- Normal physiological response to exercise
- Normal physiological response to a decrease in vagal tone (reflex tachycardia)
- Sympathetic stimulation in pathological conditions (fever, pain, hyperthyroidism, hypovolemia, sepsis, anemia, pulmonary embolism, myocardial infarction)
- Exposure to stimulants (nicotine, caffeine, amphetamines), anticholinergic drugs, beta-blocker medication withdrawal, illicit drugs (cocaine)
- Postural orthostasis: fatigue, lightheadedness, exercise intolerance
- Heart rate > 100/min with normal P waves and QRS complexes observed via electrocardiogram (ECG)
- The rate of impulses arising from the sinoatrial node is elevated.
- Sinus tachycardia is typically regular, between 100/min and 180/min.
- Determine underlying cause:
- Volume depletion versus infection versus other medical conditions
- Via CBC, WBC, thyroid-stimulating hormone (TSH), angiography, urine drug test, etc.
- Reverse the underlying cause
- If reversible causes have been excluded, consider beta-blockers, then ivabradine, then catheter ablation.
Paroxysmal Supraventricular Tachycardias (PSVTs)
- Presents in young adulthood
- Prevalence is similar in men and women and increases progressively with age.
- 60% of PSVT cases are due to atrioventricular nodal reentry tachycardia (AVNRT):
- Two different electrical pathways in the atrioventricular (AV) node form a loop that continuously conducts impulses leading to tachycardia.
- The 2 pathways form a “fast” and “slow” pathway:
- Anterograde conduction along the slow pathway
- Retrograde conduction along the fast pathway
- 30% of PSVT cases are due to atrioventricular reciprocating tachycardia (AVRT).
- The re-entry loop is formed by a normal AV node.
- Abnormal presence of an accessory conduction pathway between the atria and the ventricles
- Typified by Wolff-Parkinson-White (WPW) syndrome
- 10% of PSVT cases are due to atrial tachycardia (AT) and sinoatrial nodal reentrant tachycardia (SANRT).
- Syncope or presyncope
- Lightheadedness or dizziness
- Chest pain
- Shortness of breath
- Sudden-onset episodes of heart rate > 100/min caused by re-entry involving the atrium, AV node, or an accessory pathway
- PSVTs are typically regular and between 140 and 250/min with narrow QRS complexes (< 120 ms)
- Evaluate for signs and symptoms of hemodynamic (in)stability
- Assess ECG for the type of narrow QRS complex tachycardia present: regular vs. irregular → P wave identification → atrial rate, P wave morphology, RP relationship, and AV relationship
Treat hemodynamic instability via urgent direct current (DC) cardioversion if present.
AVNRT and AVRT:
- Attempt vagal maneuvers (Valsalva, carotid massage) to slow conduction through the AV node.
- If ineffective, IV adenosine is the first-line pharmacotherapy to terminate the rhythm.
- IV calcium-channel blockers (e.g., verapamil), IV beta-blockers (e.g., propranolol), or digoxin may be used to slow conduction through the AV node in acute or preventative treatment if adenosine is not effective.
- AVRT: Consider IV procainamide or IV amiodarone if persistent.
- Atrial impulses pass to the ventricles through both the AV node and an accessory pathway (bundle of Kent): leads to ventricular pre-excitation
- Accessory pathway is often congenital in origin: failure of resorption of the myocardial syncytium at the annulus fibrosis during development
- Characteristic ECG findings in WPW are observed due to the accessory pathway activating the ventricle slightly before the AV nodal pathway:
- Shortened PR interval (< 0.12 s)
- Slurred QRS upstroke (delta wave)
- Widened QRS (> 120 ms)
- The majority of patients are asymptomatic.
- Patients can develop wide QRS-complex atrial fibrillation with rapid ventricular response (RVR) as part of the AVRT re-entry tachyarrhythmia.
- Accompanying palpitations, lightheadedness or dizziness, syncope or presyncope, chest pain, or sudden cardiac arrest can be present.
- Short PR interval (< 0.12 s) and a delta wave: confirming the diagnosis of the WPW pattern on ECG
- Invasive electrophysiology testing: confirming the diagnosis in rare circumstances (e.g., short effective refractory periods in competitive athletes)
Treatment is indicated in patients with symptomatic tachyarrhythmias to prevent RVR.
- Do not use AV-blocking agents to treat the tachyarrhythmia as slowed conduction through the AV node will worsen conduction through the accessory pathway and can be fatal.
- Drugs for aborting the arrhythmia:
- Catheter ablation of the accessory pathway for long-term control
- Digoxin and calcium channel blockers are dangerous in WPW because they block the normal AV node and force conduction in an abnormal pathway.
Atrial Flutter and Atrial Fibrillation
- Rapid, regular atrial activity at a rate of 180–300/min
- Varying degrees of conduction block at the AV node (due to the refractory period)
- Generally caused by re-entry over a circuit of tissue along the tricuspid valve annulus → depolarizes large amounts of the atria throughout the cycle
- Diffuse atrial polarization leads to its characteristic “sawtooth” pattern on ECG
- Irregular atrial rate so fast that there are no discernable P waves on ECG
- Patients have an “irregularly irregular” ventricular rhythm.
- Generally caused by re-entry in random circuits around the atria caused by abnormal electrical discharges that originate in the pulmonary veins
- Complications: stroke, secondary to thrombus formation in the left atria
Multifocal Atrial Tachycardia (MAT)
- 60% of cases are associated with significant pulmonary disease
- Chronic obstructive pulmonary disease (COPD) > pneumonia, pulmonary embolism, etc.
- Associated cardiac disease (coronary, valvular, hypertensive)
- Can also be associated with hypokalemia, hypomagnesemia, medications (e.g., isoproterenol, aminophylline, theophylline), chronic renal failure
- Multiple atrial origin sites cause different and unique P wave morphology.
- Symptoms predominantly relate to the underlying precipitating illness rather than the arrhythmia.
- Multifocal atria tachycardia can worsen systemic oxygenation in patients with advanced pulmonary disease and exacerbate heart disease.
- Cardiac decompensation: angina, dyspnea, orthopnea
- Atrial rate > 100/min
- Three or more distinct P-wave morphologies on ECG
- Each unique P wave morphology indicates a different atrial origin site.
- P waves return to baseline, separated by isoelectric intervals.
- P-P intervals, P-R duration, and R-R intervals that vary
- Aimed at underlying disease: magnesium and potassium replacement
- Calcium channel blockers (e.g., verapamil) and beta-blockers (e.g., metoprolol) can be used with caution related to the underlying disease (avoid beta-blockers in lung disease)
- Rarely required as episodes are brief and resolve with correction of the underlying abnormality
- Indicated in persistent symptomatic MAT if the patient does not respond to or cannot tolerate pharmacotherapy
The following conditions may be associated with the development of tachyarrhythmias:
- Hyperthyroidism: an excess of thyroid hormones T3 and T4. Can promote the development of tachyarrhythmias, particularly atrial fibrillation.
- Structural heart disease: can be arrhythmogenic; patients should be evaluated with echocardiography. Structural abnormalities may be a consequence of congestive heart failure, myocardial infarction, or valvular heart disease.
- COPD: a spectrum of conditions characterized by irreversible airflow limitation correlated to smoking. The condition is a result of obstructive inflammation of the small airways as well as changes in the lung parenchyma and pulmonary vasculature. Advanced pulmonary disease is associated with the development of multifocal atrial tachycardia.
- Intoxication/ingestion: Numerous pharmacologic and illicit drugs may lead to sinus tachycardia or promote arrhythmias.
- Electrolyte abnormalities: Several abnormalities are associated with the development of ventricular tachyarrhythmias, including hypokalemia and hypomagnesemia.