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Biomedical subjects

D B O'Keeffe

Publications and source records attributed to D B O'Keeffe.

8 recordsLinked to original sources
PubMed1992

Hemodynamic effects of different temporary pacing modes for the management of bradycardias complicating acute myocardial infarction.

Twelve patients requiring temporary pacing following acute myocardial infarction (AMI) (10 heart block, 2 junctional bradycardia) had hemodynamic measurements taken with ventricular demand pacing at 80 ppm (VVI80), ventricular demand pacing at the atrial rate (VVIa), physiological pacing (DDD), and spontaneous (intrinsic) rhythm. VVI80 mode did not improve any hemodynamic parameter compared with spontaneous rhythm. VVIa mode improved diastolic and mean arterial pressures only. DDD mode improved most hemodynamic parameters compared with spontaneous rhythm (cardiac output by 29% [P less than 0.0001]; blood pressure: diastolic by 24% [P less than 0.01], systolic by 19% [P less than 0.01], mean by 21% [P less than 0.005]; pulmonary wedge pressure by 10% [P = 0.057] and right atrial pressure by 24% [P less than 0.005]) and also significantly improved some parameters compared with VVIa (cardiac output by 20% [P less than 0.001], systolic blood pressure by 11% [P less than 0.01] and right atrial pressure by 15% [P less than 0.01]). Physiological pacing is hemodynamically superior both to ventricular pacing and spontaneous rhythm for patients requiring temporary pacing following AMI. Ventricular pacing at 80 ppm has little hemodynamic advantage over spontaneous rhythm.

Adult↗
PubMed1991

Effect of atrial pacing on the frequency of tachycardia in patients with recurrent junctional tachycardia.

In order to assess whether atrial pacing reduced the frequency of tachycardia in patients with recurrent junctional tachycardias, ten patients with recurrent junctional tachycardias with atrial Intertach antitachycardia pacemakers in situ were paced in a random order in atrial demand mode at 50 ppm (AAI 50), 80 ppm (AAI 80), and 100 ppm (AAI 100) for a period of up to 1 month. The numbers of tachycardias detected by the pacemaker over this period were recorded and compared with the number seen when unpaced (000). Correct arrhythmia detection by the pacemaker was confirmed by Holter monitoring. The number of tachycardias in 000 was 44.7 +/- 19.8 (mean +/- SEM). No significant reduction in tachycardia frequency was seen in any pacing mode. Back-up atrial pacing at 50 ppm tended to reduce the frequency of tachycardias (32.3 +/- 12.8 tachycardias; P = 0.06). The higher pacing rates increased the number of tachycardias (AAI 80; 57.1 +/- 24.6 tachycardias, P = 0.20: AAI 100; 81.8 +/- 30.2 tachycardias; P = 0.31). Symptoms increased with each pacing mode and palpitations were statistically more severe in AAI 100 mode. Four patients had disabling symptoms at this rate and had to drop out. Atrial back-up pacing may be of use in some patients with junctional tachycardia, but overdrive pacing is not helpful.

Adult↗
PubMed1990

Management of acute coronary occlusion during percutaneous transluminal coronary angioplasty: experience of complications in a hospital without on site facilities for cardiac surgery.

OBJECTIVE: To determine whether percutaneous transluminal coronary angioplasty may be safely performed in cardiology centres in the United Kingdom without immediate on site cardiac surgical cover for complications arising at angioplasty. DESIGN: Retrospective review of coronary angioplasties and complications in a hospital without on site cardiac surgical cover. SETTING: All angioplasties were performed in the catheterisation laboratory of the Belfast City Hospital. Revascularisation surgery for complicated coronary angioplasty was performed in the cardiac surgical unit of the Royal Victoria Hospital, 2.4 km away from the catheterisation laboratory. PATIENTS: 540 Coronary angioplasties were performed on 512 patients between late 1982 and November 1988. Indications included stable angina, unstable rest angina, and suitable coronary disease at coronary arteriography after myocardial infarction. MAIN OUTCOME MEASURES: In hospital mortality after complicated coronary angioplasty and delay to surgical revascularisation after acute coronary occlusion at angioplasty. RESULTS: Coronary angioplasty was successful in 444 cases (82%). Acute coronary occlusion occurred in 35 cases (6.5%). Twelve patients required urgent revascularisation surgery and were transferred safely to the surgical unit; none of these patients died. A mean delay of 268 minutes (range 180-390 minutes) occurred before revascularisation compared with 273 minutes (range 108-420 minutes) in the Royal Victoria Hospital, where on site surgical cover was available. The principal cause of delay was the wait for a cardiac operating theatre to become available and not the transfer time between hospitals. Five deaths occurred after coronary angioplasty, a mortality of 0.9%. Three deaths were related to acute coronary occlusion. The absence of immediate surgical help did not influence the outcome in any patient. CONCLUSION: With careful selection of patients coronary angioplasty may be safely performed in a hospital without on site cardiac surgical facilities, provided that these are available at a nearby centre.

Acute Disease↗
PubMed1990

Intravenous streptokinase for acute myocardial infarction reduces the occurrence of ventricular late potentials.

The occurrence of ventricular late potentials in survivors of acute myocardial infarction treated with intravenous streptokinase was compared with that in a conservatively treated group and the relation between ventricular late potentials and patency of the infarct related artery was examined. Of 115 patients admitted with a first infarct, 55 were treated with intravenous streptokinase (streptokinase group) and 60 were treated conservatively (non-streptokinase group). A signal averaged electrocardiogram was recorded in all patients and coronary angiography was performed in 45 (81.8%) of the streptokinase group and in 21 (35%) of the non-streptokinase group. At a 40 Hz filter setting ventricular late potentials were significantly less common in patients treated with streptokinase (9 (16.4%) of 55) than in those who were not (26 (43.3%) of 60). A total of 66 patients underwent angiography. Of the 26 who had closed infarct-related arteries, 17 had ventricular late potentials at a 40 Hz filter setting (sensitivity 65.4%, specificity 95%) and 38 of the 40 patients with a patent infarct-related artery did not have ventricular late potentials (sensitivity 80.9%, specificity 89.5%). Patients with acute myocardial infarction treated with intravenous streptokinase were significantly less likely to have ventricular late potentials than conservatively treated patients and the absence of ventricular late potentials at 40 Hz filter setting was a good non-invasive predictor that the infarct-related artery was patent.

Arrhythmias, Cardiac↗
PubMed1989

Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction.

At necropsy five of eight patients (mean age 57 years) who died after intravenous streptokinase treatment for severe acute myocardial infarction (mean Peel index = 18) were found to have a patent infarct related coronary artery. Coronary artery stenoses were caused by fibrofatty atheromatous plaques; there were no residual thrombi in the lumen or acute intimal lesions. Three of these infarcts were of partial thickness (less than two thirds wall width) with sparing of the outer third of the myocardium and subendocardial zones. In the other three patients the infarct related coronary arteries remained histologically closed with residual lumen thrombi and underlying intimal lesions. Two infarcts were transmural. Six of the eight infarcts were noticeably haemorrhagic. Myocardial haemorrhage was confined to areas of necrotic myocardium and did not affect viable regions. These findings suggest that thrombus overlying a complex lesion may be more difficult to lyse than thrombus overlying a simple fibrofatty plaque. They also suggest that myocardial haemorrhage outside the infarct area, which might lead to cardiac rupture or delayed healing, does not usually occur.

Acute Disease↗
PubMed1988

Relation of coronary arterial patency and left ventricular function to electrocardiographic changes after streptokinase treatment during acute myocardial infarction.

One hundred and eighty-eight patients with evolving acute myocardial infarction were treated with intravenous streptokinase. Serial 12-lead electrocardiograms were recorded for 3 hours after treatment and inspected for rapid repolarization changes of the ST segment and T wave. Abrupt electrocardiographic repolarization changes were observed in 106 patients (56%) and were strongly predictive for an open infarct-related coronary artery at a mean of 6 days after treatment (predictive value = 0.92, sensitivity = 0.67). Abrupt electrocardiographic changes were not observed in 82 patients (44%). This absence was not a good predictor of an occluded infarct-related coronary artery (predictive value = 0.4). There was no relation between the presence or absence of abrupt electrocardiographic changes and global or regional left ventricular function after streptokinase treatment. Abrupt repolarization changes after thrombolytic treatment indicate a high probability of an open infarct-related artery. When abrupt repolarization changes do not occur, the patency of the infarct-related coronary artery cannot be predicted with accuracy. Serial electrocardiographic recordings do not provide sufficient information about coronary patency to eliminate the need for coronary arteriography.

Aged↗
PubMed1979

The effects of physostigmine on amitriptyline induced cardiotoxicity in dogs.

When 0.5 mgs of physostigmine salicylate was injected intravenously into adult beagle dogs which had been severely poisoned with amitriptyline, a transient improvement in cardiac output, systolic blood pressure, intraventricular conduction and in the maximum rate of rise of arterial blood pressure (arterial dP/dT max.) was observed. These effects were maximal at 15-20 minutes after injection and had largely disappeared 30 to 35 minutes after the injection.

Amitriptyline↗