eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Syncope: Treatment & Medication

Author: M Silvana Horenstein, MD, Consulting Staff, Department of Pediatrics, University of Texas Medical School Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc
Coauthor(s): Robert Murray Hamilton, MD, MSc, FRCPC, Section Head, Electrophysiology, Director, High-Risk Hereditary Heart Conditions Clinic, Labatt Family Heart Centre; Professor, Department of Pediatrics, Associate Scientist, Physiology and Experimental Medicine, The Hospital for Sick Children and Research Institute, University of Toronto, Canada
Contributor Information and Disclosures

Updated: Nov 11, 2009

Treatment

Medical Care

Typical neurocardiogenic syncopes rarely require medication in childhood. In general, addressing certain behavioral aspects with the patient is sufficient as the only therapeutic measure. However, for many individuals, treatment outcome may be difficult to predict; a significant patients continue to experience syncope despite medical therapy.

  • For patients with typical features of neuroregulatory syncope, the most important initial step is to reassure the patient and to provide instructions regarding avoidance of both dehydration and postural hypotension.
  • Therapy aimed at preventing an exaggerated reflex may be achieved by increasing intravascular volume with an increased dietary salt intake, prescribed sodium chloride tablets, or salt-retaining fluorinated corticosteroid.
  • Alternately, peripheral venous pooling and cardiac hypercontractility can be avoided with beta-blockers. Cardiac hypercontractility and the vagal portion of the autonomic reflex can also be inhibited with negative inotropic anticholinergic medication (eg, disopyramide).
  • Alpha-adrenergic agents have also been effective in patients with cardioinhibitory syncope.
  • Specialized permanent pacing designs have been effective in revealing the paradoxical relative bradycardia of the Bezold-Jarisch reflex and respond with high-rate dual-chamber pacing.

Consultations

Consider consultation with a neurologist for patients with syncope that remains unexplained following complete cardiac investigations.

Diet

Salt substitutes should be avoided. Salt may be added to the diet of an individual with neuroregulatory syncope (ie, common faint) who cannot voluntarily maintain adequate hydration.

Activity

Patients should avoid situations in which syncope might result in injury while they are undergoing evaluation or if an effective therapy has not been identified.

Medication

Electrolytes

These agents are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance. They are used to reestablish osmotic equilibrium of specific ions.


Sodium chloride

Sodium is the principle cation of extracellular fluid, and chloride is the principle anion of extracellular fluid.

Adult

900-1000 mg PO tid; titrate to maintain electrolyte homeostasis

Pediatric

15 mg/kg PO tid; titrate to maintain electrolyte homeostasis

May decrease levels of lithium when administered concurrently

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Caution in CHF, hypertension, edema, liver cirrhosis, renal insufficiency, and sodium toxicity

Mineralocorticoids

These agents are used to treat syncope secondary to orthostatic hypotension. They act on fluid and electrolyte balance and enhance sodium reabsorption in the kidney, resulting in expanded extracellular fluid volume. They increase renal excretion of potassium and hydrogen ions.


Fludrocortisone (Florinef)

Increases standing blood pressure. Acts to increase sodium retention and expand plasma volume.

Adult

0.1-0.2 mg/d PO

Pediatric

0.05-0.1 mg/d PO

Antagonizes effects of anticholinergics; rifampin, hydantoins, and barbiturates decrease effects of fludrocortisone; decreases salicylate levels

Documented hypersensitivity; systemic fungal infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Taper dose gradually when therapy is discontinued; caution in Addison disease, potassium loss, and sodium retention

Beta-adrenergic blocking agents

These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation. Peripheral venous pooling and cardiac hypercontractility can be avoided through the use of beta-blockers.


Propranolol (Inderal)

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

Adult

10-30 mg PO tid/qid; alternatively, administer total daily dose as SR product qd

Pediatric

0.5-1 mg/kg/d PO divided q6-8h initially; titrate upward q3-5d prn; typical dose is 2-4 mg/kg/d; not to exceed 16 mg/kg/d or 60 mg/d
In older children, total daily dose may be administered as SR product qd

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely


Atenolol (Tenormin)

Selectively blocks beta1 receptors with little or no effect on beta2 receptors.

Adult

50 mg PO qd; increase to 100 mg/d prn

Pediatric

0.8-1.5 mg/kg PO qd; not to exceed 2 mg/kg/d

Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity of atenolol

Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during an IV, carefully monitor BP, heart rate, and ECG

Alpha-adrenergic agonists

These agents may improve the hemodynamic status in patients with cardioinhibitory syncope by increasing myocardial contractility and heart rate, resulting in increased cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.


Midodrine (ProAmatine, Amatine)

Active metabolite, desglymidodrine, is an alpha1 agonist. Desglymidodrine is structurally similar to methoxamine and produces alpha-adrenergic receptor stimulation of arterial and venous systems.

Adult

10 mg PO tid; administer doses 4 h apart

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Drugs that stimulate alpha-adrenergic agonists may enhance or potentiate pressor effects of midodrine; coadministration with cardiac glycosides psychopharmacologic agents, or beta-blockers may enhance or precipitate bradycardia, AV block, or arrhythmia

Documented hypersensitivity; acute renal disease; severe organic heart disease; pheochromocytoma; urinary retention; persistent and excessive supine hypertension

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in diabetes or visual complications; discontinue midodrine and reevaluate if any signs or symptoms suggesting bradycardia occur

Vagal inhibitors

Cardiac hypercontractility and the vagal portion of the autonomic reflex can be inhibited with a negative inotropic anticholinergic medication (eg, disopyramide).


Disopyramide (Norpace)

Class 1A antiarrhythmic. Possesses anticholinergic, peripheral vasoconstrictive, and negative inotropic effects. Decreases conduction velocity and myocardial excitability.

Adult

<50 kg: 100 mg PO q6h or 200 mg q12h if controlled release
>50 kg: 150 mg PO q6h or 300 mg q12h if controlled release
Not to exceed 400 mg PO q6h for severe refractory VT

Pediatric

<1 year: 10-30 mg/kg/d PO divided q6h
1-4 years: 10-20 mg/kg/d PO divided q6h
4-12 years: 10-15 mg/kg/d PO divided q6h
>12 years: 6-15 mg/kg/d PO divided q6h

Phenytoin, rifampin, and phenobarbital may decrease effects; toxicity increases with erythromycin and sparfloxacin; levels of digoxin increase

Documented hypersensitivity; preexisting second or third-degree AV block; coadministration with sparfloxacin; history of complete heart block; sick sinus syndrome; cardiogenic shock; CHF; prolonged baseline QTc (>460 ms)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in preexisting urinary retention, hypotension during initiation of therapy, and angle-closure glaucoma (including family history)

More on Syncope

Overview: Syncope
Differential Diagnoses & Workup: Syncope
Treatment & Medication: Syncope
Follow-up: Syncope
Multimedia: Syncope
References

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Further Reading

Keywords

syncope, faint, common faint, loss of consciousness, vasovagal syncope, vasodepressor syncope, neuroregulatory syncope, neurogenic syncope, neurocardiogenic syncope, presyncope, atrial fibrillation, supraventricular tachycardia, SVT, pulmonary hypertension

Contributor Information and Disclosures

Author

M Silvana Horenstein, MD, Consulting Staff, Department of Pediatrics, University of Texas Medical School Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc
M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Robert Murray Hamilton, MD, MSc, FRCPC, Section Head, Electrophysiology, Director, High-Risk Hereditary Heart Conditions Clinic, Labatt Family Heart Centre; Professor, Department of Pediatrics, Associate Scientist, Physiology and Experimental Medicine, The Hospital for Sick Children and Research Institute, University of Toronto, Canada
Robert Murray Hamilton, MD, MSc, FRCPC is a member of the following medical societies: American Heart Association, Canadian Cardiovascular Society, Canadian Medical Association, Canadian Medical Protective Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Ontario Medical Association, Pediatric Electrophysiology Society, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Ira H Gessner, MD, Professor Emeritus, Pediatric Cardiology
Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

John W Moore, MD, MPH, Professor of Clinical Pediatrics, Section of Pediatric Cardiology, Department of Pediatrics, University of California San Diego School of Medicine; Director of Cardiology, Rady Children's Hospital
John W Moore, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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