- Published on
Emergency and Acute Medicine - Supraventricular Tachycardia
Supraventricular tachycardia (SVT) refers to a tachyarrhythmia that originates above the His bundle and produces a heart rate of 100 beats per minute or greater. It may present as a regular narrow-complex rhythm, an irregular narrow-complex rhythm, or a wide-complex rhythm if conduction occurs outside the normal His-Purkinje system. Irregular narrow-complex SVT includes atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. Regular narrow-complex SVT includes atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), atrial tachycardia, and atrial flutter. A wide-complex SVT may occur when an accessory pathway or bundle branch block is present, but any wide-complex tachycardia should be assumed to be ventricular tachycardia unless there is strong evidence otherwise.
The causes of SVT vary by rhythm type. Atrial tachycardias may be triggered by premature beats, hypoxia, electrolyte abnormalities, theophylline toxicity, or increased atrial pressure. Junctional tachycardias may result from AV nodal re-entry, myocardial ischemia, structural heart disease, or pre-excitation syndromes. Wolff-Parkinson-White syndrome involves an accessory pathway and can predispose to dangerous tachyarrhythmias. Atrial fibrillation is associated with hypertension, coronary disease, thyroid abnormalities, alcohol use, mitral valve disease, chronic lung disease, pulmonary embolism, digoxin toxicity, sepsis, and pericardial disease. Atrial flutter is often linked to ischemic heart disease, valvular disease, heart failure, myocarditis, cardiomyopathy, or pulmonary disease.
Patients commonly present with palpitations, which are the most frequent symptom. They may also report lightheadedness, dyspnea, diaphoresis, dizziness, weakness, chest discomfort, or syncope. Some patients describe abrupt onset palpitations and head pressure, while others present more gradually with fatigue, malaise, or exercise intolerance. Prominent neck vein pulsations, the so-called “frog sign,” may be seen. Signs of instability include altered mental status, ischemic chest pain, acute pulmonary edema, and hypotension.
Evaluation begins with assessment of airway, breathing, and circulation, followed by rapid determination of whether the patient is stable or unstable. History should focus on onset, prior episodes, cardiac history, medication use, stimulants, decongestants, and illicit drug exposure. Physical examination should assess heart rhythm regularity, blood pressure, respiratory status, and evidence of heart failure such as jugular venous distention or pulmonary rales. An ECG is essential for diagnosis. Atrial fibrillation typically shows an irregularly irregular rhythm without discernible P waves. Atrial flutter demonstrates sawtooth flutter waves, often with 2:1 block. Multifocal atrial tachycardia shows at least three different P-wave morphologies. Atrial tachycardia usually has abnormal but visible P waves before each QRS. Junctional tachycardia often has absent or retrograde P waves. In adults, ventricular rates over 200 beats per minute strongly suggest an accessory pathway such as WPW.
Laboratory evaluation may include CBC, electrolytes, cardiac enzymes, BNP, and occasionally thyroid studies. Chest radiography is more useful in atrial fibrillation or flutter to assess cardiac size or pulmonary pathology. The main diagnostic challenge is distinguishing SVT with aberrancy from ventricular tachycardia. If there is uncertainty, the rhythm should be treated as ventricular tachycardia.
Management depends on the rhythm type and the patient’s hemodynamic status. Unstable patients require immediate synchronized cardioversion. In stable atrial fibrillation or atrial flutter, rate control is the priority, typically with beta-blockers or calcium channel blockers, while amiodarone or digoxin may be used in selected cases. Cardioversion should generally be avoided in stable atrial fibrillation of more than 48 hours or uncertain duration because of embolic risk. In WPW with atrial fibrillation, AV nodal blocking drugs such as adenosine, beta-blockers, calcium channel blockers, and digoxin should be avoided, and agents such as procainamide or amiodarone, or direct current cardioversion, are preferred.
For regular narrow-complex SVT, vagal maneuvers should be attempted first. Valsalva is most effective when performed with the patient lying flat. Carotid massage may be considered in selected patients, and the diving reflex with ice to the face may be used in children. If vagal maneuvers fail, adenosine is the first-line medication and successfully terminates many episodes. If adenosine transiently slows but does not terminate the rhythm, escalating the dose further is usually not useful and another agent should be chosen. In wide-complex tachycardia of uncertain origin, treatment should proceed as for ventricular tachycardia, usually with amiodarone and sometimes procainamide if an accessory pathway is suspected. Verapamil should not be used in uncertain wide-complex tachycardia.
In children, SVT is the most common arrhythmia seen without structural heart disease. Initial treatment again includes vagal maneuvers, with ice to the forehead in infants or blowing through a straw in older children. Synchronized cardioversion is used for unstable patients. In pregnancy, adenosine is considered safe, and cardioversion is also safe if needed.
Patients may be admitted if there is concern for ischemia, persistent SVT, pre-excitation syndrome, or an underlying metabolic abnormality. Those whose rhythm is successfully terminated and who have no signs of organ hypoperfusion or serious underlying disease may often be discharged with outpatient follow-up. They should be advised to return for faintness, neurologic symptoms, trouble speaking or seeing, or recurrent episodes, and to avoid high-risk activities such as swimming, diving, or piloting until further evaluation. A key pitfall is misidentifying atrial fibrillation in WPW or any wide-complex tachycardia as benign SVT. When in doubt, treat the rhythm as ventricular tachycardia.
Supraventricular tachycardia (SVT) refers to a tachyarrhythmia that originates above the His bundle and produces a heart rate of 100 beats per minute or greater. It may present as a regular narrow-complex rhythm, an irregular narrow-complex rhythm, or a wide-complex rhythm if conduction occurs outside the normal His-Purkinje system. Irregular narrow-complex SVT includes atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. Regular narrow-complex SVT includes atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), atrial tachycardia, and atrial flutter. A wide-complex SVT may occur when an accessory pathway or bundle branch block is present, but any wide-complex tachycardia should be assumed to be ventricular tachycardia unless there is strong evidence otherwise.
The causes of SVT vary by rhythm type. Atrial tachycardias may be triggered by premature beats, hypoxia, electrolyte abnormalities, theophylline toxicity, or increased atrial pressure. Junctional tachycardias may result from AV nodal re-entry, myocardial ischemia, structural heart disease, or pre-excitation syndromes. Wolff-Parkinson-White syndrome involves an accessory pathway and can predispose to dangerous tachyarrhythmias. Atrial fibrillation is associated with hypertension, coronary disease, thyroid abnormalities, alcohol use, mitral valve disease, chronic lung disease, pulmonary embolism, digoxin toxicity, sepsis, and pericardial disease. Atrial flutter is often linked to ischemic heart disease, valvular disease, heart failure, myocarditis, cardiomyopathy, or pulmonary disease.
Patients commonly present with palpitations, which are the most frequent symptom. They may also report lightheadedness, dyspnea, diaphoresis, dizziness, weakness, chest discomfort, or syncope. Some patients describe abrupt onset palpitations and head pressure, while others present more gradually with fatigue, malaise, or exercise intolerance. Prominent neck vein pulsations, the so-called “frog sign,” may be seen. Signs of instability include altered mental status, ischemic chest pain, acute pulmonary edema, and hypotension.
Evaluation begins with assessment of airway, breathing, and circulation, followed by rapid determination of whether the patient is stable or unstable. History should focus on onset, prior episodes, cardiac history, medication use, stimulants, decongestants, and illicit drug exposure. Physical examination should assess heart rhythm regularity, blood pressure, respiratory status, and evidence of heart failure such as jugular venous distention or pulmonary rales. An ECG is essential for diagnosis. Atrial fibrillation typically shows an irregularly irregular rhythm without discernible P waves. Atrial flutter demonstrates sawtooth flutter waves, often with 2:1 block. Multifocal atrial tachycardia shows at least three different P-wave morphologies. Atrial tachycardia usually has abnormal but visible P waves before each QRS. Junctional tachycardia often has absent or retrograde P waves. In adults, ventricular rates over 200 beats per minute strongly suggest an accessory pathway such as WPW.
Laboratory evaluation may include CBC, electrolytes, cardiac enzymes, BNP, and occasionally thyroid studies. Chest radiography is more useful in atrial fibrillation or flutter to assess cardiac size or pulmonary pathology. The main diagnostic challenge is distinguishing SVT with aberrancy from ventricular tachycardia. If there is uncertainty, the rhythm should be treated as ventricular tachycardia.
Management depends on the rhythm type and the patient’s hemodynamic status. Unstable patients require immediate synchronized cardioversion. In stable atrial fibrillation or atrial flutter, rate control is the priority, typically with beta-blockers or calcium channel blockers, while amiodarone or digoxin may be used in selected cases. Cardioversion should generally be avoided in stable atrial fibrillation of more than 48 hours or uncertain duration because of embolic risk. In WPW with atrial fibrillation, AV nodal blocking drugs such as adenosine, beta-blockers, calcium channel blockers, and digoxin should be avoided, and agents such as procainamide or amiodarone, or direct current cardioversion, are preferred.
For regular narrow-complex SVT, vagal maneuvers should be attempted first. Valsalva is most effective when performed with the patient lying flat. Carotid massage may be considered in selected patients, and the diving reflex with ice to the face may be used in children. If vagal maneuvers fail, adenosine is the first-line medication and successfully terminates many episodes. If adenosine transiently slows but does not terminate the rhythm, escalating the dose further is usually not useful and another agent should be chosen. In wide-complex tachycardia of uncertain origin, treatment should proceed as for ventricular tachycardia, usually with amiodarone and sometimes procainamide if an accessory pathway is suspected. Verapamil should not be used in uncertain wide-complex tachycardia.
In children, SVT is the most common arrhythmia seen without structural heart disease. Initial treatment again includes vagal maneuvers, with ice to the forehead in infants or blowing through a straw in older children. Synchronized cardioversion is used for unstable patients. In pregnancy, adenosine is considered safe, and cardioversion is also safe if needed.
Patients may be admitted if there is concern for ischemia, persistent SVT, pre-excitation syndrome, or an underlying metabolic abnormality. Those whose rhythm is successfully terminated and who have no signs of organ hypoperfusion or serious underlying disease may often be discharged with outpatient follow-up. They should be advised to return for faintness, neurologic symptoms, trouble speaking or seeing, or recurrent episodes, and to avoid high-risk activities such as swimming, diving, or piloting until further evaluation. A key pitfall is misidentifying atrial fibrillation in WPW or any wide-complex tachycardia as benign SVT. When in doubt, treat the rhythm as ventricular tachycardia.
0 Comments
