Is a person who suddenly fainted, fainted or cardiac arrest? Is the risk high or low? Do you need CPR? How to evaluate and treat patients with fainting? Dr. Zhou Peng, Chairman of the Academic/Education Committee of the Chinese Heart Association (CNAHA) and Director of the Department of Internal Medicine at Beijing Mingde International Hospital, answered the above questions in combination with the brief version of the "Symptom Handbook" of the Massachusetts General Hospital affiliated to Harvard University, and interpreted the "2017 Guidelines for Assessment and Management of Patients with ACC/AHA/HRS" and the "2018 Guidelines for Diagnosis and Management of ESC".
1. Comparison and overall evaluation of European and American guidelines
"2017 Guidelines for Assessment and Management of Patients with Syncose" is the first syncope guide in the United States, focusing on the diagnosis and treatment strategies of syncope. The 2018 ESC Syncose Diagnosis and Management Guide is a relatively mature guide, an update to the 2009 version, with the top priority being to help prevent unnecessary hospitalizations and examinations, emphasizing the cost-benefit ratio. The two guides for
are slightly different in terms of recommendation level and evidence level. In terms of specific content, the two are the same principles, and some contents are different, such as the recommendation for beta-blockers for vasovagal syncope. In addition, European guidelines mention hypotension susceptibility, syncope units, etc. Both
guides provide good strategies, citing a large amount of literature, with very detailed content, strong practical guidance and operability, but not high level of evidence.
2. Overview of syncope
syncope is a sudden, complete, and short-term loss of consciousness caused by insufficient brain perfusion, which can be completely restored. A sign of fainting refers to a sign of dizziness, but no sign of fainting. Syncose accounts for 1% to 3% of emergency cases and 6% of hospitalized patients; the risk of syncope in an individual in their lifetime is 11% to 33%. The causes of syncope of
are complex, and the prognosis of syncope caused by different causes varies greatly. Overall, a single objective auxiliary examination is not of great value to the diagnosis of the cause. Careful medical history collection and physical examination, including vital signs in lying position and standing position, have the best cost-benefit ratio in diagnosis.
After excluding cardiogenic (20%) and neurogenic (10%) causes, the remaining vasovagal syncope (25%), orthostatic hypotension (10%) had better prognosis.
3. How to distinguish between syncope and cardiac arrest/ sudden cardiac death ?
sudden loss of consciousness can be seen in several clinical situations: fainting, cardiac arrest (SCA)/sudden cardiac death (SCD), and epilepsy. How to identify patients who have sudden loss of consciousness? When will cardiopulmonary resuscitation (CPR) begin?
fainting and cardiac arrest can be manifested as sudden falls. Is it that someone who suddenly fell to the ground fainting? Or SCA? Do you need CPR? The "Symptom Manual" gives a realistic and practical answer: those who wake up and stand up without CPR are fainting, because fainting is sudden and short, rarely exceeding 20 seconds; those who require CPR and defibrillation are SCD or SCA; the prognosis of the two is very different. When will
start CPR? Seeing a person fall, according to the latest CPR guidelines from the American College of Cardiology and the American Heart Association (ACC/AHA), witnesses should start CPR immediately after judging whether the environment is safe. Because fainting is short and reversible, it will not exceed 20 seconds in most cases and will recover on its own, while SCD or SCA is fatal, and it is irreversible if cardiopulmonary resuscitation is not promptly.
syncope, SCD and SCA were all retrospectively diagnosed. Seeing a person suddenly fall down and follow the ACC/AHA guidelines is the correct solution.
In addition, 80% of the initial rhythms in SCD are ventricular speed or ventricular fibrillation. If you do not defibrillate in time, it is difficult to succeed by relying on heart compression alone. Therefore, most of the people who have not recovered from defibrillation are dysfunction caused by fainting or other conditions.
4. The causes of syncope
The various guidelines and textbooks have different classifications of the causes of syncope.
1. Neurocardiogenic
is also known as vasovagal syncope or reflex syncope, accounting for about 25% of the causes of syncope. When coughing, swallowing, defecate or urinating, the vagus nerve tension increases, which can induce fainting.
2. Orthostatic hypotension (Orthostatic hypotension)
accounts for 10% of the causes of fainting. It can be seen in: (1) volume reduction caused by diuretics, vasodilator drugs, especially when combined with negative potency change drugs; (2) Autonomous neuropathy: ① Primary: Parkinson's disease , multisystem atrophy/Shy-Drager syndrome, Lewy body dementia, orthostatic tachycardia syndrome (POTS), ② Secondary: diabetes, alcohol dependence, amyloidosis and chronic kidney disease.
3. Cardiovascular (Cardiovascular)
accounts for 20% of the causes of syncope, and more men than women. Including: (1) arrhythmia , accounting for 15% of syncope; (2) mechanical, accounting for 5% of syncope.
Arrhythmias include: (1) Bradycardia: pathological sinoatrial syndrome, high atrioventricular block, drug and pacemaker failure during negative change; (2) Tachocardia: ventricular tachycardia, supraventricular tachycardia, unless combined with structural heart disease or pre-excitation syndrome.
Mechanical causes include: (1) Endaria/valvular: aortic valve stenosis, mitral valve stenosis , pulmonary valve stenosis, thrombosis of prosthetic valve and myxoma; (2) Myocardium: pump dysfunction after myocardial infarction, outflow tract obstruction of hypertrophic obstructive cardiomyopathy (more caused by ventricular velocity); (3) Pericardial: pericardial tamponade; (4) Vascular vessels: pulmonary embolism, pulmonary hypertension , aortic dissection, rupture of abdominal aortic aneurysm and subclavian blood thieves.
4. Neurologic
accounts for 10% of syncope, including posterior circulation ischemia, cerebral artery dissection, subarachnoid hemorrhage, transient ischemia attack/stroke and migraine.
5. Other causes of loss of consciousness (but not fainting)
includes convulsions/epilepsy, hypoglycemia, hypoxemia, narcolepsy, cardiac loss of consciousness, etc.
Dr. Zhou Peng mentioned that the two European and American guidelines did not mention or downplay neurogenic syncope. European Guidelines mention transient loss of consciousness (TOLC), a retrospective diagnosis.
5. Initial evaluation of syncope in
1. Medical history and physical examination
lying position and standing position vital signs have the best cost-benefit ratio. Other contents include:
Current medical history: The information provided by witnesses is very important, including the activities, posture, and posture of the patient before fainting.
trigger factors: (1) Labor induction: suggests aortic valve stenosis, hypertrophic obstructive cardiomyopathy and pulmonary hypertension; (2) Change in position: indicates orthostatic hypotension; (3) Coughing, defecation, urination and swallowing: indicates neurocardial (vasovagal syncope); (4) Head position change (turning back or shaving): indicates carotid sinus sensitivity; (5) Upper limb movement: subclavian artery stole blood.
prodromal symptoms: such as sweating, nausea, blurred vision, etc.; cardiogenic 5 seconds, vagus 5 seconds; incontinence indicates short-term brain hypoperfusion, usually less than 10 seconds, spasms and convulsions may occur, similar to epilepsy seizures.
Personal history: (1) previous fainting, previous cardiovascular and neurological diseases; (2) If the patient has no basic cardiovascular disease background, 5% is cardiogenic and 25% is vasovagal; (3) If the patient has basic cardiogenic and 25% is cardiogenic and 10% is vasovagal.
can be used as a drug for syncope: (1) ɑ receptor blockers, nitrates, ACEI/ARB, calcium antagonists, hydralazines, phenothiazines; (2) diuretics, negative time-changing agents such as beta receptor blockers; (3) Pro-arrhythmic effects of QT interval prolongation and antiarrhythmic drugs: IA, IC and III antiarrhythmic drugs; (4) Psychiatric drugs: antipsychotic drugs, tricyclic antidepressants, barbiturates, benzodiazepine drugs.
Family history: cardiomyopathy , family history of sudden cardiac death and fainting, vasovagal syncope may have genetic susceptibility.
Physical examination: A comprehensive physical examination was found and positive signs were found. Contents: (1) Vital signs (blood pressure); (2) Cardiac examination; (3) Vascular examination; (4) Nervous examination.
2. ECG
In terms of electrocardiogram recommendations and evaluation, European and American guidelines are consistent with the "Symptom Manual".
50% of patients with syncope have abnormal electrocardiograms, but the electrocardiogram changes that can determine the cause of syncope are less than 10%. The overall sensitivity of the ECG is high, but the specificity is very low.
Sinus arrhythmias and conduction blocks: sinus bradycardia, sinus arrest, atrioventricular block, bundle branch block, indoor conduction block, etc. Low sensitivity, but high specificity.
Arrhythmias: ectopic heart rhythm, prolongation or shortening of QT interval, pre-excitation syndrome (WPW), Brugada syndrome, arrhythmic right ventricular cardiomyopathy (Epsilon wave), supraventricular speed and ventricular speed. Low sensitivity, but high specificity.
3. Laboratory test
output value is low. Including blood sugar, hemoglobin, pregnancy test (female childbearing age), D-dimer, troponin (if there are no other symptoms and signs, the diagnostic value is small).
European and American syncope guide on initial evaluation is the same as the syncope manual (Figure 1). The 2018 European syncope guideline emphasizes the clinical pathways that determine patients based on initial assessment, and the 2017 American syncope guideline also proposes a flowchart of initial assessment post-processing (Figure 2). Data show that 50% of patients with fainting were hospitalized, and in the following 7 to 30 days, 0.8% of patients died, 3.6% had serious consequences and 6.9% had non-fatal serious consequences.
Figure 1 Initial evaluation of syncope (2017 US syncope Guide)
Figure 2 Processing process after initial evaluation of patients with syncope (2017 US syncope Guide)
6. Further objective examination
1. Dynamic electrocardiogram monitoring (if arrhythmia is suspected to cause syncope)
Event Recorder: Syncose is a sudden event, and the event recorder needs to be started by the patient. Only patients with obvious prodromal symptoms are useful.
In vitro event recorder: can continuously store heart rhythm and be activated after arrhythmia events occur. Suitable for patients who estimate events occur within a short period of time (such as within 1 month) (regardless of prodromal symptoms); it can also be coupled with mobile-remote ECG devices; event recording can be triggered by professionals.
implantable long-range event recorder (ILR): subcutaneously implanted, recording time can be up to 1 year. More than 55% of cases can be diagnosed, suitable for those with repeated syncope, but infrequent and no prodromal symptoms, such as syncope events once a month. The 2018 European syncope guideline recommends ILR (I, A) in patients with suspected cardiogenic syncope.
2. Echocardiography
is used to rule out structural heart disease (including hypertrophic obstructive cardiomyopathy and arrhythmic cardiomyopathy), valvular disease (aortic valve stenosis, mitral valve stenosis and mitral valve prolapse, etc.), myxoma, amyloidosis, pulmonary hypertension or coronary malformation.
3. Exercise load test, CT coronary angiography and catheter examination
, especially labor-induced syncope, rule out ischemic heart disease or catecholamine-induced arrhythmia.
4. Electrophysiological examination
Electrophysiological examination can be used to consider high-risk patients who are the cause of fainting but cannot be confirmed. If the patient has cardiovascular disease, 50% of the patients have abnormal electrophysiological examinations (induced ventricular speed, conduction abnormalities), but its importance remains controversial. If the electrocardiogram is abnormal, 3% to 20% of patients have abnormal electrophysiological examination; if the patient's heart or electrocardiogram is normal, 1% of patients have abnormal electrophysiological examination.
5. Tilt test (TTT)
The "Symptom Manual" points out that TTT is highly controversial due to its low sensitivity, specificity and repeatability; it is only used to consider patients with vaginosis but whose medical history is not certain.Dr. Zhou Peng believes that this view lacks scientificity, while European and American guidelines are more scientific.
TTT positive can reveal "hypotensive susceptibility" and can be seen in other syncopes, including cardiogenic syncope, and TTT helps with treatment options such as pacemaker implantation.
6. Cardiac MRI
If the electrocardiogram indicates cardiomyopathy and echocardiography have right heart insufficiency or a family history of sudden cardiac death, cardiac MRI is helpful in diagnosing arrhythmic cardiomyopathy.
7. Neurology examination
If the medical history and physical examination support, cerebrovascular examinations, CT, MRI and EEG examinations should be performed, but the value of helping diagnose is very limited. The 2017 US syncope guideline also believes that in terms of syncope assessment and management, routine neurological examinations are very costly to diagnose but have low diagnostic rates. The guidelines recommend that concurrent monitoring of EEG and hemodynamic parameters during tilt tests can help identify syncope, pseudosyncope, and epilepsy (IIa, C-LD).
Figure 3 Technical route for further examination after initial evaluation (2017 American syncope Guide)
7. High-risk characteristics of syncope
High-risk characteristics listed in the "Symptom Manual":
➤ Age 60 years old, coronary artery disease, cardiac insufficiency/cardiomyopathy, valvular disease or congenital heart disease, arrhythmia background, family history of sudden cardiac death;
➤ Syncope with heart causes (lack of prodromal symptoms, labor-induced, heart trauma) or recurrence;
➤ Patients complain of chest pain or dyspnea, abnormal signs of heart, respiratory and neurological examination;
➤ Electrocardiogram indicates abnormal conduction, arrhythmia or ischemia;
➤ Patients with pacemaker implantation or cardiac reversion defibrillator implantation.
Table 1 Related medical history characteristics that suggest cardiogenic and non-cardiogenic syncope
Table 2 Examples of serious diseases that require further hospitalization evaluation and treatment
8. Treatment of syncope
1. Cardiac or neurogenic syncope
treatment of underlying causes. Treatment of cardiac syncope includes: (1) cardiac inhibitory: pacemaker; (2) rapid arrhythmia: ablation or ICD+ ablation. ICD cannot reduce syncope load, and those that can be ablated before ICD should be ablated as much as possible. In terms of treatment plans, European and American guidelines and "Symptom Manual" are similar.
Figure 4 Overall framework for syncope treatment (2018 European syncope guide)
2. Vascular syncope
"Symptom Manual" recommends:
➤ Flucolithone, Midojson and the choice of serotonin reuptake inhibitor (SSRI) are controversial;
➤ Diisopropyramide and beta blockers have no preventive benefits;
➤ Have prodromic symptoms and drink 450-500ml of water before the onset, which is controversial;
➤ Three syncope events in two years, and the implantable event recorder records cardiac arrest for 3 seconds, and the benefits of pacemaker implantation are also controversial;
➤ If the tilt test is positive and there is no arrhythmia, pacemaker implantation is likely to be unhealthy.
Regarding the role of beta blockers in vaginosis, the recommendations of the US guidelines are inconsistent with those of the European guidelines and the syncope manual.
Table 3 Recommendations for treatment of vaginosis (2017 American Syncose Guide)
3. Syncose caused by orthostatic hypotension
syncope manual recommended treatment measures include: fluid capacity supplementation (500 ml of water every morning); if it is a chronic condition, you must wake up slowly; elastic stockings; midojal, atomoxetine (the effect is still controversial), fluorocortisone; increase the sodium-containing diet.
Figure 5 Treatment process for syncope caused by orthostatic hypotension (2017 American Syndrome Guidelines)
9. Prognosis of syncope
The overall recurrence rate of idiopathic syncope is 22%, and the recurrence rate in other situations is 3%. The incidence of SCD in patients with cardiogenic syncope is 20% to 40%, and the median survival time is 6 years. Vascular syncope does not increase the risk of death, myocardial infarction and stroke. The mortality rate of patients with syncope that cannot be explained by
has increased by 1.3 times, but it is not cardiogenic, with normal electrocardiogram, no ventricular speed, no history of heart failure and age 45 years of age, with a low recurrence rate and a 1-year SCD incidence rate of 5%.
Key points review
➤The causes of fainting are complex, and the prognosis is very different due to different causes.
➤ Careful medical history collection and physical examination, including the vital signs of lying position and standing position, has the best cost-benefit ratio in diagnosis.
➤ Overall, a single objective auxiliary examination is not of great value to the diagnosis of the cause.
➤There is a sword in the chest - After excluding cardiogenic and neurogenic causes, the prognosis of vasovagal syncope and "unexplained syncope" that accounts for 40% of syncope is good.
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