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PubMed1978

[Vagal tone in symptomatic sinus node dysfunction (author's transl)].

Under investigation in this study were the role of vagal tone in symptomatic sinus node dysfunction and the relationship between hypersensitive carotid sinus reflex (HCSR) and sick sinus syndrome (SSS). In 168 symptomatic patients (pts) resting heart rate (HR), maximal corrected sinus node recovery time (CSRTmax) and maximal carotid sinus pressure results (CSPmax) were determined before and after Atropine, 1 mg i.v. (A). According to test results, 103 pts had HCSR (1), 33 had HCSR + SSS (II), 30 pts had isolated SSS (III) and 20 pts with normal test results served as controls (IV). Mean age was the same in groups I--IV (p greater than 0.05). Groups I--III had a HR less than or equal to 60 bpm, rising 31% after A in groups I--IV, but absolute values were below those in group IV. In groups I--III CSP normalized after A and CSRT remained unchanged (p greater than 0.05). We conclude that increased vagal tone plays but one role in groups I--III and the combination HCSR + SSS seems rather frequent. Specific testing clearly separated HCSR from SSS.

Adult↗

PubMed1977

[Studies on the differential diagnosis of carotid sinus syndrome and sick sinus syndrome (author's transl)].

55 patients suffering from syncopes or dizziness were investigated by atrial pacing and carotid sinus reflex. In 17 pts. the only pathologic finding was a prolonged sinus node recovery time, in 8 pts. a pathologic carotid sinus reflex. In 7 pts. both pathologic findings were present, a prolonged sinus node recovery time and a pathologic carotid sinus reflex. In 3 pts. suffering from atrial fibrillation in addition a pathologic carotid sinus reflex was found. In 20 pts. the findings were normal. It is concluded that sick sinus syndrome and carotid sinus syndrome are different diseases, which can be separated clearly.

Aged↗

PubMed1976

The abnormal upper gastrointestinal vagovagal reflexes that affect the heart.

The clinically important upper gastrointestinal-cardiac vagovagal reflexes are mainly those initiated by swallowing and rapid gastric distention. Pre-existing-heart disease has little to do with determining susceptibility to upper gastrointestinal stimuli. The dangerous cardiac repercussions concern diminished coronary artery flow and the arrhythmias. The latter can be subcategorized as swallow tachycardia, pharyngeal disease with arrhythmia, glossopharyngeal neuralgia with swallow syncope, spontaneous swallow syncope and swallow bradycardia. Iatrogenic arrhythmias are particularly tragic potential hazards of all pharyngoesophagogastric manipulations.

Adolescent↗

PubMed1979

Carotid sinus syncope induced by malignant tumors in the neck. Emergence of vasodepressor manifestations following pacemaker therapy.

Three patients had carotid sinus syncope secondary to malignant neoplasms in the neck. Pacemaker therapy controlled the cardioinhibitory reflex with bradycardia, but the patients manifested varying episodes of hypotension due to a vasodepressor reflex that most likely resulted from persistent irritation of the carotid sinus by the tumor. These episodes seemed to be self-limiting. Surgical treatment in resistant cases is a possibility.

Carcinoma, Squamous Cell↗

PubMed1978

[The significance of electrophysiologic findings and clinical course in symptomatic sinus node dysfunction (author's transl)].

Under investigation in this study were the relationship between hypersensitive carotid sinus reflex (HCSR) and sick sinus snydrome (SSS), the significance of clinical symptomatology versus electrophysiologic test results and the natural course of both syndromes. In 186 symptomatic patients (pts) resting heart rate, maximal corrected sinus node recovery time (CSRTmax) and maximal carotid sinus pressure results (CSPmax) were determined. According to test results, 103 pts had HCSR (I), 33 had HCSR + SSS (II), 30 pts had SSS (III), and 20 pts with normal test results served as controls (IV). Mean age was the same in groups I--IV (p greater than 0.05). Groups I--III had a heart rate less than or equal to 60 bpm. There was no correlation between patients test data and the occurrence of syncopes in each of groups I--III (p greater than 0.05). In 16 pts with SSS, test results remained unchanged 16 months later (p greater than 0.05). More pts (31%) in group II died in a shorter period of time after pacer application (1.4 +/- 1 year) than pts with AV III degrees block (25%, 1.8 +/- 1.6 years) after pacer application. We conclude that the combination HCSR + SSS seems rather frequent. Specific testing separated HCSR from SSS, but failed to predict syncopes and thereby cannot aid in the indication for pacer application. The 16 months prognosis of SSS proved unfavorable. Mortality after pacer application in HCSR + SSS seems less favorable than in AV III degrees block (p less than 0.05), but depends largely on the severity of associated diseases.

Adult↗

PubMed1975

Postural reflexes in chronic Chagas's heart disease. Heart rate and arterial pressure responses.

Studies of heart rate and blood pressure responses to 70 degrees head-up tilt and 30 degrees head-down tilt were conducted in normal subjects and in chronic cardiac chagasic patients without past or present cardiac decompensation. During steady state of tilt, heart rate alterations were less marked in the chagasic than in the control group. Vasodepressor syncope supervened in three cardiac chagasic patients, two of whom showed the distinctive feature of hypotension without reflex bradycardia. In these patients, vagal control of cardiac rate could not be demonstrated either following a full blocking dose of atropine or during sudden elevation of systemic arterial blood pressure. These results are interpreted in the context of the pathologic and functional derangements of autonomic control which occur in Chagas' heart disease.

Adult↗

PubMed1978

A patient with repeated syncopal attacks after using isosorbide dinitrate.

The case of a patient with repeated attacks of collapse induced by sublingual isosorbide dinitrate is reported. The patient was an 81 year-old female who was admitted to Yura Hospital because of attacks of precordial pain. Several minutes after the sublingual administration of isosorbide dinitrate (10 mg) for an anginal attack, she developed a sensation of general weakness, and thereafter because unconscious. Arterial blood pressure fell and became unmeasurable. Electrocardiograms recorded during the syncopal attack showed sinus tachycardia and significant elevation of ST-segment in right precordial leads. In response to a drip infusion of noradrenaline, arterial blood pressure returned to normal with recovery of consciousness. Two similar syncopal attacks induced by sublingual isosorbide dinitrate occurred in the next three days. These attacks were not due to augmentation of the vagal reflex. Decrease of venous return probably was the primary etiological factor.

Aged↗

PubMed1978

Reflex anoxic seizures ('white breath-holding'): nonepileptic vagal attacks.

From clinical history 58 children were diagnosed as having reflex anoxic seizures secondary to provoked cardioinhibition (also known as white breath-holding attacks). Before referral, these seizures were commonly misdiagnosed as epileptic either because the provocation was ignored, not recognised, or was a febrile illness, or because there was no crying, no obvious breath-holding, little cyanosis, and often no pallor to suggest syncope and cerebral ischaemia. The duration of cardiac asystole after ocular compression was measured in these children and in 60 additional children with other paroxysmal disorders. In 45 (78%) of the 58 with reflex anoxic seizures asystole was 2 seconds or over, and in 32 (55%) it was 4 seconds or greater, an abnormal response. Review of the literature supports the concept that these seizures result from vagal-mediated reflex cardiac arrest which can if necessary be prevented by atropine. The simple name 'vagal attack' is proposed. Ocular compression under EEG and ECG control supports the clinical diagnosis if asystole and/or an anoxic seizure is induced; the procedure described is safe and should be routine in seizure or syncope evaluation, when a meticulous history still leaves room for doubt.

Adolescent↗

PubMed1975

[Treatment of carotid sinus syncope by demand electro-systolic cardiac pacing].

The observations of 2 patients having carotid sinus syncopes treated by temporary (1 case), or definitive (1 case) endovenous demand cardiac pacing are correlated with 15 similar observations found in the literature. In all these patients, cardiac pacing is more effective than all the other treatments cutting off the hyperactive reflex. Indeed, carotid sinus hypersensibility seems to be good, though unusual indication of cardiac pacing.

Aged↗

PubMed1977

Profound reflex bradycardia produced by transient hypoxia or hypercapnia in man.

A quadraplegic patient was able to breathe adequately for the first 3 days after his cervical spinal cord was transected by a bullet. However, for several days thereafter spontaneous ventilation became inadequate, most likely due to edema of the cord, and mechanical ventilation was required. When the ventilator was disconnected for required tracheal aspiration, before there was any tracheal stimulation, profound bradycardia, hypotension and syncope occurred within a few seconds. The bradycardia could be diminished by atropine and its onset delayed by prior ventilation with oxygen. Because of the rapid onset of the hemodynamic changes and their correlation with relatively small changes in PaO2 and PaCO2, it is suggested that this vagally mediated bradycardia represents the primary cardiac reflex response to peripheral chemoreceptor stimulation, which, although extensively studied in experimental animals, has not before been described in man. Just as in animals, it seems likely that the inability to hyperventilate permitted the primary cardiac reflex to occur rather than the usual response of tachycardia to chemoreceptor stimulation which is prepotent with spontaneous ventilation. An understanding of this reflex was important in the clinical mangement of this patient.

Adult↗

PubMed1975

Vagal role and pacemaker indication in hypersensitive carotid sinus reflex.

The effect of carotid sinus pressure (CSP) on sinus rate was studied in 24 patients with sinoatrial pauses below 3 sec (control) and 23 patients with sinoatrial pauses above 3 sec (hypersensitive carotid sinus reflex equal to (HCSR). For registration of P waves, intraatrial electrograms were used. CSP was applied several times before and after atropine. Patients with HCSR showed inconstant response to CSP. The maximal result was considered diagnostic. No difference in the lengths of sinoatrial pauses was found between patients without dizziness or syncopes in the presence of HCSR and patients with dizziness that proved clinically to be based on the existence of HCSR. It was concluded that CSP-induced asystole can serve neither as a differential diagnostic criterion nor as an indication for pacemaker application. Sick sinus syndrome, and thereby dysfunction of the sinus node, were excluded by rapid atrial stimulation. Patients with HCSR showed overall higher age, slower resting heart rate before and after atropine and less atropine response during CSP compared to control. Hypersensitivity of the carotid sinus reflex was interpreted as a part of the physiological augmentation of vagal tone in elderly people.

Adult↗

PubMed1977

[Sublingual isosorbide dinitrate-induced severe hypotension, bradycardia and prelypothymia in patients with acute myocardial infarction (author's transl)].

100 patients with acute myocardial infarction were given 5 mg of sublingual isosorbide dinitrate within 36 hours by the onset of their symptoms. 86 patients did not show any unusual effect after the administration of the drug; their heart rate was only slightly increased and their arterial pressure slightly reduced. 14 patients developed severe systemic arterial hypotension, associated with absolute or relative bradycardia, within 30 minutes of receiving the drug. All the patients complained of fainting and sweating, 1 patient developed a syncope. Symptoms were relieved by raising patients legs in 10 cases, by 0.5 mg Atropina e.v. in 4 cases, 1 case required also external cardiac massage. There was no significant difference between the two groups as regard to the location of myocardial infarction nor to the functional class (according to Killip classification). Possible mechanism producing bradycardia, hypotension and lipothymia after nitrates administration are considered. A vagally mediate reflex possibly elicited by a fall in venous return is the most acceptable hypothesis. The study emphasizes the importance of carefull observation of patients receiving sublingual nitrates during acute myocardial infarction, and the rapid response of bradycardia, hypotension and lipothymia following nitrates administration, to a simple therapy, which avoids other potentially hazardous treatments.

Aged↗

PubMed1977

The mechanism of orthostatic and haemorrhage fainting.

In order to study the adjustment of central circulation to postural changes and the mechanism of orthostatic fainting, the pressure in the brachial artery, the pulmonary artery, the right ventricle and heart rate (HR) were recorded in sixteen healthy young men, both supine and after tilting to 45 degrees and 90 degrees head up, before (normovolaemic, NV) as well as after (hypovolaemic, HV) withdrawal and reinfusion of (mostly) 950 g blood (about 15% of blood volume, BV). Two subjects fainted in supine HV, two in 90 degrees NV, four disclosed impending symptoms of fainting, and two fainted in 90 degrees HV. 'Fainters' differed from the others by smaller BV in relation to body height, higher HR in 90 degrees NV and lower arterial mean pressure in HV. In the three fainting situations, right ventricular enddiastolic pressure (PRveD) was markedly lowered to or below 0 mmHg. Arterial diastolic pressure (PaD) was not correlated with PRveD, but the pulse pressure decreased with the fall in PRveD. In 90 degrees HV, PaD fell in the six subjects who fainted or disclosed impending symptoms. Irrespective of the situation, the fainting attack involved a sudden decrease of HR and arterial pressure, concomitantly with a first unchanged then increased PRveD and/or pulmonary artery diastolic pressure. A reflex control of the filling volume/pressure of the heart is assumed to precipitate fainting by counteracting the arterial blood pressure regulation.

Adult↗

PubMed1975

Sinoatrial block. Autonomic influences and clinical assessment.

Seventeen patient with sinoatrial block and 16 healthy volunteers were investigated with recently developed autonomic tests of atrial pacemaker function. Only one patients was found to be entirely normal in comparison with normal subjects, while another patients had supernormal responses. Fifteen patients had reduced responses relative to the controls implying impaired atrial pacemaker function or sinoatrial disease. It is suggested that while in some cases sinoatrial block may be of physiological origin, it is more often due to sinoatrial disease. The latter group are liable to Adams-Stokes syncope and may have additional atricventricular conduction abnormalities. The possible mechanisms and treatment of sinoatrial block are discussed relative to the autonomic and pacemaker function abnormalities described.

Adams-Stokes Syndrome↗

PubMed1976

[Relation between training status and orthostatic tolerance].

Investigations on orthostatic tolerance and physical fitness prior to and after 6-8 h immersion experiments surprisingly revealed that all untrained subjects endured pre- and postimmersion tilt table tests without subjective complaints, whereas after immersion all trained participants collapsed within the first minutes of erect position displaying symptoms of a vasovagal syncope. Assuming that this impaired orthostatic tolerance of trained subjects can partially be referred to influences of an altered blood pressure control system we decided to record the blood pressure characteristics of both groups. Thereby, the transmural pressure of the carotid artery was changed by applying from outside either reduced or exceeding pressures. The controller sensitivity in the untrained group was almost twice as high as in the trained one. This implies a better regulatory response to disturbing interference in the untrained. Under normal conditions the controlling capacity of both groups is sufficient to cope with body position changes. However, during stress situations--in this case, reduction of aldosterone concentration as well as losses of plasma volume due to the 'Gauer-Henry-Reflex'--blood pressure regulation first fails in the trained subjects.

Blood Pressure↗