Sinus-node recovery times were measured, before and after atropine administration, in 21 patients with the clinical diagnosis of sick-sinus syndrome. The results were compared with those reported by other workers. It is concluded that sinus-node recovery times of more than 1 400 ms are most likely due to sinus-node damage (sick-sinus syndrome); normal recovery times are rare in such patients. The diagnosis of the syndrome is strengthened if the recovery time remains abnormally long even after atropine. Further useful diagnostic information can be obtained from the total stimulation phase (duration until restoration of the basic rhythm), this being overall longer in patients with the syndrome than in normal subjects. The increased incidence of A-V nodal rhythms before restoration of the basic rhythm is another indication of organic damage to the sinus node, especially if it also occurs after atropine. The significance of a recovery time which is prolonged before but normal after atropine is less clear: a raised sensitivity to vagotonic influences may be the determining factor here.

Adult↗

PubMed1975

The effect of carotid sinus nerve stimulation on muscle and skin nerve sympathetic activity in man.

Microelectrode recordings of multi-unit sympathetic activity were made in the right peroneal nerve of 4 awake human subjects during carotid sinus nerve stimulation. 36 periods of CSN-stimulation gave in all cases an inhibition of the muscle nerve sympathetic activity and there was good temporal agreement between this effect and the reduction of heart rate and blood pressure. The neural inhibition was marked during the first part of the stimulation but with continued stimulation the sympathetic activity reappeared, in most cases with reduced strength. In contrast, 20 periods of CSN-stimulation had no reproducible effect on skin nerve sympathetic activity. In most cases, the neural activity remained unchanged but both increases and decreases could occur. The results demonstrate that stimulation of carotid sinus baroreceptors in man has different effects on sympathetic outflow to different regions: a clear inhibition of the outflow to the muscles but no discernable effect on impulses destined to the skin.

Adult↗

PubMed1975

Resection of lef ventricular aneurysm-late results.

A survey of 22 patients operated on with left ventricular (LV) infarctectomy during 1967-72 is given. Clinical, haemodynamic and angiographic results are discussed. In most patients, in whom pre- and postoperative examination was possible, there was improvement concerning anginal pain, dyspnoea and attacks of ventricular tachycardia. Exercise studies revealed a lower heart rate at follow-up. In general, heart size had decreased. Angiographically, there was a decrease in end-diastolic and end-systolic heart volume postoperatively, with an increased LV ejection fraction.

Adult↗

PubMed1975

Central and peripheral circulation immediately after pulmonary surgery as related to sympathodrenal activity.

Catecholamine output and circulation were observed in connection with pulmonary surgery in one group of ten patients who were anaesthetized with halothane-N20-02-d-tubocurarine and who breathed spontaneously after operation. In another group of four patients who received a modified neurolept anaesthesia with phenoperidine-N2O-O2-d-tubocurarine and who were mechanically ventilated also after operation, catecholamine output and temperature were observed. In both patient groups, catecholamine output was normal during iperation. Adrenaline output increased by 400% the first postoperative hours, while noradrenaline output remained normal. Thereafter, noradrenaline output increased, while adrenaline output started to decrease. A subnormal body temperature was seen at the end of the operation. In two patients from the neurolept group, adrenaline output and temperature were recorded hour by hour; maximal adrenaline output concided with maximal temperature rise. In the patients from the halothane group, the pstoperative change in foot, calf and forearm blood flow correlated well with the change in catecholamine output. The central circulatory response to the symptahoadrenal stimulation was, however, found to be less pronounced than is ordinarily seen.

Adult↗

PubMed1975

[Sinus node syndrome].

Recently disorders of sinus node function have found increasing interest in clinical medicine thanks to new diagnostic and therapeutic developments. This paper represents a comprehensive review of these conditions, combined under the name "Sick Sinus Syndrome" (SSS). Besides a detailed analysis of 63 cases seen at our institution, the results of other groups are compared and extensively discussed. The clinical picture of the SSS is characterized by a wide variety of bradycardiac and tachycardic atrial arrhythmias, occurring separately or in combination. These can be classified in three subgroups: Patients with exclusive sinus bradycardia; patients with sinoatrial exit block or transient episodes of sinus arrest with or without AV escape rhythms; and finally patients with the bradycardia/tachycardia-syndrome, which are complicated by additional atrial tachyarrhythmias. The symptomatology of the SSS is multiform and extends from symptomless cases and those with only general signs of reduced cardiac function to patients with recurrent severe syncopal attacks which may lead to cerebral damage and even death. Besides the typical history, the diagnosis of the SSS primarily rests upon the ECG, especially the long term ECG recorded continuously on a 24 hrs. tape (Holter technique). Also the exercise ECG is of some value, characteristically showing an inadequate increase in the sinus rate, sometimes with AV escape systoles and -rhythms. In addition various provocative tests have been devised which are of help to differentiate between a pathologic and a normal sinus node function. Among these the determination of the sinus node recovery time following overdrive atrial pacing has gained wide acceptance. In most cases the exact etiology of the SSS is not known. In addition to coronary and inflammatory heart diseases a primarily degenerative lesion of the sinus node, comparable to cases with "primary heart block" are discussed. There is also a remarkably frequent past history diththeria. Rarer causes of the condition represent cases with cardiomyopathy, thyreotoxic heart disease, collagen and other disorders and also a familial manifestation of the SSS has been described. Therapeutically, pharmacologic treatment with vagolytic, beta-adrenergic or the common antiarrhythmic drugs is often unsuccessful, especially in the treatment of the Brady-Tachy-Syndrome. Digitalis glycosides, however, are frequently of some value, as they represent an effective prophylactic agent against atrial tachyarrhythmias without prolonging the sinus node recovery time or reducing significantly the sinus rate. While a few patients do not require any treatment, an artificial cardiac pacemaker has to be inserted in most cases. Atrial stimulation may be superior to ventricular on-demand pacing in some patients, and also a special system for the treatment of the SSS combined with significant AV block (binodal disease) has been designed, the bifocal sequential pacemaker.

Age Factors↗

PubMed1975