Tachycardia 

Tachycardia is defined as a heart rate above 100 beats per minute, but symptomatic tachycardia generally involves rates over 150 beats per minute, unless underlying ventricular dysfunction exists. Management of tachyarrhythmias is determined by the presence of clinical symptoms and signs caused by the rapid heart rate. 

 

The fundamental approach is as follows: First determine if the patient is unstable (eg: manifests ongoing ischemic chest pain, acute mental status changes, hypotension, signs of shock, or evidence of acute pulmonary edema). Hypoxemia is a common cause of tachycardia. 

 

If instability is present and appears related to the tachycardia, treat immediately with synchronized cardioversion, unless the rhythm is sinus tachycardia. Some cases of supraventricular tachycardia may respond to immediate treatment with a bolus of adenosine (6 to 12 mg IV) without the need of cardioversion. Whenever possible, assess whether the patient can perceive the pain associated with cardioversion, and if so provide appropriate sedation and analgesia. 

 

 

Ref: ACLS guidelines

 

Narrow complex tachycardia: 

Two main categories: 
1. AV node independent 

1. Sinus tachycardia  
2. Atrial tachycardia (unifocal/multifocal) 
3. Atrial fibrillation 
4. Atrial flutter 

2. AV node dependent 

1. AV node re-entry tachycardia  
2. AV re-entry tachycardia  
3. Junctional tachycardia 

 

Regular narrow complex

Sinus tachycardia and supraventricular tachycardia are the major causes of a regular narrow complex arrhythmia. Other causes are junctional tachycardia, atrial tachycardia, PSVT. Sinus tachycardia is a common response to fever, anemia, shock, sepsis, pain, heart failure, or any other physiologic stress. No medication is needed to treat sinus tachycardia; care is focused on treating the underlying cause.  

Junctional tachycardia is uncommon in adults and is generally the result of an ectopic focus in the AV junction that manifests enhanced automaticity. It is usually a manifestation of digitalis toxicity or excessive use of exogenous catecholamines or theophylline; these agents should be withdrawn. Electric cardioversion should not be used in these situations, as it is ineffective for terminating arrhythmias due to enhanced automaticity.  

Supraventricular tachycardia (SVT) is a regular tachycardia most often caused by a reentrant mechanism within the conduction system. Vagal maneuvers like carotid sinus massage or valsalva, which may block conduction through the AV node and result in interruption of the reentrant circuit, may be employed on appropriate patients while other therapies are prepared. SVT refractory to vagal maneuvers is treated with adenosine.  

Because of its extremely short half-life, adenosine (6 to 12 mg IV) is injected as rapidly as possible into a large proximal vein, followed immediately by a 20 mL saline flush and elevation of the extremity to ensure the drug enters the central circulation before it is metabolized. If the first dose of adenosine does not convert the rhythm, a second and third dose of 12 mg IV may be given. Prior to injection, warn the patient about transient side effects from adenosine, including chest discomfort, dyspnea, and flushing, and give reassurance that these effects are very brief. Perform continuous ECG recording during administration. If adenosine fails to convert the SVT, consider other etiologies for this rhythm, including atrial flutter or a non-reentrant SVT, which may become apparent on the ECG when AV nodal conduction is slowed. 

 

If conversion attempts fail, initiate rate control with either an intravenous nondihydropyridine calcium channel blocker or a beta blocker. 

 

The recommended initial biphasic energy dose for cardioversion of atrial fibrillation is 120 to 200 J. The initial monophasic dose for cardioversion of atrial fibrillation is 200 J. Cardioversion of adult atrial flutter and other supraventricular rhythms generally requires less energy; an initial energy of 50 to 100 J with either a monophasic or a biphasic device is often sufficient. 

 

 

Irregular narrow complex 

 

Irregular narrow-complex tachycardias may be caused by atrial fibrillation, atrial flutter with variable AV block, multifocal atrial tachycardia (MAT), or sinus tachycardia with frequent premature atrial beats. 

 

The initial goal of treatment in stable patients is to control the heart rate using either a nondihydropyridine calcium channel blocker (diltiazem 15 to 20 mg IV over two minutes, repeat every 15 minutes, or a beta blocker (eg: metoprolol 5 mg IV for 3 doses every two to five minutes; then up to 200 mg PO every 12 hours). For atrial fibrillation associated with hypotension, amiodarone may be used (150 mg IV over 10 minutes, followed by 1 mg/min drip for six hours, and then 0.5 mg/min for 18 hours. However, we can give some additional boluses of 150mg in between. The total loading dose is usually 10gm spread over 7-10 days, but the possibility of conversion to sinus rhythm must be considered. For atrial fibrillation associated with acute heart failure, amiodarone or digoxin may be used for rate control. Treatment of MAT includes correction of possible precipitants, such as hypokalemia and hypomagnesemia. 

 

Atrial tachycardia with multiple foci (MAT) must be distinguished from atrial fibrillation since both present with an irregularly irregular rhythm. Cardioversion and standard antiarrhythmic drugs are typically ineffective in MAT and are usually ineffective for typical atrial tachycardia. 

 

Cardioversion of stable patients with irregular narrow complex tachycardias should NOT be undertaken without considering the risk of embolic stroke. If the duration of atrial fibrillation is known to be less than 48 hours, the risk of embolic stroke is low, and the clinician may consider electrical or chemical cardioversion.  

 

 

Regular wide complex 

 

A regular, wide-complex tachycardia is generally ventricular in etiology. Aberrantly conducted supraventricular tachycardias may also be seen. Because differentiation between ventricular tachycardia (VT) and SVT with aberrancy can be difficult, assume VT is present. Treat clinically stable undifferentiated wide-complex tachycardia with antiarrhythmics or elective synchronized cardioversion.  

 

In cases of regular, wide-complex tachycardia with a monomorphic QRS complex, adenosine may be used for diagnosis and treatment. Do not give adenosine to patients who are unstable or manifest wide-complex tachycardia with an irregular rhythm or a polymorphic QRS complex. In patients with an accessory pathway capable of antegrade (atrium to ventricle) conduction, AF can degenerate into ventricular fibrillation. As a result, caution should be used when giving adenosine if an accessory pathway with antegrade conduction is a possible mechanism, and emergency resuscitation equipment should be available. Adenosine is unlikely to affect ventricular tachycardia but is likely to slow or convert SVT with aberrancy.  

 

SVT with aberrancy, if definitely identified (eg, old ECG demonstrates bundle branch block), may be treated in the same manner as narrow-complex SVT, with vagal maneuvers, adenosine, or rate control.  

 

 

Irregular wide complex 

 

A wide complex, irregular tachycardia may be atrial fibrillation with preexcitation (eg, Wolf Parkinson White syndrome), atrial fibrillation with aberrancy (bundle branch block), or polymorphic ventricular tachycardia (VT)/Torsades de pointes.

 

Use of atrioventricular (AV) nodal blockers in wide complex, irregular tachycardia of unclear etiology may precipitate ventricular fibrillation (VF) and patient death, and is contraindicated. Such medications include beta blockers, calcium channel blockers, digoxin, and adenosine. To avoid inappropriate and possibly dangerous treatment, the 2010 ACLS Guidelines suggest against assuming that any wide complex, irregular tachycardia is caused by preexcited atrial fibrillation. 

 

Treat polymorphic VT with emergent defibrillation. Interventions to prevent recurrent polymorphic VT include correcting underlying electrolyte abnormalities (eg, hypokalemia, hypomagnesemia) and, if a prolonged QT interval is observed or thought to exist, stopping all medications that increase the QT interval. 

 

 

Sinus tachycardia 

 

The most common causes of sinus tachycardia are the normal response to exercise and conditions in which catecholamine release is physiologically enhanced: flight, fright, anger, or stress. Other causes are Hyperthyroidism, Fever, Hypovolemia, Anxiety, Pheochromocytoma, Sepsis , Anemia, Hypotension and shock, Pulmonary embolism, Acute coronary ischemia and myocardial infarction, Heart failure, Chronic pulmonary disease, Hypoxia and Exposure to stimulants (nicotine, caffeine) or illicit drugs.  

 

Symptoms— Sinus tachycardia is often asymptomatic, although the patient may complain of a rapid heartbeat. However, a very rapid heart rate can: 

• Decrease the cardiac output by shortening ventricular filling time 
• Exacerbate coexisting myocardial and/or valvular heart disease 
• Increase myocardial oxygen consumption 
• Reduce coronary blood flow 

Diagnosis — The diagnosis of sinus tachycardia is usually easily established from the ECG. However, the P waves may be difficult to identify at heart rates above 140 beats per minute, since they are often superimposed on the preceding T wave. As a result, a sinus tachycardia can be confused with a paroxysmal supraventricular tachycardia or atrial flutter with 2:1 block. 

 

Carotid sinus massage, other vagal maneuvers, Valsalva or intravenous AV nodal blocking agents (eg, adenosine, verapamil) may help in the identification of the arrhythmia by inducing one or more of the following: 

• Slowing the sinus rate to allow proper identification of the sinus P waves 
• Causing transient AV nodal block to make atrial flutter with 2:1 block apparent 
• Termination of a paroxysmal supraventricular tachycardia (atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia 

 

A.Fib/A.Flutter: 

 

Duration <48 hours — Electric cardioversion is the preferred treatment for the restoration of sinus rhythm. Patients who do not have valvular heart disease, an enlarged left ventricle or heart failure, or a prior history of an embolic event are at low risk for embolism ; as a result, cardioversion does not need to be delayed for chronic anticoagulation. Recommended agents (class IIa) include  amiodarone,  ibutilide,  flecainide, propafenone, and procainamide. 

 

Duration ≥48 hours or unknown — When AF is of longer duration, there is an increased risk of embolism from an atrial thrombus; as a result, pharmacologic or electric cardioversion should be delayed until there has been at least three weeks of adequate anticoagulation (INR 2 to 3). Adequate anticoagulation should be continued for at least four weeks thereafter because of “atrial stunning” and the potential risk for embolism despite sinus rhythm. 

 

For patients who might benefit from earlier cardioversion because of hemodynamic problems, early cardioversion is an option. However, in such patients the presence of an atrial thrombus must be excluded. Intravenous heparin is begun immediately and a TEE is performed to exclude left atrial thrombus; in the absence of thrombus, cardioversion is performed within 24 hours and anticoagulation with warfarin is continued for four weeks. 

 

The initial single shock success rate is 14% with 100J, 39% with 200J, and 95% with 360J in patients with AF for more than 48 hours. Am J Cardiol. 2000 Aug 1;86(3):348-50

 

A.Fib with WPW — Most patients with atrial fibrillation or atrial flutter associated with WPW have normal left ventricular function and the preferred approach is cardioversion. However, if cardioversion is not feasible, antiarrhythmic drugs that have direct on the accessory pathway conduction and refractoriness are acceptable alternatives for rate control; Recommended drugs include amiodarone,  flecainide,  procainamide, or sotalol. The drug of choice for more immediate effect is intravenous procainamide. Drugs that block AV node like beta blockers and CCB’s can kill the patient.  

 

    

Ref: ACLS guidelines

 

Non Sustained V.Tach 

 

A variety of definitions of NSVT have been published, but the most commonly used definition is as follows: 

• Three or more consecutive ventricular beats 
• A rate of >120 beats/min 
• A duration of less than 30 seconds 

Options for the treatment of symptomatic NSVT include: 

• Beta blockers — Beta blockers are favored for the initial treatment of symptomatic NSVT.  
• Nondihydropyridine calcium channel blockers — Calcium channel blockers can be useful, particularly in patients who do not have structural heart disease.  
• Antiarrhythmic medications —Sotalol, amiodarone, and dofetilide are the agents most commonly used for suppression of symptomatic NSVT.  
• Catheter ablation — In patients who have very frequent, monomorphic NSVT not controlled by medications or unable or unwilling to take medications, catheter ablation can be effective for reducing or eliminating NSVT and associated symptoms 

 

PEARLS: 

• Adenosine should be used only for regular rhythm, either narrow complex or wide complex. 
• For patients with A.fib who are unsuitable for or choose not to take an oral anticoagulant (for reasons other than concerns about major bleeding), we recommend combination therapy with aspirin and clopidogrel rather than aspirin (75 mg to 325 mg once daily) (Grade 1B). 
• For patients with AF and stable coronary artery disease (eg, no acute coronary syndrome within the previous year) and who choose oral anticoagulation, we suggest adjusted-dose VKA therapy alone (target INR of 2.0-3.0) rather than the combination of adjusted-dose VKA therapy and aspirin (Grade 2C) . 
• For patients with AF at high risk of stroke (eg, CHADS 2 score of 2 or greater) during the first month after placement of a bare-metal stent or the first 3 to 6 months after placement of a drug-eluting stent, we suggest triple therapy (eg, VKA therapy, aspirin, and clopidogrel) rather than dual antiplatelet therapy (eg, aspirin and clopidogrel) (Grade 2C). After this initial period of triple therapy, we suggest a VKA (INR 2.0-3.0) plus a single antiplatelet drug rather than VKA alone (Grade 2C). At 12 months after intracoronary stent placement, antithrombotic therapy is suggested as for patients with AF and stable coronary artery disease 
• For patients with AF at intermediate to high risk of stroke (eg, CHADS 2 score of 1 or greater) who experience an acute coronary syndrome and do not undergo intracoronary stent placement, we suggest for the first 12 months, adjusted-dose VKA therapy (INR 2.0-3.0) plus single antiplatelet therapy rather than dual antiplatelet therapy or triple therapy (Grade 2C) . After the first 12 months, antithrombotic therapy is suggested as for patients with AF and stable coronary artery disease. 
• For patients with AF being managed with a rhythm control strategy (pharmacologic or catheter ablation), we suggest that antithrombotic therapy decisions follow the general risk-based recommendations for patients with AF , regardless of the apparent persistence of normal sinus rhythm (Grade 2C) . 
• For patients with AF of greater than 48 h or unknown duration undergoing elective electrical or pharmacologic cardioversion, we recommend therapeutic anticoagulation for at least 3 weeks before cardioversion or a transesophageal echocardiography (TEE)-guided approach with abbreviated anticoagulation before cardioversion rather than no anticoagulation (Grade 1B) . We recommend therapeutic anticoagulation for at least 4 weeks after successful cardioversion to sinus rhythm rather than no anticoagulation, regardless of the baseline risk of stroke (Grade 1B). 
• For patients with AF of documented duration of 48 h or less undergoing elective cardioversion (electrical or pharmacologic), we suggest therapeutic anticoagulation for at least 4 weeks after cardioversion, regardless of baseline stroke risk 
• In Paroxysmal A.fib, the highest risk of embolization is after converting from A.fib to sinus rhythm, as atrial kick returns in sinus rhythm and may dislodge the clot. 
• For patients with rheumatic mitral valve disease complicated by the presence of left atrial thrombus, we recommend VKA therapy (target INR, 2.5; range, 2.0-3.0) over no VKA therapy 
• In patients with nonbacterial thrombotic endocarditis and systemic or pulmonary emboli, we suggest treatment with full-dose IV UFH or SC LMWH over no anticoagulation (Grade 2C). 
• Always, try to find the cause of A.fib, which can be structural heart disease, ischemia, alcohol, electrolyte issues, hyperthyroidism, lung pathology and hypertrophy and sympathomimetic drugs. 
• Digoxin toxicity can cause A.flutter with variable block.  T wave inversion (Inverted check sign) is a sign of normal digoxin therapy. 
• V1 is the best lead to look for P-waves: it sits right over the SA node!  Also more likely to be seen in V2 and lead II 
• Always assume a wide complex tachycardia as Vtach first.  Why? Because the treatment for VTach will work for all the other diagnoses in your DDx, however, the treatment for SVT with aberrancy will kill the patient with VTach. 
• Adenosine dosing for SVT generally begins with 6mg IV push (fast with a rapid flush afterwards), followed by a 12 mg push.  The dose can be 3mg if the patient has a central line, had a heart transplant, or is taking carbamazepine, theophylline or dipyrimadole. If pt. is taking strong doses of caffeine, start with 12mg instead of 6mg. 
• If the patient has more than 4 seconds of asystole after giving adenosine, have them cough. 
• Flutter atrial rate is usually around 300bpm. 
• If BP drops after giving CCB for rate control, we can give 1 gm of calcium gluconate. In a study by Moser, administration of calcium salts before giving verapamil prevented verapamil induced hypotension. Am Heart J. 1992 Jul;124(1):231-2 , J Cardiovasc Pharmacol 22 (2), 273-279. 8 1993 , 
• Adenosine is safe in pregnancy 
• ST depression in the setting of SVT is common and has no clinical significance. It doesn’t predict underlying CAD. 
• ST elevation in aVR is a sign of left main coronary disease. 
• HR>150 is unlikely to be sinus tachycardia 
• Magnesium 2-4 g over 10 minutes has similar effects of CCB and B-Blockers in controlling rate as well as rhythm conversion. (Am J Cardiol. 1989 May 1;63(15):1129-31 and J Am Coll Cardiol. 1986 Jun;7(6):1356-62). 
• In a study, magnesium was superior to amiodarone in the conversion of acute atrial tachyarrhythmias, while initial slowing of ventricular response rate in nonconverters appears equally efficacious with both agents. Crit Care Med. 1995 Nov;23(11):1816-24 
• In another study, magnesium 2.5 gm over 15 min vs cardizem 25 mg over 15 min was equally effective for rate control but magnesium was more effective for conversion to sinus rhythm.  International Journal of Cardiology 2001, 79(2-3):287-291
• PAC resets everything but PVC is followed by a compensatory pause. 
• SVT means that it originates above the bundle of his.  
• Brugada Syndrome: ST segment elevation in the pre-cordial leads V1-V3 accompanied by a morphology of the QRS complex resembling a right bundle branch block; 
• V.Tach: the rate is usually >120. If not, it usually is bundle branch block. 
• AV nodal blockers are only contraindicated when there is atrial fib with WPW 
•