The severity of signs and symptoms associated with an irregular tachycardia varies depending on the ventricular rate, how long the rhythm has been present, and the patient ’s cardiovascular status. The patient may be asymptomatic and not require treatment or may experience serious signs and symptoms.
It is best to seek expert consultation when treating a patient who has an irregular tachycardia.
Multifocal Atrial Tachycardia [Objectives 1, 2, 3]
Multifocal AT (MAT) is an automatic tachycardia that is the result of the random and chaotic firing of multiple ectopic sites in the atria. At least three different P wave configurations (seen in same lead) are required for a diagnosis of MAT ( Table 5.10, Fig. 5.12). MAT is an irregular rhythm with a ventricular rate faster than 100 beats/min; it is most often found in patients with advanced pulmonary disease.
Because MAT can be difficult to treat, it is best to consult a cardiologist before starting treatment.
Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG.
The treatment of MAT is directed at the underlying cause (eg, hypoxia, acidosis, electrolyte distur-bances). If the rhythm persists, evaluate the clinical signif icance of the tachycardia before considering the use of antiarrhythmics (Mottram & Svenson, 2011). Because MAT does not involve reentry through the AV node, it is unlikely that vagal maneuvers or giving adenosine will terminate the rhythm. Metoprolol has been shown to be effective for rate control, but it should be avoided in patients with impaired left ventricular function or bronchospastic pulmonary disease; in such cases, amiodarone may be preferred (Mottram & Svenson, 2011; Olgin & Zipes, 2012). MAT is unresponsive to cardioversion (Link, et al., 2015).
TABLE 5.10 Characteristics of Multifocal Atrial Tachycardia
Regularity Irregular; the pacemaker site shifts from the SA node to ectopic atrial locations or the AV junction
Rate Ventricular rate faster than 100 beats/min
P waves Size, shape, and direction may change from beat to beat; at least three different P wave configurations (seen in same lead) are required for a diagnosis of MAT
PR interval Varies; the pacemaker site shifts from the SA node to ectopic atrial locations or the AV junction QRS duration 0.11 sec or less unless abnormally conducted
AT, atrial tachycardia; AV, atrioventricular; MAT, multifocal atrial tachycardia; SA, sinoatrial.
Atrial Flutter [Objectives 1, 2, 3]
Atrial flutter is a macroreentrant AT in which an irritable site within the atria fires regularly at a very rapid rate ( Table 5.11). Because of this extremely rapid stimulation, atrial waveforms are produced that resem-ble the teeth of a saw, or a picket fence; these are called flutter waves or F waves (Fig. 5.13).
Typical atrial flutter is caused by reentry in which an impulse circles around a large area of tissue, such as the entire right atrium in a counterclockwise direction. F waves are predominantly negative in leads II, III, and aVF, and positive in V 1 ( January, et al., 2014). The atrial rate is typically 240 to 300 beats/min ( January, et al., 2014).
It is best to consult a cardiologist when considering treatment options. Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG. Vagal maneuvers may help to identify the rhythm by temporarily slowing AV conduction and revealing the underlying flutter waves (see Fig. 5.13). When vagal maneuvers are used in the management of atrial flutter, the response is usuallysudden slowing and then a return to the former rate. Vagal maneuvers will not usually convert atrial flutter because the reentry circuit is located in the atria, not the AV node.
ACLS Pearl
The two primary treatment strategies used to control symptoms associated with atrial flutter or AFib are rate control and rhythm control. With rate control, the patient remains in atrial flutter or AFib but the ventricular rate is controlled to decrease acute symptoms, reduce signs of ischemia, and reduce or prevent signs of heart failure from developing. With rhythm control, sinus rhythm is reestablished.
When a rate control strategy is considered for the patient with atrial flutter and a rapid ventricular response, medications such as beta-blockers or nondihydropyridine calcium channel blockers (eg, verap-amil, diltiazem) are the drugs of choice (Link, et al., 2015). When a rhythm control strategy is consid-ered, it is best to consult a cardiologist (Link, et al., 2015). The short-acting antiarrhythmic ibutilide ( Table 5.12) may be ordered for pharmacologic rhythm control, provided there are no contraindications to its use (Bontempo & Goralnick, 2011). Successful pharmacologic cardioversion with ibutilide has reportedly occurred in 60% to 90% of episodes of atrial flutter (Olgin & Zipes, 2012). Excessive QT Fig. 5.12 MAT. (From Braunwald E, Libby P, Zipes DP, et al.: Heart disease: a textbook of cardiovascular medicine, ed 6, St.
Louis, 2001, Mosby.)
TABLE 5.11 Characteristics of Atrial Flutter
Regularity Atrial: regular; ventricular: regular or irregular, depending on AV conduction and blockade Rate The atrial rate generally ranges from 240 to 300 beats/min; the ventricular rate varies and is
determined by AV blockade; the ventricular rate will usually not exceed 180 beats/min as a result of the intrinsic conduction rate of the AV junction
P waves No identifiable P waves; saw-toothed“flutter” waves are present PR interval Not measurable
QRS duration 0.11 sec or less but may be widened if flutter waves are buried in the QRS complex or if abnormally conducted
AV, atrioventricular
144 CHAPTER 5 Tachycardias
interval prolongation, which can cause torsades de pointes (TdP), is a potential complication that can occur during and shortly after ibutilide administration. Because most episodes of ibutilide-induced TdP occur within 1 hour after treatment and almost all occur within 6 hours, continuous ECG
monitoring is essential throughout ibutilide administration and for 6 to 8 hours thereafter (Bontempo & Goralnick, 2011; Olgin & Zipes, 2012). Other medications that are useful for the phar-macologic cardioversion of atrial flutter or AFib include flecainide, dofetilide, and propafenone ( January, et al., 2014).
Prompt synchronized cardioversion should be considered for any patient who is hemodynamically unstable (Link, et al., 2015). If synchronized cardioversion is performed, atrial flutter can be successfully converted to a sinus rhythm with the use of low energy levels. Sedation should be considered when cir-cumstances permit.
Atrial Fibrillation [Objectives 1, 2, 3]
AFib is a SVT characterized by uncoordinated atrial activation and consequently ineffective atrial con-traction ( January, et al., 2014). It occurs because of altered automaticity in one or several rapidly firing sites in the atria or reentry involving one or more circuits in the atria ( Table 5.13, Fig. 5.14). Cardiac output is decreased because of various mechanisms including the loss of effective atrial contraction, irreg-ular cardiac cycle length, rapid heart rates, and decreased coronary blood flow (Goel, et al., 2013).
Patients who experience AFib are at increased risk of atrial thrombus formation, leading to stroke, peripheral thromboembolism, or both ( January, et al., 2014).
II
A
II
B
II CSM
C
Fig. 5.13 Atrial flutter. A, This rhythm strip shows a narrow-QRS tachycardia with a ventricular rate just under 150 beats/min. B, The same rhythm shown in A with arrows added indicating possible atrial activity. C, When CSM is performed, the rate of conduction through the AV node slows, revealing atrial flutter. (From Grauer K: A practical guide to ECG interpre- tation, ed 2, St Louis, 1998, Mosby.)
Atrial flutter or AFib that has a rapid ventricular rate is described as uncontrolled (Figs. 5.15, 5.16).
Atrial flutter or AFib with a rapid ventricular response is commonly called Aflutter with RVR or AFib with RVR.
Obtaining a thorough medical history and patient assessment are important. When obtaining the patient ’s history, asking about the number of episodes of AFib, their frequency, the nature of the patient ’s symptoms, and possible triggers may help to determine the pattern of the dysrhythmia.
It is best to consult a cardiologist when considering specific therapies. Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG.
TABLE 5.13 Characteristics of Atrial Fibrillation
Regularity Ventricular rhythm usually irregularly irregular
Rate Atrial rate usually 400 to 600 beats/min; ventricular rate variable
P waves No identifiable P waves; fibrillatory waves present; erratic, wavy baseline
PR interval Not measurable
QRS duration 0.11 sec or less unless abnormally conducted
II
MCLI
Fig. 5.14 AFib. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.) TABLE 5.12 Ibutilide (Corvert)
Class Class III antiarrhythmic Mechanism of
Action
• Potassium channel blocker; prolongs action potential duration and QT interval
• Mild slowing of the sinus rate and AV conduction
• Rhythm conversion usually occurs within 30 min but may take up to 90 min after the start of the infusion (Gahart, et al., 2016a)
Indications Rapid conversion of recent onset AFib or atrial flutter to sinus rhythm
Dosage 1 mg IV over 10 min; if the dysrhythmia does not terminate within 10 min after the end of the initial dose, a repeat dose of 1 mg may be administered 10 min after completion of the first infusion (Olgin & Zipes, 2012)
Considerations • Avoid if the QTc is longer than 0.44 sec or when uncorrected hypokalemia or bradycardia exists (Olgin & Zipes, 2012)
• Should not be given concurrently with Class IA antiarrhythmics or other Class III antiarrhythmics (eg, amiodarone, sotalol).
• Lengthens the QT interval, increasing the risk of ventricular dysrhythmias, including TdP and monomorphic VT
• During administration, resuscitation equipment must be immediately available and continuous ECG monitoring is essential; ECG monitoring should be continued for at least 4 hours after administration (January, et al., 2014).
• Pretreatment with IV magnesium may reduce the risk of ventricular dysrhythmias (January, et al., 2014).
AFib, atrial fibrillation; AV, atrioventricular; ECG, electrocardiogram; IV, intravenous; QTc, corrected QT interval; TdP, torsades de pointes; VT, ventricular tachycardia
146 CHAPTER 5 Tachycardias
With a rate control strategy, the ventricular rate associated with the AFib is slowed without termi-nation of the AFib and it is achieved using medications that prolong the refractory period of the AV node or catheter ablation (Fuster, et al., 2011; Bontempo & Goralnick, 2011). Treatment of precipitating or reversible causes of AFib is recommended before starting antiarrhythmic therapy ( Wann, et al., 2011).
IV administration of beta-blockers (eg, esmolol, metoprolol, propranolol) or nondihydropyridine cal-cium channel blockers (eg, verapamil, diltiazem) is recommended to slow the ventricular response to AFib ( Anderson, et al., 2013; January, et al., 2014). These medications must be used with caution in patients with hypotension or heart failure. IV amiodarone can be useful for rate control in critically ill patients without preexcitation, but it is less effective than nondihydropyridine calcium channel blockers ( January, et al., 2014).
Rhythm control, that is, termination of AFib and restoring sinus rhythm, is achieved using a com-bination of approaches including pharmacologic or electric cardioversion and radiofrequency catheter ablation. Because pharmacologic or electric cardioversion carries a risk of thromboembolism, anticoagu-lation is recommended before attempting conversion of AFib to a sinus rhythm when the duration of the AFib exceeds 48 hours ( January, et al., 2014). Shorter durations of AFib do not exclude the possibility of
thromboembolism (Link, et al., 2015). For patients who are symptomatic and stable, but the duration of atrial flutter or AFib is unknown, issues with regard to anticoagulation are important. Rate control can be attempted while expert consultation is sought.
Patients who are hemodynamically unstable (eg, angina, heart failure, symptomatic hypotension, ongoing myocardial ischemia, shock, pulmonary edema) should receive prompt synchronized cardiover-sion ( January, et al., 2014). Sedation should be considered when circumstances allow. Anticoagulation should be started as soon as possible and continued for at least 4 weeks after cardioversion unless contra-indicated ( January, et al., 2014).
Although atrial flutter often converts to a sinus rhythm with the use of low energy levels during syn-chronized cardioversion, higher energy levels are required for AFib (Fuster, et al., 2011). Although resus-citation guidelines have traditionally recommended that the energy used during the cardioversion of AFib be increased in successive increments, experts state that the initial use of a higher-energy shock is more effective and may minimize the number of shocks required, as well as the duration of sedation ( January, et al., 2014). Pretreatment with selected antiarrhythmic medications such as ibutilide can be useful to enhance the success of synchronized cardioversion, prevent recurrent AFib, and increase the likelihood of maintenance of sinus rhythm ( January, et al., 2014). For cardioversion of AFib, a biphasic waveform is more effective than a monophasic waveform ( January, et al., 2014). Some, but not all, studies
II
Fig. 5.15 AFib with a rapid ventricular response. (From Aehlert B: ECGs made easy study cards, St. Louis, 2004, Mosby.)
Lead I
Fig. 5.16 AFib with a rapid ventricular response and left BBB. (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed 7, St. Louis, 2006, Mosby.)
have shown anterior – posterior electrode placement superior to anterolateral placement. If cardioversion is attempted using one electrode placement and fails, experts recommend using the alternative placement before attempting another shock ( January, et al., 2014).
Polymorphic Ventricular Tachycardia [Objectives 1, 2, 3]
With PMVT, the QRS complexes vary in shape and amplitude from beat to beat and appear to twist from upright to negative or negative to upright and back, resembling a spindle (Fig. 5.17). The ECG characteristics of PMVT are shown in Table 5.14.
Several types of PMVT and their possible causes have been identified. PMVT that occurs in the pres-ence of a long QT interval (generally, 0.50 second or more) is called torsades de pointes (TdP). A long QT interval may be congenital, acquired (typically precipitated by antiarrhythmic drug use or hypokalemia, which are typically associated with bradycardia), or idiopathic (neither familial nor with an identifiable
acquired cause). PMVT that occurs in the presence of a normal QT interval is simply referred to as poly-morphic VT or normal-QT PMVT.
The signs and symptoms associated with PMVT are usually related to the decreased cardiac output that occurs because of the fast ventricular rate. Signs of shock are often present. The patient may expe-rience a syncopal episode or seizures. The rhythm may occasionally terminate spontaneously and recur after several seconds or minutes, or it may deteriorate to VF. The patient with sustained PMVT is rarely hemodynamically stable.
Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG. It is best to seek expert consultation when treating the patient with PMVT because of the diverse mechanisms of PMVT, for which there may or may not be clues as to its specific cause at the time of the patient ’s presentation. Treatment options vary and can be contradictory. For example, a medication that may be appropriate for the treatment of TdP may be con-traindicated when treating another form of PMVT. In general, if the patient is symptomatic because of the tachycardia, treat ischemia (if it is present) and correct electrolyte abnormalities. If the QT interval is prolonged, the cause of the long QT should be determined and corrected, if possible (Olgin & Zipes, 2012). Discontinue any medications that the patient may be taking that prolong the QT interval. Gen-erally, IV magnesium ( Table 5.15) is the initial treatment for the stable patient with PMVT associated with a long QT interval (ie, TdP). Beta-blockers may be effective for certain forms of PMVT
Fig. 5.17 When the QRS complexes of VT vary in shape and amplitude, the rhythm is called PMVT. (From Aehlert B: ECGs made easy study cards, St. Louis, 2004, Mosby.)
TABLE 5.14 Characteristics of Polymorphic Ventricular Tachycardia
Regularity Ventricular rhythm may be regular or irregular
Rate Ventricular rate is 150 to 300 beats/min; typically 200 to 250 beats/min P waves None
PR interval None
QRS duration 0.12 sec or more; there is a gradual alteration in the amplitude and direction of the QRS complexes; a typical cycle consists of 5 to 20 QRS complexes
148 CHAPTER 5 Tachycardias
(eg, ischemic PMVT, congenital long-QT syndrome PMVT, catecholaminergic PMVT). Amiodarone may be effective for PMVT with a normal QT interval. PMVT that is associated with Brugada syndrome may be responsive to isoproterenol (Link, et al., 2015). Adenosine should not be given for PMVT because it may cause degeneration of the dysrhythmia to VF (Link, et al., 2015).
Because the QRS complexes of PMVT are disorganized (ie, they differ in amplitude and direction), synchronized cardioversion is generally not possible when managing an unstable patient with this rhythm. Therefore if the patient with PMVT is unstable or has no pulse, proceed with defibrillation as for VF. The tachycardia algorithm is shown in Fig. 5.18.
TABLE 5.15 Magnesium Sulfate
Class Antiarrhythmic, electrolyte Mechanism
of Action
• Essential for activity of many enzyme systems
• Plays an important role with regard to neurochemical transmission and muscular excitability
Indications PMVT with prolonged QT interval
Dosage • If pulseless, give 1 to 2 g IV diluted in 10 mL D5W.
• If pulse present, give 1 to 2 g IV diluted in 50 to 100 mL D5W over 15 min.
Considerations • Use with caution in patients receiving digitalis, patients with impaired renal function, and patients with preexisting heart blocks.
• Calcium is the antidote for magnesium toxicity.
D5W, dextrose 5% in water; IV, intravenous; PMVT, polymorphic ventricular tachycardia
Fig. 5.18 Tachycardia algorithm. (American Heart Association tachycardia algorithm. Reprinted with permission. 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 7: Adult Advanced Cardiovascular Life Support. ECC guidelines.heart.org. © Copyright 2015 American Heart Association, Inc.)