Carotid sinus syndrome. Vascular reflex. Hypersensitive Carotid Sinus and Carotid Sinus Syndrome See also Atherosclerosis
Name: Carotid node syndrome
Carotid node syndrome
In carotid node syndrome, stimulation of one or both of the hypersensitive carotid nodes located at the bifurcation of the common carotid arteries leads to short episodes of syncope. There are 4 types.Risk factors
Clinical picture
Diagnostics
Treatment:
Lead tactics. The method of choice is the setting of a pacemaker (2-chamber).Drug therapy
Complications
Synonyms
See also Atherosclerosis
ICD. G90.0 Idiopathic peripheral autonomic neuropathy Clinically, it is very important to distinguish between carotid node hypersensitivity syndrome and sick sinoatrial node syndrome.In carotid node syndrome, stimulation of one or both of the hypersensitive carotid nodes located at the bifurcation of the common carotid arteries leads to short episodes of syncope. There are 4 types.
Frequency. 50% of examined patients over 65 years of age with frequent episodes of dizziness or syncope in history. Prevailing age- elderly. Predominant sex- male.
Etiology
Risk factors
Clinical picture
Diagnostics
differential diagnosis.
Vagal reactions, postural hypotension, primary insufficiency of the autonomic nervous system, hypovolemia, arrhythmias, pathological sinus syndrome and other conditions accompanied by low cardiac output, cerebrovascular insufficiency, emotional disorders.
TREATMENT
Tactics of conducting. The method of choice is the setting of a pacemaker (two-chamber).
Drug therapy
Complications
Current and forecast.
With atheromatous lesions of the carotid or basilar artery, the prognosis is not very favorable.
Concomitant pathology
Prevention.
Exposure to provoking factors that can stimulate the carotid node (tight collar, shaving, turning the head in this direction, straining during defecation) should be avoided.
Synonyms
In occurrence carotid sinus syndrome cardiac, vasomotor and cerebral factors are involved. Already in the norm, a test with pressure on the sinus region (mechanical irritation of the accumulation of nerve endings in the area of the carotid sinus) causes a decrease in blood pressure, bradycardia, peripheral vasodilation, and changes in the chemical composition of the blood (especially changes in CO2 tension). In pathology, these reflexes are so sharply increased that, even with mild irritation of the carotid sinus, cardiac arrest can be observed for several seconds and a drop in blood pressure to 50 mm Hg (Rossier).
Heart failure and a drop in blood pressure clinically often leads to a short-term loss of consciousness. However, after irritation of the carotid sinus, a short-term loss of consciousness is also observed without a simultaneous change in the pulse rate or blood pressure, so one should think about the complicity of the cerebral factor.
Depending on whether they come to the fore slowing down of cardiac activity, a drop in blood pressure, or a more difficult to detect effect on the brain centers, distinguish between vagal, vasomotor and cerebral types, and the vasomotor type is almost always combined with the vagal type.
In patients with so-called carotid sinus syndrome with various movements that can cause irritation of the carotid sinus - turning the head, tilting the head backwards, too narrow collars, in severe cases, attacks of loss of consciousness occur, which occasionally can also be accompanied by convulsions, so that differential diagnostics should be distinguished not only from other cardio -vascular forms, but also from epilepsy. In milder cases, it does not come to loss of consciousness, but there are more or less severe dizziness, sensations of heaviness in the limbs, general malaise and vomiting. Only occasionally does involuntary defecation occur.
Diagnosis is based primarily on the results of a pressure test on the carotid sinus: if, with slight compression of the carotid sinus, which, as a rule, is located at the level of the angle of the mandible, significant bradycardia or even cardiac arrest occurs within a few seconds, the diagnosis of carotid sinus syndrome becomes reliable. At the same time, the mechanism that directly causes seizures in the patient (often in a stereotypical way), sometimes associated with professional activities (for example, a strong tilt of the head forward during certain actions), is also easily revealed.
At the heart of the pathological increase reflex excitability of the carotid sinus almost always lie atherosclerotic changes, less often pathological processes near the sinus (lymphomas, tumors) or psychoneurosis.
Violations predominantly vascular functions(peripheral vasomotor collapse). Again and again attempts are made to distinguish between collapse and shock as different forms of peripheral circulatory failure. However, this kind of differentiation is not feasible at the bedside. Clinically for collapse, resp. shock, the following phenomena are characteristic: pallor of the skin, a drop in arterial and venous pressure, blackout of consciousness up to loss of it, tachycardia, but also sharp bradycardia, sluggish wide pupils, shallow and accelerated breathing, a tendency to vomit and sweat; subjectively, patients experience a feeling of coldness of the hands and feet, a very sharp weakness and often a peculiar feeling of pressure in the abdomen.
post-traumatic collapse with or without loss of blood is caused by various kinds of injuries and is easily recognized (see also crush syndrome).
Vago-vasal reflex(synonym: vasopressor reflex). The fall in blood pressure in this form appears to be due to reflex dilation of the arterioles. The exact mechanism is unknown. It is only reliable that the reverse venous flow to the heart is sharply reduced. The occurrence of this reflex depends on many factors. First of all, the reflex mechanism is activated by mental factors (accident, venipuncture, unpleasant message, etc.). Everyone is familiar with this situational collapse in highly sensitive people. In contrast to a hysterical seizure, there is a true drop in blood pressure, which is crucial for the diagnosis.
As a reflex shock the state of collapse after severe injuries of the abdomen is well known (corresponding to the experience of Goltz with beating the abdomen of a frog). This group also includes a rare reflex collapse during pleural punctures and a pulmonary reflex with a sudden increase in pressure in the pulmonary circulation due to pulmonary embolism. A strong blow to the area of the carotid sinus causes a reflex "knockout" - collapse.
Educational video of the causes of loss of consciousness and types of collapse
In case of problems with viewing, download the video from the pageIt occurs quite often (1-2% among other causes of syncope). Most often, the pathology is observed in older men with coronary heart disease or arterial hypertension. Loss of consciousness can occur with sharp turns of the head, overextension of the neck, while eating. This is additionally facilitated by wearing shirts with a tight collar, tightly tying a tie.
With the cardioinhibitory variant, there is a sharp decrease in heart rate up to asystole (reflex stop of the sinus node or high-degree AV blockade). With the vasodepressor variant, there is a drop in blood pressure without the development of bradyarrhythmias. In the cerebral variant, loss of consciousness occurs without changes in heart rate and blood pressure, accompanied by the appearance of focal neurological symptoms.
Certain medications may increase the carotid reflex:
- cardiac glycosides, obzidan (cardioinhibitory reaction);
- diuretics, vasodilators (increased vasodepressor component).
Diagnosis of carotid sinus syndrome
Massage of the carotid sinus (the test is contraindicated in the presence of noise over the carotid arteries) is performed in the supine position with simultaneous ECG recording and blood pressure measurement. Massage in the area of pulsation of the carotid arteries is carried out alternately on each side, gradually increasing the degree of pressure, but not more than 20 seconds.
Normally, young people have a slight decrease in heart rate and a decrease in blood pressure by less than 10 mm Hg. Art., in the elderly, a decrease in blood pressure sometimes reaches 20-40 mm Hg. Criteria for increased sensitivity of the carotid sinus: the occurrence of an asystole period of more than 3 s (cardioinhibitory variant) and a decrease in systolic blood pressure by more than 50 mm Hg. Art. (vasodepressor variant).
In the absence of these signs, the test is carried out in the patient's sitting position (detection of the vasodepressor component). With the development of a cardioinhibitory variant, the test should be repeated after the administration of 1 mg of atropine (to exclude the concomitant vasodepressor component). Absolute proof of the presence of carotid sinus syndrome is only the occurrence of fainting during the test.
Literature:
Pozdnyakov Yu.M., Krasnitsky V.B. Urgent cardiology - M.: Shiko, 1997, -249s.
Sick sinus syndrome (SSS) develops, as a rule, in the elderly due to sclero-degenerative processes affecting the conduction system of the heart (PSS), atherosclerotic (including post-infarction) cardiosclerosis. Electrophysiologically, SSSU is manifested by a decrease in the automatism function of the sinus node (SA) and/or disturbances in sinoauricular (SA) conduction.
It is important to emphasize that in the initial stages of SSSU development, a decrease in the automatism of SS more often leads not to severe bradycardia, recorded at night with Holter monitoring (HM) ECG, but to the lack of an adequate increase in heart rate in response to exercise - to the so-called "chronotropic insufficiency". This is probably due to the influence of a compensatory increase in sympathetic activity, which still makes it possible to avoid severe bradycardia, but no longer provides an increase in heart rate during exercise.
Constant hypersympathicotonia in such patients manifests itself in rhythm rigidity - the absence of proper fluctuations in heart rate during the day, a decrease in heart rate variability (HRV), detected using methods of mathematical analysis.
SSSU, as a rule, requires differential diagnosis with the so-called vagotonic dysfunction of the SU (VDS), which is based on an increase in the tone of the parasympathetic division of the autonomic nervous system and/or an increase in the sensitivity of the SU to parasympathetic influences. As a rule, such an increase in parasympathetic tone is associated with pathological viscero-visceral reflexes and, in most cases, can be eliminated with atropine drugs.
A special type of sinus dysfunction is the carotid sinus syndrome (SCS), in which severe depression of the sinus tract (up to arrest) develops, for example, during mechanical action on the carotid sinus zone.
Differential diagnosis of SSSU, VDSU and SCS requires an integrated approach - a thorough history taking, physical examination, ECG registration, dynamic ECG, a number of samples and an electrophysiological study (EPS) with drug denervation (MD). Here is a clinical observation of a patient in whom a comprehensive examination revealed a combination of SSS and SCS.
Patient F., aged 45, was admitted to the clinic of the institute on 22.10.99 with complaints of fatigue, weakness, rare dizziness. In the anamnesis for 3 years, he notes an increase in blood pressure to 190/120 mm Hg. July 30, 1999 suffered an acute myocardial infarction of the lower wall of the left ventricle. The acute period proceeded without complications.
Since September 1999, ECG against the background of sinus bradycardia on inspiration began to record periods of asystole lasting up to 3800 ms. Daily ECG monitoring was performed repeatedly, during which sinus rhythm (SR) was recorded during the day with a heart rate of 43 to 102 beats/min. with pauses up to 2054 ms, no other significant arrhythmias were detected. To clarify the diagnosis and determine the management tactics, the patient was hospitalized in the clinic of the Institute.
On admission to the hospital, the patient's condition was satisfactory. On physical examination, the pulse was 52 beats/min, rhythmic, blood pressure was 150/110 mm. rt. Art., a moderate increase in the size of the heart to the left, heart sounds are muffled, rhythmic, otherwise - without deviations from the norm. General blood and urine tests without pathology, lipid metabolism indicators - cholesterol 4.5 mmol / l, B- and pre-B-lipoproteins - 80 conventional units, electrolytes within the normal range (K - 4.3 mmol / l, Na - 138.6 mmol/l), glucose - 4.0 mmol/l, prothrombin - 90%.
The standard ECG shows moderate sinus bradycardia with a heart rate of 57 beats/min. Cicatricial changes in the area of the posterior wall of the hypertrophied left ventricle. Enlargement of the left atrium. Pauses of up to 3400 ms were recorded during inspiration due to 2nd degree SA blockade, periods of a replacement rhythm from the atrioventricular junction (see Fig. 1a).
Rice. Fig. 1. ECG of patient F., 45 years old: a - breath holding test (maximum RR interval reaches 2900 ms),
b- massage of the carotid sinus on the right (pause value 4300 ms).
With 3-day ECG monitoring from 25 to 27.10.99 heart rate from 43 to 96 beats / min. Attention was drawn to the lack of an adequate increase in heart rate (maximum heart rate for physical activity - 96 beats / min), post-extrasystolic pauses up to 2600 ms. In the analysis of HRV, there was a pronounced decrease in such indicators as sigma, RR50, especially at night, when rigid bradycardia was noted in the non-REM sleep phase.
Echocardiographic study ejection fraction - 62%, marked hypertrophy of the left ventricle, hypokinesia of the upper and middle parts of the lower wall of the left ventricle.
To exclude hypersensitivity of the carotid sinus, a test was performed with a massage of the carotid sinus zone under ECG control. The following results were obtained: when massaging the carotid sinus, an asystole period lasting 4300 ms was recorded on the right, and a pause lasting 2340 ms was recorded on the left (see Fig. 1b).
Consulted by an oculist. When examining the fundus, signs of hypertensive angiopathy of the retinal vessels were revealed. On October 29, 1999, to clarify the function of the SU, a transesophageal EPS with MD was performed, during which data were obtained indicating an organic lesion of the SU. The increase in the recovery time of the SU function (VVFSU) reached 1560 ms against the background of the initial rhythm and 1640 ms after MD, and the corrected EVFSU (CVVFSU) - initially 510 ms and 540 ms after denervation.
Restoration of the activity of pacemakers of the second order was registered, the appearance of secondary pauses after MD (Fig. 2). The patient underwent a test with a rapid intravenous injection of adenosine triphosphate (ATP) according to the method developed by us. With the introduction of 20 mg of ATP after atropinization, the maximum interval P-P=2020 ms was registered (Fig. 3), which, according to our data, indicates an organic pathology of SU.
Rice. Fig. 2. Some results of transesophageal EPS with MD in patient F., 45 years old: a - determination of VVFSU against the background of the initial rhythm (the value of the secondary pause is 1560 ms), b - ECG after atropinization (PP = 640 ms), c - ECG after MD ( RR reaches 1100 ms), d - determination of VVFSU after MD (1680 ms).
Rice. 3. ECG of patient F., 45 years old. - conducting a test with a rapid intravenous injection of 20 mg of ATP after atropinization. The value of the maximum RR interval is 2020 ms. Explanations in the text.
Thus, on the basis of a comprehensive examination, the patient was diagnosed with SSSU. At the same time, the results of the massage of the carotid sinus indicated that the patient had an independent pathology - the carotid sinus syndrome, and pronounced pauses recorded against the background of breath holdings suggest that it is based on the hypersensitivity of the SU to parasympathetic influences.
Thus, based on the anamnesis, clinical data, examination results, the diagnosis was made: IHD. Postinfarction cardiosclerosis (MI at 07.99 g). Hypertension stage 2. Circulatory failure 0 tbsp. SSSU. Carotid sinus syndrome.
Taking into account that quite often the cause of SSSU is coronary artery disease, and the patient has a history of myocardial infarction of the lower wall, the next step should have been coronary angiography to assess the state of the coronary arteries. In the future, with damage to the coronary artery supplying the SU, surgical treatment with a re-evaluation of the SU function is possible. However, the patient categorically refused coronary angiography, therefore, despite the absence of absolute indications, due to the high risk of sudden death, the installation of PEKS was proposed. On November 5, 1999, the patient was transferred to the cardiac surgery clinic for PEKS implantation in physiological mode.
LITERATURE
1. Kushakovsky M.S. Arrhythmias of the heart. - St. Petersburg: ICF "Foliant", 1999-640 p.
2. Cardiac arrhythmias: Mechanisms, diagnosis, treatment, in 3 volumes / ed. B.J. Mandela; M., Medicine, 1996.
3. Shulman V.A., Egorov D.F., Matyushin G.V., Vygovsky A.B. Sick sinus syndrome. S.Pb, Krasnoyarsk, 1995, 439 p.
4. Gukov A.O., Zhdanov A.M. Neurocardiogenic (vasovagal) syncope. Russian medical journal, 1999, N6.
5. Chireikin L.V., Medvedev M.M., Biskup A.B. On the effect of rapid intravenous administration of adenosine triphosphate on the conduction system of the heart Bulletin of Arrhythmology 1994, N3, p. 10-16.