Asystole following butane gas inhalation.
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Adolescent↗
Biomedical subjects
A A Adgey
Publications and source records attributed to A A Adgey.
Clinical Q fever in Northern Ireland 1962-1989.
Q fever was diagnosed in 443 patients in Northern Ireland between 1962 and 1989. From 1986 onwards there was an increase, which peaked in 1989 with 107 cases of whom 47 were infected in Ballycastle, Co Antrim. There were three outbreaks and 21 clusters of patients with Q fever. Most cases were in April and May which correlated with the peak lambing and calving season. Q fever mainly affected males in the 40-49 year old age group. County Antrim had the highest prevalence rate of 40/100,000 population and also had the most sheep. The number of sheep in Northern Ireland has doubled in the past ten years. Q fever was strongly associated with occupation and animal contact. Eighty-seven patients (19.6%) drank unpasteurized milk. The commonest presenting illnesses were pneumonia (62.8%), influenza-like illness (24.6%), involvement of the heart (9.0%) and hepatitis (1.6%). Thirty-two patients (7.2%) had endocarditis, 20 of whom had prosthetic valves and three of whom died. Coxiella burnetii was present on valves removed from seven patients.
Adolescent↗
Electrode pad size, transthoracic impedance and success of external ventricular defibrillation.
Electrode pad size is an important determinant of transthoracic current flow during external countershock. Self-adhesive, dual function electrocardiogram/defibrillator pads were used to assess the effect of electrode pad size on defibrillation success with low energy (200 J) shocks. The study analyzed 123 cardiac arrests due to primary ventricular fibrillation (VF) in 105 patients (74 men, 31 women) ages 40 to 84 years (mean 64). Transthoracic impedance was measured before defibrillation using a low amplitude 30-kHz current passed through the chest by way of the electrocardiogram/defibrillator pads applied anteroanteriorly. Pad diameters were small (8/8 cm) in 26 cardiac arrests, intermediate (8/12 cm) in 63 arrests and large (12/12 cm) in 34 cardiac arrests. Transthoracic impedance decreased with increasing pad size (112 +/- 17 vs 92 +/- 22 vs 72 +/- 14 omega, respectively, p = 0.0001). Only the first episode of primary VF during a cardiac arrest was analyzed. A single shock of 200 J (delivered energy) was successful in 8 of 26 (31%) arrests using small pads, in 40 of 63 (63%) with intermediate pads and in 28 of 34 (82%) with large pads (p = 0.0003). A second 200-J shock increased the cumulative defibrillation rates to 12 of 26 (46%), 50 of 63 (79%) and 33 of 34 (97%), respectively (p less than 0.0001). In primary VF, larger self-adhesive electrocardiogram/defibrillator pads are associated with a lower transthoracic impedance and improved defibrillation success rates with low energy shocks.
Adhesives↗
Transthoracic defibrillation threshold of sine and trapezoidal waveforms in defibrillation.
The transthoracic defibrillation threshold of trapezoidal (2.5-, 5-, 10-, 15-, 20-, 40-, and 55-msec duration) and damped sine waveforms were established in groups of anesthetized greyhounds. Of the seven trapezoidal waveforms, the threshold current was lowest for the 20-msec pulse but was not significantly different for the 5-20-msec pulses (p greater than 0.05). The threshold delivered energy was not significantly different for the 2.5-20-msec waveforms. The 40- and 55-msec pulses had significantly greater delivered energies than the shorter pulses (p less than 0.01). The transthoracic defibrillation threshold of two trapezoidal (5- and 20-msec) and three damped sine waves (Lown, Edmark, and Belfast) showed that the threshold transthoracic current and energy were not significantly different for the 5-msec trapezoid and three sine waves (p greater than 0.05). The threshold transthoracic energy for the 20-msec trapezoid was significantly greater than that of the four other waveforms. The threshold current for the 20-msec trapezoid was significantly less than that of the Belfast and Edmark waveforms only. Thus, none of the three damped sine waveforms was superior, with the 5-msec trapezoid producing similar results. Although the 20-msec trapezoid had the lowest threshold current, it had the highest delivery energy.
Animals↗
High dose nalbuphine in early acute myocardial infarction.
Twenty patients with moderate or severe pain of suspected myocardial infarction received nalbuphine 50 mg intravenously as analgesia in 2 divided doses of 30 mg and 20 mg with 10 mg metoclopramide and were observed for 2 hours. Eighteen patients received nalbuphine outside hospital. The median time from onset of pain to treatment was 73 minutes. Within 30 minutes of the drug's administration 90% of all patients reported satisfactory pain relief (grade 0 or 1). For those with definite myocardial infarction 83% reported satisfactory pain relief at 30 minutes. There were no significant adverse cardiorespiratory effects observed or serious side-effects reported. Nalbuphine is effective and safe when used in this higher dose, although no additional analgesic effect was demonstrated when compared with lower established doses used early in acute myocardial infarction.
Chest Pain↗
Cardiac injury with damped sine and trapezoidal defibrillator waveforms.
To assess defibrillator-induced cardiac damage, 49 anaesthetized greyhounds received either no shocks (control group) or five shocks from a defibrillator delivering one of five waveforms (Lown, Edmark, Belfast damped sine waveforms: 5 and 20 ms trapezoidal waveforms). At 3 days the hearts of the 36 surviving dogs were examined for macroscopic damage. The Belfast and Edmark waveforms caused significantly more damage (mean 21.1 +/- SEM 2.9 g and 16.0 +/- 3.7 g) respectively than the Lown waveform (3.5 +/- 1.3 g) P less than 0.01. The 20 ms trapezoid caused significantly more damage (8.1 +/- 3.1 g) than the 5 ms pulse (0.7 +/- 1.3 g) P less than 0.05). The ventricular ectopic counts per minute were not significantly different in the three sine wave and 20 ms trapezoidal groups at 24 and 48 h (P greater than 0.05), but at 2 and 72 h were significantly greater in the Belfast and Edmark groups than in the Lown group (2 h, Belfast P less than 0.01, Edmark P less than 0.05: 72 h P less than 0.05). At 15 min there was more right chest ST-segment elevation in the Belfast than in the Lown, Edmark and 20 ms trapezoid groups (P less than 0.01), while left chest ST elevation was greater in the Belfast and Edmark than in the Lown (P less than 0.05) and 20 ms trapezoid groups (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Metabolic changes and mitochondrial dysfunction early following transthoracic countershock in dogs.
The mechanisms of myocardial injury and necrosis following transthoracic shocks from a direct current cardiac defibrillator were investigated in adult greyhounds. Myocardial lactate extraction became negative maximally at 1 minute, following two (mean -22% +/- SEM23) or five (-193% +/- 135) shocks and returned to baseline in 6-15 minutes. Myocardial necrosis assessed at 4 hours following the shock period was 0.05 g (+/- 0.03) after two shocks, 6.69 g (+/- 1.76) after five shocks and zero in controls. In further experiments, dogs received five or zero (dummy) shocks and mitochondria were isolated from their hearts following excision within 1 minute of receiving the final shock. Maximal oxygen consumption in right ventricular mitochondria was lower than the unshocked controls with both glutamate (66.9 +/- 9.4 nanoatoms of oxygen/mg per minute, n = 9 vs 86.6 +/- 13.6 nanoatoms/mg per minute, n = 7) and succinate (96.2 +/- 8.7 nanoatoms/mg per minute, n = 9 vs 119.5 +/- 14.4 nanoatoms/mg per minute, n = 7) as substrates. Using electron spin resonance spectroscopy, an increase in a peroxyl-free radical with g = 2.031 was detected in myocardial tissue after two internal shocks (50 joules stored energy, 0.5-minute intervals). We conclude that mitochondrial dysfunction and free-radical generation are likely contributors to cellular injury following multiple countershocks.
Animals↗
A double blind placebo controlled study of early and late administration of recombinant tissue plasminogen activator in acute myocardial infarction.
Within four hours of the onset of acute myocardial infarction 57 consecutive patients were randomised blindly to infusion of 150 mg recombinant tissue plasminogen activator (rt-PA) (group 1) over five hours or placebo (group 2) when they were first seen outside hospital or in the accident and emergency department. When they were admitted to the coronary care unit patients in group 1 also had placebo infused and those in group 2 were treated with rt-PA as well as placebo. Treatment with rt-PA started at a mean of 119 minutes (range 38-235) after the onset of pain in group 1 and 187 minutes (range 80-285) after the onset of pain in group. In 19 (79%) of 24 in group 1 and 16 of 25 (64%) in group 2 cardiac catheterisation 10-14 days after infarction showed thrombolysis in myocardial infarction grades 2 or 3. There was mean percentage shortening of the infarct related segments (Leighton method) of 16% in group 1 and 10.3% in group 2. For patients with anterior infarction mean percentage shortening was 20.5% in group 1 and 12.2% in group 2. Although there was no significant difference in global ejection fraction as assessed by contrast ventriculography or radionuclide ventriculography the infarct related regional third ejection fraction (a measure of the function of the territory of the affected coronary artery) was significantly improved by early treatment (41% group 1 and 28% group 2). Assessment of infarct size by the QRS scoring method of Palmeri showed QRS score less than or equal to 15/25 patients in group 1 and 8/27 in group 2. Nine patients developed 11 episodes of ventricular fibrillation; all patients in whom ventricular fibrillation developed during treatment with rt-PA were successfully resuscitated. There was no clinically significant bleeding. In seven (12%) patients clinical and electrocardiographic criteria suggested reocclusion. Five patients died from cardiac causes. Prehospital administration of rt-PA was feasible and significantly reduced the delay before thrombolysis was started. Earlier treatment improved myocardial function in the the infarct area and reduced the infarct size.
Adult↗
Initial experience with a microprocessor controlled current based defibrillator.
Intramyocardial current flow is a critical factor in successful ventricular defibrillation. The main determinants of intramyocardial current flow during transthoracic countershock are the selected energy and the transthoracic impedance of the patient. To optimise the success of the first shock and to titrate energy dosage according to each patient's transthoracic impedance, a microprocessor controlled current based defibrillator was developed. It was compared with a conventional energy based protocol of 200 J (delivered energy), 200 J, then 360 J if required in 42 consecutive episodes of ventricular fibrillation in 33 men and seven women. The mean (SD) predicted transthoracic impedance was 69.9 (14.0) omega. First shock success with the standard protocol was 80.9%, and first or second shock success was 95.2%. The microprocessor controlled current based defibrillator automatically measured transthoracic impedance and calculated the energy required to develop a selected current in each patient. A current protocol of 30 A, 30 A, then 40 A, if required, was used in 29 men and 12 women with 41 episodes of ventricular fibrillation. Transthoracic impedance (mean 65.1 (15.9) omega) was similar to that in the energy protocol group and success rates for first shock (82.9%) and first or second shocks (97.5%) were also similar. The mean delivered energy per shock with the current based defibrillator for first or second shock success was significantly less (144.8 J) with the energy protocol (200 J). The mean peak current of successful shocks was also significantly reduced (29.0 v 31.9 A). A current based defibrillator titrates energy according to transthoracic impedance; it has a success rate comparable to conventional defibrillators but it delivers significantly less energy and current per shock.
Cardiography, Impedance↗
A randomised dose ranging study of recombinant tissue plasminogen activator in acute myocardial infarction.
To assess the thrombolytic efficacy and the effect on the systemic fibrinolytic system of recombinant tissue plasminogen activator doses of 20 mg, 50 mg, and 100 mg were compared in a randomised study. Tissue plasminogen activator was infused intravenously over 90 minutes in 50 consecutive patients with acute myocardial infarction of four hours' duration or less; on average the infusion was started 135 minutes (range 20 to 240) after the onset of pain. The affected artery was patent at the end of the 90 minute infusion in 14/17 (82%) of those who received 100 mg, 12/17 (71%) of those who received 50 mg, and 8/16 (50%) of those who received 20 mg. Regardless of dose, reperfusion rates were significantly better for patients treated within two hours of the onset of symptoms (81%) than for those treated in the third and fourth hours (54%). At the end of the infusion serum fibrinogen concentrations fell to 86% of the preinfusion value after 20 mg, 75% after 50 mg, and 63% after 100 mg, and similar dose dependent changes occurred in plasminogen, (alpha 2 anti-plasmin, and fibrinogen and fibrin degradation products. The mean infarct related regional third ejection fraction was 46% for patients with grade 2 or 3 reperfusion and 35% for those with grade 0 or 1. Ventricular fibrillation occurred in six (12%) patients during the infusion of tissue plasminogen activator, but no late ventricular fibrillation occurred. Bleeding was minimal, reocclusion occurred in three patients, and four patients died from cardiac causes. Recombinant tissue plasminogen activator is an effective thrombolytic agent which produces better reperfusion rates after a 50 or 100 mg dose than after a 20 mg dose. The effect on the systemic fibrinolytic system is dose dependent. Successful reperfusion results in improvement of left ventricular function.
Adult↗
Thrombolytic therapy for myocardial infarction.
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Anistreplase↗
Assessment of a device for trans-telephonic control of defibrillation.
The safety and efficacy of a device allowing the trans-telephonic control of defibrillation have been assessed in 32 attempted defibrillations performed in 29 patients. The initial rhythm was atrial fibrillation in 27; ventricular tachycardia in 4; and ventricular flutter in 1. Satisfactory voice and ECG transmission were established in all cases. The mean time taken by the patient unit to dial and activate the base station was 20.3 seconds. The mean defibrillator charge time was 5.5 seconds to 50 joules and 9.3 seconds to 360 joules. A total of 84 synchronised and 5 unsynchronised shocks were delivered satisfactorily. Lay persons were trained to use the patient unit, and were able to operate the device at home. This device has the potential for rapid defibrillation of patients who develop ventricular fibrillation outside hospital.
Adult↗
Fourier analysis of ventricular fibrillation and synchronization of DC countershocks in defibrillation.
Spectral analysis of the first 40 seconds of ventricular fibrillation confirmed the presence of a large periodic component in fibrillation, with a dominant frequency of 9.9 +/- 0.7 Hz and a narrow bandwidth. To determine whether less energy was required for defibrillation at any particular phase of the ventricular fibrillation cycle, the authors studied the effect of synchronization of the countershock to the peaks and troughs of the ventricular fibrillation waveform in 12 dogs anesthetized with sodium pentobarbitone (35 mg/kg iv). There was no significant difference in threshold-delivered energy or threshold-delivered current between shocks synchronized to the peaks of ventricular fibrillation, shocks synchronized to the troughs of ventricular fibrillation, and unsynchronized shocks.
Animals↗
Myocardial infarction in pregnancy.
Three cases of myocardial infarction occurring in the third trimester of pregnancy are presented. The method of delivery in each case was individualised with no maternal or fetal mortality. Each patient had significant risk factors for coronary arterial disease or thrombosis. One patient had normal coronary arteries demonstrated at coronary arteriography.
Adult↗
Death and damage caused by multiple direct current shocks: studies in an animal model.
Patients who require multiple defibrillator shocks have a poor prognosis. In healthy greyhounds the acute mortality increased as the number of transthoracic shocks (400 J) applied increased (one shock 0/6: five shocks 8/18: 10 shocks 12/17 dogs died acutely from asystole or electromechanical dissociation). The appearance on electron microscopy of the myocardium of these dogs showed few specific abnormal features to account for the total contractile failure that occurs in these dogs. In the survivors, significant ST segment elevation was recorded from the precordial leads of the dogs receiving five and 10 shocks, but not those receiving a single shock. At three days there was significantly more macroscopic cardiac damage in the 10-shock (13.1 +/- 1.8 g) than in the five-shock (7.2 +/- 2.0) group (P less than 0.05). One shock caused little damage. Hence a single high-energy shock was well tolerated in this model. Multiple shocks caused cardiac injury and acute pump failure. These studies indicate the need to reassess why patients die following multiple shocks, and re-emphasise the need for optimized first-shock effectiveness.
Animals↗
Effect of nifedipine on arrhythmias in the acute phase of myocardial infarction.
In a double-blind placebo-controlled trial to study the effect of nifedipine on ventricular arrhythmias among patients with acute myocardial infarction, 434 patients with suspected myocardial infarction were randomized within 6 h from the onset of chest pain to treatment with nifedipine (p = 217) or placebo (p = 217). During the 48-h treatment period, a 10-mg capsule containing active drug or placebo was administered sublingually every 4 h for 24 h, then orally every 4 h for the next 24 h. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). Twenty-four hour ECG tape analysis during 1-5 h from onset of chest pain showed that there was no significant difference in the number of patients with ventricular ectopics, ventricular couplets, ventricular tachycardia (3-9 beats), self terminating or sustained ventricular tachycardia between the two treatment groups. Also during the greater than 5-24 h from onset of chest pain, the numbers of patients with ventricular ectopics, multifocal, bigeminal or couplets, self-terminating ventricular tachycardia or sustained ventricular tachycardia did not differ significantly. However, there was a significant reduction in the number of patients with short runs of ventricular tachycardia (3-9 beats) in the nifedipine-treated group. There was no significant difference among patients with ventricular fibrillation between the two treatment groups.
Adult↗
Effect of nifedipine on enzymatically estimated infarct size in the early phase of acute myocardial infarction.
In a double blind placebo controlled trial, 434 patients with suspected myocardial infarction were randomised to treatment with nifedipine (n = 217) or placebo (n = 217) within six hours from the onset of chest pain. During the treatment period of 48 hours, a 10 mg capsule containing nifedipine or placebo was given sublingually every four hours for 24 hours, then orally every four hours for the next 24 hours. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). The median delay time to intervention with nifedipine in patients with acute myocardial infarction was 111 minutes. Infarct size was assessed by the estimation of release of creatine kinase isoenzyme MB and creatine kinase from blood samples taken every four hours for 48 hours. The total mean (SEM) creatine kinase MB released was 406.4 (27.2) IU/l in the nifedipine group and 345.7 (20.5) IU/l in the placebo group. Total mean (SEM) creatine kinase released was 2749.6 (165.1) IU/l in the nifedipine group and 2698.4 (145.9) IU/l in the placebo group. In hospital mortality was similar for both the nifedipine and placebo groups (6.6% and 5.8% respectively). Treatment with nifedipine in the early phase of acute myocardial infarction seems to have no effect on enzymatically measured infarct size.
Aged↗
Thallium scintigraphy in patients with angina at rest.
Sixty six patients with angina at rest were investigated by exercise electrocardiography, thallium scintigraphy, and coronary arteriography. A positive exercise electrocardiogram was highly predictive (93%) but poorly sensitive (52%) of coronary artery disease (greater than or equal to 50% stenosis). Thallium scintigraphy was as predictive of the presence of coronary artery disease (91%) but was also highly sensitive (91%). The diagnostic contribution of the thallium scan was greatest in those patients with an inconclusive exercise electrocardiogram without Q waves.
Adrenergic beta-Antagonists↗