Arrhythmias

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

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

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

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

• 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)

• 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.