Which adverse hemodynamic effects typically occur when a client develops tachycardia

Narrow Complex Tachyarrhythmias

Sinus tachycardia is one of the most common perioperative tachyarrhythmias. Assess if the patient has an adequate circulating blood volume and adequate pain control. These should be addressed first and can often correct the abnormality. Once these are ruled out, or corrected, then an agent to control the accelerated rate could be considered if the patient would be thought to have an increased cardiac risk. Rate control for the sake of rate control in each and every patient is unnecessary and could actually combat this compensatory mechanism from another unrecognized etiology.

There is an array of other narrow complex tachyarrhythmias including accelerated junctional rhythm, paroxysmal supraventricular tachycardia, and certainly the most common arrhythmia in this category and worth mention is atrial fibrillation. In general, atrial fibrillation is very well tolerated in most patients. The loss of atrial contraction and atrial-ventricular dyssynchrony only results in hemodynamic instability when there is a setting of decreased ventricle filling capacity. Should the patient become unstable with hemodynamic compromise or develop severe cardiopulmonary symptoms (angina, dyspnea, etc.), then you are hard-pressed to take action. Rarely, a patient with paroxysmal atrial fibrillation in this clinical scenario will need light sedation and electrical cardioversion per ACLS protocol. It should be mentioned that attempting cardioversion in a patient with long-standing persistent or permanent atrial fibrillation will be unsuccessful and, in our opinion, a waste of precious time. More commonly, these patients will require the administration of a vasopressor such as phenylephrine or norepinephrine to stabilize the blood pressure and then receive an intravenous agent such as amiodarone (Table 3) for rate control while attempts are made to correct other causes such as electrolyte abnormalities or addressing causes of myocardial ischemia. Amiodarone protocols usually include a 150 mg IV loading bolus over 10 minutes followed by an amiodarone drip at 1 mg/min for 6 hours and then 0.5 mg/min for another 18 hours. Additional amiodarone boluses of 150 mg IV can be given during the infusion period, each over 10 minutes. Digoxin can also be considered in these patients, particularly if the patient has severe pulmonary disease or has already demonstrated a hypersensitivity to amiodarone. We also often use another underappreciated, and rather benign antiarrhythmic, intravenous magnesium sulfate (2–6 g IV). This can be considered as long as the patient does not have corresponding severe acute or chronic renal dysfunction or elevation of other intracellular cations (potassium). We initially target rate control for less than 100 beats/min. If this is tolerated, we then lower our target to 80 beats/min, which in our experience seems helpful for chemical cardioversion.

Stable patients with new-onset atrial fibrillation can often be managed in a stepwise manner. Again, the goal is rate control over rhythm control. The ventricular rate is usually controlled first with a parenteral dose of β-blocker (usually metoprolol) or calcium channel blocker (diltiazem). β-blockers are especially preferred if the patient has known ischemic heart disease. A single or series of IV doses can also be used to achieve more rapid HR control in acute settings. Once the maximum dose has been given, then a second agent will need to be added to either the diltiazem or metoprolol. If the patient is still hypertensive, then we often add the other agent (add diltiazem if metoprolol given first). Or rather, if the blood pressure is more marginal now, consider adding either digoxin or amiodarone. Either an IV or parental route can be used to load amiodarone. Ten grams is needed if using the oral dosing regimen and 5 g is needed for the IV route. Once the agent is loaded a standard maintenance dose can be given (usually 200 mg PO every day). Digoxin is usually avoided for patients with decreased creatinine clearances because of its renal clearance (or a dose adjustment to avoid digoxin toxicity). Amiodarone is usually avoided in patients with a prior sensitivity or severe lung disease. Last, one must use caution when adding a third high dose nodal blocking agent and using amiodarone in combination with digoxin.

Introduction

Tachyarrhythmia is defined as a heart rhythm with a ventricular rate of 100 beats/min or greater. Tachyarrhythmias are broadly categorized as narrow complex tachycardia (NCT; < 120 ms) or wide complex tachycardia (≥ 120 ms). NCT reflects rapid activation via the normal His–Purkinje system and therefore tachycardia origin above or within the His bundle [i.e., supraventricular tachycardia (SVT)].1,2 However, wide complex tachycardia (WCT) indicates abnormally slow ventricular activation.3 Tachycardia origin can be below the His bundle within bundle branches, Purkinje system, or ventricular myocardium [i.e., ventricular tachycardia (VT)]. Otherwise, it may reflect SVT with preexisting bundle branch block (BBB), rate-dependent aberrancy, or conduction over an accessory pathway.

Prevention and Termination of Tachyarrhythmias

In some patients with long-QT syndrome, continuous pacing can prevent recurrent tachyarrhythmias. In addition, paroxysmal reentrant tachyarrhythmias can be terminated in some patients through programmed stimulation and short bursts of rapid pacing. However, the guidelines do not provide support for the routine use of antitachycardia pacemakers without extensive testing before implantation (Table 41G.5), but continue to consider bradycardia pacing appropriate (class I indication) for patients with sustained pause-dependent ventricular tachycardia (VT, unrelated to a drug whose use can be discontinued), with or without a prolonged QT interval, if the efficacy of temporary pacing has been demonstrated (Table 41G.6). However, some patients have or are at risk for other types of VT. In these patients an ICD may be more appropriate.

Narrow QRS complex tachycardia

A narrow QRS complex tachycardia (QRS duration < 120 ms and rate > 100 bpm) indicates a supraventricular origin with ventricular activation occurring via the fast-conducting His-Purkinje system. The acute management of a regular narrow QRS complex tachycardia will depend on the hemodynamic state of the patient. In most but certainly not all instances the patient remains hemodynamically stable even if the rhythm is rapid; this is especially the case if the patient is younger and otherwise healthy; however, AV nodal and AV reentry tachycardias (Fig. 4.1) can cause severe symptoms of presyncope and frank syncope at any rate because of the retrograde atrial depolarization and atrial contraction against closed AV valves; this in turn produces not only loss of stroke volume but also, via atrial stretch receptor activation, reflex systemic hypotension, which can be refractory.

If the patient is stable, the first thing to try is a Valsalva maneuver (bearing down with closed mouth) or carotid sinus massage (if there is no carotid bruit or known vascular disease). If this is ineffective, it should be repeated with the patient in the Trendelenburg position or in combination. If this is ineffective, then adenosine between 6 mg or escalating doses of 12 mg or 18 mg given as an intravenous (IV) bolus followed by a saline “chaser” should be used; this will be expected to either terminate the tachycardia if it is dependent on the AV node for its maintenance or be diagnostic for what the atrial rhythm is during tachycardia, if the tachycardia is AV node independent. For example, sometimes a narrow QRS complex tachycardia, thought to be AV node or AV reentry, in fact turns out to be atrial flutter; adenosine, by producing AV block, thus allowing the atrial rhythm to be visible, will be diagnostic.

In some instances, adenosine is ineffective (sometimes due to the presence of theophylline or high levels of caffeine). If this is the case, a second option would be to give IV verapamil 5 to 15 mg; it is important to know that verapamil should not be given to the patient with a wide QRS complex tachycardia. If neither of these therapies is effective, a DC shock given with anesthesia may be effective; however, it should be recognized that adenosine and verapamil are indeed highly effective in terminating almost all supraventricular tachycardias (SVTs) and that if they do not work it is entirely possible that that the tachycardia is not an SVT but might be sinus tachycardia. IV digoxin is rarely given to terminate narrow QRS complex tachycardias because its action is not that of a direct AV nodal blocker but produces AV block through vagal mechanisms. Adenosine should not be given to heart transplant patients because prolonged asystole may follow; the effects of adenosine can be longer lasting in these patients than would be expected. The normal duration of action of adenosine is 10 to 20 seconds. Whereas theophylline and caffeine diminish the effects of adenosine, dipyridamole accentuates them. Adenosine can cause bronchospasm and atrial fibrillation; if the latter occurs in a patient with WPW syndrome, the atrial fibrillation can be potentially lethal.

Tachyarrhythmias

Tachyarrhythmias are broadly characterized assupraventricular tachycardia (SVT),1 defined as a tachycardia in which the driving circuit or focus originates, at least in part, in tissue above the level of the ventricle (i.e., sinus node, atria, AV node, or His bundle). Atrial fibrillation is discussed inChapter 38. Ventricular tachycardia (VT) is defined as a tachycardia in which the driving circuit or focus originates solely in ventricular tissue (including valves and root of the great arteries) or Purkinje fibers (seeChapter 39). Because of differences in prognosis and management, distinction between SVT and VT is critical early in the acute management of a tachyarrhythmia.2 In general, with the exception of the idiopathic form, VT often carries a much poorer prognosis, usually implies the presence of significant heart disease, results in more profound hemodynamic compromise, and therefore requires immediate attention and measures to revert to sinus rhythm. SVT is not usually lethal and often does not result in hemodynamic collapse; therefore more conservative measures can be applied initially to convert to sinus rhythm.1,3

Distinction between SVT and VT can generally be made on the basis of the electrocardiogram (ECG) obtained during tachycardia (seeChapter 35). It is important to obtain a 12-lead ECG during tachycardia if possible and to obtain 12-lead (or at least multilead) rhythm strips during any intervention aimed at termination of the tachycardia, because examining the termination (and initiation) can help identify the specific arrhythmia. If the QRS is narrow (duration <120 msec, often referred to asnarrow-complex tachycardias), the ventricle is usually being activated through the normal His-Purkinje system, and thus the origin of the tachycardia is supraventricular4 (Fig. 37.1). A wide QRS (duration >120 msec) during tachycardia suggests VT, although in some common scenarios, SVT can produce a wide QRS complex. Therefore a more descriptive term, wide-complex tachycardia (WCT), is often used when the precise arrhythmia mechanism cannot be determined. For example, SVT with a concurrent bundle branch block (BBB) or intraventricular conduction defect can produce WCTs despite a supraventricular origin, as can preexcited tachycardias (tachycardias in which the ventricle is activated in whole or in part over an accessory pathway). Therefore, although a narrow-complex tachycardia almost always makes the diagnosis of SVT, a WCT can be supraventricular or ventricular. Fusion or capture beats and AV dissociation are diagnostic of VT but are often not present or are difficult to detect. Criteria and algorithms have been developed to determine whether a WCT is more likely to be SVT or VT (Table 37.2; seeChapter 39). The general principles behind these algorithms rest on the assumption that the closer the QRS morphology is to a typical BBB pattern, the more likely it is an SVT and assumes that the septum is still rapidly activated in a WCT caused by SVT.

DIFFERENTIAL DIAGNOSIS

Tachycardia-Bradycardia Syndrome

Tachycardia-bradycardia syndrome, frequently referred to as sick sinus syndrome, is a common manifestation of SND, and it refers to the presence of intermittent sinus or junctional bradycardia alternating with atrial tachyarrhythmias (Fig. 8.5). The atrial tachyarrhythmia is most commonly paroxysmal AF, but AT, AFL, and occasionally atrioventricular nodal reentry tachycardia or AVRT can also occur.

Apart from underlying sinus bradycardia of varying severity, these patients often experience prolonged sinus arrest and asystole on termination of the atrial tachyarrhythmia, resulting from overdrive suppression of the sinus node and secondary pacemakers by the tachycardia. Long sinus pauses that occur following electrical cardioversion of AF constitute another manifestation of SND.

Therapeutic strategies to control the tachyarrhythmias often cause SND and result in the need for pacemaker therapy (Fig. 8.6). On the other hand, long sinus pauses occurring following tachycardia episodes can be reversible in some patients once the tachyarrhythmia is eliminated, thus obviating the need for pacing.

Atrial Reentrant Tachycardia

Abstract

Tachyarrhythmias are abnormal heart rhythms with a ventricular rate of 100 or more beats per minute. These rhythms are classified as either narrow or wide-complex tachycardia with further subdivision into regular or irregular rhythm. Patients are frequently symptomatic presenting with palpitations, diaphoresis, dyspnea, chest pain, dizziness, and syncope. Sudden cardiac death may occur with certain arrhythmias. Recognizing tachyarrhythmia and understanding its management is important as a wide spectrum of neurologic complications have been associated with such arrhythmias. The purpose of this chapter is to provide a comprehensive overview on the neurologic complications of tachyarrhythmias, neurologic adverse events of antiarrhythmic interventions, and neurologic conditions that can precipitate tachyarrhythmia.