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J Tarnow

Publications and source records attributed to J Tarnow.

At least 19 recordsLinked to original sources

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

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

[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

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

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

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

[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

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

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

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

[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

Comparison of phentolamine and urapidil in controlling acute intra-operative hypertension in patients subjected to coronary artery bypass surgery.

Intra-operative hypertensive episodes are a frequent problem in patients undergoing coronary artery bypass grafting. The haemodynamic effects of the alpha-adrenergic blocking drugs phentolamine and urapidil, two alpha-adrenergic blocking drugs with a different alpha-receptor subtype specificity, when used to control intra-operative hypertension were evaluated. Ten patients received phentolamine (about 25 micrograms kg-1 min-1) and ten patients received urapidil (about 100 micrograms kg-1 min-1) to return arterial blood pressure to control levels. Both drugs decreased arterial pressure to baseline values within 2-3 minutes by reducing the elevated systemic vascular resistance. Treatment with phentolamine was accompanied by a marked increase in heart rate with a concomitant increase in cardiac index and the rate-pressure product. Urapidil caused no change in heart rate, but the cardiac index increased. Urapidil lowered the rate-pressure product significantly. Both drugs reduced mean pulmonary artery and pulmonary capillary wedge pressures. The different selectivity of phentolamine and urapidil to alpha 1-and alpha 2-adrenergic receptors induces the diverse haemodynamic effects. We conclude that the use of urapidil is the superior regimen when an alpha-adrenergic blocking agent is favoured as a vasodilator.

Acute Disease

Haemodynamic effects of dopamine and dopamine combined with nitroglycerin in patients subjected to coronary bypass surgery.

The haemodynamic effects of dopamine and dopamine with nitroglycerin were evaluated in eight patients with coronary heart disease who underwent aortocoronary bypass surgery. The study was performed under anaesthesia and before surgery. Dopamine 8 micrograms kg-1 min-1 alone produced a marked increase of the cardiac index from 2.47 to 3.47 litre min-1 m-2 but only small changes in heart rate (from 65 to 68 beat min-1). This improvement in cardiac performance was accompanied by an increase of the mean pulmonary artery pressure from 10.9 to 21.3 mm Hg and in the left ventricular filling pressure from 6.1 to 13.8 mm Hg with unchanged systemic and pulmonary vascular resistance. Mean arterial pressure increased from 72 to 103 mm Hg. Simultaneous infusion of dopamine (8 micrograms kg-1 min-1) and nitroglycerin (mean dose 0.5 microgram 21.3 to 14.4 mm Hg) and of left ventricular filling pressure (from 13.8 to 7.9 mm Hg). Cardiac index (from 3.47 to 3.34 litre min-1 m-2) and mean arterial pressure (from 103 to 95 mm Hg) were not reduced to the same extent by the addition of nitroglycerin. The combined treatment of dopamine with nitroglycerine seems to be of value in patients with pre-existing high left ventricular filling pressure or with pulmonary hypertension.

Adult

[The haemodynamic effects of dobutamine and dopamine in patients with coronary artery disease. A study performed under general anaesthesia (author's transl)].

The haemodynamic effects of dobutamine (2 microgram/kg . min and 4 microgram/kg . min) and dopamine (4 microgram/kg . min and 8 microgram/kg . min) were studied in 17 patients with coronary artery disease prior to coronary bypass surgery. The study was performed under general anaesthesia (modified neurolept analgesia) and controlled ventilation. Dopamine improved cardiac index significantly, increased mean aortic pressure slightly while heart rate and total peripheral resistance remained unchanged. Dobutamine failed to increase cardiac and stroke index significantly, but increased mean aortic pressure distinctly due to an elevated total peripheral resistance. Both catecholamines increased left ventricular filling and mean pulmonary artery pressure. The HR x ASP-product which is closely related to left ventricular oxygen consumption was found to be augmented to a greater extent during dobutamine. For the above reasons dopamine should be favoured for increasing cardiac output in patients undergoing aortocoronary bypass surgery. Our study does not confirm earlier results which have shown dobutamine to be the preferable catecholamine. The possible reasons for this discrepancy are discussed.

Adult

[Flunitrazepam-pretreatment for prevention of adverse cardiovascular effects following ketamine].

In 18 patients with documented ischaemic heart disease the cardiovascular effects of ketamine (1.5 mg/kg iv) were studied under three different conditions: 1. in awake premedicated patients (n = 6); 2. after the previous administration of flunitrazepam (0.015 mg/kg iv, n = 6) and 3. under conditions of neuroleptanalgesia and muscle relaxation (n = 6). Flunitrazepam prevented or at least attenuated the increases in heart rate (30%), mean arterial pressure (37%), mean pulmonary artery pressure (165%), left ventricular filling pressure (230%), total peripheral resistance (50%), pulmonary vascular resistance (100%) and in the rate-pressure product (66%) which were associated with the use of ketamine as the sole anaesthetic agent. In addition, the flunitrazepam-pretreatment abolished the fall in cardiac index and stroke index which occured in patients given ketamine alone. Flunitrazepam therefore appears to be a promising drug to prevent adverse cardiovascular reactions, when ketamine should be chosen for induction of anaesthesia. Neuroleptanalgesia and muscle relaxation also proved effective in controlling the sympathomimetic actions of ketamine. The response of the mean pulmonary artery pressure and of the ventricular filling pressures to ketamine in this group was even more damped than in the patients pretreated with flunitrazepam alone.

Adult