Tag: supraventricular tachycardia

Tachyarrhythmias (2024)

~ iEM Education Project Team ~ Leave a comment

by Keith Sai Kit Leung, Rafaqat Hussain & Abraham Ka Cheung Wai 

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You have a new patient!

A 28-year-old female patient presented with 3 weeks history of palpitations. She started with a new-onset shortness of breath and dizziness this morning, which prompted her to attend ED. The patient also complains of recent unintentional weight loss, restlessness, insomnia, passing loose stool more frequently, menstrual disturbances, and some degree of chest pain. No other significant medical history was noted. On physical examination, she looks well-perfused, with bilateral equal air entry and normal vesicular breath sounds throughout, heart sound I+II with no added sound. Vital signs monitoring showed a temperature of 38.1°C, heart rate of 142 bpm, respiratory rate of 21, blood pressure of 155/98, peripheral CRT of 3s, and SpO2 96% on air. ECG is shown below:

(Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8496558/)

What do you need to know?

Tachyarrhythmia is an abnormal heart rate over 100 bpm. It can be classified by site of origin (sinus, supraventricular, ventricular), in relation to QRS complexes (narrow or board-complex), or regularity.

Importance

Tachycardia is an extremely common finding in patients presenting to the emergency department; it involves a wide range of differential diagnoses, from normal variants to physiological responses to life-threatening conditions like shock and cardiac arrest. Studies have shown that patients with tachycardia have an increased risk of post-discharge mortality [1, 2], with higher rates of future re-visit to ED [3].

Epidemiology and Pathophysiology

Sinus tachycardias usually occur as part of a normal physiological response (e.g., exercise, pregnancy) or a compensatory pathological response to secondary underlying conditions (e.g., pulmonary embolism, hyperthyroidism, anemia, infection). It is important to note that sinus tachycardia can be abnormal, secondary to cardiac dysautonomia. These conditions are postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Supraventricular tachycardias is an umbrella term that includes a number of arrhythmias that arise above the bundle of His, i.e., the sinoatrial (SA) node, atria, and atrioventricular (AV) node; these are typically narrow complex tachycardia except WPW syndrome. The most prevalent types of SVTs, in descending order, are atrial fibrillation, atrial flutter, atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), with atrial tachycardia (AT) and junctional tachycardia being the least common types [4, 5]. Three arrhythmogenic mechanisms have been proposed: Re-entry, enhanced automaticity, or triggered activity [6].

Starting with atrial fibrillation (AF) and atrial flutter (AFL), the latest data from the Global Burden of Disease Study 2019 showed that there are 59.7 million affected individuals worldwide [7], with a male predominance in the older population. Common causes of AF include PIRATES [Mnemonic for Pulmonary embolism, Ischaemic heart disease/Idiopathic, Rheumatic valvular disorder, Anaemia/Alcohol, Thyroid (hyperthyroidism), Electrolytes imbalance/Elevated BP (hypertension), Sepsis/Sick sinus syndrome]. The arrhythmogenic mechanism of AF is by increased automaticity, leading to ectopic focal activities and the creation of micro re-entrant circuits in the atrial muscles. Without organized contractility, blood pools in the atria, predisposing to thrombus formation and increasing stroke risk.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial flutter is less common than AF, but they both share similar aetiologies and may coexist. The difference between both is that AF presents with an irregularly irregular heartbeat, while AFL presents with a regularly irregular heartbeat, as a macro re-entrant circuit exists in the atrium, producing a rapid regular atrial rate at 300 bpm. Depending on the conduction ratio, affected patients have a fixed ventricular rate at 150 bpm (2:1), 100 bpm (3:1), or 75 bpm (4:1).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular nodal re-entrant tachycardia (AVNRT) has a prevalence of 2.25 cases per 1000 people in the general population, with a female/male ratio of 2:1 among all age groups [8]. It is the most common cause of paroxysmal SVT and occurs in about 50% of cases. Hence, it is often used synonymously with the term SVT. AVNRT is usually idiopathic, i.e., patients have structurally normal hearts. In AVNRT, re-entry is the main arrhythmogenic mechanism. Naturally, the AVN has dual pathways with different conduction velocities (a fast and slow pathway). Usually, conduction passes via the fast pathway, which blocks incoming current from the slow pathway, while in SVT, the slow pathway becomes the dominant anterograde conduction pathway, uses the fast pathway for retrograde conduction, and creates a re-entrant loop. 90% of AVNRT is slow-fast type [9].

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular re-entrant (or reciprocating) tachycardia (AVRT) is another form of paroxysmal SVT, accounting for 30% of cases. It is caused by an anatomical re-entrant circuit with the normal AV conduction system and an AV accessory tract. The most commonly known accessory pathway is called Bundle of Kent, causing Wolff-Parkinson-White (WPW) pre-excitation syndrome; hence, WPW and AVRT are often used interchangeably. It has been estimated to affect 1-3 persons per thousand people. [10]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial tachycardia (AT) accounts for the remaining 10-20% of cases, as opposed to other subtypes; it is usually caused by increased atrial automaticity independent from the AV conduction system or accessory pathways. Other causes include sinoatrial scarring, digoxin toxicity, or conditions that cause atrial dilation (COPD, CHF). Note that there are 2 types of AT, focal and multifocal AT; the former is caused by one ectopic arrhythmogenic focus and later with multiple arrhythmogenic foci within the atria. The firing rate of the ectopic focus is faster than that of the SA node, which overrides its activity. [11]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Junctional tachycardia occurs when there is increased automaticity in the AV node and decreased automaticity in the SA node. This causes ECG changes, which commonly present as retrograde p waves around the QRS complex. [12]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Ventricular arrhythmias are life-threatening conditions that cause sudden cardiac death (SCD); subtypes include monomorphic and polymorphic ventricular tachycardia (VT), Torsades de Pointes (TdP, variant of PVT), ventricular fibrillation (VF). It has been estimated that over 356,000 people suffer from out-of-hospital cardiac arrest in the USA annually, nearly 1000 cases each day [13], and SCD remains the world’s leading cause of death, costing 17 million lives each year [14]. Over the years, VT/VF has decreased incidence; they account for 23% of initial cardiac arrest rhythm, with the most commonly encountered ones being asystole (39%) and PEA (37%). This trend is likely due to the advancement of devices like implantable cardiac defibrillators and improvement in preventative cardiology practice [15]. The most common causes of VT/VF include acute coronary syndrome, cardiomyopathies, congenital channelopathies (BrS, LQTS, CPVT), QT-prolonging drugs (macrolides, TCA), electrolytes imbalance, etc. (Consider 4H 4T causes in cardiac arrest).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

The diagram below shows a decision-making algorithm.

(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Medical History

As tachyarrhythmias present with an extensive list of differential diagnoses, a detailed history taking is essential to direct clinicians to the next-step management. The most common clinical presentations in patients suffering from tachycardias include palpitations (84%), chest pain (47%), dyspnoea (38%), syncope (26%), light-headedness (19%) and sweating (18%) [16]. Symptoms can be explored with a simple mnemonic SOCRATES (site/specify, onset, character/change, rhythm/radiation, associated features, timing, exacerbating and relieving factors, severity). As patients often confuse medical terms with other meanings, it is important to ask and clarify what the term means to them (palpitations vs heart attack). Understanding the onset and progression of symptoms would allow us to determine the acuity and chronicity of the presentation. For timing, we need to ask if the presentation constantly existed since the onset, if it is intermittent, and if it comes on at a particular time of the day. In terms of exacerbating and relieving factors, when it comes to cardiac problems, it is particularly important to ask about the difference between exertion and rest and whether the patient tried anything over the counter. As non-cardiac problems cause tachycardia too, it is necessary to perform a systems review from head to toe to rule out other causes (for example, diarrhea, weight loss, heat intolerance, menstrual disturbance in hyperthyroidism). Past medical and family history should never be missed; these help us to identify risk factors, e.g., hypertension, diabetes, familial hypercholesteremia (predispose to MI), and HOCM (predispose to SCD). In the end, remember to ask for medication history (both prescribed and illicit) and social history (especially smoking and alcohol intake).

If the patient is unconscious, collateral histories from friends and family members are ideal candidates to gain some basic understanding of the patient’s background. It is also worthwhile to communicate with EMTs and paramedics and see if any other valuable information can be obtained.

Adverse features (red flags) for tachyarrhythmias are mainly myocardial infarction, syncope, new-onset heart failure, and deteriorating vital signs, i.e., increased capillary refill time, hypotension (indicative of shock), altered consciousness/reduced GCS.

Physical Examination

If the patient is unconscious or has no palpable pulse, manage the patient with basic life support and advanced life support protocols.

Evaluation of all other patients with the A-E approach is critical as they are still undifferentiated. If the patient is conscious, start inspecting the patient. Key features to observe include cyanosis (poor perfusion peri-arrest), pallor (anemia), dyspnea (heart failure, myocardial infarction/injury), diaphoresis (myocardial infarction/injury), and peripheral edema (heart failure). Start peripherally at hands, observe for clubbing (indicative of infective endocarditis, congenital heart diseases, hyperthyroidism), and assess radial and carotid pulse for its rate, rhythm, and volume. Look for visible jugular venous pulse (elevated – heart failure), presence of corneal arcus (familial hypercholesterolemia) in eyes, and scars on the chest (sternotomy, pacemaker). To assess murmurs, auscultate in all 4 valvular areas (2ndICS left sternal border – pulmonary area, 2nd ICS, right sternal border – aortic area, 4th ICS left sternal border – tricuspid area, 5th ICS mid-clavicular line – mitral area). Be sure to examine other systems, including respiratory, neurological, and ENT.

Alternative Diagnoses

As mentioned above, most tachyarrhythmias are idiopathic or secondary to cardiac and non-cardiac causes. It is extremely important to keep an open mind and an extensive list of differentials so we won’t miss the actual diagnosis. The table below lists differentials for palpitations, the chief complaint of tachyarrhythmias.

Causes of Palpitations

Cardiac Causes

Noncardiac Causes

Atrial fibrillation/flutter

Atrial myxoma

Atrial premature contractions

Atrioventricular reentry

Atrioventricular tachycardia

Autonomic dysfunction

Cardiomyopathy

Long QT syndrome

Multifocal atrial tachycardia

Sick sinus syndrome

Supraventricular tachycardia

Valvular heart disease

Ventricular premature contractions

Ventricular tachycardia

Alcohol

Anemia

Anxiety/stress

Beta-blocker withdrawal

Caffeine

Cocaine

Exercise

Fever

Medications

Nicotine

Paget disease of bone

Pheochromocytoma

Pregnancy

Thyroid dysfunction

(Reuse from Wexler RK, Pleister A, Raman SV. Palpitations: Evaluation in the Primary Care Setting. Am Fam Physician. 2017;96(12):784-789.) – Open Access (https://www.aafp.org/pubs/afp/issues/2017/1215/p784.html)

Acing Diagnostic Testing

Any patients with adverse features and life-threatening presentations should be placed in a resuscitation bay with a multi-parameter vitals monitor/defibrillator connected and a point-of-care portable ultrasound ready. For stable patients, stepwise management should be initiated. Proceed with bedside tests: perform a 12-lead ECG, measure heart rate, assess SpO2 with an oximeter, and record blood pressure. Collect blood samples, including a Full Blood Count, Urea and Electrolytes, serum Magnesium, Calcium, Thyroid Function Tests, Liver Function Tests, and a coagulation panel. Additional tests can be considered based on the clinician’s clinical decision and the patient’s presentation, for example, Troponin for suspected MI, D-dimer for suspected PE, etc. Chest X-rays should be performed in any patients presenting with chest pain. Advanced imaging again depends on clinical presentation, coronary angiogram for Myocardial Infarction, Computed Tomography Pulmonary Angiography for Pulmonary Embolism, etc. The risk stratification tool (more details in the section below) can be used to facilitate decisions for advanced interventions involving intensive care input. Cardiology input will be required for further investigations involving Holter monitoring, implantable loop recorder, electrophysiological study, echocardiogram, cardiac Magnetic Resonance Imaging, etc.

Management

Sinus Tachycardia

Sinus tachycardia is often a physiological response to an underlying cause such as sepsis, hypovolemia, or anemia. Management should focus on identifying and addressing these causes rather than targeting the heart rate itself. For example, in a septic patient, early fluid resuscitation and antibiotics are critical, while in a patient with anemia, blood transfusion or treatment of iron deficiency may resolve the tachycardia. Clinicians should avoid unnecessary use of beta-blockers or calcium channel blockers unless sinus tachycardia persists after the underlying cause has been addressed.

Atrial Fibrillation

Management of atrial fibrillation requires a careful evaluation of the patient’s hemodynamic stability, symptom duration, and underlying comorbidities.

  1. Hemodynamically Stable Patients with Symptoms >48 Hours or Uncertain Timeline:

    • Rate control is the priority to prevent further decompensation. Start with beta-blockers (e.g., bisoprolol) or calcium channel blockers (e.g., diltiazem).
    • Consider digoxin for patients with congestive heart failure who may not tolerate beta-blockers.
    • Avoid cardioversion without anticoagulation if the symptom duration is >48 hours or unclear, as this increases the risk of thromboembolic events.

  2. Hemodynamically Stable Patients with Symptoms <48 Hours or a Reversible Cause:

    • Focus on rhythm control with cardioversion, which can be electrical or pharmacological (e.g., flecainide or amiodarone).
    • Ensure anticoagulation with heparin before cardioversion unless contraindicated.
    • Use an echocardiogram to rule out structural abnormalities, as this guides drug selection (e.g., flecainide for structurally normal hearts; amiodarone for structural heart disease).

  3. Patients with Adverse Features (Shock, Syncope, Acute Heart Failure, or Myocardial Ischemia):

    • Immediate electrical cardioversion is required, typically using synchronized shocks. Time is critical—any delay could worsen outcomes.

  4. Paroxysmal AF:

    • Counsel patients on the use of “pill-in-the-pocket” therapies such as flecainide or sotalol for intermittent symptoms. Ensure they understand the signs of structural heart disease, which would contraindicate these medications.

Always consider underlying conditions such as hyperthyroidism, electrolyte disturbances, or alcohol-related atrial fibrillation (Holiday Heart Syndrome). Addressing these causes can prevent recurrence. In elderly patients or those with heart failure, weigh the benefits of rhythm versus rate control.

Atrial Flutter

Management of atrial flutter parallels that of atrial fibrillation. Rate control is often sufficient in stable patients, but rhythm control may be prioritized for symptomatic relief. In acute settings, electrical cardioversion may be more effective than pharmacological approaches.

Atrial flutter is frequently associated with underlying structural heart disease or atrial enlargement. Evaluate for these conditions with echocardiography and address them to improve long-term outcomes.

AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

AVNRT is often well-managed with non-pharmacological measures in stable patients.

Conservative Management:

  • Initiate vagal maneuvers (e.g., Valsalva maneuver or carotid massage). These can terminate the tachycardia in many cases. Ensure the patient is monitored for safety, especially in older adults where carotid massage could induce complications.

Pharmacological Management:

  • Administer IV adenosine, starting at 6 mg and escalating to 12 mg or 18 mg if needed. Warn the patient about the transient sensation of chest discomfort or flushing.
  • If adenosine is contraindicated (e.g., in asthmatic patients), use a calcium channel blocker such as verapamil.

Persistent Cases:

  • Consider beta-blockers, digoxin, or amiodarone if initial treatments fail.

Hemodynamically Unstable Patients:

  • Proceed with immediate cardioversion to stabilize the patient.

In recurrent AVNRT, evaluate for underlying triggers such as excessive caffeine or stimulant use. Discuss long-term options such as catheter ablation for definitive treatment.

AVRT/WPW (Atrioventricular Reentrant Tachycardia/Wolff-Parkinson-White Syndrome)

In patients with WPW, rapid and accurate diagnosis is critical to avoid inappropriate treatment.

Stable Patients:

  • Treat with amiodarone, flecainide, or procainamide. Avoid digoxin and calcium channel blockers, as these can worsen pre-excitation and lead to ventricular fibrillation.

Unstable Patients:

  • Immediate cardioversion is indicated.

In young patients presenting with sudden palpitations and syncope, always consider WPW and obtain a 12-lead ECG for diagnosis. Educate patients on avoiding stimulants that may precipitate episodes.

Atrial Tachycardia

For atrial tachycardia, management depends on the patient’s stability. Rate control is often effective for stable patients, while cardioversion may be required in unstable cases.

Investigate underlying causes such as digoxin toxicity or structural heart disease, as addressing these may resolve the tachycardia.

Ventricular Tachycardia (VT)

Management of VT hinges on the patient’s hemodynamic stability.

Stable VT:

    • Administer amiodarone (300 mg IV STAT followed by a 900 mg infusion over 24 hours). Monitor for potential side effects such as hypotension or bradycardia.

Unstable VT, pulse positive:

    • Follow the ALS (Advanced Life Support) algorithm, prioritizing cardioversion.

VT, no pulse:

  • Follow the ALS (Advanced Life Support) algorithm, prioritizing defibrillation and CPR.

In patients with recurrent VT, assess for underlying ischemic heart disease or electrolyte abnormalities. Long-term management may require ICD placement or catheter ablation.

Ventricular Fibrillation (VF)

VF is a life-threatening emergency requiring immediate intervention. Follow the ALS algorithm, which includes high-quality CPR and defibrillation.

Always assess for reversible causes of VF, such as acute myocardial infarction or electrolyte imbalances (e.g., hypokalemia or hypomagnesemia), and treat these aggressively to prevent recurrence.

Tachycardia and advanced life support algorithms are provided below.

(Reuse from Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. DOI:10.1016/j.resuscitation.2021.02.010) – Open Access (https://www.cprguidelines.eu/)
(Reuse from Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. DOI:10.1016/j.resuscitation.2021.02.010) – Open Access (https://www.cprguidelines.eu/)

Special Patient Groups

The management of most tachyarrhythmias is similar among pregnant women and pediatric populations, with the exception of ventricular cardiac arrest rhythms.

Pregnant Patients (Obstetric Cardiac Arrest ) [17]

  • A normal supine position will result in aortocaval compression from the gravid uterus; this reduces cardiac output. Hence, placing the patient in a left lateral position is crucial, especially at> 20 weeks gestation.
  • The position of the rescuer’s hands for chest compression ideally should be slightly higher than usual, taking the elevation of the diaphragm and abdominal contents caused by the gravid uterus into account.
  • The defibrillator pad position should be adjusted to maintain the left lateral position.
  • Magnesium sulfate (4 g IV) should be given in patients with eclampsia.
  • Patients should be intubated early due to the higher risk of pulmonary aspiration and Mendelson syndrome from gastric contents.
  • Emergency delivery of the fetus (>20 weeks) with resuscitative hysterotomy should happen within 5 minutes in the event of cardiac arrest, given that the initial resuscitation attempt has failed. This is a definitive procedure to decompress IVC to facilitate venous return and increase cardiac output.
  • As this is an obstetric emergency, get help from the OB/GYN and neonatal team early; resuscitative hysterotomy should not wait even if not all surgical equipment is immediately available; one scalpel is enough to start the procedure.

Pediatrics (Cardiac Arrest) [17]

  • Most pediatric cardiac arrests are secondary to respiratory failure; hence, giving 5 rescue breaths is essential prior to chest compressions.
  • Pulse checks use brachial or femoral pulses as opposed to carotid pulses in adults.
  • It is a similar compression site but with a compression: breath ratio of 15:2, as opposed to 30:2 in adults.
  • In infants, compress the chest using two fingers or an encircling technique (two thumbs). For children over one year old, use one or two hands.
  • Intraosseous (IO) access is preferred for circulation access, as obtaining venous access can be difficult in children.
  • Adrenaline is given in 10 mcg/kg, and Amiodarone is given in 5 mg/kg.
  • Note that PALS is different from newborn life support (NLS), which is not mentioned here.

* Please refer to European Resuscitation Council (ERC) Paediatric Life Support and Special Circumstances Guidelines (https://www.cprguidelines.eu/)

Risk Stratification

There is no single risk stratification tool for tachyarrhythmias, developed scoring systems are usually condition-specific or presentation-specific. We listed some of the important ones related to tachyarrhythmias below:

  • Cardiac Arrest Hospital Prognosis (CAHP) score – predicts prognosis in patients suffering from out-of-hospital cardiac arrest. [18]
  • Cardiac Arrest Risk Triage (CART) Score – predicts the risk of in-hospital cardiac arrest in hospitalized patients. [19]
  • CHA₂DS₂-VASc Score – calculate stroke risk in patients with atrial fibrillation and guide initiation of anticoagulation therapy. [20]
  • HEART score – predicts patients presenting with chest pain for a 6-week risk of major adverse cardiac events (MACE). It can also classify patients into low, moderate, and high-risk groups to facilitate decisions for discharge from ED, admission for observation, or urgent intervention required. [21]
  • Thrombolysis In Myocardial Infarction (TIMI) score and Global Registry of Acute Coronary Events (GRACE) score – estimate mortality for patients with acute coronary syndrome, guide decision for coronary revascularisation needs. [22]
  • Well’s Score – calculate the clinical probability of DVT/PE and guide the decision to consider alternative diagnosis or perform immediate CTPA/anticoagulation. [23]
  • Pulmonary Embolism Rule Out Criteria (PERC) – effectively rules out PE if scored 0. [24]
  • Pulmonary Embolism Severity Index (PESI) – predicts 30-day mortality in patients with PE. [25]
  • Emergency Heart Failure Mortality Risk Grade (EHMRG) estimates 7-day mortality in patients with congestive heart failure and guides the decision to admit them [26].
  • San Francisco syncope rule (SFSR), Canadian syncope risk score (CSRS), and Evaluation of Guidelines in SYncope Study (EGSYS) Score – both SFSR and CSRS predict adverse outcomes in patients presenting with syncope (7-day and 30-day, respectively), EGSYS helps determine whether syncope is cardiac or non-cardiac cause (these includes vasovagal, situational, postural hypotension). [27-29]
  • Multi-parametric models – predict the prognosis of patients with Brugada syndrome for future major arrhythmic events (VT/VF) and guide decisions for implantable cardioverter defibrillator placement. [30]

* Please browse these calculators on MDCalc website (https://www.mdcalc.com/)

When To Admit This Patient

Patients with adverse features and hemodynamic instability require immediate intervention and admission. The aforementioned risk stratification tools can be used based on clinical signs and symptoms. If initial investigations yielded no clinical significance, patients could be discharged with education, reassurance, and safety netting advice. Explain that palpitations are usually transient and harmless; if they are recurring, ask patients to note down the onset, timing, and duration and measure BP and HR if monitoring is available at home. Advise them to reattend ED if symptoms persist or worsen or new-onset red flag symptoms emerge; lifestyle advice, for example, avoid certain known stimulants like caffeine, alcohol, and nicotine. If the patient is known to have SVT, educate about self-performing Valsalva maneuver to try terminating it before medical assistance arrives. Arrange follow-up with a family physician and review the need for further investigations and specialist input. Patients should be referred urgently for detailed investigations, including Holter monitoring if non-specific new clinical findings are yielded. Other options may be explored, such as an echocardiogram, implantable loop recorder, and electrophysiology study. [31, 32]

Revisiting Your Patient

The case reminds us that tachyarrhythmias can be secondary to non-cardiac causes. This is a classical presentation of hyperthyroidism, with ECG showing fast-rate atrial fibrillation. Atrial fibrillation occurs in 15% of patients with hyperthyroidism. A detailed history taking with appropriate systems review (as symptoms suggest) would point us towards hyperthyroidism. Clinical examination may reveal clubbing (thyroid acropachy), exomphalos (thyroid eye disease), pretibial myxoedema, goiter, and an irregular heartbeat with mid-systolic scratchy murmur (Means–Lerman scratch) might be heard on auscultation. The investigation here, starting from bedside, would be to obtain a complete set of vital signs (blood pressure, heart rate, respiratory rate, temperature, SpO2), 3-lead continuous monitoring, and 12-lead ECG; blood including complete blood count, urea and electrolytes, thyroid function tests, troponin (serial), venous blood gas, other electrolytes (Ca2+). The management approach of this patient is to treat the underlying hyperthyroidism primarily. Hence, endocrinologist referral will be required, with cardiologists’ input on managing the fast Atrial Fibrillation. Propranolol (reduces peripheral conversion of T4 to T3) and anti-thyroid drugs like carbimazole (inhibits thyroid peroxidase action) are the mainstay management (details see thyroid disorder chapter). However, as the patient also complains of anginal pain, rate control with cardio-selective beta-blockers should be initiated as well. It also helps with alleviating symptoms of hyperthyroidism, including palpitations, tremors, anxiety, heat intolerance, etc., due to the increased sympathetic tone caused by excess thyroid hormone production. The need for anticoagulation is assessed on an individual basis. In most cases, Atrial Fibrillation reverses to sinus rhythm spontaneously after the euthyroid state has been achieved. However, if Atrial Fibrillation persists, cardioversion may be considered. This, nevertheless, would be a cardiologist’s decision. [33]

Authors

Picture of Keith Sai Kit Leung

Keith Sai Kit Leung

Keith is an academic foundation doctor (emergency medicine themed) in the UK. He graduated both BSc and MBChB with distinction, and has published over 30 peer-reviewed articles till date. He is interested in Pre-Hospital Emergency & Retrieval Medicine, Intensive Care, Cardiology and Medical Education. He main research interests are arrhythmias and cardiac electrophysiology, cardiac arrest and resuscitation, ACS, POCUS, ECMO, airway and trauma management. He aims to work as an academic PHEM/HEMS physician and pursue a MD (Res)/PhD in the near future.

Picture of Rafaqat Hussain

Rafaqat Hussain

Dr Rafaqat Hussain is working as Specialty Doctor in Emergency Department at SWBH NHS trust. He had done MBBS.MRCEM. FRCEM.EBCEM. He has involved in training and teaching for junior doctors and medical students at University of Birmingham. He is enthusiastic in pursuing his career in being an Emergency Medicine Consultant.

Picture of Abraham Ka Cheung Wai

Abraham Ka Cheung Wai

Dr Abraham Wai, Clinical Associate Professor at the University of Hong Kong (HKU), is a dynamic force in the field of emergency medicine. His journey from specialist training to impactful research and innovative teaching has left an indelible mark on the healthcare landscape.

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References

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  9. George SA, Faye NR, Murillo-Berlioz A, Lee KB, Trachiotis GD, Efimov IR. At the Atrioventricular Crossroads: Dual Pathway Electrophysiology in the Atrioventricular Node and its Underlying Heterogeneities. Arrhythm Electrophysiol Rev. 2017;6(4):179-185. doi:10.15420/aer.2017.30.1
  10. Chhabra L, Goyal A, Benham MD. Wolff Parkinson White Syndrome. [Updated 2023 Jan 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554437/
  11. Liwanag M, Willoughby C. Atrial Tachycardia. [Updated 2022 Jun 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542235/
  12. Hafeez Y, Grossman SA. Junctional Rhythm. [Updated 2023 Feb 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507715/
  13. Srinivasan NT, Schilling RJ. Sudden Cardiac Death and Arrhythmias. Arrhythm Electrophysiol Rev. 2018;7(2):111-117. doi:10.15420/aer.2018:15:2
  14. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2022 Update: A Report From the American Heart Association [published correction appears in Circulation. 2022 Sep 6;146(10):e141]. Circulation. 2022;145(8):e153-e639. doi:10.1161/CIR.0000000000001052
  15. Keller SP, Halperin HR. Cardiac arrest: the changing incidence of ventricular fibrillation. Curr Treat Options Cardiovasc Med. 2015;17(7):392. doi:10.1007/s11936-015-0392-z
  16. Yetkin E, Ozturk S, Cuglan B, Turhan H. Clinical presentation of paroxysmal supraventricular tachycardia: evaluation of usual and unusual symptoms. Cardiovasc Endocrinol Metab. 2020;9(4):153-158. doi:10.1097/XCE.0000000000000208
  17. Maupain C, Bougouin W, Lamhaut L, et al. The CAHP (Cardiac Arrest Hospital Prognosis) score: a tool for risk stratification after out-of-hospital cardiac arrest. Eur Heart J. 2016;37(42):3222-3228. doi:10.1093/eurheartj/ehv556
  18. Banerjee, A., & Oliver, C. (2017). Revision notes for the FRCEM intermediate SAQ paper (2nd). Oxford University Press.
  19. Churpek MM, Yuen TC, Park SY, Meltzer DO, Hall JB, Edelson DP. Derivation of a cardiac arrest prediction model using ward vital signs. Crit Care Med. 2012;40(7):2102-2108. doi:10.1097/CCM.0b013e318250aa5a
  20. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137(2):263-272. doi:10.1378/chest.09-1584
  21. Brady W, de Souza K. The HEART score: A guide to its application in the emergency department. Turk J Emerg Med. 2018;18(2):47-51. doi:10.1016/j.tjem.2018.04.004
  22. de Araújo Gonçalves P, Ferreira J, Aguiar C, Seabra-Gomes R. TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interaction with revascularization in NSTE-ACS. Eur Heart J. 2005;26(9):865-872. doi:10.1093/eurheartj/ehi187
  23. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001;135(2):98-107. doi:10.7326/0003-4819-135-2-200107170-00010
  24. Freund Y, Cachanado M, Aubry A, et al. Effect of the Pulmonary Embolism Rule-Out Criteria on Subsequent Thromboembolic Events Among Low-Risk Emergency Department Patients: The PROPER Randomized Clinical Trial. JAMA. 2018;319(6):559-566. doi:10.1001/jama.2017.21904
  25. Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172(8):1041-1046. doi:10.1164/rccm.200506-862OC
  26. Lee DS, Lee JS, Schull MJ, et al. Prospective Validation of the Emergency Heart Failure Mortality Risk Grade for Acute Heart Failure. Circulation. 2019;139(9):1146-1156. doi:10.1161/CIRCULATIONAHA.118.035509
  27. Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006;47(5):448-454. doi:10.1016/j.annemergmed.2005.11.019
  28. Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ. 2016;188(12):E289-E298. doi:10.1503/cmaj.151469
  29. Kariman H, Harati S, Safari S, Baratloo A, Pishgahi M. Validation of EGSYS Score in Prediction of Cardiogenic Syncope. Emerg Med Int. 2015;2015:515370. doi:10.1155/2015/515370
  30. Chung CT, Bazoukis G, Radford D, et al. Predictive risk models for forecasting arrhythmic outcomes in Brugada syndrome: A focused review. J Electrocardiol. 2022;72:28-34. doi:10.1016/j.jelectrocard.2022.02.009
  31. Moulton KP, Bhutta BS, Mullin JC. Evaluation Of Suspected Cardiac Arrhythmia. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK585054/
  32. RCEMLearning. https://www.rcemlearning.co.uk/reference/palpitations/. Published July 27, 2021. Accessed April 13, 2023.
  33. Parmar MS. Thyrotoxic atrial fibrillation. MedGenMed. 2005;7(1):74.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Question Of The Day #27

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod27
756.1 - palpitation - SOB

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Intravenous Adenosine
  • B) Valsalva maneuver
  • C) Intravenous Metoprolol
  • D) Intravenous Diltiazem

This patient has a narrow-complex, regular tachycardia that is causing the sensation of palpitations. The clinical history, rapid heart rate, and 12-lead EKG provide enough information to diagnose this patient with supraventricular tachycardia, also known as “SVT.” Supraventricular tachycardias refer to a broad range of arrhythmias, including sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and AV nodal re-entry tachycardia. This scenario specifically depicts an AV nodal re-entry tachycardia (AVNRT). AVNRT is a common type of SVT that can occur spontaneously or is triggered by sympathomimetic agents (i.e., cocaine, amphetamines), caffeine, alcohol, exercise, or beta-2 agonists using in asthma treatment (i.e., albuterol, salbutamol). AVNRTs are narrow-complex tachycardias with rates that range from 120-280bpm. P waves are typically absent in AVNRTs, but rarely they may be present as retrograde inverted P waves located immediately before or after the QRS complex. Symptoms experienced by the AVNRT patient may include pre-syncope, syncope, dizziness, palpitations, anxiety, or mild shortness of breath. Patients with AVNRTs are more likely to be young and female over male.

QRS complexes in AVNRTs are often narrow (<120msec), however, wide QRS complexes may be present in AVNRTs if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AVNRTs are often stable and do not require electric cardioversion. Signs that indicate instability and necessitate cardioversion are hypotension (SBP <90mmHg), altered mental status, or ischemic chest pain (more common if known history of ischemic heart disease). This patient lacks all of these signs and symptoms.

Treatment of AVNRT focuses on restoring the patient to normal sinus rhythm, which leads to resolution of symptoms. First-line medications for AVNRTs are short-acting AV nodal blocking agents, like adenosine (Choice A). Beta-blockers or calcium channel blockers act as second-line agents for patients who do not respond to adenosine. Metoprolol is a beta-blocker (Choice C) and Diltiazem is a calcium channel clocker (Choice D). Prior to any medications, vagal maneuvers should always be attempted first in a stable patient with AVNRT. The Valsalva maneuver (Choice B), or “bearing down,” is a commonly used vagal maneuver in the termination of AVNRTs. Other vagal maneuvers include the carotid massage or the Diving reflex (place bag of ice and water on face). Correct Answer: B

Want Another Question?

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685

  • Burns, E. (2020). Supraventricular Tachycardia (SVT). Life in the Fast Lane. Retrieved from https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

[cite]

The EKG Case of No Symptoms

the ecg case of no symptoms
~ Anthony Rodigin, USA ~ Leave a comment

Case Presentation

A 52-year-old woman presents to the ED from an outpatient dialysis center with a rather vague history. She has no symptoms and feels normal, but she was told something “was either too low or too high” on her vital signs at dialysis, so dialysis staff did not perform her scheduled dialysis session. No one had called ahead to alert the emergency department, and the patient had driven herself to the ED, as she was instructed. Vitals show a normal temperature, respiratory rate, oxygen saturation, blood pressure of 102/47 mm Hg, and a heart rate of 138 beats per minute. The physical exam is normal besides a mild regular tachycardia and a working AV dialysis fistula on the right arm. EKG is done, and a representative portion is shown below:

EKG from the prior year is shown for comparison.

How would you interpret the first EKG, and what are your next steps?

Discussion

While you are thinking, I will discuss a few of my practical observations from working in the pit. I want to focus not so much on the diagnosis but on working with these types of scenarios.

Treat the patient and not the chief complaint, vitals, labs, EKGs, studies, or referral information.

Anthony Rodigin Tweet

When they are feeling great and have no symptoms, they are feeling great and have no symptoms! Your nurses will not necessarily think this way, but one does not feel great while having a real STEMI apparent on the triage EKG. So what is it then, if the patient is here for a contact lens stuck in their eye, but has an EKG STEMI? Worst case – a prior STEMI that never corrected or evolved on the EKG. A ventricular aneurysm? Leads misplaced? Did your EKG tech do an EKG on themselves? A silent MI can occur, but an incidental STEMI is unlikely. 

Of course, the patient has to be alert, competent, and not intoxicated. They should not be lying about or hiding their symptoms and should not have a secondary interest like the need to make it to a daughter’s wedding - live or die. The easiest thing is to ask directly.

What is the rhythm's rate doing when it is left alone?

Afibs and MATs will tend to vary greatly in the second to second heart rate, sinus tachycardias will fluctuate some, while A-flutters and SVTs will tend to stick to a single number no matter what you do and no matter if the patient is walking, talking, or snoozing. Stable Vtachs will depend on a number of factors like being monomorphic or polymorphic – but we are talking about narrow QRS dysrhythmias or ones with an obvious bundle. 

So if you cannot tell from the EKG – observe what the thing does while left alone. As long as the patient is otherwise stable or has had symptoms for a while, you have some time.

Adenosine – not just for SVT conversion

“SVT = adenosine” should not be an automatic equation. First of all, there are contraindications to adenosine based on past history or current medications taken. But adenosine can also be used to “stretch out” weird or equivocal fast rhythms to make flutter waves or hidden P waves come out, so you can see and diagnose the arrhythmia vs. sinus. 

You have to have continuous EKG recording going or printing the monitor strip to spot the temporary effect.

Hypotension + tachy-dysrhythmia: does not necessarily add up to Joules.

The textbook mantra of shocking any dysrhythmia associated with hypotension does not hold up in reality. In reality, you will find that most of your Afibs with a rapid response, your new-onset atrial flutters and your SVTs will have a lousy blood pressure: systolic of 80s and 90s are almost to be expected, and may even dip down to 70s on occasion. It also depends on a prior BP baseline, if the person is petite or dehydrated. But if the patient is mentating well and is not suffocating or experiencing crushing chest pain with diaphoresis, please don’t feel like you have to shock them. The body is not used to the new arrhythmia, and the rapid rate compromises the cardiac output. 

Yes, you can still use your rate and rhythm controllers. Give the patient a gentle fluid bolus if you must. Of course, pacer pads do have to be on ahead of time.

Be afraid of shocking dialysis patients. Check electrolytes.

Hypotension with normal mentation is much better than a PEA arrest. Shocking extremes of electrolyte and acid/base abnormalities, whether due to TCA and other overdoses or in dialysis patients, will give you exactly that. This is especially true for the so-called “slow-X” arrhythmias: slow Afib, slow SVT, or even V-slow (Vtach with a rate of 130) that dialysis patients like to present in. 

Just like airplane travel in transportation, electricity is in general the safest rhythm conversion strategy. But there are exceptions, and you only need to crash once.

A-flutter and the stuck rate of 150

You already know this, but just as a reminder. If the rate is a steady 150, plus or minus, and it is stuck there, you should think of atrial flutter. 

Even if you do not see obvious classic flutter waves, there is a high chance of 2:1 conduction. In this case, I thought of it. Fortunately, it did not think of me.

Adenosine (again)….the 6, the 12…the 24??

Sometimes adenosine is not pushed correctly, but sometimes it just does not work or only works for a few seconds. Sometimes the patient’s Mom knows best what works, so you should listen. Sometimes the last time it was used, the patient really did feel like they were going to die – so they do not ever want it again. Ever. That you should try 6mg, then 12mg, then stop is generally true, but it is also a dead-end. What is your back up plan? Electricity? In the past I have given the doses in reverse, combined 6mg with the Valsalva maneuver and had given a preemptive beta-blocker or calcium channel blocker dose 10-15 minutes before adenosine to massage a stubborn heart into adenosine submission. It is ok to experiment a little. Another practical point – how much does your ED freak an SVT patient out while he or she is being triaged and roomed? I still do not completely understand why an SVT tends to be rushed up in the same fashion as a STEMI with cardiogenic shock and bradycardia, judging from staff adrenaline levels. 

Calm the patient down, turn the lights off and let them change. It's like a kid with croup. Remember, it is lack of the sympathetic influx that we want, not an excess. Otherwise, why try the Valsalva at all? Has anyone attempted a stellate ganglion block Vfib-style for a refractory SVT? An overkill, I know….but could be fun, and practice for the real deal.

Aren’t all AVNRTs verapamil sensitive?

Years ago, in my first year of solo practice, I had a case of a refractory SVT in a young teenager, which a pediatric cardiologist consulting by phone called a “verapamil-sensitive AVNRT” based on the EKG alone. I was impressed. Hours later, I decided to flash my newly acquired cool knowledge and relayed the same to my in-house cardiologist, who looked at me with a grin and a raised eyebrow and said, “Anthony, all AVNRTs are verapamil sensitive”. At that time, I was also sensitive, and so my feelings were hurt. Lately I have gotten into the habit of treating my SVTs with diltiazem – as a purer verapamil relative. With generally good results and no need to stand in front of the patient during administration by the nurse. 

The bottom line is – you have choices. Especially, if the patient is already on a beta-blocker or a calcium channel blocker, give them a beta or a calcium blocker IV, see what happens.

Case Concluded

Despite a single nadir of blood pressure of 75 systolic, the rest holding steadily in the high 90s, the patient received a single dose of IV diltiazem and a small IV fluid bolus. Labs reviewed prior showed normal potassium, calcium, sodium, magnesium and the rest of them. Her average heart rate reduced to about 106 and a repeat EKG is shown, accidentally capturing an event: 

She, of course, had a “verapamil sensitive” SVT. The patient’s new right bundle block had also improved to an incomplete, proving to be either SVT- or rate-related. The patient had never experienced any symptoms while in the ED. She was observed for a short time, scheduled for an out-of-sequence dialysis the next day and discharged home with a normal heart rate. I guess, in this case, we did treat the EKG and not the patient.

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Want to read more, take a look this post from September

Drop the Beat! – Adenosine in SVT

Drop the Beat! – Adenosine in SVT
~ Mohammad Anzal Rehman, UAE ~ Leave a comment

Supraventricular tachycardia (SVT) is defined as a dysrhythmia that originates proximal to (or ‘above’) the atrioventricular (AV) node of the heart. It commonly manifests as a regular, narrow complex (QRS interval < 120ms) tachycardia in affected patients. It is most frequently attributable to re-entrant electrical conduction through accessory pathways in the heart, with typical Electrocardiogram (ECG) findings depicting ventricular rates of 150 to 250 beats/min without the preceding P wave usually seen in sinus tachycardias. [1,2]

In the stable adult patient presenting with SVT, where no ‘red flags’ such as shock, altered mental state, ischemic chest pain or hypotension are present, management typically begins with an attempt to convert the rhythm back to its baseline sinus state using vagal manoeuvres.[3] Vagal manoeuvres such as the carotid sinus massage and the Valsalva manoeuvre are effective first-line therapies, terminating approximately 25% of spontaneous SVTs,[4] with the newer, modified Valsalva manoeuvre showing even greater efficacy of 43% conversion.[5] When these fail or are otherwise not feasible to use in patients, management involves the administration of a drug called Adenosine.

The Evolution of Adenosine Use for SVT

In 1927, studies found that the injection of extracts from cardiac tissue into animals appeared to decrease heart rates and that this effect was attributable to an ‘adenine compound’.[6] This compound was later identified as Adenosine, comprised of the purine-based nucleobase Adenine attached to a ribose sugar. Fifty years after its initial discovery, Adenosine began to emerge as a treatment for stabilizing SVTs and has remained a mainstay in its management ever since.[7]

Current guidelines recommend Adenosine for the management of SVT, usually administered through a peripheral intravenous (IV) access initially as a 6 mg bolus. Adenosine has an extremely short half-life (less than 10 seconds) and is therefore rapidly metabolized soon after it enters the body.[8] Therefore, IV dosage is commonly followed by a 20 mL rapid saline flush to facilitate the drug’s transport to cardiac tissue where it can act before being broken down into inactive metabolites. If the 6mg dose does not convert the SVT back to sinus rhythm, subsequent doses are given at 12 mg, also followed by 20-mL saline for rapid infusion.

Pro-Tip: Single syringe technique

Before we dive into the concept of the single syringe method of administering Adenosine, take a look at the segment above. How would you give 6 mg of Adenosine through an IV site, making sure a total of 20 mL saline follows right after, in enough time to make sure you don’t waste that precious 10-second half-life of Adenosine? In many places, one of the two methods are used to make this happen:

  1. Use an IV line to push Adenosine > remove syringe > push 10 mL saline using a pre-filled syringe > remove syringe > push 10mL saline using a second pre-filled syringe.
  2. Fancier places use what’s known as a stopcock, a device usually with 3 ports attached to the IV site. Adenosine syringe is attached to one port and a 10 mL saline flush is attached at a separate port. The process looks something like this: Push adenosine through stopcock port > turn stopcock to open saline port’s access to IV site > push 10 mL saline flush > push an additional 10 mL saline using second syringe or remainder of a 20 mL prefilled syringe.

Now we all know that nurses are indistinguishable from ninjas at times when handling IV medication. However, even the most experienced practitioner is not immune to the occasional stumble when switching between the various syringes and swivels required in the methods above. In fact, a study in 2018 found that, in pediatric patients, adenosine given using the stopcock method delivered suboptimal doses.[9]

In an attempt to improve administration time, a potential work-around was proposed where adenosine could be combined with the flush solution in one 20 mL syringe and pushed altogether.[10] This potentially eliminates any time wasted changing syringes and manipulating stopcocks, but does it still work the same? Fortunately, a few studies have demonstrated the feasibility of the single syringe method, with non-inferior efficacy compared to standard methods of drug administration.[11,12]

Caveats: Coffee Conundrums

Let’s talk a bit about dosage. We mentioned above that guidelines recommend starting at 6 mg and moving to 12 mg for subsequent dosages. These dosages assume uninhibited action of adenosine at its receptors which, unfortunately, may not always be the case in patients. What would inhibit adenosine’s activity, I hear you ask? You’ll want to put down that Caramel Macchiato because the answer (pause for dramatic effect) … is coffee – caffeine to be exact.

Caffeine is known to work by antagonizing adenosine receptors, thereby decreasing adenosine’s biologic effect.[13] A component in many frequently consumed beverages, such as coffee, tea, energy drinks and sodas, and with a half-life of approximately 4-5 hours, caffeine is very likely to be present in the bloodstreams of many Emergency Department patients (and doctors). A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT. [14]

This makes it all the more important to not only include information on any known recent beverage consumption during history taking for patients presenting with SVT, but also to potentially increase dosage for patients with a confirmed or suspected recent ingestion of caffeine. In such cases, it would be reasonable to start at 12 mg adenosine as the first dose, followed by 18 mg subsequent dosages to manage SVT.[15]

A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT.

A. Rehman Tweet

References and Further Reading

  1. Bibas, L., Levi, M., & Essebag, V. (2016). Diagnosis and management of supraventricular tachycardias. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(17-18), E466–E473. https://doi.org/10.1503/cmaj.160079
  2. Mahtani, A. U., & Nair, D. G. (2019). Supraventricular Tachycardia. The Medical clinics of North America, 103(5), 863–879. https://doi.org/10.1016/j.mcna.2019.05.007
  3. Advanced Cardiac Life Support Provider Manual, American Heart Association, Mesquite 2016
  4. Lim, S. H., Anantharaman, V., Teo, W. S., Goh, P. P., & Tan, A. (1998). Comparison of Treatment of Supraventricular Tachycardia by Valsalva Maneuver and Carotid Sinus Massage. Annals of emergency medicine, 31(1), 30–35.
  5. Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A., Lobban, T., Dayer, M., Vickery, J., Benger, J., & REVERT trial collaborators (2015). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet (London, England), 386(10005), 1747–1753. https://doi.org/10.1016/S0140-6736(15)61485-4
  6. Drury, A. N., & Szent-Györgyi, A. (1929). The physiological activity of adenine compounds with especial reference to their action upon the mammalian heart. The Journal of physiology, 68(3), 213–237. https://doi.org/10.1113/jphysiol.1929.sp002608
  7. Delacrétaz E. (2006). Clinical practice. Supraventricular tachycardia. The New England journal of medicine, 354(10), 1039–1051. https://doi.org/10.1056/NEJMcp051145
  8. Kazemzadeh-Narbat, M., Annabi, N., Tamayol, A., Oklu, R., Ghanem, A., & Khademhosseini, A. (2015). Adenosine-associated delivery systems. Journal of drug targeting, 23(7-8), 580–596. https://doi.org/10.3109/1061186X.2015.1058803
  9. Weberding, N. T., Saladino, R. A., Minnigh, M. B., Oberly, P. J., Tudorascu, D. L., Poloyac, S. M., & Manole, M. D. (2018). Adenosine Administration With a Stopcock Technique Delivers Lower-Than-Intended Drug Doses. Annals of emergency medicine, 71(2), 220–224. https://doi.org/10.1016/j.annemergmed.2017.09.002
  10. Hayes, B.D. (2019). ‘Trick of the Trade: Combine Adenosine with the Flush’. Academic Life in Emergency Medicine Blog Post https://www.aliem.com/trick-of-trade-combine-adenosine-single-syringe/
  11. Choi, S.C., Yoon, S.K., Kim, G.W., Hur, J.M., Baek, K.W., & Jung, Y.S. (2003). A Convenient Method of Adenosine Administration for Paroxysmal Supraventricular Tachycardia. Journal of the Korean society of emergency medicine, 14, 224-227.
  12. McDowell, M., Mokszycki, R., Greenberg, A., Hormese, M., Lomotan, N., & Lyons, N. (2020). Single-syringe Administration of Diluted Adenosine. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 27(1), 61–63. https://doi.org/10.1111/acem.13879
  13. Ribeiro, J. A., & Sebastião, A. M. (2010). Caffeine and adenosine. Journal of Alzheimer’s disease : JAD, 20 Suppl 1, S3–S15. https://doi.org/10.3233/JAD-2010-1379
  14. Cabalag, M. S., Taylor, D. M., Knott, J. C., Buntine, P., Smit, D., & Meyer, A. (2010). Recent caffeine ingestion reduces adenosine efficacy in the treatment of paroxysmal supraventricular tachycardia. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17(1), 44–49. https://doi.org/10.1111/j.1553-2712.2009.00616.x
  15. Hayes, B.D. (2012). ‘Is the 6-12-12 adenosine approach always correct?’ Academic Life in Emergency Medicine Blog Post https://www.aliem.com/is-6-12-12-adenosine-approach-always/
[cite]

Question Of The Day #10

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod10 palpitation

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) IV Adenosine 6mg
  • B) Synchronized cardioversion
  • C) IV Amiodarone 150mg
  • D) Vagal maneuvers

This patient has a narrow-complex tachycardia with a regular rhythm. A narrow QRS complex is defined as a QRS interval less than 120msec. This is a normal finding. The differential diagnoses for regular narrow complex tachycardia include sinus tachycardia, atrial tachycardia, atrial flutter, and supraventricular tachycardia (“SVT”). SVTs are typically associated with narrow QRS complexes, unless there is a concurrent bundle branch block, other aberrant conduction, or the existence of electrical accessory pathways as in Wolff Parkinson White (WPW) syndrome. The heart rate of an SVT can vary from 140-280 beats/min. Intravenous Adenosine (Choice A) is a hallmark of SVT treatment, however, Adenosine is given after vagal maneuvers have been attempted and have failed. Synchronized cardioversion (Choice B) is a last-ditch effort treatment in a patient with SVT. Vagal maneuvers and medications are attempted prior to using cardioversion. However, if the patient is hypotensive, cardioversion should be employed. Intravenous Amiodarone (Choice C), beta-blockers, calcium channel blockers, or other antiarrhythmics can be used to terminate SVTs if vagal maneuvers and adenosine are not effective. Vagal maneuvers (Choice D), such as the Valsalva maneuver (“bearing down”) or carotid massage, are the initial treatment for SVTs. Correct Answer: D 

References

Burns, E. (2019, March 30). Supraventricular Tachycardia (SVT). Life in the Fast Lane. https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Nickson, C. (2019, March 24). Narrow Complex Tachycardia. Life in the Fast Lane. https://litfl.com/narrow-complex-tachycardia/

[cite]

Acute Management of Supraventricular Tachycardias

Acute management of SVT
~ Elif Dilek Cakal, Turkey ~ Leave a comment

The term “supraventricular tachycardia (SVT)” expresses all kinds of rhythms that meet two criteria: Firstly, the atrial rate must be faster than 100 beats per minute at rest. Secondly, the mechanism must involve tissue from the His bundle or above. Mechanism-wise, atrial fibrillation resembles SVTs. However, supraventricular tachycardia traditionally represents tachycardias apart from ventricular tachycardias (VTs) and atrial fibrillation (1,2).

Supraventricular tachycardias are frequent in the ED!

The SVT prevalence is 2.25 per 1000 persons. Women and adults older than 65 years have a higher risk of developing SVT! SVT-related symptoms include palpitations, fatigue, lightheadedness, chest discomfort, dyspnea, and altered consciousness.

How to manage supraventricular tachycardia?

In clinical practice, SVTs are likely to present as narrow regular complex tachycardias. Concomitant abduction abnormalities may cause SVTs to manifest as wide complex tachycardias or irregular rhythms. However, 80% of wide complex tachycardias are VTs. Most importantly, SVT drugs may be harmful to patients with VTs. Therefore, wide complex tachycardias should be treated as VT until proven otherwise (1,2).

The chart below summarizes acute management of regular narrow complex tachycardias:

Acute Management of Regular Narrow Tachycardias
SVT ECGs
Sinus Tachycardia
Chest Pain
iEM Top 10

References and Further Reading

  1. Brugada, J., Katritsis, D. G., Arbelo, E., Arribas, F., Bax, J. J., Blomström-Lundqvist, C., … & Gomez-Doblas, J. J. (2019). 2019 ESC Guidelines for the management of patients with supraventricular tachycardia: the Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). European Heart Journal, 00, 1-66.
  2. Page, R. L., Joglar, J. A., Caldwell, M. A., Calkins, H., Conti, J. B., Deal, B. J., … & Indik, J. H. (2016). 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology, 67(13), e27-e115.