120. Classification of arrhythmias depending on the location and mechanism of their occurrence 121Differential diagnosis of sinus arrhythmia. 122Extrasystole: types and their impact on cardiac activity. 123Diagnostic criteria for atrial fibrillation (atrial fibrillation) 124Diagnostic criteria for ventricular fibrillation 125Diagnostic criteria for sinoatrial block: mechanisms and ECG signs. 126Diagnostic criteria for AV block: mechanisms and ECG signs. 127Diagnostic criteria for first-degree AV blocks. 128Diagnostic criteria for second-degree AV blocks. Mobits type 1.
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Arrhythmias: Classification, Diagnosis & ECG Criteria (Topics 120–128)
120. Classification of Arrhythmias by Location and Mechanism
By Location of Origin
| Location | Examples |
|---|---|
| Sinoatrial (SA) node | Sinus tachycardia, sinus bradycardia, sinus arrhythmia, SA block, sick sinus syndrome |
| Atria | Atrial extrasystoles, atrial tachycardia, atrial flutter, atrial fibrillation |
| AV junction | Junctional (nodal) extrasystoles, AV nodal re-entry tachycardia (AVNRT), junctional rhythm |
| Ventricles | Ventricular extrasystoles, ventricular tachycardia (VT), ventricular flutter, ventricular fibrillation (VF) |
| Conduction system | Bundle branch blocks, SA block, AV block (I–III degree) |
By Mechanism
| Mechanism | Description | Examples |
|---|---|---|
| Enhanced/abnormal automaticity | Increased spontaneous depolarization of ectopic foci | Ectopic atrial tachycardia, accelerated idioventricular rhythm |
| Triggered activity | Early (EAD) or delayed (DAD) afterdepolarizations | Torsades de pointes, digitalis-induced arrhythmias |
| Re-entry | Electrical impulse re-enters and cycles through a circuit | AF, atrial flutter, AVNRT, VT in scar tissue |
| Conduction disturbances | Block or delay in impulse propagation | SA block, AV block |
By Rate
- Tachyarrhythmias (HR > 100 bpm)
- Bradyarrhythmias (HR < 60 bpm)
- Normosystolic arrhythmias (irregular rhythm at normal rate)
121. Differential Diagnosis of Sinus Arrhythmia
Sinus arrhythmia is a normal variant characterized by cyclic variation in the heart rate driven by the sinoatrial node — the rhythm is irregular but every complex is of sinus origin.
Types
| Type | Mechanism | Feature |
|---|---|---|
| Respiratory (phasic) | Vagal tone fluctuates with the respiratory cycle | HR increases on inspiration, decreases on expiration |
| Non-respiratory | Unrelated to breathing (vagal tone, digoxin effect) | Irregular, independent of respiratory phase |
| Ventriculophasic | Seen in complete AV block; PP intervals containing a QRS are shorter | Associated with 3rd-degree AV block |
ECG Criteria for Sinus Arrhythmia
- P wave present before each QRS, normal morphology (positive in I, II, aVF)
- PR interval constant
- PP interval variation > 0.12 s (120 ms) or > 10% of the longest PP interval
- Rate variation tied to respiration (respiratory type)
Differential Diagnosis
| Condition | Key Distinguishing Feature |
|---|---|
| Sinus arrhythmia | P waves all identical, PR constant, variation with breathing |
| Wandering atrial pacemaker | P wave morphology changes (≥ 3 different P-wave shapes), PR varies |
| Atrial extrasystoles | Premature P wave with different morphology, compensatory pause |
| SA block (Type II) | Sudden missing P-QRS complex (pause = 2× PP interval) |
| Sick sinus syndrome | Prolonged pauses, alternating tachy/brady, not respiratory |
| 2nd-degree AV block | P waves present but some not conducted; PR changes (Wenckebach) |
122. Extrasystole: Types and Their Impact on Cardiac Activity
Extrasystole (premature beat) = an impulse arising prematurely from an ectopic focus outside the SA node.
Classification by Location
| Type | Origin | ECG Features |
|---|---|---|
| Sinoatrial (SA) | SA node discharges early | Normal P-QRS-T; difficult to distinguish from sinus arrhythmia; incomplete compensatory pause |
| Atrial | Atrial ectopic focus | Premature, abnormal P wave (P'); normal (narrow) QRS; incomplete compensatory pause |
| AV junctional | AV node / His bundle | Retrograde P' (negative in II, III, aVF) before, during, or after QRS; narrow QRS |
| Ventricular | Ventricular myocardium / Purkinje | Wide (≥ 0.12 s), bizarre QRS; no preceding P wave; ST-T in opposite direction; full compensatory pause |
Classification by Frequency / Pattern
| Pattern | Definition |
|---|---|
| Bigeminy | Every other beat is an extrasystole |
| Trigeminy | Every 3rd beat is an extrasystole |
| Quadrigeminy | Every 4th beat is an extrasystole |
| Couplet | Two consecutive extrasystoles |
| Salvos / Run | ≥ 3 consecutive extrasystoles (→ short VT if ventricular) |
Classification by Morphology (for VES)
- Monomorphic: identical QRS morphology → single focus
- Polymorphic: different QRS morphologies → multiple foci
Impact on Cardiac Activity
| Impact | Description |
|---|---|
| Hemodynamic | Premature beats occur before adequate filling → reduced stroke volume; post-extrasystolic beat has enhanced contractility (post-extrasystolic potentiation) |
| Compensatory pause | Full (ventricular) or incomplete (atrial/junctional) — allows recovery |
| Risk | "R-on-T" phenomenon (VES falling on T wave) can trigger VF, especially in ischemic myocardium |
| Frequent VES (> 10,000/day or > 10%) can cause tachycardia-induced cardiomyopathy | |
| Interpolated VES (no pause) minimally affect hemodynamics |
123. Diagnostic Criteria for Atrial Fibrillation (AF)
Definition
AF is a supraventricular tachyarrhythmia characterized by chaotic, disorganized atrial electrical activity with no effective atrial contraction.
ECG Diagnostic Criteria
| Feature | Finding |
|---|---|
| P waves | Absent; replaced by fibrillatory (f) waves — irregular, low-amplitude oscillations at 350–600 bpm, best seen in V1 and II |
| RR intervals | Irregularly irregular — the hallmark |
| QRS complex | Usually narrow (< 0.12 s) unless aberrant conduction or pre-existing BBB |
| Ventricular rate | Typically 100–180 bpm (uncontrolled); can be slow if AV block co-exists |
| Baseline | Undulating, no clear isoelectric line between complexes |
Classification (ESC 2020)
- First detected: any first episode regardless of duration
- Paroxysmal: self-terminating, usually < 48 h (up to 7 days)
- Persistent: > 7 days, requires cardioversion
- Long-standing persistent: > 12 months, cardioversion attempted
- Permanent: accepted, no rhythm control pursued
Clinical Significance
- Loss of atrial "kick" → up to 20–30% reduction in CO (critical in heart failure, HCM)
- Thromboembolic risk (LAA thrombus) → stroke; assessed by CHA₂DS₂-VASc score
124. Diagnostic Criteria for Ventricular Fibrillation (VF)
Definition
VF is a life-threatening arrhythmia characterized by completely chaotic, disorganized ventricular depolarization with no effective cardiac output — a cause of sudden cardiac death.
ECG Diagnostic Criteria
| Feature | Finding |
|---|---|
| QRS complexes | Absent — no identifiable QRS, T waves, or P waves |
| Baseline | Chaotic, irregular, undulating waves of varying amplitude and frequency |
| Amplitude | Coarse VF: high-amplitude waves (> 0.5 mV) — earlier phase, more likely to respond to defibrillation |
| Fine VF: low-amplitude waves (< 0.5 mV) — later phase, worse prognosis | |
| Rate | Apparent oscillations at 150–500 "per minute" (not true complexes) |
| Rhythm | Completely disorganized |
Clinical Context
- No pulse, no CO → immediate CPR + defibrillation required (unsynchronized shock)
- Often preceded by VT ("VT → VF degeneration") or by R-on-T phenomenon
- Causes: acute MI, cardiomyopathy, channelopathies (Long QT, Brugada), electrolyte disturbances, hypothermia
125. Diagnostic Criteria for Sinoatrial (SA) Block: Mechanisms and ECG Signs
Definition
SA block = failure of the SA node impulse to depolarize the atria due to a block at the SA node–atrial junction.
Types and ECG Signs
Type I SA Block (Wenckebach)
- Mechanism: Progressive prolongation of SA conduction time until one impulse is completely blocked
- ECG: Progressive shortening of PP intervals until a PP pause occurs (the pause < 2× preceding PP); P morphology normal; no direct ECG equivalent of the SA node discharge is visible
- Diagnosed by PP interval analysis
Type II SA Block (Mobitz)
- Mechanism: Sudden block of one SA impulse without prior warning
- ECG:
- Sudden absence of one P-QRS-T complex
- Pause = exactly 2× (or multiple: 3×, 4×) the normal PP interval
- No change in PR interval before or after the pause
- Normal P-QRS-T in all other beats
Type III SA Block (Complete)
- Mechanism: No SA impulses conducted → atrial standstill
- ECG: No P waves; escape rhythm from AV junction (narrow QRS) or ventricles (wide QRS)
Key Distinction: SA Block vs. Sinus Pause/Arrest
| Feature | SA Block (Type II) | Sinus Arrest |
|---|---|---|
| Pause duration | Exact multiple of PP (2×, 3×) | NOT a multiple of PP |
| Mechanism | Conduction failure out of SA node | SA node fails to fire |
126. Diagnostic Criteria for AV Block: Mechanisms and ECG Signs
Definition
AV block = delay or failure of impulse conduction from the atria to the ventricles through the AV node or His-Purkinje system.
General Classification
| Degree | Conduction | PR Interval | QRS dropped? |
|---|---|---|---|
| 1st degree | All impulses conducted but delayed | Prolonged (> 0.20 s) | No |
| 2nd degree | Some impulses not conducted | Variable | Yes (intermittent) |
| 3rd degree (complete) | No impulses conducted | AV dissociation | All P waves blocked |
Mechanisms
| Level of Block | Features |
|---|---|
| AV nodal | Narrow QRS escape; generally benign; responds to atropine |
| Infranodal (His/Purkinje) | Wide QRS escape; unstable; does NOT respond to atropine; may need pacemaker |
General ECG Approach
- Identify P waves and measure PR interval
- Check whether every P wave is followed by a QRS
- Measure the relationship between P waves and QRS complexes
- Assess QRS width (narrow = junctional escape; wide = ventricular escape)
127. Diagnostic Criteria for First-Degree AV Block
Definition
Every atrial impulse is conducted to the ventricles but with abnormally prolonged AV conduction time.
ECG Criteria
| Feature | Finding |
|---|---|
| PR interval | > 0.20 s (> 200 ms) in adults; constant in all beats |
| P wave | Present before every QRS; normal morphology |
| QRS complex | Normal (narrow), follows every P wave |
| Rhythm | Regular |
| Dropped beats | None |
Key Points
- Not truly a "block" — all beats are conducted; it is a conduction delay
- PR interval can be very prolonged (up to 0.40–0.60 s in severe cases)
- Usually asymptomatic; no treatment required
- Can progress to higher-degree block in the setting of acute inferior MI (AV nodal ischemia), myocarditis, or drug toxicity (digoxin, beta-blockers, calcium channel blockers)
- Level of block: most often AV node
128. Diagnostic Criteria for Second-Degree AV Block — Mobitz Type I (Wenckebach)
Definition
Progressive prolongation of AV conduction with intermittent non-conduction of a P wave. Block is at the level of the AV node.
ECG Criteria
| Feature | Finding |
|---|---|
| PR interval | Progressively lengthens with each beat |
| RR intervals | Progressively shorten (despite lengthening PR — because each PR increment is smaller) |
| Dropped QRS | One QRS suddenly absent (P wave not conducted) |
| Pause | The pause containing the dropped beat is less than 2× the preceding PP interval |
| First PR after pause | Shortest PR in the cycle; cycle then repeats |
| P waves | All present, regular PP intervals |
| QRS morphology | Usually narrow (block at AV node level) |
Conduction Ratio
- Expressed as atrial:ventricular ratio — e.g., 4:3 (4 P waves, 3 QRS complexes), 3:2, 5:4, etc.
Typical Pattern (e.g., 4:3 block)
PR: short → longer → longest → [no QRS] → short → ...
RR: longer → shorter → shorter → [pause] → longer → ...
Mechanisms
- AV nodal fatigue: decremental conduction in the AV node — each successive impulse finds the node in a more refractory state until one impulse fails entirely, followed by a recovery period
- Causes: increased vagal tone (athletes, inferior MI with AV nodal ischemia via RCA), AV nodal drugs (digoxin, beta-blockers, verapamil), myocarditis, after cardiac surgery
Clinical Significance
| Feature | Mobitz Type I (Wenckebach) | Mobitz Type II |
|---|---|---|
| Level of block | AV node | His bundle / bundle branches |
| QRS | Narrow | Wide (usually) |
| Stability | Generally benign, stable | Unpredictable, may → complete block |
| Atropine response | Yes | No |
| Pacemaker | Usually not needed | Often required |
| Association | Inferior MI, vagotonia | Anterior MI, structural disease |
Summary Mnemonic for Wenckebach:
"Longer, longer, longer, DROP — then you have a Wenckebach block."
Sources: Harrison's Principles of Internal Medicine, 21st ed. (pp. 7089–7100); Braunwald's Heart Disease, 12th ed.; ACC/AHA/HRS 2018 Arrhythmia Guidelines; ESC 2020 AF Guidelines; Marriott's Practical Electrocardiography.
129Diagnostic criteria for second-degree AV blocks. Mobits 2 130Diagnostic criteria for grade II AV blocks. 131Type 3 Diagnostic criteria for third degree AV blocks. 132Differential diagnostics of SA block and AV block. 133 Diagnostic criteria for arrhythmia associated with impaired automaticity 134 Diagnostic criteria for an attack of atrial paroxysmal tachycardia 135 Principles and types of ECG diagnostics of arrhythmias 136Principles of drug therapy of arrhythmias. 137 Use of glycosides in the treatment of arrhythmias: indications and limitations.
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second degree AV block Mobitz type 2 third degree complete AV block ECG criteria differential diagnosis SA block
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AV Blocks, Arrhythmia Diagnostics & Drug Therapy (Topics 129–137)
129. Second-Degree AV Block — Mobitz Type II
Definition
Sudden, unexpected failure of AV conduction without any preceding PR prolongation. The block is located below the AV node — in the His bundle or bundle branches (infranodal).
ECG Criteria
| Feature | Finding |
|---|---|
| PR interval | Constant and fixed in all conducted beats (normal or slightly prolonged) |
| Dropped QRS | Sudden absence of QRS after a P wave — without prior PR lengthening |
| PP intervals | Regular |
| RR intervals | Regular except for the pause containing the dropped beat |
| Pause | = exactly 2× the normal RR interval (the dropped beat doubles the cycle) |
| QRS morphology | Usually wide (≥ 0.12 s) — bundle branch block pattern — because block is infranodal |
| Conduction ratio | 2:1, 3:1, 4:1 (fixed ratios are common) |
Mechanism
- Block at the His bundle or bilateral bundle branches — the conduction tissue is structurally diseased and fails suddenly without the decremental AV nodal fatigue seen in Wenckebach
- Does not respond to atropine (infranodal)
- Prone to progress to complete (3rd-degree) AV block — unpredictable and potentially fatal
Clinical Significance
| Feature | Mobitz Type I | Mobitz Type II |
|---|---|---|
| Location of block | AV node | His/bundle branches |
| QRS | Narrow | Wide (usually) |
| PR before drop | Progressive lengthening | Constant — no warning |
| Stability | Benign, stable | Unstable, may → complete block |
| Response to atropine | Yes | No |
| Pacemaker need | Rarely | Usually required |
| Association | Inferior MI, vagotonia | Anterior MI, fibrosis, Lenegre disease |
130. Diagnostic Criteria for 2:1 AV Block (High-Degree / Advanced Second-Degree)
Note: This topic ("Grade II AV blocks" with 2:1) covers the 2:1 AV block and high-degree (advanced) AV block, which are sometimes listed separately because they are difficult to classify as Mobitz I or II.
2:1 AV Block
Definition: Every other P wave is blocked — 2 P waves for every 1 QRS complex.
ECG Criteria
| Feature | Finding |
|---|---|
| Atrial:ventricular ratio | 2:1 — one P wave conducts, the next does not, alternating |
| PP interval | Regular |
| PR interval | Constant in all conducted beats |
| QRS | May be narrow (AV nodal level) or wide (infranodal level) |
| Cannot determine Mobitz I vs II | Because there is only one conducted beat per cycle — no progressive PR change can be observed |
How to Distinguish Level of Block in 2:1
| Clue | Suggests AV nodal (Mobitz I) | Suggests Infranodal (Mobitz II) |
|---|---|---|
| QRS width | Narrow | Wide (BBB pattern) |
| PR interval | Long (> 0.20 s) | Normal or borderline |
| Response to atropine | Improves (ratio may → 1:1) | No improvement |
| Response to carotid massage | Worsens | May improve (slowing atrial rate) |
| Associated with | Inferior MI, increased vagal tone | Anterior MI, His-Purkinje disease |
High-Degree (Advanced) AV Block
- Definition: ≥ 2 consecutive P waves fail to conduct (e.g., 3:1, 4:1) but the block is not complete (some P waves still conduct)
- Escape rhythms are common
- High risk of hemodynamic compromise and progression to complete block
- Pacemaker indicated
131. Diagnostic Criteria for Third-Degree (Complete) AV Block
Definition
No atrial impulses are conducted to the ventricles. The atria and ventricles beat completely independently — AV dissociation is complete.
ECG Criteria
| Feature | Finding |
|---|---|
| P waves | Present, regular PP intervals; normal sinus P waves |
| QRS complexes | Present, regular RR intervals — but completely independent of P waves |
| PR intervals | No fixed relationship — PR constantly varies; P waves "march through" QRS complexes |
| Atrial rate | Faster than ventricular rate (e.g., atrial 75 bpm, ventricular 40 bpm) |
| Ventricular escape rhythm | Regular, slow |
| AV dissociation | Complete — hallmark finding |
Escape Rhythm Determines Level of Block
| Level of Block | Escape Pacemaker | QRS Width | Rate |
|---|---|---|---|
| AV node / proximal His | AV junction | Narrow (< 0.12 s) | 40–60 bpm |
| Infranodal (His-Purkinje) | Ventricular myocardium | Wide (≥ 0.12 s), bizarre | 20–40 bpm — unreliable |
Causes
- Acute inferior MI (AV nodal ischemia via RCA — often transient, narrow QRS escape)
- Acute anterior MI (widespread infranodal destruction — wide QRS escape, dangerous)
- Degenerative fibrosis (Lenegre/Lev disease)
- Congenital complete AV block (associated with maternal anti-Ro/SSA antibodies)
- Infiltrative disease (sarcoidosis, amyloid), endocarditis, Lyme disease
- Drug toxicity (digoxin, beta-blockers, Ca²⁺-channel blockers)
Clinical Features
- Syncope (Stokes-Adams attacks): sudden LOC due to ventricular asystole at the moment of block
- Signs of low CO: hypotension, heart failure
- Cannon A waves in JVP (atrial contraction against closed tricuspid valve)
- Pacemaker implantation is indicated in symptomatic or wide-complex complete AV block
132. Differential Diagnosis of SA Block vs. AV Block
| Feature | SA Block (Type II) | AV Block (2nd/3rd degree) |
|---|---|---|
| What is blocked | Impulse from SA node → atria | Impulse from atria → ventricles |
| P waves during pause | Absent (entire P-QRS-T dropped) | Present (P waves visible, QRS absent — in 2nd degree) |
| Pause duration | Exact multiple of PP interval (2×, 3×) | In 2nd degree: pause = 2× RR; In 3rd degree: regular PP and RR but independent |
| Escape rhythm | Atrial or junctional (narrow QRS) | Junctional or ventricular (wide QRS in low blocks) |
| PR interval | Normal in remaining beats | Prolonged or variable (depending on degree) |
| Distinguishing clue | No P waves in the pause | P waves present but not always followed by QRS |
Summary Table
| Parameter | SA Block II | Mobitz II AV Block | Complete AV Block |
|---|---|---|---|
| P waves present? | No (pause) | Yes, all beats | Yes, independent |
| QRS dropped? | Yes (full complex absent) | Yes (QRS drops after constant PR) | All P waves dissociated |
| Pause = 2× PP? | Yes | Pause = 2× RR | Not applicable |
| PR interval | Constant (beats present) | Constant before drop | No fixed PR |
| Escape? | Sometimes junctional | Sometimes junctional/ventricular | Always present (slow) |
133. Diagnostic Criteria for Arrhythmias Associated with Impaired Automaticity
Automaticity arrhythmias arise from abnormal spontaneous depolarization (Phase 4 depolarization) of pacemaker or latent pacemaker cells.
A. Arrhythmias from Increased Automaticity
| Arrhythmia | ECG Features | Mechanism |
|---|---|---|
| Sinus tachycardia | Normal P, PR, QRS; rate > 100 bpm; gradual onset/offset | Enhanced SA node automaticity (sympathetic, fever, anemia, hyperthyroidism) |
| Sinus bradycardia | Normal P, PR, QRS; rate < 60 bpm | Reduced SA node automaticity (vagal, hypothyroidism, athletes) |
| Ectopic atrial tachycardia | Abnormal P morphology; rate 100–240 bpm; "warm-up/cool-down" | Abnormal automaticity of atrial focus |
| Accelerated idioventricular rhythm (AIVR) | Wide QRS (0.12–0.14 s), rate 60–100 bpm, regular; no P wave | Enhanced ventricular automaticity (reperfusion arrhythmia) |
| Junctional tachycardia | Retrograde P or absent P; narrow QRS; rate 70–130 bpm | Enhanced AV junctional automaticity (digoxin toxicity, post-cardiac surgery) |
B. Arrhythmias from Decreased Automaticity (Escape Rhythms)
| Arrhythmia | Rate | QRS | Trigger |
|---|---|---|---|
| Junctional (AV nodal) escape | 40–60 bpm | Narrow | SA node failure or AV block |
| Idioventricular escape | 20–40 bpm | Wide (bizarre) | Complete AV block, SA arrest |
| Sinus arrest / SA block | Pause, then escape | Narrow (junctional) | SA node failure |
Key ECG Feature of Automaticity Arrhythmias
- Gradual onset and offset ("warm-up" and "cool-down") — differentiates from re-entry arrhythmias which start and stop abruptly
- Sensitive to autonomic tone (atropine increases rate, vagal maneuvers decrease rate)
- NOT terminated by overdrive pacing (unlike re-entry)
134. Diagnostic Criteria for an Attack of Atrial Paroxysmal Tachycardia
Paroxysmal Supraventricular Tachycardia (PSVT) / Atrial Paroxysmal Tachycardia (APT)
Definition
Sudden-onset, sudden-offset regular narrow-complex tachycardia originating above the bundle of His, lasting seconds to hours.
ECG Diagnostic Criteria
| Feature | Finding |
|---|---|
| Onset | Abrupt — triggered by a premature atrial beat (PAC) |
| Rate | 160–250 bpm (typically 180–220 bpm) |
| Rhythm | Strictly regular RR intervals |
| P waves | Present but often hidden in QRS or just after QRS (retrograde P'); may be negative in II, III, aVF |
| P-P relationship | RP' interval short (< 70 ms in AVNRT); RP' > PR in atypical forms |
| QRS complex | Narrow (< 0.12 s) — unless aberrant conduction or pre-existing BBB |
| ST changes | Possible ST depression (rate-related ischemia) |
| Termination | Abrupt — may terminate spontaneously or with vagal maneuver/adenosine |
Forms of Paroxysmal SVT
| Type | Mechanism | P wave location |
|---|---|---|
| AVNRT (most common, ~60%) | Re-entry within AV node (slow-fast pathway) | P buried in or just after QRS (RP' < 70 ms) |
| AVRT (WPW, ~30%) | Re-entry via accessory pathway | P after QRS, RP' > 70 ms |
| Focal atrial tachycardia (~10%) | Ectopic atrial focus (automaticity/triggered) | P before QRS, abnormal morphology |
Clinical Features of a Paroxysmal Attack
- Sudden onset palpitations, dizziness, presyncope
- Polyuria at termination (ANP release)
- Vagal maneuvers (Valsalva, carotid sinus massage) may terminate AVNRT/AVRT
- Adenosine 6–12 mg IV — drug of choice for acute termination; causes transient AV block, breaks re-entry circuit
135. Principles and Types of ECG Diagnostics of Arrhythmias
Principles of ECG Analysis in Arrhythmias
A systematic approach is mandatory:
- Paper speed and calibration (standard: 25 mm/s, 1 mV = 10 mm)
- Identify P waves: present? morphology? axis? rate?
- Measure PR interval (normal: 0.12–0.20 s)
- Measure QRS duration (normal: < 0.10 s)
- Determine atrial rate (PP interval)
- Determine ventricular rate (RR interval)
- Assess P:QRS relationship (1:1? AV dissociation?)
- Evaluate rhythm regularity (regular, regularly irregular, irregularly irregular)
- Assess QT interval (corrected QTc = QT / √RR)
- Identify ST-T changes
Types of ECG Diagnostics
| Method | Description | Indication |
|---|---|---|
| Standard 12-lead ECG | 10 electrodes, 12 views; resting 10-second strip | Any arrhythmia evaluation |
| Rhythm strip | Single or dual lead (II, V1) continuous recording | Monitoring, arrhythmia characterization |
| Holter monitoring | 24–48–72 h ambulatory ECG | Paroxysmal arrhythmias, correlation with symptoms |
| Event recorder | Patient-activated; records only during symptoms | Infrequent paroxysmal arrhythmias |
| Loop recorder (implantable) | Subcutaneous, up to 3 years of monitoring | Unexplained syncope, cryptogenic stroke |
| Exercise stress test ECG | ECG during graded exercise (Bruce protocol) | Exercise-induced arrhythmias, CPVT |
| Electrophysiology study (EPS) | Intracardiac catheters; maps conduction | Complex arrhythmias, pre-ablation evaluation |
| Signal-averaged ECG | Detects late potentials (ventricular substrate for VT) | Post-MI risk stratification |
| T-wave alternans | Microvolt alternation in T wave amplitude | SCD risk assessment |
Key Measurements
| Interval | Normal Range | Significance |
|---|---|---|
| PR | 0.12–0.20 s | Prolonged → AV block; Short → accessory pathway |
| QRS | < 0.10 s (< 0.12 s) | Wide → BBB, VT, accessory conduction |
| QT (corrected) | ≤ 0.44 s (men), ≤ 0.46 s (women) | Prolonged → Torsades risk |
| PP | Reflects atrial rate | |
| RR | Reflects ventricular rate |
136. Principles of Drug Therapy of Arrhythmias
Vaughan Williams Classification of Antiarrhythmic Drugs
| Class | Mechanism | Examples | Primary Use |
|---|---|---|---|
| Ia | Na⁺ channel block (intermediate kinetics) + ↓ repolarization (↑ QT) | Quinidine, Procainamide, Disopyramide | AF, VT, WPW |
| Ib | Na⁺ channel block (fast kinetics) — shortens AP | Lidocaine, Mexiletine | Ventricular arrhythmias, VT (especially post-MI) |
| Ic | Na⁺ channel block (slow kinetics) — markedly slows conduction | Flecainide, Propafenone | AF (no structural heart disease), PSVT |
| II | Beta-adrenergic blockade — ↓ automaticity, ↓ AV conduction | Metoprolol, Atenolol, Propranolol | SVT, rate control in AF, post-MI VT suppression |
| III | K⁺ channel block — prolongs repolarization (↑ QT, ↑ ERP) | Amiodarone, Sotalol, Dronedarone, Ibutilide | AF/AFL cardioversion and maintenance, VT/VF |
| IV | Ca²⁺ channel block — ↓ AV node conduction | Verapamil, Diltiazem | Rate control in AF/AFL, AVNRT |
| V (other) | Various mechanisms | Digoxin, Adenosine, Magnesium, Atropine | Specific indications |
General Principles of Antiarrhythmic Drug Therapy
- Treat the underlying cause first — electrolyte imbalance (K⁺, Mg²⁺), ischemia, thyroid disease, drugs
- Risk-benefit assessment — all antiarrhythmics are proarrhythmic (can induce new arrhythmias); Class Ic drugs increase mortality in structural heart disease (CAST trial)
- Rate control vs. rhythm control in AF — rate control preferred in older, asymptomatic patients; rhythm control for younger, symptomatic patients (ESC 2020)
- Acute vs. chronic therapy — different agents for termination vs. prevention
- Structural heart disease constrains choice:
- EF < 35%: amiodarone or dofetilide (not Class Ic)
- No structural disease: wide choice (Ic, III, etc.)
- Monitor QT interval with Class Ia, III agents — risk of Torsades de Pointes
- Drug interactions — amiodarone inhibits CYP2D6/3A4; increases digoxin levels, warfarin effect
- Non-pharmacological alternatives: catheter ablation (1st-line for WPW, AVNRT, typical flutter), ICD for VT/VF prevention, pacemaker for bradyarrhythmias
137. Use of Cardiac Glycosides in the Treatment of Arrhythmias: Indications and Limitations
Mechanism of Action
- Inhibit Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → ↑ intracellular Ca²⁺ (via Na⁺/Ca²⁺ exchanger)
- Cardiac effects:
- Positive inotropy (↑ contractility)
- Negative chronotropy (↓ heart rate) — via enhanced vagal tone
- Negative dromotropy (↓ AV node conduction velocity) — key antiarrhythmic effect
- ↑ automaticity of ectopic foci at toxic doses (paradoxical proarrhythmia)
Indications in Arrhythmia Treatment
| Indication | Role |
|---|---|
| Atrial fibrillation (AF) with heart failure (reduced EF) | Rate control — slows ventricular response via AV nodal blockade; preferred when beta-blockers are contraindicated |
| Atrial flutter | Rate control; rarely used alone (partial AV block gives 2:1 ratio) |
| Heart failure with AF | Dual benefit: rate control + positive inotropy (improves symptoms) |
| PSVT (AVNRT) — historically | Now replaced by adenosine and verapamil; sometimes used for chronic prevention |
Limitations and Contraindications
| Limitation | Detail |
|---|---|
| Narrow therapeutic index | Therapeutic: 0.5–2.0 ng/mL; toxic: > 2.0 ng/mL (especially > 2.5 ng/mL) |
| Ineffective at rest | Vagotonic mechanism works poorly during exercise — heart rate control inadequate with exertion (unlike beta-blockers) |
| Toxicity — arrhythmias | Paradoxically proarrhythmic at toxic doses: any arrhythmia possible; classic: PAT with block, junctional tachycardia, bidirectional VT, VF |
| Toxicity — ECG signs | "Reverse tick" (sagging) ST depression; shortened QT; PR prolongation; various arrhythmias |
| Toxicity — systemic | Nausea, vomiting, xanthopsia (yellow-green vision), confusion |
| Renal impairment | Digoxin is renally excreted — dose reduction required; accumulates in CKD |
| Hypokalemia | ↓ K⁺ dramatically increases digoxin toxicity (compete for Na⁺/K⁺-ATPase binding) |
| Hypomagnesemia | Also potentiates toxicity |
| Drug interactions | Amiodarone, verapamil, quinidine increase digoxin levels (↑ toxicity risk) |
| Absolute contraindications | WPW with AF (blocks AV node → forces conduction via accessory pathway → VF), ventricular tachycardia, 2nd/3rd-degree AV block (without pacemaker), hypertrophic obstructive cardiomyopathy |
Digoxin Toxicity Management
- Stop digoxin; correct electrolytes (K⁺, Mg²⁺)
- Digoxin-specific Fab antibody fragments (Digibind/DigiFab) — for severe toxicity or life-threatening arrhythmias
- Avoid electrical cardioversion if possible (may precipitate VF in digoxin toxicity)
- Temporary pacing for severe bradycardia/AV block
Sources: Harrison's Principles of Internal Medicine, 21st ed. (pp. 6970, 7005, 7089); Braunwald's Heart Disease, 12th ed.; ACC/AHA/HRS 2018 Guidelines on Bradycardia and Cardiac Conduction Delay; ESC 2020 Atrial Fibrillation Guidelines; Vaughan Williams EM, 1984 classification; CAST Trial (NEJM 1989).
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