Arrhythmias

Categories: Cardiology

Arrhythmias

Kunal Patel, Madeline Rukavina


Acute management of arrhythmias

  • 12-lead EKG if possible and have defib pads on patient
  • Is the patient unstable (hypotensive, signs/symptoms of hypoperfusion)?
  • Is the information real?
  • Review tele strips if stable: VUMC Web Resources -> VUH PIICiX Philips Web -> patient selection -> alarm review (vuhphilipsweb.app.vumc.org)
  • Review past EKGs to determine if patient has had this rhythm before
  • Ensure pt has good IV access
  • Labs: BMP, Mg, TSH, and +/- troponin, tox screen

Bradyarrhythmias

Kunal Patel


Background

  • Broadly classified as sinus node dysfunction (pacing defect) or atrioventricular block (conduction defect)
  • Clinical presentation varies widely based on underlying cause, timing, degree of block/dysfunction
  • Unlikely to cause symptoms if HR >50
  • Symptoms include syncope/presyncope, dyspnea, angina

Etiologies

  • Infection/sepsis
  • Ischemia
  • Rheumatologic/Inflammatory
  • Post-cardiac surgery
  • Hypothyroidism
  • Sleep apnea
  • Infiltration (amyloid, hemochromatosis)
  • High vagal tone (pain, nausea)
  • Medications: Antihypertensives, antiarrhythmics, psychoactive meds, anesthetics, cannabis, muscle relaxants, etc.

Sinus node dysfunction

  • Symptomatic sinus bradycardia, tachy-brady syndrome, chronotropic incompetence, sinus pause, SA exit block
  • Asymptomatic sinus bradycardia (esp in young/healthy patient) is unlikely to be true bradyarrhythmia

AV Block

AV block

Evaluation

  • TTE if structural disease suspected
  • Ambulatory cardiac monitoring if frequently symptomatic

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:
  • Atropine (0.5 mg every 3 to 5 minutes; maximum total dose: 3 mg)
    • Do NOT use in heart transplant
    • Call CCU Fellow
    • Dopamine (5 to 20 mcg/kg/minute) OR Epi (2 to 10 mcg/min)
    • Transvenous pacing (Pacer pads on the defib device are capable of pacing, but don’t forget to sedate!)

Tachyarrhythmias - Narrow complex

Kunal Patel


Background

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

Tachyarrhythmia differential

tachyarrhythmia

Evaluation

  • Unstable tachyarrhythmia
  • Start with treatment, determine type later
  • Synchronized cardioversion: place defibrillator pads, consider 0.5-2mg IV midazolam for sedation, prepare for synchronized cardioversion at 200J (can ↑ to 300-360 J)

Management

  • Sinus tachycardia
    • Almost always secondary
    • Address underlying causes: fever/sepsis, hypo/hypervolemia, anxiety, anemia, PE, ACS, hypoxia, pain, urinary retention, withdrawal
  • Atrial Fibrillation/Flutter – See Atrial fibrillation section
  • AVNRT/Orthodromic AVRT
    • Look for p buried in QRS, rate 150-250, AVRT will have delta waves when NSR
    • Vagal maneuvers (1st line): Sit patient upright have them blow into tip of 10cc syringe for 10-15 seconds rapidly lay supine and raise legs
    • Adenosine (2nd line): therapeutic (break AVRT/AVNRT) and diagnostic (allows visualization of underlying rhythm)
      • Do NOT give in heart transplant, severe COPD, pre-excitation causing wide complex tachycardia (WPW antidromic AVRT)
      • Peripheral line 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 line: cut dose in half to 3mg x1, 3mg x1, 6mg x1
  • Multifocal atrial tachycardia
    • 3 or more p wave morphologies. Seen in cardiac and pulmonary disease
    • Usually does not cause hemodynamic instability
    • BBs and non-DHP CCBs can be effective, need to address underlying issue
Drug Dosing Benefits Side Effects
Metoprolol

5mg IV q5m x3

PO metoprolol tartrate 12.5mg q6 hours ↑ every 6 hr to target

Good 1st line agent

Less BP effect than dilt

Hypotension,

Negative inotropy

Diltiazem

10-20 mg IV over 2m q15m x2

drip = 5-15 mg/hr

Good 1st line w/ normal EF with drip needed

Hypotension

Avoid in HFrEF

Esmolol

500 mcg/kg bolus

drip = 50-200 mcg/kg/min

Rapid onset/offset

RBC metabolism

Hypotension
Amiodarone 150 IV over 10-30m, then 1 mg/m for 6h, then 0.5mg/m for 18h

Minimal BP effects

Long lasting; Relatively fast onset (acute effect is mostly beta blockade)

Pulmonary and thyroid toxicity

Cardioversion

Digoxin 500mcg IV x1, then 250mcg IV q6h x2-3 Great for reduced EF, positive inotropy

Slow onset

Depends on vagal tone – poor in hyper- adrenergic states

Procainamide 20-50 mg/min loading, 1-4 mg/min maintenance Use in pre-excitation syndromes (i.e. WPW), does not inhibit AV nodal conduction

Lupus-like syndrome

Hypotension

Tachyarrhythmias - Wide Complex

Madeline Rukavina


Definitions

Ventricular tachycardia (VT): a run of 3+ PVCs

  • Sustained VT: VT for 30 seconds or shorter if it requires intervention
  • Nonsustained VT (NSVT): VT 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
    • Ischemia until proven otherwise
  • Torsades de Pointes (TdP): a form of polymorphic VT with a continually varying QRS that appears to spiral around the baseline of the ECG in a sinusoidal pattern
  • Ventricular fibrillation (VF): chaotic rhythm characterized by undulations that are irregular in timing and morphology, without discrete QRS complexes

Ventricular Tachycardia vs. SVT with aberrancy

  • VT: The action potential originated in the ventricles (ex: VT)
  • Supraventricular tachycardia with aberrancy: the action potential originates from a focus above the ventricles & conducts through the AV node with a delay or block resulting in a wide QRS (mimics VT)
  • Ex: sinus tachycardia w/ bundle branch block (block may be rate dependent), AF w/ LBBB

Many ways to differentiate VT vs. SVT w/ aberrancy

  • Consult cardiology for assistance
  • Look for ECG features suggestive of VT
  • Very broad complexes >160 ms
  • RsR’ complex with a taller left rabbit ear In V1/2
  • AV dissociation (P/QRS dissociation)
  • Capture Beats: native QRS complexes making a cameo during the VT
  • Fusion Beats: QRS which appears like a signal average of VT and native complex

capture beat fusion beat

  • There are more advanced criteria to help distinguish. The aVR (Vereckie) criteria is one example that is fast and accurate

Management

Unstable

  • Sedate with midazolam 1-2mg
  • Cardioversion for monomorphic VT. Synchronized shock at 100-200J
  • Defibrillation if VF/polyVT

Stable

  • Medications (as below)
Drug Name Dosing Mechanism Side Effects
Amiodarone 150mg IV over 10 min, then 1mg/min for 6 hours; repeat bolus if VT recurs

Class III

-K+ channel blocker; has class Ia, II, & IV effects

Bradycardia, hypotension (acutely)
Lidocaine 1-1.5 mg/kg (usually 75-100 mg) at a rate of 25-50mg/min; lower doses of .5-.75mg/kg can be repeated every 5-10 min as needed

Class IB

-fast Na+ channel blocker-> slows conduction

Slurred speech, AMS, seizures, bradycardia
Procainamide 20-50mg/min until arrhythmia terminates or max dose 17mg/kg is reached

Class IA

-fast Na+ channel blocker -> slows conduction

-K+ channel blocker-> prolongs repolarization

Bradycardia, hypotension, torsades, drug-induced lupus

Avoid in HF pts, prolonged QT

  • Cardioversion If refractory to medical management

  • Treatment of underlying cause if identifiable

    • Ischemia, electrolyte disturbances, heart failure, drugs

Premature Ventricular Complexes (PVCs)

Madeline Rukavina


Background

  • Premature Ventricular Complex (PVC): early ventricular depolarization +/- mechanical contraction
  • PVC burden: % of beats of ventricular origin / total beats over a 24h period
  • PVCs are common: Up to 80% of apparently healthy people have PVCs
  • Normal number of PVCs in an adult is <500 in 24h

Etiologies

  • HTN with LVH, prior MI/scar, HF, myocarditis, ARVC, HCM, idiopathic VT, OSA, pHTN, COPD, thyroid disease, substance use (EtOH, nicotine, stimulants, caffeine)

Inpatient Evaluation & Management

  • 12 lead EKG: conduction disease, long QT syndrome, Brugada syndrome, ARVC
  • Labs: K, Mg, TSH, drug screen
  • Evaluate for QT prolonging agents (risk of Torsades)
  • Evaluate tele for PVC burden
  • Inpt 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 none recent.

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