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Biomedical subjects

S H Taylor

Publications and source records attributed to S H Taylor.

At least 163 records · Page 9Linked to original sources
PubMed1983

Professional disclosure in the counseling profession: a review of the literature.

Professional disclosure is a vehicle by which clients can become informed about the services they may receive in a professional setting, including those in the allied health fields. This paper reviews the literature on professional disclosure from the viewpoints of shaping client expectations, promoting counselor accountability, and being ethically responsible. A written professional disclosure statement can be provided that satisfies these requirements.

Community Participation↗
PubMed1983

Diuretics and digitalis in the treatment of chronic heart failure.

The evaluation of the long-term treatment of heart failure is complicated by many biological, clinical and technical problems. Chronic heart failure results from a variety of causes, each resulting in fundamentally different histopathological profiles. Once established chronic heart failure is unremitting, but the speed of progression of the haemodynamic derangement varies widely between different individuals. Moreover, the extent of the haemodynamic disorder correlates poorly with the severity of symptoms. The metabolism of drugs and the response of the damaged myocardium to these drugs is often quite different in the patient with heart failure than in the normal subject. Finally chronic heart failure is a terminal condition of relatively short duration so that clinical trials designed to test the efficacy of a drug treatment will fail if they are continued for more than a brief period, as all patients will die. It is against this complex biological background that the long-term clinical efficacy of diuretics and digitalis in the treatment of chronic heart failure must be evaluated.

Administration, Oral↗
PubMed1983

Haemodynamic effects of frusemide and its influence on repetitive rapid volume loading in acute myocardial infarction.

The haemodynamic effects of intravenous frusemide (1 mg/kg) were studied in 22 male patients with left ventricular failure following acute myocardial infarction. Radiographic pulmonary oedema was present in all patients and their average left heart filling pressure was 20 mmHg. Bolus injection of the drug was followed by immediate increases in systemic arterial pressure (P less than 0.05) and heart rate (less than 0.05); these declined to pre-injection values after 60 min. Following frusemide there were progressive reductions in left heart filling pressure (P less than 0.01), thermodilution cardiac output (P less than 0.01) and stroke volume (P less than 0.05) and a progressive increase in the derived systemic vascular resistance (P less than 0.05). There was an average diuresis of 860 ml during the 90 min following the frusemide injection. The influence of frusemide on left ventricular performance was studied by comparing the circulatory effects of passive leg raising in the control period with those at 30, 60 and 90 min after the drug. In the control period this manoeuvre increased left heart filling pressure, but not heart rate, cardiac output, stroke volume or systemic vascular resistance. Ninety minutes after frusemide, but not before, passive leg raising resulted in a significant increase in cardiac output (P less than 0.01) and stroke volume at a similar increment in filling pressure and a significant reduction in the systemic vascular resistance (P less than 0.05). These circulatory actions of intravenous frusemide are compatible with initial arteriolar constriction and venodilatation followed by depletion of blood volume with subsequent change in left ventricular pumping performance.

Adult↗
PubMed1983

Observations on the mechanism underlying the differences in exercise and isoprenaline tachycardia after cardioselective and non-selective beta-adrenoceptor antagonists.

1 Differences in ability to attenuate isoprenaline tachycardia between the cardioselective beta-adrenoceptor antagonist atenolol and the non-selective drug propranolol, when administered in equivalent anti-exercise tachycardia oral doses, were measured in four normal volunteers. 2 Propranolol at all dose comparisons showed a greater potency in antagonism of isoprenaline tachycardia than atenolol; this ranged from 6 at the lowest doses (40 and 50 mg respectively) to 13 at the highest doses (320 and 400 mg respectively). 3 After doses of each drug which produced equal inhibition of exercise tachycardia, isoprenaline induced a greater increase in heart rate and greater decrease in diastolic blood pressure after pre-treatment with atenolol than after propranolol. 4 The contribution of this isoprenaline induced vasodilatation to the reduced tachycardia response, 1 h after 25 mg oral atenolol, was measured in the same four subjects by correction of the hypotension with an intravenous angiotensin infusion. Reversal by angiotensin of the 17 mm Hg average fall in diastolic blood pressure during the sustained isoprenaline infusion did not reduce the tachycardia. 5 The hypotension that results from isoprenaline stimulation of unblocked vasodilator beta 2-adrenoceptors in normal subjects pre-treated with atenolol appears to make a negligible contribution to the tachycardia response and does not explain the different abilities of cardioselective and non-selective beta-adrenoceptor blocking drugs to antagonise isoprenaline tachycardia. Our results are compatible with the presence of beta 2-adrenoceptors in human atria.

Adult↗
PubMed1983

Haemodynamic dose-response effects of i.v. penbutolol in angina pectoris.

The haemodynamic dose-response effects of intravenous penbutolol, a newer beta-adrenoceptor antagonist with intrinsic sympathomimetic activity but without cardioselectivity, were evaluated in 10 patients with angiographically documented coronary artery disease. Following four logarithmetically cumulative i.v. boluses (0.5-4 mg dosage range) there was a log linear increase in plasma penbutolol concentration; the levels achieved (51 +/- 8 to 219 +/- 19 ng/ml) were in the therapeutic range (12 to 250 ng/ml). Penbutolol resulted in a linear decrease in heart rate (maximum delta HR - 4 beats/min; P less than 0.01); there was a small increase in pulmonary artery occluded pressure which reached its maximum at the lower doses (maximum delta PAOP + 1 mm Hg; P less than 0.01). The resting cardiac output, blood pressure and calculated systemic vascular resistance were unchanged. During 4 min steady-state supine bicycle exercise there was attenuation of exercise cardiac output (delta C.I. - 0.6 1 min-1 m-2; P less than 0.01) and systolic pressor response (delta SBP - 13 mm Hg; P less than 0.01) compared with control observations without change in other measured or derived variables. The haemodynamic profile of penbutolol compared favourably with other beta-adrenoceptor antagonists previously evaluated under similar conditions in patients with ischaemic heart disease. Over the i.v. dose-range evaluated penbutolol attenuated exercise-induced angina with a relatively modest depression of cardiac performance; the small change induced in resting haemodynamic variables may, in part, have been contributed to by the intrinsic sympathomimetic activity of penbutolol.

Adult↗
PubMed1983

Haemodynamic effects of intravenous beta-blocking drugs in coronary heart disease.

Intravenous beta-blocking drugs are being increasingly used in early myocardial infarction but little is known of the comparative haemodynamic effects of drugs with different ancillary pharmacological properties. In patients with stable coronary heart disease all intravenous beta-blocking drugs reduce left ventricular pumping function in a dose-response fashion. The reduction in cardiac mechanical activity is directly related to the dose and inversely related to the degree of intrinsic sympathomimetic activity possessed by each drug; it is independent of the property of 'cardioselectivity'. The lesser depression of left ventricular pumping performance after beta-blocking drugs with intrinsic sympathomimetic activity is probably due to two primary pharmacodynamic effects: a) increased myocardial contractile activity due to stimulation of post-synaptic beta 1- and presynaptic beta 2-adrenoceptors in the sinus node and ventricular myocardium; b) reduction in left ventricular afterload consequent upon the fall in systemic vascular resistance resulting from stimulation of vasodilator beta 2-adrenoceptors in peripheral resistance vessels. A similar but less marked haemodynamic separation of beta-blocking drugs with and without intrinsic sympathomimetic activity is observed in patients with acute myocardial infarction. The quantitative difference in the haemodynamic effects of intravenous beta-blocking drugs in angina pectoris compared to their effects in acute myocardial infarction is probably due to the higher level of sympathetic stimulation and sensitivity to beta-blockade in the latter. It has yet to be shown by formal clinical trial that the haemodynamic advantages attributable to the possession of intrinsic sympathomimetic activity by a beta-blocking drug are translated into clinical benefit.

Adrenergic beta-Antagonists↗
PubMed1983

Beta-blockade in ischaemic heart disease--influence of concomitant ISA or alpha-blockade on haemodynamic profile.

To test the hypothesis that the depression of cardiac performance induced by competitive blockade of sympathetic stimulation at beta-adrenoceptors could be attenuated by the addition of a high level of intrinsic sympathomimetic activity (ISA) or concomitant alpha- and beta-blockade, the haemodynamic dose-response effects of propranolol (non-cardioselective, no ISA), pindolol (non-cardioselective, high ISA) and labetalol (non-cardioselective, alpha-blocker) were compared in a randomized study of 30 patients with stable coronary artery disease. Following 4 intravenous (i.v.) doses of each drug given according to a logarithmic cumulative dosage schedule, changes in circulatory variables were measured 2-4 min following each i.v. bolus and during bicycle exercise following the maximum dose of each drug. At rest propranolol induced dose-related reductions in heart rate, cardiac output and increases in pulmonary artery occluded pressure and systemic vascular resistance. The only change in resting haemodynamic variables following pindolol was a small dose-related increase in pulmonary artery occluded pressure. Labetalol induced dose-related falls in systemic blood pressure and vascular resistance with linear increase in cardiac output and pulmonary artery occluded pressure. During exercise the depression of cardiac output and increase in pulmonary artery occluded pressure which occurred in patients randomized to propranolol was effectively attenuated in the pindolol and labetalol groups. These observations on cardiac performance following beta-blockade in ischaemic heart disease suggest a rational basis for the use of compounds with added vasodilator or intrinsic sympathomimetic properties.

Adult↗
PubMed1983

Haemodynamic dose-response effects of intravenous labetalol in acute myocardial infarction.

The haemodynamic consequences of combined alpha- and beta-adrenoceptor blockade with intravenous labetalol were evaluated in 21 males with either high (n = 6), normal (n = 9) or low (n = 6) systemic arterial pressure, 4-17 hours after acute myocardial infarction without heart failure. Labetalol 190 +/- 18 mg (range 62-300 mg) infusion resulted in dose-related falls in systolic (P less than 0.01) and diastolic (P less than 0.05) arterial pressure in all patients. The rate of pressure reduction per mg of infused labetalol was directly proportional to the control systolic arterial pressure. Cardiac output (thermodilution) was reduced (P less than 0.05) with low dose labetalol (39 +/- 5 mg) without change on continued infusion. Left heart filling pressure (pulmonary artery occluded pressure) was unchanged throughout infusion in all patients. In conclusion, the vasodilating properties of labetalol appeared to offset the beta-blocker induced depression of cardiac function. The increased sensitivity to the effects of labetalol in those patients with hypertension may be related to excessive alpha-adrenoceptor mediated vasoconstriction in this patient group.

Dose-Response Relationship, Drug↗
PubMed1983

Management of acute heart failure following myocardial infarction: hemodynamic advantages of isosorbide dinitrate over frusemide.

The immediate hemodynamic effects of intravenous frusemide (1 mg/kg) and intravenous isosorbide dinitrate (50-200 micrograms/kg/h) were compared in a prospective, randomized, between-group study in 28 men with radiographic and hemodynamic evidence of left ventricular failure following acute myocardial infarction. The diuresis induced by frusemide reduced the left-heart filling pressure and cardiac output and transiently raised systemic blood pressure. In contrast, isosorbide dinitrate was accompanied by a reduction in systemic blood pressure and peripheral resistance, with the result that the cardiac output was not decreased despite a large fall in the pulmonary vascular and left-heart filling pressures. The results indicate that reduction of excessive preload by venodilatation may be hemodynamically superior to that induced by diuresis in terms of both reducing myocardial oxygen consumption and maintaining peripheral perfusion. The influence of these contrasting treatments on the prognosis of these high-risk patients warrants further study.

Adult↗
PubMed1982

A long-term prevention study with oxprenolol in coronary heart disease.

We carried out a randomized double-blind controlled secondary-prevention trial of oxprenolol over seven years. Forty milligrams of oxprenolol or placebo was given twice daily to 1103 men 35 to 65 years old who had an acute myocardial infarction between 1 and 90 months previously. Overall, there was no difference in mortality or cardiac events between the placebo and oxprenolol groups. The major influence on prognosis was the time at which treatment was started after infarction. In 417 patients in whom treatment was started within four months of infarction oxprenolol increased the six-year cumulative survival rate from 77 to 95 per cent (P less than 0.001). In 274 patients with treatment starting between 5 and 12 months of infarction the survival rate was similar in the two groups, but in 412 patients entered between 1 and 7 1/2 years after their first infarction oxprenolol reduced the six-year survival rate from 92 to 79 per cent (P = 0.002). The increased mortality in this latter group mainly occurred late after withdrawal from active treatment. The value of low-dose oxprenolol in secondary prevention appears to be confined to patients treated relatively soon after myocardial infarction.

Adult↗
PubMed1982

Haemodynamic advantages of combined alpha-blockade and beta-blockade over beta-blockade alone in patients with coronary heart disease.

The acute haemodynamic effects of beta-blockade with propranolol and combined alpha-blockade and beta-blockade with labetalol were compared in a randomised study in 12 patients with coronary artery disease proved by angiography. Propranolol induced significantly greater depression of left ventricular function both at rest and during exercise than labetalol. This difference was probably attributable to the vasodilator activity of labetalol and the associated reduction in afterload offsetting the haemodynamic disadvantages of blockade of cardiac beta-adrenoceptors alone. The haemodynamic advantages of combined alpha-blockade and beta-blockade over beta-blockade alone may thus have therapeutic implications for the use of these treatments in patients with coronary heart disease.

Adult↗
PubMed1982

Intravenous beta-blockade in coronary heart disease: is cardioselectivity or intrinsic sympathomimetic activity hemodynamically useful?

Beta-blocking drugs are increasingly prescribed in coronary heart disease, but controversy surrounds the hemodynamic relevance of their ancillary pharmacologic properties--cardioselectivity and intrinsic sympathomimetic activity. We therefore compared the effects of four intravenous beta-adrenoreceptor antagonists with different ancillary properties on left ventricular function in 24 patients with coronary heart disease. All four drugs depressed the relation between left ventricular filling pressure and cardiac output at rest and during exercise. However, practolol and oxprenolol, which have intrinsic sympathomimetic activity, induced significantly less depression of left ventricular function than either propranolol or metoprolol, which do not have this activity. Cardioselectivity, a property of both practolol and metoprolol, had no discernible hemodynamic advantage. Beta-blocking drugs that have intrinsic sympathomimetic activity appear to be more effective in maintaining cardiac function than drugs without this property, when given intravenously to patients with coronary heart disease.

Adrenergic beta-Antagonists↗