ECG and Heart Rhythm – Basic Interpretation and Common Arrhythmias

Electrocardiogram

The ECG shows the electrophysiological process of the heartbeat. The different waves in the heartbeat are labeled P, Q, R, S, and T.

• P wave: This shows atrial depolarization, meaning the electrical activity that triggers the contraction of the atria (the upper chambers of the heart).
• QRS complex: This represents ventricular depolarization, which triggers the contraction of the ventricles (the lower chambers).
  • The Q wave is the initial downward deflection.
  • The R wave is the next upward deflection.
  • The S wave is the following downward deflection.
• T wave: This indicates ventricular repolarization, the process of the ventricles recovering electrically in preparation for the next contraction.

Each of these waves gives important information about the heart’s rhythm and function.

The PQRST Complex – Basics of the Electrocardiogram (ECG)

The electrocardiogram (ECG) is a graphical representation of the electrical activity of the heart over time. The normal ECG waveform consists of the P wave, PR segment, QRS complex, and T wave, each corresponding to a specific phase of cardiac electrical activation and mechanical function.

P Wave – Atrial Depolarization

The P wave represents atrial depolarization. It begins when the sinoatrial (SA) node generates a spontaneous action potential, which then spreads through the atrial myocardium. This electrical activation causes the atria to contract, contributing to ventricular filling.

PR Segment – AV Nodal Delay

The PR segment reflects the time during which the electrical impulse reaches and passes through the atrioventricular (AV) node, where conduction is temporarily slowed.
This physiological delay is essential because it:

• Allows the atria to complete their contraction
• Permits adequate filling of the ventricles before ventricular contraction begins

QRS Complex – Ventricular Depolarization

The QRS complex represents ventricular depolarization. After leaving the AV node, the impulse travels rapidly through:

• The bundle of His
• The right and left bundle branches
• The Purkinje fiber network

This coordinated electrical activation leads to rapid and synchronous contraction of the ventricles, resulting in ventricular systole and blood ejection into the pulmonary artery and aorta.

T Wave – Ventricular Repolarization

The T wave corresponds to ventricular repolarization, also known as the recovery phase. During this phase:

• Ventricular muscle cells restore their resting membrane potential
• The ventricles relax, allowing diastole to begin

This relaxation prepares the heart for the next cardiac cycle.

Summary

In summary, the PQRST complex reflects the precise sequence of electrical events that underlie effective cardiac contraction and relaxation. Understanding the relationship between ECG waveforms and cardiac physiology is fundamental for interpreting normal and pathological ECG findings.

PM: Rapid and Systematic ECG Interpretation

Purpose

To ensure a structured and safe approach to ECG interpretation, allowing identification of arrhythmias, conduction abnormalities, hypertrophy, and ischemic changes.

Stepwise ECG Interpretation (CHECKLIST)

1. Check

• Confirm patient identity (name, age, sex)
• Paper speed: 25 mm/s
• Calibration: 10 mm/mV
• 1 small box = 40 ms, 0.1 mV

2. Rate

• Regular rhythm: 300 / number of large boxes between R–R
• Irregular rhythm: count QRS complexes over 10 seconds × 6
• Normal heart rate: 60–100 bpm

3. Rhythm

Sinus rhythm if:

• One P wave before every QRS and one QRS after each P
• P wave positive in leads I and II
• Regular rhythm with rate 60–100 bpm

4. Axis

• Normal axis: QRS positive in leads I and II
• Left axis deviation: QRS positive in I, negative in II
• Right axis deviation: QRS negative in I, positive in II

5. Intervals

PR interval

• Normal: 120–200 ms
• Prolonged → AV block
• Short → WPW, ectopic atrial rhythm

QRS duration

• Normal: <120 ms
• Wide QRS → bundle branch block, VT, WPW, paced rhythm

QTc interval

• Men <420 ms, women <440 ms
• >500 ms = high risk of torsades de pointes

6. Hypertrophy

Atrial enlargement

• LAE: broad or biphasic P wave (V1), P >100 ms
• RAE: tall, peaked P wave in lead II (>2.5 mm)

Left ventricular hypertrophy (LVH)

• R in V5 + S in V1 >35 mm
• Common causes: hypertension, aortic stenosis

Right ventricular hypertrophy (RVH)

• R > S in V1, right axis deviation

7. Ischemia / Infarction (brief reminder)

• ST elevation → acute ischemia / STEMI
• ST depression or T-wave inversion → ischemia
• Pathological Q waves → previous myocardial infarction

Key Memory Rule

“Check – Rate – Rhythm – Axis – Intervals – Hypertrophy – Ischemia”

Calculate QT-c Interval

Short QT Interval

• Short QT: < 300–360 ms
• Associated with: ↑ Calcium (hypercalcemia)

Long QTc Interval

• QTc:
  • < ½ of the RR interval, or
  • Men < 420 ms, women < 440 ms
  • There is no completely “safe” cutoff, but
  • > 500 ms = DANGEROUS (high risk of malignant arrhythmias)
• Causes of Long QT (“antis and hypos”):
  • Antibiotics
  • Antipsychotics
  • Antidepressants
  • TCAs (tricyclic antidepressants)
  • Antihistamines
  • Antiarrhythmics
  • Hypokalemia (low K⁺)
  • Hypomagnesemia (low Mg²⁺)
  • Congenital long QT syndrome
  • Myocardial infarction
  • Increased intracranial pressure (ICP)

Common Cardiac Rhythms and Arrhythmias – A Clinical Overview

Normal Sinus Rhythm

ECG features

• Regular rhythm
• P wave before every QRS complex
• Constant PR interval
• Heart rate 60–100 bpm

Clinical relevance

• Normal cardiac rhythm originating from the sinus node.

Sinus Tachycardia

ECG features

• Sinus rhythm
• Heart rate >100 bpm
• Regular rhythm

Common causes

• Pain, fever, hypovolemia, anxiety
• Anemia, hypoxia, sepsis

Clinical relevance

• A physiological response → treat the underlying cause, not the rhythm itself.

Sinus Bradycardia

ECG features

• Sinus rhythm
• Heart rate <60 bpm

Common causes

• Well-trained athletes, sleep
• Medications (β-blockers, digoxin)
• Hypothyroidism, inferior myocardial infarction

Clinical relevance

• Often benign
• Treatment only if symptomatic (e.g. dizziness, syncope).

Premature Atrial Contractions (PACs)

ECG features

• Early atrial beat
• Abnormal P-wave morphology
• Usually narrow QRS
• Incomplete compensatory pause

Clinical relevance

• Common and usually benign
• May trigger atrial fibrillation.

Atrial Flutter

ECG features

• Saw-tooth flutter waves (atrial rate ~300 bpm)
• Regular or regularly irregular ventricular response
• Common 2:1 conduction → ventricular rate ~150 bpm

Clinical relevance

• Increased risk of thromboembolism
• Often requires treatment (rate or rhythm control, anticoagulation).

Atrial Fibrillation

ECG features

• Irregularly irregular rhythm
• No distinct P waves
• Irregular RR intervals

Clinical relevance

• Most common sustained arrhythmia
• Stroke risk → assess with CHA₂DS₂-VASc
• Rate control and anticoagulation are key management strategies.

Atrioventricular (AV) Block

First-Degree AV Block

ECG features

• PR interval >200 ms
• All P waves conducted to QRS

Clinical relevance

• Usually benign
• Common with medications or increased vagal tone.

Second-Degree AV Block Type I (Wenckebach / Mobitz I)

ECG features

• Progressive PR prolongation
• Eventually a dropped QRS complex

Clinical relevance

• Usually benign
• Common in young individuals or inferior myocardial infarction.

Second-Degree AV Block Type II (Mobitz II)

ECG features

• Constant PR interval
• Sudden dropped QRS complexes

Clinical relevance

• More serious
• Risk of progression to complete heart block
• Often an indication for pacemaker implantation.

Third-Degree AV Block (Complete Heart Block)

ECG features

• Complete AV dissociation
• Atrial and ventricular rhythms are independent
• Slow ventricular escape rhythm

Clinical relevance

• Potentially life-threatening
• Usually requires urgent pacemaker therapy.

Practical Tips for Interns and Residents

• Always start with rhythm and heart rate
• Irregularly irregular rhythm → think atrial fibrillation
• Regular tachycardia around 150 bpm → suspect atrial flutter with 2:1 conduction
• Dropped QRS complexes → consider AV block
• Always assess the patient before the ECG (symptoms, blood pressure, consciousness)

ECG Changes in Bundle Branch Blocks and Fascicular Blocks

The cardiac conduction system consists of the AV node, the bundle of His, and the right and left bundle branches. The left bundle branch further divides into an anterior and a posterior fascicle. Disturbances in this system result in characteristic ECG changes known as bundle branch blocks or fascicular blocks.

Right Bundle Branch Block (RBBB)

In right bundle branch block, conduction to the right ventricle is delayed, resulting in sequential ventricular activation where the left ventricle is depolarized first.

ECG findings:

• QRS duration ≥ 120 ms
• rsR’, rSR’, or rsr’ pattern in leads V1–V2
• Broad S waves in leads I, V5, and V6
• Usually normal electrical axis
• Secondary ST–T changes in right precordial leads

RBBB may be a benign finding but is also seen in conditions such as pulmonary embolism, ischemic heart disease, and structural heart disease.

Left Bundle Branch Block (LBBB)

In left bundle branch block, conduction through the left bundle is interrupted, significantly altering the depolarization pattern of the left ventricle.

ECG findings:

• QRS duration ≥ 120 ms
• Deep and broad S wave or QS complex in leads V1–V2
• Broad, notched (“clumsy”) positive R waves in leads V5–V6
• Absence of normal septal q waves in lateral leads
• Marked secondary ST–T changes

LBBB is more often associated with underlying heart disease, such as hypertension, cardiomyopathy, or ischemic heart disease.

Left Anterior Fascicular Block (LAFB)

Blockage of the anterior fascicle causes the posterior fascicle to activate the ventricle first, resulting in marked left axis deviation.

ECG findings:

• Normal QRS duration (< 120 ms)
• Left axis deviation
• qR complex in lead aVL
• rS complexes in leads II, III, and aVF
• qR pattern often seen in leads V5–V6

LAFB is relatively common and may occur in isolation or in combination with other conduction disturbances.

Left Posterior Fascicular Block (LPFB)

This is less common and involves blockage of the posterior fascicle, leading to right axis deviation.

ECG findings:

• Normal QRS duration (< 120 ms)
• Right axis deviation
• rS complexes in leads I and aVL
• qR complexes in leads II, III, and aVF
• A q wave is always present in leads III and aVF

LPFB should raise suspicion of underlying heart disease and is often associated with other pathological findings.

The Cardiac Cycle – Wiggers Diagram Explained

The Wiggers diagram illustrates the relationship between electrical activity, pressure changes, volume changes, valve motion, and heart sounds during one complete cardiac cycle. It integrates mechanical and electrical events of the heart over time, primarily focusing on the left ventricle.

Phases of the Cardiac Cycle

1. Atrial Systole

The cardiac cycle begins with atrial systole, which follows atrial depolarization (P wave on ECG).

• The atria contract, pushing additional blood into the ventricles
• Ventricular volume reaches its maximum, known as end-diastolic volume (EDV)
• A slight increase in ventricular pressure occurs

2. Isovolumetric Contraction

After ventricular depolarization (QRS complex), the ventricles begin to contract.

• AV valves (mitral and tricuspid) close, producing the first heart sound (S1)
• Both AV and semilunar valves are closed
• Ventricular pressure rises rapidly
• Ventricular volume remains constant

This phase is called isovolumetric because contraction occurs without a change in volume.

3. Ventricular Ejection

When ventricular pressure exceeds aortic pressure:

• The aortic valve opens
• Blood is ejected into the aorta
• Ventricular pressure rises to its peak and then begins to fall
• Ventricular volume decreases as blood is expelled

This phase represents systole, during which cardiac output is generated.

4. Isovolumetric Relaxation

Following ventricular repolarization (T wave):

• Ventricular pressure falls rapidly
• The aortic valve closes, producing the second heart sound (S2)
• All valves are closed again
• Ventricular volume remains unchanged at end-systolic volume (ESV)

This brief phase marks the transition from systole to diastole.

5. Ventricular Filling

When ventricular pressure falls below atrial pressure:

• AV valves open
• Blood flows passively into the ventricles

This phase is divided into:

• Rapid filling – quick inflow due to pressure gradient
• Diastasis – slower filling as pressures equalize

The cycle then repeats with the next atrial systole.

Electrical, Mechanical, and Acoustic Correlation

• Electrical events (ECG) precede mechanical contraction
• Mechanical events are reflected in pressure and volume changes
• Heart sounds result from valve closure (S1 and S2), not from blood flow

The diagram highlights that electrical conduction triggers mechanical activity, but they are not perfectly synchronized in time.

Summary

The Wiggers diagram provides a comprehensive visualization of how electrical signals, valve movements, pressure changes, volume shifts, and heart sounds are tightly coordinated during each heartbeat. Understanding this diagram is fundamental for interpreting cardiac physiology, heart sounds, and hemodynamic changes in both normal and pathological states.

Electrocardiographic Patterns Suggestive of Acute Coronary Occlusion (OMI) and Important Differentials

Acute coronary occlusion may present with electrocardiographic findings that do not meet traditional ST-elevation myocardial infarction (STEMI) criteria. Recognition of these Occlusion Myocardial Infarction (OMI) patterns is critical, as delayed diagnosis may result in missed opportunities for urgent reperfusion therapy. In addition, several non-ischemic ECG patterns may mimic acute coronary occlusion and must be distinguished to avoid misdiagnosis.

OMI and STEMI-Equivalent Patterns

Wellens Syndrome (Patterns A and B)
Wellens syndrome reflects critical proximal left anterior descending (LAD) artery stenosis. Pattern A shows biphasic T waves in leads V2–V3, while Pattern B demonstrates deeply inverted, symmetric T waves in the same leads. These findings often occur during pain-free intervals and indicate imminent large anterior myocardial infarction.

Hyperacute T Waves
Hyperacute T waves are broad-based, bulky, and disproportionately tall relative to the QRS complex. They may appear in any lead and often represent the earliest ECG manifestation of acute coronary occlusion, preceding ST elevation.

De Winter T-Wave Pattern
The De Winter pattern is characterized by upsloping ST depression (1–3 mm) at the J point in the precordial leads, accompanied by tall, symmetric T waves. This pattern is a STEMI equivalent, most commonly associated with acute proximal LAD occlusion.

Aslanger Pattern
This pattern includes ST elevation in lead III, ST depression in leads V4–V6 with terminally positive T waves, and greater ST deviation in V1 than in V2. It is associated with inferior myocardial infarction and concurrent multivessel ischemia.

South African Flag Sign
This sign consists of ST elevation in leads I, aVL, and V2 with reciprocal ST depression in lead III. It suggests high lateral or proximal LAD involvement and may be overlooked when relying solely on contiguous lead criteria.

New-Onset Bifascicular Block
The combination of right bundle branch block and left anterior fascicular block in the setting of ischemic symptoms may indicate extensive anterior myocardial infarction due to LAD occlusion.

Posterior OMI
Posterior myocardial infarction typically presents with horizontal ST depression maximal in leads V1–V4, often with tall R waves. These changes represent reciprocal findings of posterior ST elevation and require a high index of suspicion.

Terminal QRS Distortion
Terminal QRS distortion is defined by the absence of both the S wave and the J wave in leads V2–V3 during anterior myocardial infarction. It is a marker of severe ischemia and is not present in benign early repolarization.

Modified Sgarbossa–Smith Criteria
In patients with left bundle branch block or ventricular pacing, acute myocardial infarction can be diagnosed using the modified Sgarbossa criteria, particularly an ST/S ratio ≥25% in discordant leads.

Precordial Swirl Pattern
This pattern describes ST elevation in right precordial leads (V1–V2) with simultaneous ST depression in lateral leads (V5–V6), producing a swirling ST-vector appearance suggestive of acute ischemia.

Northern OMI Pattern
Characterized by ST elevation in aVR and/or aVL with negative T waves, together with widespread ST depression in inferior and lateral leads, this pattern suggests left main coronary artery occlusion or severe proximal multivessel disease.

Important Differential Diagnosis: Brugada Syndrome

Brugada Syndrome is an inherited cardiac channelopathy associated with an increased risk of ventricular arrhythmias and sudden cardiac death. It is not caused by myocardial ischemia but may mimic anterior STEMI or OMI on ECG.

The characteristic ECG findings are seen in the right precordial leads (V1–V3) and include:

• Type 1 (diagnostic): Coved ST elevation ≥2 mm followed by a negative T wave.
• Type 2 and 3: Saddleback-shaped ST elevation with varying degrees of ST elevation.

Brugada ECG patterns are typically static or intermittent, not associated with reciprocal ST depression, and are often unaccompanied by ischemic symptoms or troponin elevation. Fever, sodium channel–blocking drugs, and metabolic disturbances may unmask the pattern.

Correct differentiation between Brugada syndrome and acute coronary occlusion is essential, as management strategies differ fundamentally. Brugada syndrome does not require reperfusion therapy but may necessitate electrophysiological evaluation and implantable cardioverter-defibrillator (ICD) consideration.

Conclusion

A wide range of ECG patterns represent STEMI equivalents and indicate acute coronary occlusion despite the absence of classic ST elevation. Clinicians must also recognize non-ischemic mimics, such as Brugada syndrome, to avoid inappropriate management. Mastery of these ECG patterns is essential for timely diagnosis, appropriate treatment, and improved patient outcomes.

Electrolyte Abnormalities and Their Effects on the Electrocardiogram (ECG)

Electrolyte imbalances significantly affect cardiac electrophysiology and may produce characteristic changes on the electrocardiogram (ECG). Early recognition of these patterns is essential, as severe disturbances can lead to malignant arrhythmias and hemodynamic instability.

Hypokalemia

Low serum potassium levels increase myocardial excitability and delay ventricular repolarization. Typical ECG findings include:

• ST-segment depression
• Flattened or inverted T waves
• Prominent U waves, often best seen in the precordial leads

Severe hypokalemia increases the risk of atrial and ventricular arrhythmias, including ventricular tachycardia.

Hyperkalemia

Elevated serum potassium levels reduce myocardial conduction velocity and impair depolarization. Progressive ECG changes may include:

• Peaked, tall (“tented”) T waves
• ST-segment elevation
• Prolonged PR interval
• Widened QRS complexes, which may progress to sine-wave morphology

Advanced hyperkalemia can result in ventricular fibrillation, asystole, or cardiac arrest.

Hypocalcemia

Low calcium levels primarily affect the duration of ventricular repolarization. The hallmark ECG feature is:

• Prolonged QT interval, mainly due to ST-segment prolongation

In severe cases, hypocalcemia may predispose to ventricular tachyarrhythmias.

Hypercalcemia

Excess calcium shortens ventricular repolarization. Typical ECG findings include:

• Shortened QT interval
• Shortened ST segment
• Occasionally widened or flattened T waves

Marked hypercalcemia may be associated with bradyarrhythmias and heart block.

Hypomagnesemia

Magnesium deficiency often coexists with hypokalemia and contributes to electrical instability. Common ECG changes include:

• ST-segment depression
• T-wave inversion
• Prolonged QT interval

Hypomagnesemia is strongly associated with torsades de pointes and other ventricular arrhythmias.

Hypermagnesemia

Elevated magnesium levels depress atrioventricular conduction and myocardial excitability. ECG manifestations may include:

• Prolonged PR interval
• Widened QRS complexes

Severe hypermagnesemia can lead to advanced heart block and cardiac arrest.

Clinical Significance

Electrolyte-related ECG changes can mimic acute ischemia or other cardiac pathologies. Prompt identification and correction of electrolyte disturbances are critical to prevent life-threatening arrhythmias and to guide appropriate clinical management, particularly in critically ill patients.

Ischemic Regionality on the Electrocardiogram (ECG)

The electrocardiogram (ECG) is a fundamental diagnostic tool in the evaluation of suspected acute coronary syndrome. By analyzing which ECG leads demonstrate ischemic changes (ST elevation, ST depression, or T-wave abnormalities), it is possible to determine the myocardial region affected by ischemia and to infer the most likely culprit coronary artery.

Inferior Wall

Ischemia or infarction of the inferior (diaphragmatic) wall of the heart is reflected in leads II, III, and aVF. This regional pattern is most commonly associated with occlusion of the right coronary artery (RCA), although in some cases it may be caused by a dominant left circumflex artery.

Anterior Wall

Changes in leads V1–V4 indicate ischemia involving the anterior wall of the left ventricle. This territory is primarily supplied by the left anterior descending artery (LAD). Anterior ischemia is often associated with a larger infarct size and a higher risk of complications.

Lateral Wall

Ischemia affecting the lateral wall is seen in leads I, aVL, V5, and V6. This pattern is typically related to involvement of the left circumflex artery (LCX) or diagonal branches of the LAD.

Posterior Wall

Posterior myocardial ischemia or infarction is frequently more difficult to detect on a standard 12-lead ECG. It should be suspected in the presence of ST depression in leads V1–V2, which represents reciprocal changes to posterior ST elevation. The diagnosis can be confirmed by recording posterior leads V7–V9. Posterior infarction is most often caused by occlusion of the RCA or LCX, depending on coronary dominance.

Clinical Significance

Understanding ischemic regionality on the ECG allows for rapid identification of:

• the location of myocardial ischemia or infarction
• the most likely culprit coronary artery
• the risk of associated complications (e.g., atrioventricular block in inferior infarction)

This information is essential for timely clinical decision-making, selection of reperfusion strategy, and risk stratification in patients with suspected or confirmed myocardial infarction.

Antiarrhythmic Drugs – Mechanisms of Action in Relation to the Cardiac Action Potential

Antiarrhythmic drugs are commonly classified according to the Vaughan Williams classification, which groups agents based on their primary effects on ion channels and receptors within the cardiac conduction system. These drugs modify specific phases of the cardiac action potential and are used in the treatment of supraventricular and ventricular arrhythmias.

The Cardiac Myocyte Action Potential

The action potential of a cardiac myocyte is divided into five phases (0–4):

• Phase 0 (Depolarization): Rapid influx of sodium ions (Na⁺)
• Phase 1: Initial rapid repolarization (K⁺/Cl⁻ efflux)
• Phase 2 (Plateau phase): Influx of calcium ions (Ca²⁺)
• Phase 3 (Repolarization): Efflux of potassium ions (K⁺)
• Phase 4 (Resting phase): Stable resting membrane potential, maintained mainly by potassium “rectifier” channels

Different classes of antiarrhythmic drugs exert their effects by modifying one or more of these phases.

Class I – Sodium Channel Blockers

Class I agents inhibit fast sodium channels, thereby reducing the slope of phase 0 and slowing conduction velocity.

Subclasses:

• Class IA (e.g. Procainamide, Quinidine, Disopyramide)
  • Moderate Na⁺ channel blockade
  • Prolong action potential duration and refractory period
• Class IB (e.g. Lidocaine, Mexiletine)
  • Weak Na⁺ channel blockade
  • Shorten action potential duration
  • Preferentially act on ischemic or depolarized tissue
• Class IC (e.g. Flecainide, Propafenone)
  • Strong Na⁺ channel blockade
  • Markedly slow conduction with minimal effect on action potential duration

Class I agents are used in both supraventricular and ventricular arrhythmias but require careful patient selection due to proarrhythmic risk.

Class II – Beta-Adrenergic Blockers

Examples include Metoprolol, Bisoprolol, Propranolol and Esmolol.

These drugs block β-adrenergic receptors, reducing sympathetic stimulation of the heart. Their primary effects are:

• Reduced automaticity (phase 4)
• Slowed AV nodal conduction
• Decreased heart rate

They are commonly used for rate control in atrial fibrillation and other supraventricular tachyarrhythmias.

Class III – Potassium Channel Blockers

Examples include Amiodarone, Dronedarone, Dofetilide, Sotalol, Ibutilide, and Vernakalant.

These agents block potassium efflux during phase 3, resulting in:

• Prolonged repolarization
• Increased action potential duration
• Prolonged refractory period

Class III drugs are effective in both atrial and ventricular arrhythmias but may increase the risk of QT prolongation and torsades de pointes (drug-specific risk).

Class IV – Calcium Channel Blockers

Examples include Verapamil and Diltiazem.

These drugs inhibit L-type calcium channels, particularly in the AV node, leading to:

• Slowed AV nodal conduction
• Reduced heart rate
• Shortened phase 2 activity

They are primarily used in supraventricular tachycardias involving the AV node.

Summary

Antiarrhythmic drugs exert their effects by altering ion fluxes across the cardiac cell membrane, thereby modifying the electrical activity of the heart on a beat-to-beat basis. Understanding which phase of the cardiac action potential is affected is essential for appropriate drug selection and safe management of cardiac arrhythmias.

Table of antiarrhythmic drugs

Clinical Decision Algorithm: Antiarrhythmic Drugs

(Which drug, when, and why)

STEP 1: Is the patient hemodynamically unstable?

(Hypotension, shock, ischemia, pulmonary edema, altered mental status)

✅ YES → Immediate synchronized cardioversion

• Drug therapy is not first-line
• Antiarrhythmics may be used after stabilization to maintain rhythm

❌ NO → Proceed to Step 2

STEP 2: Identify QRS width

🔹 Narrow QRS (<120 ms) → Likely supraventricular

→ Go to Step 3A

🔹 Wide QRS (≥120 ms) → Possible ventricular or SVT with aberrancy

→ Go to Step 3B

STEP 3A: Narrow QRS Tachycardia (SVT)

A) Regular narrow-complex tachycardia

(AVNRT, AVRT)

First-line

• Vagal maneuvers
• Adenosine (acute termination)

If recurrent or prevention needed

• β-blocker (Class II) → slows AV nodal conduction
• Verapamil / Diltiazem (Class IV) → AV nodal block

Why?
AV-node–dependent reentry → treat the AV node

B) Atrial fibrillation / atrial flutter

1️⃣ Rate control (most patients)

• β-blocker (Class II)
• Verapamil / Diltiazem (Class IV)

Why?
Slows AV nodal conduction → controls ventricular rate

2️⃣ Rhythm control (selected patients)

• Amiodarone (Class III)
• Flecainide / Propafenone (Class IC)
  ⚠️ Only if structurally normal heart

Why?
Suppress atrial reentry and prolong refractoriness

STEP 3B: Wide QRS Tachycardia

A) Monomorphic ventricular tachycardia (VT)

First-line

• Amiodarone (Class III)

Alternatives

• Procainamide (Class IA)
• Lidocaine (Class IB) (especially post-MI)

Why?
Ventricular arrhythmias require drugs that:

• slow conduction
• prolong refractoriness
• suppress ectopic ventricular foci

B) Polymorphic VT / Torsades de Pointes

Immediate treatment

• Magnesium sulfate (IV)

Additional measures

• Correct electrolytes (K⁺, Mg²⁺)
• Stop QT-prolonging drugs

Why?
Triggered activity due to prolonged repolarization

STEP 4: Special clinical contexts

🔹 Structural heart disease / heart failure

• Amiodarone (safest antiarrhythmic)
• Avoid Class IC

🔹 Post–myocardial infarction VT

• Lidocaine (Class IB)
• Amiodarone

🔹 High sympathetic tone (stress, ischemia)

• β-blockers (Class II)

🔹 AV nodal–dependent arrhythmias

• Class II or IV

QUICK SUMMARY TABLE (MENTAL MAP)

• AV node problem? → Class II or IV
• Atrial rhythm control? → Class IC or III
• Ventricular arrhythmia? → Class III (± IB/IA)
• Structural heart disease? → Amiodarone
• QT prolongation? → Avoid Class IA & III

ONE-LINE MEMORY RULE

“Node = II & IV, Atria = IC & III, Ventricles = III, Unstable = Shock.”