Authors: Vivian Nwike, MD (EM Resident, Mizzou); Alexander Hamilton, MD (EM Resident, Mizzou); Jessica Pelletier, DO, MHPE (Assistant Professor of EM/Associate Residency Director, Mizzou – Columbia, MO) // Reviewed by: Sophia Görgens, MD (EM Physician, BIDMC, MA); Cassandra Mackey, MD (Assistant Professor of Emergency Medicine, UMass Chan Medical School); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)
Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.
A 28-year-old female presented to the emergency department (ED) with complaints of palpitations, shortness of breath, and dizziness. The patient reported that she had been experiencing these symptoms for the past 3 hours. She denied any chest pain or syncope. VS were as follows: HR 180 bpm, BP 110/70 mmHg, RR: 22 breaths/min, O2 sat 96% on RA. On physical exam, the patient appeared anxious and tachypneic. Cardiovascular examination revealed a rapid, regular heart rhythm but no murmurs or gallops. Other systemic examinations were normal. Laboratory results, including a complete blood count (CBC), basic metabolic panel (BMP), and a thyroid-stimulating hormone (TSH) were within normal limits. 12-lead ECG revealed:
What is the diagnosis?
Answer: Supraventricular Tachycardia (SVT)
Background
- Tachycardia is generally defined as a heart rate ≥100 bpm and may be a normal physiological response to a systemic process or a manifestation of underlying pathology.1,2
- Tachydysrhythmias range from benign to malignant rhythms. Emergency physicians must be able to accurately diagnose these conditions to deliver appropriate and timely interventions to prevent potential deleterious complications.
- Some forms of tachycardia (such as rapid atrial fibrillation), if untreated, can lead to stroke, heart failure (i.e. tachycardia-induced cardiomyopathy), cardiovascular collapse, and death.3
- Several methods of classification of tachyarrhythmia are helpful to organize and manage tachycardias. These include:
- Sinus versus non-sinus cause
- Narrow versus wide-complex tachycardias
- Regular versus irregular arrhythmias
- Atrial versus junctional versus ventricular arrhythmias1
Etiology
Regular tachycardia has multiple etiologies, including cardiac and non-cardiac pathology.1,4
- Cardiac causes:
- Cardiomyopathy
- Coronary artery disease
- Heart failure
- Ischaemic heart disease
- Myocardial infarction
- Myocarditis
- Pericarditis
- Structural heart problem
- Non-cardiac causes:
- Anxiety
- Dehydration/Hypovolemia
- Drug-induced (e.g., amiodarone, amphetamines, beta-blockers, cocaine, digoxin)
- Electrolyte abnormalities (especially hypo/hyperkalemia, hypo/hypercalcemia, hypo/hypermagnesemia)
- Fever
- Hypoglycemia
- Hypo/hyperthermia
- Hypo/hyperthyroidism
- Sepsis
- Shock
- Stress
- Trauma
Epidemiology
- Sinus tachycardia is the most common tachyarrhythmia, as it is usually a normal physiological response to emotional or physical stimulation.5 The prevalence of inappropriate sinus tachycardia is not well known, and the underlying mechanisms are likely to be multifactorial, but patients are often younger (age 15 to 50 years) and female.2
- The prevalence of SVT is 2.25/1000 persons, with a female predominance of 2:1 across all age groups.6
- The patients are often younger, although the disorder can present at any age.7
- SVT can be the source of significant morbidity, including disabling symptoms and frequent hospital visits.7
- Paroxysmal SVT (PSVT), defined as intermittent SVT (AV node re-entry tachycardia, AV reentrant tachycardia, or atrial tachycardia), has an incidence of 57.8 cases per 100,000 person-years and a prevalence of 1.26 million people in the US.8
- Females are twice as likely to develop PSVT, and the incidence is five times greater in people older than 65 years compared with younger people.9
- Most cases of SVT are due to AV nodal re-entrant tachycardia (60% of cases); the remainder are due to AV reciprocating tachycardia (30%) and atrial tachycardia (10%).10
- The incidence of atrial flutter has been reported as 88 cases per 100,000 person-years; it is more common in men, with increasing age, and in those with heart failure or chronic obstructive pulmonary disease (COPD).6
- The prevalence of ventricular tachyarrhythmia is highly dependent on its type and duration. In patients with a history of previous myocardial infarction (MI), the incidence of sustained monomorphic ventricular tachyarrhythmia depends on the size of the infarction and the overall left ventricular function.11,12
Clinical Presentation
- Regular tachycardia can present with a wide range of symptoms, from asymptomatic to severe.
- The specific symptoms and severity can vary depending on the underlying cause and the individual’s overall health and psychological state at the initiation of 13
- Symptoms include:14
- Anxiety
- Chest pain
- Dyspnea
- Fatigue
- Light-headedness
- Nausea
- Orthopnea
- Palpitations
- Syncope
- Vomiting
- Signs include:14
- Bibasilar crackles
- Decreased level of consciousness/altered mentation
- Evidence of poor perfusion (e.g., hypotension, delayed capillary refill time, decreased urinary output)
- Elevated jugular venous pressure (JVP)
- Tachypnea
- Tachycardia with regular rhythm
Evaluation
- Electrocardiogram (ECG)
- Laboratory testing:14
- Basic metabolic panel (BMP)
- CBC
- Magnesium level
- Phosphorus level
- C-reactive protein (CRP)
- Coagulation profile
- Liver function tests (LFTs)
- TSH (followed by free T4 if abnormal)
- Venous blood gas (VBG) vs. arterial blood gas (ABG) if intubated/critically ill
- If there is shortness of breath, consider CXR, viral testing (i.e. COVID-19, influenza).
- If concerns for infectious etiology/sepsis, blood cultures should be obtained.
- If there are signs and symptoms of volume overload, consider pro-BNP.
- If there are risk factors for pulmonary embolism (PE), D-dimer vs. computed tomography (CT) angiography of the chest.
- +/- bedside ECHO, if there are concerns for congestive heart failure (CHF), MI, PE, or pericardial effusion.
- This can also be used to evaluate volume status and determine whether dehydration or volume overload is an underlying trigger of the tachycardia.
Diagnosis
- Is the patient clinically or hemodynamically unstable?3
- The most important clinical determinant in a patient presenting with a tachyarrhythmia.
- Signs/symptoms of instability include:
- Chest pain suggestive of coronary ischemia
- Altered Mentation
- Hypotension
- Shortness of breath
- A reasonable approach to diagnosing tachyarrhythmias is to obtain a quality ECG and assess the QRS complex duration (<120 milliseconds is narrow, 120 milliseconds is wide) and the rhythm (regular or irregular based on the RR interval). This initial categorization will help narrow the differential diagnosis and guide management.3
- Determining whether a patient’s symptoms are related to the tachycardia depends upon several factors, including age and the presence of underlying cardiac disease.3
- In patients presenting with symptomatic tachyarrhythmias, a 12-lead ECG should be obtained while a brief initial assessment of the patient’s overall clinical condition is performed.3
Differential Diagnosis
- Commonly encountered differential diagnoses in the ED for regular narrow-complex tachycardia include:3
- Sinus tachycardia (Fig. 1) – This occurs due to enhanced automaticity from the SA node. It is the most common tachycardia as it is a normal response to physiologic, pathologic stressors, or sympathomimetics and some drugs.3
- SVT – A heterogeneous group of arrhythmias that describe tachycardias involving cardiac tissue at or above the level of the bundle of His.2
- Atrioventricular (AV) nodal re-entrant tachycardia (AVNRT) (Fig. 2-3) – A re-entrant circuit that develops within an AV node that contains two pathways for impulses to travel through; a “slow” pathway with a short (i.e fast) refractory period (referred to as the “slow-fast” pathway), and a “fast” pathway with a long (i.e slow) refractory period (referred to as the “fast-slow” pathway.3
- AV re-entrant tachycardia (AVRT) (Fig. 4) – A re-entrant tachydysrhythmia with the circuit consisting of the AV node (AVN) (slow conduction and short refractory period) and an accessory pathway bypassing the AVN connecting the atria to the ventricles (with fast conduction and long refractory period).3 It is further classified into:
- Orthodromic AVRT (Fig. 5) – Referring to electrical impulses travelling anterogradely through the AVN toward the ventricles, then retrograde through the AP to the atria. It accounts for 90-95% of SVT occurring in patients with an AP.3
- Antidromic AVRT (Fig. 6) – Electrical impulses traveling in the opposite direction of orthodromic AVRT, where ventricular depolarization begins at the connection site of the AP, resulting in a regular wide complex tachycardia (WCT). It is much less common than orthodromic AVRT and accounts for 5% of SVT in patients with an AP.3
- Atrial flutter with fixed conduction (Fig. 7) – there should be a sawtooth pattern of P waves; these may have differing morphology throughout, and P waves should outnumber QRS complexes.3
- Focal atrial tachycardia (AT) – fast rhythm originating from a single focus in the atria that is NOT the sinus node. There will be discrete P waves, and other than when the tachyarrhythmia is “ramping up” or “ramping down,” it will be very regular.3
- In this ED setting, it is hard to distinguish sinus tachycardia from AT based on the heart rate (AT may be faster).
- Suspect this in patients who have no obvious cause for sinus tachycardia and for whom the heart rate does not slow down with treatment of any reversible underlying causes.
- It is ultimately diagnosed via electrophysiology studies.
- Treatment in the ED setting is the same as for SVT.
- In this ED setting, it is hard to distinguish sinus tachycardia from AT based on the heart rate (AT may be faster).
- The differential diagnosis of regular wide complex tachycardia (WCT) includes three major categories:15
- Ventricular tachycardia (VT) (Fig. 8) – arrhythmia originating from the ventricles and does not require any supraventricular tissues for its maintenance. VT is the most common etiology, accounting for about 80 % of WCT16
- SVT with aberrancy (Fig. 9) – referring to any tachycardic rhythm with a left or right bundle branch block that is NOT ventricular tachycardia.
- Preexcited tachycardia – these are conducted antegradely over an accessory pathway.
Treatment
- The management of tachycardia depends on morphology (wide versus narrow complex), whether or not the person is stable or unstable, and whether the instability is due to the tachycardia.18
- Guidelines on the management of SVTs are available from the American College of Cardiology/American Heart Association (2015),1 the European Heart Rhythm Association (2017),6the European Society of Cardiology Scientific Group (2017),2 and the European Society of Cardiology (2019).19
Initial Management
- Assess the patient using the airway, breathing, circulation, disability, and exposure (ABCDE) approach.
- Identify and treat reversible causes e.g., electrolyte abnormalities, volume overload/depletion, etc.
- As sinus tachycardia is often a response to a physiologic or pathologic process, management should be directed toward correcting the underlying cause.3
- Regular Narrow complex tachycardias (QRS duration <0.12 s) – e.g. SVT3
-
- In hemodynamically unstable patients:
- For patients with adverse features such as shock, heart failure, syncope, myocardial ischemia, arrange for emergency synchronized direct current (DC) cardioversion under conscious sedation, when appropriate. Some patients may not tolerate sedation due to instability.
- The fastest method to break the circuit and restore sinus rhythm is synchronized electrical cardioversion.
- If the initial shock is unsuccessful, repeat two subsequent shocks at increasing increments.
- Starting dose should be 50-100 J; the initial dose should be doubled if this is not successful.
- If still unsuccessful, administer a loading dose of amiodarone 150 mg IV over 10-20 minutes and repeat DC cardioversion followed by amiodarone 900 mg IV over 24 hours.
- For patients with adverse features such as shock, heart failure, syncope, myocardial ischemia, arrange for emergency synchronized direct current (DC) cardioversion under conscious sedation, when appropriate. Some patients may not tolerate sedation due to instability.
- In hemodynamically stable patients:
- Acute management of paroxysmal SVT involves regulating the heart rate and preventing hemodynamic instability.
- The goal of treatment in paroxysmal SVT is to disrupt the re-entrant circuit by altering conduction through the AV node, which is a part of the circuit in both AVNRT and AVRT.
- This can be done with vagal maneuvers (via activating baroreceptors), medications (such as adenosine, calcium channel blocker [CCB], and beta-blockers), or electrical cardioversion. This approach aims to terminate the tachycardia and restore a normal heart rhythm.
- In hemodynamically unstable patients:
- Attempt vagal maneuvers:
-
-
- Vagal maneuvers are first-line treatment in stable patients before advancing to medications. They include Valsalva maneuver, modified Valsalva with straight leg raise, carotid sinusmassage, and the diver reflex via ice to the face. Their benefits include: ease of performance, low cost, association with minimal risk, and they have been found to terminate paroxysmal SVT with success in up to 50% of cases.20
- Carotid massage can slow AV nodal conduction. Massaging the carotid sinus for several seconds on the nondominant cerebral hemisphere side.20
- This maneuver is usually reserved for young patients. Due to the risk of stroke from emboli, auscultate for bruits before attempting this maneuver.
- Bilateral concurrent carotid massage is not recommended.
-
- If this fails, short-term pharmacologic management:
-
-
- Of the medications that alter conduction through the AV node, adenosine, CCB, and beta-blockers are recommended (in that respective order).6,7
- Adenosine 6 mg IV.6
- Warn patients of transient unpleasant side effects: flushing, nausea, chest tightness, ‘feeling of impending doom.’
- Avoid in patients with asthma (due to rare risk of bronchoconstriction) and denervated hearts (as it is unlikely be effective).
- Adenosine should also be avoided in patients with suspected WPW as it can potentiate the pre-excitation and increase the risk of ventricular arrhythmias.
- Often ineffective if the patient has consumed theophylline, dipyridamole, or carbamazepine.
- If 6 mg is unsuccessful, an additional dose of adenosine 12 mg IV can be administered.6,7
- If adenosine is ineffective and there are no concerns for pre-excitation, consider:6
- Beta blockers – contraindicated in patients with bronchospastic conditions such as asthma or chronic obstructive pulmonary disease (COPD), or patients with decompensated CHF.
- Esmolol 0.5 mg/kg bolus or 0.05-0.3 mg/kg/min gtt
- Metoprolol 2.5-15 mg in 2.5 mg boluses
- Calcium channel blockers – not preferred in patients with heart failure with reduced ejection fraction (HFrEF).
- Diltiazem 20 mg over 2 minutes
- Verapamil 5-10 mg over 2 minutes
- Beta blockers – contraindicated in patients with bronchospastic conditions such as asthma or chronic obstructive pulmonary disease (COPD), or patients with decompensated CHF.
- If none of these strategies are effective:6,7
- Synchronized DC shock up to 3 attempts.
- Sedation or anesthesia if the patient is conscious.
- Of the medications that alter conduction through the AV node, adenosine, CCB, and beta-blockers are recommended (in that respective order).6,7
-
- Regular WCTs (QRS duration >0.12 s)
-
- In hemodynamically unstable patients:
- Patients should be promptly cardioverted back into normal rhythm, using synchronized electrical direct current.15
- Hitting the patient on the chest, also called “thump version or precordial thump,” can sometimes terminate a WCT presumably by mechanically inducing a premature ventricular complex that interrupts the reentrant circuit of the tachycardia.15
- In hemodynamically stable patients:
- As mentioned above, from a statistical standpoint, the most likely diagnosis in patients with WCT is VT. Assuming this diagnosis even in the hemodynamically stable patient until proven otherwise is the safest approach to management.
- Any WCT should be treated as VT unless the patient has an old ECG with a clear previous bundle branch block of unchanged morphology.20
- If likely monomorphic VT (or uncertain rhythm):
- Give amiodarone 150 mg IV over 20-30 min followed by amiodarone 900 mg IV over 24 hours.
- Amiodarone can terminate both SVT and VT.
- Amiodarone (class III) is the agent of choice for stable WCT (particularly if the etiology is uncertain).
- It is also particularly useful in patients with poor ejection fraction, such as impaired left ventricular function, heart failure, or structural heart disease, as it has a favorable hemodynamic profile.21
- Procainamide (Class IA) can also be used in the initial treatment of hemodynamically stable WCT.
- Its main disadvantage is that it cannot be administered rapidly secondary to hypotension.
- Lidocaine (Class IB) is useful for VT of ischemic origin.
- It does not terminate SVT, however, and can result in confusion at high doses.
- Amiodarone can terminate both SVT and VT.
- Give amiodarone 150 mg IV over 20-30 min followed by amiodarone 900 mg IV over 24 hours.
- If there are concerns for SVT with aberrancy (i.e. Bundle branch blocks):
- Try adenosine; similar to regular narrow complex tachycardias.
- If ineffective:
- Synchronized DC cardioversion up to 3 attempts (with sedation or anesthesia if the patient is conscious).
- In hemodynamically unstable patients:
Prognosis
- The prognosis for regular tachycardia depends on the underlying cause, type of tachycardia, presence of underlying heart disease, and effectiveness of treatment.1
- While some forms are benign, others can lead to serious morbidity and mortality, such as heart failure, pulmonary edema, myocardial ischemia, myocardial infarction, and sudden cardiac death.
- One study found that 1/3 of patients with SVT experienced syncope or required cardioversion.22
- Repeated episodes or poorly managed chronic SVT can cause tachycardia-induced cardiomyopathy.3
Pearls
- For regular tachycardia, it’s crucial to quickly assess the patient’s hemodynamic status and determine what type it is.
- Stabilizing the patient takes priority over determining the underlying rhythm.
- Unstable? Cardiovert. Potentially VT? Cardiovert.
- Typical SVT can be treated with vagal maneuvers or adenosine.
