Diagnostic Testing

    • Symptoms: palpitations, dizziness, syncope, decreased exercise tolerance.
    • ECG: look for pre-excitation, heart block, long QT.
    • Often Echo: to evaluate LV size/function, and look for structural heart disease.
    • Cardiac MRI: evaluate for sarcoidosis and cardiomyopathy (causes of arrhythmia).  
        (Same info as echo, but allows evaluation of infiltrative causes.)
    • Invasive EP setting: to provoke and map arrhythmia.

    Rhythm Recorders:

    • 24-48hr Holter
      • For frequent and asymptomatic arrhythmia capturing (occurring in 24-48hr period) while device is worn.
    • Event Recorder
      • If episodes are less frequent, but within few weeks period.
      • Triggered by the patient.
    • Loop Event Recorder
      • For brief episodes (too brief to capture on event recorder).
      • Records and saves last 1min or so when button is triggered.
    • Implantable Loop Recorder
      • Can be placed subcutaneously and interrogated.  Store up to 42min of data and have battery life up to 3 years can capture very infrequent episodes.
    • MCOT (Mobile Cardiac Outpatient Telemetry)
      • Continuously monitor EKG and automatically recognized arrhythmias and transmit EKG to health care provider. (Central monitoring station).  
      • Allows even longer (>1mo) duration of rhythm analysis.



    • Types:
      • Sinus node dysfunction
      • AV node dysfunction
      • His-purkinje system.
    • Causes:
      • Drugs
      • High K+
      • Lyme disease
      • Hypothyroidism     

    Sinus bradycardia

    • Most common, often not pathologic.
    • Athletes (low resting HR) and no symptoms, and naturally while asleep (can be as low as 30bpm).
    • Pathologic:
      • Fibrotic replacement of SA node during agents.
      • MI sinus node damage
      • Cardiac surgery
      • Infiltrative process (amyloid, sarcoid)
      • Increased vagal tone
      • Vomiting
      • Medications (B-blockers, calcium channel blockers)
      • Genetic Rare disease
    • Manifest as sick sinus syndrome, sinus arrest, or chronotropic incompetence. 


    AV Block

    • 3 types: 1-3rd degree.
    • 1st degree: PR > 200ms
    • 2nd degree
      • Type 1 - Progressively narrowing PR intervals with dropped beats
        • Considered as a "supra-hisian" (AV node) block, which may be vagally induced
      • Type 2 - No PR lengthening, dropping QRS complexes.
        • More worrisome, suggesting his-purkinje disease. ("infra-hisian")
        • Mobitz type II - high risk of progressing to complete heart block.
        • 2:1 block -> impossible to say if Type 1 or 2.
          • Often wait and treat reversible causes (discontinue AV blocking agents)
          • If persists..Can potentially use exercise treadmill (supervised).
            • If block improves with exercise: consider Type I (benign),
            • If block does not improve or becomes high grade --> Type II (will likely need pacing)
      • "High grade heart block" occurs when two or more non-conducted P-waves occur for each QRS
    • 3rd degree (complete) heart block
      • When no relationship between P waves and QRS.
      • Reversible causes are medications and lyme disease.
      • Often require a pacemaker (higher risk of wide QRS escape - less stable escape).
    • Transient heart blocks are common post-MI (especially after anterior infarcts and sometimes posterior).  Have to wait several days post-MI to see if block is temporary.


    • Treatment of symptomatic bradycardia or heart block without reversible causes.
    • Indications for permanent pacing:
      • Symptomatic bradycardia (heart rate <40/min) or sinus pauses

        Symptomatic complete heart block or second-degree heart block (type 1 or 2)

        Asymptomatic complete heart block or advanced second-degree heart block

        Atrial fibrillation with pauses of ≥5 seconds

        Alternating bundle branch block

    • Usually put in L-pectoral area, into subclavian vein into R-side of heart.
    • Electrocautery during surgery can inhibit pacemaker.
      • If ever undergoes cardiac surgery, device should be reprogrammed for asynchronous pacing mode. (put magnet over it).
    • MRI contraindicated for most pacemakers, should only be performed with close monitoring.
    • Patients paced from RV apex all the time can develop LV dysfunction or atrial fib due to mechanical dissynchrony.
    • New algorithms developped to minimize pacing.



    • Sinus tachycardia is most common (pain, fever, anxiety, anemia).
    • Symptoms: SOB, CP, syncope, presyncope
    • Hemodynamic stability does not help with etiology.


    Ventricular Arrhythmias


    • 75% of people have PVCs, report "skipped" or "extra strong" beat due to compensatory pause after PVC.
    • No need for intervention (in absence of structural heart disease, FMHx of early cardiac death, syncope).
    • For frequent PVCs
      • Risk of cardiomyopathy (reversible with treatment)
      • Risk Factors: HTN, LVH, HF, myocardial ischemia/infarction.
    • If very symptomatic:
      • B-blocker or CCB.
      • Anti-arrhythmic agents rarely required.
      • Catheter ablation only if medical therapy failed.

    Ventricular Tachycardia

    • Rhythm >100bpm originating in ventricles.
    • Classified as:
      • "Non-sustained"
      • "Sustained" when >30s or produces hemodynamic collapse.
    • Also classified as:
      • "Monomorphic" - regular
        • Due to: Structural (prior MI, or cardiomyopathy) 
        • Structural heart disease patients with VT have high risk of sudden cardiac death.
    • If low EF, and rapid tachycardia, hypotension and syncope --> cardiac arrest
    • If normal EF, slow v-tach can have minimal symptoms (dizziness, CP, palpitations, dyspnea).
    • If VT with structural heart disease:
      • Prevention with Beta-Blocker (reduces mortality/sudden death, in those with HF and ischemic disease)
    • VFib, hemodynamically unstable VT, or stable VT with structural heart disease
      • ICD improves survival.
      • Antiarrhythmic therapies can be used in addition to prevent shocks, but no mortality benefit.
      • In those with HF, amiodarone has the best efficacy.
      • Sotalol can be used if intolerant to amiodarone, but B-blocking properties can precipitate HF decompensation.
    • In pts with dizziness, syncope, palpitations with possible VTach diagnosis --> EP study can be useful.
      • For recurrent VTach catheter ablation can be performed to reduce ICD shocks, but no effect on mortality.
    • NOTE: Amiodarone helps prevent VT, but if in effective, can add on Lidocaine IV.
    • NOTE: Alternatively Procainamide can be used, but it is a negative inotrope, so do not use in low EF patients, also risk of QT prologation and increased AV conduction.


    Idiopathic VT

    • Occurs in normal hearts.
    • Better prognosis than VT with structural heart disease.
    • Patient reports palpitations, syncope is unusual.  Can be provoked with exercise or emotional stress.
    • Usually monomorphic, originating from RV outflow tract. (positive in inferior leads)
    • Differential
      • Arrhythmogenic RV cardiomyopathy / dysplasia (ARVC/D)
      • Baseline EKG should be obtained in all pts to look for prior infarction, TWI, epsilon waves (suggestive of ARVC/D).
      • Do treadmill test to attempt provoke the tachycardia.  Can also evaluate ischemia.
      • Echo to look for structural heart disease.
      • Treatment:
        • No treatment is necessary with mild symptoms.
        • If severe symptoms: CCB or BB should be started, and if ineffective -> use Class I or III antiarrhythmic agents.  OR catheter ablation if refactory(high rate of success).
        • ICD IS NOT INDICATED (benign prognosis, and efficacy of other therapies).
    • ARVTD.png


    Inherited Arrhythmias

    Inherited Arrhythmia Syndromes



    Characteristic Findings


    Long QT syndrome

    Syncope, QTc interval usually >460 msec, torsades de pointes

    β-Blockers, ICD

    Short QT syndrome

    Syncope, QTc interval usually <350 msec, atrial fibrillation, VT, VF


    Brugada syndrome

    Syncope, VF, coved ST-segment elevation in leads V1-V3


    Catecholaminergic polymorphic VT

    Syncope, polymorphic or bidirectional VT during exercise or emotional stress

    β-Blockers, ICD


    Syncope, T-wave inversions from lead V1 to at least V3, monomorphic VT, epsilon waves, abnormal signal-averaged electrocardiogram, frequent PVCs, abnormal right ventricular size and function on echo/CMR imaging

    ICD, β-blockers, sotalol, amiodarone

    ARVC/D = arrhythmogenic right ventricular cardiomyopathy/dysplasia; 


    • Long QT channelopathy; affects 1/5000 persons.

      • Polymorphic VT risk, causing syncope.
      • Most genes that make this are in genes that affect ion channels. (depends on specific channel).
      • Various triggers: exercise, sudden loud noises, sleep.
      • Largest risk: sudden cardiac arrest in past, recent syncope, QTc > 500ms.
      • R/O reversible causes (drugs, electrolytes).
      • Treatment:
        • B-blockers are mainstay of therapy.
        • Avoud QT prolonging drugs (i.e. Sotalol, erythromycin, haloperidol.... see
        • ICD - if :
          • Hx of cardiac arrest
          • Syncope
          • VT while on Beta-blockers
          • Strong family hx of sudden death.
    • Short QT interval (very rare)

      • QTc < 350ms.
      • Predisposed to AFib, syncope, polymorphic VT, VFib.
      • Treatment:
        • Quinidine is beneficial by prolonging QT.
        • High risk of sudden death, should be offered ICD.
    • Brugada Syndrome

      • Electrocardiographic abnormality characterized by
        • ≥2mm J-point elevation on ECG
        • Coved ST-elevation
        • T-wave inversions in V1-3.
      • EKG findings often intermittent
        • Infusion of sodium channel blocker can sometimes bring out this pattern. (i.e. Ajmaline/Flecainide challenge)
        • Those with spontaneous EKG findings are at high risk of cardiac events.
        • Other things like fever, hypo/hyperkalemia, tricyclic antidepressants, cocaine, EtOH use can provoke ECG changes.
      • High risk of:
        • Syncope, VFib, sudden cardiac arrest.
      • Mechanism:
        • Potassium channel abnormality associated with this.
        • Genetic cause unknown, but likely channelopathy.
      • Brugada.png
      • Treatment:
        • In absense of symptoms --> controversial. 
        • Recent data: qunidine can be effective.
        • ICD for high risk patients.


    • Catecholaminergic Polymorphic VT

      • Usually <20yo.
      • VT during times of high adrenergic tone.
      • High risk of sudden cardiac death...
      • ECG normal at baseline, but demonstrates polymorphic VT or biventricular VT during exericse or emotional stress.
        • QRS often alternating between two morphologies between every other beat.
      • Treatment:
        • Avoid exercise
        • Beta-Blockers to avoid synchopal events.
        • ICD if B-blockers not affected.
    • ARVC/D

      • Arrhythmic RV cardiomyopathy / dysplasia
      • Charcterized by fibrofatty infiltration of RV, causing desmosome dysfunction.
      • Symptoms:
        • Syncope, sudden cardiac arrest caused by VT originating in RV.
      • As disease progresses RV dysfunction and eventual LV dysfunction can occur
      • ECG:
        • TWI V1-3 leads, may show epsilon wave (high frequency signal) at the end of QRS.
      • Continuous ambulatory EKG shows VT or >500 PVCs in 24hr period.
        • ARVTD.png
      • Echo: enlarged RV size and dysfunction.
        • CMR can image RV, and should be performed when ARVC/D is suspected.
        • If dx is in doubt, RV biopsy shows reduction in myocyte number with fibrotic replacement.
      • Management:
        • Discourage exercise (High risk of VTach, and accelrated disease progression)
        • ICD for:
          • sudden cardiac arrest, family hx, syncope, sustained VT, or extensive RV or any LV involvement.
        • No medical therapy to prevent progression (B-Blockers, sotalol, amio, catheter ablation can be used to reduce ICD shocks).
    • Idiopathic VF

      • No identifiable cause.
      • Inferolateral early repolarization on EKG (common benign finding), no futher workup needed.
      • Treatment:
        • ICD
        • Limited studies: Class IA antiarrhythmic agents, and BB's to reduce ICD shocks. 


    Sudden Cardiac Arrest

    • Cessation of cardiac activity, progression to death if no treatment is performed.
    • Affects 300,000-450,000 ppl in US annually.
    • Main mechanism: ventricular tachyarrhythmias.
    • Associated conditions: older age, FMHx, male sex, postmenopausal, obesity, HTN, lipidemia, obesity etc..
    • CPR initiated --> 2min before rhythm check.
    • Treatment:
      • ICD is indicated if sustained (>30s) for tachyarrhytmic event and for high risk sudden death.


    Device Notes

    • NOTE: Surgical electrocautery can generate interference that is sensed by ICD -->inappropriate discharge (should have ICD turned off during OR by using magnet).
    • Magnet on ICD --> turns off shock delivery, but pacing unaffected (will pace if hits low treshold)
    • Magnet on Pacemaker --> inhibit sensing, goes into asynchronous mode that delivers constant pacing (magnet turns off sensing, can can assess sensing).
    • Pacemaker
      • Nomenclature
        • 1st Letter - chamber being paced
        • 2nd Letter - chamber being sensed
        • 3rd Letter - Response - 
        • 4rth Letter - Respond to increased metabolic activity
        • "VVIR" (ventricle pacing, ventricle sensing, natural conduction inhibits pacemaker, has accelerometer to modulate rate based on movement)
          • Tested CO2 and accelerometer for movement, but accelerometer was better.
        • AAIR (atrium paced, atrium sensed [same lead], Inhibited, Rate modulating).
          • Sick sinus syndrome.  But high risk of developing AV block 5%/year, so now put in DDDR devices.
          • Risk of infection opening  (3-5% each time)
          • DDDR device (dual [two leads - atrium + vent], dual sensing, Dual [inhibit and trigger], rate modulating.
        • (intrinsic conduction is always better, paced conduction desynchronizes the heart).
        • DDD MODE, can have 4 modes of operation:
          • AP-VP
          • AS-VP (if intrinsic heart rate picks up artrial activity, Atrial sensing, ventricular pacing)
          • AP-VS (preferred for sick sinus, senses ventricles to see if conducted, but if AV block will pace both).
          • AS-VP (atrial sensing to generate ventricular beat when atria contract).
            • In AV block.
            • Sometimes atrial tachycardia, device pacest fast.  Set upper tracking limit to 130 or so (to prevent overdrive, which looks like VTach).
            • NEW: 2:1 pacing (smooth changes in heart rate)
    • In ER: if signs of infection of pocket, DO NOT stick a needle in the pacemaker pocket.  Just start broad spectrum abx.
    • QT interval in paced QRS is associated with depolarization abnormality we generated (abnormal repolarization).
    • Beeping device:
      • Typically ICD beeping requires a call to the Arrhythmia Sevice, can mean several things:
        • Battery dead (rare - patients get very close follow-up)
        • Lead impedance (most likely cause) - issue with connection of device with lead, lead itself, or lead connection to heart (erosion)
    • ASSERT Paper...?
    • For a long time DDD thought to be better for AV block, but VVI shown to be similar.
      • No hemodynamic changes, VVI (one lead)
      • One lead - less complications than two lead.
    • In sick sinus: why not put AAI pacemaker (atrially paced, atrially sensed, Inhibited)
      • Can develop AV block, (1 in 2 developed AV block?)
      • 1:2 % progression to complete AV block with AAI. (used to check if AV conduction present at 120bpm).
    • Troubleshooting:
      • Dislodgement.
        • (even milimeters change, not seen on CXR, can be dislodged).
      • Perforation  <1% with new leads, extremely rare. (Sudden change of impedance, i.e. increase in conduction b/c perforated).
      • Sensing (under/over)
        • Ignores underlying rhythm, paces anyways.
        • Threshold to detect P-wave can change, have autosensitivity modes, but consume battery. 
        • 1. Inappropriately programmed sensitivity (above)
        • 2. Lead dislodgement.
        • 3. Lead Failure (insulation break, conductor fracture) - some devices recalled, and need to be replaced either immediately or at time of battery change).
        • 4. Lead maturation - OLD 25-35y leads.
        • 5. Change in native signal.
          • Change in signal when electrolyte changes, or infarcted area of capture.
        • Oversensing:
          • asystole when using microwave etc... (patients drop)
          • (Poor connection todevice, change in ecg... i.e hyperkalemia makes tall T, sensed as QRS).
          • Intereference very rare nowadays with new algorithms.  In the old days microwaves could do that, but some case reports of electric water heaters in shower, etc..  MRI is common for interference. 
      • non-capture
      • no output
      • Pseudomalfunction.
    • 5% risk of infection when opening a pocket, so minimize!
    • Putting leads no longer in apex, but going against gravity into the outflow tract.
    • Paper: SELECT approach (Circ arrhythmia 2012, JC arrhythmia 2011)
      • Randomized 
      • Clinical outcome better, (BNP, etc..) 
    • Pacemaker Syndrome
      • Put pacemaker, and come back short of breathe. 
      • Several possibilities (unknown reason).  Initially thought V-A conduction (depol of atrum against closed AV valve?)
        • But later thought to be due to desynchronization of ventricles.
        • So started putting leads --> screwing them into the RV outflow tract to increase intrinsic conduction. 

    Device Infections

    • Present as:
      • Localized pocket erosion or abscess
      • Vegetation on a lead.
      • Unexplained bacteremia.
    • DO NOT aspirate device site (can damage leads).
    • Management:
      • Blood cultures
      • Transthoracic echo
      • (If blood cultures positive, TEE for lead and valve examination).
    • Treatment:
      • Extraction of entire system (including leads) followed by antibiotics.
      • Decision ti re-implant depends on risks/benefits.


    Beta Blocker Toxicity

    • Generally slows down SA and AV nodes, negative inotropy.
    • Treatment:
      • 1st line:
        • Atropine 0.5mg as per ACLS
        • Fluids (to improve BP)
        • Glucagon 3-5mg (if response --> 3-5mg/hr IV infusion)
          • Careful: glucagon causes lots of NAUSEA!!! (use gravol, not ondansetron)
          • Insulin + D50 has some benefit (some reports show high-dose insulin [i.e. up to 1 unit/kg/hr with D50 drip] as very effective, but BE CAREFUL! very little experience with this.  Considering DKA insulin is 0.1 u/kg/hr.
      • 2nd line:
        • Calcium (chloride or gluconate, but twice more available Ca in chloride than gluconate)
          • (i.e. 1amp has 1g of CaCl OR 2g of CaGluconate)
        • Inotropes/Chronotropes
          • Isoproterenol (B1 agonist)  + add a1 agent such as norepinephrine.
          • Dopamine (2.5-10 mcg/kg/min)
          • Dobutamine + a1 agent such as norepinephrine.
      • May need pacing (transcutaneous or transvenous).
      • Lipophilic B-blockers are dialyzable.
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