Increase In Minute Ventilation Research Articles

Methylphenidate Actively Induces Emergence from General Anesthesia

Although accumulating evidence suggests that arousal pathways in the brain play important roles in emergence from general anesthesia, the roles of monoaminergic arousal circuits are unclear. In this study, the authors tested the hypothesis that methylphenidate (an inhibitor of dopamine and norepinephrine transporters) induces emergence from isoflurane general anesthesia. Using adult rats, the authors tested the effect of intravenous methylphenidate on time to emergence from isoflurane general anesthesia. They then performed experiments to test separately for methylphenidate-induced changes in arousal and changes in minute ventilation. A dose-response study was performed to test for methylphenidate-induced restoration of righting during continuous isoflurane general anesthesia. Surface electroencephalogram recordings were performed to observe neurophysiological changes. Plethysmography recordings and arterial blood gas analysis were performed to assess methylphenidate-induced changes in respiratory function. Intravenous droperidol was administered to test for inhibition of methylphenidate's actions. Methylphenidate decreased median time to emergence from 280 to 91 s. The median difference in time to emergence without methylphenidate compared with administration of methylphenidate was 200 [155-331] s (median, [95% CI]). During continuous inhalation of isoflurane, methylphenidate induced return of righting in a dose-dependent manner, induced a shift in electroencephalogram power from delta (less than 4 Hz) to theta (4-8 Hz), and induced an increase in minute ventilation. Administration of intravenous droperidol (0.5 mg/kg) before intravenous methylphenidate (5 mg/kg) largely inhibited methylphenidate-induced emergence behavior, electroencephalogram changes, and changes in minute ventilation. Methylphenidate actively induces emergence from isoflurane general anesthesia by increasing arousal and respiratory drive, possibly through activation of dopaminergic and adrenergic arousal circuits. The authors' findings suggest that methylphenidate may be useful clinically as an agent to reverse general anesthetic-induced unconsciousness and respiratory depression at the end of surgery.

Switching control of sympathetic activity from forebrain to hindbrain in chronic dehydration

We investigated the mechanisms responsible for increased blood pressure and sympathetic nerve activity (SNA) caused by 2-3 days dehydration (DH) both in vivo and in situ preparations. In euhydrated (EH) rats, systemic application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to remove the hypothalamus) significantly reduced thoracic (t)SNA. In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transections, failed to reduce tSNA, whereas transection at the medulla-spinal cord junction massively reduced tSNA. In DH but not EH rats, selective inhibition of the commissural nucleus tractus solitarii (cNTS) significantly reduced tSNA. Comparable data were obtained in both in situ and in vivo (anaesthetized/conscious) rats and suggest that following chronic dehydration, the control of tSNA transfers from supra-brainstem structures (e.g. hypothalamus) to the medulla oblongata, particularly the cNTS. As microarray analysis revealed up-regulation of AP1 transcription factor JunD in the dehydrated cNTS, we tested the hypothesis that AP1 transcription factor activity is responsible for dehydration-induced functional plasticity. When AP1 activity was blocked in the cNTS using a viral vector expressing a dominant negative FosB, cNTS inactivation was ineffective. However, tSNA was decreased after pre-collicular transection, a response similar to that seen in EH rats. Thus, the dehydration-induced switch in control of tSNA from hypothalamus to cNTS seems to be mediated via activation of AP1 transcription factors in the cNTS. If AP1 activity is blocked in the cNTS during dehydration, sympathetic activity control reverts back to forebrain regions. This unique reciprocating neural structure-switching plasticity between brain centres emphasizes the multiple mechanisms available for the adaptive response to dehydration.

Intrathecal neuromedin U induces biphasic effects on sympathetic vasomotor tone, increases respiratory drive and attenuates sympathetic reflexes in rat

Neuromedin U (NMU) is a brain-gut peptide that plays regulatory roles in feeding, anxiety, smooth muscle contraction, blood flow, pain and adrenocortical function via two receptors, the NMU receptor 1 and NMU receptor 2. NMU has several known functions in the periphery, but its role in central cardiorespiratory regulation remains poorly understood. Experiments were conducted on urethane-anaesthetized, vagotomized and artificially ventilated male Sprague-Dawley rats (n= 42) to determine if NMU modulates sympathetic vasomotor output at the spinal level or modulates baro-, chemo- and somato-sympathetic reflexes. Intrathecal (i.t.) injections of NMU (2.5-20 nmol) caused a dose-dependent biphasic response, initially a brief period of hypertension and sympatho-excitation followed by prolonged hypotension and sympatho-inhibition. Peak excitatory as well as inhibitory responses were observed at 20 nmol. NMU (20 nmol) initially increased mean arterial pressure and splanchnic sympathetic nerve activity by 24 mmHg and 27% and then reduced these by 37 mmHg and 47%, respectively. NMU also dose-dependently increased respiratory drive, as indicated by a rise in phrenic nerve amplitude, an increase in neural minute ventilation and a shortening of the inspiratory period. Both sympatho-excitatory peaks of the somato-sympathetic reflex were abolished by i.t. NMU. Pressor, sympatho-excitatory and tachycardiac responses to chemoreceptor activation (100% N₂) were blocked or significantly reduced following i.t. NMU. NMU also reduced barosensitivity. The data demonstrate that NMU, acting in the spinal cord, differentially contributes to the control of sympathetic tone and adaptive sympathetic reflexes.

Use of Heliox in the Management of Neonates with Meconium Aspiration Syndrome

Background: Helium-oxygen mixture (heliox) ventilation has been known as an alternative treatment in patients with airway obstruction. Because of the physical properties of heliox, mechanical ventilation with this gas mixture may offer advantages in the management of respiratory failure associated with meconium aspiration syndrome (MAS). Objectives: The purpose of this pilot study was to assess the effect of short-term mechanical ventilation with heliox in newborns with MAS on vital signs, oxygenation, acid-base balance and respiratory function parameters. Methods: The study was carried out in newborns with respiratory failure requiring mechanical ventilation due to MAS. Eight patients were ventilated using pressure-controlled synchronized intermittent mandatory ventilation. Parameters of respiratory function, oxygenation, acid-base balance and vital signs were recorded at baseline, then twice during 1 h of heliox ventilation and finally twice during 1 h after switching back to air-oxygen ventilation. Results: Mechanical ventilation with heliox did not affect vital signs and the infants’ clinical condition remained stable during the study. Heliox ventilation was associated with a nonsignificant increase in tidal volume, minute ventilation and peak expiratory flow rate values. Mechanical ventilation with heliox allowed the use of significantly lower FiO₂, with a significant decrease in alveolar-arterial oxygen tension difference and a decrease in the oxygenation index which was not statistically significant. There was also a significant increase in the PaO₂/FiO₂ ratio during heliox ventilation. Conclusions: Ventilation with a helium and oxygen mixture had a positive effect on the selected parameters of oxygenation, while its effects on other respiratory parameters were relatively small.

Ventilatory Inefficiency Reflects Right Ventricular Dysfunction in Systolic Heart Failure

An increased minute ventilation (VE)/carbon dioxide production (VCO2) relationship, an expression of ventilatory inefficiency (VI), is associated with increased morbidity and mortality in patients with left ventricular systolic dysfunction (LVSD). A direct link between VI and a specific cardiac abnormality has not been established. We analyzed cardiopulmonary exercise test (CPET) data from patients (N=83) with severe LVSD (ischemic and nonischemic; left ventricular ejection fraction [LVEF] 19%±7%) and at least moderate exercise intolerance. Subjects were stratified into two groups based on the (VE/VCO2 ratio at anaerobic threshold (VE/VCO2@AT) (group 1 VE/VCO2@AT≤34; group 2 VE/VCO2@AT>34). Clinical, CPET, echocardiographic, and hemodynamic data were compared between groups. Group 2 subjects had lower exercise capacity (peak (VO2, 45.7%±11.8% vs 50.4±8.9% predicted; P<.05), with a significantly lower oxygen pulse (71.6%±24.5% vs 85.4±18.5% predicted) and maximum systolic BP (122±19 mm Hg vs 138±22 mm Hg; P<.001 for both), suggesting a more blunted stroke volume to exercise vs group 1. There were no differences in left ventricular (LV) size, LVEF, or mitral regurgitation between the two groups. In sharp contrast, group 2 had larger right ventricular (RV) dimensions (4.5±1.1 cm vs 3.9±0.8 cm) and more severe RV systolic dysfunction (RV fractional area change 26%±11% vs 33%±12%; tricuspid annular plane systolic excursion [TAPSE] 1.6±0.5 cm vs 2.0±0.5 cm; all P<.001) vs group 1. Multivariable analysis revealed that only TAPSE and Doppler-estimated pulmonary artery systolic pressure were independently associated with VE/VCO2@AT and the (VE/VCO2slope. The VE/VCO2@AT, VE/VCO2 slope, and TAPSE had nearly identical predictive value for death or transplant. The present study suggests that VI is a functional, noninvasive marker of more advanced right-sided heart dysfunction in patients with severe LVSD.

Intrathecal orexin A increases sympathetic outflow and respiratory drive, enhances baroreflex sensitivity and blocks the somato‐sympathetic reflex

Intrathecal (i.t.) injection of orexin A (OX-A) increases blood pressure and heart rate (HR), but the effects of OX-A on sympathetic and phrenic, nerve activity, and the baroreflex(es), somato-sympathetic and hypoxic chemoreflex(es) are unknown. Urethane-anaesthetized, vagotomized and artificially ventilated male Sprague-Dawley rats were examined in this study. The effects of i.t. OX-A (20 nmol 10 µL⁻¹) on cardiorespiratory parameters, and responses to stimulation of the sciatic nerve (electrical), arterial baroreceptors (phenylephrine hydrochloride, 0.01 mg kg⁻¹ i.v.) and peripheral (hypoxia) chemoreceptors were also investigated. i.t. OX-A caused a prolonged dose-dependent sympathoexcitation, pressor response and tachycardia. The peak effect was observed at 20 nmol with increases in mean arterial pressure, HR and splanchnic sympathetic nerve activity (sSNA) of 32 mmHg, 52 beats per minute and 100% from baseline respectively. OX-A also dose-dependently increased respiratory drive, as indicated by a rise in phrenic nerve amplitude and a fall in phrenic nerve frequency, an increase in neural minute ventilation, a lengthening of the expiratory period, and a shortening of the inspiratory period. All effects of OX-A (20 nmol) were attenuated by the orexin receptor 1 antagonist SB 334867. OX-A significantly reduced both sympathoexcitatory peaks of somato-sympathetic reflex while increasing baroreflex sensitivity. OX-A increased the amplitude of the pressor response and markedly amplified the effect of hypoxia on sSNA. Thus, activation of OX receptors in rat spinal cord alters cardiorespiratory function and differentially modulates sympathetic reflexes.

Effects of Bronchoconstriction, Minute Ventilation, and Deep Inspiration on the Composition of Exhaled Breath Condensate

Exhaled breath condensate (EBC) is composed of droplets of airway surface liquid (ASL) diluted by water vapor. The goal of this study was to determine if the composition of EBC is affected by changes in airway caliber, minute ventilation, or forceful exhalation, factors that may differ among subjects with asthma in cross-sectional studies. In a group of subjects with asthma, we measured the effects of the following: (1) a series of three deep-inspiration and forceful-exhalation maneuvers; (2) a doubling of minute ventilation; and (3) acute bronchoconstriction induced by methacholine on EBC volume, dilution of ASL, and concentration of cysteinyl leukotrienes (CysLTs). With the exception of an increase in EBC volume with increased minute ventilation, there were no significant changes in the volume, dilution, or levels of CysLTs in EBC introduced by each of these factors. The CIs surrounding the differences introduced by each factor showed that the maximum systematic errors due to these factors were modest. These results indicate that changes in airway caliber, minute ventilation, or breathing pattern among subjects with asthma do not significantly alter the measurements of mediator concentrations in EBC.

Influence of codeine on lobeline-induced respiratory reflexes and sensations and on ventilation with exercise in healthy subjects

In 15 healthy subjects, the effect of 60 mg oral codeine and placebo was examined on intravenously injected lobeline-elicited respiratory reflexes and sensations. Its influence was also studied on ventilation and appearance of distressful respiratory sensations with modest but incremental exercise. After placebo, tachypnoea and respiratory sensations were evoked with 12.1 ± 1.9 μg/kg of lobeline i.v. (mean threshold dose) and after codeine, by significantly higher doses i.e., 18.0 ± 3.1 μg/kg (P < 0.05). Additionally after codeine, in response to incremental doses of lobeline the respiratory reflex was notably attenuated and the magnitude of respiratory sensations, subdued. Dry cough seen in 66% of the subjects with suprathreshold doses of lobeline i.e., 22.0 ± 3.4 μg/kg (mean), appeared post codeine, with significantly higher doses i.e., 27.0 ± 3.9 μg/kg (mean) (P < 0.05) and in a fewer subjects (60%). Mean increase in minute ventilation at the end of 8 min of incremental treadmill walking after codeine was 21% less than after placebo (P < 0.05); 60% of the subjects continued to walk for an additional 4 min and the onset of respiratory discomfort was delayed by 1-5 min. This is the first report of an attenuation of lobeline-elicited respiratory reflexes and sensations that are attributable to J receptors (pulmonary C fibres) by a pharmacological entity. It also suggests that codeine decreased these receptors' known contribution to respiratory augmentation and motor inhibition during exercise, which was seen as a delay in the onset of, and a decrease in the magnitude of respiratory discomfort during treadmill walking and an increase in the duration walked by more than half the subjects.

Nitrous oxide for pneumoperitoneum: No laughing matter this! A prospective single blind case controlled study

Background The search for the perfect insufflating gas has been elusive. Even though Carbon dioxide (CO 2) is the most commonly used gas, it has numerous cardiovascular, respiratory and hemodynamic side effects, which have often been taken for granted. In the current scenario of ever expanding and complex indications for Laparoscopic Surgery these changes have an increasing implication of placing the patient at risk. Nitrous Oxide (N 2O) has now made a comeback and shown by recent studies to be as safe as CO 2 for creating pneumoperitoneum (PP). The purpose of our study is to determine whether benefits of N 2O (PP) outweigh those of CO 2 PP in Laparoscopic Surgery. Material and methods All patients undergoing Laparoscopic Surgery over an 8 week period were divided into two groups. Data were collected prospectively for Group I {N 2O( n = 38)} and Group II {CO 2 PP( n = 39)}. Heart rate, Mean Arterial Blood Pressure, End-Tidal CO 2, Arterial pH, Peak Airway Pressure, Minute Ventilation and O 2 Saturation were recorded before PP, 15 minutes after PP and 10 minutes after exsufflation. Intraoperative anesthetic agent and postoperative pain medication use was recorded. Pain was assessed by means of visual analog scale (VAS) at postoperative hours 2 and 4 and on day1. Results tabulated and analyzed statistically. Results There was no statistical difference in age, sex, weight, complexity of surgery (type of procedure and duration of PP), Anesthetic risk, and duration of hospitalization between the two groups. Mean End-Tidal CO 2 increase was greater despite a greater mean intraoperative increase in Minute Ventilation in group II, Heart Rate, Arterial pH, Mean Arterial Pressure under anesthesia were significantly higher in group II. The quantum of intraoperative anesthetic agent and postoperative pain (as assessed by Visual Analog Scale) was less in group I. Conclusion This is an initial study assessing the use of N 2O for insufflation; the results of our study suggest N 2O PP has a definitive advantage over CO 2 PP. Further multicentric randomized trials are necessary before N 2O becomes the standard insufflating agent.

Effect of intracerebroventricular injection of interleukin-1-beta on the ventilatory response to hyperoxic hypercapnia.

ObjectiveOxidative stress developed at several disease states and strenuous resistive breathing lead to the elevation of plasma and cerebral levels of proinflammatory cytokines. We hypothesized that the elevation of the cytokine level in body fluids would modulate breathing pattern and the ventilatory response to stimulation of central chemoreceptors by hypercapnia.Materials and methodsIn experiments on anesthetized, tracheostomized, spontaneously breathing rats, the effects of intracerebroventricular injection of the human recombinant interleukin-1β (IL-1β) (0.5 g/rat) on breathing were studied.ResultsDuring resting breathing IL-1β evoked a significant increase in minute ventilation and in mean inspiratory flow. Furthermore, injection of IL-1β into the cerebral-spinal fluid decreases the responses of ventilation, tidal volume, and of mean inspiratory flow to carbon dioxide.ConclusionsThe elevation of a proinflammatory cytokine in cerebrospinal fluid intensifies ventilation by modulation of breathing pattern, but weakens the chemoreflex sensitivity to hypercapnia. The results suggest the participation of cytokines in the central control of breathing and in the mechanisms of central chemoreception.

506 Heliox in the Management of Neonates with Meconium Aspiration Syndrome (MAS)

The aim of the study was to asses the influence of short-term mechanical ventilation with heliumoxygen mixture (heliox) in newborns with MAS on basic vital signs, oxygenation, acid-base balance and respiratory mechanics.The study was carried out in newborns with respiratory failure requiring mechanical ventilation due to MAS. Patients were ventilated using PC-SIMV. Parameters of mechanical ventilation, respiratory mechanics, oxygenation, acid-base balance and vital signs were recorded during three periods of one hour before, during and after heliox ventilation.Nine newborns with MAS were enrolled in the study. Mechanical ventilation with heliox did not affect vital signs, and infants' general condition remained stable during and after ventilation with heliox. Mechanical ventilation with heliox was associated with a statistically significant increase in dynamic compliance(mean 0,4 vs 0,53ml/cmH2O). Heliox caused an increase in tidal volume(mean 5,57 vs 6,84ml/kg)and minute ventilation(mean 0,87 vs 0,95l)but this was not statistically significant. Mechanical ventilation with heliox allowed the use of significantly lower fractions of inspired oxygen(mean 0,62 vs 0,35), with a significant decrease in the oxygenation index(mean 8,09 vs 4,26)and alveolararterial oxygen tension difference(mean 320,04 vs 127,65mmHg).A significant increase in pH(mean 7,34 vs 7,38) was also observed with a concomitant decrease in PaCO2(mean 43,4 vs 39,9)which was not statistically significant. Beneficial effects of heliox reversed after ventilation with this gas mixture was stopped. Patients required higher FiO2(mean 0,35 vs 0,38), OI(mean 4,26 vs 5,27)and AaDO2(mean 127,65 vs 159,6)increased. There was also a significant decrease in oxygen saturation(mean 93,69 vs 91,63).Ventilation with heliox had a positive effect on the selected parameters of oxygenation, acid-base balance and respiratory mechanics in newborns with MAS.

Ventilation-limited exercise capacity in a 59-year-old athlete

Aerobic exercise performance may be limited by the respiratory system in fit elderly adults whose lungs undergo the normal ageing process or who develop lung diseases but can maintain high pulmonary blood flows and ventilatory requirements. Here we describe a 59-year-old athlete demonstrating high aerobic exercise performance limited by his relatively low ventilatory capacity. The male hobby cyclist (59 years, 176 cm, 83 kg), undergoing cardiopulmonary exercise testing, reported no complaints except a history of dyspnoea and exercise intolerance at high altitude (> 2000 m). Lung function testing indicated mild airway obstruction (FEVC: 4.22 l, FEV1: 2.91 l, FEV1/FEVC: 69%) which was not reversed post-bronchodilator. However, FEV1/FEVC was slightly above the 5th percentile and thus not confirming the diagnosis of COPD. The athlete completed 300 W (3.6 W/kg) and his maximal oxygen uptake was 45 ml/min/kg (156% predicted!). Above 250 W he was unable further increasing minute ventilation, and oxygen pulse and oxygen uptake even decreased. The related changes of the respiratory pattern (increase of breathing frequency, decreases of inspiratory capacity and tidal volume) indicated dynamic lung hyperinflation resulting in cardiac output constraint, arterial oxygen desaturation, severe dyspnoea and exercise limitation. This case report delineates the pathophysiological situation of ventilation-limited exercise capacity in a well-trained middle-aged subject. However, beneficial adaptations to regular exercise may have helped maintain high aerobic performance without any adverse symptoms during submaximal exercise.

Contrasting pressure-support ventilation and helium–oxygen during exercise in severe COPD

Helium-oxygen mixtures and pressure-support ventilation have been used to unload the respiratory muscles and increase exercise tolerance in COPD. Considering the different characteristics of these techniques, we hypothesized that helium-oxygen would be more effective in reducing exercise-induced dynamic hyperinflation than pressure-support. We also hypothesized that patients would experience greater increases in respiratory rate and minute ventilation with helium-oxygen than with pressure-support. The hypotheses were tested in ten patients with severe COPD (FEV(1) = 28 ± 3% predicted [mean ± SE]) during constant-load cycling (80% maximal workrate) while breathing 30% oxygen-alone, helium-oxygen, and pressure-support in randomized order. As hypothesized, helium-oxygen had greater impact on dynamic hyperinflation than did pressure-support (end-exercise; p = 0.03). For the most part of exercise, respiratory rate and minute ventilation were greater with helium-oxygen than with pressure-support (p ≤ 0.008). During the initial phases of exercise, helium-oxygen caused less rib-cage muscle recruitment than did pressure-support (p < 0.03), and after the start of exercise it caused greater reduction in inspiratory reserve volume (p ≤ 0.02). Despite these different responses, helium-oxygen and pressure-support caused similar increases in exercise duration (oxygen-alone: 6.9 ± 0.8 min; helium-oxygen: 10.7 ± 1.4 min; pressure-support: 11.2 ± 1.6 min; p = 0.003) and similar decreases in inspiratory effort (esophageal pressure-time product), respiratory drive, pulmonary resistance, dyspnea and leg effort (p < 0.03). In conclusion, helium-oxygen reduced exercise-induced dynamic hyperinflation by improving the relationship between hyperinflation and minute ventilation. In contrast, pressure-support reduced hyperinflation solely as a result of lowering ventilation. Helium-oxygen was more effective in reducing exercise-induced dynamic hyperinflation in severe COPD, and was associated with greater increases in respiratory rate and minute ventilation than pressure-support.

Field and laboratory exercise challenges for identifying exercise-induced bronchoconstriction

Educational aimsTo define necessary conditions for a successful exercise challenge.To provide operational procedures for performing an exercise challenge in the laboratory or the field for the identification of exercise-induced bronchoconstriction.To compare positive and negative attributes of each challenge.To provide spirometric cut-off criteria for positive challenge tests.SummaryExercise challenge tests are often used for identification of exercise-induced bronchoconstriction (EIB). Optimal test conditions are: absolute humidity of &lt;10 mg H2O per L; exercise intensity resulting in a sustained increase in minute ventilation to 14–21 times the forced expiratory volume in 1 s or heart rate (HR) to 80–90% of the estimated maximal HR; and exercise duration of 6–8 min. Variability in fitness level and age necessitate individualisation of the exercise protocol. Field tests are subject to variability in test conditions and may have poorer repeatability than laboratory tests that require expensive equipment. However, either challenge test can be employed for the diagnosis of EIB in conjunction with a critical clinical assessment.

Autoregulation of ventilation with neurally adjusted ventilatory assist on extracorporeal lung support

Extracorporeal membrane oxygenation (ECMO) can support oxygenation and carbon dioxide elimination in severe lung failure. Usually it is accompanied by controlled mechanical ventilation. Neurally adjusted ventilatory assist (NAVA) is a new mode of ventilation triggered by the diaphragmatic electrical activity and controlled by the patient's respiratory centre, which may allow a close interaction between ventilation and extracorporeal perfusion. This pilot study intended to measure the physiologic ventilatory response in patients with severe lung failure treated with ECMO and NAVA. We hypothesized that the combination of both methods could automatically provide a protective ventilation with optimized blood gases. We report a case series of six patients treated with ECMO for severe lung failure. In the recovery phase of the disease, patients were ventilated with NAVA and ventilatory response and gas exchange parameters were measured under different sweep gas flows and temporarily inactivated ECMO. Tidal volumes on ECMO ranged between 2 and 5 ml/kg predicted body weight and increased up to 8 ml/kg with inactivated ECMO. Peak inspiratory pressure reached 19-29 cmH(2)O with active, and 21-45 cmH(2)O with inactivated ECMO. Ventilatory response to decreased sweep gas flow was rapid, and patients immediately regulated PaCO(2) tightly towards a physiological pH value. Increase in minute ventilation was a result of increased breathing frequency and tidal volumes, and protective ventilation was only abandoned if pH control was not achieved. With NAVA ventilatory response to decreased ECMO sweep gas flow was rapid, and patients immediately regulated PaCO(2) tightly towards a physiological pH value. Therefore, combination of NAVA and ECMO may permit a closed-loop ventilation with automated protective ventilation.

Ventilatory and muscular assessment in healthy subjects during an activity of daily living with unsupported arm elevation

Patients with chronic obstructive pulmonary disease (COPD) report dyspnea when performing activities of daily living (ADLs) with elevated upper limbs. To elucidate the determinants of dyspnea, it is important to study the changes in the respiratory pattern of these patients and the electromyographic activity of their accessory muscles of respiration during ADLs. In the literature, there are no reports of a normative parameter, therefore it is necessary to study how these variables behave in healthy subjects. To verify, in healthy subjects, the existence of changes in the respiratory pattern and activation of the sternocleidomastoid (SCM) muscle during an ADL with unsupported arm elevation. Thirteen male subjects, 60.57 (± 6.42) years old, with normal spirometry values for age and sex, were evaluated using surface electromyography (EMG) and respiratory inductive plethysmography (RIP) collected at rest and during the activity of combing their hair with elevated and unsupported upper limbs. The data distribution was assessed using Shapiro-Wilk's test. ANOVA was used to compare the phases, and when the difference was significant (p<0.05), Tukey's test was applied. The RIP during the ADL showed a significant increase in tidal volume, minute ventilation, respiratory frequency and mean inspiratory flow. Thoracoabdominal asynchrony was identified in percentage of asynchrony in inspiration, expiration, and Phase Angle (p<0.05). The EMG showed an increase in SMC muscle recruitment (p<0.05). Healthy subjects increased their SCM muscle activation and changed their breathing pattern when performing the ADL with unsupported arm elevation, resulting in thoracoabdominal asynchrony.

The cardiovascular, respiratory, and metabolic effects of a long duration electronic control device exposure in human volunteers

Electronic control devices (ECD) have become popular in law enforcement because they have filled a gap left by other law enforcement devices, tactics, or tools and have been shown to reduce officer and suspect injuries. Civilians are using the same technology for defensive purposes. TASER C2 is the latest generation civilian-marketed device from the manufacturer. Unlike the law enforcement devices, the device discharges for 30s continuously. This study is the first to look at the cardiovascular, respiratory, and metabolic effects of this device on human subjects. This was a prospective, observational study of human subjects involved in a training course. Subjects were exposed for 30s on the anterior thorax. Vital signs, ECG, troponin I, pH, lactate, and creatine kinase (CK) were measured before and immediately after the exposure. Troponin I, pH, lactate, and CK were measured again 24h after the exposure. Continuous spirometry was used to evaluate the respiratory effects. Echocardiography was also performed before, during, and immediately after the exposure to determine heart rate and rhythm. Eleven subjects completed the study. There were no clinically important electrocardiogram changes and no positive troponins. Spirometry showed an increase in minute ventilation during the exposure. There was no important change in CK at 24h. Lactate was slightly higher and pH was slightly lower after the exposure, but similar to the effects of physical exertion. Echocardiography was performed in 6 subjects. In half of these subjects, the rhythm was determined to be "sinus" and in the other half the rhythm was indeterminant. In our study, the civilian device caused a mild lactic acidosis. No other important physiologic effects were found.

Breathing patterns during cardiac arrest

The absence of respiratory movements is a major criterion recommended for use by bystanders for recognizing an out-of-hospital cardiac arrest (CA), as the persistence of eupneic breathing is considered to be incompatible with CA. The basis for CA-related apnea is, however, uncertain, since brain stem Po(2) is not expected to drop immediately to the critical level where anoxic apnea occurs. It is therefore essential on both clinical and physiological grounds to determine whether and when breathing stops after the onset of CA. In eight patients, we measured the ventilatory response at the onset of ventricular fibrillation (VF) for 12-15 s during the placement of an implantable cardioverter-defibrillator device. We found that regular eupneic breathing was maintained unchanged despite the cessation of systemic and pulmonary blood flow generated by the heart. We extended these findings in adult sheep and found that, as in humans, the normal ventilatory pattern persists unchanged for the first 15 s despite the drop in blood pressure, followed by a progressive increase in minute ventilation, which was sustained for up to 164 s. The ensuing apnea was disrupted by typical gasps occurring at a very slow frequency. These observations suggest a complete "decoupling" between the return of CO(2) to the pulmonary circulation and continued effective respiratory activity, contrary to what we predicted. This delayed cessation of eupneic breathing during the absence of cardiac pump function is likely related to the time needed for brain stem anoxia to develop. These findings challenge the notions that 1) ventilation stops as pulmonary blood flow/cardiac output ceases and 2) the presence of eupneic breathing is a reliable sign of effective cardiac pumping activity.

Baroreflex unloading blunts chemoreceptor sensitivity in Postural Tachycardia Syndrome (POTS)

POTS have increased minute ventilation (VE) and decreased end tidal carbon dioxide (ETCO2) compared to healthy subjects. Chemoreceptor sensitivity was measured in 18 POTS (14F, 4M), 10 healthy controls (6F, 4M) 16–35 years old by exposing them to eucapneic hyperoxia‐30%oxygen, eucapneic hypoxia (10%oxygen) and hypercapnia 30%oxygen+5%carbon dioxide) in supine and HUT70 position. We measured heart Rate (HR), mean arterial pressure (MAP) oxygen saturation, ETCO2, mean cerebral blood flow velocity (mCFV) and VE. Chemoreflex sensitivity was ascertained by comparing slopes determined from eucapneic hypoxia‐hyperoxia to measure peripheral chemoreflex sensitivity, and hyperoxic hypercapnia –eucapnia to measure central chemoreflex sensitivity. POTS had significantly higher resting HR, lower MAP, stroke volume (SV) and mCFV as compared to controls (p&lt;0.05). Hypoxia and hypercapnia increased the HR, MAP, CO, mCFV and VE (p&lt;0.05). POTS had increases in VE during supine hypoxia (POTS vs. controls, 3.6± 0.9 vs. 1.6± 0.2, p=0.003) which reversed in HUT70 (1.96± 0.3 vs. 5.4± 1.2). In both POTS and controls, hypercapnia resulted in similar increases in VE when supine but no further increases when HUT70. POTS have higher peripheral chemoreflex sensitivity than controls which attenuates during unloading of baroreflexes.

Reversible severe pulmonary hypertension in obesity hypoventilation and Mohr syndrome

A young overweight patient with Mohr–Claussen Syndrome was admitted to our department with the clinical diagnosis of pulmonary hypertension complaining about dyspnea at rest and excessive daytime sleepiness. Pulmonary function testing indicated severe airflow limitation and respiratory insufficiency. Pulmonary artery (PA) pressure was markedly increased. Pulmonary embolism, Alpha-1-antitrypsin-deficiency, emphysema and anatomical obstructions were excluded. Polysomnography showed recurrent oxygen desaturations compatible with alveolar hypoventilations. Hypercapnic ventilatory response testing (HCVR) indicated a missing increase in minute ventilation when exposed to hypercapnia. After 6 weeks of nocturnal non-invasive ventilation therapy, her clinical condition markedly improved. Furthermore, PA pressure returned to normal values. HCVR testing showed an adequate response to hypercapnia. Mohr–Claussen syndrome is a rare genetic disease affecting the mouth, face and digits. Adult patients are usually very obese; exposing them at risk for obesity hypoventilation syndrome (OHS). OHS is described as a combination of obesity and awake arterial hypercapnia (PaCO 2 > 45 mmHg) in the absence of other known causes of chronic alveolar hypoventilation. Unclear pulmonary hypertension in overweight patients should raise the suspicion for OHS.