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

A patient had repetitive ventricular fibrillation preceded by alternating ST segment depression and elevation. The ECG changes were confined to the precordial leads only, reflecting subendocardial and transmural ischemia, respectively. It is speculated that the patient exhibited consecutive episodes of subtotal and total coronary occlusion, both episodes being critical enough to induce lethal arrhythmias.
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PMID:Repetitive ventricular fibrillation preceded by both ST segment depression and elevation during acute myocardial ischemia. 278 22

In general, the cardiovascular system is more resistant to the toxic actions of local anaesthetics than is the central nervous system. However, if sufficient doses and blood levels of local anaesthetics are achieved, signs of profound cardiovascular depression may be observed. Differences exist between local anaesthetics in terms of their relative potential for cardiotoxicity. The CC/CNS ratio for bupivacaine and etiodcaine is less than for lidocaine. In addition, bupivacaine may precipitate ventricular arrhythmias and ventricular fibrillation. Local tissue toxicity can occur following the administration of local anaesthetics. In general, neural tissue appears to be relatively resistant to the irritant effects of local anaesthetic drugs. However, large dosages of chloroprocaine solutions administered intrathecally have been associated with prolonged sensory-motor deficits in a few patients due probably to the low pH and presence of sodium bisulfite in the chloroprocaine solutions. In general, the incidence of toxic reactions to local anaesthetic agents is extremely low. However, as with any class of pharmacological agents, local anaesthetics may cause severe toxic reactions, due usually to the improper use of these drugs.
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PMID:Recent advances in local anaesthesia. 352 4

This is the second of a two-part series on the effects of cognitive stress on cardiovascular disease. This paper reviews the relationship between cognitive stress and cardiovascular reactivity as it relates to the development of atherosclerosis and arrhythmias. In addition, the moderation of cardiovascular reactivity by the opportunity to exercise control over the stressor is discussed. The findings may be summarized as follows. First, recent animal work has suggested that the magnitude of heart rate change in the presence of a conditioned aversive stimulus is positively correlated with the extent of coronary atherosclerosis under diets high and low in atherogenic potential. Second, cardiovascular reactivity in humans may be related to several factors that could have an influence on the pathogenesis of atherosclerosis. These factors include: increased beta-adrenergic driving, increased shearing force on the intimal lining of the vessels, changes in pulsatile flow and the subsequent smooth muscle reparatory process. Cognitive (psychological) stress has also been related to ST segment depression, rate-pressure product changes, and changes in cardiac contractility. Animal studies have shown that the susceptibility to ventricular fibrillation may be enhanced by the presence of a conditioned aversive stimulus and may be reduced through adaptation to the aversive environment. The balance between sympathetic and parasympathetic influences on the myocardium may also play a critical role in the susceptibility of an already diseased heart to succumb to fatal arrhythmias during a behavioral stressor. Finally, studies in which subjects may exercise some control over an aversive stimulus suggest that cardiovascular reactivity may be pronounced and sustained in situations requiring frequent adjustment to changes in the criteria for successful performance, and/or the presence of positive incentives.
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PMID:Cognitive stress and cardiovascular reactivity. II. Relationship to atherosclerosis, arrhythmias, and cognitive control. 353 65

The major cause of cardiac mortality in the United States is sudden cardiac death, most often the result of ventricular tachycardia-ventricular fibrillation. Transient risk factors for sudden cardiac death include psychiatric conditions mediated through the CNS. Major advances in the evaluation and treatment of patients who have survived malignant ventricular arrhythmias have been accompanied by challenging management and therapy issues for the psychiatrist involved in the care of such patients. The authors suggest ways to meet these challenges, especially in the care of patients with concomitant anxiety, depression, delirium, or psychosis.
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PMID:Psychiatric aspects of patients with malignant ventricular arrhythmias. 353 12

Sudden death is a rather frequent occurrence in patients with hypertrophic cardiomyopathy, yet the mechanism is uncertain in most cases. We describe a case of an 18 years old patient with a family history of hypertrophic cardiomyopathy and sudden death in whom ventricular fibrillation could be repeatedly induced by means of transesophageal atrial stimulation with 1:1 AV conduction at a rate of 200 beats min-1 and prevented by pharmacological depression of AV node. The not particularly high ventricular rate at which VF occurred could suggest that in hypertrophic cardiomyopathy a major role in favouring VF induction is played by the electrophysiological properties of the myocardium and that sudden death can occur as a consequence of different atrial tachyarrhythmias.
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PMID:Ventricular fibrillation induced by transesophageal atrial pacing in hypertrophic cardiomyopathy. 366 49

The effects of an ethanol extract of the plant Sophora flavescens Ait. on haemodynamics and ventricular fibrillation threshold were studied in pentobarbitone-anaesthetized dogs. It was found that intravenous injection of the extract, 120 mg/kg, caused transient but significant depression in systolic and diastolic blood pressure, heart rate, left ventricular pressure and dLVP/dtmax, as well as elevation of ventricular fibrillation threshold. These preliminary findings suggest that the ethanol extract of Sophora flavescens Ait. possesses pharmacological activities resembling those of antiarrhythmic agents, but the mechanisms of action are unclear.
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PMID:Effects of Sophora flavescens Ait. on haemodynamics and ventricular fibrillation threshold in anaesthetized dogs. 368 40

Sodium azide (NaN3) is a highly reactive, toxic, widely used chemical. Although industrial exposure is common, fatal ingestion is rare. We describe the case of a 30-year-old man who ingested 15 to 20 g of sodium azide. He became comatose within two hours and eventually expired from a combination of acidosis, respiratory depression, and ventricular fibrillation. In sufficient doses, sodium azide is rapidly fatal and there is no effective treatment.
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PMID:Suicidal sodium azide ingestion. 368 3

The focus of this article is hypokalemia, its electrophysiologic properties, and clinical arrhythmias. The effects of potassium on the electrophysiologic properties of the heart have been extensively studied and clearly are arrhythmogenic. Hypokalemia increases resting membrane potential and increases both the duration of the action potential and the duration of the refractory period, the latter to a greater degree than the former. This combination is conducive to the genesis of reentrant arrhythmias. Hypokalemia also increases threshold potential as well as automaticity, thus providing the context for automatic arrhythmias as well. Lastly, hypokalemia decreases conductivity, which also predisposes to arrhythmias of the reentrant type. The electrocardiographic criteria for hypokalemia include the presence of U waves greater than 1 mm and U waves larger than the T wave in the same lead (with associated ST-segment depression). Other criteria have been a T:U ratio of 1 or less and a U wave greater than 0.5 mm in electrocardiographic lead II or greater than 1.0 mm in lead V3. The relationship between hypokalemia and clinical arrhythmias has long been recognized. In 1949, Bellet et al reported extrasystoles with hypokalemic alkalosis that decreased with potassium administration. These observations were confirmed by several groups in the early 1950s. In 1953, Surawicz and Lepeschkin described a series of patients with hypokalemia and frequent junctional and ventricular premature beats; in all cases the arrhythmias disappeared with administration of potassium. These clinical observations were strengthened by the 1962 findings of Gettes et al, who employed microelectrode techniques to show that perfusion of low potassium solutions resulted in ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation. In more recent years, several studies have evaluated the relationship between potassium levels and arrhythmias in patients with and without hypertension who were receiving diuretic therapy. These studies have demonstrated that there is an increased incidence of ventricular arrhythmias associated with the hypokalemia induced by diuretic therapy, an observation with obvious clinical implications.
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PMID:Hypokalemia and arrhythmias. 370 49

To ascertain if myocardial ischemia is the mechanism of out-of-hospital ventricular fibrillation (VF), left ventricular (LV) function was assessed at rest and during submaximal exercise in 15 patients who survived out-of-hospital VF. They were separated into asymptomatic (9 patients, group A) and symptomatic (6 patients, group S) groups for a history of angina or myocardial infarction. Both groups had significant (at least 70% diameter stenosis) coronary artery disease. At catheterization no patient had angina during exercise, but 12 of 15 had ST depression or increased ST depression (group A, 1.9 +/- 1.4 mm; group S, 1.1 +/- 1.2 mm) and 11 had abnormal wall motion. From rest to exercise, patients in group S had increased LV end-diastolic pressure (from 21 +/- 9 to 37 +/- 11 mm Hg, p = 0.009) and volume (from 100 +/- 25 to 107 +/- 26 ml/m2, p = 0.006), with no significant change in LV ejection fraction (from 40 +/- 13 to 42 +/- 12%). In group A LV end-diastolic pressure increased from 19 +/- 4 to 31 +/- 8 mm Hg (p = 0.001), but neither end-diastolic volume nor ejection fraction changed significantly (from 83 +/- 13 to 92 +/- 23 ml/m2 and from 55 +/- 13% to 46 +/- 13%, respectively). Thus, patients with coronary artery disease who survive out-of-hospital VF may have evidence of myocardial ischemia during exercise without pain. Painless ischemia may have a role in out-of-hospital VF.
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PMID:Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation. 382 32

The prevalence of exercise-induced ischemia was determined by thallium-201 (TI-201) scintigraphic criteria in patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) inducible by programmed electrical stimulation. Thirty-eight patients (age 57 +/- 19 years), of whom 87% had angiographic coronary artery disease, underwent quantitative TI-201 exercise scintigraphy within 14 days of invasive electrophysiologic testing. The mean rest ejection fraction was 38 +/- 9%. Eighty percent of patients had 1 or more regions with akinetic or dyskinetic wall motion. Thallium-201 scan segments were scored as normal or containing redistribution defects or mild or severe persistent defects. Only 4 patients (10%) had only redistribution defects and 9 (24%) had both redistribution defects and persistent defects; 32 of 38 patients (84%) had 1 or more persistent defects, of which 26 had at least 1 severe, persistent defect (more than 50% reduction in TI-201 activity). Patients with and without exercise-induced VT had a similar prevalence of redistribution. Redistribution defect prevalence was similar in patients with polymorphic VT (3 of 13) and monomorphic VT (10 of 25) during programmed electrical stimulation (difference not significant). Thus, patients with VT or VF induced by programmed ventricular stimulation have extensive TI-201 scintigraphic abnormalities on exercise scintigrams, predominantly those suggesting scar, with associated severe regional wall motion abnormalities at rest. The scintigraphic prevalence of exercise-induced ischemia is low and TI-201 redistribution and exercise ST depression are observed with equal frequency in patients with and those without VT induced during exercise.
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PMID:Prevalence of ischemia by quantitative thallium-201 scintigraphy in patients with ventricular tachycardia or fibrillation inducible by programmed stimulation. 382 44


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