Critical Care Medicine

Supraventricular tachycardia (non-cardiac surgery)

Supraventricular tachycardia (non-cardiac surgery)

Also known as:

  1. SVT, which incorporates supraventricular arrhythmias (SVA)

  2. Paroxysmal SVT, a subset of SVTs commonly used to describe those with a sudden or paroxysmal onset, such as AV nodal re-entrant tachycardias (AVNRT), AV re-entrant tachycardias (AVRT), and atrial tachycardias

  3. Atrial arrhythmias

Related to:

  1. Sinus tachycardia

  2. Atrial fibrillation

  3. Atrial flutter (macro-re-entrant tachycardia)

  4. AV nodal re-entrant tachycardia (AVNRT)

  5. AV re-entrant tachycardia (AVRT) (eg, Wolff-Parkinson-White syndrome and accessory pathways)

  6. Junctional tachycardias

  7. Atrial tachycardias, including focal atrial tachycardia, multifocal atrial tachycardia

1. Description of the problem

Supraventricular tachycardias constitute all tachycardias that arise from above, or involving, the bundle of His. This includes arrhythmias that originate from the sinus node, the atrial tissue (atrial flutter and atrial tachycardias), and the AV node. The management of SVT in the setting of non-cardiac surgery is discussed in this topic, with several key features common to both cardiac and non-cardiac surgery also discussed in a separate topic (“SVT in a Cardiac Surgery Patient” chapter).

The type of non-cardiac surgery is also important, and can be classified into low, medium, and high risk. High-risk surgery, associated with >5% risk of death or MI at 30 days, involves either peripheral vascular disease procedures, major aortic or vascular procedures (due to underlying comorbidities, large volumes of blood loss), and may be physiologically more proarrhythmic than lower-risk types of surgery (eg, breast, dental, gynecology).

The occurrence of an SVT in the perioperative period may be the first sign of a physiological abnormality (hypoxia, acidosis, use of pro-arrhythmic drugs), and may be more common (in particular atrial fibrillation) in patients undergoing surgery due to increased sympathetic activity. Correction of the underlying disturbance may terminate the SVT and make recurrence less likely.

Clinical symptoms of SVT

  1. May be asymptomatic

  2. Regular, episodic, or irregular palpitations

  3. Chest pain at rest or with exertion

  4. Dyspnea at rest or with exertion

  5. Weakness or fatigue

  6. Lightheadedness

  7. Exercise intolerance

  8. Dizziness, syncope, or decreased level of consciousness

Clinical signs of SVT

1. Circulatory compromise- hypotension, postural hypotension, or shock

2. Acute pulmonary edema or pulmonary congestion (radiological or on physical examination)

3. Rate-related ischemic ventricular arrhythmias or ischemic ECG changes

4. Tachycardia, which may be irregular, regular; and persistent or paroxysmal

Key management points

See ACLS initial management overview (ACLS tachycardia algorithm).

1. Assess and support vital signs- Airway, Breathing, Circulation.

2. Monitor ECG and identify rhythm.

3. Determine hemodynamic stability- if circulatory instability, then consider immediate DC cardioversion (see ACLS flowchart, DC cardioversion subsection).

4. Is the arrhythmia a wide QRS complex (>0.12 sec) or narrow QRS (<0.12 sec) morphology?

5. Is the tachycardia regular or irregular?

6. Treat as appropriate, using agents as described.

7. Consider the need for long-term pharmacological therapy, or catheter ablation with specialist referral.

2. Emergency Management

The emergency management of a patient with any SVT, and demonstrating hemodynamic compromise, should follow standard Advanced Cardiac Life Support protocols (see ACLS tachycardia algorithm).

Most patients with SVT are usually stable, and ventricular rate control is the mainstay of therapy. This has 2 major effects: reduce myocardial oxygen demand, and improve ventricular filling and improving hemodynamics. In an emergency situation, direct current cardioversion is the default treatment recommended for any unstable patient, in the appropriate setting.

ESC/AHA guidelines recommend the following treatments:

(All recommended medications are administered intravenously, unless otherwise stated).

In a hemodynamically stable patient with a regular tachycardia, recommended management consists of one or a combination of:

1. Vagal maneuvers and/or adenosine

2. Non-dihydropyridine calcium channel antagonists (verapamil, diltiazem)

3. Beta-blockers

4. Amiodarone

5. Digoxin (recommended only for patients with chronic heart failure in the perioperative setting, as has limited vagotonic effects in the setting of high adrenergic states encountered during surgery)

In patients with wide QRS complex (>120 msec) tachycardia due to:

(i) SVT and bundle branch block (BBB), or

(ii) pre-excited SVT/atrial fibrillation:

1. Consider first-line therapies above

2. Flecainide* (and consider concurrent beta-blocker to ensure dual AV node and accessory pathway conduction is blocked)

3. Procainamide*

4. Ibutilide*

5. DC cardioversion

* Avoid use with reduced LV systolic function

In patients with wide QRS complex tachycardia of unknown origin, recommended management consists of:

1. Amiodarone

2. Procainamide

3. Sotalol

4. DC cardioversion

5. Lidocaine

6. Adenosine (avoid in severe coronary disease as may precipitate ischemia in vulnerable territory)

In patients with wide QRS complex tachycardia of unknown origin, and known LV systolic dysfunction, recommended management consists of:

1. Amiodarone

2. Lidocaine

3. DC cardioversion

Vagal maneuvers

Vagal maneuvers along with adenosine are the preferred first-line treatment for termination of stable re-entrant SVT, and vagal maneuvers alone may terminate up to 25% of re-entrant SVTs.They consist of:

1. Valsalva maneuver: with patient sitting, ask him or her to take a deep breath, hold it, then bear down and strain, for 15-30 secs.

2.Carotid sinus massage (CSM): Avoid in patients with known carotid arterial disease, carotid bruit, or history of stroke or transient ischemic attack. Turn patient's head to left, and the right carotid sinus is located in line with the patient's mandibular angle, above the sternocleidomastoid muscle. Use two fingers to firmly massage the carotid sinus, in a longitudinal manner, for 5-10 secs. Repeat on the left side if unsuccessful. Never do bilateral CSM. Transient cerebral complications for CSM have been reported in fewer than 1%.


Adenosine is administered intravenously, and acts on cardiac adenosine receptors to transiently slow conduction in AV nodal tissue by delaying repolarization. It can be used diagnostically to assess underlying atrial rhythm (atrial fibrillation/flutter), or therapeutically to terminate re-entrant SVT. It does not terminate atrial fibrillation, atrial flutter, or ventricular tachycardia (VT) but may transiently slow ventricular response immediately following administration.

Adenosine has a half-life of 10 seconds, after which it is cleared by cellular uptake in whole blood, and it may produce transient side effects such as dyspnea, flushing, or chest pain. It may also cause acute bronchospasm, so care should be taken in patients with asthma or chronic obstructive airways disease.

Caution should be taken when used concurrently with other drugs such ascarbamazepine, dipyridamole, verapamil and beta-blockers, when the dose should be decreased. The initial dose should be reduced to 3 mg if being given through central venous catheters (may cause decreased peripheral resistance in large doses) or to patients with transplanted hearts.

1. ACLS tachycardia algorithm (Figure 1)

Figure 1.

ACLS tachycardia algorithm

2. Hemodynamically stable SVT algorithm (Figure 2)

Figure 2.

Hemodynamically stable SVT algorithm

3. Differential diagnosis for narrow complex tachycardia (Figure 3)

Figure 3.

Differential diagnosis for narrow QRS tachycardia

3. Diagnosis

The mainstay of SVT diagnosis is the electrocardiogram (ECG), or a definitive electrophysiological study. Nonetheless, the ECG between SVT episodes may be normal.

The baseline ECG should be evaluated for evidence of pre-excitation, defined by a short PR interval (<120 ms) and a delta wave (slurred upstroke at the onset of the QRS). These findings would suggest the presence of Wolff-Parkinson-White syndrome (WPW), although it must be remembered that in certain cases of pre-excitation, the resting 12-lead ECG may be normal.

In perioperative patients, heart rates above 100 beats per minute should raise the suspicion of the occurrence of an SVT. For SVT, the QRS morphology on the ECG is usually normal (QRS <120 msec) or narrow (<90 msec). In certain circumstances, such as myocardial infarction, rate-related bundle branch block, or underlying conduction disturbance, the QRS may be wide (>120 msec).

In the case of a patient with a wide complex rhythm who is hemodynamically unstable, ventricular tachycardia should be suspected*.

(* see Differential diagnosis for narrow QRS tachycardia algorithm)

Specific forms of SVT

1. Sinus tachycardia

In the setting of any type of surgery, most patients will demonstrate increased sympathetic activity and therefore increased heart rate, due to autonomic regulation of the sinus node. Inappropriate sinus tachycardia is defined as a “persistent increase in resting heart rate unrelated to the level of physical, emotional, pathological or pharmacological stress”, and relates to enhanced automaticity (increased sympathetic stimulation, decreased parasympathetic stimulation, or both) of the sinus node.

Thus a heart rate >100 beats/minute, in the absence of primary causes (such as infection, thyroid disorders, hemodynamic variation, pulmonary embolism, abrupt withdrawal of beta blockers), should prompt consideration of inappropriate sinus tachycardia. Characteristically, these patients have a more exaggerated heart rate response to exercise, stress, etc. as well.

The majority of patients with inappropriate sinus tachycardia are asymptomatic, but some patients may have significant symptoms, ranging from regular palpitations to extreme lethargy and fatigue. Postural orthostatic tachycardia syndrome (POTS) is a specific sinus tachycardia response to standing upright.

Specific ECG findings of sinus tachycardia

(i) Heart rate > 100 beats per minute

(ii) Normal P wave and QRS complex morphology

(iii) Positive P wave in leads II, III, aVF, and negative in aVR

2. Atrial fibrillation (AF)

Unlike other SVTs, AF may be permanent, paroxysmal, or new onset in the setting of triggers related to surgery-specific conditions (such as pyrexia, hypoxia and ischemia). AF is common, and thought to be due to multiple re-entrant circuits in the left atrium, with ectopic foci often originating from the vicinity of the pulmonary veins.

AF is commonly associated with valvular heart disease, pericarditis, cardiac surgery, myocardial ischemia, thyrotoxicosis, and alcohol. AF is also associated with increased risk of thromboembolism and stroke, as well as sudden death in patients with WPW.

Specific ECG features of AF

(i) P-QRS dissociation, or absent P waves

(ii) irregular R-R interval (ventricular rate)

3. Atrial flutter (macro-re-entrant tachycardia)

Typical atrial flutter (AFlutter) occurs due to re-entrant circuits occurring in the right atrium, which can occur in a clockwise or counterclockwise fashion. It can also be categorized into Type 1 AFlutter, which is slower, and terminated by rapid atrial pacing, and Type 2 AFlutter, which is fast and unresponsive to atrial pacing. Most AFlutter circuits involve the isthmus, an area of tissue between the tricuspid valve and inferior vena cava, which represents a target for radiofrequency ablation.

Specific ECG features of atrial flutter

(i) Typical counterclockwise atrial flutter: negatively directed 'sawtooth' P waves seen best in the inferior leads (II, III, and aVF) as well as lead V1

(ii) Clockwise atrial flutter: atrial depolarizations are positive in inferior leads

(iii) Ventricular rates are often regular but may be irregular due to variable 2:1 and 4:1 conduction.

4. AV Nodal Re-entrant Tachycardia (AVNRT)

AVNRT affects women more commonly, and can also occur in children. It is a re-entry tachycardia that affects both the AV node as well as the surrounding atrial tissue (interatrial septum, left atrium and/or coronary sinus). The re-entry circuit consists of two distinct pathways, the slow pathway (long conduction time), which is located near the tricuspid annulus, and the fast pathway (short conduction time), which is located near Koch's triangle, at the superior portion of the AV node.

During typical AVNRT (slow-fast re-entry pathway, 90-95% cases), conduction occurs antegradely down the slow pathway, and then retrogradely back up the fast pathway. The reverse occurs during atypical AVNRT (fast-slow re-entry pathway, 5-10%).

Specific ECG findings for AVNRT

(i) Ventricular rates may be from 120 to 200 beats per minute, depending on the pathway suspected.

(ii) Typical AVNRT (slow-fast pathway): P wave close to QRS complex, if seen at all (<70 msec). Pseudo R' wave in lead V1.

(iii) Atypical AVNRT (fast-slow pathway): negative P waves in III and aVF, with long R-P interval. Retrograde (inverted) P waves may also be seen.

5. (a) AV Re-entrant Tachycardia (AVRT) and pre-excitation syndromes

AVRT and pre-excitation syndromes occur when electrical isolation between the atria and the ventricles (by the annulus fibrosus) is incomplete and allows for accessory pathways to conduct via bypass tracts. If these tracts conduct retrogradely, then they form the retrograde limb of the AVRT circuit, while conduction through the AV node and bundle of His is the other portion.

Unlike AVNRT, the AVRT circuit always involves one of the ventricles; thus, bundle branch blocks can occur more commonly in AVRT than AVNRT. Atrial fibrillation occurs in 15-40%. There are 2 main types of AVRT, the more common being orthodromic AVRT (95%), a narrow complex tachycardia, where the AV node is the antegrade limb and the accessory pathway is the retrograde limb of the circuit.

In the other type of AVRT, known as antidromic AVRT (5%), a wide-complex tachycardia occurs where the antegrade limb is the accessory circuit and the AV node the retrograde limb.

Specific ECG features for AVRT

(i) P waves are often inscribed on the T wave or ST segment.

(ii) Orthodromic AVRT is characterized by a narrow QRS complex.

(iii) Antidromic AVRT is characterized by a wide QRS complex.

(iv) RP segment > 100 msec

5 (b). Pre-excitation syndromes including WPW

Activation of the ventricle via atrial impulse occurs almost simultaneously via the bypass tract and the normal conducting system, leading to pre-excitation of the ventricle and the so-called 'delta wave'. It is frequently an atrial premature complex that triggers the AVRT in the setting of WPW.

The majority of anomalous pathways are found in patients with structurally normal hearts, but are more common in right-sided congenital heart defects such as Ebstein's anomaly, occurring in up to 10% of patients.

WPW is the most common subtype where pre-excitation and tachycardias occur together. Two other forms of pre-excitation are also commonly described: (i) Mahaim re-entry tachycardia, where the accessory pathway is located near the AV node or the His-Purkinje system, and (ii) permanent AV junctional re-entry tachycardia (PJRT), where the accessory pathway behaves similarly to the AV node.

Specific ECG findings for WPW

(i) PR interval < 120 msec duration

(ii) initial upstroke of the QRS complex, known as a 'delta wave', or pre-excitation component

(iii) QRS complex =>120 msec duration

Sudden Cardiac Death and WPW

There is an increased risk of sudden death in patients with untreated WPW, estimated at approximately 0.2-0.4% per decade. Factors associated with increased risk of sudden death in WPW are the presence of multiple accessory pathways, history of syncope or recurrent tachycardias, short R-R interval during atrial fibrillation episodes, or Ebstein's anomaly.

6. Junctional tachycardias

Arrhythmias originating from the atrioventricular junction (in association with the AV node and bundle of His) are known as junctional rhythms. Myocardial tissue in this area is capable of intrinsic conduction and may produce solitary premature junctional complexes, escape rhythms, or focal junctional tachycardias.

Junctional escape rhythms occur when the impulse from the sinus node or AV node is blocked, and an accelerated junctional rhythm (narrow complex < 100 bpm) often occurs in the setting of myocardial ischemia and reperfusion, valve surgery, pulmonary disease, and electrolyte disturbances.

Specific ECG findings for junctional tachycardias

(i) inverted P waves in inferior leads (II, III, aVF)

(ii) narrow QRS

(iii) atrioventricular dissociation

7. Atrial tachycardias, including focal atrial tachycardia and multifocal atrial tachycardia

Atrial tachycardias (AT) originate from atrial tissue, and in older people are usually associated with digoxin toxicity, electrolyte disturbances, myocardial ischemia and structural heart disease. Focal atrial tachycardias have multiple mechanisms, such as delayed after-depolarizations and enhanced automaticity, and may sometimes demonstrate a 'warm-up' phenomenon where tachycardia rates speed up after initiation.

Chronic focal AT can be a cause of tachycardia-mediated cardiomyopathy. Multifocal atrial tachycardia is most often associated with extensive pulmonary disease, and is diagnosed when there is evidence of 3 or more P-wave morphologies present. It usually occurs in older patients, and the atrial rate is greater than 100 bpm.

Specific ECG findings for atrial tachycardias

(i) Focal AT: P waves of uniform morphology; rate acceleration at initiation of tachycardia; ventricular rates from 120 to 280 bpm

(ii) Multifocal AT: atrial rate > 100 bpm; P waves with 3 or more different morphologies, best diagnosed from inferior leads (II, III, aVF) and V1

1. Distinguishing between AVRT and AVNRT: the gold standard is an electrophysiology study. Using the 12-lead ECG, several features may help to distinguish between one and the other. If the R-R interval is regular, with no P waves or atrial activity visible, then it is most likely AVNRT. AVRT is present if the P wave is noted within the ST segment, and > 70 msec from the QRS complex.

2. Distinguishing between SVT with aberrancy and ventricular tachycardia (VT): Brugada proposed the following distinguishing features for the presence of VT: (i) evidence of AV dissociation, capture, or fusion beats; (ii) RS complex in precordial leads; (iii) more QRS complexes than P waves; (iv) morphology criteria for VT in V1 and V6 (RBBB V1, LBBB V6 where RT > RS).

See flow diagrams for narrow complex tachycardia.

Confirmatory tests

The definitive diagnostic investigation, if the 12-lead ECG in unhelpful, is an electrophysiological study.

4. Specific Treatment

Determine whether hemodynamically stable or unstable.

Most patients with PSVT are hemodynamically stable, allowing for appropriate clinical examination, 12-lead ECG, and blood pressure monitoring.

The goals of short-term management are to terminate the tachycardia, which can often be achieved using vagotonic maneuvers (Valsalva maneuver, carotid sinus massage), which have the effect of prolonging AV nodal refractoriness to induce transient AV nodal block (see previous section). Facial immersion in cold water also has a similar effect in increasing vagal tone.

The rationale behind the use of adenosine, as an AV nodal blocker, also helps to distinguish between several different types of SVT. SVT that occurs with re-entry within the atrial tissue only, such as atrial fibrillation or atrial flutter, will not terminate using AV nodal blockade, but will transiently slow AV conduction, thus uncovering pure atrial activity (regular or irregular non-conducted P waves).

This also occurs with atrial tachycardias (often seen in the setting of advanced congenital heart disease). Any SVTs that require the AV node for conduction may be terminated with adenosine use, as well as for junctional tachycardias. Ventricular arrhythmias will not respond to adenosine as conduction is distal to the AV node.

If vagal stimulation is unsuccessful, then the recommended regime includes:

1. Adenosine

2. Non-dihydropyridine calcium channel antagonists (verapamil, diltiazem)

3. Beta-blockers

4. Amiodarone

5. Digoxin (recommended only for patients with chronic heart failure in the perioperative setting, as has limited vagotonic effects in the setting of high adrenergic states encountered during surgery).

Preoperative decisions:

For patients with pre-existing AF: preoperative and postoperative goal is rate control.

Continuation of oral anti-arrhythmics before surgery is recommended, particularly in the case of beta-blockers, where rebound tachycardias may occur with abrupt withdrawal (eg, with patients fasting preoperatively).

Specific arrhythmia treatments

1. Sinus tachycardia

Beta-blockers form the mainstay of treatment, where elimination of primary causes has been addressed. Alternatively, non-dihydropyridine calcium channel antagonists (verapamil, diltiazem) should be considered for patients with a contraindication to beta blockers. Postural orthostatic tachycardia syndrome should not be treated with anti-arrhythmics; instead, therapies targeted at retaining sodium and water have been shown to be effective.

2. Atrial fibrillation

Specific therapy for AF follows 3 main areas: (i) For patients with new-onset AF during the perioperative period, restoration of sinus rhythm should be achieved within 48 hours to reduce the risk of long-term complications with anticoagulants. This can be achieved by DC cardioversion or anti-arrhythmic medications, such as amiodarone, flecainide, or propafenone. These drugs have also been shown to improve effectiveness of DC cardioversion in patients with persistent AF.

(ii) For patients with chronic AF, ventricular rate control is achieved using drugs that slow conduction through the AV node (beta-blockers, calcium channel antagonists, digoxin).

(iii) Thromboembolic stroke prevention: warfarin is currently the gold standard for reducing risk of stroke in patients with AF, although newer thrombin inhibitors may also demonstrate clinical utility in the future, and are the subject of ongoing trials. The CHADS2 score (Congestive heart failure, Hypertension, Age > 75 yrs, Diabetes Mellitus, Stroke) is currently the most validated scoring system for determining potential cardioembolic risk. With 1 point for each of the criteria, and 2 points for stroke or transient cerebrovascular event, long-term anticoagulation is recommended for patients with a score of >1.

(See subsection on anticoagulation in the perioperative period)

3. Atrial Flutter

Medical therapy for AFlutter is similar to that for AF, with similar cardioembolic risks and decisions for anticoagulation. Adenosine can be used to differentiate between AF and AFlutter, when 2:1 conduction is present, and atrial activity is difficult to visualize. DC cardioversion is the preferred choice of therapy for AFlutter and is often more effective than medical therapy alone.

Termination of AFlutter can be achieved with lower doses of electricity (eg, 25 Joules) than for AF. Pharmacologic or DC cardioversion should be carried out within 48 hours of AFlutter initiation in the perioperative period. For patients with isthmus-dependent AFlutter, radiofrequency ablation is considered a safe and effective cure.

4. AV Nodal Re-entrant Tachycardia (AVNRT)

Treatment options for AVNRT depend on frequency of symptoms and patient preference. Pharmacological therapy consists of standard narrow complex SVT regimen as described in Figure 2 (Hemodynamically stable SVT algorithm), consisting of AV nodal blocking therapy: beta0blockers, calcium channel antagonists, or Class 1c agents such as flecainide or propafenone where primary AV nodal blockade is ineffective.

Catheter ablation is the alternative option for AVNRT and may be up to 95% effective, with an approximately 1% incidence of procedure-induced AV nodal blockade and possible need for permanent pacing. The slow pathway is usually ablated first, as this is further away from the AV node, with the fast pathway being targeted in resistant cases.

5. AVRT and pre-excitation syndromes (WPW)

For AVRT with no evidence of pre-excitation, flecainide, sotalol, amiodarone or propafenone can be used if vagal manuevers are unsuccessful. Catheter ablation is recommended for AVRT that is poorly tolerated.

For patients with acute pre-excitation tachycardias, vagal maneuvers are useful as first-line treatments. Current ESC guidelines for WPW recommend the use of flecainide, procainamide, or ibutilide; these agents slow conduction through the accessory pathway.

Digoxin is absolutely contraindicated in patients with pre-excitation, as it shortens conduction through the bypass tract (by shortening the refractory period). Caution must be used in any drug that may block the AV node (beta-blockers, verapamil, diltiazem), as these may enhance conduction through the bypass tract.

Prevention of arrhythmias may be achieved by radiofrequency catheter ablation of the bypass tract, and may be considered in patients with recurrent tachycardias, syncope, short pre-excitation periods, Ebstein's anomaly, or for occupational reasons.

6. Junctional tachycardias

Medical therapy for focal junctional tachycardias includes beta-blockers, flecainide, or amiodarone.

7. Atrial tachycardias

Focal atrial tachycardia (FAT): Adenosine is effective for terminating the majority of FATs, with DC cardioversion showing variable effects depending on the etiology. Propranolol also has demonstrated efficacy. In resistant cases, radiofrequency ablation is successful in 70-90% of cases, depending on location of FAT.

Multifocal atrial tachycardia (MAT): Therapy is directed at any underlying causes (electrolytes, improving ventilatory capacity). Calcium channel blockers form the mainstay of pharmacological therapy, with limited success for radiofrequency ablations due to multiple foci.

Anticoagulation in the perioperative period

Patients with high perioperative risk of thromboembolic events (who are taking oral vitamin K antagonists [VKA]) require bridging therapy with unfractionated heparin (UFH) or therapeutic-dose low-molecular-weight heparin (LMWH).

This includes patients with AF and CHADS2 score 2 or greater, mechanical or bioprosthetic valves, recent venous thromboembolism and thrombophilia, and patients with recentmitral valve surgery within 3 months. In this case, oral VKA is usually stopped 5 days before planned surgery, with bridging UFH or therapeutic-dose LMWH. For patients with prosthetic heart valves, UFH isrecommended, with cessation 4 hours before surgery.

Special considerations: pregnancy

The management of hemodynamically unstable SVT in pregnancy is unchanged, and should be guided by ACLS algorithms, where DC cardioversion is the treatment of choice. For pharmacological cardioversion of hemodynamically stable AF, quinidine or procainamide may be considered.

For control of ventricular rate in patients with AF and pregnancy, there is Level C evidence for use of digoxin, beta-blockers, ornondihydropyridine calcium channel antagonists. Where possible, drugs should be avoided in the first trimester, due to potential teratogenic risks.

Drugs and dosages


Rapid dose over 1-3 secs, followed by saline flush. Blood pressure and ECG should be monitored during administration of adenosine. Transient AV nodal block occurs within 15-30 seconds of administration. Adenosine clears from the circulation within seconds due to rapid cellular and hepatic metabolism.

3 mg IV- lowest dose for patients taking concurrent drugs with interaction profiles, as well as for patients with heart transplants, or those to receive the drug via central venous routes (due to more rapid onset of action and potential reduction in peripheral resistance).

6 mg IV- standard dose used, successful in 60% cases.

9-12 mg IV- successful in 90% cases.

Recommended regimen is 6 mg (or 3 mg for special precaution patients as above), followed by 12 mg if termination does not occur, and a further 12 mg. There is no evidence that any further doses are effective.


Blood pressure and ECG should be monitored during administration of intravenous calcium channel antagonists.

5-10 mg over 2-3 minutes

Monitor for evidence of hypotension or bradycardia.


IV: Initial dose 0.25 mg/kg over 2 min, BP and ECG monitoring. Further doses of 0.35 mg/kg after 15 mins if required.


IV: initial 100-mg bolus over 2 min, up to 25 mg/min to 1 gram in first hour; subsequently 2-6 mg/min.


IV: 150 mg over 10 min bolus, then maintenance 360 mg over 6 hours, 540 mg over remaining 24 hrs. 0.5 mg/min thereafter, or switch to oral.


IV: 0.25 mg every 2 hours, to a maximum of 1.5 g (loading). Maintenance dose 0.125 mg daily, or switch to oral.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

The long-term management of PSVT depends on the frequency of occurrence, the presence of other underlying structural abnormalities, and the impact on quality of life. For patients with minimally symptomatic and infrequent episodes, long-term pharmacological therapy may not be warranted.

Definitive treatment is usually reserved for patients with:

(i) WPW and symptoms of SVT

(ii) Recurrent episodes with symptoms

(iii) Patients with high-risk features such as syncope, or those who may require definitive therapies due to occupational reasons (professional drivers, etc.).

Definitive treatment consists of radiofrequency catheter ablation, in suitable patients. In patients unsuitable for radiofrequency ablations, or having SVT recurrences, long-term pharmacologic therapy is often required.


All patients with complicated SVT (recurrent, symptomatic, causing hemodynamic compromise) should be initially followed up in a specialist cardiology center, specifically focusing on several key aspects: ambulatory heart rate monitoring to assess for asymptomatic arrhythmias either on or off treatment, cardiac ultrasound to assess for the presence of structural heart disease, which may be associated with increased risk of sudden death, and duration and type of long-term therapy (if necessary) ranging from pharmacological to catheter-based radiofrequency ablations.


The incidence of SVT is estimated at approximately 35 per 100,000/year, with an estimated prevalence of 2.25 episodes per 1000 of the population. AF is the most common of the SVTs, occurring in approximately 0.4-1.0% of the general population, increasing to 10-15% in the over-80-yrs-old group.

AFlutter is the second most common SVT, occurring in approximately 0.5% of the population. In one epidemiologic study for AFlutter, only 1-2% of patients had no evidence of structural heart disease, and 58% has associated AF. The incidence of AFlutter also increases with age. Atrial tachycardias then account for 15-20% of all tachycardias, particularly in the elderly population.

What's the evidence?

ESC compendium of abridged guidelines in Cardiovascular Medicine 2008. Lippincott Williams and Wilkins. 2008.

"Guidelines for preoperative cardiac risk assessment and perioperative cardiac management in non-cardiac surgery". Eur Heart J. vol. 30. 2009. pp. 2769-812.

Antunes, E, Brugada, J, Steurer, G. "The differential diagnosis of a regular tachycardia with a wide QRS complex on the 12-lead ECG: ventricular tachycardia, supraventricular tachycardia with aberrant intraventricular conduction, and supraventricular tachycardia with anterograde conduction over an accessory pathway". Pacing Cardiac Electrophysiol. vol. 17. 1994. pp. 1515-24.

Thompson, A, Balser, JR. "Perioperative cardiac arrhythmias". Br J Anaesthesia. vol. 93. 2004. pp. 86-94.

Opie, L, Gersch, B. Drugs for the Heart. Saunders Elsevier. 2009.

Blomstrom-Lundqvist, C. "ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias- executive summary: a report of the American College of Cardiology/American Heart Association task force on practice guidelines and the European Society of Cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias)". J Am Coll Cardiol. vol. 42. 2003. pp. 1493-531.

Fox, D, Tischenko, A. "Supraventricular tachycardia: diagnosis and management". Mayo Clin Proc. vol. 83. 2008. pp. 1400-11.

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