A heart rate > 100 bpm in an adult is called tachycardia. However, significant signs and symptoms are unlikely with heart rates < 150 bpm.

As with the treatment of bradycardias, it is essential to determine whether the patient’s symptoms are related to having a fast heart rate. Patients with significant signs and symptoms related to tachycardia often require cardioversion, while it is appropriate to treat stable patients with medications first.

Students must be able to identify the following rhythms to master this case:

• Sinus tachycardia

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• Atrial fibrillation

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• Atrial flutter

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• Supraventricular tachycardia (SVT)

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• Wide complex tachycardia
  • Monomorphic VT
  • Polymorphic VT

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Adult Tachycardia

Short Description

This algorithm outlines the steps to guide the team to efficiently assess the patient and manage tachycardia with a pulse.

Algorithm at a Glance

• The responder identifies tachycardia and assesses the patient to determine if the heart rate is appropriate for the patient’s condition.
• If possible, the responder identifies and treats the cause of the tachycardia.
• Vagal maneuvers may be attempted if the patient’s condition allows it.
• If the patient is symptomatic, the team considers administering sedation followed by synchronized cardioversion.

Goals for the Management of Adult Tachycardia

The team must succeed in the following goals to successfully manage tachycardia:

• Identify the tachycardic rhythms, including:
  • Sinus tachycardia
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardia (SVT)
  • Wide complex tachycardia

• Identify symptomatic tachycardia with a pulse.
• Appropriately treat the patient with symptomatic tachycardia with a pulse.

The Adult Tachycardia Algorithm

This algorithm was created to outline the steps for assessing patients presenting with symptoms and managing their tachycardia.

Adult Tachycardia With a Pulse Algorithm

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Box 1: Assessing Appropriateness of Heart Rate for Patient’s Condition

A fast heart rate may be due to a physiologic response to stress, such as dehydration or fever. Significant tachyarrhythmia, however, is a heart rate > 150 bpm. Clinicians agree that when the heart rate is < 150 bpm, patients are unlikely to experience symptoms and instability unless there is preexisting impaired ventricular function.

When diagnosing a patient, the clinician must distinguish whether the tachyarrhythmia is a primary cause of the patient’s symptoms or a result of physiologic stress from other disease conditions.

Some causes of tachycardia are tachyarrhythmia and physiologic stress.

Box 2: Identifying and Treating the Underlying Cause

Hypoxemia can cause tachycardia, which is quite common. The team treats symptomatic patients based on the signs and symptoms of increased breathing effort (e.g., tachypnea and intercostal retractions). Oxygen saturation should be determined immediately using a pulse oximeter and oxygen administered to the hypoxemic patient.

The patient should be monitored carefully using a cardiac monitor and with intermittent blood pressure readings. A 12-lead ECG can better evaluate the tachyarrhythmia diagnosis, but cardioversion should not be delayed if it is indicated.

At this stage, the team looks at the possible causes of tachyarrhythmia and treats it promptly. A decision to seek expert help may be made at any time during the management of tachycardia.

Box 3: Tachycardia with Persistent Symptoms

After initial evaluation and treatment with airway and oxygen supplementation, the patient may have ongoing symptoms. The clinician determines that the symptoms are due to the tachyarrhythmia and diagnoses it as the primary cause.

Unstable symptoms are secondary to reduced cardiac output, as the heart beats too fast or ineffectively due to a lack of coordination between the atria and ventricles. Especially when persistent, this arrhythmia can cause hypotensive symptoms, altered mental status, chest discomfort, acute heart failure, and signs of shock.

If the patient is hemodynamically stable, the team proceeds to Box 4. If hemodynamically unstable, they proceed to Box 5.

Box 4: Synchronized Cardioversion

Before administering synchronized cardioversion to a patient with unstable tachyarrhythmia, the team attempts to establish IV or IO access for possible sedation. Although sedation is preferable for the conscious patient, cardioversion should not be delayed if the patient is unstable, as cardiac arrest may ensue.

Synchronized cardioversion is a method of delivering a shock that is in sync with the QRS complex (delivered at the peak of the R wave). A shock during the relative refractory period of the cardiac cycle in tachyarrhythmias can produce VF, thus worsening the condition of the patient.

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If the tachyarrhythmias have polymorphic QRS complexes (i.e., torsades de pointes) in the ECG tracing, synchronization cannot occur. Thus, attempting synchronized cardioversion would be ineffective, and the team should treat torsades de pointes like VF with unsynchronized defibrillation.

Some patients with a regular, narrow complex tachycardia may respond to adenosine administration rather than cardioversion.

No data are available to recommend one type of biphasic defibrillator over another. Responders should follow the manufacturer’s recommended energy level to maximize the chances of first shock success.

Box 5: Is the QRS Complex Regular or Wide?

Wide-Complex Tachycardia

If the patient is stable and does not require immediate cardioversion, it must be determined whether the QRS is normal or wide (> 0.12 seconds).

An unstable patient diagnosed with wide complex tachycardia should be presumed to have VT, and the appropriate treatment is cardioversion. The team proceeds to Box 6.

If a defibrillator is not immediately available in a case of witnessed, monitored unstable ventricular tachycardia, the responder can attempt a precordial thump unless doing so would delay definitive treatment.

If the QRS is < 0.12 seconds, the team proceeds to Box 7.

VT is a common form of wide-complex tachycardia. SVT with aberrancy, pre-excited tachycardias, and ventricular paced rhythms are also wide-complex tachycardias that can either be VT or SVT with aberrancy. The only difference is that SVT with aberrancy is, as the name suggests, supraventricular.

To distinguish between the two, the team can treat SVT with aberrancy with AV-nodal blocking agents. However, patients with VT may suffer precipitous hemodynamic deterioration if erroneously administered an AV-nodal blocking agent. An electrocardiographic differentiation between the two is not always possible. It is critical to seek expert consultation when there is difficulty in determining the patient’s rhythm.

The team must determine if the wide-complex tachycardia has a regular or irregular rhythm. If it has a regular rhythm, then it is likely due to VT or SVT with aberrancy. An irregular rhythm is due to atrial fibrillation (AF) with aberrancy, pre-excited AF, or torsades de pointes. Teams may need to seek expert help in diagnosing wide-complex tachycardia. 

Box 6: Therapy for Wide-Complex Tachycardia

It is ideal first to identify if the wide-complex tachycardia is due to VT or SVT with aberrancy and determine the proper treatment as suggested in the algorithm. If the team is unable to distinguish between the two, it is reasonable to treat the patient with IV adenosine to provide a diagnostic benefit if the patient is stable.

Continuous ECG monitoring is necessary. If the rhythm changes to sinus after adenosine, then the wide-complex tachycardia was due to SVT with aberrancy. If the rhythm does not improve, then adenosine has not affected the rhythm (apart from idiopathic VT, which is rare).

Adenosine 6 mg is administered as a rapid IV push followed by a 20 mL normal saline flush. If the rhythm fails to convert, then it can be followed with 12 mg of adenosine. A defibrillator is always on standby when giving this treatment. At this point, the team leader considers an antiarrhythmic infusion and expert consultation.

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If the patient is unstable, adenosine might cause the rhythm to revert to VF, which is more detrimental, causing hemodynamic failure. Hence, unstable wide-complex tachycardia is a contraindication for adenosine.

Verapamil should not be used for wide-complex tachycardia unless it is supraventricular in origin.

It is appropriate to give IV antiarrhythmics such as procainamide, amiodarone, or sotalol for wide-complex tachycardias. However, for patients with prolonged QT intervals, procainamide and sotalol should be avoided.

Whenever antiarrhythmic therapy fails, it is appropriate to try cardioversion, and the team leader should consider expert consultation.

Procainamide can terminate hemodynamically stable monomorphic VT.⁴³ It can be administered via IV infusion at a rate of 20–50 mg/min until termination of the arrhythmia or an adverse reaction occurs. Common adverse reactions include hypotension and an increase in QRS duration. The maintenance infusion should be set at a rate of 1–4 mg/min. Patients with congestive heart failure or a prolonged QT interval should not be given procainamide.

Sotalol is given at a dosage of 100 mg (1.5 mg/kg) via slow IV push over 5 minutes. This is an appropriate treatment for monomorphic VT in hemodynamically stable patients. It is not to be used in patients with prolonged QT intervals.

Amiodarone can be used to prevent recurrent monomorphic VT or to treat patients with coronary artery disease with low ejection fraction and refractory ventricular arrhythmias. In ACLS, amiodarone is now considered a first-line antiarrhythmic for cardiac arrest since studies show it increases the chance of ROSC.

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Amiodarone Administration Guidelines

Regular Narrow-Complex Tachycardia

Sinus Tachycardia

Sinus tachycardia is a product of physiologic stimulus from clinical conditions such as fever, anemia, or shock. It is defined as a rate > 100 bpm.

Patients with sinus tachycardia do not require specific drug treatment. However, when symptoms persist, treatment is indicated depending on the underlying cause.

In cases with reduced cardiac function, the cardiac output might be reliant on a fast heart rate. And treating these patients to normalize heart rate may cause more harm.

Supraventricular Tachycardia

Most SVT rhythms are caused by a reentrant circuit, which produces impulses that travel circularly within the myocardium. QRS complexes < 0.12 seconds are considered narrow and are characteristic of SVT. SVT can also present with wide QRS complexes (> 0.12 seconds) if there is a pre-existing bundle branch block or a rate-dependent aberrancy.

These reentrant circuits can occur above the ventricles, such as in the atrial myocardium, causing atrial fibrillation (AF) or atrial flutter (AFL). They can also occur in the AV node itself.

If the circuit has both limbs in the AV node, it results in an AV-nodal reentry tachycardia (AVNRT). If the circuit has one limb in the AV node and the other is an accessory pathway, it is known as an AV reentry tachycardia. Combined, these are known as paroxysmal supraventricular tachycardia (PSVT). They create a regular rate exceeding 150 bpm. AVNRT does not exhibit a P wave.

An excited automatic focus can cause supraventricular tachycardias. The focus forms a gradual increase or decrease in the heart rate, similar to impulses in the sinoatrial (SA) node. They can also cause ectopic atrial tachycardias, multifocal atrial tachycardias (MATs), and junctional tachycardias. They are challenging to treat and do not respond to synchronized cardioversion. Regulating them with drugs can slow the conduction through the AV node, which slows the ventricular rate.

Box 7: Narrow Complex Tachycardia

For a narrow-complex tachycardia, the team obtains IV or IO access and a 12-lead ECG. It is reasonable to attempt vagal maneuvers and adenosine. The team leader may order β-blockers or calcium channel blockers and call for an expert consultation.

Box 8: Persistent Tachycardia

In the presence of refractory tachycardia, the team determines the underlying cause and considers adding antiarrhythmic medications.

Vagal Maneuvers

Vagal maneuvers and adenosine are the preferred initial management for PSVT. Maneuvers such as the Valsalva or carotid massage can terminate up to 25% of PSVTs.⁴⁴ However, for other SVTs, these maneuvers or adenosine will only temporarily slow the ventricular rate and do not terminate the tachyarrhythmia.

Vagal maneuver.

Adenosine

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Adenosine is the preferred treatment for PSVT. It is given as a dose of 6 mg via rapid IV push in a large vein, followed immediately by a 20 mL NS flush due to its short half-life.

In patients that may have Wolff-Parkinson-White syndrome, adenosine should be used with caution because it can cause AF. A defibrillator should be on standby during administration. Like vagal maneuvers, adenosine is a temporary intervention for treating SVTs other than PSVT.

Amiodarone is a substitute for adenosine in treating PSVT. It also has the same efficacy. However, amiodarone has a slower therapeutic effect compared with adenosine, and it also has a risk for proarrhythmic effects. Therefore, most clinicians select adenosine over amiodarone.

Adenosine is safe to use in pregnancy but contraindicated in patients with asthma. The dose should be reduced to 3 mg if administered via a central line or if a patient has taken dipyridamole or carbamazepine. Higher doses may be necessary for patients who have high levels of theophylline, caffeine, or theobromine.

After successful cardioversion with adenosine, the patient needs to be monitored continuously. If there is a recurrence of PSVT, adenosine can be given again as a 12 mg dose.

Another substitution is a longer-acting AV nodal blocking agent such as diltiazem or β-blockers. If, after treatment with adenosine, the patient develops another form of SVT, the clinician may consider using longer-acting AV nodal blocking agents to produce a longer-lasting control of the ventricular rate.

Calcium Channel Blockers and Beta-Blockers

The clinician should use calcium blockers (diltiazem or verapamil) or β-blockers to treat persistent PSVT, recurring PSVT, or other forms of SVT produced after treatment of PSVT.

These medications act on AV nodal-dependent PSVT by causing nodal tissue to terminate the reentry, and they block AV nodal conduction in SVT. A long durational effect results in a sustained termination of PSVT and control of atrial tachyarrhythmias. Studies have shown that verapamil and diltiazem convert PSVT to normal sinus rhythm.⁴⁵,⁴⁶,⁴⁷ 

Verapamil is given at a dose of 2.5–5 mg IV bolused over 2 minutes. For older individuals, it is given over 3 minutes. Repeated doses of 5–10 mg every 15 to 30 minutes may be necessary to achieve the desired effect. Verapamil should be reserved for patients with narrow-complex reentry SVT or other arrhythmias that are supraventricular in origin. Verapamil is contraindicated in patients with wide-complex tachycardias or heart failure.

Diltiazem is given at a dose of 15–20 mg as a slow IV push over 2 minutes. It can be repeated at a dose of 20–25 mg if the desired effect does not occur within 15 minutes. The maintenance infusion dose is 5–15 mg/hour titrated to achieve the desired heart rate.

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Metoprolol, atenolol, propranolol, esmolol, and labetalol can be used to treat SVT. These medications work by antagonizing the nodal tissue’s sympathetic tone, resulting in slowing of the conduction. They also have negative inotropic effects that can potentially reduce cardiac output. These medications are used with caution in patients with heart failure or obstructive pulmonary disease. Other side effects of β-blockers include bradycardia, AV conduction delays, and hypotension.

The use of adenosine, calcium channel blockers, or β-blockers in patients with pre-excited AF or AFL that conducts to the ventricles through the AV node and an accessory pathway is unlikely to slow the ventricular rate and may even increase it. These drugs should not be administered in these situations.

Combining AV nodal blocking agents may cause profound bradycardia if given serially. Hence, the clinician must avoid overlapping these treatments, keeping in mind that doing so can potentiate their effects.

Irregular Tachycardias

Atrial Fibrillation and Flutter

If the rate is irregular, a narrow-complex or wide-complex tachycardia is most likely AF with an uncontrolled ventricular response. A 12-lead ECG should be obtained to get a more accurate diagnosis.

Therapy

The focus of treatment for AF is on rate control and conversion to sinus rhythm or both. If this rhythm lasts for more than 48 hours, patients are at risk of a cardioembolic event. Electrical or pharmacologic cardioversion should only be undertaken in patients who are adequately anticoagulated unless they are unstable.

Other strategies suggest combining cardioversion and heparin anticoagulation, which involves the use of transesophageal echocardiography to ensure that a thrombus has not yet formed.