I. General principles
The principles of treatment for syncope are to prolong the patient’s life, prevent somatic damage, and prevent recurrence.
The etiology of syncope is crucial to the choice of treatment. Assessment of the etiology and mechanism of syncope should generally be performed simultaneously to determine the appropriate treatment plan to be ultimately adopted. The standard treatment for syncope should address the cause of the whole brain hypoperfusion. However, in cases where the etiology is unclear or where current treatments are not effective (e.g., no specific treatment for degenerative AV block), treatment should be directed at the pathogenesis of the whole-brain hypoperfusion (e.g., pacing should be performed for degenerative AV block). Appropriate treatment should be administered according to risk stratification (Figure 3).
II. Reflex syncope
The main goals of treatment are to prevent recurrences and associated injuries and to improve quality of life.
1. Prevention strategies.
Education is the cornerstone of nonpharmacologic treatment of reflex syncope, convincing patients that it is a benign condition and understanding the disorder, avoiding triggers (e.g., stuffy and crowded environment, hypovolemia), recognizing prodromal symptoms early, taking certain maneuvers to terminate the episode (e.g., supine position), and avoiding medications that cause lower blood pressure (including alpha blockers, diuretics, and alcohol). Although there are many mechanisms that cause this type of syncope, all prevention strategies apply.
Other treatments need to be given for unpredictable and frequent syncope, especially when the episodes are very frequent and affect the quality of life, when there are no or only very brief precursors of syncope for recurrent syncope, when there is a risk of trauma, and when the syncope occurs in high-risk operations (e.g., driving, operating machines, flying, competitive sports, etc.).
2.Treatment methods.
(1) Physical therapy [physical counterpressure maneuver (PCM)]: Non-pharmacological “physical” therapy has become the first-line treatment for reflex syncope. Isometric muscle contractions of the legs (legs crossed) or upper extremities (hands clasped and upper extremities tensed) can significantly raise blood pressure during reflex syncope episodes and in most cases allow patients to avoid or delay loss of consciousness. Tilt training: In highly sensitive young patients, when the upright position induces symptoms of vascular vagal excitation, forcing upright, gradually prolonging the time, “tilt training” can reduce the recurrence of syncope.
(2) Drug therapy: Many drugs that have been tried to treat reflex syncope are ineffective. These include beta-blockers, propylamine, scopolamine, theophylline, ephedrine, etiflorine, midodrine, colistin, and 5-hydroxytryptamine reuptake inhibitors.
Because peripheral vasculature often fails to constrict appropriately during reflex syncope, treatment with alpha agonists (etifolin and midodrine) has been used in the past; however, long-term use of alpha agonist drugs alone in patients with reflex syncope is less effective, and long-term treatment is not recommended for episodic patients.
A single dose of the drug (keep 1 tablet strategy handy) is recommended 1 h before prolonged standing or engaging in syncope inducing activities, and this treatment may be effective in some patients in addition to lifestyle and physical counterpressure maneuvers.
Fludrocortisone is widely used in adult patients with reflex syncope, but there is no trial evidence to support this. It has been postulated that the application of beta-blockers may be effective, but five of the six long-term follow-up studies confirmed beta-blocker ineffectiveness. One placebo-controlled study confirmed the effectiveness of paroxetine. Paroxetine is a psychotropic drug that reduces patient anxiety in response to unexpected events and should be used with caution in patients without serious psychiatric illness.
(3) Cardiac pacing: Cardiac pacing is rarely used in the treatment of reflex syncope, unless severe bradycardia is found. Pacing may be beneficial for carotid sinus syncope.
III. Postural hypotension and upright intolerance syndrome
1. Non-pharmacological treatment: Health education and lifestyle changes can likewise significantly improve the symptoms of upright hypotension, even if the increase in blood pressure is small (10-15 mmHg), which is sufficient to produce a significant functional improvement within the body’s own regulation.
The principles of treatment of drug-induced ANF are elimination of drug effects and expansion of extracellular fluid volume. Patients without hypertension should be instructed to consume sufficient salt and water, up to 2-3 L of fluid and 10 g of sodium chloride per day. Elevation of the head of the bed during sleep (10°) prevents nocturnal polyuria, maintains good fluid distribution, and improves nocturnal blood pressure.
Gravitational venous stasis in elderly patients can be treated with a lap band or compression stockings. Patients with premonitory symptoms should be encouraged to perform “physical counterpressure maneuvers” such as lower limb crossing and squatting.
2.Medication: In contrast to reflex syncope, in patients with chronic ANF, the alpha agonist Midodrine should be used as first-line treatment. However, it is not curable and the efficacy varies, and is only effective in some patients. Midodrine increases blood pressure in both the prone and upright positions, thereby slowing the symptoms of postural hypotension. Midodrine dosage is 5 to 20 mg/dose 3 times a day. Fludrocortisone (0.1 to 0.3 mg/d) is a salt corticosteroid that promotes sodium retention and fluid expansion. The patient’s symptoms decrease and blood pressure increases after the administration of the drug.