Overcoming noise in quantum teleportation with multipartite hybrid entanglement.

Quantum entanglement and decoherence are the two counterforces of many quantum technologies and protocols. For example, while quantum teleportation is fueled by a pair of maximally entangled resource qubits, it is vulnerable to decoherence. Here, we propose an efficient quantum teleportation protocol in the presence of pure decoherence and without entangled resource qubits entering the Bell-state measurement. Instead, we use multipartite hybrid entanglement between the auxiliary qubits and their local environments within the open-quantum system context. With a hybrid-entangled initial state, it is the decoherence that allows us to achieve high fidelities. We demonstrate our protocol in an all-optical experiment.

Eucapnic voluntary hyperventilation test decreases exhaled nitric oxide level in children.

BACKGROUND: Exhaled nitric oxide (FeNO) measurements and eucapnic voluntary hyperventilation (EVH) tests have been used as diagnostic tools for asthma. Data on the impact of hyperventilation on the level of FeNO are limited. AIM: We aimed to evaluate whether EVH tests affect the level of FeNO in children aged 10-16 years. METHODS: A total of 234 children aged 10-16 years had a 6-min EVH test performed. In total, FeNO values for 153 of 234 children were measured before the test and within 15 min after the test. According to a baseline FeNO level of 20 ppb, children were divided into two groups: those with low values (FeNO < 20 ppb) and those with high values (FeNO ≥ 20 ppb). RESULTS: The median age of the children was 13.4 years (interquartile range 12.3-15.3 years); 58% were boys and 42% were girls. Of these children, 51% were sensitized to aeroallergens. In 101 of 153 children (66%), the FeNO values decreased after the EVH test. In children with low and high baseline levels, the median level of FeNO decreased after the EVH test: 10.5 ppb before versus 9.5 ppb after (p < .011), and 31.0 ppb before versus 28.0 ppb after (p < .011), respectively. The decrease in FeNO after EVH test was not associated with induced bronchoconstriction expressed as a change in FEV1 (Rs  = .19). CONCLUSIONS: The EVH test decreases FeNO levels. Therefore, FeNO should be measured before an EVH test is performed.

Cut-off values to evaluate exercise-induced asthma in eucapnic voluntary hyperventilation test for children.

BACKGROUND AND AIM: The eucapnic voluntary hyperventilation (EVH) testing is a diagnostic tool for diagnostics of exercise-induced bronchoconstriction; while the testing has become more common among children, data on the test's feasibility among children remain limited. Our aim was to investigate EVH testing feasibility among children, diagnostic testing cut-off values, and which factors affect testing outcomes. METHODS: We recruited 134 patients aged 10-16 years with a history of exercise-induced dyspnoea and 100 healthy control children to undergo 6-min EVH testing. Testing feasibility was assessed by the children's ability to achieve ≥70% of the target minute ventilation of 30 times forced expiratory volume in 1 s (FEV1). Bronchoconstriction was assessed as a minimum of 8%, 10%, 12%, 15% or 20% fall in FEV1. Patient characteristics were correlated with EVH outcomes. RESULTS: Overall, 98% of the children reached ≥70%, 88% reached ≥80%, 79% reached ≥90% and 62% reached ≥100% of target ventilation in EVH testing; of children with a history of exercise-induced dyspnoea, the decline percentages were as follows: 24% (≥8% fall), 17% (≥10% fall), 10% (≥12% fall), 6% (≥15% fall) and 5% (≥20% fall) in FEV1, compared to 11%, 4%, 3%, 1% and 0% among the healthy controls, respectively. Healthy controls and boys performed testing at higher ventilation rates (p < .05). CONCLUSION: Eucapnic voluntary hyperventilation testing is feasible among children aged 10-16 years and has diagnostic value in evaluating exercise-induced dyspnoea among children. A minimum 10% fall in FEV1 is a good diagnostic cut-off value. Disease status appears to be important covariates.

Alterations in heart rate variability in patients with peripheral arterial disease requiring surgical revascularization have limited association with postoperative major adverse cardiovascular and cerebrovascular events.

OBJECTIVE: Obstructive sleep apnea (OSA) is common in peripheral arterial disease (PAD) and associates with high mortality after surgery. Since abnormal heart rate variability (HRV) is predictive of postoperative complications, we investigated the relations of HRV with PAD, OSA and major adverse cardiovascular and cerebrovascular events (MACCE). MATERIALS AND METHODS: Seventy-five patients (67±9 years) scheduled for sub-inguinal revascularization and 15 controls (63±6 years) underwent polysomnography and HRV analyses. OSA with an apnea-hypopnea index (AHI) ≥20/hour was considered significant. HRV was measured during wakefulness, S2, S3-4 and rapid eye movement (REM) sleep with time and frequency domain methods including beat-to-beat variability, low frequency (LF) and high frequency (HF) power, and detrended fluctuation analysis (DFA). MACCE was defined as cardiac death, myocardial infarction, coronary revascularization, hospitalized angina pectoris and stroke. RESULTS: Thirty-six patients (48%) had AHI≥20/hour. During follow-up (median 52 months), 22 patients (29%) suffered a MACCE. Compared to controls, fractal correlation of HRV (scaling exponent alpha 1 measured with DFA) was weaker during S2 and evening wakefulness in all subgroups (+/-AHI≥20/hour, +/-MACCE) but only in patients with AHI≥20/hour during morning wakefulness. The LF/HF ratio was lower in all subgroups during S2 but only in patients with AHI ≥20/hour during evening or morning wake. In the covariance analysis adjusted for age, body mass index, coronary artery disease and PAD duration, the alpha 1 during morning wakefulness remained significantly lower in patients with AHI≥20/hour than in those without (1.12 vs. 1.45; p = 0.03). Decreased HF during REM (p = 0.04) and S3-4 sleep (p = 0.03) were predictive of MACCE. In analyses with all sleep stages combined, mean heart rate as well as very low frequency, LF, HF and total power were associated with OSA of mild-to-moderate severity (AHI 10-20/hour). CONCLUSIONS: HRV is altered in patients with PAD. These alterations have a limited association with OSA and MACCE.

Eucapnic voluntary hyperventilation test in children.

BACKGROUND: In children, exercise-induced dyspnea is a common symptom that can be due to dysfunctional breathing. EVH test has bee used especially in elite athletes as bronchoprovocation test. Currently, there are only few studies on the EVH test. New research methods are required alongside the traditionally used tests especially due to dysfunctional breathing disorder. PURPOSE: The purpose of the "pilot study" was to study the usability of the EVH test with real time biofeedback in children of 10-16 years of age in the diagnostics of exercise-induced dyspnea. METHODS: Six 10-16-year-old teenagers with history of exercise-induced dyspnea and three healthy control subjects were selected for the study. A 6-minute EVH test with realtime biofeedback was performed on the patients and the diagnosis was confirmed on the basis of clinical findings and spirometry follow-up either as normal, asthma or dysfunctional breathing. RESULTS: The study was successful in the patients. In the spirometry follow-up, three patients had bronchoconstriction (FEV1 decline over 10%), dysfunctional breathing condition was observed in three patients and three control patients experienced no symptoms. Only two DFB-patients didn't reach the target level of minute ventilation due to a clinical symptom (inspiratory stridor). CONCLUSION: The EVH test was successful in the 10-16-year-old children having participated in the study and the test was well tolerated. Through the study, it was possible to provoke both dysfunctional breathing disorder and bronchoconstriction in the symptomatic patients. Based on the pilot study, EVH test seems to be usable in the diagnostics of pediatric exercise-induced dyspnea but larger studies are warranted to confirm our preliminary findings.

Automated Detection of Atrial Fibrillation Based on Time-Frequency Analysis of Seismocardiograms.

In this paper, a novel method to detect atrial fibrillation (AFib) from a seismocardiogram (SCG) is presented. The proposed method is based on linear classification of the spectral entropy and a heart rate variability index computed from the SCG. The performance of the developed algorithm is demonstrated on data gathered from 13 patients in clinical setting. After motion artifact removal, in total 119 min of AFib data and 126 min of sinus rhythm data were considered for automated AFib detection. No other arrhythmias were considered in this study. The proposed algorithm requires no direct heartbeat peak detection from the SCG data, which makes it tolerant against interpersonal variations in the SCG morphology, and noise. Furthermore, the proposed method relies solely on the SCG and needs no complementary electrocardiography to be functional. For the considered data, the detection method performs well even on relatively low quality SCG signals. Using a majority voting scheme that takes five randomly selected segments from a signal and classifies these segments using the proposed algorithm, we obtained an average true positive rate of [Formula: see text] and an average true negative rate of [Formula: see text] for detecting AFib in leave-one-out cross-validation. This paper facilitates adoption of microelectromechanical sensor based heart monitoring devices for arrhythmia detection.

Respiratory modulation of human autonomic function on Earth.

KEY POINTS: We studied healthy supine astronauts on Earth with electrocardiogram, non-invasive arterial pressure, respiratory carbon dioxide concentrations, breathing depth and sympathetic nerve recordings. The null hypotheses were that heart beat interval fluctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs. R-R interval fluctuations at usual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea. The subjects' responses to apnoea could not be attributed to changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve burst areas, frequencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pulmonary stretch receptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympathetic activity). Apnoea responses of healthy subjects may result from changes of central respiratory motoneurone activity. ABSTRACT: We studied eight healthy, supine astronauts on Earth, who followed a simple protocol: they breathed at fixed or random frequencies, hyperventilated and then stopped breathing, as a means to modulate and expose to view important, but obscure central neurophysiological mechanisms. Our recordings included the electrocardiogram, finger photoplethysmographic arterial pressure, tidal volume, respiratory carbon dioxide concentrations and peroneal nerve muscle sympathetic activity. Arterial pressure, vagal tone and muscle sympathetic outflow were comparable during spontaneous and controlled-frequency breathing. Compared with spontaneous, 0.1 and 0.05 Hz breathing, however, breathing at usual frequencies (∼0.25 Hz) lowered arterial baroreflex gain, and provoked smaller arterial pressure and R-R interval fluctuations, which were separated by intervals that were likely to be too short and variable to be attributed to baroreflex physiology. R-R interval fluctuations at usual breathing frequencies disappear during apnoea, and thus cannot provide evidence for the existence of a central respiratory oscillation. Apnoea sets in motion a continuous and ever changing reorganization of the relations among stimulatory and inhibitory inputs and autonomic outputs, which, in our study, could not be attributed to altered chemoreceptor, baroreceptor, or pulmonary stretch receptor activity. We suggest that responses of healthy subjects to apnoea are driven importantly, and possibly prepotently, by changes of central respiratory motoneurone activity. The companion article extends these observations and asks the question, Might terrestrial responses to our 20 min breathing protocol find expression as long-term neuroplasticity in serial measurements made over 20 days during and following space travel?

Respiratory modulation of human autonomic function: long-term neuroplasticity in space.

KEY POINTS: We studied healthy astronauts before, during and after the Neurolab Space Shuttle mission with controlled breathing and apnoea, to identify autonomic changes that might contribute to postflight orthostatic intolerance. Measurements included the electrocardiogram, finger photoplethysmographic arterial pressure, respiratory carbon dioxide levels, tidal volume and peroneal nerve muscle sympathetic activity. Arterial pressure fell and then rose in space, and drifted back to preflight levels after return to Earth. Vagal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations rose and then fell in space, and descended to preflight levels upon return to Earth. Sympathetic burst frequencies (but not areas) were greater than preflight in space and on landing day, and astronauts' abilities to modulate both burst areas and frequencies during apnoea were sharply diminished. Spaceflight triggers long-term neuroplastic changes reflected by reciptocal sympathetic and vagal motoneurone responsiveness to breathing changes. ABSTRACT: We studied six healthy astronauts five times, on Earth, in space on the first and 12th or 13th day of the 16 day Neurolab Space Shuttle mission, on landing day, and 5-6 days later. Astronauts followed a fixed protocol comprising controlled and random frequency breathing and apnoea, conceived to perturb their autonomic function and identify changes, if any, provoked by microgravity exposure. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, tidal carbon dioxide concentrations and volumes, and peroneal nerve muscle sympathetic activity on Earth (in the supine position) and in space. (Sympathetic nerve recordings were made during three sessions: preflight, late mission and landing day.) Arterial pressure changed systematically from preflight levels: pressure fell during early microgravity exposure, rose as microgravity exposure continued, and drifted back to preflight levels after return to Earth. Vagal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations (root mean square of successive normal R-R intervals; and proportion of successive normal R-R intervals greater than 50 ms, divided by the total number of normal R-R intervals) rose significantly during early microgravity exposure, fell as microgravity exposure continued, and descended to preflight levels upon return to Earth. Sympathetic mechanisms also changed. Burst frequencies (but not areas) during fixed frequency breathing were greater than preflight in space and on landing day, but their control during apnoea was sharply altered: astronauts increased their burst frequencies from already high levels, but they could not modulate either burst areas or frequencies appropriately. Space travel provokes long-lasting sympathetic and vagal neuroplastic changes in healthy humans.

Human hair in the identification of cocaine abuse with cantilever-enhanced photoacoustic spectroscopy and principal component analysis.

In this study, a novel approach combining different techniques, including Fourier transform infrared (FT-IR) spectroscopy, photoacoustic spectroscopy (PAS) with an interferometric cantilever microphone, and principal component analysis (PCA) along with a proper data preprocessing procedure, have been used in the investigation of hair samples for cocaine abuse. Hair fibers from cocaine-overdose patients have been measured using a simple procedure involving cantilever-enhanced photoacoustic Fourier transform infrared spectroscopy. In addition, a reference group of hair samples from subjects with no cocaine abuse has been measured. We present a first approach to discriminate the cocaine users from the reference group with the photoacoustic method and PCA. With proper data preprocessing methods, the two groups were successfully separated according to their spectra. The results were confirmed with two different classification methods independent of the principal component data analysis.

Baroreflex physiology studied in healthy subjects with very infrequent muscle sympathetic bursts.

Because it is likely that, in healthy human subjects, baroreflex mechanisms operate continuously, independent of experimental interventions, we asked the question, In what ways might study of unprovoked, very infrequent muscle sympathetic bursts inform baroreflex physiology? We closely examined arterial pressure and R-R interval responses of 11 supine healthy young subjects to arterial pressure ramps triggered by large isolated muscle sympathetic bursts. We triggered data collection sweeps on the beginnings of sympathetic bursts and plotted changes of arterial pressure (finger volume clamp or intra-arterial) and R-R intervals occurring before as well as after the sympathetic triggers. We estimated baroreflex gain from regression of R-R intervals on systolic pressures after sympathetic bursts and from the transfer function between cross-spectra of systolic pressure and R-R intervals at low frequencies. Isolated muscle sympathetic bursts were preceded by arterial pressure reductions. Baroreflex gain, calculated with linear regression of R-R intervals on systolic pressures after bursts, was virtually identical to baroreflex gain, calculated with the cross-spectral modulus [mean and (range): 24 (7-43) vs. 24 (8-45) ms/mmHg], and highly significant, according to linear regression (r(2) = 0.91, P = 0.001). Our results indicate that 1) since infrequent human muscle sympathetic bursts are almost deterministically preceded by arterial pressure reductions, their occurrence likely reflects simple baroreflex physiology, and 2) the noninvasive low-frequency modulus reliably reproduces gains derived from R-R interval responses to arterial pressure ramps triggered by infrequent muscle sympathetic bursts.

Delta entropy of heart rate variability along with deepening anesthesia.

BACKGROUND: Conventional time and frequency domain measures of heart rate variability (HRV) are strongly influenced by anesthetic drugs, and are therefore not able to detect subtle changes in HRV, even during light anesthesia. Approximate entropy of R-R intervals is an HRV measure that has a tendency to decrease during anesthesia, but it is severely compromised by low-frequency variations of the signal. However, the negative effect of the low-frequency variations can be eliminated by differentiating the R-R interval tachogram before analysis. We designed this study to investigate characteristics of a novel HRV measure, named δ entropy (dEn), during deepening anesthesia. METHODS: Eight healthy subjects were anesthetized with sevoflurane and 8 with propofol in a stepwise manner using 3 escalating concentrations (2%, 3%, and 4% end-tidal concentration and 7.4 ± 1.7, 12.3 ± 2.6, and 18.3 ± 5.0 µg/mL plasma concentration, respectively) at 30-minute intervals. A third group of 8 subjects received a supramaximal IV dose of glycopyrrolate without anesthesia to examine the effect of cardiac vagal activity on dEn. We computed dEn at baseline, during each step of anesthesia and during the anticholinergic blockade. RESULTS: The dEn decreased along with deepening levels of sevoflurane and propofol anesthesia up to 33% (95% confidence interval [CI] 21%-44%) and 38% (95% CI 28%-48%), respectively. At each anesthesia level, dEn differed significantly (P < 0.05) from that measured at the preceding level, similarly in both the sevoflurane and propofol groups. Parasympathetic blockade by glycopyrrolate was found to decrease dEn by 17% (95% CI 6%-28%). CONCLUSIONS: The dEn is a novel HRV measure able to detect subtle sympathetic- and parasympathetic-mediated alterations in HRV both during deepening levels of sevoflurane and propofol anesthesia and during exceedingly deep anesthesia.

Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans.

Activation of sympathetic efferent traffic is essential to maintaining adequate arterial pressures during reductions of central blood volume. Sympathetic baroreflex gain may be reduced, and muscle sympathetic firing characteristics altered with head-up tilt just before presyncope in humans. Volume redistributions with lower body negative pressure (LBNP) are similar to those that occur during haemorrhage, but limited data exist describing arterial pressure-muscle sympathetic nerve activity (MSNA) relationships during intense LBNP. Responses similar to those that occur in presyncopal subjects during head-up tilt may signal the beginnings of cardiovascular decompensation associated with haemorrhage. We therefore tested the hypotheses that intense LBNP disrupts MSNA firing characteristics and leads to a dissociation between arterial pressure and sympathetic traffic prior to presyncope. In 17 healthy volunteers (12 males and 5 females), we recorded ECG, finger photoplethysmographic arterial pressure and MSNA. Subjects were exposed to 5 min LBNP stages until the onset of presyncope. The LBNP level eliciting presyncope was denoted as 100% tolerance, and then data were assessed relative to this normalised maximal tolerance by expressing LBNP levels as 80, 60, 40, 20 and 0% (baseline) of maximal tolerance. Data were analysed in both time and frequency domains, and cross-spectral analyses were performed to determine the coherence, transfer function and phase angle between diastolic arterial pressure (DAP) and MSNA. DAP-MSNA coherence increased progressively and significantly up to 80% maximal tolerance. Transfer functions were unchanged, but phase angle shifted from positive to negative with application of LBNP. Sympathetic bursts fused in 10 subjects during high levels of LBNP (burst fusing may reflect modulation of central mechanisms, an artefact arising from our use of a 0.1 s time constant for integrating filtered nerve activity, or a combination of both). On average, arterial pressures and MSNA decreased significantly the final 20 s before presyncope (n = 17), but of this group, MSNA increased in seven subjects. No linear relationship was observed between the magnitude of DAP and MSNA changes before presyncope (r = 0.12). We report three primary findings: (1) progressive LBNP (and presumed progressive arterial baroreceptor unloading) increases cross-spectral coherence between arterial pressure and MSNA, but sympathetic baroreflex control is reduced before presyncope; (2) withdrawal of MSNA is not a prerequisite for presyncope despite significant decreases of arterial pressure; and (3) reductions of venous return, probably induced by intense LBNP, disrupt MSNA firing characteristics that manifest as fused integrated bursts before the onset of presyncope. Although fusing of integrated sympathetic bursts may reflect a true physiological compensation to severe reductions of venous return, duplication of this finding utilizing shorter time constants for integration of the nerve signal is required.

Rapid prediction of trauma patient survival by analysis of heart rate complexity: impact of reducing data set size.

Heart rate complexity (HRC) is an emerging "new vital sign" for critically ill and injured patients. Traditionally, 800-beat data sets have been used to calculate HRC variables, thus limiting their practical use in an emergency. We sought to investigate whether data set reductions diminish the use of HRC to predict mortality in prehospital trauma patients. Ectopy-free, 800-beat sections of electrocardiogram (EKG) were collected from 31 prehospital trauma patients during their helicopter transport to a level 1 trauma center. Twenty patients survived (survivors) and 11 died (nonsurvivors) after admission. HRC was assessed via approximate entropy (ApEn), sample entropy (SampEn), and similarity of distributions (SOD). The amplitude of high-frequency oscillations was measured via the method of complex demodulation. This analysis was repeated in data sets of 800, 600, 400, 200, and 100 beats. For 800 beats, ApEn and SampEn were lower in nonsurvivors than in survivors, and SOD was higher. With data set reduction, ApEn in survivors and nonsurvivors gradually approached each other but remained different until the 200-beat dataset. Sample entropy did not change with data shortening and remained lower in nonsurvivors in all data sets. Similarity of distributions was nearly constant within groups for all data sets and discriminated survivors from nonsurvivors in 800- and 100-beat data sets. High-frequency amplitude distinguished survivors from nonsurvivors in 400-, 200-, and 100-beat data sets. Logistic regression was performed for the 800-, 200-, and 100-beat data sets, retaining SampEn as a predictor of mortality (area under the receiver-operating-characteristic curves, 0.821-0.895). HRC decreased in nonsurvivors versus survivors. This finding was confirmed for data sets as short as 100 beats by computationally different metrics. SampEn, SOD, and complex demodulation were relatively unaffected by data set reduction. These metrics may be useful for rapid identification of trauma patients with potentially lethal injuries using short EKG data sets.

Cardiac repolarization and striatal dopamine transporter function are interrelated.

OBJECTIVE: In Parkinson's disease, striatal dopamine transporter (DAT) binding and cardiac sympathetic function are disturbed. In addition, heart rate (HR)-corrected cardiac repolarisation time (QTc interval), which is partly under autonomic control, is prolonged. Whether there is physiological coupling between striatal DAT binding and QTc time (QTc-DAT relation) is not known. The purpose of this study is to evaluate QTc-DAT relation in healthy young adults. METHODS: Thirty-five participants (18 women, age 26.4+/-1.8 years; mean+/-SD) were studied with iodine-123 labelled 2beta-carbomethoxy-3beta-(4-iodophenyl) nortropane single photon emission tomography. Signal-averaged ECG was recorded at rest from each participant. QTc interval was computed with Bazett's correction and with the approach by Karjalainen, getting QTc and QTk intervals, respectively. RESULTS: Mean striatal DAT binding, as (striatum-cerebellum)/cerebellum, was 2.63+/-0.31. Mean HR, QT, QTc and QTk intervals were 66+/-9 bpm, 340+/-25 ms, 354+/-18 ms and 351+/-16 ms, respectively. HR-QT correlation was -0.63, P value of less than 0.001. HR was not related to striatal DAT binding. QTc-DAT and QTk-DAT relations were significant, r = -0.50, P = 0.004 and r = -0.59, P = 0.0002, respectively. In linear regression model, striatal DAT binding explained 35% of the variance of QTk interval (95% confidence interval: -46.9 to -13.0, P = 0.0002). CONCLUSION: This study suggests significant physiological QTc-DAT relation in young healthy adults. QTc interval measurements might carry diagnostically important information in clinical conditions, which have an effect on both striatal DAT binding and cardiac sympathetic function.

Heart-rate complexity for prediction of prehospital lifesaving interventions in trauma patients.

BACKGROUND: Traditional vital signs often fail to identify critically injured patients soon enough to permit timely intervention. To improve our ability to forecast the need for prehospital lifesaving interventions (LSIs), we applied heart-rate complexity (HRC) analysis to the electrocardiogram (ECG) of patients en route to trauma centers. METHODS: Analysis of ECG and clinical data from 374 patients en route by helicopter to three urban Level I trauma centers was conducted. Waveforms from 182 patients were excluded (because of ectopy, noise, or inadequate length). Of the remaining 192 patients, 54 received 66 LSIs in the field (LSI group): intubation (n = 52), cardiopulmonary resuscitation (n = 5), cricothyroidotomy (n = 2), and pneumothorax decompression (n = 7); 138 patients did not (non-LSI group). In the field, heart rate, blood pressure, and the Glasgow Coma Scale score (GCS(TOTAL)) and its motor component (GCS(MOTOR)) were recorded. ECG was recorded during flight. Ectopy-free, 800-beat sections of ECG were identified off-line and analyzed by HRC methods including Sample Entropy (SampEn) and Detrended Fluctuations Analysis (DFA). RESULTS: There was no difference between LSI and non-LSI patients in heart rate or blood pressure. SampEn was lower in LSI than in non-LSI (0.88 +/- 0.03 vs. 1.11 +/- 0.03), as was DFA (1.09 +/- 0.05 vs. 1.33 +/- 0.03) and GCS(MOTOR) (3.4 +/- 0.4 vs. 5.7 +/- 0.1) (all p < 0.0001). By logistic regression, SampEn, DFA, and GCS(MOTOR) were independently associated with LSIs (area under the receiver operating characteristic curve, 0.897). CONCLUSIONS: Decreased HRC is associated with LSIs in prehospital trauma patients. HRC may be useful as a new vital sign for identification of the severely injured.

Assessment of cardiovascular regulation after burns by nonlinear analysis of the electrocardiogram.

Critical illness and hypovolemia are associated with loss of complexity of the R-to-R interval (RRI) of the electrocardiogram, whereas recovery is characterized by restoration thereof. Our goal was to investigate the dynamics of RRI complexity in burn patients. We hypothesized that the postburn period is associated with a state of low RRI complexity, and that successful resuscitation restores it. Electrocardiogram was acquired from 13 patients (age 55 +/- 5 years, total body surface area burned 36 +/- 6%, 11 +/- 5% full thickness) at 8, 12, 24, and 36 hours during postburn resuscitation. RRI complexity was quantified by approximate entropy (ApEn) and sample entropy (SampEn) that measure RRI signal irregularity, as well as by symbol distribution entropy and bit-per-word entropy that assess symbol sequences within the RRI signal. Data (in arbitrary units) are means +/- SEM. All patients survived resuscitation. Changes in heart rate and blood pressure were not significant. ApEn at 8 hours was abnormally low at 0.89 +/- 0.06. ApEn progressively increased after burn to 1.22 +/- 0.04 at 36 hours. SampEn showed similar significant changes. Symbol distribution entropy and bit-per-word entropy increased with resuscitation from 3.63 +/- 0.22 and 0.61 +/- 0.04 respectively at 8 hours postburn to 4.25 +/- 0.11 and 0.71 +/- 0.02 at 24 hours postburn. RRI complexity was abnormally low during the early postburn period, possibly reflecting physiologic deterioration. Resuscitation was associated with a progressive improvement in complexity as measured by ApEn and SampEn and complementary changes in other measures. Assessment of complexity may provide new insight into the cardiovascular response to burns.

Prehospital loss of R-to-R interval complexity is associated with mortality in trauma patients.

BACKGROUND: To improve our ability to identify physiologic deterioration caused by critical injury, we applied nonlinear analysis to the R-to-R interval (RRI) of the electrocardiogram of prehospital trauma patients. METHODS: Ectopy-free, 800-beat sections of electrocardiogram from 31 patients were identified. Twenty patients survived (S) and 11 died (NonS) after hospital admission. Demographic data, heart rate, blood pressure, field Glasgow Coma Scale (GCS) score, and survival times were recorded. RRI complexity was assessed via nonlinear statistics, which quantify entropy or fractal properties. RESULTS: Age and field heart rate and blood pressure were not different between groups. Mean survival time (NonS) was 129 hours +/- 62 hours. NonS had a lower GCS score (8.6 +/- 1.7 vs. 13.2 +/- 0.8, p < 0.05). RRI approximate entropy (ApEn; 0.87 +/- 0.06 vs. 1.09 +/- 0.07, p < 0.01), sample entropy (SampEn; 0.80 +/- 0.08 vs. 1.10 +/- 0.05, p < 0.01) and fractal dimension by dispersion analysis (1.08 +/- 0.02 vs. 1.13 +/- 0.01, p < 0.05) were lower in NonS. Distribution of symbol 2 (Dis_2), a symbol-dynamics measure of RRI distribution, was higher in NonS (292.6 +/- 34.4 vs. 222 +/- 21.3, p < 0.10). For RRI data, logistic regression analysis revealed ApEn and Dis_2 as independent predictors of mortality (area under the receiver-operating characteristic curve = 0.96). When GCSMOTOR was considered, it replaced Dis_2 whereas ApEn was retained (area under curve = 0.92). When Injury Severity Score was considered, it replaced GCSMOTOR; ApEn was retained. CONCLUSIONS: Prehospital loss of RRI complexity, as evidenced by decreased entropy, was associated with mortality in trauma patients independent of GCS score or Injury Severity Score.

The role of heart rate variability in risk stratification for adverse postoperative cardiac events.

There is growing evidence of a strong association between the compromised autonomic nervous system and sudden cardiac death. Heart rate variability (HRV) measures are widely used to measure alterations in the autonomic nervous system. Several studies with cardiac patients show that decreased HRV as well as baroreceptor dysfunction are more powerful predictors for sudden cardiac death than established clinical predictors such as left ventricular ejection fraction. One-third of all postoperative complications and more than half of the deaths are due to cardiac complications. Several risk indices are useful for immediate perioperative short-term, but not for long-term outcome risk stratification of an individual patient. Currently, there are no clinically assimilated methods for long-term postoperative risk assessment. Recently, few studies have shown that preoperatively decreased HRV can independently predict postoperative long-term mortality. Further studies with surgical patients are needed to establish a possible predictive value of preoperative baroreceptor dysfunction, alone and combined with HRV, for short- and long-term postoperative outcome.

Sympathetic nerve activity and heart rate variability during severe hemorrhagic shock in sheep.

INTRODUCTION: In this study we explored direct and indirect measures of autonomic nervous system function, as well as changes in cardiovascular complexity, during hemorrhagic shock (HS). METHODS: HS was induced in anesthetized sheep (n=8) by removing 40 ml/kg of blood in four 10 ml/kg steps over 40 min. Resuscitation was performed with lactated Ringer's and re-infusion of shed blood. Renal sympathetic nerve activity (RSNA) was measured by microneurography. Spectral analysis of heart rate variability (HRV) employed fast-Fourier transformation of the R-to-R interval (RRI) of the EKG. This generated the normalized high-frequency (HFnu) and low-frequency (LFnu) powers of the RRI, and their ratio (LFnu/HFnu, a proposed index of sympatho-vagal balance). Additionally, non-linear methods were applied: RRI complexity was measured by approximate (ApEn) and sample (SampEn) entropy methods; RRI fractal dimension was measured by curve lengths (FDCL). Plasma catecholamines were determined by HPLC. RESULTS: The model caused profound HS; 2/8 animals survived till the end of resuscitation. RSNA increased in 7/8 sheep and, as HS progressed, multiple burst complexes were identified followed by sympathetic withdrawal. Concomitant decreases in HFnu and increases in LFnu/HFnu occurred after 20 ml/kg blood loss. ApEn and FDCL decreased after withdrawal of 40 ml/kg of blood. Catecholamine concentrations increased throughout HS. LFnu/HFnu and RSNA were not linearly correlated. CONCLUSIONS: HS led to an increase in RSNA with subsequent withdrawal. LFnu/HFnu increased during HS in association with vagal withdrawal and loss of RRI complexity. RRI complexity may in part reflect vagal modulation of the heart rate. Changes in directly measured tonic sympathetic traffic do not correlate with non-invasive measures of autonomic modulation of the heart.

Effects of cellular phone use on ear canal temperature measured by NTC thermistors.

The earlier studies using phantom models and human subjects concerning warming effects during cellular phone use have been controversial, partly because radiofrequency (RF) exposures have been variable. In this randomized, double-blind, placebo-controlled crossover trial, 30 healthy subjects were submitted to 900 MHz (2W) and 1800 MHz (1W) cellular phone RF exposure, and to sham exposure in separate study sessions. Temperature signals were recorded continuously in both ear canals before, during and after the 35-min RF exposure and the 35-min sham exposure sessions. Temperature was measured by using small-sized NTC thermistors placed in the ear canals through disposable ear plugs. The mean temperature changes were determined during a set cardiovascular autonomic function studies: during a 5-min controlled breathing test, during a 5-min spontaneous breathing test, during 7-min head-up tilting, 1-min before, during and after two consecutive Valsalva manoeuvres and during a deep breathing test. Temperatures in the exposed ear were significantly higher during RF exposures compared with sham exposure in both 900 and 1800 MHz studies with maximum differences of 1 x 2 +/- 0 x 5 degrees C (900 MHz exposure) and 1 x 3 +/- 0 x 7 degrees C (1800 MHz exposure). Temperatures in the RF-exposed ear were also significantly higher during the postexposure period compared with post-sham exposure period with maximum differences of 0 x 6 +/- 0 x 3 degrees C for 900 MHz and 0 x 5 +/- 0 x 5 degrees C for 1800 MHz. The results of this study suggest that RF exposure to a cellular phone, either using 900 or 1800 MHz with their maximal allowed antenna powers, increases the temperature in the ear canal. The reason for the ear canal temperature rising is a consequence of mobile phone battery warming during maximal antenna power use. The earlier published articles do not indicate that temperature rising in the ear canal has any significant contribution from the RF fields emitted from mobile phones.