Syncope is a common clinical condition. For many years, the diagnosis and treatment of syncope are confusing, and there is not much clinical research data. The guidelines for the management of syncope published by the European Society of Cardiology are based on recent clinical practice to find more favorable evidence to guide the diagnosis and treatment of syncope, further standardizing the steps for the diagnosis of syncope and making the treatment more scientific, rational and effective.
I. Definition and epidemiology of syncope
Syncope is a sudden, transient loss of consciousness caused by a variety of causes, which can recover on its own. It is a common clinical syndrome, the mechanism of which is transient cerebral hypoperfusion. Syncope may be preceded by aura such as mild dizziness, nausea, sweating and weakness, and visual abnormalities, but most manifest as sudden attacks and therefore often cause falls, especially in the elderly.
The Framingham study showed that the incidence of syncope is 3% in men, 3.5% in women, and 6% in the elderly. About 20-30% of people experience syncope or a precursor to syncope at least once in their lifetime. Some syncope is often indicative of a poor prognosis, such as syncope with cardiac arrhythmias. 9-34% of syncope is of cardiac origin and can lead to sudden death in severe cases. The mortality rate within one year is 30%. The causes of syncope are numerous and the mechanisms are complex, and physicians are often faced with a number of challenges when dealing with specific patients. In recent years, foreign research on the etiology and mechanism of syncope has progressed faster, and the upright tilt test, electrophysiological examination, telephone ECG, signal-averaged ECG and other examinations have been commonly carried out in the clinic, and the application of these methods has made certain syncope with unknown causes traceable, and the etiological diagnosis and treatment of syncope have been greatly improved.
Second, the etiology and classification of syncope
Cardiac syncope
Arrhythmogenic
1, pathological sinus node syndrome (including slow fast syndrome)
2.Atrioventricular block
3.Supraventricular tachyarrhythmias
4.Ventricular tachyarrhythmia
5.Long QT syndrome
6.Brugada syndrome
7.Related to pacemakers and ICDs
8.Drug arrhythmogenic effect
Hemodynamic
1, heart valve lesions: such as aortic and aortic valve stenosis, pulsatile and pulmonary valve stenosis, mitral valve stenosis, prosthetic valve dysfunction.
2, acute myocardial infarction and/or ischemia
3, hypertrophic obstructive cardiomyopathy
4, atrial mucinous aneurysm
5, acute aortic coarctation
6, acute pericardial tamponade
7, pulmonary embolism and pulmonary hypertension
Non-cardiac syncope
Neurally mediated syncope
1.Vascular vagal
2.Carotid sinus syndrome
3.Other reflex syncope
①coughing ②gagging ③urination ④defecation
Orthostatic hypotension
1.Primary autonomic dysfunction
2.Secondary autonomic dysfunction
Cerebrovascular disease
Subclavian steal syndrome
Unexplained syncope
III. Diagnosis and differential diagnosis of syncope
Clinical assessment (1) Initial assessment: whether the syncope is real or not, through history, physical examination, ECG
(2) Suspicious diagnosis: further auxiliary examination
(3) Define the cause, determine the diagnosis and treatment
(A) Medical history
1. Causes.
(1) Position-related syncope: syncope in the recumbent position when prominently standing up: upright hypotension. Syncope after change of position: atrial mucinous tumor.
(2) Syncope related to neck activity: mostly due to carotid and vertebral artery stenosis, or allergic syncope of the vertebral sinus.
(3) Syncope occurring in the prone position: As syndrome, hyperventilation syndrome.
(4) Syncope occurring during starvation: hypoglycemia.
(5) Syncope occurring in special environments (situational): e.g. urination, coughing, bathing, diving syncope: mostly neuroreflex syncope.
(6) Syncope preceded by palpitations: suggestive of arrhythmogenicity.
(7) Syncope at the time of exercise: common in aortic stenosis.
(8) Syncope shortly after exercise: hypertrophic cardiomyopathy.
(9) Induced during arm exercise: subclavian steal syndrome.
(10) Drug-related syncope: antihypertensive drugs, hypoglycemic drugs, antiarrhythmic drugs, digitalis drugs, diuretics, etc.
(11) Family history of sudden death: long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy.
2.Prodromal symptoms
General syncope can be preceded by symptoms of vagal hyperfunction: such as pallor, sweating, nausea, vomiting, palpitations due to rapid arrhythmias, hyperventilation syncope: first dyspnea (accelerated frequency) then tachycardia, numbness in the end of the extremities and around the mouth. Cerebrovascular syncope: preceded by neurological symptoms, such as hemiparesis and symptoms of cranial nerve damage: such as dysarthria, diplopia, vertigo. Some cardiac arrhythmias and postural hypotensive syncope may have no antecedent symptoms.
3. Duration: syncopal episodes are mainly brief loss of consciousness, with varying duration, but mostly within one minute, and up to 2-3 minutes in long cases.
(B) Physical examination: pay attention to the mental state, body position, facial color, blood pressure, heart rate.
1, vasovagal syncope: pale face, but no cyanosis, may have blood pressure and/or slowed heart rate.
2, Aortic stenosis, left atrial mucus aneurysm: corresponding characteristic murmur.
3, As syndrome: pale face, mostly cyanosis, deep and slow breathing, or sigh-like breathing, or even cardiac respiratory arrest, and facial flushing when the heartbeat is restored.
4, congestive heart failure: often with a drop in blood pressure.
5, due to hypertension: blood pressure is elevated.
6, hysterical syncope: face and blood pressure are normal.
7, subclavian steal syndrome or arterial entrapment: unequal blood pressure in both arms.
8, epilepsy: impaired consciousness > 5 minutes, spontaneous tonic clonus, tongue biting, and cyanotic face.
(iii) Electrocardiogram
The presence of abnormal ECG (excluding non-specific ST-T changes) suggests that syncope may be related to arrhythmias. ECG abnormalities are independent predictors of cardiac syncope and increased mortality, and the following are abnormal ECG manifestations that may be associated with arrhythmic syncope.
1, double branch block (left bundle branch, right bundle branch combined with left anterior or left posterior branch block)
2, other intraventricular block (QRS time limit >= 0.12s)
3.Second degree type II or higher AVB.
4.Severe sinus bradycardia of 3s.
5, Pre-excitation syndrome.
6, QT prolongation.
7.V1-3ST elevation with right bundle branch block.
8, T wave in the right thoracic lead leading to positive epsilon wave and late ventricular potentials, suggesting arrhythmogenic right ventricular dysplasia (ARVD).
9, Abnormal Q waves: suggesting myocardial infarction.
(iv) Further relevant tests
1.Electrocardiogram: The patient’s subjective complaints are objectively confirmed.
2.Electrocardiogram with exercise stress
Syncope with double bundle branch block: induce atrioventricular block.
Ischemic heart disease: induced out ventricular tachycardia.
Vaso-vagal syncope: vaso-vagal response is enhanced during the recovery period of exercise test, and syncope is likely to occur.
3.Echocardiography: detect heart valve or structural abnormalities, such as valve stenosis, incomplete closure, prolapse, tendon rupture, hypertrophic cardiomyopathy, pericardial effusion, congenital heart disease, atrial mucinous aneurysm, aortic coarctation, post-myocardial infarction ventricular wall aneurysm, etc.
4, ventricular late potential (VLP): high-frequency, low-amplitude fragmented electrical activity on the terminal part of the QRS wave and ST segment, its presence suggests the existence of slow conduction zones within the ventricle, with potential folding pathways, and folding ventricular tachycardia may occur under suitable conditions.
Significance
(1) Syncope without cause: Positive VLP indicates the cause of ventricular tachycardia.
(2) Heart attack, cardiomyopathy: positive VLP, risk of sudden death.
(3) Recurrent sustained ventricular tachycardia: positive VLP, indicating a folding mechanism.
(4) Recurrent syncopal ventricular tachycardia: positive VLP with antiarrhythmic pacemaker.
(5) Persistent ventricular tachycardia: VLP negative, suggesting that the ventricular tachycardia mechanism is not folding.
5.Heart rate variability (HRV)
It refers to the degree of sinus arrhythmia, and is used for the assessment of sympathetic and parasympathetic regulation disorders. For people prone to syncope, sympathetic activity is hyperactive and HRV is low; for hypertension, coronary heart disease and heart failure, sympathetic activity is enhanced and vagal activity is diminished and HRV is low.
6.Cardiac electrophysiological examination
(1) Atrioventricular esophageal pacing.
(2) Intracardiac electrophysiological examination: standard electrogram, programmed stimulation method.
(3) Significance: (1) Auxiliary diagnosis of diseased sinus: esophageal pacing to determine the recovery time of sinus node, sinus conduction time, etc. (2) Assessment of atrioventricular node function; (3) Assessment of Hipp’s fiber system function; (4) Assessment of the characteristics of atrioventricular bypass; (5) Induced termination of supraventricular and ventricular arrhythmias associated with syncope. (6) Differential diagnosis of wide QRS tachycardia. (⑦Screening of antiarrhythmic drugs. ⑧Provide diagnostic means for radiofrequency ablation.
7.Electroencephalogram
Mainly used for the diagnosis of epilepsy and differential diagnosis of syncope.
8.Radiological examination
(1) Cardiovascular angiography.
(2) Cerebral angiography.
(3) Digital subtraction angiography (DSA): is a combination of electronic computer and angiography, digitized and subtracted by the electronic computer to remove unnecessary images, so that the conventional cardiac and cerebral angiography images are clearer and have better contrast.
(4) CT ① intracranial occupancy ② cerebrovascular accident: hemorrhage, infarction. (3) Determine or exclude intracerebral hematoma, contusion, distinguish epidural, subdural. ④In combination with imaging, diagnose spinal cavernous disease, spinal cord occupying lesions. ⑤ Aortic coarctation hematoma.
9.Magnetic resonance imaging (MRI)
Using the strong difference in magnetic resonance signals between normal and diseased tissues in the human body, tomographic images are obtained using scanning and computer reconstruction. Compared with CT, because it can obtain cross-sectional, coronal, and sagittal images, it makes the image anatomical structure realistic, lesions are clearly displayed, and the localization and qualitative diagnosis of lesions are accurate. MRI is also prominent in the examination of the head, spinal canal, spinal cord and blood vessels because it can image normal or abnormal blood vessels without contrast because of the low signal (dark shadow) of blood vessels during MRI examination. The diagnosis of pericardial disease, cardiomyopathy and pericardial calcification is reliable, and the diagnosis of the extent of aortic coarctation, entrance and exit, the presence of calcification and branch lesions is accurate and reliable.
10.Upright tilt test (TTT)
Mechanism: In normal people, lower limb congestion during uprightness decreases the amount of return blood, ventricular filling decreases, aortic pressure decreases, and through the carotid sinus and aortic arch pressure receptors, reflexively causes sympathetic excitation, heart rate increases, heart contraction strengthens and peripheral vasoconstriction and keeps blood pressure normal. In patients with vasovagal syncope, a sudden reduction in return blood volume can cause an excessive increase in catecholamine secretion and a significant increase in myocardial contraction, resulting in a highly contracted state of near-complete ventricular emptying, which in turn overstimulates mechanoreceptor C fibers in the inferior posterior wall of the left ventricle, and afferents to the medullary cardiovascular center via the vagus nerve and the glossopharyngeal nerve, thereby inhibiting the normal state of sympathetic nerve Therefore, the afferent signals from the cardiovascular center are dominated by the parasympathetic component, and the parasympathetic nerve is clearly dominant when the afferent signals are sent to the heart and blood vessels, which eventually leads to abnormal vasodilation, blood pressure drop, and heart rate slowdown, and the above mechanism also produces paradoxical cerebral vasoconstriction, causing insufficient blood supply to the brain and prompting syncope. Isoprenaline enhances myocardial contractility and increases the sensitivity of afferent fibers, resulting in an increased positive test rate.
Objective: To evaluate neurally mediated syncope, diagnose unexplained syncope, except for organic heart disease such as severe hypertension, coronary artery disease, main stenosis, pulmonary hypertension, hypertrophic obstructive cardiomyopathy, pacemaker interventional tachycardia, and syncope whose etiology is clear before the test.
11.Carotid sinus massage test
Mechanism: When the pressure in the carotid sinus increases, the excitation of pressure receptors causes reflex vagal excitation, heart rate slows down, and blood pressure decreases. There are three types of carotid sinus massage: cardiac suppression type: cardiac arrest ≥ 3S; vascular decompression type: decrease in systolic blood pressure ≥ 50 mmHg; mixed type.
Purpose: It is mainly used for the diagnosis of carotid sinus allergic syncope.
Contraindications to carotid sinus massage: ①have severe atherosclerosis and carotid stenosis. ② Have a stroke within 3 months.
12.Rising test in prone position
Mechanism and purpose: The mechanism is the same as the upright tilt test, but this test is to observe the immediate response of blood pressure and heart rate after uprightness to diagnose upright hypotension or upright tachycardia.
Determination of results: Normal individuals may have a mild transient decrease in systolic blood pressure after uprightness, but = 30 mmHg or syncope or near syncope.
Upright tachycardia: increase in heart rate >= 25 beats/min after uprightness.
13.Drug test
(1) Atropine test: release the inhibition of the sinus node by the vagus nerve, used as an adjunct to the examination of pathological sinus node syndrome.
(2) Isoprenaline test: used for the differential diagnosis of sinus bradycardia and pathological sinus node syndrome.
(3) Phentolamine test: used for the auxiliary diagnosis of pheochromocytoma.
14.Measurement of blood and endocrine metabolites
(1) Blood glucose: hypoglycemic syncope.
(2) Cardiac enzymes, troponin measurement: acute heart attack.
(3) Blood and urine catecholamine and its metabolite concentration determination.
(4) Blood routine: severe anemic syncope.
(5) Blood electrolytes: electrolyte abnormalities such as low potassium for the diagnosis of arrhythmogenic syncope.
(E) Risk stratification of syncope
There are five variables for predicting the risk of syncope: (1) age older than 45 years; (2) history of heart failure; (3) history of ventricular arrhythmias, especially ventricular tachycardia and ventricular fibrillation episodes; (4) specific electrocardiogram changes, such as Q-T prolongation, Brugada syndrome electrocardiogram changes; (5) special occupations such as driving and piloting.
IV. Characteristics of various diseases causing syncope
(A) Cardiac syncope
It refers to syncope caused by sudden reduction or suspension of cardiac output due to cardiac disorders, mostly caused by arrhythmia and/or organic heart disease. The common features are: seizures can occur in any position, triggers are mostly related to exertion, asymptomatic or palpitations before the seizure, changes in heart rhythm during the seizure, cyanosis or pallor, dyspnea, recurrent syncope, and a history of heart disease.
1. Cardiac arrhythmia: Both too fast and too slow heart rates can lead to syncope. In normal people, the heart rate to maintain cerebral blood flow in the prone position is 35~190 beats/min. If it is greater than 190 beats/min, syncope occurs due to insufficient filling of ventricular diastole and a significant decrease in cardiac output, which leads to inadequate cerebral blood supply, and the situation is more serious if cardiac insufficiency; if the heart rate is too slow, less than 35 beats/min or arrest, the cardiac output is reduced or interrupted, which can also cause syncope.
(1) Morbid sinus node syndrome: syncopal episodes can manifest as slow arrhythmias such as severe sinus bradycardia, sinus block, and ventricular arrest. It can also be in rapid arrhythmias such as paroxysmal atrial fibrillation, when atrial flutter is abruptly terminated after an episode (fast-slow syndrome). Electrocardiogram during the attack, atropine test and atrial pacing during the inter-episode period can provide a diagnostic basis.
(2) Atrioventricular block: II degree type II and III degree house block cause syncope and convulsion due to slow heart rate and arrest, called A-S syndrome.
(3) Tachyarrhythmia: Transient supraventricular tachycardia, paroxysmal atrial fibrillation, atrial flutter and paroxysmal supraventricular tachycardia are prone to syncope when the ventricular rate is greater than 190 beats/min especially when the cardiac function is poor, mostly occurring at the beginning or termination of tachyarrhythmia.
Electrocardiogram during the attack is of diagnostic significance. The cause of syncope can be found in about 85% of patients if the interval is combined with dynamic ECG, exercise test and electrophysiological examination if necessary.
(4) Long Q-T interval syndrome: can be divided into two categories: primary and secondary, primary, also known as congenital, familial, is a congenital disorder, often early sudden death and repeated syncope familial, sometimes with deafness, secondary often due to electrolyte abnormalities (low potassium, low magnesium, low calcium), drugs (anti-arrhythmic drugs, anti-psychotic drugs, antimony, etc.), central nervous system injury, autonomic function The diagnosis is based on the electrocardiogram at the time of the attack.
The diagnosis is mainly based on the electrocardiographic recording of tip-twisting ventricular tachycardia and prolonged Q-T interval between episodes.
(5) Brugada syndrome: recurrent ventricular fibrillation without a diagnosis of organic heart disease, characterized by (1) ST-segment elevation in specific right thoracic leads (V1-V3) with ST-segment multiplicity with or without RBBB; (2) no significant abnormalities in cardiac structure; and (3) a tendency to recurrent fatal ventricular tachyarrhythmias.
(6) Pacemaker-induced syncope: There are three categories; pacemaker failure, pacing syndrome and pacemaker-mediated tachycardia. Pacemaker syndrome refers to symptoms such as syncope and hypotension occurring at the same time as retrograde conduction after ventricular pacing, and the diagnosis of pacing syndrome is established when the symptoms disappear after stopping pacing or changing to sequential atrioventricular pacing (without atrioventricular block).
(7) Arrhythmogenic effects of drugs
Anti-arrhythmic drugs can lead to malignant arrhythmias due to their arrhythmogenic effects, which can produce life-threatening syncope, such as quinidine, cardioplegia, digitalis poisoning due to severe rapid or slow arrhythmias, even ventricular fibrillation, syncope and even death.
2.Hemodynamic
(1) Aortic stenosis: left ventricular ejection is severely blocked, and cardiac output is fixed at a low level and does not increase with activity, so it is called “exertional syncope”. The main points of diagnosis: ① syncope is related to exertion and can be accompanied by angina pectoris. The syncope lasts for a long time and is often followed by chest tightness, weakness, palpitations and other symptoms. ③There is a systolic murmur in the aortic valve area, which conducts toward the neck. (④Echocardiography may help in the diagnosis.
(2) Hypertrophic obstructive cardiomyopathy, also known as idiopathic subaortic stenosis. Episodes of syncope are associated with ventricular outflow tract obstruction or/and sympathetic excitation, and occur mostly after exertion and emotional stress. There is mostly a family history, and the diagnosis is not difficult to confirm by physical and echocardiographic examination.
(3) Atrial mucinous tumor: It is common in the left atrium. Syncope often occurs when the position is changed, when sitting or standing from the prone position, the mucinous tumor or thrombus is embedded in the atrioventricular valve orifice, causing temporary obstruction and interruption of blood drainage. Clinical features: (1) syncope occurs during position change; (2) apical murmur changes with position; (3) embolism, fever, heart failure and other symptoms may be present; (4) echocardiography has characteristic changes.
(4) Aortic coarctation: syncope occurs mostly at the early stage of the disease. Syncope can be caused by upward expansion of the aortic coarctation hematoma, which compresses the carotid artery or the unnamed artery and reduces the blood supply to the brain, or by rupture of the coarctation to the pericardium, causing acute pericardial tamponade. Diagnostic points: ① severe tearing-like pain in the chest or abdomen. ②There are clinical shock-like manifestations, but the blood pressure does not drop significantly or increases. ③A sudden diastolic murmur in the aortic valve area on auscultation. ④Previous history of hypertension. ⑤ Aortography can provide a definite basis, and CT and MRI have high diagnostic specificity.
(5) Acute pericardial tamponade: syncope is mainly caused by a sudden increase in pericardial cavity pressure, obstruction of blood return and reduced blood displacement. Echocardiography is a specific diagnostic method.
(6) Acute pulmonary embolism: acute massive pulmonary embolism causes syncope due to increased pulmonary vascular resistance and reduced left ventricular filling. Diagnostic points: ①Previous organic heart disease with a history of atrial fibrillation or/and thrombosis. ②Sudden onset of dyspnea, chest pain, hemoptysis, cyanosis, syncope, or acute right heart failure. (③Pulmonary arteriography or spiral CT may provide a confirmatory basis for diagnosis.
(7) Acute myocardial infarction and/or ischemia: It is a rare cause of syncope and is associated with vagal hyperfunction and sudden arrhythmias. ECG and myocardial enzymology, coronary angiography, and other tests may help in the diagnosis.
(8) Congenital heart disease: a rare cause of syncope, mainly including tetralogy of Fallot, Eisenmenger syndrome, primary pulmonary hypertension and pulmonary valve stenosis, etc. The diagnosis is easily confirmed by physical examination and echocardiography.
(B) Non-cardiac syncope
1, neurally mediated syncope: the most common cause of syncope, common features: no evidence of organic heart disease, the attack is related to posture or physiological action, there can be syncopal aura before the attack, the attack is brief and can recover on its own.
(1) Vasovagal syncope: accounts for most of the unexplained syncope (about 70%). Characteristics: (1) Most often seen in young and frail women. (2) There are mostly clear causes: mental stimulation, emotional stress, acute trauma and long-term chronic diseases, etc. ③Seizures are position-related, rarely occurring in the prone position, but mostly in the standing or sitting position, with aura of syncope before the seizure, and can recover quickly when lying down immediately after the onset of symptoms. ④According to the change of blood pressure and heart rhythm during the attack, there are three types: cardiac suppression type, blood pressure suppression type and mixed type, with mixed type being the most common. (5) Upright tilt test can confirm the diagnosis.
(2) Carotid sinus syncope: Syncope caused by hyperreflexia and increased sensitivity of carotid sinus caused by various reasons. The most common causes of syncope are the compression of the carotid sinus by tissue lesions around the neck (inflammation, occupancy, trauma, etc.), which causes abnormal reflexes; increased sensitivity of the carotid sinus in hypertension, coronary artery disease, diabetes mellitus, etc.; certain drugs, such as digitalis and certain parasympathetic drugs, can also cause hyperreflexia of the carotid sinus, resulting in syncope. Predisposing factors are related to pressure on the carotid sinus (e.g. too high collar, too tight, neck compression test) and excessive strain on the carotid sinus.
Diagnostic points: ① History of syncopal attacks, related to the above-mentioned etiology and precipitating factors. ② Most often seen in middle-aged men, carotid sinus massage test can induce the same symptoms. The main manifestation of the attack is a decrease in heart rate or blood pressure. (3) Syncope rarely occurs in the prone position, but mostly occurs in the standing or sitting position.
(3) Other reflex syncope
①Cough syncope: refers to a brief loss of consciousness that occurs after coughing and can be recovered quickly without sequelae. Patients often experience syncope after a violent cough and recover on their own in a few seconds to minutes. The mechanism may be increased intrathoracic pressure, decreased venous return, and decreased cardiac output, leading to ischemic attack and syncope.
Urinary syncope: It is syncope that occurs at the beginning, during, at the end and immediately after the end of urination, usually without prodromal symptoms, and can recover on its own. The mechanism may be related to factors such as high vagal tone of the patient, sudden change of position, sudden decrease in blood volume and air-abandonment action.
(iii) Diving syncope: sudden syncope and even sudden death during underwater diving. Hypoxia and vagus nerve hyperfunction are the pathogenesis.
Swallowing and lingual-pharyngeal neuralgia syncope: some patients with lingual-pharyngeal neuralgia can have syncope or even convulsions during painful episodes, and some patients with esophageal, pharyngeal and mediastinal disorders can have syncope or even convulsions during swallowing, which usually last for a short period of time, 10-15 seconds. The mechanism is related to reflex cardiac depression of the vagus nerve, causing severe sinus bradycardia, sinus arrest or atrioventricular block, decreased cardiac output, resulting in cerebral ischemia and syncopal episodes.
2.Upright hypotensive syncope
When a healthy person rises from the prone position, the cardiac output decreases and the blood pressure falls, stimulating the pressure receptors of the carotid sinus and the aortic arch, which are transmitted to the vasomotor center, causing sympathetic excitation, increased secretion of catecholamines and renin, so the vasoconstriction and tachycardia occur, and the blood pressure rises, ensuring the blood supply to the brain. Impaired or impaired regulation of any of the above regulatory mechanisms can lead to postural hypotension and cause syncopal episodes. Several types.
(1) Physiological disorders: seen when standing stationary for a long time, pregnant women and those who suddenly rise from bed for a long time. Syncope can also occur in normal people when they are engaged in strenuous activity and suddenly stop, which is associated with a sudden drop in cardiac blood displacement and a lag in vascular regulation.
(2) Idiopathic upright hypotension (primary autonomic dysfunction): also known as shy-Drager syndrome, clinical features are: (1) onset in middle age or older, with significantly more male patients than female. The clinical features are: (1) the onset of upright hypotension in middle age or older, with significantly more men than women. (2) the onset of syncope and syncope on standing, but rarely with facial changes and nausea, with progressive worsening of symptoms. It is accompanied by impotence and absence of sweating. Symptoms of extrapyramidal and cerebellar lesions are also present. (3) The standing prone test helps to diagnose the disease, and the blood pressure drops significantly during the attack without significant heart rate changes.
(3) Acquired postural hypotension (secondary autonomic dysfunction): seen with certain drugs (such as chlorpromazine, guanethidine, diuretics and calcium antagonists), after sympathectomy and certain systemic diseases, such as spinal cord damage, polyneuritis, diabetic neuropathy, chronic dystrophy, etc.
(C) Cerebrovascular disease
1, transient ischemic attack (TIA): TIA is due to the impaired circulation of the vertebral basilar artery leading to syncope, accounting for 7.7% of syncope. in addition to loss of consciousness, TIA attacks can also have vertigo, ataxia and sensory impairment.
2, medullary syncope: lesions and dysfunction of the medullary cardiovascular center can lead to syncope attacks. It is mainly seen in certain diseases involving the cardiovascular center (such as myelitis, poliomyelitis, Guillain-Barre syndrome, rabies, etc.).
3. Migraine: In some young women, migraine attacks during menstruation can be accompanied by syncopal attacks. It is characterized by a slow development of loss of consciousness and may be followed by severe pain in the occipital region. The mechanism is unknown and may be related to brainstem ischemia due to basilar artery spasm or inhibition of the cardiovascular motor center due to excessive dopamine receptor response.
(iv) Subclavian steal syndrome (stealsyndrome): When the subclavian artery is narrowed, the blood flow of the affected ipsilateral vertebral artery is reversed during arm movement, resulting in syncope due to vertebrobasilar artery ischemia. The main diagnostic basis: ① the blood pressure of the affected upper limb is about 20 mmHg lower than that of the healthy side. ② the pulsation of the radial artery on the affected side is diminished or absent, and most of the vascular murmurs can be heard in the path of the affected subclavian artery. ③Motion of the affected upper extremity may induce or aggravate the symptoms. (iv) Vertebral artery angiography can establish the diagnosis.
(E) Mental disorder syncope
1, hysterical syncope: not true syncope. Rather, it is a narrowing of the range of consciousness, and its episodes can be terminated or intensified by implication.
2, hyperventilation syndrome: mostly seen in young women. The mechanism is due to emotional stress or hysterical attack caused by enhanced respiration and hyperventilation, carbon dioxide emission increases, which can lead to respiratory alkalosis and cerebral vasoconstriction, cerebral hypoxia, mostly manifested as chest tightness and suffocation, tachycardia, end of limbs, facial and perioral numbness, hand and foot twitching, and blurred consciousness.
(F) Blood and endocrine metabolism abnormalities cause syncope
1, hypoxia: refers to the cerebral circulation of blood flow does not necessarily reduce the oxygen saturation, oxygen partial pressure reduction or red blood cell reduction, so that brain cells are hypoxic and cause syncope. Such as tetralogy of Fallot, primary pulmonary hypertension, when the activity is intense and crying. Syncope can occur after activity in patients with severe anemia.
2, hypoglycemia: spontaneous, secondary and the application of hypoglycemic drugs, especially insulin overdose caused by severe hypoglycemia can produce syncope or even coma. The onset of syncope has nothing to do with body position, tachycardia during the attack, blood pressure is normal, and syncope occurs gradually, mostly accompanied by weakness, sweating, and low blood sugar measured at the time can confirm the diagnosis. The symptoms are relieved soon after the application of glucose.
V. Treatment principles and prognosis of syncope
(A) Cardiac syncope: The main treatment is for the original disease. For syncope caused by blocked cardiac drainage, surgical treatment is the main treatment; for syncope caused by arrhythmia, drugs, artificial pacemakers and catheter radiofrequency ablation are used according to their different types; for syncope caused by pacemakers, the causes should be investigated, troubleshooting, and pacemakers should be replaced if necessary.
(B) Neurally mediated syncope
1.General treatment
(1) Patient education, understanding the triggers of syncope, and avoiding triggering factors.
(2) In patients with recurrent vasovagal syncope, gradually extending the standing time (called tilt exercise) can reduce the syncope attacks.
(2) Pharmacological treatment: many drugs can be used for vasovagal syncope, including ① β-blockers: reduce sympathetic stimulation and C-fiber stimulation, ② α-agonists: increase peripheral resistance and effective blood volume, ③ anticholinergics: reduce vagal tone, ④ salt corticosteroids: increase Na+ reabsorption and increase blood volume, ⑤ theophyllines: block adenosine, increase heart rate and raise blood pressure.
3.Pacing therapy: For vasovagal syncope, it was thought that pacing therapy was limited because it could not prevent the onset of syncope in the tilt test, but the results of a multicenter clinical trial showed that pacing therapy was effective in some patients. In patients with vasovagal syncope of the cardiac depression type, dual-chamber pacemaker therapy may be considered when the effect of general therapy is not obvious. For patients with carotid sinus syndrome, high collar and overly tight shirts should be avoided, neck compression maneuvers should be avoided, and atropine, epinephrine, and sedatives should be used to treat different types of syncope during attacks. Double-chamber pacing is recommended for some patients with bradycardia, and care should be taken to avoid the use of vasodilator drugs.
(iii) Upright hypotensive syncope
The main goal of treatment of upright hypotensive syncope is to reduce the symptoms associated with cerebral hypoperfusion (syncope, near syncope, and confusion, etc.). Avoid factors that affect blood pressure, such as sudden changes in position, prolonged standing, standing to urinate, hyperventilation, high temperatures, strenuous exercise, large amounts of food (especially carbohydrates), alcohol, and drugs that cause vasodepression. Other treatments include: (1) methods to increase blood volume, encouraging adequate daily intake of salt and fluids, and small doses of glucocorticoids; (2) reducing blood volume accumulation in the lower part of the body: using a lap band, pantyhose, etc.; (3) eating fewer meals and reducing the amount of carbohydrates; (4) crossing or squatting the lower extremities; and (5) exercises to exercise the lower extremities or abdominal muscles, such as swimming.
(iv) cerebrovascular syncope: mainly for the treatment of the original disease, according to the conventional treatment of cerebrovascular disease, pay attention to moderate hypotension (with hypertension), intracranial occupancy feasible surgical treatment.
(e) Subclavian artery steal syndrome: direct surgery or angioplasty is effective.
(F) Syncope caused by psychiatric factors: mainly by suggestive therapy and sedation if necessary.
(vii) Syncope due to blood and endocrine metabolism: the main treatment is also the primary disease. And the drug effect causes syncope is mainly to stop the relevant drugs.
The prognosis of syncope is directly related to its etiology, and the prognosis of syncope with different underlying lesions varies greatly. In general, the prognosis of cardiogenic syncope is the worst, with a one-year mortality rate of 30%, which is worse with malignant arrhythmias and abnormal cardiac function; non-cardiogenic syncope is the second worst, with a one-year mortality rate of 0%-12%, with cerebral syncope having a higher mortality rate than other syncopes, and reflex syncope and syncope caused by psychiatric factors having a relatively good prognosis. The prognosis of unexplained syncope is better than the above 2 categories, with a one-year mortality rate of 6%. Therefore, the diagnosis of the etiology of syncope is important for the choice of its treatment and prognosis.