Anterior cerebral blood velocity and end-tidal CO2 responses to exercise differ in children and adults.

Little is known about the response of the cerebrovasculature to acute exercise in children and how these responses might differ with adults. Therefore, we compared changes in middle cerebral artery blood velocity (MCAVmean), end-tidal Pco2 ([Formula: see text]), blood pressure, and minute ventilation (V̇e) in response to incremental exercise between children and adults. Thirteen children [age: 9 ± 1 (SD) yr] and thirteen sex-matched adults (age: 25 ± 4 yr) completed a maximal exercise test, during which MCAVmean, [Formula: see text], and V̇e were measured continuously. These variables were measured at rest, at exercise intensities specific to individual ventilatory thresholds, and at maximum. Although MCAVmean was higher at rest in children compared with adults, there were smaller increases in children (1-12%) compared with adults (12-25%) at all exercise intensities. There were alterations in [Formula: see text] with exercise intensity in an age-dependent manner [F(2.5,54.5) = 7.983, P < 0.001; η2 = 0.266], remaining stable in children with increasing exercise intensity (37-39 mmHg; P > 0.05) until hyperventilation-induced reductions following the respiratory compensation point. In adults, [Formula: see text] increased with exercise intensity (36-45 mmHg, P < 0.05) until the ventilatory threshold. From the ventilatory threshold to maximum, adults showed a greater hyperventilation-induced hypocapnia than children. These findings show that the relative increase in MCAVmean during exercise was attenuated in children compared with adults. There was also a weaker relationship between MCAVmean and [Formula: see text] during exercise in children, suggesting that cerebral perfusion may be regulated by different mechanisms during exercise in the child.NEW & NOTEWORTHY These findings provide the first direct evidence that exercise increases cerebral blood flow in children to a lesser extent than in adults. Changes in end-tidal CO2 parallel changes in cerebral perfusion in adults but not in children, suggesting age-dependent regulatory mechanisms of cerebral blood flow during exercise.

Nitric oxide-sensitive guanylyl cyclase signaling affects CO2-dependent but not pressure-dependent regulation of cerebral blood flow.

Cerebrovascular CO2 reactivity is affected by nitric oxide (NO). We tested the hypothesis that sildenafil selectively potentiates NO-cGMP signaling, which affects CO2 reactivity. Fourteen healthy males (34 ± 2 yr) were enrolled in the study. Blood pressure (BP), ECG, velocity of cerebral blood flow (CBF; measured by transcranial Doppler), and end-tidal CO2 (EtCO2) were assessed at baseline (CO2 ~39 mmHg), during hyperventilation (CO2 ~24 mmHg), during hypercapnia (CO2 ~46 mmHg), during boluses of phenylephrine (25-200 µg), and during graded head-up tilting (HUT). Measurements were repeated 1 h after 100 mg sildenafil were taken. Results showed that sildenafil did not affect resting BP, heart rate, CBF peak and mean velocities, estimated regional cerebrovascular resistance (eCVR; mean BP/mean CBF), breath/min, and EtCO2: 117 ± 2/67 ± 3 mmHg, 69 ± 3 beats/min, 84 ± 5 and 57 ± 4 cm/s, 1.56 ± 0.1 mmHg·cm-1·s-1, 14 ± 0.5 breaths/min, and 39 ± 0.9 mmHg, respectively. Sildenafil increased and decreased the hypercapnia induced in CBF and eCVR, respectively. Sildenafil also attenuated the decrease in peak velocity of CBF, 25 ± 2 vs. 20 ± 2% (P < 0.05) and increased the eCVR, 2.5 ± 0.2 vs. 2 ± 0.2% (P < 0.03) during hyperventilation. Sildenafil did not affect CBF despite significant increases in the eCVRs that were elicited by phenylephrine and HUT. This investigation suggests that sildenafil, which potentiates the NO-cGMP signaling, seems to affect the cerebrovascular CO2 reactivity without affecting the static and dynamic pressure-dependent mechanisms of cerebrovascular autoregulation.

Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed.

Ultrasound tagged near infrared spectroscopy does not detect hyperventilation-induced reduction in cerebral blood flow.

INTRODUCTION: Continuous non-invasive monitoring of cerebral blood flow (CBF) may be important during anaesthesia and several options are available. We evaluated the CerOx monitor that employs ultrasound tagged near infrared spectroscopy to estimate changes in a CBF index (CFI). METHODS: Seven healthy males (age 21-26 years) hyperventilated and were administered phenylephrine to increase mean arterial pressure by 20-30 mmHg. Frontal lobe tissue oxygenation (ScO2) and CFI were obtained using the CerOx and mean blood flow velocity in the middle cerebral artery (MCAv mean) was determined by transcranial Doppler. Blood flow in the internal and external carotid artery (ICAf and ECAf) was determined using duplex ultrasonography and forehead skin blood flow (SkBF) and oxygenation (S skin O2) by laser Doppler and white light spectroscopy. RESULTS: During hyperventilation MCAv mean and ICAf decreased by 44% (median; interquartile range 40-49; p = 0.016) and 46% (40-53; p = 0.03), respectively. Conversely, CFI increased by 9% (2-31; p = 0.016), while no significant change was observed in ScO2. SkBF increased by 19% (9-53; p = 0.016) and S skin O2 by 6% (1-7; p = 0.047), although ECAf was unchanged. Administration of phenylephrine was not associated with any changes in MCAv mean, ICAf, ECAf, ScO2, SkBF, S skin O2, or CFI. CONCLUSION: The CerOx was able to detect a stable CBF during administration of phenylephrine. However, during hyperventilation MCAv mean and ICAf decreased while CFI increased, likely due to an increase in superficial tissue oxygenation. Thus, CFI does not provide an unbiased evaluation of changes in CBF.

Effects of hyperventilation on cerebral oxygen saturation estimated using near-infrared spectroscopy: A randomised comparison between propofol and sevoflurane anaesthesia.

BACKGROUND: Near-infrared spectroscopy estimates cerebral regional tissue oxygen saturation (rSO2), which may decrease under hyperventilation. Propofol and sevoflurane act differently on cerebral blood vessels. Consequently, cerebral blood flow during hyperventilation with propofol and sevoflurane anaesthesia may differ. OBJECTIVES: The first aim of this study was to compare the changes in rSO2 between propofol and sevoflurane anaesthesia during hyperventilation. The second aim was to assess changes in rSO2 with ventilation changes. DESIGN: A randomised, open-label study. SETTING: University of Yamanashi Hospital, Yamanashi, Japan from January 2014 to September 2014. PARTICIPANTS: Fifty American Society of Anesthesiologists physical status 1 or 2 adult patients who were scheduled for elective abdominal surgery were assigned randomly to receive either propofol or sevoflurane anaesthesia. Exclusion criterion was a known history of cerebral disease such as cerebral infarction, cerebral haemorrhage, transient ischaemic attack and subarachnoid haemorrhage. INTERVENTIONS: After induction of anaesthesia but before the start of surgery, rSO2, arterial carbon dioxide partial pressure (PaCO2) and arterial oxygen saturation were measured. Measurements were repeated at 5-min intervals during 15 min of hyperventilation with a PaCO2 around 30 mmHg (4 kPa), and again after ventilation was normalised. MAIN OUTCOME MEASURES: The primary outcome was the difference of changes in rSO2 between propofol anaesthesia and sevoflurane anaesthesia during and after hyperventilation. The second outcome was change in rSO2 after the initiation of hyperventilation and after the normalisation of ventilation. RESULTS: Changes of rSO2 during hyperventilation were -10 ±â€Š7% (left) and -11 ±â€Š8% (right) in the propofol group, and -10 ±â€Š8% (left) and -9 ±â€Š7% (right) in the sevoflurane group. After normalisation of PaCO2, rSO2 returned to baseline values. Arterial oxygen saturation remained stable throughout the measurement period. The rSO2 values were similar in the propofol and the sevoflurane groups at each time point. CONCLUSION: The effects of hyperventilation on estimated rSO2 were similar with propofol and sevoflurane anaesthesia. Changes in rSO2 correlated well with ventilation changes. TRIAL REGISTRATION: Japan Primary Registries Network (JPRN); UMIN-CTR ID; UMIN000010640.

The effect of rebreathing and hyperventilation on retinal and choroidal vessels measured by spectral domain optical coherence tomography.

OBJECTIVE: The purpose of this study was to examine the vasoreactivity in retina and choroid of the healthy eyes in response to experimentally altered partial arterial pressure of carbon dioxide (PaCO(2)) using a non-invasive technique, spectral domain optical coherence tomography (SD-OCT). MATERIALS AND METHODS: The study included non-smoking participants between 18 and 35 years of age, having visual acuity of 20/20 and with no systemic and ocular diseases. At baseline, the participants breathed room air (normocapnia). Hypocapnia was created with the help of hyperventilation; for this, the participants were instructed to draw deep and quick breaths, resulting one breathing cycle per 2 s. To create hypercapnia subjects rebreathed from a 5 l bag at least 3 min. Choroidal thickness and retinal artery diameter were measured at baseline, and hyperventilation and rebreathing conditions by SD-OCT. RESULTS: Twenty eyes of 20 healthy subjects were included in this study. Their mean age was 24.90 ± 5.32 years. Hyperventilation caused a significant reduction in choroidal thickness, compared with baseline, at all points; whereas rebreathing caused no significant change at all points. The mean diameters of the arteries were 151.80 ± 7.88 µm, with a significant decline to 148.90 ± 7.25 µm at hyperventilation condition and a significant increase to 153.50 ± 7.88 µm at rebreathing condition (p = 0.018, p = 0.043, respectively). CONCLUSION: This study demonstrated that, SD-OCT was a useful tool in measuring the ocular vascular response under hypercapnia and hypocapnia conditions. These findings may be helpful for further understanding the physiological nature of ocular blood flow and this preliminary study provides a basis for future studies.

Hypocapnia in women with fibromyalgia.

OBJECTIVES: The purpose of this study was to investigate whether people with fibromyalgia (FM) have dysfunctional breathing by examining acid-base balance and comparing it with healthy controls. METHODS: Thirty-six women diagnosed with FM and 36 healthy controls matched for age and gender participated in this cross-sectional study. To evaluate acid-base balance, arterial blood was sampled from the radial artery. Carbon dioxide, oxygen, bicarbonate, base excess, pH and lactate were analysed for between-group differences. Blood gas analyses were performed stepwise on each individual to detect acid-base disturbance, which was categorized as primary respiratory and possible compensation indicating chronicity. A three-step approach was employed to evaluate pH, carbon dioxide and bicarbonate in this order. RESULTS: Women with FM had significantly lower carbon dioxide pressure (p = 0.013) and higher lactate (p = 0.038) compared to healthy controls at the group level. There were no significant differences in oxygen pressure, bicarbonate, pH and base excess. Employing a three-step acid-base analysis, 11 individuals in the FM group had a possible renally compensated mild chronic hyperventilation, compared to only 4 among the healthy controls (p = 0.042). CONCLUSIONS: In this study, we could identify a subgroup of individuals with FM who may be characterized as mild chronic hyperventilators. The results might point to a plausible dysfunctional breathing in some women with FM.

Somatic mosaicism in a mother of two children with Pitt-Hopkins syndrome.

Pitt-Hopkins syndrome (PTHS) is a neurodevelopmental disorder characterized by intellectual disability, unusual face and breathing abnormalities and can be caused by haploinsufficiency of TCF4. The majority of cases are sporadic. Somatic mosaicism was reported infrequently. We report on a proband with typical manifestations of PTHS and his younger brother with a less striking phenotype. In both, a heterozygous frameshift mutation (c.1901_1909delinsA, p.Ala634AspfsX67) was found in exon 19 of TCF4. The same mutation was found at low levels in DNA extracted from the mother's blood, urine and saliva. This report of familial recurrence with somatic mosaicism in a healthy mother has important consequences for genetic counseling. We suggest careful studies in parents of other patients with PTHS to determine the frequency of germline and somatic mosaicism for TCF4 mutations.

Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study.

BACKGROUND: While the decrease in blood carbon dioxide (CO2 ) secondary to hyperventilation is generally accepted to play a major role in the decrease of cerebral tissue oxygen saturation (SctO2 ), it remains unclear if the associated systemic hemodynamic changes are also accountable. METHODS: Twenty-six patients (American Society of Anesthesiologists I-II) undergoing nonneurosurgical procedures were anesthetized with either propofol-remifentanil (n = 13) or sevoflurane (n = 13). During a stable intraoperative period, ventilation was adjusted stepwise from hypoventilation to hyperventilation to achieve a progressive change in end-tidal CO2 (ETCO2 ) from 55 to 25 mmHg. Minute ventilation, SctO2 , ETCO2 , mean arterial pressure (MAP), and cardiac output (CO) were recorded. RESULTS: Hyperventilation led to a SctO2 decrease from 78 ± 4% to 69 ± 5% (Δ = -9 ± 4%, P < 0.001) in the propofol-remifentanil group and from 81 ± 5% to 71 ± 7% (Δ = -10 ± 3%, P < 0.001) in the sevoflurane group. The decreases in SctO2 were not statistically different between these two groups (P = 0.5). SctO2 correlated significantly with ETCO2 in both groups (P < 0.001). SctO2 also correlated significantly with MAP (P < 0.001) and CO (P < 0.001) during propofol-remifentanil, but not sevoflurane (P = 0.4 and 0.5), anesthesia. CONCLUSION: The main mechanism responsible for the hyperventilation-induced decrease in SctO2 is hypocapnia during both propofol-remifentanil and sevoflurane anesthesia. Hyperventilation-associated increase in MAP and decrease in CO during propofol-remifentanil, but not sevoflurane, anesthesia may also contribute to the decrease in SctO2 but to a much smaller degree.

Serial monitoring of CO2 reactivity following sport concussion using hypocapnia and hypercapnia.

PRIMARY OBJECTIVE: This study examined the effects of mild traumatic brain injury (mTBI) on cerebrovascular reactivity (CVR). RESEARCH DESIGN: A repeated measures design was used to examine serial changes in CVR. METHODS AND PROCEDURES: Twenty subjects who recently suffered a mTBI were subjected to a respiratory challenge consisting of repeated 20 s breath-holds (BH) and hyperventilations (HV). Testing occurred on days 2 (D2), 4 (D4) and 8 (D8) post-injury as well as a baseline (BASE) assessment (after return-to-play). Transcranial Doppler was used to assess mean cerebral blood velocity (vMCA) and expired gas analysis provided end-tidal carbon dioxide (PETCO2) levels. RESULTS: There was no significant difference in resting vMCA across all testing days for mTBI. No significant differences in PETCO2 were found throughout the testing protocol. A significant effect (p < 0.001) of testing day on vMCA was found during BH and HV challenges for mTBI. Post-hoc analysis revealed significant differences (p < 0.05) in vMCA between D2 and the other testing days. CONCLUSIONS: These data suggest that, following mTBI: (1) CVR is not impaired at rest; (2) CVR is impaired in response to respiratory stress; and (3) the impairment may be resolved as early as 4 days post-injury.

Low serum concentrations of vitamin B6 and iron are related to panic attack and hyperventilation attack.

Patients undergoing a panic attack (PA) or a hyperventilation attack (HVA) are sometimes admitted to emergency departments (EDs). Reduced serotonin level is known as one of the causes of PA and HVA. Serotonin is synthesized from tryptophan. For the synthesis of serotonin, vitamin B6 (Vit B6) and iron play important roles as cofactors. To clarify the pathophysiology of PA and HVA, we investigated the serum levels of vitamins B2, B6, and B12 and iron in patients with PA or HVA attending an ED. We measured each parameter in 21 PA or HVA patients and compared the values with those from 20 volunteers. We found that both Vit B6 and iron levels were significantly lower in the PA/HVA group than in the volunteer group. There was no significant difference in the serum levels of vitamins B2 or B12. These results suggest that low serum concentrations of Vit B6 and iron are involved in PA and HVA. Further studies are needed to clarify the mechanisms involved in such differences.

Mild hypercapnia with hyperventilation attenuates recovery from anesthesia in elderly patients.

PURPOSE: Mild hypercapnia with hyperventilation has been reported to significantly decrease recovery time from inhaled anesthesia in young and middle-aged patients. However, its efficacy has not yet been clarified in elderly patients, although delayed emergence can deteriorate their quality of recovery. METHODS: We enrolled 30 elderly patients (≥65 years) and 30 middle-aged patients (45-64 years) who were scheduled for ophthalmic surgery and allocated them to the control or the device group. Anesthesia was maintained with 1.5% sevoflurane. Mild hypercapnic hyperventilation was induced by the ANEclear anesthesia recovery device. The primary outcome was the time from vaporizer shut-off to initial response (eye or mouth opening, nodding, or grasping hand) in elderly patients. The secondary outcomes were the time to extubation and leaving the operating room (OR), the time to reach 50% of the difference between BIS at extubation and vaporizer shut-off (BIS ET50), and interaction between the recovery measures and patient age. RESULTS: The ANEclear significantly reduced the time to initial response, extubation, leaving the OR, and BIS ET50 in both age groups: their means and 95% CI of the ratio of two means (Mean(ANEclear)/Mean(control)) were 0.576 (0.500, 0.660), 0.595 (0.523, 0.673), 0.713 (0.622, 0.812), and 0.547 (0.444, 0.663), respectively, in the elderly group, and 0.717 (0.591, 0.849), 0.723 (0.609, 0.842), 0.855 (0.736, 0.982), and 0.631 (0.463, 0.813), respectively, in the middle-aged group. The recovery measures were shortened equally in both age groups: P values for the interaction were 0.060679, 0.062534, 0.069215, and 0.420061, respectively. CONCLUSIONS: Recovery time was significantly decreased by the ANEclear in the elderly group. This reduction was comparable to the time for middle-aged patients.

Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise.

We examined the effects of inspiratory muscle training (IMT) upon volitional hyperpnoea-mediated increases in blood lactate ([lac(-)](B)) during cycling at maximal lactate steady state (MLSS) power, and blood lactate and oxygen uptake kinetics at the onset of exercise. Twenty males formed either an IMT (n = 10) or control group (n = 10). Prior to and following a 6-week intervention, two 30 min trials were performed at MLSS (207 ± 28 W), determined using repeated 30 min constant power trials. The first was a reference trial, whereas during the second trial, from 20 to 28 min, participants mimicked the breathing pattern commensurate with 90% of the maximal incremental exercise test minute ventilation ([Formula: see text]). Prior to the intervention, the MLSS [lac(-)](B) was 3.7 ± 1.8 and 3.9 ± 1.6 mmol L(-1) in the IMT and control groups, respectively. During volitional hyperpnoea, [Formula: see text] increased from 79.9 ± 9.5 and 76.3 ± 15.4 L min(-1) at 20 min to 137.8 ± 15.2 and 135.0 ± 19.7 L min(-1) in IMT and control groups, respectively; [lac(-)](B) concurrently increased by 1.0 ± 0.6 (+27%) and 0.9 ± 0.7 mmol L(-1) (+25%), respectively (P < 0.05). Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac(-)](B) during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (-28%) and phase II oxygen uptake (-31%) kinetics time constants at the onset of exercise and the MLSS [lac(-)](B) (-15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.

Elevated lactate during psychogenic hyperventilation.

STUDY OBJECTIVE: Elevated arterial lactate levels are closely related to morbidity and mortality in various patient categories. In the present retrospective study, the relation between arterial lactate, partial pressure of carbon dioxide (Pco(2)) and pH was systematically investigated in patients who visited the emergency department (ED) with psychogenic hyperventilation. METHODS: Over a 5-month period, all the patients who visited the ED of a university hospital with presumed psychogenic hyperventilation were evaluated. Psychogenic hyperventilation was presumed to be present when an increased respiratory rate (>20 min) was documented at or before the ED visit and when somatic causes explaining the hyperventilation were absent. Arterial blood gas and lactate levels (reference values 0.5-1.5 mmol/l) were immediately measured by a point-of-care analyser that was managed and calibrated by the central laboratory. RESULTS: During the study period, 46 patients were diagnosed as having psychogenic hyperventilation. The median (range) Pco(2) for this group was 4.3 (2.0-5.5) kPa, the pH was 7.47 (7.40-7.68) and the lactate level was 1.2 (0.5-4.4) mmol/l. 14 participants (30%) had a lactate level above the reference value of 1.5 mmol/l. Pco(2) was the most important predictor of lactate in multivariate analysis. None of the participants underwent any medical treatment other than observation at the ED or had been hospitalised after their ED visit. CONCLUSIONS: In patients with psychogenic hyperventilation, lactate levels are frequently elevated. Whereas high lactates are usually associated with acidosis and an increased risk of poor outcome, in patients with psychogenic hyperventilation, high lactates are associated with hypocapnia and alkalosis. In this context, elevated arterial lactate levels should not be regarded as an adverse sign.

Is venous blood a more reliable description of acid-base state following simulated hypo- and hyperventilation?

BACKGROUND: ABGs are performed in acute conditions as the reference method for assessing the acid-base status of blood. Hyperventilation and breath-holding are common ventilatory changes that occur around the time of sampling, rapidly altering the 'true' status of the blood. This is particularly relevant in emergency medicine patients without permanent arterial catheters, where the pain and anxiety of arterial punctures can cause ventilatory changes. This study aimed to determine whether peripheral venous values could be a more reliable measure of blood gases following acute changes in ventilation. METHODS: To allow for characterisation of ventilatory changes typical of acutely ill patients, but without the confounding influence of perfusion or metabolic disturbances, 30 patients scheduled for elective surgery were studied in a prospective observational study. Following anaesthesia, and before the start of the surgery, ventilator settings were altered to achieve a + 100% or - 60% change in alveolar ventilation ('hyper-' or 'hypoventilation'), changes consistent with the anticipation of a painful arterial puncture commonly encountered in the emergency room. Blood samples were drawn simultaneously from indwelling arterial and peripheral venous catheters at baseline, and at 15, 30, 45, 60, 90 and 120 s following the ventilatory change. Comparisons between the timed arterial (or venous) samples were done using repeated-measures ANOVA, with post-hoc analysis using Bonferroni's correction. RESULTS: Arterial blood pH and PCO2 changed rapidly within the first 15-30s after both hyper- and hypoventilation, plateauing at around 60s (∆pH = ±0.036 and ∆PCO2 = ±0.64 kPa (4.7 mmHg), respectively), with peripheral venous values remaining relatively constant until 60s, and changing minimally thereafter. Mean arterial changes were significantly different at 30s (P < 0.001) when compared to baseline, in response to both hyper- and hypoventilation. CONCLUSION: This study has shown that substantial differences in arterial and peripheral venous acid-base status can be due to acute changes in ventilation, commonly seen in the ER over the 30s necessary to sample arterial blood. If changes are transient, peripheral venous blood may provide a more reliable description of acid-base status.

Causes of breathing inefficiency during exercise in heart failure.

BACKGROUND: Patients with heart failure (HF) develop abnormal pulmonary gas exchange; specifically, they have abnormal ventilation relative to metabolic demand (ventilatory efficiency/minute ventilation in relation to carbon dioxide production [V(E)/VCO2]) during exercise. The purpose of this investigation was to examine the factors that underlie the abnormal breathing efficiency in this population. METHODS AND RESULTS: Fourteen controls and 33 moderate-severe HF patients, ages 52 ± 12 and 54 ± 8 years, respectively, performed submaximal exercise (∼65% of maximum) on a cycle ergometer. Gas exchange and blood gas measurements were made at rest and during exercise. Submaximal exercise data were used to quantify the influence of hyperventilation (PaCO2) and dead space ventilation (V(D)) on V(E)/VCO2. The V(E)/VCO2 relationship was lower in controls (30 ± 4) than HF (45 ± 9, P < .01). This was the result of hyperventilation (lower PaCO2) and higher V(D)/V(T) that contributed 40% and 47%, respectively, to the increased V(E)/VCO2 (P < .01). The elevated V(D)/V(T) in the HF patients was the result of a tachypneic breathing pattern (lower V(T), 1086 ± 366 versus 2003 ± 504 mL, P < .01) in the presence of a normal V(D) (11.5 ± 4.0 versus 11.9 ± 5.7 L/min, P = .095). CONCLUSIONS: The abnormal ventilation in relation to metabolic demand in HF patients during exercise was due primarily to alterations in breathing pattern (reduced V(T)) and excessive hyperventilation.

Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET.

BACKGROUND: Arterial carbon dioxide tension (PaCO(2)) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia-induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). METHODS: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H(2)(15)O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. RESULTS: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO(2) was decreased from 5.5 + or - 0.7 to 3.8 + or - 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. CONCLUSIONS: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia.

Cardiopulmonary changes during clarinet playing.

Since playing wind instrument impedes normal respiratory functions, its effect on expiratory and blood gases as well as on cardiac function was investigated. In 15 skilled clarinettists expiratory PO(2) and PCO(2) were measured in gas drawn from a modified clarinet barrel when playing a composition (Robert Schumann's "Phantasiestücke" Op. 73 for clarinet and piano) with increasing difficulty from movement 1 to movement 3. Blood gases were measured in arterialized ear lobe blood at the end of each movement and the electrocardiogram was recorded continuously. From the expiratory gas pressures one may conclude that the most advanced players adapt their ventilation to the requirements of the composition and sustain expiration during difficult parts of the composition until hypoxic alveolar PO(2) values are reached (minimum 77 mmHg). Less trained clarinettists tend to hyperventilation or shallow breathing. Oxygen saturation in arterialized blood showed a slight step-wise decrease from movement to movement [control 96.6 ± 0.5 (SD)%, end of concert 95.6 ± 1.0%]. SO(2) was significantly higher because of possibly more effective ventilation in instrumentalists with practise time exceeding 2 h daily. Mean heart rate increased to values like during moderate to heavy physical exercise depending on artistic fitness and the difficulty of the movement (maximal individual value 173 beats/min). Additionally, a large variation might be caused through intrathoracic pressure changes, changing exertion, respiratory influences and emotion. The electrocardiogram showed no pathological events. In general, clarinet playing at a professional level imposes strain on ventilation and circulation but usually not on a pathophysiological level.

High fliers: the physiology of bar-headed geese.

Up to half the world's population of bar-headed geese (Anser indicus) migrate between central Asia and India and fly between 5000 m and 9000 m above sea level as they cross the Himalayas. The partial pressures of oxygen at these altitudes are, respectively, about 50% and 30% those at sea level. Flapping flight is energetically expensive, so how are bar-headed geese able to migrate at such altitudes? The haemoglobin of bar-headed geese has a greater affinity for oxygen than those of lowland birds, and birds are able to hyperventilate to a greater extent than mammals during severe hypoxia. Together, these mean that the concentration of oxygen in the arterial blood at a given altitude is greater in bar-headed geese than in lowland birds and mammals. The low partial pressure of CO(2) in arterial blood (hypocapnia) that accompanies hyperventilation does not cause reduction of cerebral blood flow in birds as it does in mammals, thus there is greater oxygen delivery to the brain in hypoxic birds, including bar-headed geese, than in mammals. Captive bar headed geese could not maintain elevated aerobic metabolism during exercise at a simulated altitude of 8500 m and their cardiac stroke volume was much lower than that during exercise at sea level. This suggests that if some individuals of this species of geese do really manage to fly over Mt Everest, they may only do so if they receive assistance from vertical air movements, for example from lee waves downwind from the mountains.

A 19-month-old boy with recurrent respiratory distress.

We present a 19-month-old boy with a history of asthma who presented to the pediatric emergency department with noisy breathing and tachypnea partially responsive to albuterol. He was discharged to routine care at home. His parents brought him back the next day for persistent respiratory distress despite routine home albuterol. A check of electrolytes showed a low bicarbonate level.