{"title":"Psychological factors in cardiac arrhythmias.","authors":"G Härtel","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Autonomic nervous control of the heart and the blood vessels is essential for optimal physical performance. Afferent nerves conduct impulses to the vasomotor and cardioaccelerator and cardioinhibitor centres resulting in efferent sympathetic and vagus output. Information inputs also from the environment and the person's thought processes are mediated from the cortex by the hypothalamus, the limbic system, and the autonomic nervous system to the heart and blood vessels. Emotional factors like anger, anxiety, and fear increase sympathetic output and influence heart rate. On the other hand, fear and the feeling of being in a helpless situation causes intensive vagal activation with ensuing severe bradycardia or asystole and vasovagal syncope. Although psychologic factors can cause extreme grades of tachy- or bradycardia they usually have no acute deleterious effects in the normal heart. In the diseased heart, however, consequences may be hazardous. Emotional factors are known to increase ventricular arrhythmias either directly or indirectly by increasing heart rate and causing ischaemia as in coronary heart disease. In animal experiments ventricular fibrillation threshold is lowered by aversive conditions. In heart diseases with sudden death as a well known complication increased sympathetic activity may give rise to fatal arrhythmias. In man the evidence of psychologic factors as the cause of life-threatening arrhythmias and sudden death is mostly anecdotal or circumstantial. Well designed studies are needed to evaluate the role of psychologic factors in arrhythmias.</p>","PeriodicalId":8084,"journal":{"name":"Annals of clinical research","volume":"19 2","pages":"104-9"},"PeriodicalIF":0.0000,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of clinical research","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Autonomic nervous control of the heart and the blood vessels is essential for optimal physical performance. Afferent nerves conduct impulses to the vasomotor and cardioaccelerator and cardioinhibitor centres resulting in efferent sympathetic and vagus output. Information inputs also from the environment and the person's thought processes are mediated from the cortex by the hypothalamus, the limbic system, and the autonomic nervous system to the heart and blood vessels. Emotional factors like anger, anxiety, and fear increase sympathetic output and influence heart rate. On the other hand, fear and the feeling of being in a helpless situation causes intensive vagal activation with ensuing severe bradycardia or asystole and vasovagal syncope. Although psychologic factors can cause extreme grades of tachy- or bradycardia they usually have no acute deleterious effects in the normal heart. In the diseased heart, however, consequences may be hazardous. Emotional factors are known to increase ventricular arrhythmias either directly or indirectly by increasing heart rate and causing ischaemia as in coronary heart disease. In animal experiments ventricular fibrillation threshold is lowered by aversive conditions. In heart diseases with sudden death as a well known complication increased sympathetic activity may give rise to fatal arrhythmias. In man the evidence of psychologic factors as the cause of life-threatening arrhythmias and sudden death is mostly anecdotal or circumstantial. Well designed studies are needed to evaluate the role of psychologic factors in arrhythmias.