[Peripartum aortic dissection]. / Peripartale Aortendissektion.

A 29-year-old primagravida developed severe chest pains during labor. An emergency caesarean section was performed as the symptoms persisted. Imaging diagnosis immediately after delivery revealed an acute proximal (type A) aortic dissection. The patient was transferred to the nearest cardiothoracic surgery centre and successful emergency surgical aortic repair was performed. The perioperative course of a type A aortic dissection during pregnancy and labor is complicated by time pressure, diagnostic restrictions until delivery and potentially fatal uterine bleeding during cardiopulmonary bypass and hypothermic cardiac arrest. This case report describes the diagnosis and the surgical, anesthesiological and gynecological management of this life-threatening peripartum complication.

Aerobic exercise capacity is normal in obesity with or without metabolic syndrome.

BACKGROUND: Obesity might be a cause of limited aerobic exercise capacity. It is often associated with metabolic syndrome (MS) that includes cardiovascular comorbidities as arterial hypertension. Cardiopulmonary exercise testing (CPET) is the gold-standard to assess aerobic capacity and discriminate causes of dyspnea. AIM: To evaluate aerobic capacity in obesity and if MS or hypertensive treatment impacts on the CPET profile. METHODS: CPET of 146 obese patients, whom 33 and 31 were matched for MS and antihypertensive medication, were analyzed. VO2peak (mL/min/Kg) was reported in percentage of predicted value, or, divided by body weight, fat free mass (FFM) or body weight expected for a body mass index of 24 (BMI24). RESULTS: VO2peak (20,8 ± 4,4 mL/min/Kg) was normal when expressed in percentage predicted for obesity (111 ± 22%pred) or divided by FFM and weightBMI24 (33,6 ± 5,6 and 30,6 ± 6,2 respectively). The latter correlated better with maximal work rate (r = 0,7168, p < 0,001). Obese patients showed normal ventilatory efficiency (ventilation to carbon dioxide production slope: 28 ± 4), VO2 to work rate (10,2 ± 1,6 mLO2/Watt) and, slightly elevated heart rate to VO2 slope (4,0 ± 1,1 bpm/mL/min/Kg). Compared to normotensives, hypertensive medicated patients had higher blood pressure at anaerobic threshold (142 ± 23 vs 158 ± 26 mmHg, p = 0,001) but not at maximal exercise (189 ± 31 vs 201 ± 23 mmHg, p = NS), and, had lower actual maximal heart rate (155 ± 23 vs 143 ± 25 bpm, p = 0,03). There was no difference between obese patients with or without MS. CONCLUSION: Obese people with or without MS present with similar and normal aerobic profile related to the excessive body weight. VO2peak divided by weightBMI24 is an easy and clinical meaningful index for obese patients.

Comparison of two preoperative indices to predict perioperative mortality in non-cardiac thoracic surgery.

OBJECTIVE: The preoperative classifications: physical status of the American Society of Anesthesiologists (ASA-PS) and/or cardiac risk index (CRI) of Goldman are widely used to estimate the perioperative risk in patients undergoing noncardiac throacic surgery. We tried to determine the validity of both methods in predicting the perioperative mortality in 845 consecutive patients scheduled for major elective noncardiac thoracic surgery. METHODS: Preoperatively, each patient was assigned 2 independent estimations of risk according to the ASA-score (ASA grade, I-IV) and CRI score (CRI grade, I-IV), respectively. RESULTS: Twenty-five patients died within 4 weeks after the operation, the others survived the perioperative period. The grading according to ASA as well as to the CRI score showed a direct correlation with the outcome: The higher the preoperative score, the higher was the mortality rate. When various combinations of ASA and CRI were tested, the lowest mortality rate was found in presence of ASA < or = III and CRI = I. Multivariate regression analysis showed that the ASA score had an independent correlation with perioperative mortality, whereas such a relationship was absent for CRI. CONCLUSIONS: The subjective assessment by an experienced anesthesiologist as expressed by the ASA-score is a valid method in the determination of the perioperative risk. CRI does not contribute additional information for the general perioperative risk.

Regulation of alveolar gas conductance by NO in man, as based on studies with NO donors and inhibitors of NO production.

AIM: Nitric oxide (NO) is a mediator of the pulmonary vessel tone and permeability. We hypothesized that it may also regulate the alveolar-capillary membrane gas conductance and lung diffusion capacity. METHODS: In 20 healthy subjects (age = 23 +/- 3 years) we measured lung diffusion capacity for carbon monoxide (DLco), its determinants (membrane conductance, D(m), and pulmonary capillary blood volume, V(c)), systolic pulmonary artery pressure (PAPs) and pulmonary vascular resistance (PVR). Measurements were performed before and after administration of N(g)-monomethyl-L-arginine (L-NMMA, 0.5 mg kg(-1) min(-1)), as a NO production inhibitor, and L-arginine (L-Arg, 0.5 mg kg(-1) min(1)) as a NO pathway activator. The effects of L-NMMA were also tested in combination with active L-Arg and inactive stereoisomer D-Arg vehicled by 150 mL of 5%d-glucose solution. For L-Arg and L-NMMA, saline (150 mL) was also tested as a vehicle. RESULTS: L-NMMA reduced D(m) (-41%P < 0.01), DLco (-20%, P < 0.01) and cardiac output (CO), and increased PAPs and PVR. In 10 additional subjects, a dose of L-NMMA of 0.03 mg kg(-1) min(1) infused in the main stem of the pulmonary artery was able to lower D(m) (-32%, P < 0.01) despite no effect on PVR and CO. D(m) depression was significantly greater when L-NMMA was vehicled by saline than by glucose. L-Arg but not D-Arg abolished the effects of L-NMMA. L-Arg alone increased D(m) (+14%, P < 0.01). CONCLUSION: The findings indicate that NO mediates the respiratory effects of L-NMMA and L-Arg, and is involved in the physiology of the alveolar-capillary membrane gas conductance in humans. NO deficiency may cause an excessive endothelial sodium exchange/water conduction and fluid leakage in alveolar interstitial space, lengthening the air-blood path and depressing diffusion capacity.

Atorvastatin therapy improves exercise oxygen uptake kinetics in post-myocardial infarction patients.

BACKGROUND: Statins represent a modern mainstay of the drug treatment of coronary artery disease and acute coronary syndromes. Reduced aerobic work performance and slowed VO(2) kinetics are established features of the clinical picture of post-myocardial infarction (MI) patients. We tested the hypothesis that statin therapy improves VO(2) exercise performance in normocholesterolaemic post-MI patients. MATERIALS AND METHODS: According to a double-blinded, randomized, crossover and placebo-controlled study design, in 18 patients with uncomplicated recent (3 days) MI we investigated the effects of atorvastatin (20 mg day(-1)) on gas exchange kinetics by calculating VO(2) effective time constant (tau) during a 50-watt constant workload exercise, brachial artery flow-mediated dilatation (FMD) as an index of endothelial function, left ventricular function (echocardiography) and C-reactive protein (CRP, as an index of inflammation). Atorvastatin or placebo was given for 3 months each. RESULTS: Atorvastatin therapy significantly improved exercise VO(2) tau and FMD, and reduced CRP levels. We did not observe changes in cardiac contractile function and relaxation properties during all study periods in either group. CONCLUSIONS: In post-MI patients exercise performance is a potential additional target of benefits related to statin therapy. Endothelial function improvement is very likely implicated in this newly described therapeutic property.

[Coronary stents, dual antiplatelet therapy and peri-operative problems]. / Koronare Stents, duale Antiplättchentherapie und die perioperative Problematik.

Up to 90% of all percutaneous coronary interventions include coronary artery stenting. Dual antiplatelet therapy, usually involving acetylsalicyl acid combined with clopidogrel, is mandatory for patients with coronary artery stents. The duration of antiplatelet therapy for bare metal stents is 3-4 weeks, for drug eluting stents 6-12 months. Preoperative discontinuation of both drugs increases the risk of stent thrombosis, continuation the risk of relevant bleeding. According to the recommendations of anaesthesiological and cardiological societies, perioperative management has to balance the risk of bleeding vs stent thrombosis. Surgery involving a high risk of bleeding can require the discontinuance of both substances. In cases of high thrombosis risk, at least the acetylsalicyl acid should be continued until the day of surgery. For patients under antiplatelet therapy scheduled for local anaesthesia, national recommendations exist. A close collaboration between the anaesthesiologist, cardiologist and surgeon is essential for appropriate pre-, intra- and postoperative management.

Coronary artery stenting and non-cardiac surgery--a prospective outcome study.

BACKGROUND: A 45% complication rate and a mortality of 20% were reported previously in patients undergoing non-cardiac surgery after coronary artery stenting. Discontinuation of antiplatelet drugs appeared to be of major influence on outcome. Therefore we undertook a prospective, observational multicentre study with predefined heparin therapy and antiplatelet medication in patients undergoing non-cardiac procedures after coronary artery stenting. METHODS: One hundred and three patients from three medical institutions were enrolled prospectively. Patients received coronary artery stents within 1 yr before non-cardiac surgery (urgent, semi-urgent or elective). Antiplatelet drug therapy was not, or only briefly, interrupted. Heparin was administered to all patients. All patients were on an intensive/intermediate care unit after surgery. Main outcome was the combined (cardiac, bleeding, surgical, sepsis) complication rate. RESULTS: Of 103 patients, 44.7% (95% CI 34.9-54.8) suffered complications after surgery; 4.9% (95% CI 1.6-11.0) of the patients died. All but two (bleeding only) adverse events were of cardiac nature. The majority of complications occurred early after surgery. The risk of suffering an event was 2.11-fold greater in patients with recent stents (<35 days before surgery) as compared with percutaneous cardiac intervention more than 90 days before surgery. CONCLUSIONS: Despite heparin and despite having all patients on intensive/intermediate care units, cardiac events are the major cause for new perioperative morbidity/mortality in patients undergoing non-cardiac surgery after coronary artery stenting. The complication rate exceeds the re-occlusion rate of stents in patients without surgery (usually <1% annually). Patients with coronary artery stenting less than 35 days before surgery are at the greatest risk.

Incidence of bradycardia during recovery from spinal anaesthesia: influence of patient position.

We administered 0.5% plain bupivacaine 4 ml intrathecally (L2-3 or L3-4) in three groups of 20 patients, according to the position in which they were nursed in the post-anaesthesia care unit (PACU): supine horizontal, 30 degrees Trendelenburg or hammock position (trunk and legs 30 degrees elevated). Patients were observed until anaesthesia descended to less than S1. The incidence of severe bradycardia (heart rate < 50 beat min-1) in the PACU was significantly higher in patients in the Trendelenburg position (60%) than in the horizontal (20%, P < 0.01) or hammock (10%, P < 0.005) position. After 90 min, following admission to the PACU, only patients in the hammock position did not have severe bradycardia. In this late phase, the incidence of severe bradycardia in the Trendelenburg group was 35% (P < 0.005) and 10% in patients in the supine horizontal position. In four patients, severe bradycardia first occurred later than 90 min after admission to the PACU. The latest occurrence of severe bradycardia was recorded 320 min after admission to the PACU. We conclude that for recovery from spinal anaesthesia, the Trendelenburg position should not be used and the hammock position is preferred.

Transesophageal versus surface pulse oximetry in intensive care unit patients.

OBJECTIVES: To compare oximetric readings from the esophagus (STEO2) and the skin (finger, SSO2) with those obtained from arterial blood samples (SaO). In addition, to compare the influences of mean arterial pressure (MAP) and body temperature to the accuracy of STEO2 and SSO2 readings. DESIGN: Prospective, single-center study. SETTING: Surgical intensive care unit of an academic, teaching, and community hospital in Austria. PATIENTS: A total of 40 consecutive, severely traumatized or diseased, intensive care unit patients requiring mechanical ventilatory support and deep analgosedation. Patients had to be nonpregnant, > or =19 yrs of age, and without a disease or a trauma of the esophagus. INTERVENTIONS: Placement of an esophageal and a finger-pulse oximetry probe and a radial artery catheter. MEASUREMENTS AND MAIN RESULTS: STEO2, SSO2, MAP, and esophageal temperature were recorded continuously during a 4-hr period, and SaO2 was measured every 30 mins. The first outcome variable was the deviation of STEO2 and SSO2 from SaO2. The second outcome variable was the influence of MAP and body temperature on STEO2 and SSO2 regression analysis and repeated measures. Analysis of variance was used for statistics (p < .05 was accepted as significant). In patients with a MAP ranging from 29 to 111 mm Hg and a temperature ranging from 33.4 degrees C (92.1 degrees to 39.2 degrees C (102.6 degrees F), SSO2 measurements underestimate SaO2 by 2% to 4%. Whereas STEO2 matches SaO2, STEO2 was not dependent on MAP or temperature, but increased temperature or low MAP were associated with falsely low SSO2 readings. CONCLUSIONS: Assuming correct positioning of the probe, readings from the esophagus are more consistent with arterial oxygen saturation than readings from surface pulse oximetry. MAP or temperature changes do not influence STEO2, but they do affect SSO2. In critically ill patients, STEO2 appears to be a more reliable variable than SSO2.

Ketamine has stereospecific effects in the isolated perfused guinea pig heart.

BACKGROUND: S(+)-Ketamine is judged to produce more potent anesthesia than either the racemate or the R(-) ketamine isomer because of differential activation of specific cerebral receptors. Other than central nervous system effects, the most important side effects of ketamine occur in the cardiovascular system. We examined the direct cardiac effects of the isomers and the racemate of ketamine in the isolated perfused guinea pig heart. METHODS: Twenty-three guinea pig hearts were perfused by the Langendorff technique with modified 37 degrees C Krebs-Ringer's solution (97% oxygen and 3% carbon dioxide) at a constant perfusion pressure. Eight animals were pretreated with reserpine to deplete hearts of catecholamines. These pretreated hearts were also perfused with Krebs-Ringer's solution containing propranolol, phenoxybenzamine, and atropine to block any remaining effects of catecholamines and of acetylcholine. Five additional hearts were perfused with naloxone to block cardiac opioid receptors. Ten hearts were not treated. All 23 hearts were then exposed to four increasing equimolar concentrations of each isomer and the racemate of ketamine for 10 min. Heart rate, atrioventricular conduction time (AVCT), left ventricular pressure, coronary flow, and inflow and outflow oxygen tensions were measured. Percentage oxygen extraction, oxygen delivery, and oxygen consumption were calculated. RESULTS: Both isomers and the racemate caused a concentration-dependent depression of systolic left ventricular pressure and an increase in AVCT. In the untreated hearts, S(+)-ketamine decreased heart rate and left ventricular pressure and, at higher concentrations, oxygen consumption and percentage oxygen extraction significantly less than R(-)-ketamine independent of blocked or unblocked opioid receptors. Racemic ketamine depressed cardiac function to a degree intermediate to that produced by the isomers. Coronary flow and AVCT were equally affected by the isomers and by the racemic mixture. In the catecholamine-depleted hearts both isomers and the racemate caused equipotent depression of all variables. In these hearts cardiac depression was greater, and AVCT, coronary flow, and oxygen delivery were significantly greater than in untreated and opioid receptor-blocked hearts. CONCLUSIONS: Lesser cardiac depression by the S(+) isomer is attributable to an increased availability of catecholamines, because previous depletion of catecholamine stores and autonomic blockade completely inhibited these differences. The inability of cardiac tissue to reuptake released catecholamines into neuronal or extraneuronal sites during exposure to ketamine is stereoselective and caused predominantly by the S(+) isomer. Cardiac opioid receptors are apparently not involved in this phenomenon.

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. I. Methodology, conscious state, and halothane anesthesia: comparison with and without muscarinic blockade during exposure to epinephrine.

BACKGROUND: Supraventricular dysrhythmias are common during anesthesia, but have been incompletely investigated. Mechanisms may involve altered automaticity of subsidiary pacemakers and participation of vagal reflexes. The following hypotheses were tested: (1) shifts from the sinoatrial (SA) node to subsidiary pacemakers require intact vagal reflexes and (2) halothane sensitizes the heart to epinephrine-induced atrial pacemaker shifts. METHODS: Epicardial electrodes were implanted in eight dogs on both atrial appendages, the right ventricle, along the sulcus terminalis, and at the His bundle. Weekly testing awake (control), awake with atropine methylnitrate, with 1 and 2 micrograms epinephrine.kg-1.min-1 (3 min-infusions), and under 1.25 and 2 MAC halothane was performed. Electrograms were analyzed for the site of earliest activation (SEA), which was scored 1-6 depending on the distance from the SA node, and expressed as the SEA value. RESULTS: In conscious dogs (control) and at 1.25 MAC halothane, epinephrine increased the SEA values (shifted activation from SA node) and blood pressure, and decreased heart rate; however, with atropine, SEA values were unaffected by epinephrine, although blood pressure and heart rate were elevated. At 2 MAC, atropine did not affect the epinephrine-induced increase in SEA values. Halothane increased SEA values when combined with 1 micrograms epinephrine.kg-1.min-1. CONCLUSIONS: Pacemaker shifts account for atrial dysrhythmias in the conscious state and during 1.25 MAC halothane with epinephrine, and require vagal participation. Halothane sensitizes the heart to epinephrine-induced atrial dysrhythmias. Atropine and halothane facilitate His bundle beats during exposure to epinephrine.

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. II. Effects of enflurane and isoflurane during exposure to epinephrine with and without muscarinic blockade.

BACKGROUND: Atrial dysrhythmias precede ventricular dysrhythmias during epinephrine-anesthetic sensitization, and may be caused by an altered relationship between automaticity of primary and subsidiary pacemakers. The following hypotheses were tested: (1) epinephrine-induced pacemaker shifts with enflurane or isoflurane require intact vagal reflexes and (2) these anesthetics sensitize the atrial myocardium to epinephrine-induced dysrhythmias. METHODS: Eight dogs were instrumented for chronic electrophysiologic investigation, including electrodes at the SA node, atrial appendages, right ventricle, and His bundle, and along the sulcus terminalis. After conscious-state testing, dogs were anesthetized with isoflurane or enflurane and exposed to epinephrine, with or without atropine methylnitrate. Eight-channel ECG recordings were analyzed before and during epinephrine infusions. Atrial pacemakers were assigned values 1-6 with increasing distance from the SA node, normalized and expressed as the site of earliest activation value (SEA). RESULTS: Epinephrine increased SEA values during enflurane or isoflurane anesthesia. Atropine enhanced this increase during enflurane anesthesia, but abolished the increase during isoflurane anesthesia. Enflurane increased SEA values only when combined with atropine. Isoflurane did not increase SEA values under any test conditions. CONCLUSIONS: With enflurane, epinephrine-induced atrial pacemaker shifts in chronically instrumented dogs are caused by direct depression of SA node automaticity or a relative increase of automaticity in subsidiary atrial pacemakers. With isoflurane, pacemaker shifts are caused by reflex-induced vagal suppression of SA node automaticity and escape of latent pacemakers. Enflurane sensitizes the atrial myocardium to dysrhythmias when combined with muscarinic blockade; isoflurane does not sensitize the atrium.

First clinical experience with the rapid-, short-acting amiodarone derivative E 047/1 after cardiac surgery.

BACKGROUND AND OBJECTIVE: Amiodarone is very effective against a variety of dysrhythmias but has poor pharmacodynamic properties and many undesired side-effects. Its short- and rapid-acting derivative E 047/1 may circumvent some of these drawbacks. It is easier to titrate while retaining the high efficacy of amiodarone and may have acceptable influences on haemodynamics and cardiac conduction in patients who develop serious, destabilizing ventricular tachydysrhythmias after cardiac surgery. METHODS: Testing E 047/1 was performed prospectively in two consecutive phase II open, clinical studies. Out of 504 patients scheduled for surgery using cardiopulmonary bypass for coronary artery grafting and/or valve repair, 35 developed serious, haemodynamically destabilizing ventricular dysrhythmias (Lown 2-Lown 4b) after surgery and were treated with a 1 mg kg(-1) (pilot study, n = 15) or randomized to a 2 or 3 mg kg(-1) bolus of E 047/1, followed by a 1 mg kg(-1) h(-1) continuous infusion for 2 h (n = 10 in each group). Dysrhythmias, PQ, QTc intervals and haemodynamics using the thermodilution technique were evaluated for up to 24 h after drug initiation. RESULTS: At the time of final inclusion the patients had between 6 and 12 (or more) ventricular ectopics per minute. Within the first 2-3 min of application in the pilot trial E 047/1 induced a decrease of ventricular dysrhythmias to between 0 and 4 per min, a decrease that held for the duration of treatment. The area under the curve decreased from 434 (322, 855; median, quartiles) to 114 (9, 477, P < 0.01) events per hour. In the randomized trial, E 047/1 administered in either dose rapidly reduced ventricular dysrhythmias at least as effectively as in the pilot trial 565 (478, 701) to 33 (8, 238, P < 0.05) after a 2 mg bolus; 482 (339, 482) to 95 (13, 540, P < 0.01) events per hour after a 3 mg bolus. Approximately 4-6 h after drug termination, dysrhythmias reappeared in the majority of patients. In only three patients did the incidence of dysrhythmias return to inclusion criteria levels. In contrast to the pilot trial, in the randomized trial there was a slight increase of mean pulmonary artery pressure, central venous pressure and pulmonary arterial wedge pressure and a slight decrease of LCWI in both groups. E 047/1 did not cause QTc prolongation. CONCLUSIONS: E 047/1 appears to be a safe alternative to amiodarone in the perioperative setting of cardiac surgery when serious, destabilizing dysrhythmias occur.

Anesthetics and automaticity in latent pacemaker fibers. IV. Effects of isoflurane and epinephrine or norepinephrine on automaticity of dominant and subsidiary atrial pacemakers in the canine heart.

BACKGROUND: Anesthesia and surgery may be associated with atrioventricular junctional or ventricular rhythm disturbances. These may be caused by alteration of automaticity of primary and subsidiary pacemakers. METHODS: The direct effects of isoflurane, alone or in combination with epinephrine (E) and norepinephrine (NE), as well as single effects of E and NE, were examined on automaticity of primary and subsidiary atrial pacemakers (SAP) using a perfused canine right atrial preparation (n = 29). Preparations were perfused with oxygenated Krebs' solution at a constant perfusion pressure of 87 mmHg and a temperature of 36.5 +/- 0.5 degrees C. Delivered concentrations of isoflurane of 1.4 and 2.8% corresponded to measured perfusate concentrations of 315 +/- 7 and 617 +/- 16 microM in experiments with E (n = 14), and 316 +/- 10 and 610 +/- 26 microM in experiments with NE (n = 15). Epinephrine or NE perfusate concentrations were 2 and 5 micrograms/l or 5 and 10 micrograms/l, respectively. To determine the site of earliest activation, extracellular recordings were made from the SA node region and distal sites (approximately 1, 2, and 3 cm) along the sulcus terminalis, the previously reported locations of SAP. Sites of earliest activation shifts from SA node to SAP were scored 1, 2, or 3 depending on the distance from the control pacemaker. The summed shift scores (magnitude score) were normalized by dividing by the total number of preparations for each experimental condition. RESULTS: Exposure to isoflurane, NE, or E alone did not produce a significant increase in the incidence of pacemaker shifts or normalized pacemaker shift scores. Only the high dose of E significantly increased the incidence of pacemaker shifts and normalized shift scores. Dysrhythmogenic potential of E and NE tended to be greater after earlier exposure to isoflurane. Every combination of isoflurane with E or NE produced a significant increase in the incidence of pacemaker shifts and normalized shift scores. CONCLUSIONS: It was concluded that isoflurane with E or NE acts synergistically to increase dysrhythmic potential in the arterial tissue.

The comparative effects of equimolar sevoflurane and isoflurane in isolated hearts.

The aim of this study was to compare the direct effects of equivalent molar concentrations of sevoflurane (SEVO) and isoflurane (ISO) on electrophysiology, mechanical function, metabolism, and perfusion in isolated hearts, independent of neuronal, humoral, or hemodynamic influences. Three equimolar concentrations of SEVO or ISO were administered randomly in each of 14 guinea pig hearts perfused by the Langendorff technique. Spontaneous heart rate (HR), atrioventricular (AV) conduction time, left ventricular pressure (LVP), and coronary flow (CF) were measured directly. To differentiate a direct vasodilatory effect from an indirect metabolic effect due to autoregulation of CF, arterial and coronary sinus oxygen tension were measured continuously to calculate oxygen delivery (Do2), myocardial oxygen consumption (MVo2), percent O2 extraction, and cardiac efficiency. Linear slope analysis (cardiac effect as a function of 0.1 mM anesthetic concentration) was used to compare anesthetic effects. Only AV time was increased more (P < 0.05) by ISO (+1.8 ms per 0.1 mM) than by SEVO (+1.1 ms per 0.1 mM). CF tended to be higher with ISO (+0.7 mL.g-1.min-1 per 0.1 mM) than SEVO (0.4 mL.g-1.min-1 per 0.1 mM) but this was not significant. HR (ISO, -1.4% per 0.1 mM; SEVO, -1.7% per 0.1 mM), LVP (ISO, -5.8% per 0.1 mM; SEVO, -5.1% per 0.1 mM), and percent O2 extraction (ISO, -6.1% per 0.1 mM; SEVO, -5.8% per 0.1 mM) were decreased similarly by both anesthetics and these effects were accompanied by proportional decreases in MVo2 (ISO, -34% +/- 4%, SEVO, -37% +/- 6%) at the highest concentrations (0.53 mM). Neither anesthetic altered cardiac efficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

[Coronary arterial stent implantation proceeding noncardiac surgical procedures. Is it safe; can we recommend it?]. / Koronararterielle Stentimplantation vor nichtkardiochirurgischen Eingriffen. Wiegen wir uns fälschlich in Sicherheit?

Patients undergoing non-cardiac surgical procedures who carry coronary artery stents have to be classified as high risk patients. Perioperative myocardial infarction and severe bleeding are possible. Therefore, anaesthetic management directed by invasive monitoring, ECG ST analysis, transesophageal echocardiography and referral to an intensive care unit are absolutely justified. The urgency of the surgical procedure, perioperative risk and an antiplatelet regimen have to be discussed with the patient and the surgeon in advance. In the case of cardiac complications, rapid therapy by an interventional cardiologist must be available.

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. IV. Dysrhythmias after sinoatrial node excision.

BACKGROUND: Subsidiary atrial pacemakers assume control after sinoatrial (SA) node excision, and anesthetic-catecholamine interactions can produce severe bradycardia during isoflurane anesthesia. We hypothesized that epinephrine enhances atrial, atrioventricular junctional, and ventricular dysrhythmias after SA node excisions in dogs and that inhalation anesthetics would facilitate such dysrhythmias. METHODS: In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, at the His bundle, and along the sulcus terminalis. Site of the earliest atrial activation and incidences of nonatrial beats were determined in the conscious state, with methylatropine, with epinephrine, and during halothane, isoflurane, or enflurane anesthesia. RESULTS: After SA node excision, a stable, regular subsidiary atrial pacemaker rhythm resulted. Epinephrine and halothane shifted the site of earliest activation to more remote atrial sites. Epinephrine-induced ventricular escape was increased by all anesthetics tested, but atropine prevented ventricular escape. Epinephrine-induced His bundle (atrioventricular junctional) and premature ventricular beats were increased by halothane and enflurane. After SA node excision, ventricular escape occurred as a result of epinephrine-anesthetic interactions, especially during anesthesia with isoflurane. CONCLUSIONS: In dogs with excised SA nodes, anesthetic-catecholamine interaction facilitates ventricular escape, His bundle dysrhythmias, and premature ventricular beats. In addition, halothane and enflurane, more than isoflurane, facilitate ectopic ventricular tachydysrhythmias with epinephrine. Compared to intact dogs, dogs with excised SA nodes may be more susceptible to epinephrine anesthetic dysrhythmias. If findings can be extrapolated to humans, intrinsic SA node dysfunction may facilitate severe cardiac dysrhythmias with inhalation anesthetics and catecholamines.