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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

13 male patients suffering from arteriosclerotic heart disease and/or arterial hypertension were monitored continuously before and after vascular surgical procedures using an arrhythmia computer. Heart rate, paroxysmal supraventricular tachycardias, ventricular extrasystoles, ventricular tachycardias, ventricular fibrillation and prematurity index (QnQe/QTn) were recorded numerically. Ventricular arrhythmias were detected as follows preoperatively in 12 patients, after operation in all patients, paired ventricular extrasystoles or episodes of ventricular tachycardia were found in 5 cases before and in 7 after operation, ventricular fibrillation in one case. The incidence of ventricular dysrhythmias increased significantly (p less than 0.05) early after operation, as did the heart rate during the observed postoperative period (p less than 0.001). The prematurity index dropped below 1.0 during the two days following operation. This differed significantly from the preoperative value (p less than 0.05). The incidence of ventricular extrasystoles was related to postoperative myocardial infarction and heart failure (p less than 0.01), which occurred in 6 cases, with a lethal outcome in three. Only occasionally controlled by trained staff in a normal surgical ward the "Servomed Dysrhythmiemonitor" yielded reliable numerical results during the main part of the monitored period. In two cases it led to immediate detection and rapid institution of treatment of severe tachyar rhythmias.
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PMID:[Postoperative cardiac arrhythmias (author's transl)]. 8 Sep 61

Variations in central hemodynamics of dogs were compared with the outcome of resuscitation of 18 dogs subjected to 12-minute reversible circulatory arrest because of ventricular fibrillation. Nine survived dogs with completely recovered neurological status during the first 10 minutes after resuscitation had moderate hypertension, the mean arterial pressure (MAP) being 175.0 + 8.9 mm Hg. In the dogs who died within 24-48 hours after resuscitation, the MAP did not rise during this period as compared to the initial level; 2 dogs developed excessive hypertension (MAP about 200 mm Hg). There were also found certain differences in other parameters of central hemodynamics. Moderate hypertension in the first 10 minutes of the postresuscitation period leads to rapid restoration of the adequate level of peripheral blood flow in organs and tissues, thus favouring survival of animals subjected to a long circulatory arrest.
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PMID:[Central hemodynamics of dogs in the early postresuscitation period and the outcome of resuscitation]. 54 Jan 36

The incidence, circumstances, and mechanism of development of cardiac arrest in 786 patients with myocardial infarction treated at a coronary care unit within a five-year period were studied and clinical factors are analysed with respect to success of resuscitation. One or more episodes of cardiac arrest occurred in a total of 156 patients (19.8%). Of these, 25 (16.0%) were successfully resuscitated and 131 (84.0%) died. At the clinical ward where the patients had been transferred after the acute stage, cardiac arrest occurred in additional 22 patients, of whom two were successfully resuscitated. Thus, the total number of successfully resuscitated patients throughout the five-year period was twenty-seven. The results of resuscitation were poorer in elderly patients, in those with anterior infarction, and above all in patients with severe symptoms of mechanical heart failure. Anamnestic factors (chronic angina pectoris, previous myocardial infarction, hypertension, diabetes mellitus, ischaemic disease of the lower limbs) were not significantly associated with the results of resuscitation. Primary ventricular fibrillation was the principal mechanism of cardiac arrest in 24 of the 27 patients successfully resuscitated, and its total incidence in the investigated group was 3%. The prognosis of resuscitation in patients with primary ventricular fibrillation was very good, and in all of them the resuscitation was successful and permanent.
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PMID:Incidence of circulatory arrest in patients with acute myocardial infarction in coronary unit. Mechanism of their genesis and factors conditioning successful resuscitation. 67 95

The presented analysis deals with the physiopathological mechanisms of the debelopment of postinfarction cardiac insufficiency and the clinical peculiarities of its manifestations. It is emphasized that the leading cause of cardiac insufficiency consists in a reduction of the contractile function of the left ventricular myocardium due to the development of asynergy in the cicatrical zone. The addition of several accompanying factors, such as heart mitralization, tachysystolic form of ventricular fibrillation, repeated infarction with a growing asynergic zone, aggravate the course of cardiac insufficiency providing for the development of hypertension in the general circulation system.
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PMID:[Cardiac insufficiency in ischemic heart disease]. 78 66

A total cardiac supplementation through a simple by-pass of the left ventricle was performed on hearts in ventricular fibrillation on 51 dogs not treated with heparin. The right-sided circulation was passive to avoid introducing added disturbing parameters. A bi-valved supple prosthesis was set in motion by a pneumatic pump regulated on the left atrial pressure and the arterial tree proper rate. The 44 cases which survived from 7 to 27 hours were limited by a slow and regular lowering of the blood pressure without notable decrease of the output. This lowered pressure was due to the action of the atrial and pulmonary mechanical receptors responding to a left atrial hypertension, secondary to a mild leak of the inflow valve. The mild haemolysis and the total absence of thrombosis should be related with the rate-regulation of the pump on the arterial tree rate, thus providing a maximal yield.
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PMID:[Interpretation of the limits of survival during circulatory support in the dog]. 81 10

Sudden coronary death from ventricular fibrillation is the biggest and possibly the most remediable of the major public health problems at the moment. Most of those liable to sudden death can be identified and it is possible that by the use of beta-adrenergic blocking or other antiarrhythmic drugs, by reducing the consumption of cigarettes and perhaps, by different therapies for hypertension, a substantial proportion of coronary deaths might be prevented or, at least, postponed.
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PMID:Toward preventing coronary death from ventricular fibrillation. 82 Apr 86

The effects of ventricular fibrillation and subsequent resuscitation on the microcirculation of the verebral cortex were studied with microangiographic and fluorescent protein tracer techniques. Immediately after revival, a transient period of impaired cerebral perfusion occurred before complete recovery from circulatory arrest was obtained. A circulatory arrest of longer than ten minutes, followed by four to six hours of resuscitation, caused defects of cortical capillary filling in both microangiography and Trypan blue fluorescence. This was considered to represent impairment of cortical perfusion, most likely due to edema. Cardiac arrest up to 12 minutes and subsequent resuscitation per se caused no blood-brain barrier damage. Minimal blood-brain barrier damage occurred in one dog following uncomplicated revival from a 14-minute arrest and in animals with prolonged hypertension post-resuscitation. Up to three consecutive carotid angiographies did not cause blood-brain barrier damage in the postischemic brain.
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PMID:Cerebral circulation after cardiac arrest. Microangiographic and protein tracer studies. 84 82

The effect of acute elevation of arterial blood pressure on the ventricular fibrillation threshold was examined in 19 closed chest dogs anesthetized with chloralose during 10 minutes of occlusion followed by abrupt reperfusion of the left anterior descending coronary artery. Ventricular fibrillation threshold was determined using two methods of electrical testing: sequential R/T pulsing and the train of stimuli method. Blood pressure was increased with an intravenous injection of the alpha adrenergic stimulator phenylephrine. Acute hypertension significantly diminished the enhanced vulnerability associated with coronary occlusion. After denervation of the carotid sinus and aortic arch baroreceptors, elevation of blood pressure failed to affect vulnerability during occlusion. In both intact and denervated animals, the predisposition to ventricular fibrillation after reperfusion was unchanged by the increase in blood pressure. It is suggested that withdrawal of sympathetic tone mediated by the baroreceptor reflex is the basis for the protection against ventricular fibrillation resulting from elevation of blood pressure. The failure of acute hypertension to alter vulnerability during reperfusion suggests that the predisposition to ventricular fibrillation during reperfusion is due to mechanisms other than those operating during coronary occlusion.
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PMID:Acute blood pressure elevation and ventricular fibrillation threshold during coronary occlusion and reperfusion in the dog. 84 36

The effect of posterior hypothalamic stimulation on cardiac susceptibility to ventricular fibrillation (VF) was studied in 34 dogs. VF threshold was determined by inducing a sequence of early extrasystoles (R/T pulsing). Hypothalamic stimulation was associated with sinus tachycardia, systemic hypertension, and a 40% reduction in VF threshold. The effects of hypothalamic stimulation on the VF threshold persisted when heart rate acceleration and the pressor response were prevented. Cervical vagotomy and bilateral adrenalectomy were likewise without effect on fibrillation threshold changes. However, the decrease in threshold was abolished by beta-adrenergic blockade. It is concluded that the reduction in VF threshold associated with hypothalamic stimulation derives from the direct action of sympathetic nerves upon the myocardium, rather than from secondary hemodynamic effects.
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PMID:Effect of posterior hypothalamic stimulation on ventricular fibrillation threshold. 111 57

A 36-year-old white patient is described. He received treatment for hypertension and showed slightly increased excretion of 17-OHCS- and 17-ketosteroids but no increase in values for 3-methoxy-4-hydroxymandelic acid in the urine. He was admitted to hospital for a myocardial infarction, which was found to be situated in the anterior wall. During his stay in hospital a sudden increase in blood pressure occurred, together with a typical attach of perspiration, loss of consciousness, and ventricular fibrillation. The assay by 3-methoxy-4-hydroxymandelic acid now showed markedly increased amounts. A phaeochromocytoma was thought to be the most probably diagnosis, but now withstanding therapy the patient died from cerebral lesions. At necropsy a recent anteroseptal myocardial infarction and some minor lesions were found but no tumour and notably no phaechromocytoma, neither in the adrenals nor elsewhere. Using Dobbie's morphometric technique, as described by Munro Neville (1969), changes in the adrenals were demonstrated, which were considered to represent primary adrenal medullary hyperplasia. Criteria for the diagnosis of this syndrome are discussed. Until now it had been presumed to be present in a number of cases but never convincingly demonstrated.
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PMID:Bilateral adrenal medullary hyperplasia: a clinicopathological entity. 112 22


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