A Practical Approach to Palpitations in Internal Medicine: Pearls, Pitfalls, and Evidence-Based Strategies

 

A Practical Approach to Palpitations in Internal Medicine: Pearls, Pitfalls, and Evidence-Based Strategies

Dr Neeraj Manikath , claude.ai

Abstract

Palpitations represent one of the most common presenting complaints in internal medicine, accounting for approximately 16% of primary care consultations. While often benign, palpitations may herald life-threatening arrhythmias or underlying structural heart disease. This review provides a systematic, evidence-based approach to evaluating patients with palpitations, highlighting diagnostic pearls, common pitfalls ("oysters"), and practical management strategies for internists and trainees.

Introduction

Palpitations are defined as an unpleasant awareness of the heartbeat, described variably as "fluttering," "pounding," or "skipping." The challenge for internists lies in distinguishing benign from potentially fatal causes while avoiding unnecessary investigations. Approximately 40% of patients with palpitations have cardiac causes, 30% have psychiatric origins, and the remainder have metabolic, pharmacologic, or unknown etiologies.

Initial Assessment: History is King

The Art of Characterization

Pearl #1: The "Tap Test" is invaluable. Ask patients to tap out their palpitation rhythm on the desk. Regular tapping suggests supraventricular tachycardia (SVT) or ventricular tachycardia (VT), while irregular tapping indicates atrial fibrillation (AF) or frequent ectopy. This simple maneuver has demonstrated 87% sensitivity for identifying arrhythmias in prospective studies.

Pearl #2: Abrupt onset and offset ("on-off like a light switch") strongly suggests re-entrant SVT, particularly atrioventricular nodal re-entrant tachycardia (AVNRT) or atrioventricular re-entrant tachycardia (AVRT). Gradual onset suggests sinus tachycardia secondary to anxiety, hyperthyroidism, or pheochromocytoma.

Oyster #1: Don't dismiss "skipped beats." While premature atrial contractions (PACs) and premature ventricular contractions (PVCs) are usually benign, frequent PVCs (>10,000/24 hours) can cause PVC-induced cardiomyopathy, which is reversible with ablation or suppression.

Critical Historical Elements

Duration matters. Palpitations lasting seconds suggest ectopy, while episodes lasting minutes to hours indicate sustained arrhythmias. Document associated symptoms meticulously: syncope or near-syncope suggests hemodynamically significant arrhythmia, chest pain may indicate ischemia, and dyspnea could reflect heart failure or pulmonary embolism.

Pearl #3: Ask about the "vagal maneuver response." Patients with SVT often discover inadvertently that bearing down, drinking cold water, or changing position terminates their palpitations—this is pathognomonic for re-entrant SVT and can guide management.

The medication history is crucial. Common culprits include beta-agonists (albuterol), sympathomimetics (pseudoephedrine), anticholinergics, thyroid hormone excess, and stimulants. Proton pump inhibitors can cause hypomagnesemia-induced arrhythmias—an increasingly recognized phenomenon.

Oyster #2: Remember recreational substances. Cocaine, methamphetamine, and increasingly, synthetic cannabinoids can trigger malignant arrhythmias. Energy drinks containing high caffeine concentrations (up to 500mg per serving) are underappreciated triggers, particularly in adolescents and young adults.

Family History: The Hidden Risk Stratifier

Pearl #4: A three-generation cardiac family history is essential. Specifically inquire about sudden cardiac death before age 50, unexplained drowning (possible long QT syndrome), or recurrent syncope. Conditions like hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and channelopathies (Brugada syndrome, long QT syndrome) have genetic inheritance patterns.

Physical Examination: Often Normal but Occasionally Revealing

The physical examination during palpitations is rarely achievable but can be diagnostic. Between episodes, focus on signs of structural heart disease: irregular rhythm (AF), murmurs (mitral valve prolapse, aortic stenosis), elevated JVP, displaced apex (cardiomyopathy), and evidence of thyrotoxicosis.

Pearl #5: Check for a midsystolic click and late systolic murmur (mitral valve prolapse), which affects 2-3% of the population and is associated with increased PACs, PVCs, and rarely, SVT. The Valsalva maneuver accentuates the click and murmur.

Oyster #3: Always palpate the thyroid and check for tremor and tachycardia. Hyperthyroidism causes palpitations in 89% of cases and may be subtle in elderly patients ("apathetic thyrotoxicosis"). New-onset AF in patients over 60 should prompt thyroid function testing.

Diagnostic Investigations: Strategic and Stepwise

The 12-Lead ECG: More Than Rhythm

While the resting ECG captures arrhythmias in only 2-3% of cases, it provides crucial structural and electrophysiologic information:

  • Pre-excitation (delta waves): Wolff-Parkinson-White syndrome with risk of AF conducting rapidly down the accessory pathway
  • Short PR interval with normal QRS: Possible Lown-Ganong-Levine syndrome
  • Prolonged QTc (>460ms women, >440ms men): Risk of torsades de pointes
  • Epsilon waves (ARVC): Rare but lethal if missed
  • Brugada pattern (coved ST elevation V1-V2): Requires sodium channel blocker challenge if suspected
  • Deep Q waves or T-wave inversions: Suggesting structural disease

Pearl #6: Calculate the QTc manually in patients with palpitations. Automated measurements can be inaccurate. Use Bazett's formula: QTc = QT/√RR interval. Drug-induced long QT is an underdiagnosed cause of polymorphic VT.

Ambulatory Monitoring: Matching Symptoms to Rhythm

The 24-48 hour Holter monitor is ideal for daily symptoms but captures arrhythmias in only 30% of patients with palpitations occurring less than daily.

Event recorders (30-day monitors) have 66% diagnostic yield for weekly symptoms. Patients activate the device during symptoms, storing 30-60 seconds before and after activation.

Pearl #7: Consider implantable loop recorders (ILRs) for infrequent but concerning symptoms, especially if syncope accompanies palpitations. ILRs have 90% diagnostic yield over 3 years and are cost-effective compared to repeated external monitoring.

Mobile cardiac telemetry (MCT) continuously monitors and auto-triggers for arrhythmias, combining Holter and event recorder advantages. A recent meta-analysis showed MCT has 61% diagnostic yield versus 23% for Holter monitors in patients with palpitations.

Oyster #4: Smartphone-based single-lead ECG devices (like KardiaMobile) are excellent patient-initiated tools but have limitations in detecting subtle arrhythmias and should complement rather than replace physician-ordered monitoring when clinical suspicion is high.

Laboratory Investigations

Basic metabolic panel (potassium, magnesium, calcium), CBC (anemia), thyroid function tests, and troponin (if chest pain present) constitute the essential first-tier investigations.

Pearl #8: Check serum magnesium even if the patient is not on diuretics. Intracellular magnesium deficiency can exist despite normal serum levels. Consider RBC magnesium if clinical suspicion is high. Hypomagnesemia predisposes to both atrial and ventricular arrhythmias.

For selected patients: urine metanephrines (pheochromocytoma—classically causes "spells"), cortisol (Cushing's), and toxicology screen.

Echocardiography: Structural Assessment

Transthoracic echocardiography should be performed in patients with:

  • Abnormal cardiovascular examination
  • Abnormal ECG
  • Risk factors for structural heart disease
  • Sustained palpitations with hemodynamic compromise

Oyster #5: Don't over-rely on normal left ventricular systolic function. Look specifically for diastolic dysfunction, left atrial enlargement (substrate for AF), regional wall motion abnormalities, and valvular disease. ARVC may show RV dysfunction with preserved LV function.

Exercise Stress Testing

Pearl #9: Exercise testing is particularly useful for exercise-induced arrhythmias, catecholaminergic polymorphic VT (bidirectional VT with exercise), and unmasking ischemia. It also helps assess chronotropic competence and reproduce symptoms in a controlled setting.

Risk Stratification: Who Needs Urgent Evaluation?

High-risk features requiring urgent cardiology referral:

  • Syncope with palpitations
  • Family history of sudden cardiac death
  • Known structural heart disease
  • Abnormal ECG suggesting arrhythmia substrate
  • Sustained palpitations (>30 seconds documented)
  • Palpitations triggered by exercise
  • Short-coupled PVCs on monitoring (R-on-T phenomenon)

Pearl #10: The "3-3-3 rule" for PVCs: Consider further evaluation if >3000 PVCs per 24 hours, >3 consecutive PVCs, or PVCs comprising >3% of total beats. These thresholds suggest increased risk of PVC-induced cardiomyopathy.

Management Strategies: Tailored to Etiology

Benign Ectopy

For patients with structurally normal hearts and PACs/PVCs:

  • Reassurance is therapeutic—emphasize benignity
  • Reduce triggers: caffeine, alcohol, stress, sleep deprivation
  • Beta-blockers (metoprolol 25-50mg twice daily) if symptomatic
  • Rarely, catheter ablation for highly symptomatic patients with frequent ectopy

Hack #1: Magnesium supplementation (400mg daily) reduces PAC/PVC burden in 50% of patients and is safe, cheap, and worth trying before pharmacologic suppression.

Supraventricular Tachycardia

Hack #2: Teach patients the modified Valsalva maneuver (bearing down for 15 seconds in semi-recumbent position, then lying flat with legs elevated for 15 seconds)—this terminates AVNRT in 43% versus 17% with standard Valsalva.

For recurrent SVT:

  • Acute: Adenosine 6mg IV push (12mg if ineffective)—warn patients of "impending doom" sensation
  • Chronic prevention: Beta-blockers, calcium channel blockers (diltiazem/verapamil)
  • Definitive: Catheter ablation (95% success rate for AVNRT/AVRT)

Atrial Fibrillation

Rate control versus rhythm control depends on symptom burden, comorbidities, and left atrial size. CHA₂DS₂-VASc scoring mandates anticoagulation consideration—remember that "female sex" adds a point only if other risk factors exist.

Pearl #11: Early rhythm control (within one year of AF diagnosis) improves cardiovascular outcomes compared to initial rate control strategy, per the EAST-AFNET 4 trial. Consider this approach in appropriate patients.

Ventricular Arrhythmias

Asymptomatic isolated PVCs in structurally normal hearts require no treatment. Symptomatic PVCs or NSVT warrant beta-blockade. Sustained VT or VF requires ICD consideration and specialist management.

Oyster #6: Outflow tract PVCs (RVOT or LVOT) have characteristic morphologies (LBBB pattern with inferior axis for RVOT) and are generally benign but may respond to ablation if symptomatic despite medical therapy.

Special Populations

Pregnant patients: Palpitations increase due to physiologic increases in heart rate and stroke volume. PACs and occasional PVCs are normal. Beta-blockers (labetalol, metoprolol) are safe; avoid atenolol. Adenosine is safe for acute SVT.

Athletes: Distinguish physiologic adaptations (resting bradycardia, early repolarization) from pathology. Sudden cardiac death risk stratification requires careful evaluation including exercise testing and possibly cardiac MRI.

Elderly patients: Lower threshold for investigation due to higher prevalence of structural disease and AF. Consider amyloidosis in elderly patients with unexplained heart failure and arrhythmias.

Conclusion

Palpitations require a systematic, evidence-based approach balancing diagnostic yield against cost and invasiveness. History remains the cornerstone of evaluation. Risk stratification identifies the minority requiring urgent intervention while reassuring the majority with benign causes. Extended monitoring technologies have revolutionized diagnostic capabilities. The modern internist must integrate clinical acumen with appropriate technology utilization, always remembering that patient education and reassurance are powerful therapeutic tools.

Key Takeaway Pearls

  1. The tap test reveals rhythm patterns
  2. Abrupt on-off suggests re-entrant SVT
  3. Vagal response is pathognomonic for SVT
  4. Three-generation family history identifies inherited arrhythmia syndromes
  5. Manually calculate QTc
  6. ILRs for infrequent concerning symptoms
  7. Check magnesium routinely
  8. Exercise testing unmasks catecholaminergic arrhythmias
  9. Modified Valsalva has superior SVT termination
  10. Early rhythm control benefits new-onset AF
  11. The 3-3-3 PVC rule guides further evaluation

Disclosure: No conflicts of interest.


Selected References:

  1. Raviele A, et al. Management of patients with palpitations: a position paper from the European Heart Rhythm Association. Europace. 2011;13(7):920-934.

  2. Thavendiranathan P, et al. Does this patient with palpitations have a cardiac arrhythmia? JAMA. 2009;302(19):2135-2143.

  3. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl J Med. 1998;338(19):1369-1373.

  4. Weber BE, Kapoor WN. Evaluation and outcomes of patients with palpitations. Am J Med. 1996;100(2):138-148.

  5. Kirchhof P, et al. Early rhythm-control therapy in patients with atrial fibrillation. N Engl J Med. 2020;383(14):1305-1316.

  6. Appelboam A, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015;386(10005):1747-1753.

  7. Barsky AJ. Palpitations, arrhythmias, and awareness of cardiac activity. Ann Intern Med. 2001;134(9 Pt 2):832-837.

  8. Giada F, et al. Recurrent unexplained palpitations (RUP) study comparison of implantable loop recorder versus conventional diagnostic strategy. J Am Coll Cardiol. 2007;49(19):1951-1956.

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