Tuesday, October 1, 2013

Symptomatic Tachycardia in Cardiovascular Emergencies

      Patients who are pulseless or clinically unsable with the tachycardia require immediet defibrillation  with unsynchronized high-energy shocks (200, 300, 360 Joule) followed by appropriate ABC attention of ACLS. The cardiac rhythm is briefly assessed between shocks.
Administer epinephrine (1 mg IV every 3-5 minutes) or vasopressin (pitressin, 40 U IV once). Amiodarone (Cordarone, pacerone, 300 mg IV once, repeat at 150 mg IV once) or lidocaine (1,0 – 1,5 mg/kg IV, repeat in 3 – 5 minutes to maximum dose, 3 mg/kg) should be given for continued pulseless ventricular tachycardia (VT). 360 Joule shocks should continue every 30 to 60 seconds the VT (tachycardia) or VF (fibrillation) continues. Procainamide 20 mg/min can also be considered. If Hyperkalemia is suspected, Calcium gluconas and Natrium Bicarbonat should be administered.

If the patient has a pulse and is cliically stable, analysis of the ECG dictates the next management steps:
•    Narrow – QRS complex (Supraventricular tachy cardia or SVT) tachycardias (QRS < 0,12
      second) in order of frequency
•    Sinus tachycardia
•    Atrial fibrillation
•    Atrial Flutter
•    AV nodal reentry
•    Acessory pathway-mediated tachycardia (AVRT)
•    Atrial tachyardia (etopic and reentrant)
•    Multifactorial atrial tachycardia (MAT)
•    Junctional tachycardia
•    Wide – QRS complex tavhycardia (QRS ≥ 0,12 second)
•     Ventricular tachycardia (VT)
•    SVT with aberrancy
•    Preexcited tachycardias (Wolff-Parkinson-White)

      Narrow-QRS complex arrhytmias are further diagnosed (and often treated) by slowing the conduction through the AV node. Essentially, AV nodal blockade will either (1) demontrate the underlying atrial rhythm without large ventricular QRS complexs obscuring the rhythm (atrial fibrillation, flutter, ectopic atrial tachycardia) or (2) stop the tachycardia if it is dependent on the AV node as part of tachycardia circuit (AVNRT, AVRT). AV node slowing can be accomplished by increasing vagal tone (carotid sinus massage) or by administering adenosine (6-12 mg IV rapid push with flush)

      Wide-QRS complex arrhytmias present more of chalengge by requiring a working diagnosis before the treatment plan is enacted. Treatment of VT is verry different than of SVT with abberancy or a preexcited tachycardia. Clues suggesting VT as the cause:
•    In patients with known structural heart disease, especially coronary disease. VT is more likely cause of wide-complex tachycardia.
•    Comparison to the ECG during sinus rhythm is helpful, as a significant  change in the QRS morphology and/or a shift in axis are more suggestive of VT.
•    Other specific findings suggestive of VT include (1) AV dissociation, (2) fusion/capture beats, (3) left bundle-branch block with right-axis deviation, and (4) positive or negative concordance of QRS in ECG leads V1 to V6.
•    Should question remain, the Brugada criteria can be used to further determine VT versus SVT.

        For patients with monomorphic VT, amiodrone (150 mg IV over 10 minutes, followed by 1 mg/min continous infusion for 6 hours and 0,5 mg/min continous infusion for the next 18 hours) should be used. Alternative options are procainamide or  or sotalol. If the patient becomes unstable, or the VT persists, a synchronized defibrillation shock should be delivered.

         Polyymorphic VT requires immediete attention, as it can become unstable quickly. A prolonged QT interval in sinus rhythm should raise concern of torsades de pointes. Immediate treatment should include adminitering  4 g IV magnesium, overdrive pacing, or IV isoproterinol at 5 µg/minute IV infuion. Amiodarone (150 mg IV over 10 minutes) may be helpful, particularly if the QT interval is normal at baseline. Undrlying medications or overdose should be investigated. Persistent torsades de pointes requires defibrillation.

        Because coronary artery disease is the most common cause of ventricular tachycardia, an urgent coronary catheterization warranted, particularly with VT refractory to antiarrhytmic medication.

5 comments:

  1. WAH KALAU BHSA ENGLIS HARUS CARI KAMUS DULU NIH

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