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Biomedical subjects

L E Oliver

Publications and source records attributed to L E Oliver.

13 recordsLinked to original sources
PubMed1995

Low energy endocardial cardioversion of atrial arrhythmias in humans.

We assessed the feasibility of low energy endocardial defibrillation in patients with atrial fibrillation or atrial flutter who had failed a trial of pharmacological reversion with amiodarone. Low energy endocardial defibrillation under general anesthesia was attempted in 9 patients, 5 with atrial flutter and 4 with atrial fibrillation (median duration of arrhythmia 3.75 months). Two large surface area endocardial leads were introduced percutaneously and sited in the right atrial appendage and at the right ventricular apex. A cutaneous patch electrode was placed on the left thorax. Biphasic shocks synchronized to the ventricular electrogram were used to terminate atrial arrhythmias. Three electrode configurations were evaluated in the following sequence at each energy level: atrial cathode to ventricular anode; ventricular cathode to atrial anode; atrial cathode to a combined ventricular and cutaneous anode. If endocardial defibrillation failed (0.5-10 J), transthoracic defibrillation using 200 joules followed by 360 joules, if required, was performed. Endocardial defibrillation was successful in all five patients with atrial flutter (0.5 J, 1.0 J, 1.0 J, 4.0 J, and 10.0 J) but in only one patient with atrial fibrillation (10 J). On no occasion did successful defibrillation occur with one configuration when it had failed with an alternate configuration at that particular energy level. Ventricular fibrillation did not occur, and there were no other significant complications. Low energy endocardial defibrillation is feasible in patients with atrial flutter using large surface area electrodes. Although the success rate of atrial defibrillation was low, further work is required, particularly in patients with more recent onset of the arrhythmia and using a right to left electrode configuration.

Adult↗
PubMed1985

Aggravation of myocardial ischaemia by nifedipine.

Three cases in which myocardial ischaemia was possibly precipitated by the administration of nifedipine are reported. It is suggested that the initial administration of nifedipine should be undertaken with caution in patients with unstable ischaemic heart disease.

Coronary Disease↗
PubMed1981

Effects of captopril (SQ 14,225) in a patient with primary pulmonary hypertension.

In a 33-year-old patient with severe primary pulmonary hypertension, the acute administration of the angiotensin-converting-enzyme inhibitor captopril (SQ 14,225) induced a rise in cardiac output, and a fall in both pulmonary and systemic vascular resistance. Subsequent chronic oral administration of captopril induced only transient clinical improvement, and the patient died. Captopril may nevertheless be useful in the treatment of less advanced cases of this disease.

Adult↗
PubMed1980

Use of dopamine and prazosin combined in the treatment of cardiogenic shock.

Seventeen patients who developed cardiogenic shock after acute myocardial infarction were treated with intravenously infused dopamine. In eight of these patients a stable blood pressure was attained, but oliguria or anuria persisted, and oral treatment with prazosin was instituted. Diuresis occurred in seven of these patients, but was followed by transient hypotension associated with a rapid rise in plasma prazosin levels in three. Four patients left hospital, and there were two long-term survivors. Prazosin may be a useful adjunct to dopamine in the treatment of cardiogenic shock.

Administration, Oral↗
PubMedDate not supplied

Haemodynamic effects of a single low dose of prazosin in patients with chronic congestive cardiac failure correlations with pharmacokinetics.

The haemodynamic effects and pharmacokinetics of a single orally administered dose of 0.5 mg of prazosin have been compared in six patients with stable severe congestive cardiac failure. Administration of prazosin induced significant decreases in mean pulmonary capillary wedge pressure (from 27.5, s.e.m. = 4.5 to 19.4, s.e.m. = 5.1 mmHg; P less than 0.001), mean arterial blood pressure (from 94.5, s.e.m. = 6.0 to 85.4, s.e.m. = 5.0 mmHg; P less than 0.01), and systemic vascular resistance (from 1690, s.e.m. = 360 to 1420, s.e.m. = 200 dyn. s/cm5; P less than 0.05) and a rise in cardiac index from 1.98 (s.e.m. = 0.07) to 2.28 (s.e.m. = 0.16) litres/min per m2 (P less than 0.05). There was a non-significant fall in heart rate. Pharmacokinetic analysis revealed maximum plasma prazosin concentrations of 4.1 (s.e.m. = 1.4) ng/ml, occurring 2.1 (s.e.m. = 0.4) h after drug ingestion. The mean elimination half-life was 5.1 (s.e.m. = 0.8) h, which is longer than that found in our previous studies in normal subjects. There was considerable interindividual variation in peak plasma prazosin concentrations, elimination half-life and area under the concentration-time curve. While mean maximal haemodynamic effects of prazosin occurred at similar times to the peak plasma concentration of the drug, there was no significant correlation between the extent of haemodynamic response and individual pharmacokinetic parameters. It is concluded that significant and potentially beneficial haemodynamic effects occur with the initial administration of 0.5 mg oral dose of prazosin in patients with stable congestive cardiac failure and it is suggested that in many patients little advantage will be achieved with higher initial doses.

Aged↗