Sinus tachycardia (Figure 18–18 and Table 18-15), the most common narrow-complex tachycardia encountered in the ED, is defined as sinus rhythm with rates greater than 100 beats/min.
Sinus tachycardia at a rate of 110 beats/min.
Table 18–15ECG Features of Sinus Tachycardia ||Download (.pdf) Table 18–15 ECG Features of Sinus Tachycardia
|Normal sinus P waves and PR interval |
|1:1 atrioventricular conduction |
|Atrial rate usually between 100 and 160 beats/min |
Sinus tachycardia should be considered a reactive rhythm, occurring in response to a triggering condition. Generally, sinus tachycardia is a benign rhythm without any end-organ dysfunction.
Because sinus tachycardia is often a compensatory mechanism resulting from a physiologic stress, address the underlying cause, not the rhythm.
ATRIAL FIBRILLATION AND ATRIAL FLUTTER
After sinus tachycardia, atrial fibrillation is the next most frequent narrow-complex tachycardia encountered in the ED; atrial flutter is a less common dysrhythmia. Atrial fibrillation occurs when there are multiple, small areas of atrial myocardium continuously discharging and contracting.20 There is no uniform atrial depolarization and contraction but, rather, only a quivering of the atrial chamber walls, resulting in less than effective ventricular filling and diminished cardiac output.
The ECG hallmarks of atrial fibrillation (Figure 18–19 and Table 18-16) include the absence of discernible P waves and an irregularly irregular ventricular rhythm. With the chaotic atrial activity, distinct P waves are not noted; rather either a flat or chaotic baseline is seen, most prominent in lead V1. The irregularly irregular ventricular rhythm results from the atrial chaos and the variable conduction of impulses through the AV node to the ventricle. The atrial rate in atrial fibrillation is often greater than 600 beats/min, whereas the ventricular rate is markedly lower due to the refractory period of the AV node; in atrial fibrillation where the AV node is unaffected by disease or medications, the ventricular rate is typically 120 to 170 beats/min. Illnesses or medications may reduce AV node conduction and markedly slow ventricular response. A very rapid ventricular response (>200 beats/min) may be seen in patients with accessory or bypass tracts (discussed later in this chapter).
Three examples of atrial fibrillation with irregular ventricular response.
Table 18–16ECG Features of Atrial Fibrillation ||Download (.pdf) Table 18–16 ECG Features of Atrial Fibrillation
|Absence of discernible P waves with flat or chaotic isoelectric baseline |
|QRS complexes narrow unless preexisting bundle-branch block or preexcitation syndrome |
|Irregularly irregular ventricular rhythm |
In contrast to atrial fibrillation, atrial flutter most often is a regular rhythm (Figure 18–20 and Table 18-17); in rare cases, it can be irregular. P waves are present and of a single morphology, typically a downward deflection, called flutter waves resembling a saw blade with a "sawtooth" pattern, best seen in the inferior ECG leads and lead V1. Most commonly, the atrial rate is regular, classically around 300 beats/min, varying between 250 and 350 beats/min. The ventricular rhythm is frequently regular and is a function of the AV block. AV ratios of 2:1 are common and produce a ventricular rate around 150 beats/min, whereas a 3:1 AV ratio will result in a ventricular rate of 100 beats/min. Although the degree of AV conduction is often fixed, it may also be variable and create an irregular ventricular response. A regular narrow-complex tachycardia at an approximate rate of 150 beats/min strongly suggests atrial flutter with 2:1 conduction.
Atrial flutter. A. Regular, narrow-complex tachycardia at a ventricular rate of 155 beats/min. B. Atrial flutter with flutter waves most visible in leads 2, 3, and AVF. C. Atrial flutter response to carotid sinus massage inducing transient AV block and unmasking flutter waves.
Table 18–17ECG Features of Atrial Flutter ||Download (.pdf) Table 18–17 ECG Features of Atrial Flutter
|Identifiable P waves |
| Single morphology |
| Negative amplitude ("flutter waves" in "sawtooth pattern") best seen in inferior ECG leads and V1 |
| Atrial rate is regular, usually at 300 beats/min |
|QRS complexes narrow unless preexisting bundle-branch block |
|Ventricular rate regular although occasional irregularity can be seen |
|Ventricular rate often 150 beats/min |
Atrial fibrillation is usually associated with ischemic or valvular heart disease; less common causes include congestive cardiomyopathy, myocarditis, alcohol binge ("holiday heart"), thyrotoxicosis, and blunt chest trauma.20,21 Left atrial enlargement is a common feature of patients with chronic atrial fibrillation. Atrial fibrillation can be paroxysmal (lasting less than 7 days, terminating either spontaneously or with treatment), persistent (sustained longer than 7 days or requiring treatment to terminate), long-standing persistent (lasting continuously longer than 1 year), or permanent (long-standing where a decision has been made not to try to restore normal sinus rhythm).20 New or recent onset is applied to symptomatic patients presenting to the ED without a prior history of atrial fibrillation.
The clinical consequences of atrial fibrillation include loss of atrial contraction, potential for rapid ventricular rates, and risk of arterial embolism. In patients with compromised cardiac function, left atrial contraction contributes significantly to left ventricular filling, so the loss of effective atrial contraction, as in atrial fibrillation, may produce heart failure in these patients. A rapid ventricular rate can impact ventricular filling as well as coronary and systemic perfusion. Atrial fibrillation increases the risk of venous and atrial thrombosis, with potential for pulmonary and systemic arterial embolism. If an atrial thrombus has formed, conversion from atrial fibrillation to sinus rhythm can propel a portion of the thrombosis out into the systemic circulation, and this risk increases with duration of the dysrhythmia. Observational studies note that conversion from new-onset atrial fibrillation that has been present for 12 hours or less carries a 0.3% risk of arterial embolism, whereas that risk is about 1% for durations of 12 to 48 hours before conversion.22 For patients with heart failure and diabetes mellitus, conversion from new-onset (duration <48 hours) atrial fibrillation carries a risk of thromboembolic events as high as 9.8%.23 Conversely, the incidence of thromboembolic events is 0.2% in patients age <60 years and no heart failure.23 After a duration of >48 hours, the risk of conversion-induced thromboembolic events is increased across all patient groups and a period of anticoagulation is recommended prior to conversion.20,24
Treatment of atrial fibrillation in the ED involves three issues: ventricular rate control, rhythm conversion, and anticoagulation to prevent arterial embolism.24-26 Treatment varies according to patient stability, duration of symptoms, and chronicity of atrial fibrillation (paroxysmal, persistent, or permanent). Review prior records to identify past episodes or treatment for atrial fibrillation. For new-onset atrial fibrillation, consider checking thyroid function.27 For patients on warfarin, check the prothrombin time. Calculate either the CHADS2 or CHA2DS2-VASc score to risk-stratify the potential for future arterial embolic complications; a CHADS2 score of 0 or a CHA2DS2-VASc score of 0 or 1 identify low-risk patients (Table 18-18).20,21
Table 18–18CHADS2 and CHA2DS2-VASc scores ||Download (.pdf) Table 18–18 CHADS2 and CHA2DS2-VASc scores
|Criteria ||CHADS2 ||CHA2DS2-VASc |
|Congestive heart failure ||1 ||1 |
|Hypertension ||1 ||1 |
|Age ≥75 y ||1 ||2 |
|Diabetes mellitus ||1 ||1 |
|Stroke, TIA, or thromboembolism ||2 ||2 |
|Vascular disease (CAD, PAD) ||– ||1 |
|Age 65–74 y ||– ||1 |
|Sex (female) ||– ||1 |
|Range ||0–6 ||0–9 |
For patients with paroxysmal atrial fibrillation or acute medical conditions producing atrial fibrillation, a period of observation and treatment in the ED is appropriate as the atrial fibrillation may spontaneously convert.12,28 Up to 70% of otherwise healthy ED patients evaluated for acute-onset atrial fibrillation will spontaneously convert within 48 to 72 hours.29 Ventricular rate control may help control symptoms until conversion. Also, it is more difficult to achieve rate or rhythm control of atrial fibrillation in patients with acute underlying medical illness, and such attempts are associated with an increased incidence of adverse events.30
For patients with recent-onset atrial fibrillation and a rapid ventricular response that is producing hypotension, myocardial ischemia, or pulmonary edema, treat with urgent electrical cardioversion.20,24,25,31 When possible, first determine if the patient has long-standing atrial fibrillation because electrical cardioversion is not likely to succeed, and instead, initiate ventricular rate control treatment. If the patient is at increased risk for embolic complications (CHADS2 or CHA2DS2-VASc scores ≥1, mechanical heart value, or rheumatic valvular disease), consider anticoagulation with heparin before or immediately after electrical cardioversion and continue that as a bridge to oral anticoagulants.31
For stable low-risk patients in the ED with new-onset atrial fibrillation, either rate-control or rhythm-conversion strategies are appropriate (Table 18-19).20,24,25 The rate-control approach consists of initiating medications that block the AV node to control the ventricular response, initiating oral anticoagulants to prevent thromboembolism (if appropriate), and re-evaluation after 3 to 4 weeks for elective cardioversion. The rhythm-conversion approach uses electrical or pharmacologic methods to convert the patient back into sinus rhythm while in the ED.
Table 18–19Typical ED Management of Atrial Fibrillation/Fluttertin_ch18fn9 ||Download (.pdf) Table 18–19 Typical ED Management of Atrial Fibrillation/Fluttertin_ch18fn9
|DILTIAZEM ||Metoprolol |
|1. Diltiazem, 15-20 milligrams IV bolus over 2 minutes; may repeat bolus if inadequate rate response. ||1. 5 mg IV; may repeat every 5 minute to total of 15 mg |
|2. Once satisfactory rate response, begin IV infusion 5-10 milligrams/hr ||2. Once satisfactory rate response, given oral metoprolol, as 12.5 mg po per 5 mg IV metoprolol |
|3. Begin transition to oral diltiazem, 60-90 milligrams po for 5 or 10 milligrams drip rate, respectively || |
|4. Stop IV infusion 2 hours after oral dose || |
| || |
|CARDIOVERSION REQUIREMENTS || |
|Atrial Flutter ||May require as little as 25-50 j |
|Atrial Fibrillation ||150-200 j |
Control of the ventricular response is done using a calcium channel blocker (diltiazem) or β-blockers (metoprolol and esmolol) with limited data favoring more effective acute rate control with diltiazem.32 If β-blockers or calcium channel blockers are ineffective, intravenous procainamide or amiodarone is an option to slow the ventricular response. The goal for rate control is a ventricular rate of <100 beats/min at rest.25
Electrical cardioversion using 150 to 200 J can terminate atrial fibrillation allowing for sinus rhythm to resume.24,31 Conversion to and retention of sinus rhythm is more likely when atrial fibrillation is of short duration (<48 hours) and the atria are not greatly dilated. Observational analysis also notes that administration of rate-control or rhythm-conversion medications prior to electrical cardioversion attempts is associated with a reduced rate of successful conversion to sinus rhythm.33 Although ED electrical cardioversion is effective in many atrial fibrillation patients34 and observational studies indicate shorter ED length of stay,26 there has been mixed acceptance of this approach.35-37 As noted above, a significant portion of patients with new-onset atrial fibrillation will spontaneously convert to sinus rhythm within 24 hours of onset and evaluation.12,28,29,38,39 This rate of spontaneous conversion coupled with the results of atrial fibrillation trials demonstrating that rate-control is similar to rhythm-control in terms of several key endpoints indicates no proven benefit for conversion of all new atrial fibrillation patients to sinus rhythm while in the ED.24,38,39 The patient with new-onset atrial fibrillation who is stable can certainly be managed with rate-control alone, either as an inpatient or outpatient depending overall clinical condition.
The antiarrhythmics procainamide, ibutilide, flecainide, propafenone, and vernakalant can chemically convert atrial fibrillation to sinus rhythm.24,40,41 Of the five, ibutilide has the highest consistent success rate for conversion. Ibutilide should not be given in the presence of hypokalemia, prolonged QT interval, or history of heart failure, as torsade de pointes may be initiated. This risk of torsade de pointes persists for 4 to 6 hours after the ibutilide is given. Pharmacologic conversion therapy is best avoided if duration is unknown or greater than 48 hours, allowing for heart clot detection and anticoagulation prior to any attempt.
Patients with recurrent paroxysmal atrial fibrillation are sometimes given oral medications (usually flecainide or propafenone) to be taken at the onset of the dysrhythmia; this "pill in a pocket" approach is successful in selected outpatients.24 This approach should only be used in patients with paroxysmal episodes after SA or AV node dysfunction, conduction disturbance (bundle branch block, Brugada syndrome), and structural heart disease have been excluded.2
Atrial flutter is managed in the same fashion as atrial fibrillation: either rhythm conversion or ventricular rate-control with β-blockers or calcium channel blockers.24 Atrial flutter is very responsive to electrical cardioversion; as little as 25 to 50 J is often effective. In general, patients in atrial flutter tend to better tolerate the dysrhythmia hemodynamically than patients with atrial fibrillation. This "hemodynamic toleration" results from the organized atrial contraction seen with atrial flutter, as opposed to the lack of organized atrial contraction with atrial fibrillation. Despite organized atrial activity, there is a risk of arterial embolism with atrial flutter,42 and corresponding recommendations for anticoagulation are based on the same criteria used for atrial fibrillation.25
Patients with chronic atrial fibrillation and planned cardioversion should be anticoagulated for 3 to 4 weeks, assuming clinical stability allows such an approach.20 Patients with permanent atrial fibrillation are at increased risk for embolic stroke, and oral anticoagulation can reduce that occurrence. The benefits of oral anticoagulation are counterbalanced by the potential adverse effects, usually hemorrhagic events. Clinical scoring tools, such as the CHA2DS2-VASc, can be used to guide the decision to initiate long-term oral anticoagulation therapy in atrial fibrillation patients.20,21
Significant regional variation for hospitalization after an ED visit for atrial fibrillation has been reported, reflecting the interplay between patient clinical, socioeconomic, and hospital characteristics.43 Admission is indicated when the patient’s clinical status identifies distress with the need for continued therapy; such as heart failure with pulmonary congestion and continued respiratory distress, or ongoing myocardial ischemia.44 Occasionally, admission is advised when ventricular rate control cannot be achieved and the patient has persistent symptoms.44 Conversely, 80% or more of patients with atrial fibrillation can be discharged from the ED after rate or rhythm control with low risk for stroke or death within 30 days.45 For patients with atrial flutter converted to sinus rhythm with electrical cardioversion, about 90% can be discharged with a very low incidence of stroke within the following year.46 A protocol is useful to ensure that the patient with persistent dysrhythmia is discharged with appropriate medications and plan for follow up (Table 18-20 and Table 18-21).47
Table 18-20.Example Protocol for Discharge of Patient with Persistent Atrial Fibrillation or Flutter ||Download (.pdf) Table 18-20. Example Protocol for Discharge of Patient with Persistent Atrial Fibrillation or Flutter
|Patient is breathing comfortably on room air with SaPO2 > 95% and BP is at baseline |
|Ventricular rate has been controlled to a rate less than 100 bpm at rest |
|For nonvalvular atrial fibrillation patients not converted to sinus rhythm, determine risk for embolic stroke by calculating the CHA2DS2-VASc score |
CHA2DS2-VASc = 0: oral anticoagulation not recommended
CHA2DS2-VASc = 1: either no anticoagulation or oral anticoagulant are acceptable
CHA2DS2-VASc ≥ 2: oral anticoagulation recommended, consult follow-up specialist for specific agent
|Consult with internist or cardiologist to arrange early follow-up (within 7 days) and choose medications for rate and/or rhythm control and oral anticoagulants upon discharge (Table 18-21) |
|Arrange outpatient echocardiography for patients with new-onset atrial fibrillation or flutter |
|Discharge patient with prescriptions for rate and/or rhythm control, and oral anticoagulant if indicated, in quantity only sufficient to last until follow-up appointment |
Table 18-21.Rate Control and Oral Anticoagulation Medications used on Discharge of Patients with Persistent Atrial Fibrillation or Flutter ||Download (.pdf) Table 18-21. Rate Control and Oral Anticoagulation Medications used on Discharge of Patients with Persistent Atrial Fibrillation or Flutter
| ||Typical Initial Dose ||Comments |
|Rate Control Medications |
|Diltiazem ||30 mg PO QID (120 mg/d) non-sustained release form, increase dose if needed for ventricular rate control up to 480 mg/d; typical maintenance dose 360 mg/d ||More effective than metoprolol in controlling heart rate and reducing dysrhythmia-related symptoms |
Avoid in patients with heart failure with reduced ejection fraction
Can switch to a slow-release/extended release dose when rate control dose established
|Metoprolol ||25 mg PO BID (50 mg/d) nonsustained release form, increase dose if needed for ventricular rate control up to 200 mg/d; typical maintenance dose 100 mg/d ||Can switch to a slow-release/extended release dose when rate control dose established |
|Oral Anticoagulants |
|Warfarin ||5 mg PO daily ||Half-life 20 – 60 hours, mean 40 hours |
Preferred regimen if CrCl < 15 mL/min
|Enoxaparin ||1 mg/kg SC q 12h |
Reduce dose if CrCl <30 mL/min
|See text comments about bridging parenteral anticoagulation |
|Dabigatran etexilate mesylate ||150 mg PO BID (if CrCl >30 mL/min) |
75 mg PO BID (if CrCl 15 - 30 mL/min)
|Half-life 12-17 hours |
|Rivaroxaban ||20 mg PO daily with evening meal (if CrCl >50 mL/min) |
15 mg PO daily with evening meal (if CrCl 15 - 50 mL/min)
|Half-life 5-9 hours |
|Apixaban ||5 mg PO BID |
2.5 mg PO BID in patients with at least 2 of the following characteristics: age ≥80 years, body weight ≤60 kg, or serum creatinine ≥1.5 mg/dL
|Half-life during repeat oral dosing 12 hours |
Oral anticoagulation is used to reduce the incidence of embolic stroke in patients with atrial fibrillation or flutter.48 Practical factors such as co-morbidities, convenience, and cost should be considered when selecting the specific oral anticoagulant. For patients at short-term high risk for thromboembolism (e.g., CHA2DS2-VASc ≥ 7, prior stroke, intracardiac thrombus, biosynthetic valve, mitral stenosis), bridging therapy with a parenteral anticoagulant, such as enoxaparin, is reasonable when starting warfarin. Enoxaparin is started at the same time as the warfarin and continued until the INR is within the therapeutic range – 2.0 to 3.0 for nonvalvular atrial fibrillation. For patients at low risk for short-term thromboembolism (e.g., nonvalvular atrial fibrillation and no prior history of thromboembolism), the incidence of a thromboembolic event during the few days required to achieve therapeutic anticoagulation upon starting warfarin is so low as to obviate the need for bridging parenteral anticoagulation. It is best to consult with the appropriate specialist who will be following the patient after ED discharge to discuss the specific agent to be used.
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
Paroxysmal supraventricular tachycardia most frequently results from sustained reentry occurring with the AV node, with an ectopic atrial focus accounting for the remaining 15% to 20%. In paroxysmal supraventricular tachycardia (Figure 18–21 and Table 18-22), the QRS complex is of normal width, rapid, and regular. P waves are "buried" within the QRS complex in about 70% of cases. In the others, a P wave (so-called "retrograde" P wave) is found immediately adjacent before, during, or after the QRS complex without a measurable PR interval.
Paroxysmal supraventricular tachycardia.
Table 18–22ECG Features of Paroxysmal Supraventricular Tachycardia ||Download (.pdf) Table 18–22 ECG Features of Paroxysmal Supraventricular Tachycardia
|Absence of normal (sinus-mediated) P waves with normal PR interval |
|Rare retrograde P wave (usually inverted P wave and immediately adjacent to QRS complex, pre or post) |
|Narrow QRS complex, usually <100 ms in duration |
|Ventricular rate usually 170–180 beats/min; the rate can range from as low as 130 beats/min to as high as 300 beats/min |
Paroxysmal supraventricular tachycardia is seen more frequently in females, with a peak in the late teenage and young adult years. The majority of patients are without active cardiovascular disease.49 Patients may be able to describe the abrupt onset of this reentrant dysrhythmia and also note when it self-terminates. Palpitations, lightheadedness, and dyspnea are common symptoms.
If applied early in the dysrhythmia course, vagal maneuvers are often effective (Table 18-3).10,11 Attention to technique is important to maximize success rate. If there is no response to vagal maneuvers, adenosine IV is recommended to convert to sinus rhythm.9 It is the rare patient who requires β-blocker or calcium channel blocker. In patients with recalcitrant paroxysmal supraventricular tachycardia or who are unstable, use electrical cardioversion to convert the dysrhythmia.
MULTIFOCAL ATRIAL TACHYCARDIA
Multifocal atrial tachycardia is an irregular rhythm resulting from at least three different atrial ectopic foci competing to pace the heart. The electrocardiographic characteristics (Figure 18–22 and Table 18-23) require at least three distinct P-wave morphologies. Due to irregularity and the chaotic appearance of atrial depolarization, multifocal atrial tachycardia is often confused with atrial fibrillation or atrial flutter.
Multifocal atrial tachycardia. Note multiple P-wave morphologies with irregular tachycardia rhythm.
Table 18–23ECG Features of Multifocal Atrial Tachycardia ||Download (.pdf) Table 18–23 ECG Features of Multifocal Atrial Tachycardia
|At least 3 distinct P-wave morphologies in a single ECG lead |
|No consistent P to P, PR, or R to R intervals |
|Irregularly irregular rhythm with rates usually 100–180 beats/min |
|Normal QRS complex unless preexisting bundle-branch blocks |
|Frequently confused with atrial fibrillation or flutter |
Multifocal atrial tachycardia is found most often in elderly patients with decompensated chronic lung disease, but may also complicate heart failure or sepsis.
Treatment is directed toward the underlying disorder. With decompensated lung disease, oxygen and bronchodilators improve pulmonary function and arterial oxygenation and decrease atrial ectopy. Antidysrhythmic treatment is not indicated, and cardioversion has no effect.