Shuji Dohi

Errors in the measurement of cardiac output by thermodilution.

Cardiac output (CO) determination by thermodilution, which was introduced by Fegler in 1954, has gained wide acceptance in clinical medicine and animal experiments because it has several advantages over other methods with respect to simplicity, accuracy, reproducibility, repeated measurements at short intervals, and because there is no need for blood withdrawal. However, errors in determination of CO by thermodilution may be introduced by technical factors and the patients’ pathological conditions. The current review summarizes these issues and provides our recommendations, based on the medical literature published between 1954–1992. To obtain more reproducible and accurate CO values by thermodilution, one should make several determinations (1) by using 10 ml injectate at room temperature for adults and 0.15 ml · kg−1 injectate for infants and children; (2) at evenly spaced intervals of the ventilation cycle; (3) when rapid intravenous fluid administration is discontinued; (4) by observing thermodilution curves so that baseline pulmonary artery temperature drift or the existence of intra- and extra-cardiac shunts are noticed. Finally, CO determination by thermodilution may be unreliable or impossible in patients with low CO slates and tricuspid or pulmonary regurgitation. Since non-invasive CO monitoring has not replaced CO determination by thermodilution, intimate knowledge of this method is crucial for anaesthetists to prevent errors in the management of patients.RésuméLa mesure du débit cardiaque par thermodilution introduite par Fegler en 1954 est largement répandue en clinique et en recherche animale grâce à ses nombreux avantages sur les autres méthodes: simplicité, précision, reproductiblé, répétivité à courts intervalles, absence de prélèvement sanguin. Cependant, dans son application il peut facilement s’introduire des erreurs d’origine technique ou pathologique. La présente revue résume ces questions et propose certaines recommandations, basées sur la littérature médicale publiée entre 1954 et 1992. Pour obtenir des mesures fiables et précises du débit cardiaque par thermodilution, il faut répéter les mesures: 1) avec 10 ml d’injectat maintenu à température de la pièce chez le adulte, 0,15 ml · kg− 1 chez l’enfant; 2) à des moments identiques du cycle respiratoire; 3) après l’arret d’une perfusion rapide de liquide intraveineux; 4) en observant les courbes de thermodilution pour pouvoir tenir compte de la dérive de la température initiale de l’artère pulmonaire et de la présence de shunts intraou extracardiaques. Finalement, le débit cardiaque par hémodilution peut manquer de fiabilité et peut même devenir impossible à mesurer chez les malades dont le débit est bas ou qui souffrent de régurgitation tricuspidienne ou pulmonaire. Comme le monitorage du débit cardiaque non invasif n’a pas encore remplacé la thermodilution, les anesthésistes doivent posséder une connaissance approfondie de cette méthode pour éviter des erreurs thérapeutiques graves.

Heart rate response to atropine in humans anaesthetized with five different techniques

Atropine, 0.01 mg·kg-1, was given intravenously before the start of surgery to 169 patients who were anaesthetized with one of five different techniques; halothane, enfturane, cervical epidural, lumbar epidural or narcotic anaesthesia in addition to nitrous oxide and oxygen. Atropine produced a significant increase in heart rate (HR) within 1 min in all patients studied; the HR increases in patients anaesthetized with halothane (37 ± 11 beats·min-1, n = 37) or narcotic (34 ± 12 beats·min-1, n = 30) were significantly greater than in those anaesthetized with enflurane (25 ± 10 beats·min-1, n = 35; P < 0.01) or epidural anaesthesia. Because of the presence of an acute cardiac sympathectomy, the patients who received cervical epidural anaesthesia were expected to have different responses to the atropine. However, there was no significant difference in the HR increases between the patient groups with cervical (19 ± 12 beats·min-1, n = 32) and lumbar (22 ± 8 beats·min-1, n = 35) epidural anaesthesia. Atropine also produced a small but significant increase in arterial pressure in all five groups of patients. These results suggest that the cardiac responses to atropine may differ depending on the individual anaesthetic agent used, and are likely dependent upon the agent’ s effect on autonomic nervous system activity.RésuméDe ľatropine 0.01 mg · kg-1 a été administré par voie intraveineuse avant le début de la chirurgie à 169 patients qui étaient anesthésiés avec ľune des cinq techniques différentes; halothane, enflurane, épidurale cervicale, épidurale lombaire ou anesthésie au narcotique additonné de protoxyde ďazote et ďoxygène. Ľatropine a produit une augmentation significative de la fréquence cardiaque (HR) en dedans ďune minute chez tous les patients étudiés. Cette augmentation de la fréquence cardiaque chez les patients anesthésiés avec ľhalothane (37 ± 11 BPM, n = 37) et narcotic (34 ± 12 BPM, n = 30) étaient significativement plus grandes que celles observées avec ľenflurane (25 ± 10 BPM, n = 35; p < 0.01) et ľanesthésie épidurale. A cause ďune sympathectomie cardiaque aiguë les patients ayant reçu une anesthésie épidurale cervicale on anticipa une réponse différente lors de ľadministration de ľatropine. Cependant on observa aucune différence statistiquement significative dans ľaugmentation de la fréquence cardiaque entre ľanesthésie épidurale cervicale (19 ± 12 BPM, n = 32) et lombaire (22 ± 8 BPM, n = 35). Ľatropine a aussi produit une petite augmentation statistiquement significative dans la pression artérielle chez les patients des cinq groupes. Ces résultats suggèrent que la réponse cardiaque à ľatropine peut varier selon ľagent anesthésique utilisé selon ľeffet de ľagent sur ľactivité du système nerveux autonome.

End-tidal carbon dioxide monitoring during awake blind nasotracheal intubation

STUDY OBJECTIVEnTo test the usefulness of the end-tidal carbon dioxide monitor in facilitating awake blind nasotracheal intubation in patients with potentially difficult airways.nnnDESIGNnRandomized, controlled comparison of regimen.nnnSETTINGnInpatient surgery clinic at a university hospital.nnnPATIENTSnSixty-one consecutive patients with potentially difficult airways.nnnINTERVENTIONSnAfter airway anesthesia with 4% lidocaine was administered to all patients, either fentanyl and diazepam (n = 30) or fentanyl alone (n = 31) was given intravenously before the awake blind nasotracheal intubation procedure.nnnMEASUREMENTS AND MAIN RESULTSnEnd-tidal carbon dioxide concentration, arterial blood pressure, heart rate, and arterial oxygen saturation (by pulse oximeter) were measured in each patient during the awake blind nasotracheal intubation procedure. The day after anesthesia and surgery, each patient was asked to assess the degree of discomfort experienced during the procedure. In 54 of 61 patients, the end-tidal carbon dioxide monitor facilitated awake blind nasotracheal intubation. End-tidal carbon dioxide was significantly higher in patients given both fentanyl and diazepam than in those given fentanyl alone (7.4% +/- 1.4% vs 5.9% +/- 0.9%, respectively; p less than 0.05), but no patient in either group recalled the awake intubation as extremely uncomfortable.nnnCONCLUSIONSnMonitoring of end-tidal carbon dioxide is useful and valuable in both facilitating blind nasotracheal intubation and avoiding profound hypoventilation.

Halothane concentrations required to block the cardiovascular responses to incision (MAC CVR) in infants and children

The purpose of this study was to determine the halothane concentration in N2O required to block the cardiovascular responses to skin incision (MAC CVR) in infants and children. We studied 64 unpremedicated ASA 1 infants and children (one month to seven years). In each infant or child, anaesthesia was induced slowly with halothane and N2O, and an endotracheal tube was placed. The MAC CVR was assessed, after a steady state end-tidal halothane concentration had been established for ten minutes, by the “up and down technique” of Dixon. Positive responses were defined as an increase in MAP or HR > 10%. The MAC CVR50 values of halothane with 60% N2O were 1.16 ± 0.23% at 1–6 mo, 1.17 ± 0.18% at 7–12 mo, 0.95 ± 0.26% at 1–3 yr, and 1.12 ± 0.16% at 4–7 yr. The value at 1–3 years children was less than those in the other age groups (P < 0.05). The changes of MAP were correlated with changes of both HR and pupillary diameter. These results indicate that the values of MAC CVR50 of halothane in infants and children are higher than those required to block motor responses (MAC). The halothane requirement to block cardiovascular responses is lowest in the children aged one to three years.RésuméL’objet de cette étude est de déterminer la concentration d’halothane et de N2O nécessaire pour bloquer les réponses cardiovasculaire à l’incision de la peau (MAC CVR) chez les enfants et les nouveau-nés. Nous avons étudié 64 nouveau-nés et enfants, non prémédiqués, ASA = 1. Chez chaque nouveauné ou enfant, l’anesthésie et été initiée lentement avec halothane et N2O, suivie d’une intubation endotrachéale. Le MAC CVR a été évalué après qu’une concentration d’équilibre de fin d’expiration d’halothane soit établie depuis 10 minutes par la technique de Dixon. Les réponses positives correspondent à une augmentation de pression artérielle moyenne ou de fréquence cardiaque supérieure à 10%. Le MAC CVR50 de l’halothane avec 60% de N2O est de 1,16 ± 0,23% de 1 à 6 mois; 1,17 ± 0,18% de 7 à 12 mois; 0,95 ± 0,26% de 1 à 3 ans; et de 1,12 ± 0,16% de 4 à 7 ans. La concentration nécessaire de 1 à 3 ans est moindre que dans les autres groupes d’âge (P < 0,05). Les variations de pression artérielle moyenne ont été correlées avec les variations de fréquence cardiaque et de diamètre pupillaire. Ces résultats indiquent que les valeurs de MAC CVR50 d’halothane chez les enfants et les nouveau-nés sont supérieures à celles requises pour bloquer la réponse motrice (MAC). Le besoin d’halothane pour bloquer les réponses cardiovasculaires est inférieures chez les enfants de 1 à 3 ans.

Nonrespiratory rhythmic fluctuations in systemic arterial pressure in anesthetized humans

STUDY OBJECTIVEnTo clarify the frequency of nonrespiratory rhythmic fluctuations in systemic arterial pressure (vasomotor waves) and to identify the clinical conditions in which the vasomotor waves develop in humans under anesthesia.nnnDESIGNnRetrospective analysis of collected data.nnnSETTINGnInpatient surgery clinic at a university hospital.nnnPATIENTSnFive hundred thirteen consecutive ASA physical status II-V patients.nnnINTERVENTIONSnDirect arterial pressure monitoring and general anesthesia, including high-dose fentanyl, enflurane, enflurane plus fentanyl, cervical or thoracic epidural, and lumbar epidural anesthesia.nnnMEASUREMENTS AND MAIN RESULTSnAmong the anesthesia techniques used, vasomotor waves occurred most frequently in patients anesthetized with high-dose fentanyl (31.1%) and least frequently in those with high-level epidural blockade (7.4%). As a result of multiple logistic analysis, the contributing factors to the appearance of vasomotor waves were the institution of cardiopulmonary bypass (CPB) and the patients age. It is also a novel finding that nearly one-third of the vasomotor waves developed in patients under stable hemodynamic conditions.nnnCONCLUSIONSnVasomotor waves are a common phenomenon in relatively high-risk patients during general anesthesia. The appearance of vasomotor waves is significantly related to CPB and patient age.

Diazepam prevents fentanyl-induced muscle rigidity

Although high-dose fentanyl-oxygen anesthesia has been widely used for cardiac surgery , the most serious and frequently encountered disadvantage of this technique is the development of truncal rigidity. Fentanyl-induced rigidity has been shown to produce hypercarbia, a potent stimulus of pulmonary vasoconstriction. Kallos et al. 4 reported that in man, increased expiratory muscle activity was present even in the absence of clinically evident rigidity. This caused a reduction of functional residual capacity and total chest compliance. Neuromuscular blocking drugs relieve the rigidity -8 . Anesthetic drugs such as thiopental, enflurane and halothane probably prevent or reduce it s. Patient awareness precludes muscle relaxant administration to prevent such rigidity. Even if the above anesthetics were able to prevent or reduce truncal rigidity during cardiac anesthesia, they may produce cardiovascular depression. To prevent awareness, diazepam has been employed as a supplement to fentanyl-oxygen anesthesia. Unlike the above drugs8 , l O,1l diazepam causes a very mild degree of ventilatory and

Haemodynamic and cerebral blood flow alterations after reduction of increased cerebrospinal fluid pressure in dogs

To clarify some of the mechanisms for the hypotension that may occur after cranial decompression, the authors examined alterations in cerebral blood flow (CBF) and systemic and pulmonary haemodynamic variables when cerebrospinal fluid (CSF) pressure was increased and then suddenly reduced in eight anaesthetized dogs. After CSF pressure was elevated to 50–85 mmHg for two hours, CBF decreased from 46.3 ± 4.4 to 31.6 ± 8.5 ml · 100 g−1 · min−1 (mean ± SD, P < 0.01). Mean systemic arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and systemic vascular resistance index (SVRI) increased by 20 ± 11 mmHg, 3.9 ± 2.5 mmHg, 5.2 ± 3.3 mmHg, and 1448 ± 1377 dynes · sec · cm−5 · m−2 from baseline values, respectively (P < 0.01). Rapid reduction of increased CSF pressure caused CBF to increase to 61.5 ± 19.1 ml · 100g−1 · min−1, whereas MAP, MPAP, PAWP, and SVRI decreased by 22 ± 11 mmHg, 2.4 ± 0.9 mmHg, 2.3 ± 2.0 mmHg, and 1289 ± 1237 dynes · sec · cm−5 · m−2 from previous values (P < 0.01) at 30 min following the decompression. However, cardiac index and pulmonary vascular resistance index remained unchanged during the study period. The present animal data indicate that the decrease in MAP after decompression is mainly a result of a reduction in systemic vascular resistance.RésuméAfin d’éclaircir certains des mécanismes de l’ hypotension pouvant survenir après decompression cérébrale, les auteurs ont examiné les altérations du flot sanguin cérébral (CBF) et les variables hémodynamiques pulmonaire et systémique quand la pression du liquide céphalo-rachidien (CSF) fut augmentée et soudainement réduite chez huit chiens anesthésies. Après l’ élévation de la pression CSF à 50–85 mmHg pour deux heures, le CBF a diminué de 46,3 ± 4,4 à 31,6 ± 8,5 ml · 100 g−1 · min−1 (moyenne ± SD, P < 0.01). La pression artérielle systémique moyenne (MAP), la pression moyenne de l’ artère pulmonaire (MPAP), la pression de l’ artère pulmonaire occluse (PAWP), et la résistance systémique vasculaire indexée (SVRI) ont augmenté de 20± 11 mmHg, 3,9 ±2,5 mmHg, 5, 2 ± 3, 3 mmHg, et 1448 ± 1377 dynes · sec · cm−5 · m−2 à partir des valeurs de contrôle, respectivement (P < 0.01). La diminution rapide de cette augmentation de la pression du CSF a amané une augmentation du CBF à 61, 5 ± 19, 1 ml · 100 g−1 · min−1, alors que la MAP, MPAP, PAWP, et SVRI ont diminué à 22 ± 11 mmHg, 2, 4 ± 0, 9 mmHg, 2, 3 ± 2, 0 mmHg, et 1289 ± 1237 dynes · sec · cm−5 · m−2 des valeurs préalables (P < 0.01) à 30 min. après la décompression. Cependant, l’ index cardiaque et la résistance vasculaire pulmonaire indexée sont demeurés inchangés durant la période d’ étude. Ces données expérimentales indiquént que la diminution de la MAP après décompression est principalement en résultat de la diminution de la résistance vasculaire systémique.

Periodic isorhythmic dissociation during enflurane anesthesia in a patient with Sinus Bradycardia

Isorhythmic dissociation is not uncommon during inhalational anesthesia, But a few reports are available, and a report described that during enflurane anesthesia isorhythmic dissociation occurred in 5 out of 12 subjects (42%)2. The etiology of this rhythm disturbance remains unclear, as does its treatment, We experienced a case in which isorhythmic dissociation developed several times in a patient with sinus bradycardia during enflurane anesthesia. The conversion from sinus rhythm to isorhythmic dissociation occurred periodically in association with acceleration of heart rate due to surgical stimulation or following intravenous atropine. Although isorhythmic dissociation has been recognized to disappear spontaneously and reappear during anesthetic course, we believe that this periodical occurrence has not been detailed in the literature.

Epidural anesthesia for a patient with acute idiopathic pandysautonomia

In patients with autonomic dysfunction, the cardiovascular instability is a common problem during anesthesia. A significant decrease in blood pressure without a compensatory tachycardia following thiopental induction or inhalation of volatile anesthetics has previously been reported to occur in patients with dysautonomial-, Shy-Drager syndromeb, or familial dysautonomia. Because these patients already have sympathetic denervation, it is assumed that regional anesthesia may not cause any further cardiovascular perturbation due to sympathetic blockade. Therefore, we speculate that regional anesthesia would provide an advantage such as cardiovascular stability in these patients during anesthesia. To date, however, there has been no report describing epidural anesthesia for patients with dysautonomia. We describe a case in which a 37-year-old patient with acute idiopathic pandysautonomia (AIPD)5,6 had a stable anesthetic course with thoracic epidural plus light general anesthesia.