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Biomedical subjects

J Tarnow

Publications and source records attributed to J Tarnow.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1985

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↗
PubMed1984

Nifedipine versus nitroprusside for controlling hypertensive episodes during coronary artery bypass surgery.

Intraoperative hypertensive episodes are a common problem in patients undergoing coronary artery bypass grafting. Twenty patients who developed acute hypertension (mean arterial pressure increase to 110 mmHg) were studied. Ten patients received nifedipine (about 3 micrograms kg-1 min-1) and ten patients nitroprusside (about 0.75 micrograms/kg-1 min-1) to return arterial blood pressure to control levels. All patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O/O2. The study compares the effects of nifedipine and nitroprusside on systemic and pulmonary haemodynamics. Both nifedipine and nitroprusside decreased arterial pressure to baseline values within about 3 min by reducing the elevated systemic vascular resistance. Cardiac filling pressures and pulmonary artery pressure decreased significantly only with nitroprusside. Following nitroprusside cardiac output remained unchanged whereas nifedipine increased cardiac output and stroke volume when blood pressure was lowered by a comparable degree. The data suggest that nifedipine primarily affects resistance vessels in the systemic circulation without significantly changing venous tone as opposed to the effect of nitroprusside. Thus, nifedipine appears to be an appropriate vasodilator for controlling arterial hypertensive episodes in patients with coronary artery disease and normal left ventricular function.

Adult↗
PubMed1984

Combined effects of halothane anesthesia and verapamil on systemic hemodynamics and left ventricular myocardial contractility in patients with ischemic heart disease.

The interaction of halothane anesthesia and intravenous verapamil (0.15 mg/kg over 10 min) was investigated in eight patients scheduled for coronary artery bypass surgery. All patients had a normal left ventricular (LV) function at rest and were on chronic beta-blocker therapy. Halothane produced a marked reduction in mean arterial pressure (MAP), cardiac index, and in LV contractility as documented by a decrease in LV peak positive dP/dt. Verapamil caused an additional depression (16%) of LV peak positive dP/dt accompanied by a small increase (3 mm Hg) in LV end-diastolic pressure. The combined negative inotropic propensities of halothane and verapamil did not produce any overt untoward effects even in the presence of chronic low dose beta-blocker therapy. The predominant hemodynamic effect of verapamil was a systemic vasodilation resulting in a further reduction in MAP (12%) while heart rate remained unaffected. Despite reducing myocardial oxygen demand, caution must be exercised in dose selection in each drug to avoid regional myocardial ischemia due to the combined hypotensive effects of halothane and verapamil.

Adult↗
PubMed1984

[Blood pressure control with an inhalation anesthetic in acute intraoperative hypertension. Hemodynamic profile of halothane, enflurane and isoflurane in coronary surgery patients].

The haemodynamic effects of isoflurane, halothane and enflurane when used to control intraoperative hypertension were evaluated in 30 patients undergoing coronary artery bypass grafting. The patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mmHg due to sternal spread or surgical manipulation of the aorta, halothane, enflurane or isoflurane were administered to return arterial pressure to control levels. Using a non-rebreathing system, inspired halothane concentrations of 1.0-1.5 vol.%, enflurane concentrations of 2.0-2.5 vol.% and isoflurane concentrations of 1.5-2.0 vol.% were necessary. Measurements were repeated during the hypertensive episodes and after treatment with halothane, enflurane or isoflurane while surgical stimulation continued. During the hypertensive episodes marked elevations in systemic vascular resistance were observed, four patients developed ischaemic ST-segment changes. Each of the three inhalational anaesthetics decreased mean arterial pressure to baseline values within 5 to 10 minutes. The fall in blood pressure caused by halothane was mainly due to a reduction in cardiac index, since the elevated systemic vascular resistance almost remained unaffected. Enflurane produced a similar fall in cardiac index, although left ventricular afterload was significantly reduced, suggesting that enflurane caused more impairment of cardiac performance than halothane. In contrast, the administration of isoflurane was associated with an increase of the cardiac index in the presence of marked systemic vasodilation and a slight decrease in left ventricular filling pressure. Halothane, enflurane and isoflurane reduced the rate-pressure product by a comparable degree and, when present, abnormalities in the ST-segments disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1983

Cardiovascular interactions of halothane anesthesia and nifedipine in patients subjected to elective coronary artery bypass surgery.

The effects of intravenous (iv) nifedipine (7.5 micrograms/kg over 10 min) on systemic hemodynamics and myocardial contractility were investigated under steady state conditions of halothane anesthesia (0.5 MAC) in 8 patients scheduled for elective coronary artery bypass surgery. All patients received long-term medication in the form of beta adrenergic receptor blockers and had a normal global left ventricular function at rest. Halothane produced a marked reduction in left ventricular contractility as documented by a considerable fall in LV max dP/dt. Nifedipine caused a small additional depression of LV max dP/dt without affecting LVEDP significantly. The slight myocardial depressant effect of nifedipine was counterbalanced by a concomitant reduction in left ventricular afterload due to a decrease in the systemic vascular resistance resulting in unchanged or even improved cardiac output. The results indicate that iv nifedipine in the doses used here is safe for patients with ischemic heart disease, even in the presence of already compromised myocardial contractility due to halothane anesthesia and chronic low-dose beta blocker therapy.

Aged↗
PubMed1983

Comparison of isoflurane and halothane when used to control intraoperative hypertension in patients undergoing coronary artery bypass surgery.

The hemodynamic effects of isoflurane and halothane when used to control intraoperative hypertension were evaluated in 20 patients undergoing coronary artery bypass grafting. The patients were anesthetized with flunitrazepam, fentanyl, pancuronium, and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mm Hg due to sternal spread or surgical manipulation of the aorta, isoflurane or halothane were used to return arterial pressure to control levels. Using a non-rebreathing system, inspired isoflurane concentrations of 1.5-2.0 vol% or halothane concentrations of 1.0-1.5 vol% were necessary. Measurements were repeated during the hypertensive episode and after treatment with isoflurane or halothane while surgical stimulation continued. Both inhalation anesthetics decreased arterial pressure to baseline values within 5-10 min. The lowering of arterial pressure with halothane was not accompanied by significant decreases in the elevated systemic vascular resistance and pulmonary capillary wedge pressure. Cardiac index and stroke volume index decreased markedly when halothane was used (18% and 25%, respectively). In contrast, isoflurane significantly decreased systemic vascular resistance (42%). This reduction of left ventricular afterload was associated with an increase in cardiac index (22%) and a decrease in left ventricular filling pressure. Heart rate did not change significantly. These findings indicate that isoflurane is superior to halothane for controlling intraoperative hypertension during coronary artery bypass surgery.

Adult↗
PubMed1982

Swan-Ganz Catheterization--application, interpretation and complications.

Considering the wide use of Swan-Ganz catheter monitoring, remarkably little serious morbidity and mortality has been reported. It is my belief that continued formal training in this technique is the best way to minimize the complication rate. Since its use involves far more important skills than the ability to insert a catheter into the venous circulation, the physician must not only know the indications and limitations but must also be prepared to recognize and treat its potential complications. He must be familiar with the calibration of manometers and amplifiers and he must be competent in the interpretation of pressure curves and the determination of therapeutic consequences. However, in spite of the importance of continued formal training, PA catheterization should never become a routine technique. Inappropriate application and subsequent overuse of Swan-Ganz catheter monitoring must be avoided. It should be used only when precise hemodynamic data cannot be derived from non-invasive or clinical evaluation.

Catheterization↗
PubMed1982

Haemodynamic responses to induction of anaesthesia using midazolam in cardiac surgical patients.

The cardiovascular effects of midazolam 0.2 mg kg-1 i.v. were studied during the induction of anaesthesia in 16 premedicated patients subjected to cardiac surgery. In eight patients with coronary artery disease in whom global resting left ventricular function was normal the haemodynamic changes were small and observations on arterial pressure, cardiac index, stroke index, cardiac filling pressures, systemic and pulmonary vascular resistance appeared to parallel those accompanying deep sleep in healthy volunteers. In eight patients with valvular heart disease and haemodynamic evidence of moderately impaired cardiac performance, pump function during induction with midazolam was maintained, probably as a result of the tendency towards a decrease in systemic vascular resistance. Midazolam appears to be a valuable alternative to conventional induction agents without adverse effects on the cardiovascular system.

Adult↗
PubMed1982

Pulmonary vascular responses to nitrous oxide in patients with normal and high pulmonary vascular resistance.

The pulmonary vascular responses to 50 per cent nitrous oxide were studied in 32 anesthetized patients ventilated to maintain normal PaCO2. One group consisted of sixteen patients with coronary artery disease (CAD) and normal pulmonary vascular resistance (PVR) about to undergo coronary artery bypass surgery. A second group consisted of 16 patients with markedly elevated PVR values due to chronic mitral valve stenosis (MVS). CAD patients showed a significant increase in PVR irrespective of whether halothane or fentanyl was used as background anesthetic. Individual changes, however, did not exceed the upper limit of normal and therefore are not considered to be of clinical importance in these patients. In patients with MVS subjected to fentanyl anesthesia, N2O caused a marked increase in PVR from 357 to 530 dyn . s. cm-5. Halothane anesthesia did not significantly attenuate the effect of nitrous oxide on the pulmonary vasculature as mean PVR increased from 351 to 451 dyn . s. cm-5. These results suggest that the preexisting PVR value is of more importance for the pulmonary vascular response to N2O than the influence of background anesthesia. We conclude that nitrous oxide should be used with caution in patients with elevated pulmonary vascular resistance, particularly in the presence of right ventricular dysfunction and/or right coronary artery disease.

Coronary Disease↗
PubMed1982

[Hemodynamic analysis of 6 different anesthesia induction procedures in coronary surgery patients].

We investigated the cardiovascular effects of intravenous thiopentone (3.0 mg/kg), etomidate (0.3 mg/kg), althesin (0.07 ml/kg), ketamine (1.5 mg/kg), diazepam (0.15 mg/kg) and flunitrazepam (0.015 mg/kg) alone and after the addition of fentanyl (0.01 mg/kg) during induction of anaesthesia in 46 premedicated patients subjected to coronary artery bypass surgery. Thiopentone, etomidate or diazepam caused only small changes in the haemodynamic determinants of myocardial oxygen supply and demand (arterial pressure, heart rate, left and right ventricular filling pressure) in patients with coronary artery disease in whom global resting left ventricular function was normal. Althesin and flunitrazepam produced a significant fall in arterial pressure, cardiac index and stroke index; heart rate increased after the administration of althesin. Ketamine markedly elevated systemic and pulmonary pressure, heart rate, systemic and pulmonary vascular resistance, right and left ventricular filling pressure. The subsequent administration of fentanyl was associated with a further decrease in arterial pressure in the althesin and flunitrazepam group. The circulatory stimulating effects of ketamine were largely abolished by fentanyl. None of the induction procedures was associated with cardiovascular stimulation during laryngoscopy and tracheal intubation.

Alfaxalone Alfadolone Mixture↗
PubMed1981

[The role of vasodilators in the treatment of congestive heart failure and myocardial ischaemia (author's transl)].

The introduction fo vasodilators has greatly expanded the therapeutic armamentarium for the management of severe heart failure. Although such agents have been employed for many years to treat hypertension and myocardial ischaemia, only recently has their use become widely popular in the therapy of pump failure. Since there is a large spectrum of therapeutically effective vasodilators, a rational selection of vasodilator, inotropic or combined therapy has to consider the pathophysiology of the underlying heart disease, the haemodynamic effects of the drugs and the possible hazards associated with their use. On this basis we discuss the intraoperative use of vasodilator and combined therapy in cardiac surgical patients with acutely disturbed pump performance due to various types of heart disease.

Coronary Disease↗
PubMed1981

[Monitoring of cerebral electrical activity during cardiac surgery (author's transl)].

Continuous recording of cerebral activity by the Cerebral Function Monitor is a useful supplementation to anaesthetic monitoring in cardiac surgery. It is a simple and reliable method for early detection of cerebral damage during heart surgery and in other situations with possible cerebral impairment. The operating principles of the Cerebral Function Monitor and the interpretation of the electrical activity tracings are presented. Therapeutic considerations to minimize or to prevent anoxic brain damage are offered.

Age Factors↗
PubMed1981

[Systemic and coronary haemodynamic effects of dobutamine and norepinephrine during metabolic acidosis].

The effects of clinical doses of dobutamine (5 microgram/kg x min) and norepinephrine (0.2 microgram/kg x min) on systemic haemodynamics and coronary circulation were studied during normal pH and during metabolic acidosis (pH 7.0) induced by hydrochloric acid in 9 anaesthetized closed chest dogs. Metabolic acidosis per se failed to show any significant depression of cardiac function, indicating that animals with intact sympathoadrenal system are highly resistant to acidaemia. Our results further demonstrated that a significant circulatory response to clinical doses of dobutamine and norepinephrine was still present during metabolic acidosis. However, the increase in cardiac output, max dp/dt and mean arterial pressure after dobutamine was found to be significantly reduced at low pH-values, whereas the vasopressor response to norepinephrine was not affected. From these results it may be speculated that metabolic acidosis differently influences the responsiveness of alpha- and beta-adrenergic receptors. Finally our results show that metabolic acidosis did not compromise the coronary adjustment to catecholamine-induced increases in myocardial oxygen demand.

Acidosis↗