Arrhythmias

Background

• Sinus node dysfunction (pacing defect) vs atrioventricular block (conduction defect). 
• Clinical presentation: 
  • A sinus HR > 50 bpm or a sinus pause < 3 seconds is unlikely to cause symptoms. 
  • Symptoms include syncope/presyncope, dyspnea, angina.

Etiologies 

• Older age (most common) 
• Ischemia (can’t miss) 
• Metabolic: Hypothyroidism, hyper/hypokalemia, hypermagnesemia (generally > 8 mg/dL) 
• Infection: Perivalvular abscess, Lyme, Toxoplasmosis 
• Inflammatory/infiltrative: Myocarditis, SLE, cardiac sarcoidosis, amyloidosis, hemochromatosis 
• latrogenic: cardiac surgery/valvular procedures 
• High vagal tone (e.g., pain, nausea, athletes) 
• Sleep apnea (should be considered in nocturnal sinus bradycardia) 
• Medications: Beta blockers, verapamil, diltiazem, digoxin, antiarrhythmics, alpha-2 agonists, antiepileptics, propofol, cannabis, etc.

AV Block Morphology

Management

• Avoid nodal blocking agents: adenosine, beta-blockers, CCBs, digoxin. 
• Observation if asymptomatic.
• Treat identified underlying causes. 
• If symptomatic or high-grade block (Mobitz II or complete heart block), EP consult for pacemaker evaluation 
• If unstable: 
  • Call CCU Fellow IV atropine (1 mg every 3 to 5 minutes; maximum total dose: 3 mg).  Do NOT use in heart transplant. 
  • Dopamine (5 to 20 mcg/kg/minute) OR Epi (2 to 10 mcg/min). 
  • Transvenous pacing.

Background

• Three causes of tachyarrhythmias: 
  • Re-entry: pt with structural heart disease (e.g. post-infarction scar). 
  • Abnormal Automaticity: electrolyte derangement or acute ischemia (Purkinje fibers). 
  • Triggered Activity: early and late after depolarizations. (e.g. Hypokalemia, ischemia, infracts, excess calcium and drug toxicity).

Evaluation

• Is the QRS narrow or wide (see Tachyarrhythmias – Wide Complex section). 
• Is the rhythm regular or irregular? 
• Look for P waves (location, axis, morphology). 
• Compare to baseline ECG.

Regular

• Sinus tachycardia - Maximum rate = 220 - patient age. Management: Address underlying causes (eg, fever/sepsis, hypo/hypervolemia, anxiety, anemia, PE, ACS, hypoxia, pain, urinary retention, withdrawal). 
• AVNRT – Originates from a reentrant loop that involves the AV node and the atrial tissue causing simultaneous depolarization of the atrium and the ventricle. P waves are rarely seen (buried in QRS). 
• Orthodromic AVRT - Involves an accessory pathway that bypasses the normal insulation provided by the atrioventricular valves, allowing conduction between the atria and ventricles. Can see P waves after QRS (note: antidromic is wide complex and P waves are typically buried in T waves). 
• Junctional Tachycardia - Arises from abnormal automaticity of an ectopic focus in the atrioventricular (AV) junction, including the AV node and His bundle.
• Focal atrial tachycardia – regular atrial rhythm > 100 bpm with discrete P waves (with abnormal morphology) caused by increased automaticity at an atrial focus or reentrant circuit in the atria.

Irregular

• Atrial Fibrillation/Flutter – See Atrial fibrillation section. 
• Multifocal atrial tachycardia - ≥3 p wave morphologies. Irregular rhythm. Gradual onset and termination. Rate = typically 100-150. 
  • Mechanism/etiologies: multiple atrial premature beats from hypoxia/increased atrial pressure. 
  • Management: BBs and non-DHP CCBs can be effective, address underlying issue.

Management

• If unstable -> synchronized cardioversion. Place defibrillator pads, consider 0.5-2mg IV midazolam for sedation, prepare for synchronized cardioversion at 200J (can ↑ to 300-360 J). 
• If stable: 
  • 1. Try vagal maneuvers, of which modified Valsalva is the most effective (Sit pt upright à have patient blow into tip of 10cc syringe for 10-15 seconds à rapidly lay supine and raise legs). 
  • 2. Try administering adenosine, which can be both therapeutic (break AVRT/AVNRT and 80% of atrial tachycardias) and diagnostic (allows visualization of underlying rhythm). 
  • Would try and have continuous 12 lead EKG on while pushing adenosine to try and catch the underlying rhythm 
    • Do NOT give in heart transplant, severe COPD, pre-excitation causing wide complex tachycardia (WPW → antidromic AVRT). 
    • Peripheral at AC or above w/ arm elevated: 6mg x1 → 6mg x1 (if not effective after 1-2 min) →12mg x1 (if refractory to 6mg). 
    • Central: cut dose in half to 3mg x1 → 3mg x1 → 6mg.

Dosing

Definitions

• Premature Ventricular Complex (PVC): early ventricular depol +/- mechanical contraction. 
• PVCs are common: Up to 80% of apparently healthy people have PVCs. 
  • PVC induced cardiomyopathy may be present with PVC burden >10-20%. 
  • Inpt Eval: Order 12 lead EKG to look for conduction disease (Long QT, brugada), K, Mg, TSH, Drug screen (EtOH, nicotine, stimulants, caffeine), med rec for QT prolonging agents, tele to assess PVC burden. 
  • Inpt management: consult to EP for PVCs rarely warranted unless significant PVC burden (>5 PVC/min, consistently) in setting of reduced LVEF. 
  • For pts with >5 PVC/min or pts with symptoms, discharge with Ziopatch (VA) or mobile cardiac telemetry (VU) and obtain TTE if not done in past 3 months.

Wide-complex tachycardia (WCT): QRS >0.12 seconds and HR >100 beats/min

• Differential = VT, SVT with aberrancy, ventricular paced rhythm, preexcitation syndrome, drug- and electrolyte-induced WCT (ex. HyperK).

Ventricular tachycardia: a run of 3+ PVCs originating in the ventricles at a rate >100 bpm

• Sustained VT: VT for >30 seconds or shorter if it requires intervention 
• Nonsustained VT (NSVT): >3 complexes for < 30 seconds 
• VT storm: > 3 separate episodes of sustained VT within 24 hrs. 
• VT Morphologies 
  • Monomorphic VT: similar QRS configuration from beat to beat 
    • Usually 2/2 scar-mediated VT from prior infarction 
  • Polymorphic VT: a continuously changing QRS configuration from beat to beat 
• Evaluate for ischemia with LHC 
  • Torsades de Pointes: a form of polymorphic VT occurring in the setting of QT prolongation, characterized by waxing and waning QRS amplitude with a twisting appearance around the baseline. 
  • Ventricular fibrillation (VF): chaotic rhythm characterized by irregular undulations and morphology, without discrete QRS complexes.

Wide-complex tachycardia evaluation

• - WC-caused by ventricular arrhythmias (VT, VF) or supraventricular tachycardias with aberrant conduction resulting from one of the following: disease in the His–Purkinje system, such as left or right bundle-branch block; a bypass tract (i.e., Wolff–Parkinson–White syndrome), with depolarization of the ventricle from the bypass tract; or a ventricular paced rhythm from a pacemaker. 
• - Of note, a bundle branch block may appear with faster or slower heart rates and disappear with normal heart rates (i.e., rate dependent). 

To differentiate between WCTs: 

• Use the Basel algorithm (93% sensitivity & 90% specificity).
  • VT is likely if > 2 of the criteria are present: 1. Structural heart disease (hx of MI, CHF with LVEF < 35, Device—ex, ICD, CRT), 2. Time to first peak in Lead II is > 40ms, 3. Time to first peak in Lead aVR is > 40ms. 
  • SVT is likely if only 0 or 1 criteria fulfilled.
• Regular WCT: monomorphic VT or SVT with aberrancy. 
  • VT is likely if --> AV dissociation, escape or fusion beat, concordance (QRS complexes are completely + or – in leads V1-V6), extreme axis deviation. 
  • SVT with aberrancy is likely if --> QRS complexes look identical to those seen in sinus (morphology and axis), pre-excitation is seen on baseline.
• Irregular WCT: atrial fibrillation with aberrant conduction (if same QRS morphologies) or polymorphic VT (if different QRS morphologies).

Management

• If you’re unsure that the rhythm is VT or SVT with aberrancy -> treat like VT. 
• Unstable 
  • Sedate with midazolam 1-2mg.
  • Cardioversion for monomorphic VT. Synchronized shock at 100-200J. 
  • Defibrillation if VF/polymorphic VT.

Stable:

• Anti-tachycardia pacing (ATP): if the patient is in VT and has an ICD in place, page cardiology fellow to perform ATP. 
• Cardioversion if refractory to medical management. 
• Treat underlying causes if identifiable: Ischemia, electrolyte disturbances, heart failure, drugs.