Tachyarrhythmias in the ICU ACNP/PA Critical Care Boot Camp Vanderbilt University Medical Center September 21, 2015 Ariel Kappa RN, MSN, ACNP-BC
Acute Arrhythmias are the gremlins of the ICU because they pop up unexpectedly, create some havoc, and are often gone in a flash -Paul Marino (The ICU Book, 2007)
Objectives Review EKG characteristics Initial Considerations Pharmacology Interactive Case Studies
Stable or Unstable (Shock?) Regularity? Appreciable P waves? Morphology of QRS Blocks? Infarction?
Tachycardia Regular Irregular Narrow Wide Narrow Wide Sinus Tachycardia, Atrial Tachycardia, AVNRT/AVRT, Atrial flutter Monomorphic VT, SVT with aberrancy/blo ck/pacingmediated Atrial fibrillation, MAT Polymorphic VT/VF/ Torsades, Irregular SVT with aberrancy/blo ck
Stable? Initial considerations Hypotension, AMS, signs of shock, CP 12-lead EKG Pharmacological management Non-Pharmacological management Synchronized cardioversion (50-200 J) Oxygen, airway, monitor, sedation
Class Common Examples Mechanism Clinical Use Ia Quinidine Procainamide Na+ Channel blocker; Fast (effects Pharmacology QRS) Pre-excited afib, Stable monomorphic VT Ib Lidocaine, Mexilitine, Phenytoin Na+ Channel blocker; No effect on conduction; may prolong APD VT Ic Fleicanide, Propafenone Na+ Channel blocker; (no effect on QRS) SVT, PVCs, WPW II Metoprolol, Esmolol, Propranalol Block beta-adrenergic receptors Afib rate control, Narrow Stable SVT III Amiodarone*, Sotalol*, Ibitulide K+ channel blocker SVT (Regular and Irregular) IV Verapamil, Diltiazem Non-dihydropyridine Calcium channel blocker, vasodilate, negative inotrope Misc. Digoxin, Adenosine Magnesium Dig- parasympathetic AV, + Inotrope Adenosine- AV Mag- effect Na/K transport Rate control SVT *Avoid in CHF/VT Preexited Afib Dig- SVT, Afib in HF, Adenosine- SVT, stable WCT Mg- Polymorphic VT/Torsades
Case 1 73 yo female with history of HTN, Aortic Stenosis, DMII, COPD POD 1 s/p AVRt with EF of 60% c/o SOB. Vitals: HR: 162, SBP: 131/71, RR: 26
Case 1 What does this EKG show? 1. Atrial tachycardia 2. AV nodal reentrant tachycardia 3. Atrial fibrillation 4. Atrial flutter
What is the best next step? 1. Prepare for synchronized cardioversion of atrial fibrillation. 2. Initiate IV amiodarone bolus and infusion. 3. Assess timing, electrolytes and consider IV diltiazem bolus and infusion. 4. Administer 5mg IV metoprolol.
Rate vs. Rhythm control AFFIRM TRIAL True or False: Rhythm control is more important than rate control 1. True 2. False RACE II True or False: HR less than 110 is noninferior to HR less than 80 in morbidity/mortality outcomes 1. True 2. False (AFFIRM, NEJM, 2002), (VanGelder et al., NEJM, 2010)
Atrial Fibrillation EKG Characteristics: Irregularly Irregular. Etiology: Numerous waves of depolarization spreading throughout the atria, leading to an absence of coordinated atrial contraction. Treatment: Class II, Class IV, Class III, Digoxin: HF (inotropic support). Unstable: Low voltage DCCV AFFIRM trial (NEJM, 2000): Rate control not rhythm control Race II Trial: (NEJM, 2010): Lenient rate control
Case 2 68 yo male with COPD exacerbation admitted to MICU. HR: 151, SBP: 121/73, RR: 28
Case 2 What does this EKG show? 1. Atrial tachycardia 2. Sinus tachycardia 3. Atrial fibrillation 4. Atrial flutter
Atrial Flutter EKG Characteristics: Sawtooth pattern: atrial rate ~300, ventricular rate 75-150 bpm (unless irregular). Usually with 2:1/4:1block at AV node. Rhythm constant amplitude, morphology, duration. **May be variable and irregular Etiology: Reentrant circuit in the wall of the atrium Treatment: Class III (Ibutilide, sotalol, amiodarone): prolong refractory period (not slowing conduction) *Small risk for torsades. Ventricular rate control can be difficult, AV nodal blockers prevent 1:1 conduction. Unmasking of flutter waves with adenosine. *Nonpharmacological : Rapid pacing or low voltage DC cardioversion is effective. (Blomstro m-lundqvist, et al., 2003)
Case 3 24 yo female admitted to Trauma ICU with pelvic fracture s/p MVC complaining of palpitations. Vitals: HR: 148, SBP 118/58, RR: 22
Case 3 What does this EKG show? 1. Sinus Tachycardia 2. AV nodal reentrant tachycardia 3. Atrial fibrillation 4. Atrial flutter
AV Nodal Reentrant Tachycardia (AVNRT) EKG characteristics: Rate 140-280, P wave undetected (activation atria/ventricle simultaneously), Etiology: Triggered by PACs, Micro Reentry at AV node (atrial stretch, inflammation, irritability- catecholamines) Treatment: Vagal maneuvers, Adenosine 6-12 mg IV push, Ca++ channel blockers, Digoxin, Beta blockers (Blomstro m-lundqvist, et al., 2003)
Multifocal Atrial Tachycardia (MAT) EKG characteristics: at least 3 P wave morphologies, variable intervals P-P, R-R, P-R, look for isoelectric baseline Etiology: No single dominant pacemaker, multiple atrial foci fire independently. COPD/CHF Treatment: Treat underlying cause (electrolyte derangement, hypoxemia). Rate control- Class IV- CCBs, Class II- Betablockers ST PACs
Atrioventricular Reentrant Tachycardia (AVRT) Etiology: Macrorentry through normal conduction system with accessory AV pathway; Delayed activation of atria = visible P wave Treatment: Similar to treatment of AVNRT, AV nodal blockers, eventual ablation
Sinus Tachycardia Atrial Tachycardia EKG characteristics: Constant PR interval Varies with stimulation/respiration Normal Rate 220 bpm age (yrs) Etiology: Physiologic Treatment: Fix underlying physiologic insult (Fever, anxiety, thyrotoxicosis, exogenous catecholamines, anticholinergic, LV dysfunction- MI etc. EKG characteristics: Atrial rate 150-250 Distinct P wave morphology Etiology: CHF, HTN, electrolyte abnormalities Treatment: Adenosine, Class II, Class III, *Dig toxicity?
Case 4 38 yo male with PMH: Appendectomy Presented to ED with SBO s/t incarcerated groin hernia now POD 3 s/p SBO repair. Vitals: HR 148, SBP 100/58, RR: 20 BMP: 148 19 41 2.1 21 1.6
Case 4
What is your next course of action? 1. Correct hypokalemia and prepare amiodarone for administration. 2. Grab the crash cart and prepare for emergent cardioversion. 3. Correct hypokalemia and prepare lidocaine for bolus/infusion. 4. Grab the crash cart and ask the nurse to give sotalol.
Monomorphic VT EKG characteristics: 3 consecutive beats >100 bpm, QRS >120ms Brugada criteria: Precordial leads- No RS complex or RS >100ms, AV dissociation, QRS morphology- Fusion beats Etiology: CAD, CM, Ischemia Treatment: Correct aggravating conditions (hypokalemia, ischemia) Class I: Wide QRS presumed VT if unclear ( LOE: C). *DCCV unstable ( LOE: C). Class II: Procainamide- careful in LV dysfunction, CHF, hypotensionprolong QT. Class III- Sotalol, Amiodarone (benefit IV to PO). Class IIb- IV lidocaine initial treatment associated with MI (LOE: C). (Zipes et al., 2006)
Wide Complex SVT EKG characteristics: Regular, Wide complex, Fails Brugada s Criteria (from previous slide) Etiology: BBB/IVCD, Pre-excitation, Presence of PPM/ICD Treatment: WPW- Procainamide (*Avoid AV nodal blockers) Vagal maneuvers, Adenosine, Class III, Cardioversion WPW Delta wave Pacemaker- Mediated
Which of these below is not a treatment option? 1. DC Cardioversion 2. Metoprolol 3. Amiodarone 4. Procainamide
Case 5 Lets go back to the 38 yo. male with VT Unfortunately you look up at the monitor and see this
Case 5 What do you do next? 1. Give magnesium 2. Defibrillate 3. Stop all QT prolonging medications 4. All of the above.
Irregular, Wide Complex Polymorphic VT Etiology: Ischemia, Catecholamines Treatment: Defibrillation Ventricular fibrillation, Torsades de pointes Etiology- QT prolongation, Class I, III- prolong refractory period
General Tips Narrow complex tachyarrhythmias can be diagnosed or possibly terminated in most cases with IV adenosine. If the origin of arrhythmia is unclear on a symptomatic patient, it is generally consider safe to treat as ventricular in origin.
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