Arrhythmias and ECG interpretation

After this note, you will be able to approach a patient with an arrhythmia, understand its causes, and interpret relevant investigations. Always check drug doses and local protocols against the Kenya MoH guideline and your hospital formulary.

Definition

An arrhythmia (or dysrhythmia) is any deviation from the normal cardiac rhythm, encompassing abnormalities in the rate, regularity, or site of origin of the electrical impulse, or in its conduction through the heart.

Anatomy and physiology you need

The heart's electrical activity originates in the sinoatrial (SA) node, the natural pacemaker, located in the right atrium. The impulse spreads through the atria, causing atrial contraction, and reaches the atrioventricular (AV) node. The AV node delays the impulse, allowing ventricular filling, then transmits it via the Bundle of His, left and right bundle branches, and Purkinje fibers to the ventricular myocardium, causing ventricular contraction. This coordinated sequence ensures efficient blood pumping. Cardiac cells possess automaticity (ability to spontaneously depolarize), excitability (ability to respond to a stimulus), conductivity (ability to transmit an impulse), and contractility (ability to contract). These properties are modulated by the autonomic nervous system: sympathetic stimulation increases heart rate and contractility, while parasympathetic (vagal) stimulation decreases them.

Causes and risk factors

Arrhythmias arise from abnormalities in impulse formation (e.g., enhanced automaticity, triggered activity) or impulse conduction (e.g., re-entry, heart block).

Pathophysiology

Abnormal Impulse Formation

1. Enhanced Automaticity:

SA node firing rate increases (e.g., fever, hyperthyroidism) OR Latent pacemakers (e.g., atrial, junctional, ventricular cells) spontaneously depolarize at a faster rate than the SA node (e.g., ischemia, electrolyte imbalance) $\rightarrow$ Ectopic beats or sustained tachyarrhythmias.

1. Triggered Activity:

Early afterdepolarizations (EADs) $\rightarrow$ Prolonged repolarization (e.g., hypokalemia, antiarrhythmic drugs) $\rightarrow$ Cell depolarizes before full repolarization $\rightarrow$ Torsades de Pointes. Delayed afterdepolarizations (DADs) $\rightarrow$ Intracellular calcium overload (e.g., digoxin toxicity, catecholamine excess) $\rightarrow$ Spontaneous calcium release $\rightarrow$ Cell depolarizes after full repolarization $\rightarrow$ Ventricular tachycardia.

Abnormal Impulse Conduction (Re-entry)

1. Presence of two distinct pathways for impulse conduction (e.g., accessory pathway, myocardial scar tissue, functional differences in refractory periods) $\rightarrow$
2. Unidirectional block in one pathway $\rightarrow$
3. Impulse travels down the unblocked pathway and retrogradely activates the blocked pathway $\rightarrow$
4. Continuous circuit of activation $\rightarrow$ Sustained tachyarrhythmia (e.g., Atrial Fibrillation, Atrial Flutter, AVNRT, AVRT, Ventricular Tachycardia).

Conduction Blocks

1. Damage or dysfunction in the conduction system (e.g., ischemia, fibrosis, inflammation, drug toxicity) $\rightarrow$
2. Delay or complete interruption of impulse propagation (e.g., SA block, AV block, bundle branch block) $\rightarrow$
3. Bradyarrhythmias or asystole.

Clinical features

History

• Nature of palpitations: Onset and termination (abrupt suggests paroxysmal SVT or VT; gradual suggests sinus tachycardia), regularity (regular suggests SVT, atrial flutter, VT; irregularly irregular points to atrial fibrillation), and triggers (caffeine, khat/miraa, alcohol, fever, antiretroviral therapy, anti-tuberculosis therapy, or electrolyte-wasting illnesses like acute diarrhoea).
• Haemodynamic compromise: Presyncope or frank syncope implies severe hypoperfusion from extreme rates (VT, high-grade AV block). Exertional dyspnoea, orthopnoea, and paroxysmal nocturnal dyspnoea indicate acute heart failure secondary to loss of atrial kick and shortened diastolic filling time.
• Ischaemic symptoms: Angina-like chest pain occurs when tachycardia outstrips coronary perfusion capacity.
• Systemic enquiry: Recent pharyngitis or joint pains (rheumatic heart disease), night sweats, weight loss, and chronic cough (tuberculosis, HIV-associated myocarditis), or thyroid symptoms (heat intolerance, tremor in thyrotoxicosis).

Physical examination

• Pulse assessment:
  • Rate: Bradycardia (<60 bpm) seen in sinus node dysfunction, AV nodal blocks, or digoxin toxicity; tachycardia (>100 bpm) in SVT, VT, AF.
  • Rhythm: Regularly irregular (e.g., ventricular bigeminy, second-degree AV block Mobitz type I); irregularly irregular (atrial fibrillation).
  • Pulse deficit: Difference between apical heart rate and radial pulse rate occurs in AF because early, weak contractions fail to generate an arterial pulse wave that transmits peripherally.
• Blood pressure: Hypotension marks uncompensated haemodynamic collapse due to inadequate stroke volume. Pulsus paradoxus may rarely be present if pericarditis/pericardial effusion with tamponade is the underlying trigger.
• Jugular venous pulse (JVP):
  • Cannon 'a' waves: Occur when the right atrium contracts against a closed tricuspid valve; irregular cannon waves indicate complete heart block (AV dissociation); regular cannon waves suggest AV nodal re-entrant tachycardia (AVNRT) or VT with retrograde conduction.
  • Elevated baseline JVP: Reflects right ventricular failure or volume overload complicating the arrhythmia.
• Precordial auscultation: Variable intensity of the first heart sound ($S_1$) points to complete heart block due to changing PR intervals before ventricular contraction. Murmurs may reveal underlying structural lesions (e.g., mid-diastolic murmur of mitral stenosis predisposing to AF).
• Respiratory and systemic signs: Basal fine crackles (pulmonary oedema from acute left ventricular failure); hepatomegaly, ascites, and peripheral pitting oedema (biventricular or right-sided failure). Pallor or fever may identify primary metabolic/infectious triggers.

Differential diagnosis

Investigations

Diagnosis and severity

Diagnostic synthesis

The diagnosis relies on identifying the rhythm on a 12-lead ECG (or telemetry rhythm strip) systematically:

1. Rate: Count cycles (<60 bpm bradycardia, >100 bpm tachycardia).
2. Rhythm: Assess R-R intervals (regular vs irregular).
3. QRS width:
   • Narrow complex (<0.12 s): Originates above the His bundle (sinus tachycardia, atrial fibrillation, atrial flutter, AVNRT, AVRT).
   • Broad complex ($\ge$0.12 s): Ventricular tachycardia until proven otherwise; alternatively, SVT with aberrant conduction or pre-excitation (Wolff-Parkinson-White syndrome).
4. P waves and AV relationship: Present, absent, saw-tooth (flutter), or fibrillatory. Check if P waves precede every QRS (normal conduction) or if P waves and QRS complexes are completely dissociated (third-degree AV block).

Severity classification

• Haemodynamically unstable (Life-threatening):

Characterised by any of the four "adverse features":

1. Shock: Systolic blood pressure <90 mmHg, pallor, cold extremities, diaphoresis.
2. Syncope: Transient loss of consciousness due to acute cerebral hypoperfusion.
3. Heart failure: Acute pulmonary congestion, high JVP, orthopnoea.
4. Myocardial ischaemia: Severe anginal pain, ischaemic ST changes on ECG.

Requires immediate emergency electrical or chemical intervention.

• Haemodynamically stable:

Patient is fully conscious, normotensive, and free of active ischaemic chest pain or acute heart failure. Permits a systematic, step-by-step diagnostic and pharmacological approach.

Management

Immediate Stabilisation

• Assess clinical stability: Look for shock, hypotension, altered mental status, ischemic chest pain, or acute pulmonary oedema.
• Unstable tachyarrhythmias: Provide immediate synchronised DC cardioversion. If pulseless (VT/VF), immediately start CPR and deliver unsynchronised defibrillation.
• Unstable bradyarrhythmias: Administer intravenous atropine. If no response or high-grade AV block (Mobitz II or complete heart block), initiate transcutaneous pacing followed by transvenous temporary pacing.
• Stable narrow-complex regular tachycardia (SVT):
  • Attempt vagal manoeuvres first (Valsalva manoeuvre or carotid sinus massage after excluding bruits).
  • If unsuccessful, administer intravenous adenosine via a rapid large-bore peripheral bolus with an immediate saline flush to transiently block the AV node.
• Stable narrow-complex irregular tachycardia (AF/Aflutter): Rate control is preferred acutely using intravenous beta-blockers (e.g., metoprolol) or non-dihydropyridine calcium channel blockers (e.g., diltiazem, verapamil). Use digoxin if concomitant severe systolic heart failure is present.
• Stable wide-complex regular tachycardia (presumed VT): Use intravenous amiodarone. Avoid AV nodal blockers.

Definitive Treatment and Follow-up

• Atrial fibrillation:
  • Thromboembolism prevention: Stratify risk using the CHA₂DS₂-VASc score. Initiate oral anticoagulation (direct oral anticoagulants or warfarin; target INR 2.0–3.0). In patients with rheumatic mitral stenosis, use warfarin exclusively.
  • Long-term rhythm vs. rate control: Maintain rate control with oral beta-blockers, non-dihydropyridine CCBs, or digoxin. Consider electrical/pharmacological cardioversion or catheter ablation if symptomatic despite rate control.
• Atrioventricular blocks: Symptomatic Mobitz II and third-degree AV blocks require permanent pacemaker implantation.
• Ventricular arrhythmias: Implantable cardioverter-defibrillator (ICD) placement for secondary prevention in structural heart disease; oral amiodarone or beta-blockers as adjuncts.
• Underlying cause correction: Treat severe malaria, manage sepsis, correct hypokalaemia or hypomagnesaemia, discontinue QT-prolonging medicines (e.g., macrolides, fluoroquinolones, haloperidol), and treat underlying TB pericarditis or ischaemia.

Contraindications and Safety

• Adenosine: Contraindicated in asthma and severe reactive airway disease (can precipitate bronchospasm) and pre-excited AF (Wolff-Parkinson-White syndrome).
• Verapamil/Diltiazem: Contraindicated in wide-complex tachycardia of unknown origin (can trigger ventricular fibrillation) and decompensated heart failure with reduced ejection fraction.
• Atropine: Ineffective and potentially harmful in infranodal heart blocks (Mobitz II, complete heart block) or cardiac transplant recipients.

Complications and Prognosis

• Haemodynamic: Cardiogenic shock, acute pulmonary oedema, syncope, sudden cardiac death.
• Thromboembolic: Ischaemic stroke, mesenteric ischaemia, acute limb ischaemia (primarily from AF).
• Tachycardiomyopathy: Left ventricular systolic dysfunction secondary to persistent, poorly controlled tachyarrhythmias.
• Prognosis: Favourable if secondary to reversible metabolic or infective triggers (e.g., severe malaria, electrolyte shifts). Poor in the presence of severe underlying structural heart disease, advanced rheumatic heart disease, or late-stage HIV-associated cardiomyopathy.

High-Yield Exam Points

• The "Stable VT" trap: Never administer verapamil to a patient with an undifferentiated wide-complex tachycardia; if it is ventricular tachycardia, it causes peripheral vasodilation, cardiovascular collapse, and VF.
• Pre-excited AF (WPW + AF): Recognised by an irregularly irregular, wide-complex tachycardia with variable QRS morphology. AV nodal blockers (adenosine, beta-blockers, CCBs, digoxin) are strictly contraindicated because they divert conduction down the accessory pathway, causing VF.
• Bedside physical findings in complete heart block: Examiners look for cannon a waves in the jugular venous pulse (right atrium contracting against a closed tricuspid valve) and variable intensity of the first heart sound ($S_1$).
• Stroke risk in Rheumatic AF: CHA₂DS₂-VASc does not apply to "valvular" AF (moderate-to-severe mitral stenosis or mechanical valves). These patients are universally high risk and require warfarin, not DOACs.
• Electrolytes before cardioversion: Always verify serum potassium and magnesium levels; hypokalaemia makes the myocardium irritable, refractory to cardioversion, and prone to post-procedure VT/VF.

Clinical Case

A 24-year-old female presents with sudden-onset palpitations, lightheadedness, and shortness of breath. She has a history of childhood joint pains and a known heart murmur. Blood pressure is 82/50 mmHg, pulse is 168 beats/min and irregularly irregular. Chest auscultation reveals bilateral basal crackles and a mid-diastolic rumbling murmur at the apex. ECG shows absent P waves, fibrillatory baseline, and irregularly irregular wide and narrow complexes averaging 170 beats/min.

Questions and Model Answers

1. What is the immediate management step for this patient? Immediate synchronised DC cardioversion, because the patient is haemodynamically unstable (hypotensive with acute pulmonary oedema).

2. What long-term medication must be initiated for stroke prevention, and which drug class is contraindicated? Warfarin is indicated for stroke prevention in rheumatic mitral stenosis (target INR 2.0–3.0). Direct oral anticoagulants (DOACs like rivaroxaban or apixaban) are contraindicated in moderate-to-severe rheumatic mitral stenosis.

3. Why did this patient rapidly deteriorate haemodynamically when she went into this rhythm? Rheumatic mitral stenosis causes fixed left ventricular inflow obstruction. The loss of coordinated atrial contraction ("atrial kick") and shortened diastolic filling time from severe tachycardia precipitously drop left ventricular end-diastolic volume, stroke volume, and cardiac output, while left atrial pressures surge backwards into the pulmonary circulation.

Practice Questions

Question 1

A 58-year-old male on treatment for severe pulmonary tuberculosis presents to the emergency department after a syncopal episode. His ECG shows a polymorphic ventricular tachycardia with a twisting axis and a baseline corrected QT interval (QTc) of 560 ms. Which acute intravenous intervention is most appropriate?

A. Synchronised DC cardioversion
B. Intravenous adenosine
C. Intravenous magnesium sulphate
D. Intravenous amiodarone

Answer: C. Intravenous magnesium sulphate
Explanation: The ECG demonstrates Torsades de Pointes secondary to acquired long QT syndrome (frequently worsened by antitubercular or companion antimicrobials). Intravenous magnesium sulphate stabilizes cardiac membranes and terminates the arrhythmia even if serum magnesium levels are normal; amiodarone is contraindicated as it further prolongs the QT interval.

Question 2

A 30-year-old female presents with acute palpitations. Her ECG shows a regular, narrow-complex tachycardia at 190 bpm with no visible P waves. Vagal manoeuvres fail. She has a history of mild asthma. What is the next best pharmacological choice?

A. Intravenous verapamil
B. Intravenous adenosine
C. Intravenous propranolol
D. Intravenous digoxin

Answer: A. Intravenous verapamil
Explanation: Adenosine is the first-line agent for paroxysmal supraventricular tachycardia, but it can induce severe bronchospasm in patients with asthma; a non-dihydropyridine calcium channel blocker like verapamil is the safest, effective alternative for AV nodal blockade.

Question 3

An examiner asks a student why intravenous calcium channel blockers must never be given to a patient with an irregular, wide-complex tachycardia showing delta waves. What is the correct physiological explanation?

A. They trigger extreme coronary vasospasm
B. They block the AV node and accelerate conduction down the accessory pathway
C. They lead to acute hyperkalaemia and asystole
D. They convert atrial flutter into refractory ventricular tachycardia

Answer: B. They block the AV node and accelerate conduction down the accessory pathway
Explanation: In pre-excited AF (Wolff-Parkinson-White syndrome), blocking the AV node with CCBs leaves the accessory pathway unopposed, driving 1:1 conduction of rapid atrial impulses directly to the ventricles and precipitating ventricular fibrillation.

Question 4

A 72-year-old male with symptomatic third-degree atrioventricular block and a ventricular escape rhythm of 32 bpm is awaiting transvenous pacing. He remains hypotensive. Which drug is preferred as a temporising bridge?

A. Intravenous atropine
B. Intravenous isoprenaline
C. Intravenous digoxin
D. Intravenous amiodarone

Answer: B. Intravenous isoprenaline
Explanation: Atropine acts on the vagus nerve at the AV node and is ineffective for infranodal complete heart block; a beta-agonist like isoprenaline (or adrenaline infusion) increases ventricular automaticity and heart rate while pacing is arranged.

Question 5

A 45-year-old male with newly diagnosed non-valvular atrial fibrillation has hypertension and a history of a transient ischaemic attack. Which long-term strategy for stroke risk reduction is indicated?

A. Aspirin monotherapy
B. Dual antiplatelet therapy with aspirin and clopidogrel
C. Oral anticoagulation with a direct oral anticoagulant or warfarin
D. Rate control monotherapy with metoprolol

Answer: C. Oral anticoagulation with a direct oral anticoagulant or warfarin
Explanation: The patient has a high CHA₂DS₂-VASc score (at least 3 points for age, hypertension, and prior TIA); guideline-directed therapy requires full oral anticoagulation, as antiplatelets are ineffective for cardioembolic stroke prevention in atrial fibrillation.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.