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Biomedical subjects

A A Adgey

Publications and source records attributed to A A Adgey.

At least 19 recordsLinked to original sources

Failure of countershock-type pulses in vitro to adversely alter mitochondrial oxidative phosphorylation.

STUDY OBJECTIVE: The aim of the study was to investigate a potential mechanism of myocardial injury after DC countershock. The effect of countershock-type electrical discharges on rabbit heart mitochondrial oxygen consumption was measured in vitro using a novel respiration cell. MEASUREMENTS AND MAIN RESULTS: Mitochondria were isolated from the hearts of adult Dutch and New Zealand White rabbits. Single rectangular shocks (voltage gradients 20 to 80 V/cm; 5 ms duration) caused no significant changes in state 3 oxygen consumption in standard incubation medium. Single and multiple defibrillator shocks (critically damped sine waveform; 5 ms duration) with peak voltage gradients of 242 to 659 V/cm similarly had no significant effect on state 3 oxygen consumption. CONCLUSION: At voltage gradients similar to and greater than those causing myocardial cell injury and necrosis, electrical discharges do not directly depress mitochondrial function. Therefore, the reduction in mitochondrial oxygen consumption observed following transthoracic shocks in vivo may invoke other mechanisms (eg, intracellular calcium influx, high circulating noradrenaline, or free radical formation in the intact heart).

Animals

Oxidative metabolism and myocardial blood flow changes after transthoracic DC countershocks in dogs.

Changes in oxidative metabolism and myocardial blood flow were investigated in adult greyhounds following transthoracic shocks from a DC cardiac defibrillator (400 Joules stored energy, damped sine wave, 0.5 min intervals). Myocardial lactate extraction became negative maximally at 1 min, following both two (mean -24% +/- SEM24) or five (-193% +/- 148) shocks and returned to baseline by 6-15 min. Transient reductions were also observed in myocardial extraction of pyruvate and free fatty acids but not glucose. Myocardial necrosis assessed at 4 h following the shocks was 0.05 g (+/- 0.03) after two shocks, 6.5 g (+/- 1.5) after five shocks and zero in controls. Mean peak noradrenaline levels in arterial (785 +/- 319 pg.ml-1) and coronary sinus (916 +/- 313 pg.ml-1) blood at 1 min after five shocks were higher than after 0 shocks (82 +/- 33 pg.ml-1 and 201 +/- 63 pg.ml-1 respectively), P < 0.05. Great cardiac venous blood flow was measured by a thermodilution technique, with continuous infusion of 0.9% saline, before, during and after five shocks. Mean blood flow fell from 47 +/- 13 ml.min-1 to a minimum of 36 +/- 7 ml.min-1 during shocks, and then rose to 83 +/- 17 ml.min-1 at 2 min after the fifth shock (P < 0.05). Following damaging countershocks, oxidative metabolism is depressed, in keeping with a primary disturbance of mitochondrial function. These metabolic changes are not secondary to ischaemia, since an increase in blood flow in the great cardiac vein (GCV) is observed. Vasodilatation of the coronary vascular bed must occur to account for this.

Analysis of Variance

The accuracy of decision-making of a semi-automatic defibrillator during cardiac arrest.

The accuracy of decision-making of a semi-automatic defibrillator was assessed at 57 cardiac arrests in 55 patients. The initial rhythm was ventricular fibrillation at 40 arrests and was correctly identified in 37 (sensitivity 92.5%). In the other 17 arrests initial rhythms were not ventricular fibrillation and 16 were correctly identified (specificity 94%). Continuous electrocardiographic recordings of the arrests were analysed in 8-12 s segments: of 432 segments showing ventricular fibrillation, 352 were correctly identified (sensitivity 81%); 3895 of 4139 segments showing rhythms other than ventricular fibrillation were correctly identified (specificity 94%). The percentage accuracy of detection of ventricular fibrillation varied from 0-100% (mean 91%) and for non-ventricular fibrillation from 51-100% (mean 92%). When 104 segments of ventricular fibrillation and 470 segments of non-ventricular fibrillation with cardiopulmonary resuscitation artefact were excluded from the analysis, a sensitivity of 91% and specificity of 96% were obtained. Thus the detection of cardiac arrest rhythms using a microprocessor based detection system for patients with cardiac arrest has a high sensitivity for ventricular fibrillation and specificity for non-ventricular fibrillation.

Cardiopulmonary Resuscitation

Recurrent ventricular arrhythmias complicating myocardial infarction in the presence of phaeochromocytoma.

After an acute myocardial infarction a 49 year old man developed late recurrent severe ventricular arrhythmias coincident with transient hypertensive episodes. A phaeochromocytoma was diagnosed on the basis of the urinary concentration of catecholamines and computerised tomography of the adrenal glands. After stabilisation of his cardiac rhythm and blood pressure with alpha and beta adrenergic blockade and anti-arrhythmic treatment the right adrenal gland, which contained the tumour, was successfully resected. The diagnosis of a phaeochromocytoma should be considered when recurrent ventricular arrhythmias are associated with intermittent hypertension after myocardial infarction.

Adrenal Gland Neoplasms

Mortality within hospital after resuscitation from ventricular fibrillation outside hospital.

OBJECTIVE: To determine factors related to mortality within hospital after successful resuscitation from ventricular fibrillation outside hospital by a mobile coronary care unit manned by a physician. DESIGN: Retrospective review of records of patients resuscitated and admitted to hospital between 1 January 1966 and 31 December 1987. SETTING: Mobile coronary care unit, coronary care unit, and cardiology department. PATIENTS: 281 patients (227 male), aged 14-82 (mean 58) successfully resuscitated from ventricular fibrillation outside hospital of whom 182 (65%) developed ventricular fibrillation before the arrival of the mobile coronary care unit. The aetiology of ventricular fibrillation was acute myocardial infarction in 194 patients (69%), ischaemic heart disease without infarction in 71 (25%), and other or unknown in 16 (6%). MAIN OUTCOME MEASURES: Death within hospital. RESULTS: There were 91 deaths in hospital (32%). Factors on univariate analysis significantly associated with increased mortality were patient age > or = 60 years, previous myocardial infarction or cerebrovascular disease, prior digoxin or diuretic treatment, collapse without prior chest pain or with pain lasting 30 minutes or less, defibrillation delayed by > or = 5 min, > or = four shocks required to correct ventricular fibrillation, left ventricular failure or pulmonary oedema and cardiogenic shock after successful defibrillation, and coma on admission to hospital. On multivariate analysis the most important factors (in rank order) were cardiogenic shock after defibrillation, coma on admission to hospital, age > or = 60 years and the requirement for four or more shocks to correct ventricular fibrillation. CONCLUSIONS: The in-hospital mortality of patients resuscitated from ventricular fibrillation outside hospital was related to patient characteristics before the cardiac arrest and to the immediate haemodynamic and neurological status after correction of ventricular fibrillation as well as to factors at the resuscitation itself. The in-hospital mortality of this study compares favourably with the results obtained by units staffed by paramedical workers and emergency medical technicians, although 35% (99/281) of the patients had ventricular fibrillation after the arrival of the mobile unit and defibrillation was thus rapid.

Adult

Frequency analysis of ventricular fibrillation and resuscitation success.

In 56 patients, frequency analysis of the electrocardiogram of ventricular fibrillation exhibited power spectra with a distinct dominant frequency. The greatest success for resuscitation from ventricular fibrillation is recorded when ventricular fibrillation develops after the patient comes under coronary care. Of the 41 patients in whom the onset and first 8 s of ventricular fibrillation were artefact-free the mean dominant frequency of primary ventricular fibrillation (no cardiogenic shock or cardiac failure) in 21 patients was 6.2 +/- 0.2 Hz, significantly higher than the mean dominant frequency of the first 8 s of secondary ventricular fibrillation (cardiogenic shock or heart failure) (4.0 +/- 0.2 Hz, 20 patients, p = 0.0001). In these patients the peak-to-trough amplitude (ECG) of the first 8 s of ventricular fibrillation was similar in both primary and secondary ventricular fibrillation as was the mean duration of ventricular fibrillation prior to the first DC shock. There was a significantly lower success rate for resuscitation from secondary ventricular fibrillation (6 of 20 patients) compared with resuscitation from primary ventricular fibrillation (18 of 21 patients, chi 2 17.8, p = 0.001). Of the remaining 15 patients who were collapsed between 3 and 20 min before the arrival of the mobile coronary care unit, the dominant frequency of the first 8 s of ventricular fibrillation fell with increased duration of collapse (from 5.5 Hz at 3 min to a mean of 2.1 Hz at 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

A cellular transtelephonic defibrillator for management of cardiac arrest outside the hospital.

A cellular transtelephonic defibrillator facilitates early defibrillation in remote areas and involves electrocardiographic diagnosis and defibrillation control by a physician remote from but in voice contact with the patient-unit operator. The patient unit contains a microprocessor, microphone, defibrillator, electrocardiogram/defibrillator electrode pads and cellular telephone. Activation of the patient-unit initiates automatic dialing and contact with the remotely sited base station within 35 to 50 seconds. The physician at the base station identifies the rhythm and controls defibrillator charging and discharge. The minimal interaction required between the system and the local operator makes it suitable for use by minimally trained first responders. The cellular transtelephonic defibrillator has been tested in 211 calls responded to by a physician-manned mobile coronary care unit over distances up to 15 miles in an urban area. Satisfactory electrocardiographic transmission and voice communication were established in 172 of 211 calls (81.5%). In 39 (18.5%), connection with the base station either could not be established or maintained mainly because of geographic location or battery failure. One hundred direct current shocks of 50 to 360 J were effectively administered to 22 patients with 48 episodes of ventricular fibrillation or ventricular tachycardia with successful correction of 46 of 48 episodes using 1 to 4 shocks per episode. Widespread distribution of such devices could improve survival in patients with cardiac arrest outside the hospital.

Ambulances

Congestive heart failure due to aortic incompetence with intestinal infarction due to endarteritis obliterans.

A 27-year-old man with congestive heart failure due to aortic incompetence and subsequent intestinal infarction was found at laparotomy to have extensive necrosis of the bowel due to proliferative endarteritis. Symptoms resolved following treatment with prednisolone and cyclophosphamide, and replacement of the aortic valve. The sub-total occlusion produced by endarteritis obliterans may lead to acute end-organ infarction if cardiac output is reduced.

Adult

One-year follow-up after recombinant tissue plasminogen activator administered to patients with acute myocardial infarction.

Of 106 patients seen within 4 h of chest pain with 107 episodes of acute myocardial infarction, nine died before or during hospitalization mainly from cardiogenic shock, and four died during the next year, three were sudden deaths. The 93 survivors were reviewed at a mean of 53 (range 49-70) weeks after infarction. Of these 93, 18 had had attempted angioplasty (successful in 12) and 15 had had coronary artery bypass grafting (including one patient who had coronary artery bypass grafting performed after unsuccessful angioplasty). The remaining 61 patients continued on medical therapy only. During the one-year follow-up two patients suffered reinfarction and a further 22 had one or more cardiac admissions, mostly for chest pain. At review, 22 patients had angina (16 New York Heart Association Grade I or II) and five dyspnoea (all NYHA Grade II). Forty-three patients were taking oral nitrates, 53 were receiving calcium antagonists, 54 were using betablocking agents and 73 used anti-platelet agents. However, many of these patients continued on anti-anginal therapy prophylactically after their myocardial infarction, without continuing chest pain. Thus after recombinant tissue plasminogen activator therapy and following hospital discharge the mortality rate for patients with acute myocardial infarction was four out of 97 (4.1%) and reinfarction rate among survivors was two out of 93 (2.2%). Although the incidence of cardiac symptoms was low this may be partly due to the high incidence of angioplasty and coronary artery grafting, together with the use of anti-anginal agents.

Adult

Which factors determine the development of late potentials after first myocardial infarction? A multifactorial analysis.

A multifactorial analysis was performed to study the factors that contributed to the occurrence of late potentials on the signal-averaged electrocardiogram in 106 consecutive patients with a first myocardial infarction. Ninety-three (88%) patients received intravenous thrombolytic therapy within 6 hours of symptom onset. Thirty-two (30%) patients had a late potential on the signal-averaged electrocardiogram on day 6, including 17 of 31 (55%) in whom the infarct-related artery was occluded and 15 of 75 (20%) in whom it was patent (P = 0.0004). Twenty-three variables were analyzed by a multifactorial stepwise regression analysis. Predictors of a late potential were (1) an occluded infarct-related coronary artery (t = -3.653, P = 0.0004) and (2) the extent of myocardial necrosis as indicated by the peak serum lactate dehydrogenase level (t = 3.094, P = 0.0025). The lower incidence of late potentials when the infarct-related coronary artery was patent was independent of left ventricular ejection fraction and peak enzyme levels after infarction.

Arrhythmias, Cardiac

Determinants of successful transthoracic defibrillation and outcome in ventricular fibrillation.

OBJECTIVE: To examine factors determining defibrillation success and outcome in patients with ventricular fibrillation. DESIGN: Observational prospective study of age, sex, transthoracic impedance, site of cardiac arrest, ventricular fibrillation duration and amplitude, primary or secondary ventricular fibrillation, aetiology, number of shocks to correct ventricular fibrillation, and drug treatment. SETTING: A teaching hospital and a mobile coronary care unit with a physician. PATIENTS: 70 consecutive patients (50 male, 20 female) mean age 66.5 years. INTERVENTIONS: Before the first countershock was administered transthoracic impedance using a 30 kHz low amplitude AC current passed through 8 cm/12 cm self-adhesive defibrillator electrode pads applied in the anteroapical position was measured. The first two shocks were 200 J delivered energy (low energy) and further shocks of 360 J (high energy) were given if required. MAIN OUTCOME MEASURES: Countershock success and outcome from ventricular fibrillation. RESULTS AND CONCLUSIONS: First shock success was significantly greater in inhospital arrests (37/53) than in out-of-hospital arrests (5/17) and in those receiving antiarrhythmic treatment (13/15, 86.7%) v (27/51, 52.9%). Transthoracic impedance was similar in those who were successfully defibrillated with one or two 200 J shocks (98.7 (26) omega) and those who required one or more 360 J shocks (91.4 (23) omega). Success rates with two 200 J shocks were similar in those patients with "high" transthoracic impedance (that is, greater than 115 omega) and those with transthoracic impedance (less than or equal to 115 omega) (8/12 (67%) v 44/58 (76%]. Fine ventricular fibrillation was significantly more common in the patients with a transthoracic impedance of greater than 95 omega (41% (13/32] than in those with a transthoracic impedance less than or equal to 95 omega (13% (5/38]. Death during arrest was significantly more common in patients who needed high energy shocks (14/18 (78%] than in those who needed low energy shocks (16/52 (31%]. Multiple regression analysis identified ventricular fibrillation with an amplitude of greater than or equal to 0.5 mV, age less than or equal to 70 years, and arrests that needed less than or equal to two shocks for defibrillation, in rank order as independent predictors of survival to discharge.

Aged

Factors determining success and energy requirements for cardioversion of atrial fibrillation: revised version.

Factors thought to affect the success of and energy requirements for cardioversion of atrial fibrillation were studied in 80 (49 male, 31 female) patients aged 21-88 (mean 61.5 years). Transthoracic impedance was measured in advance of the countershock using a 30 kHz low amplitude AC current passed through self-adhesive ECG/defibrillator pads (diameters 8 and 12 cm) applied to the chest in the antero-posterior (AP) position in 57 patients and the anteroapical (AA) position in 23 patients. Mean transthoracic impedance for all patients was 69.3 +/- 16 (SD) ohms (range 39-131 ohms), but transthoracic impedance was significantly greater in the AA than the AP position (75.4 +/- 13 vs. 66.7 +/- 16 ohms, p = 0.02). Initial energy was 50 J (delivered) and was gradually increased to a maximum of 360 J if required. Cardioversion was successful in 73 of 80 (91.2 per cent), and low energy shocks (< or = 200 J) were successful in 45 of 80 (56.2 per cent) patients. Using single factor analysis, sex, left atrial enlargement, electrode pad positions, aetiology of atrial fibrillation, presence of left ventricular failure, and prior treatment with verapamil or beta-adrenergic blockers were not significant determinants of cardioversion success or success of low energy shocks but prior treatment with digoxin was, both for cardioversion success and success at low energies. In patients with transthoracic impedance < or = 70 ohms, low energy shocks were more often successful (33 of 50, 66 per cent) than in patients with transthoracic impedance > 70 ohms (12 of 30, 40 per cent), p = 0.04. Using univariate analysis, cardioversion success with low energy shocks was not only significantly associated with prior treatment with digoxin but also with the duration of atrial fibrillation (24 hours to less than one month and one month to three years) and for shocks of < or = 100 J, with prior treatment with amiodarone. Multifactorial linear regression analysis selected, in rank order, only duration of atrial fibrillation of 24 hours to less than one month and one month to three years as significant predictors of both cardioversion success irrespective of shock strength, and success of low energy shocks.

Adult

Long-term survival after resuscitation from ventricular fibrillation occurring before hospital admission.

Factors related to long-term (post-discharge) outcome following successful resuscitation from pre-hospital ventricular fibrillation by a physician-manned mobile coronary care unit were studied. Between 1 January 1966 and 31 December 1987, 190 patients were resuscitated from pre-hospital ventricular fibrillation (158 male; mean age 56 years). The aetiology of ventricular fibrillation was acute myocardial infarction in 131 patients (69 per cent), ischaemic heart disease without infarction in 48 (25 per cent) and other or unknown in 11 (6 per cent). Predicted actuarial survival rates at 1, 2, 5, 10 and 20 years were 76 per cent, 66 per cent, 41 per cent, 27 per cent and 12 per cent respectively. Of 128 recorded deaths over 20 years, 85 per cent were cardiac and 48 per cent were defined as sudden death outside hospital. Factors significantly associated with increased long-term mortality (p less than 0.05), based on analysis of 10 year actuarial life tables using the Lee-Desu statistic were ventricular fibrillation due to ischaemic heart disease without infarction rather than acute myocardial infarction, a history of previous myocardial infarction, a history of hypertension, digoxin and diuretic therapy before ventricular fibrillation and digoxin as discharge medication, and failure to stop smoking after discharge from hospital by patients who had been smoking prior to ventricular fibrillation. In addition, Cox's regression analysis showed that patient age greater than or equal to 60 years was significantly associated with increased long-term mortality. On multivariate analysis, factors independently associated with increased long-term mortality were ventricular fibrillation occurring before 1977, previous myocardial infarction or hypertension and digoxin as discharge medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Out-of-hospital ventricular fibrillation in patients under the age of 40 years and the long-term prognosis.

Among patients with ventricular fibrillation outside hospital seen by our mobile coronary care unit between 1967 and 1988, 28 were aged less than 40 years (range 12-39, mean 28). Coronary artery disease was present in 11 (39 per cent) and was the most common single cause, although none of these patients was aged less than 28 years. Of 15 patients with cardiac disease, only four (27 per cent) had previously sought medical advice. Nineteen patients (68 per cent) collapsed without preceding symptoms. Survival to reach hospital was significantly associated with bystander cardiopulmonary resuscitation and early defibrillation. Eleven patients (39 per cent) survived to hospital discharge, of whom seven remain alive after 2 1/2 to 21 1/2 years, five without symptoms. Thus, as demonstrated for older patients, coronary artery disease is an important cause of sudden death in this age group, and bystander cardiopulmonary resuscitation and early defibrillation are important for survival. Most of these patients collapse without warning and are not already known to have cardiac disease.

Adolescent

Thrombolytic therapy within one hour of the onset of acute myocardial infarction.

Between 1986 and 1988, 239 consecutive patients with acute myocardial infarction received thrombolytic therapy up to 285 minutes after onset of symptoms; in 39 (17 with anterior infarction, 21 inferior, one lateral infarction) recombinant tissue plasminogen activator or anistreplase was administered a mean of 51 minutes (range 20-60 minutes) after the onset of symptoms. The patency rates (26 of 30; 87 per cent), rapid ST segment resolution (36 of 38; 95 per cent) and QRS score of less than or equal to 3 (28 of 38; 74 per cent) were statistically significantly higher for those seen and treated in the first hour in comparison with those seen and treated later. For those treated within the first hour mean peak creatine kinase was 1264 U/l for those with TIMI grade 2 or 3 (partial or complete perfusion) compared with 3005 U/l for those with TIMI grade 0 or 1 (no perfusion or penetration without perfusion) (p = 0.02): mean peak creatine kinase-MB for those with TIMI grade 2 or 3 perfusion was 115 U/l compared with 312 U/l for those with TIMI grade 0 or 1 (p = 0.01). Four of the 39 patients developed ventricular fibrillation following thrombolytic therapy, three within 24 hours of infarction and one following reinfarction on day 15. There were no significant bleeding complications. One patient died. Thrombolytic therapy within 1 hour of the onset of symptoms led to a very high angiographic patency rate, rapid ST segment resolution with preservation of left ventricular function. This therapy is without significant complications.

Anistreplase

The initial electrocardiogram in patients seen by a mobile coronary care unit.

The advent of thrombolytic therapy for patients with suspected acute myocardial infarction has highlighted the importance of the initial electrocardiogram (ECG) in decision making. Thus we analysed the initial ECGs of 94 consecutive cases with suspected myocardial infarction who were seen within six hours after the onset of chest pain by a mobile coronary care unit. The study included 91 patients (three patients admitted twice) (61 male), aged 27-83 years (mean 60.5). Median time from onset of chest pain to arrival of the mobile coronary care unit was 75 minutes (range 15-345), and mean mobile coronary care unit response time was 12.3 +/- 7 (SD) minutes (range 5-45). The majority of cases (65 of 94, 69.1 per cent) were seen within two hours of the onset of symptoms. A final diagnosis of myocardial infarction was made in 48 of 94 (51.1 per cent) cases; 38 had unstable angina and eight other diagnoses. Of the 48 with myocardial infarction the initial ECG showed ST segment elevation in 37, ST depression and or T wave inversion in six, Q waves only in three and left bundle branch block in two. No patient with an initially normal ECG had a myocardial infarction. Thrombolytic therapy was given out of hospital to 33 of 38 patients with ST segment elevation. In seven patients with ST elevation (median delay time to intensive care 60 minutes), rapid resolution of ST segment elevation occurred following thrombolytic therapy and there was no significant elevation of cardiac enzymes, suggesting that the infarct had been aborted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Transient release of lipid peroxides after coronary artery balloon angioplasty.

Free radical production may cause myocardial damage during reperfusion of ischaemic myocardial tissue; when free radicals interact with polyunsaturated fatty acids or their esters, lipid peroxides are produced. A product of lipid peroxidation, malondialdehyde, was measured in 10 subjects with stable angina who underwent angioplasty of a proximal high-grade stenosis (over 90%) of the left anterior descending coronary artery. In all subjects the duration of balloon occlusion was 60 s. Blood was withdrawn from the great cardiac vein immediately before balloon inflation (T0), immediately after balloon deflation (T60), 15 s after balloon deflation (T75), and 1 min after balloon deflation (T120). There was a significant increase in malondialdehyde at T60 compared with T0 for the first balloon inflation (mean increase 0.3 mumol/l [95% confidence limits 0.1, 0.5]), and at both T60 (0.31 mumol/l [0.15, 0.47]) and T75 (0.22 mumol/l [0.04, 0.40]) for the second balloon inflation. This model could be used to assess antioxidant effects of drugs.

Adult

Fourier analysis of ventricular fibrillation of varied aetiology.

Fast Fourier Transform analysis was used to study ventricular fibrillation induced by several different methods in 43 greyhounds anaesthetized with sodium pentobarbitone. The dominant frequency at the body surface of ventricular fibrillation induced electrically in non-ischaemic hearts was initially 9.9 +/- 0.7 Hz, remained above 9 Hz for 70 s and then rapidly fell to 5 Hz. The dominant frequency of ventricular fibrillation induced by acute occlusion (initially 12.3 +/- 0.2 Hz), or by reperfusion (12.2 +/- 0.4 Hz) of the anterior descending branch of the left coronary artery, showed a similar time-course. However, ventricular fibrillation induced by administration of potassium (4.8 +/- 0.8 Hz) or ouabain (7.1 +/- 1.1 Hz) was significantly slower. Fibrillation recorded from the endocardium of the heart initially showed a similar dominant frequency to that recorded at the body surface, but there was no significant fall in frequency over 3.3 mins. There was little difference in the time-course of fibrillation in the non-ischaemic heart recorded directly from the epicardium or from a surface lead. These findings may be of relevance to the poor response to DC countershock after prolonged ventricular fibrillation, hyperkalaemia or cardiac glycosides.

Animals