The Unsteady Beat: A Guide to Common Cardiac Arrhythmias
A firm grasp of cardiac arrhythmias is fundamental for any Malaysian house officer or medical student navigating the wards. These disturbances of the heart's electrical rhythm range from benign palpitations to life-threatening emergencies. This guide provides a practical, high-yield overview of the definition, pathophysiology, and, most importantly, the clinical management of common arrhythmias, grounding recommendations in the Malaysian context where possible.
Atrial Fibrillation (AF)
Definition
Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation, leading to an ineffective atrial contraction and an irregularly irregular ventricular response (1).
Epidemiology
The prevalence of AF is rising globally, posing a significant public health issue. In Malaysia, community-based studies have reported a prevalence of around 0.54% (2). One study in a hypertensive population in Sarawak found a prevalence of 0.75%, while another study of acute medical admissions to a single centre reported a rate of 2.8% (3). The risk of developing AF increases significantly with age and is strongly associated with conditions like hypertension, heart failure, coronary artery disease, and diabetes mellitus (1). [While these figures provide some insight, comprehensive, nationwide prevalence data for all ethnic groups in Malaysia remains limited; this should be interpreted with caution].
Pathophysiology
AF is driven by chaotic electrical impulses originating from multiple ectopic foci, most commonly within the myocardial sleeves of the pulmonary veins (4). This electrical anarchy, often at rates of 300-600 per minute, prevents organised atrial contraction. The atrioventricular (AV) node, acting as a filter, allows only a fraction of these impulses to reach the ventricles, resulting in the characteristic "irregularly irregular" pulse (4, 5). The underlying substrate often involves atrial remodelling—fibrosis and dilation—caused by chronic conditions like hypertension or heart failure (4).
Clinical Presentation
Presentation is highly variable. Some patients are asymptomatic, while others report debilitating symptoms.
Common Symptoms (>50%): Palpitations (a sense of a rapid, fluttering, or chaotic heartbeat), fatigue, and dyspnea are the most frequent complaints (1).
Less Common Symptoms (10-50%): Dizziness, reduced exercise tolerance, and chest discomfort can also occur (1).
⚠️ Red Flag Signs & Symptoms: Any new focal neurological deficit (suggesting stroke), signs of acute heart failure (e.g., severe dyspnea, orthopnea, peripheral edema), hypotension, or syncope require immediate escalation and management.
Complications
Thromboembolic: The most feared complication is ischemic stroke. Blood stasis in the non-contracting left atrial appendage promotes thrombus formation, which can embolize to the brain. AF increases stroke risk by three to five times (1, 6).
Cardiovascular: Tachycardia-induced cardiomyopathy (a decline in ventricular function due to persistently high heart rates) and exacerbation of underlying heart failure (1).
Prognosis
The prognosis of AF is closely tied to the underlying cardiac and comorbid conditions and the adequacy of stroke prevention. Effective anticoagulation significantly reduces the risk of mortality and morbidity from stroke (1, 6).
Differential Diagnosis
Atrial Flutter with Variable Block: This can present with an irregular rhythm mimicking AF. However, a careful look at the ECG, particularly the inferior leads (II, III, aVF), may reveal the classic "sawtooth" flutter waves, distinguishing it from the chaotic baseline of AF (5).
Multifocal Atrial Tachycardia (MAT): This is an irregular tachycardia characterized by at least three different P-wave morphologies, a variable PR interval, and an atrial rate over 100 bpm. It is often seen in patients with severe pulmonary disease. Unlike AF, discernible P waves are present before each QRS complex (7).
Investigations
Immediate & Bedside Tests
12-Lead ECG: This is mandatory for diagnosis. An ECG confirms the absence of discernible P waves, a chaotic baseline, and an irregularly irregular R-R interval (the action), which are the hallmark features needed to definitively identify AF (the rationale) (1).
Diagnostic Workup
Full Blood Count: Essential to identify anemia, which can exacerbate symptoms, or thrombocytopenia, which impacts anticoagulation choices (the rationale), ensuring baseline parameters are known before starting treatment (the action).
Renal Profile & Electrolytes: Crucial for guiding the choice and dosage of anticoagulants (especially Direct Oral Anticoagulants - DOACs) and rate-control agents (the rationale), as renal impairment is a key factor in drug safety and efficacy (the action) (6).
Thyroid Function Tests: Necessary to rule out hyperthyroidism, a common and reversible cause of AF (the rationale), allowing for targeted treatment of the underlying trigger (the action).
Echocardiogram: A fundamental investigation to assess for structural heart disease, valvular pathology, left ventricular function, and left atrial size (the rationale), which helps in long-term risk stratification and choosing between rate and rhythm control strategies (the action) (1).
Monitoring & Staging
Holter Monitoring: Useful in patients with suspected paroxysmal AF where a standard ECG is normal, this 24-48 hour recording can capture intermittent episodes (the action) to confirm the diagnosis and assess the patient's arrhythmia burden (the rationale) (8).
Management
The management of AF is centred on three key pillars: rate control, rhythm control, and anticoagulation to prevent stroke (1, 6).
Management Principles: The goals are to control symptoms, improve quality of life, and, most critically, prevent thromboembolic complications. An early decision on a rate versus rhythm control strategy should be made, often in consultation with a senior.
Acute Stabilisation (The First Hour)
Airway/Breathing: "Administer high-flow oxygen via a non-rebreather mask if the patient is hypoxic (SpO2 <94%) (the action) to prevent tissue hypoxia exacerbated by the rapid heart rate (the rationale)."
Circulation: "Secure IV access. For hemodynamically unstable patients (hypotension, signs of shock, acute heart failure), immediate synchronised DC cardioversion is indicated (the action) as it is the fastest way to restore sinus rhythm and improve cardiac output (the rationale) (9). Sedation should be provided if the patient is conscious and time permits."
For stable patients, the immediate goal is ventricular rate control.
Definitive Therapy
1. Anticoagulation (Stroke Prevention):
This is arguably the most critical long-term intervention. The decision is based on stroke risk, not the AF pattern (paroxysmal vs. permanent).
Risk Stratification: Use the CHA₂DS₂-VASc score to estimate stroke risk. Anticoagulation is recommended for men with a score of ≥2 and women with a score of ≥3 (10, 11). Consider it for men with a score of 1. Use the HAS-BLED score to identify and mitigate bleeding risks, not to withhold anticoagulation (1, 11).
First-Line Agent: Direct Oral Anticoagulants (DOACs) such as Apixaban, Dabigatran, or Rivaroxaban are recommended over warfarin for most patients with non-valvular AF (the action), due to their superior safety profile (lower risk of intracranial hemorrhage) and convenience (no routine INR monitoring) (the rationale) (10, 11). Check the latest MOH Drug Formulary (FUKKM) for availability and specific prescribing criteria.
Warfarin: Remains the agent of choice for patients with mechanical heart valves and moderate-to-severe mitral stenosis (11).
2. Rate Control (For Most Patients):
Goal: Lenient rate control (resting heart rate <110 bpm) is a reasonable initial target for asymptomatic patients (9).
First-Line Agents: Beta-blockers (e.g., Metoprolol, Bisoprolol) or non-dihydropyridine calcium channel blockers (e.g., Diltiazem) are the preferred agents (the action), as they effectively slow AV nodal conduction (the rationale) (1, 9).
IV Diltiazem: A common choice in the acute setting is IV Diltiazem 0.25 mg/kg (up to 20mg) over 2 minutes, followed by an infusion if needed.
Second-Line Agent: Digoxin can be considered, especially in patients with heart failure, but it is less effective for controlling heart rate during activity (1). Amiodarone may be used for rate control if other agents fail or are contraindicated (9).
3. Rhythm Control (Select Patients):
Considered for younger patients, those who remain symptomatic despite adequate rate control, or when AF is thought to be the cause of heart failure (10).
Cardioversion: Can be electrical (DC shock) or pharmacological (e.g., Amiodarone). For AF >48 hours or of unknown duration, at least 3 weeks of therapeutic anticoagulation is mandatory before elective cardioversion to prevent stroke (1).
Antiarrhythmic Drugs: Amiodarone is a broad-spectrum agent available in the MOH formulary, but has significant long-term toxicity. Flecainide or Propafenone may be considered in patients without structural heart disease (1). The choice of agent is complex and should be guided by a senior or cardiologist.
Catheter Ablation: An invasive procedure that electrically isolates the pulmonary veins. It is more effective than drugs for maintaining sinus rhythm and is increasingly used earlier in the disease course (10).
Key Nursing & Monitoring Instructions
Continuous cardiac monitoring for acute presentations.
Monitor blood pressure closely, especially after administering IV rate-control agents.
Inform medical staff if heart rate remains >110 bpm, systolic BP drops below 90 mmHg, or the patient develops new symptoms.
For patients on warfarin, ensure INR is monitored as per local protocol.
When to Escalate
Call Your Senior (MO/Specialist) if: The patient is hemodynamically unstable, develops signs of a stroke, does not respond to first-line rate control measures, or if there is any doubt about the diagnosis (e.g., possible pre-excited AF).
Supraventricular Tachycardia (SVT)
Definition
Supraventricular Tachycardia (SVT) is a general term for rapid heart rhythms originating above the ventricles. It typically involves a re-entrant circuit and is characterized by a narrow QRS complex (<120 ms) on the ECG (12). The two most common types are Atrioventricular Nodal Re-entrant Tachycardia (AVNRT) and Atrioventricular Re-entrant Tachycardia (AVRT).
Epidemiology
SVT is a common cause of emergency department visits for palpitations. AVNRT is more common in young adults, with a higher prevalence in women (13). [Specific incidence and prevalence data for SVT in Malaysia are not readily available; global figures suggest an incidence of around 35 per 100,000 person-years (13)].
Pathophysiology
AVNRT: The most common form of SVT, caused by a micro-re-entrant circuit within the AV node itself. This requires the presence of two distinct electrical pathways (a "slow" and a "fast" pathway) (12).
AVRT: This occurs in patients with an accessory pathway (an extra electrical connection between the atria and ventricles), such as in Wolff-Parkinson-White (WPW) syndrome. The re-entrant circuit uses the normal AV node for one limb and the accessory pathway for the other (12).
Clinical Presentation
Diagnostic Clues: The hallmark is its abrupt onset and termination.
Common Symptoms (>50%): Palpitations (often described as a "switch being flipped"), dizziness, and shortness of breath are very common (12, 14).
Less Common Symptoms (10-50%): Lightheadedness, anxiety, and chest discomfort can occur.
⚠️ Red Flag Signs & Symptoms: Syncope, pre-syncope, hypotension, or signs of heart failure indicate hemodynamic instability and require immediate cardioversion.
Differential Diagnosis
Sinus Tachycardia: This is a physiological response to stress, fever, or hypovolemia. Unlike SVT, it has a gradual onset and offset, and the ECG shows normal, upright P waves preceding every QRS complex (15).
Atrial Fibrillation/Flutter: While also supraventricular, AF is typically irregular. Atrial flutter is regular but usually has a characteristic "sawtooth" pattern and the atrial rate is around 300 bpm, often with a 2:1 block resulting in a ventricular rate of ~150 bpm (5).
Investigations
Immediate & Bedside Tests
12-Lead ECG: This is the key diagnostic test. Capturing the arrhythmia shows a regular, narrow-complex tachycardia, typically at a rate of 150-220 bpm (the action), which confirms the diagnosis and helps differentiate it from other tachycardias (the rationale) (12). P-waves are often absent (buried in the QRS) or retrograde (seen after the QRS).
A baseline ECG in sinus rhythm might show features of WPW (short PR interval, delta wave), suggesting AVRT as the mechanism.
Management
Management depends entirely on the patient's hemodynamic stability.
Management Principles: For stable patients, the approach is a stepwise escalation from vagal manoeuvres to pharmacological therapy. For unstable patients, the goal is immediate termination of the arrhythmia with electrical cardioversion.
Acute Stabilisation (The First Hour) - STABLE Patient
Vagal Manoeuvres: "Attempt a modified Valsalva manoeuvre first (patient strains for 15 seconds then is laid flat with legs elevated) (the action), as this is a non-invasive and often effective way to increase vagal tone and block the AV node, terminating the re-entrant circuit (the rationale) (12)."
Pharmacological Therapy (if vagal manoeuvres fail):
First-Line: "Administer Adenosine 6mg as a rapid IV bolus into a large-bore cannula, followed immediately by a 20mL saline flush (the action). Adenosine is a very short-acting AV nodal blocking agent that will terminate the majority of SVTs involving the AV node (the rationale) (12, 16)."
Escalation: If the first dose is ineffective, a second dose of Adenosine 12mg can be given.
Contraindications/Cautions: Adenosine is contraindicated in patients with severe asthma. It causes transient flushing, chest tightness, and a sense of impending doom, which patients should be warned about.
Second-Line (if Adenosine fails or is contraindicated):
"Administer an IV non-dihydropyridine calcium channel blocker like Verapamil (2.5 to 5mg IV over 2 minutes) or Diltiazem, or an IV beta-blocker like Metoprolol (the action). These agents provide a more sustained AV nodal blockade to terminate the rhythm (the rationale) (12)." Avoid Verapamil in patients with wide-complex tachycardia as it can cause hemodynamic collapse if the rhythm is actually VT.
Acute Stabilisation (The First Hour) - UNSTABLE Patient
Synchronised DC Cardioversion: "For any patient with SVT and signs of instability (hypotension, altered mental status, acute heart failure), perform immediate synchronised electrical cardioversion, starting with 50-100 Joules (biphasic) (the action). This is the most effective method to rapidly restore sinus rhythm and prevent further clinical deterioration (the rationale) (12)."
Long-Term Plan & Patient Education
For patients with recurrent or highly symptomatic SVT, long-term options include daily oral beta-blockers or calcium channel blockers.
Catheter ablation is a curative procedure with a high success rate (>95%) for AVNRT and AVRT and is often recommended as a first-line therapy for those who wish to avoid long-term medication (12).
Educate the patient on how to perform the Valsalva manoeuvre at home at the onset of an episode.
When to Escalate
Call Your Senior (MO/Specialist) if: The patient is hemodynamically unstable, the diagnosis is uncertain (especially if the QRS is wide), the patient fails to convert with vagal manoeuvres and adenosine, or if you suspect pre-excited AF (irregular, wide-complex tachycardia in a patient with known WPW).
Ventricular Tachycardia (VT)
Definition
Ventricular Tachycardia (VT) is a life-threatening arrhythmia defined as three or more consecutive beats of ventricular origin at a rate exceeding 100 bpm. It is a wide-complex tachycardia (QRS duration ≥120 ms) (17).
Epidemiology
VT most commonly occurs in patients with underlying structural heart disease, particularly those with a history of myocardial infarction (17). [Specific prevalence data for VT in the Malaysian population is not available, but its incidence is closely linked to the prevalence of coronary artery disease and heart failure].
Pathophysiology
In patients with structural heart disease, the most common mechanism is macro-reentry around an area of scar tissue from a previous heart attack. The scar provides the perfect substrate for a continuous electrical loop within the ventricles (17). In patients without structural heart disease (idiopathic VT), the mechanism is more often enhanced automaticity or triggered activity from a specific focus, often in the ventricular outflow tracts (17).
Clinical Presentation
Diagnostic Clues: The most important clinical rule is: Treat any wide-complex tachycardia in an adult as VT until proven otherwise. Mistaking VT for SVT with aberrancy and giving the wrong drugs (e.g., Verapamil) can be fatal (18).
Symptoms: Can range from palpitations and dizziness in a stable patient to syncope and cardiac arrest in an unstable patient.
⚠️ Red Flag Signs & Symptoms: Pulselessness, hypotension, altered mental status, severe chest pain, or acute heart failure are absolute emergencies.
Differential Diagnosis
SVT with Aberrant Conduction: This is the main differential. It occurs when a supraventricular impulse is conducted down the ventricles in the presence of a bundle branch block, widening the QRS complex. ECG algorithms (e.g., Brugada criteria) can help differentiate, but in an emergency, the safest assumption is VT (18).
Pre-excited Tachycardia: An antidromic AVRT in a patient with WPW can also cause a regular wide-complex tachycardia (12).
Investigations
Immediate & Bedside Tests
12-Lead ECG: This is critical for diagnosis. A wide-complex tachycardia (QRS ≥120 ms) is the key finding. Look for specific features that favour VT such as AV dissociation (P waves and QRS complexes at different rates), capture beats, or fusion beats (the action), as these signs are highly specific for VT (the rationale) (17, 18).
Management
Management is dictated by the presence or absence of a pulse and hemodynamic stability. This follows the ACLS algorithm.
Management Principles: The immediate priorities are to restore a stable rhythm, prevent cardiac arrest, and identify and treat underlying causes.
Acute Stabilisation (The First Hour)
VT WITH A PULSE - UNSTABLE (Hypotension, altered GCS, signs of shock)
Synchronised DC Cardioversion: "Perform immediate synchronised electrical cardioversion with an initial energy of 100 Joules (biphasic) (the action). This is the most effective treatment to terminate the rhythm and restore hemodynamic stability in a deteriorating patient (the rationale) (17, 18)." Provide sedation if possible, but do not delay cardioversion.
VT WITH A PULSE - STABLE
Pharmacological Therapy: "Administer an IV antiarrhythmic agent. IV Amiodarone is a first-line option. A loading dose of 150mg is given over 10 minutes, followed by an infusion (the action) as it is effective for both terminating the rhythm and preventing recurrence (the rationale) (17, 19)." Consult your senior or local cardiology protocol for specific infusion rates.
Synchronised cardioversion should be considered if drug therapy fails or the patient becomes unstable.
VT WITHOUT A PULSE (CARDIAC ARREST)
Immediate Defibrillation: "This is a cardiac arrest situation. Shout for help, start high-quality CPR, and deliver an unsynchronised high-energy shock (defibrillation) as soon as a defibrillator is available (the action). Early CPR and defibrillation are the most critical determinants of survival from VF/pulseless VT (the rationale) (19)."
Follow the ACLS algorithm for drug administration (e.g., Adrenaline 1mg every 3-5 minutes, Amiodarone 300mg IV/IO bolus after the third shock).
Long-Term Plan & Patient Education
Patients who have survived an episode of sustained VT, particularly in the setting of structural heart disease, are at high risk of sudden cardiac death.
An Implantable Cardioverter-Defibrillator (ICD) is the cornerstone of long-term management for secondary prevention of sudden cardiac death (17).
Patients require a full cardiology workup to investigate the underlying cause, often including an echocardiogram, coronary angiogram, and possibly a cardiac MRI.
When to Escalate
Call Your Senior (MO/Specialist) Immediately: For any patient presenting with a wide-complex tachycardia. These patients should be managed in a high-dependency or resuscitation area with continuous monitoring and expert oversight.
References
Ministry of Health Malaysia. (2012). Clinical Practice Guidelines: Management of Atrial Fibrillation. MOH/P/PAK/259.12(GU).
Lim, C. W., et al. (2016). Prevalence of atrial fibrillation in the Malaysian communities. Heart Asia, 8(2), 62–66. https://doi.org/10.1136/heartasia-2016-010775
Wong, Y. S., et al. (2014). Atrial fibrillation in a hypertensive population in Sarawak, Malaysia. The Medical journal of Malaysia, 69(3), 119–123.
Kirchhof, P., Benussi, S., Kotecha, D., et al. (2016). 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. European Heart Journal, 37(38), 2893–2962. https://doi.org/10.1093/eurheartj/ehw210
Life in the Fast Lane (LITFL). (n.d.). Atrial Fibrillation. Retrieved from https://litfl.com/atrial-fibrillation-ecg-library/
Hindricks, G., Potpara, T., Dagres, N., et al. (2021). 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal, 42(5), 373–498. https://doi.org/10.1093/eurheartj/ehaa612
UpToDate. (n.d.). Multifocal atrial tachycardia. Retrieved July 9, 2025.
UpToDate. (n.d.). Ambulatory ECG monitoring. Retrieved July 9, 2025.
Amboss. (n.d.). Atrial Fibrillation. Retrieved July 9, 2025.
Joglar, J. A., Chung, M. K., Armbruster, T. L., et al. (2023). 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Journal of the American College of Cardiology, 83(1), 109-279. https://doi.org/10.1016/j.jacc.2023.08.017
National Institute for Health and Care Excellence (NICE). (2021). Atrial fibrillation: diagnosis and management. (NICE guideline NG196). Retrieved from https://www.nice.org.uk/guidance/ng196
Brugada, J., Katritsis, D. G., Arbelo, E., et al. (2020). 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. European Heart Journal, 41(5), 655–720. https://doi.org/10.1093/eurheartj/ehz467
StatPearls. (2024). Supraventricular Tachycardia. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK441972/
UpToDate. (n.d.). Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation. Retrieved July 9, 2025.
Life in the Fast Lane (LITFL). (n.d.). Sinus Tachycardia. Retrieved from https://litfl.com/sinus-tachycardia-ecg-library/
UpToDate. (n.d.). Treatment of paroxysmal supraventricular tachycardia in adults. Retrieved July 9, 2025.
Zeppenfeld, K., Tfelt-Hansen, J., de Riva, M., et al. (2022). 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. European Heart Journal, 43(40), 3997–4126. https://doi.org/10.1093/eurheartj/ehac262
UpToDate. (n.d.). Wide QRS complex tachycardias: Approach to the diagnosis. Retrieved July 9, 2025.
American Heart Association. (2020). Advanced Cardiovascular Life Support (ACLS) Provider Manual.
