1. AV node independent
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Sinus tachycardia
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Atrial tachycardia (unifocal/multifocal)
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Atrial fibrillation
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Atrial flutter
2. AV node dependent
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AV node re-entry tachycardia
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AV re-entry tachycardia
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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of digitalis toxicity or excessive use of exogenous catecholamines or theophylline; these agents should be withdrawn.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.
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Decrease the cardiac output by shortening ventricular filling time
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Exacerbate coexisting myocardial and/or valvular heart disease
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Increase myocardial oxygen consumption
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Reduce coronary blood flow
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Slowing the sinus rate to allow proper identification of the sinus P waves
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Causing transient AV nodal block to make atrial flutter with 2:1 block apparent
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Termination of a paroxysmal supraventricular tachycardia (atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia
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Three or more consecutive ventricular beats
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A rate of >120 beats/min
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A duration of less than 30 seconds
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Beta blockers — Beta blockers are favored for the initial treatment of symptomatic NSVT.
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Nondihydropyridine calcium channel blockers — Calcium channel blockers can be useful, particularly in patients who do not have structural heart disease.
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Antiarrhythmic medications —Sotalol, amiodarone, and dofetilide are the agents most commonly used for suppression of symptomatic NSVT.
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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
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Adenosine should be used only for regular rhythm, either narrow complex or wide complex.
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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).
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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) .
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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
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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.
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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) .
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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).
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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
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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.
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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
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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).
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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.
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Digoxin toxicity can cause A.flutter with variable block. T wave inversion (Inverted check sign) is a sign of normal digoxin therapy.
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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
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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.
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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.
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If the patient has more than 4 seconds of asystole after giving adenosine, have them cough.
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Flutter atrial rate is usually around 300bpm.
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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.
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Adenosine is safe in pregnancy
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ST depression in the setting of SVT is common and has no clinical significance. It doesn’t predict underlying CAD.
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ST elevation in aVR is a sign of left main coronary disease.
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HR>150 is unlikely to be sinus tachycardia
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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).
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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
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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
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PAC resets everything but PVC is followed by a compensatory pause.
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SVT means that it originates above the bundle of his.
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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;
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V.Tach: the rate is usually >120. If not, it usually is bundle branch block.
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AV nodal blockers are only contraindicated when there is atrial fib with WPW
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