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J Tarnow

Publications and source records attributed to J Tarnow.

At least 19 recordsLinked to original sources
PubMed1995

The effects of prostacyclin on gastric intramucosal pH in patients with septic shock.

OBJECTIVE: To investigate whether infusing prostacyclin (PGI2) in patients with septic shock improves splanchnic oxygenation as assessed by gastric intramucosal pH (pHi). DESIGN: Interventional clinical study. SETTING: Surgical ICU in a university hospital. PATIENTS: 16 consecutive patients with septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine to maintain arterial blood pressure. INTERVENTIONS: All patients received PGI2 (10 ng/kg x min) after no further increase in oxygen delivery could be obtained by volume expansion, red cell transfusion and dobutamine infusion. The results were compared with those before and after conventional resuscitation. The patients received continuous PGI2 infusion for 33-32 days. MEASUREMENTS AND RESULTS: O2 uptake was measured directly in the respiratory gases, pHi was determined by tonometry. Baseline O2 delivery, O2 uptake and pHi were 466 +/- 122 ml/min.m2, 158 +/- 38 ml/min.m2, and 7.29 +/- 0.09, respectively. While O2 uptake remained unchanged, infusing PGI2 increased O2 delivery (from 610 +/- 140 to 682 +/- 155 ml/min.m2, p < 0.01) and pHi (from 7.32 +/- 0.09 to 7.38 +/- 0.08, p < 0.001) beyond the values obtained by conventional resuscitation. While 9 of 11 patients with final pHi > 7.35 survived, all patients with final pHi < 7.35 died (p < 0.01). CONCLUSIONS: Infusing PGI2 in patients with septic shock increases pHi probably by enhancing blood flow to the splanchnic bed and thereby improves splanchnic oxygenation even when conventional resuscitation goals have been achieved.

Adult↗
PubMed1995

Desflurane inhibits hypoxic pulmonary vasoconstriction in isolated rabbit lungs.

BACKGROUND: Inhalational anesthetics inhibit hypoxic pulmonary vasoconstriction (HPV) in vivo and in vitro with a half-maximum inhibiting effect (ED50) within concentrations applied for general anesthesia. Because it is unknown whether desflurane acts likewise, we studied its effect on HPV in isolated blood-perfused rabbit lungs and compared its ED50 with that of halothane. METHODS: Isolated blood-perfused rabbit lungs were randomly allocated to treatment with either desflurane (n = 6) or halothane (n = 6). HPV, defined as an increase in pulmonary arterial pressure (PAP) at constant flow, was elicited by decreasing inspiratory oxygen concentration from 20% to 3% for 4 min. This effect was determined without (control HPV) and with increasing concentrations of the anesthetics (fraction of inspired carbon dioxide kept constant at 4.8 +/- 0.2%, perfusate temperature at 37 degrees C, and blood flow at 100 ml.min-1). RESULTS: Before exposure to the anesthetics, PAP increased by 8.6 +/- 1.9 cmH2O for all lungs within 4 min of hypoxia (control PAP for all lungs 19.6 +/- 2.5 cmH2O). Desflurane decreased this effect in a concentration-dependent fashion with an ED50 of 14.5%, compared with that of halothane, with an ED50 of 1.7%. CONCLUSIONS: Assuming that 1 minimum alveolar concentration (MAC) values of desflurane and halothane for rabbits are 8.9% and 1.39%, respectively, this study yields ED50 values for the inhibition of HPV of approximately 1.6 MAC for desflurane and 1.2 MAC for halothane (P not statistically significant).

Anesthetics, Inhalation↗
PubMed1994

[Distal edema and hyperhidrosis of the arm. Symptoms of reflex sympathetic dystrophy (Sudeck's disease)].

Reflex sympathetic dystrophy is characterized clinically by the triad of autonomic sympathetic dysfunction, and motor and sensory disturbances of the affected extremity. Typical symptoms are distal generalized edema with cyanotic skin, pathologic function of eccrine sweat glands and diffuse dull pain. If reflex sympathetic dystrophy is not recognized an irreversible stage may be reached, with atrophic pale, cool, and anhidrotic skin, contractures and diffuse osteoporosis. The syndrome can be idiopathic but can also be precipitated by a variety of factors, including banal trauma, bone fracture, and traumatic nerve lesions. Pathophysiologically, a functional disturbance of sympathetic nerve fibres may result in a vicious circle of blood flow dysfunction, excitation of afferent nociceptors and maintenance of sympathetic dysfunction at the level of the spinal or central nervous system. In the patient presented in this paper, sympathetic dysregulation of reflex sympathetic dystrophy was cured by means of blockades of the stellate ganglion.

Adult↗
PubMed1994

Prostacyclin improves glucose utilization in patients with sepsis.

PURPOSE: In patients with sepsis, impaired glucose metabolism and altered microcirculatory blood flow are common findings. Prostacyclin (PGI2) improves tissue oxygenation, indicated by enhanced oxygen delivery (DO2) and oxygen uptake (VO2). The purpose of this study was to explore whether these effects are associated with improved glucose utilization. METHODS: In 7 patients with sepsis, glucose metabolism was analyzed using dideuterated and 13C-labeled glucose and isotope dilution mass spectrometry. All patients received total parenteral nutrition with glucose covering 60% to 70% of the predicted energy expenditure and needed continuous intravenous insulin (40 microU.kg-1.min-1) to keep blood glucose concentrations below 10 mmol.l-1.VO2 and carbon dioxide production (VCO2) were continuously measured directly from the respiratory gases via indirect calorimetry. After equilibration of the infused labeled glucose with body glucose pool, baseline variables of glucose metabolism were assessed: glucose oxidation rate was determined from the enrichment of 13CO2 in the expired gas during primed constant infusion of [U-13C]glucose, glucose turnover rate (Ra) from the plasma enrichment of simultaneously infused [6,6-2H2]glucose. Endogenous glucose production rate was calculated as the difference between Ra and glucose infusion rate. Then, we examined the effect of PGI2 infusion (5 to 12.5 ng.kg-1.min-1) on glucose metabolism and gaseous exchange. RESULTS: The PGI2-induced increase in DO2 (from 15.8 to 17.7 ml.kg-1.min-1; P < .05) resulted in an increase in directly measured VO2 from 5.0 to 5.3 ml.kg-1.min-1 (P < .01) whereas VCO2 remained unchanged. Although glucose turnover and production rates remained constant, glucose oxidation rate increased significantly from 1.21 to 1.38 mg.kg-1.min-1 (P < .02). CONCLUSIONS: Improving tissue perfusion and oxygenation with PGI2 may also modify the impaired glucose metabolism by increasing glucose oxidation rate in patients with sepsis, suggesting enhanced adenosine triphosphate production.

Adenosine Triphosphate↗
PubMed1994

High thoracic epidural anesthesia does not alter airway resistance and attenuates the response to an inhalational provocation test in patients with bronchial hyperreactivity.

BACKGROUND: The functional relevance of an intact pulmonary sympathetic innervation for airway resistance is unknown. We therefore evaluated whether or not pulmonary sympathetic denervation by thoracic epidural anesthesia decreases the threshold of an inhalational provocation with acetylcholine in 20 patients with documented bronchial hyperreactivity scheduled for elective upper abdominal or thoracic surgery. METHODS: Baseline inhalational provocation with acetylcholine was performed 2-4 days before surgery. The acetylcholine threshold concentration for a hyperreactivity response (i.e., for a 20% decrease in forced expiratory volume in 1 s and a 100% increase in total respiratory resistance by oscillometry) was determined. On the day of surgery a second inhalative provocation with acetylcholine was performed 45 min after the patients had received 6-8 ml epidural bupivacaine 0.75% (n = 10), intravenous bupivacaine (1.2 mg.min-1, n = 6), or 6-8 ml epidural saline (n = 4). The acetylcholine threshold concentration for a hyperreactive response was again determined. We also measured vital capacity, forced expiratory volume in 1 s as a percentage of vital capacity, spread of sensory blockade (pin prick), skin temperature on hand and foot (telethermography). RESULTS: During thoracic epidural anesthesia, C4-T8 skin temperature increased significantly on hand and foot indicating widespread sympathetic blockade including the lungs. Compared to values obtained immediately before pulmonary sympathetic blockade, forced expiratory volume in 1 s as a percentage of vital capacity, and total respiratory resistance by oscillometry remained unchanged, while vital capacity decreased. Compared to baseline the acetylcholine threshold concentration for the hyperreactive response increased threefold after epidural as well as after intravenous bupivacaine. Epidural saline evoked no directional changes in the acetylcholine threshold concentration. CONCLUSIONS: We conclude that in patients with bronchial hyperreactivity 1. blockade of pulmonary sympathetic innervation seems to be of no relevance for airway resistance and 2. both epidural and intravenous bupivacaine substantially attenuate the response to an inhalational provocation with acetylcholine.

Acetylcholine↗
PubMed1992

Fat emulsions containing medium chain triglycerides in patients with sepsis syndrome: effects on pulmonary hemodynamics and gas exchange.

Fat emulsions containing medium chain triglycerides (MCT) have recently been introduced into clinical practice as a component of total parenteral nutrition. Since several authors reported increased pulmonary artery pressure and impaired gas exchange during intravenous (i.v.) fat use, in particular in septic patients, we studied the pulmonary hemodynamic and gas exchange effects of i.v. fat containing MCT and long chain triglycerides (LCT) in patients with sepsis syndrome. As the effects of fat emulsions have been attributed to increased formation of prostanoids, the production of thromboxane A2 and prostacyclin was investigated by the determination of urinary thromboxane B2 and 6-keto-prostaglandin F2 alpha, respectively. The i.v. fat use did not induce any alterations in pulmonary hemodynamics and gas exchange, the distribution of ventilation and perfusion nor urinary prostaglandin content. We conclude that fat emulsions containing MCT induce little alterations in pulmonary hemodynamics and gas exchange. This result is probably due to reduced prostaglandin formation because fat emulsions containing MCT provide less prostaglandin precursors than pure LCT emulsions.

Adult↗
PubMed1992

Isoflurane does not increase the incidence of intraoperative myocardial ischaemia compared with halothane during vascular surgery.

We have studied the incidence of new intraoperative myocardial ischaemia (IMI), myocardial infarction (MI) and cardiac death (CD) in 500 consecutive patients undergoing elective major non-cardiac vascular surgery. Patients were allocated randomly to receive either halothane (n = 226) or isoflurane (n = 274) as principal anaesthetic agent. Using real-time ST segment trend analysis (leads V5 and II) IMI (halothane 39%, isoflurane 38%), MI (halothane 1.3%, isoflurane 1.5%) and CD (halothane 0.4%, isoflurane 0.7%) did not differ significantly between the two groups. Twenty-three per cent of IMI episodes were related to haemodynamic disturbances, but unrelated to the type of surgery: 148 supra-aortic (IMI = 39%), 244 abdominal aortic (IMI = 41%) and 108 lower extremity revascularizations (IMI = 33%). We conclude that the choice of volatile anaesthetic agent does not influence cardiac morbidity or mortality in this type of patient.

Adult↗
PubMed1992

[Perioperative diagnosis of acute myocardial ischemia].

The prevalence of coronary artery disease substantially affects both cardiac and noncardiac surgery. Assuming that biometric data reported from North America are representative for Germany, the following incidences can be estimated: around 1 million out of 8 million patients operated upon each year will suffer from coronary artery disease, and 15,000 of these patients will have a perioperative myocardial infarction. Since a close relationship has been shown between pre-, intra-, and postoperative myocardial ischaemia and postoperative cardiac morbidity and mortality, early diagnosis and therapy of acute perioperative myocardial ischaemia is warranted. The purpose of this review is to weigh critically the various methods for diagnosis of myocardial ischaemia in view of their practicability and cost/benefit relationship in the perioperative setting. The symptoms of angina pectoris are unreliable in the perioperative period, since patients are premedicated preoperatively, without symptoms during anaesthesia, and usually receive analgesics postoperatively. Intraoperative detection of myocardial ischaemia focuses on standard electrocardiography (ECG) with on-line registration of the ST-segment in two leads (usually leads II and V5) and automatic analysis of ST-segment deviation, achieving a sensitivity of 80% in the detection of myocardial ischaemia. Measurement of regional wall motion abnormalities with trans-esophageal echocardiography (TEE) is a more sensitive method of myocardial ischaemia detection compared to ECG. However, several reasons preclude the broader application of this method in the perioperative phase: (1) it lacks validation by an accepted and independent gold standard; (2) there is a wide spectrum of false-positive findings (considerable interindividual variations in left ventricular contraction, bundle branch blocks, hypertension, hypervolemia); (3) changes in the inferior and apical segments of the left ventricle cannot be detected by single-plane TOE. Detection in these segments might be achieved with biplane echocardiography, but few data on this improved technique are presently available; (4) the method is semi-invasive and might be not applicable during periods with a high incidence of myocardial ischaemia, e.g., intubation, the end of anaesthesia, and extubation; (5) anaesthetists seldom fulfil standard guidelines in echocardiography training; and (6) the method is expensive, which also limits its broader application. Cardiokymography, a noninvasive technique, allows analog representation of anterior wall motion.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1991

Cardiovascular effect of low-dose epinephrine infusions in relation to the extent of preoperative beta-adrenoceptor blockade.

The relationship between the extent of preoperative beta-adrenoceptor blockade and the hemodynamic properties of epinephrine was investigated in patients scheduled for elective myocardial revascularization during the immediate preoperative period under steady-state hemodynamic and anesthetic conditions. Twenty patients had been treated with beta-adrenoceptor blocking drugs for at least 3 weeks before the study; 11 unblocked patients served as control group. The extent of clinical beta-adrenoceptor blockade was quantified using the isoproterenol sensitivity test. The dose of isoproterenol required to increase heart rate by 25 beats per min was defined as the chronotropic dose 25 (CD25), representing the degree of beta-adrenoceptor blockade. Geometric mean CD25 per 70 kg was 3.0 micrograms in the control group and 21.8 micrograms in the patients receiving beta-adrenoceptor blocking drugs. The authors found a significant inverse relationship between CD25 values and changes in cardiac index in response to three epinephrine infusion rates (0.01, 0.02, and 0.04 micrograms.kg-1.min-1), the correlation coefficients being -0.71, -0.81, and -0.86, respectively. Compared to unblocked patients, almost no change, or even a decrease, of the cardiac index was observed at greater degrees of clinical beta-adrenoceptor blockade, particularly in patients receiving nonselective blockers. Moreover, there was a significant linear correlation (r = 0.76-0.86) between CD25 values and the effects of epinephrine on systemic vascular resistance index (SVRI); i.e., SVRI significantly decreased in control patients but markedly increased in patients with high degrees of preoperative beta-adrenoceptor blockade. This unmasked vasoconstrictive response to low doses of epinephrine was observed despite the fact that the majority of our patients had received cardioselective adrenergic blocking drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS.

Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng.kg-1.min-1) for 45 min. We examined whether reducing the right ventricular (RV) outflow pressures by PGI2 infusion would increase the right ventricular ejection fraction (RVEF) measured by thermodilution. PGI2 reduced the pulmonary artery pressure (PAP) from 35.6 to 29.1 mmHg (p less than 0.01). The cardiac index (CI) increased from 4.2 to 5.81.min-1.m-2 (p less than 0.01) partly due to an increased stroke volume. The decreased PAP together with the increased CI resulted in a fall of the calculated pulmonary vascular resistance index (PVRI, from 5.1 to 2.5 mmHg.min.m2.1-1, p less than 0.01). In the patients with subnormal baseline RVEF the increased stroke volume was associated with an increased RVEF (from 47.6% to 51.8%, p less than 0.05) suggesting improved RV function. This result was underscored by a significant relationship between the changes in PVRI and RVEF (r = 0.789, delta % RVEF = 2.11.delta PVRI-1.45). Despite an increased venous admixture from 27.8% to 36.9% (p less than 0.05) the arterial PO2 remained constant resulting in an increased oxygen delivery from 657 to 894 ml.min-1.m-2 (p less than 0.01). We conclude that short term infusions of PGI2 increased CI concomitant to improved RV function parameters when baseline RVEF was depressed. Since improved oxygen availability should be a major goal in the management of patients with ARDS PGI2 may be useful to lower pulmonary artery pressure in ARDS.

Adult↗
PubMed1990

Prostacyclin for the treatment of pulmonary hypertension in the adult respiratory distress syndrome: effects on pulmonary capillary pressure and ventilation-perfusion distributions.

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.

Adult↗
PubMed1990

[Preoperative treatment with beta-receptor blockers and isoflurane anesthesia. Hemodynamic interactions in patients with coronary disease].

Although many patients undergoing general anesthesia and surgery are pretreated with beta-adrenoceptor blocking drugs, hemodynamic interactions of beta-blockers and volatile anesthetics have so far only been studied in animals. We therefore designed a clinical study to evaluate the relationship between the extent of preoperative beta-adrenoceptor blockade and the hemodynamic effects of isoflurane anesthesia. Sixty-one patients with coronary artery disease (CAD) and normal global left ventricular function scheduled for elective myocardial revascularization were studied immediately prior to surgery. One group of patients (n = 39) had been treated with beta-adrenoceptor blocking agents for at least 3 weeks up to and including the day of surgery. The degree of clinical beta-adrenoceptor blockade was quantified using the isoproterenol sensitivity test. The dose of isoproterenol required to increase heart rate by 25 beats/min was defined as the chronotropic dose 25 (CD25), representing the degree of beta-adrenoceptor blockade. Hemodynamic data were collected before and during isoflurane anesthesia (0.5%-0.6% end-tidal) plus 50% nitrous oxide. Twenty-two patients without preoperative beta-blocker therapy served as a control group. Preanesthetic values of cardiac index (CI), heart rate (HR) and mean arterial pressure (MAP) were lower in patients pretreated with beta-blocking drugs, but statistically these differences were not significant when compared to data obtained in unblocked patients. Isoflurane anesthesia caused significant reductions of CI and arterial blood pressure. However, there were no significant differences in the absolute values or the percentage changes compared to baseline data obtained in awake patients between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1988

Altered hemodynamic response to dobutamine in relation to the degree of preoperative beta-adrenoceptor blockade.

The relationship between the extent of preoperative beta-adrenoceptor blockade and the hemodynamic properties of dobutamine was investigated in patients scheduled for elective myocardial revascularization during isoflurane-nitrous oxide anesthesia. Twenty patients had been treated with beta-adrenoceptor blocking drugs for at least 4 weeks before the study; 11 unblocked patients served as control group. The extent of clinical beta-adrenoceptor blockade was quantified using the isoproterenol sensitivity test. The dose of isoproterenol required to increase heart rate by 25 beats/min was defined as the CD25 (chronotropic dose 25), representing the degree of beta-adrenoceptor blockade. Geometric mean CD25/70 kg was 3.8 micrograms in the control group, and 24.5 micrograms in the patients receiving beta-adrenoceptor blocking drugs. The authors found a significant inverse relationship between CD25 values and changes in cardiac index in response to three dobutamine infusion rates (1.0, 2.0, and 4.0 micrograms.kg-1.min-1), the correlation coefficients being -0.78, -0.79, and -0.82, respectively. Compared to unblocked patients, almost no change, or even a decrease, of the cardiac index was observed at higher degrees of clinical beta-adrenoceptor blockade. Moreover, there was a significant linear correlation (r = 0.66 - 0.75) between CD25 values and the effects of dobutamine on systemic vascular resistance index (SVRI), i.e., SVRI decreased in control patients, but increased in patients with high degrees of preoperative beta-adrenoceptor blockade. This unmasked vasocontrictive response to dobutamine was observed despite the fact that the majority of our patients had received cardioselective adrenergic blocking drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1987

Effects of short-term infusion of nifedipine or verapamil on systemic hemodynamics and left ventricular myocardial contractility in patients prior to coronary artery bypass surgery.

The effects of short-term infusion (10 min) of nifedipine (7.5 micrograms . kg-1) or verapamil (0.15 mg . kg-1) on left ventricular (LV) contractility and on systemic hemodynamics in patients with coronary artery disease, chronically treated with low-dose beta-adrenergic blocking drugs, exhibiting a normal LV function at rest, are presented. In order to analyze the interaction between calcium entry blocking drugs and halothane, the results are discussed in light of data, obtained in similar patients during halothane anesthesia, using identical experimental conditions, which have already been reported. LV dP/dtmax and LV end-diastolic pressure (LVEDP) remained unaffected when nifedipine was infused in the awake patients. Verapamil significantly decreased LV dP/dtmax in patients while awake, but LVEDP did not change. Both calcium entry blocking drugs caused decreases in blood pressure and systemic vascular resistance, accompanied by increases in heart rate. The only significant differences between the awake and the anesthetized patients were the absence of changes in heart rate and the greater reduction in LV dP/dtmax following administration of the calcium entry blocking drugs during anesthesia. Possible explanations for this may include the drugs' combined interference with calcium ion fluxes within the myocardial and smooth muscle fibers, the ability of halothane to modify the response of the autonomic nervous system to the calcium entry blocking drugs and altered kinetics of the calcium entry blocking drugs induced by the volatile anesthetic. It is impossible to determine from the present investigation which of these mechanisms is predominant.

Adult↗
PubMed1986

Isoflurane improves the tolerance to pacing-induced myocardial ischemia.

Fourteen patients with normal, global, left ventricular function scheduled for elective myocardial revascularization were studied at rest and during atrial pacing before and during isoflurane anesthesia (0.5% end-tidal) plus 50% nitrous oxide. Rapid atrial pacing was performed in a stepwise fashion until the onset of angina pectoris in the awake patients. The same step increase in pacing rate was applied in the anesthetized patients. Compared with prepacing baseline values, isoflurane significantly decreased systemic blood pressure, coronary perfusion pressure, the rate-pressure product, and cardiac index. No patient had ST-segment depression while awake or during isoflurane anesthesia before pacing was started. Prepacing left and right ventricular filling pressures and wave forms were normal, both while awake and during isoflurane anesthesia. The mean pacing rate at which first signs of myocardial ischemia appeared (V5 ST-segment depression greater than or equal to 0.1 mV, increase in pulmonary capillary wedge pressure (PCWP) to greater than or equal to 15 mmHg, and prominent PCWP v-waves greater than or equal to 20 mmHg) was significantly higher during isoflurane anesthesia than in the awake patients (128 +/- 4 vs. 115 +/- 5 beats/min). With the exception of one patient, the individual pacing rates inducing first signs of ischemia in the awake patients were below the anginal threshold. None of the patients had a reduced ischemic threshold during anesthesia. Eleven anesthetized patients tolerated a higher pacing rate until initial signs of ischemia appeared. In four of these patients, the pacing rate required to induce first signs of ischemia was above the heart rate at which chest pain had been induced while they were awake. At a peak atrial pacing rate of 129 +/- 5 beats/min, which had induced angina pectoris in the awake patients, the increase in PCWP was significantly smaller during pacing with isoflurane than during control pacing. Prominent PCWP v-waves (greater than or equal to 20 mmHg) appeared in 12 of the 14 patients during initial pacing to angina and in eight patients paced during isoflurane anesthesia. In six of these eight patients, the abnormal v-waves were less prominent than those observed during control pacing. Ischemic ST-segment changes developed in 13 of 14 patients during initial pacing and in nine patients during pacing with isoflurane. Mean V5 ST-segment depression during the two pacing periods was significantly different, averaging 0.19 and 0.11 mV, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

[Circulatory effects of vecuronium as well as pancuronium under different conditions of anesthesia].

The cardiovascular effects of equipotent doses (1,25 X ED95) of vecuronium (70 micrograms/kg iv) and pancuronium (80 micrograms/kg iv) were studied in 16 patients scheduled for elective coronary artery bypass surgery during steady-state conditions of isoflurane (0,4-0,5 vol% end-tidal)-nitrous oxide anaesthesia. All patients were chronically treated with oral beta receptor-blocking agents. Vecuronium did not cause any significant cardiovascular changes whereas pancuronium produced increases in heart rate (13%), cardiac index (15%) and mean arterial pressure (4%) while systemic vascular resistance decreased (8%). In a second part of this study we analysed whether the magnitude of the vagolytic effects of pancuronium is influenced by the anaesthetic procedure and/or by preoperative beta-blocker therapy. A group of 8 patients who were pretreated with beta-receptor blockers and received fentanyl (7 micrograms/kg) during the anaesthetic procedure showed low control values of heart rate (HR), cardiac index (CI), mean arterial pressure (MAP) and the rate-pressure product (RPP) which were due to both, the antisympathetic effects of beta-blocker therapy and the central vagomimetic properties of fentanyl. The administration of pancuronium (80 micrograms/kg) caused the greatest percentage increases in HR (20%), CI (22%), MAP (8%) and RPP (31%) in this group of patients. In contrast, patients (n = 8) anaesthetized with isoflurane-nitrous oxide who were not on preoperative beta-receptor blocker medication, demonstrated higher haemodynamic control values and less increases in HR (10%), CI (10%) and RPP (15%), MAP did not change. The clinical significance of these findings is discussed.

Adrenergic beta-Antagonists↗