Tachyarrhythmias
A rapid heart rate or tachycardia in a critically ill patient is usually evidence of a problem, but the tachycardia may not be the problem (e.g., sinus tachycardia). This chapter describes tachycardias that are a problem (i.e., tachyarrhythmias), and require prompt recognition and management. Many of the recommendations in this chapter are based on the most recent clinical practice guidelines on the subject (1,2).
I. Recognition
The diagnostic evaluation of tachycardias (heart rate >100 beats/min) is based on 3 findings on the ECG: (a) the duration of the QRS complex, (b) the uniformity of the R-R intervals, and (c) the characteristics of the atrial activity. This scheme is outlined in Figure 13.1.
A. Narrow-QRS-Complex Tachycardias
Tachycardias with a narrow QRS complex (≤0.12 sec) originate from a site above the AV conduction system, and are also known as supraventricular tachycardias. These include sinus tachycardia, atrial tachycardia, AV nodal re-entrant tachycardia (also called paroxysmal supraventricular tachycardia), atrial flutter, and atrial fibrillation. The specific arrhythmia can be identified using the uniformity of the R-R interval (i.e., the regularity of the rhythm), and the characteristics of the atrial activity, as described next.
1. Regular Rhythm
If the R-R intervals are uniform in length (indicating a
regular rhythm), the possible arrhythmias include sinus tachycardia, AV nodal re-entrant tachycardia, or atrial flutter with a fixed (2:1, 3:1) AV block. The atrial activity on the ECG can identify each of these rhythms using the following criteria:
regular rhythm), the possible arrhythmias include sinus tachycardia, AV nodal re-entrant tachycardia, or atrial flutter with a fixed (2:1, 3:1) AV block. The atrial activity on the ECG can identify each of these rhythms using the following criteria:
 FIGURE 13.1 Flow diagram for the evaluation of tachycardias. |
Uniform P waves and P–R intervals are evidence of sinus tachycardia.
The absence of P waves suggests an AV nodal re-entrant tachycardia (see Figure 13.2).
Sawtooth waves are evidence of atrial flutter.
2. Irregular Rhythm
If the R-R intervals are not uniform in length (indicating an irregular rhythm), the most likely arrhythmias are multifocal atrial tachycardia and atrial fibrillation. Once again, the atrial activity on the ECG helps to identify each of these rhythms; i.e.,
Multiple P wave morphologies and variable PR intervals are evidence of multifocal atrial tachycardia (see Panel A, Figure 13.3).
The absence of P waves with highly disorganized atrial activity (fibrillation waves) is evidence of atrial fibrillation (see Panel B, Figure 13.3).
 FIGURE 13.2 Narrow-QRS-complex tachycardia with a regular rhythm. Note the absence of visible P waves (which are hidden in the QRS complex). This is an AV nodal re-entrant tachycardia, also called a “paroxysmal supraventricular tachycardia” because it has an abrupt onset. |
B. Wide-QRS-Complex Tachycardias
Tachycardias with a wide QRS complex (>0.12 sec) can originate from a site below the AV conduction system (i.e., ventricular tachycardia), or they can represent a supraventricular tachycardia (SVT) with prolonged AV conduction (e.g., from a bundle branch block). The distinction between these two arrhythmias is described later in the chapter.
 FIGURE 13.3 Narrow-QRS-complex tachycardias with an irregular rhythm. Panel A shows a multifocal atrial tachycardia, identified by multiple P wave morphologies and variable PR intervals. Panel B is atrial fibrillation, identified by the highly disorganized atrial activity (fibrillation waves). |
II. Atrial Fibrillation
Atrial fibrillation (AF) is a common arrhythmia that increases in prevalence with advancing age; the reported prevalence is 2% with age <65 years, and 9% with age ≥65 years (1).
A. Etiologies
Most patients with AF have underlying heart disease, including valvular disease.
Potentially reversible causes of AF include binge drinking, major surgery, myocardial infarction, myocarditis, pericarditis, pulmonary embolism, and hyperthyroidism.
Postoperative AF is reported in up to 45% of cardiac surgeries, up to 30% of non-cardiac thoracic surgeries, and up to 8% of other major surgeries (3).
B. Adverse Consequences
The adverse consequences of AF are impaired cardiac performance and thromboembolism.
1. Cardiac Performance
The principal threat from AF is reduced ventricular filling from loss of atrial contractions (which normally contribute 25% of the ventricular end-diastolic volume) and the rapid heart rate (which reduces the time for diastolic filling). Reduced ventricular compliance (e.g., from ventricular hypertrophy) and mitral stenosis will magnify the problem. The effect on cardiac stroke output will depend on the rate and the type and severity of underlying cardiac disease.
2. Thromboembolism
AF predisposes to thrombus formation in the left atrium, and these thrombi can dislodge and embolize in the cerebral circulation to produce an acute ischemic stroke.
The risk of thromboembolic stroke is increased when AF is accompanied by certain risk factors (e.g., heart failure, advanced age). The methods used to determine the risk of stroke are described later in the chapter.
The increased risk of embolic stroke pertains to all types of AF (paroxysmal, etc.), except first episodes of AF that are <48 hrs in duration (1).
C. Acute Rate Control
In patients with rapid AF who are hemodynamically stable, the immediate goal is to slow the ventricular rate to ≤80 beats/min using drugs that prolong AV conduction. These drugs are shown in in Table 13.1, along with the intravenous and oral (maintenance) dosing regimens. (Note: These drugs
should not be used in cases of AF due to re-entry of impulses through an accessory pathway, as described later.)
should not be used in cases of AF due to re-entry of impulses through an accessory pathway, as described later.)
Table 13.1 Drug Regimens for Rate Control in Atrial Fibrillation | ||||||||||||||||||||||||||||||||||||
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1. Diltiazem
Diltiazem is a calcium receptor antagonist that achieves satisfactory rate reduction in about 85% of cases of AF (1). The drug is given as an intravenous bolus followed by a continuous infusion (see Table 13.1), and the response is superior to that seen with IV amiodarone or digoxin (4).
Adverse effects include hypotension and cardiac depression (negative inotropic effect). Because of the latter effect, diltiazem is not recommended for patients with decompensated systolic heart failure (1).
2. β-Receptor Antagonists
β-blockers achieve successful rate control in 70% of cases of acute AF (11), and they are preferred for rate control when AF is associated with hyperadrenergic states (e.g., acute MI and post-cardiac surgery) (1,3).
Two cardioselective β-blockers that have proven efficacy in AF are esmolol and metoprolol, and their dosing regimens are shown in Table 13.1. Esmolol is an ultra-short-acting drug (with a serum half-life of 9 minutes) and is given by continuous infusion, which allows rapid dose titration to the desired effect (unlike metoprolol) (12).
Adverse effects are similar to those of diltiazem, and these agents are not advised in the setting of decompensated systolic heart failure (1).
3. Amiodarone
Amiodarone prolongs conduction in the AV node, and is an effective agent for acute rate control in critically ill patients with AF (1).
Amiodarone causes less cardiac depression than diltiazem (6), and is a preferred agent for rate control in patients with systolic heart failure (1,7). Otherwise, because of the toxic effects associated with long-term use, amiodarone is usually reserved for cases of AF that are refractory to rate control with other agents (1).
The dosing regimen for amiodarone is shown in Table 13.1. The IV regimen usually lasts only 24 hrs before a change to oral maintenance therapy.
Amiodarone is also an antiarrhythmic agent (Class III), and is capable of converting AF to a sinus rhythm. Conversion is uncommon with persistent AF (present for more than one year) (1), but the success rate for converting recent-onset AF is 55–95% when a loading dose and continuous infusion are used, and the daily dose exceeds 1500 mg (7). Unanticipated cardioversion can be problematic when patients are not adequately anticoagulated (see later).
Adverse effects of short-term IV amiodarone include hypotension (15%), bradycardia (5%), and elevated liver enzymes (3%) (8,9). (Note: IV amiodarone is available in 2 formulations: one contains polysorbate 80, a vasoactive solvent that promotes hypotension, and one contains captisol, which has no vasoactive effects.)
Amiodarone has several drug interactions by virtue of its metabolism by the cytochrome P450 enzyme system in the liver (9). These interactions include inhibition of digoxin and warfarin metabolism, which requires attention if amiodarone is continued for oral maintenance therapy.Related posts:
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