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Tachycardias, from the EMT to the EP lab. An overview of acute and long-term therapies Nikhil Joshi, MD Talk outline Narrow complex tachycardia • Regular SVT – AVNRT, AVRT, AT • Atrial Flutter/Fibrillation Wide complex tachycardia • Ventricular tachycardia • SVT with aberrant conduction (LBBB, RBBB) • Antidromic SVT (accessory pathway mediated) Supraventricular Tachycardia • AVNRT – This is a reentry tachycardia with a functional, anatomic circuit, involving predominantly the AV Node • AVRT – this is a reentry tachycardia with an anatomic circuit involving the AV Node, the ventricle and an accessory pathway • AT – this is usually a tachycardia of abnormal automaticity, resulting from firing of a focus besides the sinus node Regular, narrow complex tachycardia • Acute treatment focuses include hemodynamic stabilization and supportive care • Mostly these are well tolerated, even with heart rates approaching 200s (younger patients) • Often express symptoms of racing heart, feeling dizzy, sensation in throat • Syncope rare, consider degeneration to another rhythm, or significant hypotension AVNRT AVNRT • Most common type of regular SVT • Rates ranging from 100-280 BPM • More common in women, typically presents in mid20s, but very young and very old cases also seen • Difficult to see p-waves on ECG – “pseudo” s-wave in III – “pseudo” R’ in V1 Typical AVNRT Acute Therapy – Vagal maneuvers • Valsalva/coughing, Carotid Sinus Massage, Ice/cold water immersion • Enhance Vagal Tone • Cause slowing of conduction through the AV Node (and prolongs refractoriness) • Can be effective in terminating AVNRT via effects on either the slow or fast pathway Carotid Sinus Massage • Patient should be supine with extension of neck • Apply firm, steady pressure for 5-10 seconds • L carotid may be more effective • Be cautious in elderly patients, and avoid bilateral carotid stimulation Adenosine • Acts upon AV node in manner similar to Ach • Causes cellular hyperpolarization, also causing prolonged refractoriness • Rapid onset/offset, but warn patients about symptoms • Effective in termination of reentrant arrhytmias that are dependent upon AV nodal conduction • Sometimes can also terminate or transiently suppress focal arrhythmias • Caution of use in Wide Complex Rhythms Other considerations for SVT • Beta blockers • Calcium channel blockers • Amiodarone Less effective for acute termination, but can be considered as therapy for prevention, especially if patients prefer to avoid ablation Catheter ablation Orthodromic AVRT • Narrow complex tachycardia • Acute evaluation and treatment similar to that of AVNRT • This is still a NARROW complex tachycardia (conduction is DOWN the AV node, and UP an accessory pathway) • Vagal maneuvers, adenosine, AVN blocking agents still effective acute therapy Atrial Tachycardia • Typically an ectopic focus outside of the sinus node – likely enhanced automaticity • More likely to see in patients with underlying heart disease • Less responsive to adenosine, may slow with AV nodal blockers • Ablation focuses on localizing site of impulse initiation and ablating Atrial flutter • “sawtooth” pattern ECG – most common form with negative p-waves inferiorly, and positive pwaves in V1 (counterclockwise) • Atypical forms also exist, especially with underlying structural heart disease (mitral valve) or prior cardiac surgery/ablation • May be difficult to discern p-waves if very rapid conduction • Atrial rates often 250-350 bpm, with variable conduction to the ventricle Acute treatment • Hemodynamic stabilization • Response to pharmacologic agents is variable – Adenosine will slow transiently, can be helpful to see the “flutter” waves – AVN blockers can help slow, unlikely to convert – Amiodaroe may slow or convert (be cautious with unknown duration, unless unstable • Cardioversion if unstable only, especially if duration or anticoagulation status unknown Catheter ablation • Definitive RX for typical flutter (medications less effective, often not well tolerated) • Can be curative for various atypical forms as well, but often recur Atrial fibrillation • ECG - irregularly irregular, no clear discernable p waves (“coarse” afib can appear like p-waves) • More common in older population • Can exist in otherwise young/healthy hearts Acute treatment • Rate control with AVN blocking agents • No response to adenosine – may see transient slowing only • Electrical cardioversion if unstable, but again be weary if duration and anticoagulation status unknown Atrial Fibrillation Triggers • • • • Pulmonary Veins Superior Vena Cava IVC, Coronary Sinus, others Ablation focuses on electrical isolation of the pulmonary veins, thought to be the primary trigger for atrial fibrillation Ventricular Tachycardia • Monomorphic VT – often scar mediated • Polymorphic VT (including Torsades) – Acute ischemia – Electrolyte disturbances – scar • Ventricular Fibrillation – Acute MI – Degeneration from another rhythm SVT with aberrancy • Often AVNRT or AVRT with pre-existing or rate-related bundle branch block • Can also be atrial fibrillation or flutter • Aberrancy can be transient, having an old ECG is helpful but not always available Pre-excited tachycardia WCT • 80% is VT (wider = more likely VT) • If history of MI, structural heart disease then VT even more likely • VT often has “northwest” axis – negative in lead I and inferior leads Acute Treatment • Focus on assessing hemodynamics/perfusion • Synchronized Cardioversion or Defibrillation for any hemodynamic instability • ?Adenosine Catheter Ablation • Approach for SVT with aberrancy and Antidromic tachycardia is similar to narrow SVT ablation • VT ablation typically focuses on identifying areas of scar, that are known to be triggers • In some cases, a focal PVC or area can trigger polymorphic VT/VT and can be targeted Summary/Conclusions • Most tachycardias, both narrow and wide are amenable to some form of definitive therapy after acute stabilization • In the case of most SVTs, often catheter ablation is curative • Afib and VT tend to recur, especially in sicker patients with chronic heart conditions