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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Observations during 935 anesthesias for implantation or revision of permanent pacemakers are presented. Using different methods of anesthesia we found the light halothane anesthesia introduced by inhalation to be best, provided that only atropine was used for premedication. Applying this method we saw asystolies or ventricular fibrillation in 3% of all cases--3 patients (i.e. 0.4%) died in tabula. Tachycardia (2.4%) occuring mostly during the introduction period were successfully treated by verapamil or practolol. Hypotension (5.4%) mostly took place in the course of anesthesia after implantation of the pacemaker. This depression may be due to a normalisation of the enhanced stroke volume whedication with pethidine or induction with propanidid was followed by comparatively more complications such as exitus letalis (2% resp. 1.5%), cardiac arrest (6.5% resp. 9%) and hypotension (24% resp. 10.5%). Regional anesthesia did not bring specific advantages. The good experiences with soft halothane anesthesia for implantations or revisions of pacemakers include 125 high risk patients (ASA classification IV to VII).
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PMID:[Anesthesia in pacemaker implantation. Experiences in 935 cases of anesthesia for the implantation or revision of a cardiac pacemaker]. 86 62

Twenty-one long-term survivors of out of hospital sudden cardiac death due to ventricular fibrillation underwent radionuclide angiography and myocardial imaging with thallium-201. In 13 patients images were obtained at rest and after maximal treadmill exercise; 11 of these 13 (85 percent) had an image defect in one or both studies. Eleven of the 21 patients (52 percent) had a defect in the image obtained at rest. The magnitude of myocardial image defects was typically great; some patients had an image abnormality without other clinical evidence (angina, S-T depression) of ischemia. The mean ejection fraction, assessed in 16 patients with radionuclide angiography, was 0.41 +/- 0.15 (standard deviation); in 5 of the 16 ejection fraction was normal (more than 0.50) and in 3 it was severely abnormal (less than 0.25). Thus, noninvasive radionuclide studies defined a broad spectrum of ischemic and ventriculographic abnormalities in survivors of sudden cardiac death. Further application of these noninvasive studies may identify those at high risk.
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PMID:Myocardial imaging and radionuclide angiography in survivors of sudden cardiac death due to to ventricular fibrillation: preliminary report. 87 Nov 11

The fall in the ventricular fibrillation threshold during the first half an hour following ligation of the descending branch of the left coronary artery in dog was not influenced by the i.v. injection of trimecain (Mesokain Spofa). On the other hand, an i.v. injection of methypranol (Trimepranol Spofa) given prior to ligation increased the level of ventricular fibrillation threshold 3 to 4 times compared to control value before occlusion in all 10 studied dogs. Depression of the beta-blocking adrenergic activity may thus prevent the occurrence of ventricular fibrillation in acute myocardial ischaemia.
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PMID:Prevention of ventricular fibrillation in experimental myocardial infarction. 92 60

Cardiac arrest developed in two patients after the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal.
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PMID:Cardiac arrest due to oral potassium administration. 111 63

Depressed postoperative myocardial performance (low output syndrome) requiring inotropic drugs or balloon counterpulsation is due to subendocardial ischemic damage. Before July, 1972, we needed inotropic drugs in 30 to 52 per cent of 189 patients undergoing coronary revascularization or aortic or mitral valve replacement in whom we used ischemic arrest, profound topical hypothermia, and ventricular fibrillation. The mortality rate ranged from 10 to 17 per cent. Our experimental studies show that morbidity and death in such cases are caused by ischemic injury to the heart resulting from inadequate myocardial protection during bypass. Based on these experimental studies, we have, since July, 1972, employed the following principles clinically: (1) Maintain beating empty heart whenever possible; (2) maintain adequate coronary perfusion pressure (less than 80 mm. Hg); (3) avoid extreme hemodilution; (4) avoid ventricular fibrillation; (5) avoid prolonged hypothermic arrest, limiting ischemic periods to less than 15 minutes; (6) repay myocardial ischemic oxygen debt with total (vented) bypass; and (7) optimize DPTI/TTI (supply/demand ratio) pre- and postoperatively. These principles were followed in 189 consecutive operations, and postoperative inotropic drugs were needed in only 12. The principles were violated in 4 of the 12 patients (6 per cent), and 5 others had identifiable causes of myocardial depression; low output syndrome was unexplained in only 3 patients (1.7 per cent).
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PMID:Depressed postoperative cardiac performance. Prevention by adequate myocardial protection during cardiopulmonary bypass. 118 89

Short-term results of aggressive surgical management were compared with results of medical management in forty-three patients with preinfarction angina admitted to the coronary-care unit (CCU) over an 18 month period. These patients were selected from 1,609 consecutive admissions to the CCU because they met strict criteria for preinfarction angina: severe chest pain at rest, ST-segment elevation or depression during pain which subsided rapidly after cessation of pain, and normal serum enzymes (CPK, SGOT, and LDH). Twenty-three patients had coronary angiography, done with operating room and pump standby. One patient, who had total occlusion of the left main coronary artery, died during the study. Twenty-one of the remaining patients were considered surgical candidates, and were treated immediately after angiography with 1 to 3 vein bypass grafts. There was one late postoperative death and, of the 20 survivors, 2 had ECG evidence of acute myocardial infarction and one had mild angina at time of discharge. In contrast, of the 21 patients treated medically, 13 sustained acute MI, resulting in 8 instances of congestive heart failure and 4 cases of ventricular fibrillation. Four patients died in cardiogenic shock. With the use of rigid criteria, a small subgroup of patients with variant angina at high risk of developing AMI has been identified and categorized as having preinfarction angina. Our experience suggests that aggressive surgery immediately following coronary angiography offers a lower incidence of MI, morbidity, and death than does medical management.
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PMID:Management of preinfarction angina. Evaluation and comparison of medical versus surgical therapy in 43 patients. 124 46

This study investigated the influence of defibrillator shocks delivered directly over a coronary artery, independent of ventricular fibrillation, on cardiac hemodynamics. Thirty-six open chest, halothane anesthetized pigs were randomized to receive six shocks at one of 5.0, 7.5, or 10.0 joules (J). Shocks were delivered between two mesh electrodes (Medtronic TX-7) sutured onto the epicardium, one over the left anterior descending coronary artery and the second directly opposite on the posterobasal ventricular surface. Shock delivery was synchronized to the R wave of the cardiac cycle, to reduce the risk of inducing fibrillation, with a 5-minute stabilization period between successive shocks. Pressure from the left ventricle, the left anterior descending coronary artery, distal to the mesh electrode and the left circumflex (control) artery and contractility in the regions perfused by both arteries were measured. The shocks invariably produced an immediate (2-second postshock), but transient, depression in systolic pressure of the same magnitude for the left anterior descending coronary artery, circumflex artery and the left ventricle that recovered by 5-minute postshock. There was no dose dependent relationship to energy. Also there was no clear difference in myocardial wall motion between the area perfused by the left anterior descending coronary artery and that perfused by the circumflex artery. These results suggest that shocks up to 10 J delivered over an epicardial artery do not cause arterial spasm and do not compromise coronary artery blood flow.
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PMID:Effects of defibrillation shocks delivered directly over a major coronary artery. 127 39

Propafenone is an antiarrhythmic agent with fast sodium channel, calcium channel, and beta-adrenergic receptor blocking properties. The effects of propafenone on arrhythmias, free intracellular calcium and left ventricular performance were studied using perfused rat hearts during (i) pacing-induced ventricular fibrillation and (ii) infusion with 2.65 x 10(-6) M, 5.3 x 10(-6) M and 7.9 x 10(-6) M propafenone hydrochloride (corresponding to approximately 1, 2 and 3 mg kg-1 body weight). A bolus of 1 mg kg-1 propafenone during ventricular fibrillation resulted in a decrease in intracellular calcium, with subsequent conversion to sinus rhythm. In perfused hearts with sinus rhythm propafenone produced a dose-dependent decrease in heart rate and myocardial oxygen consumption together with a rise in left ventricular diastolic pressure, and diastolic [Ca2+]i, indicative of depression of left ventricular function. We conclude that a bolus of propafenone during ventricular fibrillation leads to a decrease in [Ca2+]i preceding conversion to sinus rhythm. In rat hearts with sinus rhythm the depressive effects of propafenone on [Ca2+]i are dose dependent.
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PMID:Effects of propafenone on pacing-induced ventricular fibrillation and intracellular calcium in rat hearts. 133 67

To determine the incidence and characteristics of ventricular dysrhythmias (premature ventricular contractions greater than 30/min, ventricular tachycardia greater than or equal to 3 beats, and ventricular fibrillation) and whether a relationship exists between ventricular tachycardia and myocardial ischemia in patients undergoing coronary artery bypass graft surgery, we continuously monitored 50 patients for 10 perioperative days using two-lead electrocardiography. Electrocardiographic changes consistent with ischemia were defined as a reversible ST depression greater than or equal to 1.0 mm, or ST elevation greater than or equal to 2.0 mm from baseline, lasting at least 1 minute. Ventricular dysrhythmias developed in 10% of patients preoperatively and in 16% intraoperatively before bypass surgery. The highest incidence occurred postoperatively, with ventricular dysrhythmias developing in 66% of patients (22% to 44% of patients on any postoperative day 0 to 7). Premature ventricular contractions were greater than 30/hr in 6% of patients preoperatively, in 8% intraoperatively before bypass, and in 34% postoperatively (6% to 23% of patients on any postoperative day). Twenty-nine patients (58%) developed 76 verified episodes of greater than or equal to 3 beats of ventricular tachycardia. Ventricular tachycardia occurred in 6% of patients preoperatively (four episodes), in 8% of patients intraoperatively prior to bypass (four episodes), and 54% of patients postoperatively (5% to 21% on any postoperative day). No patient developed ventricular fibrillation. All postoperative ventricular tachycardia episodes (after tracheal extubation) were asymptomatic. Postoperatively, 48% of patients developed ischemia, compared with 12% preoperatively and 10% intraoperatively before bypass surgery. Only 5 of 68 (7%) postoperative ventricular tachycardia episodes occurred within 3 hours of an ischemia episode.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular dysrhythmias in patients undergoing coronary artery bypass graft surgery: incidence, characteristics, and prognostic importance. Study of Perioperative Ischemia (SPI) Research Group. 137 Mar 63

In open chest anaesthetised dogs, dofetilide increased the ventricular effective refractory period over the dose range 1-100 micrograms/kg i.v. and the ventricular fibrillation threshold at doses between 3-100 micrograms/kg and was 80-1000 times more potent than sematilide, racemic sotalol, d-sotalol or quinidine. The maximal increases in ventricular fibrillation threshold induced by sematilide and quinidine were less than that induced by the other drugs. A change in the character of the induced arrhythmia from true ventricular fibrillation to a rapid ventricular flutter, with frequent spontaneous conversion, was observed following all drugs. No adverse haemodynamic effects of dofetilide, sematilide or d-sotalol were observed, but quinidine induced marked cardiac depression and racemic sotalol also impaired left ventricular contractility. All drugs reduced heart rate, though the effect of racemic sotalol was clearly greater than that of the other agents. Dofetilide is a potent class III antiarrhythmic agent with antifibrillatory properties and a favourable haemodynamic profile.
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PMID:Electropharmacology of dofetilide, a new class III agent, in anaesthetised dogs. 139 82


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