CSR. Patients with PB or CSR have greater cardiac function impairment. Mean values of lung volumes and PaO2 were similar in the three groups of patients considered. In contrast, patients with PB or CSR had an increased minute ventilation and reduced PaCO2 values. Interestingly, patients with PB or CSR had lower values of arterial content of O2 and systemic oxygen transport (SOT) than patients with a normal breathing pattern (SOT, 394+/-9.8, 347+/-9.6, 438+/-11 mL of O2/min/m2, respectively; analysis of variance p<0.001). Weak correlations were found among lung volumes, blood gases, and cardiac function parameters: ie, vital capacity was correlated inversely with pulmonary capillary wedge pressure (PCWP) (-0.25; p<0.05); PaCO2 with PCWP (r=0.26; p<0.05), lung-to-ear circulation time (LECT) (r=-0.4; p<0.05), SOT (r=-0.33; p<0.0001), and cardiac index (CI) (r=0.27; p=0.003). Multiple regression analyses showed that arterial PCO2 was significantly correlated with SOT, LECT, and CI (r=0.51; r2=0.26; p<0.000001); the correlation became stronger considering only CSR patients (r=0.64; r2=0.4; p<0.001). CONCLUSIONS: Our study shows that patients with daytime breathing disorders have chronic hypocapnia. A reduced SOT may be one of the stimuli determining increased minute ventilation in these patients.     

Face immersion increases vagal activity as assessed by heart rate variability

We examined whether the diving reflex without breath-holding (face immersion alone) increases vagal activity, as determined by heart rate variability. A group of 15 men [mean age 20 (SD 3) years, height 172 (SD 5) cm, body mass 68 (SD 9) kg] performed 12 trials at various breathing frequencies (5, 10, 15, 20, 30 breaths x min(-1) and uncontrolled breath) with or without face immersion. The R-R intervals of the ECG and gas exchange variables were recorded during the 2 min of each trial. The subjects immersed their faces in 8 10 degrees C water while breathing through a short snorkel. The subject sat in the same position either with or without face immersion. The mean R-R interval (RRmean), standard deviations (SD[RR]) and coefficient of variance (CV[RR]) of the R-R interval were calculated from the R-R intervals during 30-120 s. The face immersion significantly increased SD(RR) and CV(RR) (P < 0.05), and increased RRmean (P < 0.05) at 20 breaths x min(-1). Face immersion itself had no effect on oxygen uptake, tidal volume, end-tidal O2 and CO2 partial pressures. The diving reflex without breath-holding increased the heart rate variability, indicating that face immersion alone increases vagal activity.