Tachyarrhythmias are either the result of 1) increased automaticity 2) triggered activity or 3) reentry. Reentry is the most common clinically significant etiology. Tachyarrhythmias can also be classified as SVT (normal QRS) or ventricular (QRS > 0.12s).
Algorithm / Suggestions for Accurate Diagnosis
Narrow Complex Tachyarrhythmias (QRS < 0.12s)
First look at the rhythm and rate: Rhythm markedly irregular: A-fib or MFAT Rhythm regular, pulse < 150: sinus tach, also consider A-flutter with fixed (2:1, 3:1…) AV block Rhythm regular, pulse > 150: AV nodal re-entrant tachycardia (aka PSVT)
Then look at the atria: Uniform P waves, fixed P-R interval: sinus tachycardia Multiform P waves, variable P-R interval: MFAT Inverted P waves: AV nodal tachycardia Sawtooth P waves: A-flutter No atrial activity: AV nodal re-entrant tachycardia
Wide Complex Tachyarrhythmias (QRS > 0.12s)
Helpful markers: Pronounced irregularity: SVT with aberrant (prolonged) AV conduction Fusion beats (merging of ectopic ventricular impulse with a normal QRS complex, producing something intermediate between the two): VT AV dissociation: VT
100 – 140 bpm. Usually caused by a systemic or non-cardiac condition. Goal should be to identify and rectify this condition (ex. hypoxemia, sepsis, hypovolemia, pharmacology). If the patient had an MI, B-blockers are indicated but B-blockers should not be used in systolic heart failure. The arrhythmia itself is not urgent (although the underlying cause may be) – cardiac filling is not impaired until HR > 180. [Circulation 64: 1079, 1981]
Atrial Fibrillation / Flutter
Possible etiologies include age, coronary artery disease, dilated cardiomyopathy, recent surgery (esp. valve, lung), and acute MI. Very few of these patients actually have a thyroid disease. 30% of bypass patients will suffer AF sometime between days 2 and 4. 25% of preload is lost when the atria malfunction – this is tolerated well in a normal heart but not in an abnormal (ex. hypertrophied) heart. 15% of patients with AF > 3 days will develop a thrombus, and the annual stroke rate of patients with chronic AF who are not on anticoagulation is 5%. [Mayo Clin Proc 71: 150, 1996]
The acute management goal of AF is not conversion but rather rate control – this should include 1) normal stroke volume 2) absence of pulse deficit and 3) HR < 100 bpm. Stroke volume is the best parameter for following the effect of AF on cardiac output. If this is not available, go with the pulse deficit (precordial pulse – peripheral pulse).
In patients who are not hypotensive, many pharmaceutical agents have proven effective for treating AF. The goal here should be to lower the rate to 60-80 bpm while using systolic blood pressure (a proxy for stroke volume) as a guide. Diltiazem is an excellent first-line therapy (85% success rate, also verapamil causes too much cardiac depression and has too many side effects). β-blockers are excellent for rate control in AF when accompanied by hyperadrenergic states (ex. MI, post-cardiac surgery) – start with esmolol and convert to metoprolol. DO NOT COMBINE CCB AND β-BLOCKERS as this can produce severe myocardial depression. Amiodarone is almost as effective as diltiazem (75% success) but produces less cardiac depression, however it has more side effects (ex. hypotension in 15%) and drug interactions, especially with coumadin.
(see also Atrial flutter: Pharmacologic treatment)
There is some belief that magnesium helps control AF – a RCT of 199 adult ER patients with rapid AF showed a significant reduction in pulse rate and a significant increased likelihood of conversion when MgSO4 was added to conventional therapy (most commonly digoxin), but side effects (hypotension, bradycardia) were also increased [Ann Emerg Med 45: 347, 2005]. Another RCT of 207 post-CABG patients showed a significant reduction of AF when magnesium was added to sotalol [Card Electrophysiol Rev 7: 168, 2003]. There are, however, other recent RCTs that have failed to show benefits [Ann Thorac Surg 77:824, 2004]. Digoxin is a commonly used agent but has a delayed onset, thus is not recommended in controlling acute AF. [Ann Emerg Med 25: 127, 1995]
Ibutilide is the only pharmacologic agent that can convert the rhythm (> 50%) but carries a 4% risk of Torsades. [Cardiol Clin 22: 21, 2004]
Remember that in patients with WPW, AV blocking agents (CCB, digoxin) can actually enhance the heart rate. WPW patients should receive procainamide or DC cardioversion.
In patients who are hypotensive but awake, volume infusion can be attempted first – give volume expanders until filling pressures (CVP, PCWP) reach 20 mm Hg after which point DC cardioversion may be necessary (DC cardioversion is not immediately necessary but should be in the back of one’s mind).
DC cardioversion is indicated in the setting of AF in 1) hypotension 2) impaired vital organ function or 3) HR > 150. Always premedicate. Synchronized shocks are not necessary for AF and in fact can be harmful if they cause any sort of delay [JAMA 268: 2199, 1992]. See ACLS guidelines for dosing. DC cardioversion is 90% successful at ACLS doses.
Anticoagulation should be started based on risk factors. Patients < 60 with no heart disease (“lone A-fib”) need no therapy. Those < 60 with heart disease and EF > 0.35 and no hypertension, and those > 60 with no heart disease should be on ASA 325. Everyone else should be on coumadin. [J Am Coll Cardiol 38: 1266i, 2001]
Multi-Focal Atrial Tachycardia
Multiple P wave morphologies and variable P-R interval. Mostly seen in patients with chronic lung disease and theophylline therapy but also hypokalemia, hypomagnesemia, acute PE, MI, CHF. Management algorithm is as follows: 1) d/c theophylline if on 2) give IV magnesium if not contraindicated – 2 g in 15 min, then 6 g in 6 hrs 3) if hypokalemic, give Mg2+ first, followed by K+ 4) if previous therapy ineffective, consider metoprolol (good lungs) or verapamil (airway disease).
AV Nodal Re-entry
Paroxysmal SVT, characterized by abrupt onset and absence of identifiable atrial activity (P waves hidden in QRS). Standard treatment is to block the re-entrant pathway with either 6-12 mg adenosine (works in ~ 90% of AVRET) or CCB (cardiodepressive, try adenosine first). Note that adenosine dose is reduced 50% if introduced through a central catheter. Adenosine is contraindicated in asthma or AV block. Flushing occurs in 50%, as does bradycardia or AV block. Also dyspnea in 35% and angina in 20%.
Any wide complex tachycardia in an ICU patient should be treated as a probably VT (95% of them are). Algorithm is as follows: 1) if hypotensive, give 100/200/300/360J 2) if not hemodynamically compromised, give amiodarone [Circulation 112S: IV 67, 2005], after which you can try lidocaine 3) if not responsive to amiodarone or lidocaine, check Q-Tc and if < 0.44 give procainamide, infused slowly 4) if not responsive to amiodarone or lidocaine and Q-Tc > 0.44 give magnesium (except in renal failure). Also, if you’re not sure about VT (i.e., you think it might be SVT with aberrant conduction), try adenosine first. ACLS used to recommend bretylium but Marino disagrees, as do the Guidelines 2000 for emergency cardiac care [The International Guidelines 2000 for CPR and ECC, Circulation 102: I112, 2000]. All instances of VT must be followed with an etiologic search, including EKG, ABG, chem-12, drug levels.
Torsades is a special case of VT and is universally managed with magnesium despite only being supported by uncontrolled case studies [Circulation 77: 392, 1988]. Also correct for hypokalemia and hypocalcemia. Marino suggests managing according to etiology – if acquired, try Mg therapy, but if congenital, try ventricular pacing to HR > 100.