Tomomasa Kimura

Spectral Analysis of Heart Rate Variability during Isoflurane Anesthesia

The autonomic nervous system is an important neural control system for maintaining cardiovascular stability in humans. Analysis of heart rate variations may provide important clinical information on the influence of anesthesia on the autonomic nervous system and the central nervous system. Therefore, the effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane anesthesia on beat-to-beat heart rate variations were studied in ten patients (ASA Physical Status 1). Spectral analysis was used to determine the intensity of the variations. For each power spectrum, the frequency components were identified as follows: 1) the parasympathetically mediated respiratory component (0.15-0.4 Hz) and 2) both parasympathetically and sympathetically mediated components (0.04-0.15 Hz). The latter was subdivided into the low-frequency component (0.04-0.09 Hz) of vasomotor origin and the mid-frequency component (0.09-0.15 Hz) of baroreceptor origin. Marked reductions in the power of heart rate variations, at all frequencies, were found during isoflurane anesthesia, indicating isoflurane decreased total autonomic nervous system activity. Isoflurane decreased the high-frequency and mid-frequency components in a concentration-dependent manner. The low-frequency component increased transiently at 1.5 minimum alveolar concentrations concomitant with the burst suppression in the electroencephalogram. The ratio of mid-frequency to high-frequency components did not change significantly during isoflurane anesthesia compared with the awake period. These frequency characteristics of heart rate variations during isoflurane anesthesia suggest there are dose-related decreases in autonomic nervous system activity in both the vagus and the cardiac sympathetic nerves.

Differential effects of ketamine and midazolam on heart rate variability

Alterations in autonomic activity caused by anaesthesia can be assessed by spectral analysis of heart rate variability (HRV). This study examined the effects of ketamine and midazolam on HRV. Thirty patients of ASA PS 1 were studied. Fifteen were given ketamine (2 mg · kg−1) and 15 received midazolam (0.3 mg · kg−1), m The RR intervals of ECG were measured before and after induction of anaesthesia for ten minutes during spontaneous respiration. Power spectral density of the data was computed using fast Fourier transform. The spectral peaks within each measurement were calculated: low frequency area (LF, 0.04–0.15 Hz), high frequency area (HF, 0.15–0.5 Hz), and total power (TP, 0.04–0.5 Hz). Normalized unit power was derived as follows: low frequency area (nuLF): LF/ TP × 100%, high frequency area (nuHF): HF/TP × 100%. Both ketamine and midazolam caused reductions in all measurements of HRV power (P < 0.05). However, ketamine increased nuLF from 64 ± 14% to 75 ± 13% (P < 0.05) and decreased nuHF from 36 ± 14% to 25 ± 13% (P < 0.05), while midazolam decreased nuLF from 66 ± 15% to 54 ± 14% (P < 0.05) and increased nuHF from 34 ± 15% to 46 ± 14% (P < 0.05). These results documented that both ketamine and midazolam reduced the total power and all frequency components of power in spite of their opposing effects on autonomic nervous activity. However, normalized unit power showed the expected sympathetic activation with ketamine and sympathetic depression with midazolam since ketamine increased nuLFand midazolam decreased nuLF.RésuméIl est possible de mesurer l’activité autonome initiée par l’anesthésie au moyen de l’analyse spectrale des fluctuations de la fréquence cardiaque (FFC). Cette étude recherche les effets de la kétamine et du midazolam sur les FFC. Trente patients ASA PS I font partie de l’étude. Quinze ont reçu de la kétamine (2 mg · kg−1) et quinze du midazolam (0,3 mg · kg−1) iv. Les intervalles RR ont été mesurés à l’ECG avant et après l’induction de l’anesthésie pendant dix minutes de respiration spontanée. La densité de la puissance spectrale des données a été calculée après transformation rapide sur une échelle de Fourier. Les pointes spectrales de chaque mesure ont été calculées: zone de basse fréquence (LF, 0.04–0,15 Hz), zone de haute fréquence (HF, 0,15–0.5 Hz) et puissance totale (TP, 0,04–0,5 Hz). L’unité de puissance normalisée a été dérivee comme suit: zone de basse fréquence (nuLF): LF/TP × 100%, zone de haute fréquence (nuHF): HF/TP × 100% La kétamine et le midazolam provoquent des réductions de toutes les mesures de puissance des FFC (P < 0,05). Cependant la kétamine a augmenté nuLF de 64 ± 14% à 75 ± 13% (P < 0,05) et a diminue nuHF de 36 ± 14% à 25 ± 13% (P < 0,05), alors que le midazolam a diminué nuLF de 66 ± 14% à 54 ± 14% (P < 0,05) et a augmenté nuHF de 34 ± 15% à 46 ± 14% (P < 0,05). Ces résultats montrent que la kétamine et le diazépam réduisent tous deux la puissance totale et toutes les composantes fréquentielles de la puissance malgré leurs effets opposés sur l’activité nerveuse autonome. Cependant, l’unité de puissance normalisée a montré, comme on s’y attendait, l’activation sympathique par la kétamine et la dépression sympathique par le midazolam étant donné que la kétamine augmentait nuLF et que le midazolam diminuait nuLF.

Effects of halothane, thiamylal, and ketamine on central sympathetic and vagal tone.

The effects of increasing doses of halothane, thiamylal, and ketamine on central sympathetic tone (ST) and vagal tone (VT) in cats were studied. Compound action potentials were recorded simultaneously from the cervical sympathetic trunk and the vagus nerve. After full-wave rectification, they were integrated for continuous monitoring of the tonic levels of activity. ST and VT changed characteristically with different anesthetics. Halothane depressed ST and VT equally to approximately 70%, 60%, and 30% of the control level (70% N2O in O2) at end-tidal halothane concentrations of 0.5%, 1.0%, and 2.0%, respectively. When thiamylal was given intravenously at incremental doses (3, 6, 9, and 12 mg/kg), ST was markedly reduced to 10% of the control level. The reduction in VT was relatively small and the autonomic balance shifted in the vagodominant direction. Intravenous ketamine (2,4,6, and 8 mg/kg) changed neither ST nor VT significantly. Halothane and thiamylal markedly reduced central sympathetic and vagal outflows that play a role in peripheral homeostatic regulation. We suggest that these two anesthetics effect attenuated or altered autonomic regulation. Ketamine produced little change in central autonomic outflow.

Pretreatment with Topical 60% Lidocaine Tape Reduces Pain on Injection of Propofol

We determined whether pretreatment with topical 60% lidocaine tape reduced the incidence of pain on injection of propofol compared with mixing intravenous lidocaine with propofol.In a randomized, double-blind trial, 90 patients were allocated to one of three groups: pretreatment with a bioocclusive dressing and administration of a premixed solution of propofol 180 mg and 2 mL of normal saline (Group A); pretreatment with 60% lidocaine tape and a premixed solution of propofol and normal saline (Group B); or pretreatment with a bioocclusive dressing and a premixed solution of propofol 180 mg and lidocaine 40 mg (Group C). The incidences of pain in Groups A, B, and C were 86.7%, 33.4%, and 20%, respectively. Group B and Group C had a significantly lower incidence of pain than Group A. There was no significant difference in the incidence of pain between Group B and Group C. There was no significant difference in the distribution of site of pain on injection of propofol among the three groups. Pretreatment with topical 60% lidocaine tape reduced the incidence of pain on injection of propofol similar to that of intravenous lidocaine mixed with propofol. Implications: Pretreatment with topical 60% lidocaine tape reduces the pain associated with injection of propofol, a frequently used intravenous anesthetic. This approach should increase patient comfort during induction of anesthesia. (Anesth Analg 1997;85:672-4)

Heart rate variability during massive hemorrhage and progressive hemorrhagic shock in dogs

Purpose: To investigate the sequential changes in heart rate (HR), autonomic nervous activity presented by the spectral analysis of heart rate variability (HRV), hemodynamics and metabolism during massive hemorrhage and progressive hemorrhagic shock in dogs.Methods: Twelve dogs were subjected to acute massive hemorrhage until mean arterial pressure (MAP) reached 50 mmHg. Then bleeding was stopped and they were allowed to reach a plateau phase. They were divided, post hoc, into bradycardic or tachycardic groups according to their HR response to the acute massive hemorrhage. After reaching a plateau phase, the dogs were further bled to keep their MAP around 50 mmHg (progressive hemorrhagic shock). Their heart rate power spectra were quantified into low-frequency (LF) (0.04–0.15 Hz) and high-frequency (HF) (0.15–0.4 Hz) components.Results: In the bradycardic group, both LF and HF increased after massive hemorrhage, but during progressive hemorrhagic shock these components decreased while HR increased. In the tachycardic group, LF increased after massive hemorrhage, but during progressive hemorrhagic shock LF decreased with continuous suppression of HF.Conclusion: Massive hemorrhage caused two types of HR response: bradycardia and tachycardia. The HRV profile showed differential autonomic characteristics, and could be a valuable tool in assessing various degrees of hemorrhagic shock.RésuméObjectif: Examiner les changements de fréquence cardiaque (FC), l’activité nerveuse autonome selon l’analyse spectrale de la variabilité de la fréquence cardiaque (VFC), l’hémodynamie et le métabolisme pendant une hémorragie massive et un choc hémorragique progressif, chez des chiens.Méthode: Douze chiens ont été soumis à une hémorragie aiguë massive jusqu’à ce que la tension artérielle moyenne (TAM) atteigne 50 mmHg. Puis, on a arrêté le saignement et laissé la pression parvenir à un plateau. On a, en conséquence, réparti les animaux en groupe bradycardie ou tachycardie selon le compotement de la FC pendant l’hémorragie aiguë massive. Un plateau une fois atteint, les chiens ons subi une autre hémorragie pour amener leur TAM autour de 50 mmHg (choc hémorragique progressif). Le spectre de la puissance de la fréquence cardiaque a été quantifié en composantes de basses fréquences (BF) (0,04–0,15 Hz) et de hautes fréquences (HF) (0,15–0,4 Hz).Résultats: Dans le groupe bradycardie, les BF et HF ont augmenté après l’hémorragie massive, mais lors du choc hémorragique progressif, ces composantes ont diminué pendant que la FC augmentait. Dans le groupe tachycardie, les BF ont augmenté après l’hémorragie massive, mais lors du choc, elles ont baissé en même temps que survenait la suppression continue des HF.Conclusion: L’hémorragie massive a causé deux types de réaction de la FC: la bradycardie et la tachycardie. Le profil de VFC a affiché des caractéristiques autonomes différentielles, ce qui en fait un outil valable pour évaluer différents degrés de choc hémorragique.

Recovery of heart rate variability profile in patients after coronary artery surgery

We examined the different characteristics of heart rate variability (HRV) to define the time course of HRV profile after coronary artery surgery (CAS).Spectral analysis of HRV was performed on a 512-s segment of R-R intervals of the electrocardiogram on the preoperative day and on Postoperative Days 1, 2, 3, 4, 5, 6, 7, 14, 21, and 28. Power spectral area was divided into low (0.04-0.15 Hz; LF)-and high (0.15-0.5 Hz; HF)-frequency components. Fractal slope and sympathovagal slope of 1/f characteristics of HRV were determined in two different frequency ranges (from 0.01 to 0.15 Hz and from 0.01 to 0.5 Hz, respectively). Three recovery profiles of HRV were identified. Early HRV recovery profiles (Postoperative Days 1-6) included reduction in LF, HF, and sympathovagal slope, as well as an increase in fractal slope. Subsequent HRV recovery profiles (Postoperative Days 7-21) revealed reductions in LF, HF, and sympathovagal slope. Fractal slope became normal. Later HRV recovery profiles (Postoperative Day 28) demonstrated that all spectral components of HRV remained reduced, but sympathovagal and fractal slopes became normal. These changes in the HRV profile after CAS suggest significant postoperative alterations in cardiovascular homeostasis with significant but incomplete recovery during the first 28 postoperative days. Implications: Heart rate variability reflects normal neural regulation of cardiac function. This variability remains depressed as long as 28 days after coronary artery bypass surgery, but can recover as early as 1 wk postoperatively. Despite implied loss of normal neural regulation of cardiac function, a specific correlation between depressed heart rate variability and outcomes was not performed. (Anesth Analg 1997;85:713-8)

Heart rate variability and arterial blood pressure variability show different characteristic changes during hemorrhage in isoflurane-anesthetized, mechanically ventilated dogs.

UNLABELLED: We assessed the changes in heart rate variability (HRV) and blood pressure variability (BPV) as indices of autonomic nervous system and volume status during hemorrhage in isoflurane-anesthetized, mechanically ventilated dogs. Nine dogs were used. They were sequentially subjected to withdrawal of 30% estimated blood volume and graded isoflurane inhalation of 1% and 2% followed by discontinuation of isoflurane and retransfusion. The power spectra of HRV and BPV were computed using the fast Fourier transformation, and were quantified by determining the areas of the spectrum in two component widths: low-frequency component (LF) (0.04-0.15 Hz) and high-frequency component (HF) (0.15-0.4 Hz). During hemorrhage and isoflurane anesthesia, both HRV-LF and HRV-HF were decreased and plateaued at the smaller concentration of isoflurane, whereas BPV-LF decreased concentration-dependently. BPV-HF showed a completely different response and increased significantly during 2% isoflurane. We speculate that HRV and BPV-LF would be affected by the autonomic nervous activity, whereas BPV-HF would depend on relative/absolute change in circulating blood volume. IMPLICATIONS: Power spectra of heart rate variability (HRV) and blood pressure variability (BPV) were computed using the fast Fourier transformation. The HRV and BPV showed their differential characteristics during hemorrhage, isoflurane anesthesia, and retransfusion, and would help to assess changes in autonomic nervous system and preload under mechanical ventilation.

Alterations in Spectral Characteristics of Heart Rate Variability as a Correlate of Cardiac Autonomic Dysfunction after Esophagectomy or Pulmonary Resection

Background Both esophagectomy and pulmonary resection are associated with postoperative cardiac complications, partly because of autonomic perturbations involving the heart. This study was undertaken to determine whether heart rate variability (HRV), employed as an index of cardiac autonomic function, changes in patients undergoing esophagectomy or pulmonary resection. Methods Electrocardiographic RR intervals were measured in 20 esophagectomized patients, 10 undergoing right and 10 undergoing left pulmonary resection on the preoperative day as baseline data and on postoperative days 1, 3, 5, 7, 14, and 30. Instantaneous heart rate was calculated every 250 ms from 416-s data of RR intervals. Power spectra of HRV for 128 s were computed using a fast Fourier transform and normalized by squared mean heart rate. The averaged ten sets of normalized HRV power were obtained by integrating the following power spectral bands: the low-, (0.06-0.10 Hz), high- (0.15-0.40 Hz), and total-frequency regions (0.01-0.40 Hz). Results In the esophagectomy group, mean low-, high-, and total-frequency HRV power decreased after surgery to 17%, 6%, and 15% of their preoperative values, respectively, and these indexes remained suppressed for up to 30 days. After right pulmonary resection, low- and total-frequency HRV power decreased through 30 and 7 postoperative days, respectively. In the left pulmonary resection group, HRV remained unchanged. In the esophagectomy group, mean (+/-SEM) heart rate increased from 78 (+/-3) bpm to more than 90 bpm throughout the study, and body temperature from 36.5 (+/-0.1) degrees C to more than 37.0 degrees C through 14 postoperative days. Heart rate and body temperature remained increased for 3 days after pulmonary surgery. Mean arterial pressure remained unchanged in the three surgical groups. Conclusions Reductions in HRV after esophagectomy or right pulmonary resection indicate a substantial and prolonged surgical injury to the autonomic nervous control of pulse rate.

Heart rate and blood pressure power spectral analysis during calcium channel blocker induced hypotension

PurposeTo observe heart rate (HRV) and blood pressure variability (BPV) as indices of neurocirculatory responses to induced hypotension with diltiazem and/or nicardipine for hip surgery.MethodsThirty-six ASA I–II patients received diltiazem (group D, n = 12), nicardipine (group N, n = 12) or combination of diltiazem/nicardipine (group DN, n = 12). The intensity of HRV and BPV was determined by spectral analysis of HRV and BPV before anesthesia (T0), just before induced hypotension (T1), and at 10 and 30 min after the start of induced hypotension (T2 and T3, respectively). The logarithmic HRV and BPV were integrated: sympathetic and parasympathetic mediated low frequency area (0.06–0.1 Hz, LF), parasympathetic related high frequency area (0.15–0.4 Hz, HF) and total frequency area (0.01–0.4 Hz). Blood loss was assessed by weighing gauzes and measuring suction.ResultsGroup DN had less blood loss (466 ± 46 ml, mean ± SEM) than group D (733 ± 100 ml,P < 0.05). Diltiazem (11.4 ± 0.9 μg·kg−1·min−1), and combination of diltiazem (0.25 ± 0.01 mg·kg−1) and nicardipine (5.9 ± 0.9 μg·kg−1·min−1) decreased LF-HRV at T2 and T3 (P < 0.05vs T0 and T1), while nicardipine (8.1 ± 0.8 gmg·kg−1·min−1) showed increase in LF-HRV at T2 (P < 0.05vs T1 ). HF-HRV unchanged through hypotension except for a decrease in group N at T3 (P < 0.05 vs T1). There were no increases in HF-BPV and LF-BPV except for a diltiazem induced decrease in LF-BPV at T3 (P < 0.05vs T0 and T1).ConclusionGroup D and group DN can be used for deliberate hypotension without an increase in sympathetically mediated LF-HRVRésuméObjectifObserver la variabilité de la fréquence cardiaque (VFC) et de la tension artérielle (VTA) en tant qu’indices des réponses neurocirculatoires à l’hypotension contrôlée avec le diltiazem et/ou la nicardipine lors d’une opération de la hanche.MéthodeTrente-six patients ASA I–II ont reçu du diltiazem (groupe D, n = 12), de la nicardipine (groupe N, n = 12) ou une combinaison des deux (groupe DN, n = 12). L’intensité de la VFC et de la VTA a été déterminée par une analyse spectrale de VFC et de VTA avant l’anesthésie (T0), juste avant l’induction de l’hypotension (T1) et à 10 et à 30 min après le début de l’hypotension provoquée (T2 et T3, respectivement). Les logarithmes de VFC et VTA ont été intégrés : zone de basses fréquences d’origine sympathique et parasympathique (0,06-0, 1 Hz, BF), zone de hautes fréquences reliée au système parasympathique (0,15-0,4 Hz, HF) et zone incluant toutes les fréquences (0,01-0,4 Hz). La perte sanguine a été évaluée en pesant les compresses et en mesurant le volume aspiré par succion.RésultatsDans le groupe DN, la perte sanguine a été moindre (466 ± 46 ml, moyenne ± erreur type) que dans le groupe D (733 ± 100 ml,P < 0,05). Le diltiazem (11,4 ± 0,9μg·kg−1·min−1) et une combinaison de diltiazem (0,25 ± 0,01 mg·kg−1) et de nicardipine (5,9 ± 0,9 μg·kg−1·min−1) ont réduit la VFC-BF à T2 et à T3 (P < 0,05vs T0 et T1 ), tandis que la nicardipine (8,1 ± 0,8 μg·kg−1·min−1) a haussé la VFC-BF à T2 (P < 0,05vs T1 ). La VFC-HF n’a pas changé pendant l’hypotension sauf pour une baisse chez les patients du groupe N à T3 (P < 0,05vs T1 ). Dans le groupe D, il n’y a pas eu d’augmentation de VPS-HF et la VPS-BF a baissé à T3 (P < 0,05).ConclusionLes groupes D et DN peuvent servir de modèles dans le cas d’une hypotension contrôlée sans augmentation de la VFC-BF d’origine sympathique.

Transfer function analysis of the circulation in patients undergoing sevoflurane anesthesia

PurposeThe effects of sevoflurane anesthesia on the interactions between heart rate, blood pressure and respiration were assessed using transfer function analysis.MethodsNine ASA 1 or 2 patients undergoing elective surgery were involved. They were paralysed and their lungs were mechanically ventilated during sevoflurane anesthesia. Instantaneous heart rate (IHR) from electrocardiogram, instantaneous lung volume (ILV) by respiratory inductive plethysmography and mean blood pressure (MBP) by arterial tonometry were obtained during conscious state, and 1 MAC and 2MAC of sevoflurane anesthesia. Transfer function analysis for the relationships between ILV and IHR, ILV and MBP, MBP and IHR were made for five minute periods during which the respiratory rate was varied in a standardized fashion.ResultsIn awake patients transfer magnitudes for the relationships between ILV and IHR and between MBP and IHR in the 0.04–0.5Hz frequency band were 8.9 ± 7.7 bpm·l−1 and 0.95 ± 0.44 bpm·mmHg−1 respectively. Sevoflurane 2MAC decreased these values to 1.2 ± 0.7 (P = 0.014) and 0.26 ± 0.14 (P < 0.01) respectively, but phases were not affected. Neither transfer magnitudes nor phases between ILV and MBP were affected during sevoflurane anesthesia. Coherence for the relationships between ILV and IHR and between MBP and IHR were decreased during 1MAC sevoflurane anesthesia but not affected during 2MAC sevoflurane anesthesia.ConclusionsThe interactions between heart rate, blood pressure and respiration were altered by sevoflurane anesthesia. These findings could be explained by the attenuation of autonomic nervous system activity.RésuméObjectifÉvaluer les effets de l’anesthésie avec du sévoflurane sur les interactions entre la fréquence cardiaque, la tension artérielle et la respiration par l’analyse de la fonction de transfert.MéthodeNeuf patients de classe I ou II ASA, devant subir une intervention élective, ont été recrutés. On les a insensibilisés et placés sous ventilation mécanique pendant l’anesthésie au sévoflurane. On a obtenu la fréquence cardiaque instantanée (FCI), de l’électrocardiogramme; le volume pulmonaire instantané (VPI), de la pléthysmographie respiratoire inductive; la tension artérielle moyenne (TAM), de la tonométrie artérielle, à l’état de conscience, puis à 1CAM et à 2CAM de sévoflurane. L’analyse de la fonction de transfert a été faite pour étudier les relations entre le VPI et la FCI, le VPI et la TAM, la TAM et la FCI pour des périodes de cinq minutes durant lesquelles le rythme respiratoire était modifié d’une façon standard.RésultatsChez les patients éveillés, l’ampleur du transfert pour les relations entre le VPI et la FCI, et entre la TAM et la FCI, selon la bande de fréquences de 0,04–0,5 Hz a été de 8,9 ± 7,7 bpm·l−1 et de 0,95 ± 0,44 bpm·mmHg−1 respectivement. Sous une concentration de 2CAM de sévoflurane, ces valeurs ont baissé à 1,2 ± 0,7 (P = 0,014) et à 0,26 ± 0,14 (P < 0,01) respectivement, mais les phases n’ont pas changé. Ni l’ampleur du transfert, ni les phases entre le VPI et la TAM n’ont été modifiées pendant l’anesthésie au sévoflurane. La cohérence de la relation entre le VPI et la FCI et entre la TAM et la FCI a diminué pendant l’anesthésie avec 1 CAM de sévoflurane, mais n’a pas été modifiée pendant l’utilisation de 2CAM.ConclusionLes interactions entre la fréquence cardiaque, la tension artérielle et la respiration ont été modifiées par l’anesthésie au sévoflurane. Ces résultats peuvent s’expliquer par la réduction de l’activité du système nerveux autonome.