Cardiovascular System (CVS) ORGAN SYSTEMS

Cardiac arrhythmia

Abnormal variation from the normal heart rate and/or rhythm.

Abnormal variation from the normal heart rate and/or rhythm.

Patients with an arrhythmia may exhibit a broad spectrum of clinical presentation from being entirely asymptomatic to sudden cardiac arrest. Arrhythmias can be paroxysmal, leading to difficulty in estimating true prevalence.

Normal heart conduction:

The only normal rhythm of the heart is a normal sinus rhythm. In this rhythm, an impulse is generated in the sinoatrial (SA) node, which is conducted through and slowed down while passing through the atrioventricular node (AV). It is then conducted through the bundle of His, to the left and right bundle branches, and eventually into the Purkinje fibers. Any deviation from this conduction pathway results in arrhythmia.
A graphical representation of the Electrical conduction system of the heart showing the Sinoatrial node, Atrioventricular node, Bundle of His, Purkinje fibers, and Bachmann’s bundle. | Wikimedia Commons (Public Domain)


Electrophysiologic mechanisms:

Underlying electrophysiologic mechanisms are generally divided into 2 major categories
  • Enhanced/abnormal impulse formation (ie, focal activity)
  • Conduction disturbances (ie, reentry)
Classification of active cardiac arrhythmias. | Antzelevitch, C., & Burashnikov, A. (2011). Overview of Basic Mechanisms of Cardiac Arrhythmia. Cardiac electrophysiology clinics, 3(1), 23–45.


Afterdepolarization & Triggered Activity

Depolarizations that attend or follow the cardiac action potential and depend on preceding transmembrane activity for their manifestation are referred to as afterdepolarizations. When the after-depolarization amplitude suffices to bring the membrane to its threshold potential, a spontaneous action potential referred to as a triggered response is the result. These triggered events give rise to extrasystoles, which can precipitate tachyarrhythmias.
  • Early afterdepolarization (EAD): Interrupts or retards repolarization during phase 2 and/or phase 3 of the cardiac action potential
  • Delayed afterdepolarization (DAD): Occurs after full repolarization.
Afterdepolarization & Triggered Activity
Examples of early afterdepolarization (EAD) (A), delayed afterdepolarization (DAD) (B), and late phase 3 EAD (C). | Burashnikov A, Antzelevitch C. Late-phase 3 EAD. A unique mechanism contributing to initiation of atrial fibrillation. Pacing Clin Electrophysiol 2006;29:290–5

Reentrant arrhythmias:

Reentry is fundamentally different from automaticity or triggered activity in the mechanism by which it initiates and sustains cardiac arrhythmias.
  • Circus movement reentry: Activation wavefront propagates around an anatomic or functional obstacle or core, and reexcites the site of origin. In this type of reentry, all cells take turns in recovering from excitation so that they are ready to be excited again when the next wavefront arrives.
  • Non-circus movement reentry (reflection and phase 2 reentry): Occur in a setting in which large differences of recovery from refractoriness exist between one site and another. The site with delayed recovery serves as a virtual electrode that excites its already recovered neighbor, resulting in a reentrant reexcitation.
    • Reflection: Nonstimulated impulse due to circuitous reentry at the level of the syncytial interconnections, made possible by longitudinal dissociation of the bundle
    • Phase 2 reentry: Dome of the action potential (most commonly epicardial) propagates from sites at which it is maintained to sites at which it is abolished, causing local reexcitation of the epicardium and the generation of a closely coupled extra-systole. Severe spatial dispersion of repolarization is needed for phase 2 reentry to occur.
Ring models of reentry: (A) Schematic of a ring model of reentry. (B) Mechanism of reentry in the Wolf-Parkinson-White syndrome involving the AV node and an atrioventricular accessory pathway (AP). (C) A mechanism for reentry in a Purkinje-muscle loop proposed by Schmitt and Erlanger. The diagram shows a Purkinje bundle (D) that divides into 2 branches, both connected distally to ventricular muscle. Circus movement was considered possible if the stippled segment, A → B, showed unidirectional block. An impulse advancing from D would be blocked at A, but would reach and stimulate the ventricular muscle at C by way of the other terminal branch. The wavefront would then reenter the Purkinje system at B traversing the depressed region slowly so as to arrive at A following expiration of refractoriness. (D) Schematic representation of circus movement reentry in a linear bundle of tissue as proposed by Schmitt and Erlanger. The upper pathway contains a depressed zone (shaded) that serves as a site of unidirectional block and slow conduction. Anterograde conduction of the impulse is blocked in the upper pathway but succeeds along the lower pathway. Once beyond the zone of depression, the impulse crosses over through lateral connections and reenters through the upper pathway. | (C and D from Schmitt FO, Erlanger J. Directional differences in the conduction of the impulse through heart muscle and their possible relation to extrasystolic and fibrillary contractions. Am J Physiol 1928;87:326–47.) | Antzelevitch, C., & Burashnikov, A. (2011). Overview of Basic Mechanisms of Cardiac Arrhythmia. Cardiac electrophysiology clinics, 3(1), 23–45.


Arrhythmia is broadly categorized into bradyarrhythmias and tachyarrhythmia based on the heart rate. They are further divided according to the origin, means of transmission, and syndromes associated with it.

  • Bradyarrhythmia: HR < 60 bpm
  • Tachyarrhythmia: HR > 100 bpm


Classification based on the origin of arrhythmia:

  • Supraventricular Tachycardia (SVT): Arrhythmia originating from above AV node
    • Atrial fibrillation (AFib), flutter, tachycardia
    • Atrial premature complex (PAC)
    • Atrioventricular nodal reentrant tachycardia (AVNRT)
    • Atrioventricular reentrant tachycardia (AVRT)
    • AV junctional extrasystoles
  • Ventricular Tachycardia (VT): Arrhythmia originating below AV node.
    • Ventricular fibrillation (V-fib), tachycardia (sustained or non-sustained)
    • Ventricular premature beats (PVC) 

Classification based on QRS complex duration:

  • Narrow QRS complex tachycardia: QRS <120 ms
    • Sinus tachycardia
    • Atrial tachycardia (AT), flutter, fibrillation (irregular QRS complexes)
    • Atrioventricular nodal reentrant tachycardia (AVNRT)
    • Atrioventricular reentrant tachycardia (AVRT)
    • Junctional ectopic tachycardia
    • Sinoatrial nodal reentrant tachycardia (SANRT)
  • Wide QRS complex tachycardia: QRS ≥120
    • Monomorphic & polymorphic ventricular tachycardia
    • Ventricular fibrillation

Supraventricular Tachycardia (SVT)

Usually narrow complex tachycardias with QRS width being < 3 mm or 120 ms on the EKG strip.

Classification based on mechanism SVTs:

  • Atrioventricular reciprocating tachycardia (AVRT)
  • Atrioventricular nodal reentrant tachycardia (AVNRT)
  • Atrial tachycardia

Atrioventricular reciprocating tachycardia (AVRT):

As found in Wolff-Parkinson-White syndrome (the presence of delta wave without arrhythmia doesn’t require investigation or treatment).
  • Mechanism: Accessory pathway present outside of the AV node-Bundle of Kent.
  • Subtypes:
    • Antidromic: Conduction down accessory pathway and up to AV node leading to formation of a delta wave.
    • OrthodromicConduction down AV node into an accessory pathway with no delta wave.
  • Presentation: Palpitation, shortness of breath, or syncope
  • EKG: Slurred upstroke of the QRS, delta wave, may give an impression of the wide QRS complex.
  • Management:
    • First line: Amiodarone or procainamide
    • 2nd line: Synchronized cardioversion
    • Definitive: Accessory pathway ablation

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)

  • Mechanism: Slow & fast fibers present in AV node & peri-nodal tissue leading to re-entry.
  • Presentation: Sudden tachycardia, palpitation, shortness of breath, chest tightness, or syncope.
  • EKG: Narrow complex tachycardia with P waves hidden in T waves. HR: 150-160 bpm.
  • Management:
    • Step 1: Carotid massage/Valsalva maneuver 
    • Step 2: Adenosine
    • Step 3: Cardioversion
    • Step 4: Ablation or chronic suppressive therapy with beta-blockers and calcium channel blockers such as diltiazem/verapamil.

Atrial fibrillation (AFib)

M/C arrhythmia
  • 5 types based on their duration:
    • New-onset AFib
    • Paroxysmal AFib: Self-terminating or intermittent
    • Persistent AFib: Fails to self-terminate within 7 days and requires treatments (medical or electrical cardioversion) 
    • Long-standing persistent AFib: Lasts for ≥ 1 year
    • Permanent AFib: Persistent for ≥ 1 year despite treatment
  • Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle fibers near the proximal part of the pulmonary vein.
  • Presentation: Usually asymptomatic or can cause symptoms like palpitation, shortness of breath, irregularly irregular pulse, or even hypotension.
  • EKG: Irregularly irregular narrow complex tachycardia with no discernable P-waves.
  • Management: Rate control or rhythm control strategy (depending on hemodynamic stability, candidacy for ablation, and the presence of co-morbidities)
    • Rate Control Strategy: HR goal is < 110 bpm in patients with chronic atrial fibrillation.
      • Beta-blockers or calcium channel blockers (CCB)
      • Digoxin (adjuvant therapy in difficult to control cases)
    • Cardioversion strategy: Preferred in hemodynamically unstable or if rate control fails and in a young patient with no other co-morbidities.
      • Synchronized electric cardioversion
      • Chemical cardioversion: Flecainide, propafenone, amiodarone, or dronedarone
      • Maze procedure

The CHA2DS2VaSc score:

Determined by the presence of the following factors: Congestive heart failure (CHF) with ejection fraction (EF) less than 40%, hypertension, age > 65 years, diabetes mellitus, history of stroke (non-hemorrhagic), or transient ischemic attack (TIA), vascular disease (peripheral vascular disease – PVD), age > 75 years, female sex. Each factor adds a point to the score, except for a history of stroke/TIA, which adds 2 points.
  • If the score is 0: No anticoagulation or aspirin based on individual assessment
  • If the score is 1: Aspirin or anticoagulation based on individual assessment.
  • If the score is 2 or more: Anticoagulation is recommended if not at high risk of bleeding. 

Atrial Flutter:

  • Mechanism: Reentrant circuit usually around the tricuspid annulus in the right atrium.
  • Presentation: Can be asymptomatic, or it can cause palpitation, shortness of breath, or hypotension.
  • EKG: Regular tachycardia with Saw-tooth appearance of P wave with a variable degree of AV block.
  • Management:
    • Control of ventricular rate: AV blocking agents (beta-blockers or CCB)
    • Restoration of sinus rhythm: Cardioversion/ablation  

Multifocal Atrial Tachycardia (MAT)

  • Mechanism: Multiple automatic atrial foci due to increased sympathetic tone secondary to various causes, including hypoxemia (chronic obstructive pulmonary disease (COPD), or stimulant use.
  • Presentation: Usually asymptomatic. Patients will have symptoms of the underlying illness, such as dyspnea.
  • EKG: ≥ 3 P-wave morphologies with different PR intervals.
  • Management:
    • Oxygen therapy if hypoxemic and treatment of the underlying cause.
    • Refractory cases: Rate Control with CCBs (first choice in the setting of COPD followed by beta-blockers)

Junctional tachycardia

Arrhythmia originating from or near the AV node.
  • Mechanism: Rhythm arising from the AV node.
  • Risk Factors: Post cardiac surgery, myocardial ischemia (or during reperfusion), or digoxin toxicity.
  • Presentation: Usually well-tolerated and asymptomatic.
  • EKG Findings: Inverted P Wave in the lead 2 with short PR or No P waves with a narrow complex.
  • Management: Treat the underlying cause. 

Ventricular Tachycardia

Origin is below the AV node. It is the major cause of sudden cardiac deaths.

Non-Sustained Ventricular Tachycardia:

When the rapid ventricular rhythm terminates on its own within 30 seconds.
  • Mechanism: Channelopathies secondary to structural abnormality, electrolyte disturbances, metabolic imbalance, and the effect of pro-arrhythmic drugs.
  • Risk Factors: Structural or ischemic heart disease.
  • Presentation: Asymptomatic or palpitations.
  • EKG: Monomorphic wide complex with more than 3 beats in a row lasting < 3 seconds
  • Management: Implantable cardioverter-defibrillator (ICD) and/or medical therapy.

Sustained Ventricular Tachycardia

  • Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current. Some patients do not have structural heart disease. Approximately 10% cases are idiopathic.
  • Risk Factors: Structural heart disease and post-myocardial infarction.
  • Presentation: Palpitation, hypotension, or syncope.
  • EKG: Monomorphic wide complex tachycardia.
  • Management:
    • IV Lidocaine, amiodarone, or procainamide
    • Catheter ablation

Ventricular Fibrillation (VFib)

  • Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current leading to disorganized high-frequency excitation. Patients with Cardiomyopathies can have Ventricular fibrillation due to an increase in end-diastolic pressure, wall tension, or the presence of abnormal channels in ventricular fibers.
  • Risk Factors: Structural heart disease and post-myocardial infarction.
  • Presentation: Syncope and death if not treated immediately.
  • EKG Findings: Polymorphic fibrillatory waves.
  • Management: Unsynchronized cardioversion followed by amiodarone.

Torsades De Pointes

  • Mechanism: Usually precipitated by premature ventricular contraction leading to the “R on T phenomenon.”
  • Risk Factors: Congenital long QTc with hypokalemia and hypomagnesemia.
  • Presentation: Syncope and death if not treated immediately.
  • EKG: Polymorphic wide-complex tachycardia with HR > 300 bpm.
  • Management:
    • IV magnesium or Isoproterenol, which increases heart rate and decreases QT-duration
    • Avoid hypokalemia and hypomagnesemia
    • Chronic therapy with beta-blockers in patients with long QT syndrome


Bradyarrhythmia is defined as a heart rate below 60 beats per minute (bpm) and comprises several rhythm disorders, including atrioventricular (A-V) blocks and sinus node disorders.

Sinus Bradycardia

  • Mechanism: Increased vagal tone. It can be physiological in athletes.
  • Signs & Symptoms: Usually asymptomatic. It can lead to orthostasis or dizziness if pathological.
  • EKG Findings: Sinus rhythm with an upright P wave in lead II and biphasic in V1.
  • Management: No treatment is required unless pathological with an inadequate heart rate increase with leg raise test. Treat with isoproterenol or pacemaker if no relief. 

Atrioventricular Blocks

Atrial impulses are conducted with a delay or not at all when an electrical impulse reaches a tissue that not excitable or is in a refractory period.
  • First Degree AV Block: Caused by increased vagal tone or conduction impairment or due to medications.
    • Presentation: Generally asymptomatic but can cause dizziness.
    • EKG: PR interval is greater than 200 milliseconds.
    • Management: Usually, no need to treat.
  • Second Degree AV Block
    • Subtypes:
      • Mobitz I block: Progressive prolongation of the PR interval followed by a skipped beat
      • Mobitz II block: Randomly dropped QRS complex with fixed PR interval
    • Presentation: Can be asymptomatic, dizziness, palpitations, weakness, syncope.
    • EKG: 
      • Mobitz type I: Progressive prolongation of PR interval followed by dropped QRS complex or dropped beat
      • Mobitz type II: Randomly dropped QRS complexes
    • Management: Pacemaker (indicated in symptomatic Mobitz I and all of Mobitz II heart block)
  • Third Degree (complete) AV Block:
    • Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions.
    • Presentation: Profound bradycardia, hypotension, and can lead to asystole and cardiac arrest.
    • EKG: Bradycardia, P waves occur independently of QRS and Wide QRS for ventricular rhythm.
    • Management: Pacemaker placement.

Sinus Node Dysfunction

  • Mechanism: Senescence of the SA node, an ischemic event involving the SA node leading to impulse generation at a slower rate.
  • Sinus Pause: When the SA node has delayed impulse generation.
  • Sinus Arrest: Failure of impulse generation.
  • SA Nodal Exit Block: Failure of impulse transmission.
  • Presentataion: Bradycardia, dizziness, palpitation, or syncope.
  • EKG: P-wave not originating at a determined rate with regularity
  • Management: Symptomatic patients require pacemaker placement

Inherited cardiac arrhythmias

Rare diseases are often the underlying cause of sudden cardiac death in young individuals and result from mutations in several genes encoding ion channels or proteins involved in their regulation.

  • Long QT syndrome
  • Short QT syndrome
  • Catecholaminergic polymorphic ventricular tachycardia
  • Brugada syndrome

J Wave Syndromes:

Conditions with a common arrhythmic platform related to amplification of Ito-mediated J waves, and ECG characteristics, clinical outcomes and risk factors
  • Brugada syndrome (BrS): Rare hereditary syndrome marked by right bundle branch block (RBBB), ST-segment elevation in right precordial leads of the ECG, and a high risk of sudden cardiac death from ventricular arrhythmias.
  • Early repolarization syndrome (ERS): Presence of J-point elevation ≥ 1 mm in ≥ 2 contiguous inferior and/or lateral leads of a standard 12-lead ECG in a patient resuscitated from otherwise unexplained ventricular fibrillation/ polymorphic ventricular tachycardia.

Long QT Syndrome (LQTS):

Congenital disorder characterized by a prolongation of the QT interval on electrocardiograms (ECGs) and a propensity to ventricular tachyarrhythmias, which may lead to syncope, cardiac arrest, or sudden death

Short QT Syndrome (SQTS):

Inherited cardiac channelopathy characterised by an abnormally short QT interval and increased risk for atrial and ventricular arrhythmias.

Other causes

Hypertrophic Obstructive Cardiomyopathy

  • Mechanism: Subaortic outflow tract obstruction from abnormal hypertrophy of the septal region of the heart, leading to precipitation of ventricular arrhythmias.
  • Risk Factor: Autosomal dominant mutation in the gene coding for cardiac sarcomere(Beta myosin heavy chain). Suspect this in a patient with a family history of sudden cardiac death in 2 first-degree relatives.
  • Presentation: Syncope with exertion, palpitation, develops early heart failure symptoms. 
  • Management:
    • Beta-blockers: Mainstay of therapy
    • Surgery: Indicated for obstructive physiology with an outflow gradient greater than 50 mmHg
    • Defibrillator: Indicated for symptomatic post maximal medical therapy, abnormal systolic blood pressure response to exercise, septal thickness > 30 mm, runs of ventricular tachycardia, or ventricular fibrillation on telemetry or during the stress test


Implantable cardioverter defibrillator (ICD):

Stimulate the heart as a pacemaker to treat bradycardia (and heart failure), or terminate ventricular tachyarrhythmias with either shocks or special pacing techniques
  • Indications for ICD placements to prevent sudden cardiac death with arrhythmia:
    • CHF with EF < 35% after three months of maximal medical therapy.
    • Myocardial infarction (MI) with EF < 40% with inducible VT or VF in electrophysiological studies.
    • MI with EF < 30%
    • Patients with long QT if QTc > 500 and an episode of unexplained syncope or Holter showing NSVTs

Leave a Reply