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 (1^st line): Sit patient upright have them blow into tip of 10cc syringe for 10-15 seconds rapidly lay supine and raise legs
- Adenosine (2^nd 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 V½
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)

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.

Last update: 2022-05-29 04:32:11