Paroxysmal Supraventricular Tachycardia (PSVT)

PSVT is a common arrhythmia that occurs among all age groups in both ambulatory and inpatient settings. Although most patients with PSVT are symptomatic in some way from this arrhythmia (with lightheadedness, awareness of rapid heart beat or palpitations), hemodynamic compromise is usually not seen if the patient is otherwise healthy and does not have underlying heart disease. In contrast, sudden development of this arrhythmia is much more likely to be consequential when it occurs in older patients, in very young children, or adults with significant underlying cardiac disease. Hemodynamic decompensation is especially likely to develop in such individuals when the rate of PSVT is very rapid and/or the rhythm persists for long periods of time. 

Electrocardiographically, the diagnosis of PSVT is suggested by the finding of a regular supraventricular (narrow complex) tachycardia in which normal atrial activity is lacking on the surface ECG. Terminology of the various forms of PSVT may be confusing, because there are a number of different mechanisms that may produce a similar electrocardiographic picture. Most commonly the phenomenon of "reentry" exists, in which the electrical impulse continually circulates over a well defined reentrant pathway. In a primary care setting, the overwhelming majority of adults who present with the ECG picture of PSVT (regular narrow complex tachycardia at a rate of between 140-240 beats per minute without evidence of normal atrial activity) will have a reentrant tachycardia in which at least a portion of the reentry circuit involves the AV node. Surprisingly, up to one-third of these patients have an accessory pathway involved in reentry circuit that is "concealed" (not manifested by delta waves on the surface ECG), reflecting the fact that conduction only occurs over the accessory pathway in retrograde fashion. This reentrant form of PSVT is said to manifest orthodromic conduction, because the electrical impulse travels first down the normal AV nodal pathway and then back up the accessory pathway. As a result of this sequence of activation, the usual ECG hallmarks of an accessory pathway (short PR interval, delta wave, QRS widening) are not seen. 

Clinically, initial management of patients with PSVT from a concealed accessory pathway (i.e., with orthodromic conduction first through the AV node, and then back up the accessory pathway in retrograde fashion) is similar to management of the more common form of PSVT in which the entire reentry circuit is contained within the AV node (atrioventricular nodal reentrant tachycardia, or AVNRT). In both cases, the arrhythmia behaves as an "AV nodal dependent" tachycardia, in that interventions aimed at altering AV nodal conduction properties may interrupt the reentry circuit just long enough to block propagation of the circulating impulse, and therefore convert the arrhythmia to sinus rhythm. 

Acute treatment of patients with AV nodal dependent forms of PSVT may include use of a vagal maneuver, and/or administration of IV verapamil, diltiazem, or adenosine (Adenocard). Although each of these drugs is effective in converting PSVT more than 90 percent of the time, adenosine is often preferred in an emergency setting because of its rapid onset. Unfortunately, recurrence may be seen with this agent because of its short dura-tion of action. If this occurs, either adenosine may be repeated, or use of a longer acting agent (verapamil or diltiazem) may be tried. Alternatively, use of digoxin or a beta-blocker could be considered. The addition of an anxiolytic agent may be a helpful adjunct for treatment of PSVT because it reduces the anxiety that often accompanies this arrhythmia, as well as the physiologic effect it may have in attenuating sympathetic tone and therefore altering conduction properties in one or both arms of the reentrant pathway.

Long-term management of the patient with PSVT includes elimination of all stimulants (including caffeine), alcohol, tobacco, and other substances of possible abuse, sympathomimetic agents, and diet pills. Selected patients can be taught the Valsalva maneuver, to be performed when necessary. 

Consideration may sometimes be given to administration of drugs on an episodic basis for patients with infrequent attacks, or daily for more frequent occurrence. Intermittent therapy may be appropriate for selected individuals whose PSVT only occurs at infrequent intervals, in which the treating physician prescribes the use of verapamil, diltiazem, or a beta-blocker that may be taken by the patient at home at the time of the episode. Such therapy should not be used unless the mechanism of the arrhythmia has been clearly defined. However, when appropriate, use of intermittent therapy for treatment of PSVT is well received by patients because it restores a measure of control over their condition and avoids the need to take a medication daily when their arrhythmia only occurs at infrequent intervals. The addition of a benzodiazepine to the rateslowing regimen may be beneficial because it reduces the anxiety that accompanies PSVT during the time that it takes the oral regimen to work (usually 30 to 90 minutes). 

Several points should be emphasized regarding the management of PSVT. First, patients with frequent episodes of PSVT that do not readily respond to medical therapy should be referred for electrophysiologic study. Doing so allows identification of a group of patients who may be suitable candidates for catheter ablation therapy, a procedure that may be curative in more than 90 percent of cases with only minimal risk of complications. This evaluation and treatment course should be especially considered for patients with PSVT that is known to be associated with conduction over an accessory pathway-since such individuals may retain the potential to suddenly develop antegrade (forward) conduction down the accessory pathway in association with tachycardia. In particular, development of atrial fibrillation in such a patient with antidromic conduction over an accessory pathway may lead to excessively rapid ventricular rates (of 250 beats per minute, or more) with associated life-threatening hemodynamic compromise. Electrophysiologic study of these patients allows identification of the culprit accessory pathway in most cases, which may then be ablated with cure of the arrhythmia. 

Finally, it should be appreciated that a small percentage of patients who present with the ECG picture of PSVT in reality have an "AV nodal independent" mechanism responsible for their arrhythmia. This group of tachyarrhythmias include entities such as sinus node reentry, intra-atrial reentry, and ectopic (automatic) atrial tachycardia, as may occur with digitalis toxicity. The importance of being aware of these much less commonly occurring arrhythmias is that the usual measures used for treatment of AV nodal dependent PSVT rhythms may not be effective if the AV node is not involved in the genesis and/or maintenance of the arrhythmia. For example, withholding digoxin may be all that is needed for resolution of atrial tachycardia with block that arises as a manifestation of digoxin toxicity. Clinically, sinus node reentrant tachycardia and intra-atrial reentrant tachycardia are both often resistant to treatment with standard antiarrhythmic agents. Early referral for electrophysiologic study should be strongly considered for such patients.

Read More

Ventricular Arrhythmias

 Ventricular arrhythmias are a broad category of conditions that include premature ventricular contractions (PVCs), ventricular tachycardia, accelerated idioventricular rhythm, torsades de pointes, ventricular flutter and
fibrillation.

Premature Ventricular Contractions. Prudent medical practice dictates that therapy for PVCs be based on "the company they keep". They are common in the general population, and if no heart disease is present, they are generally benign. Accompanying conditions that increase catecholamine levels, as well as hypoxia, electrolyte abnormalities, and drug toxicity, should be treated.

If, however, the PVCs occur with acute ischemic heart disease or any other organic heart disease, they may be of greater signifi-cance. PVCs themselves are not a cause of mortality, unless they lead to sustained VT or VF. Clinically, one should look first for disorders associated with increased catecholamine levels, hypoxia, electrolyte abnormalities, drug toxicity, HF, and ischemia. These conditions should be corrected if they exist. If PVCs persist, Holter monitoring could be considered in an attempt to determine if more malignant forms are present. In the absence of underlying heart  disease, PVCs, even if frequent, are generally benign and need not be treated. If the patient is symptomatic from such PVCs, a beta-blocker is the antiarrhythmic agent of choice.

In contrast, if PVCs occur in a patient who does not have underlying heart disease, cardiovascular risk is increased. The problem is that with rare exceptions, antiarrhythmic therapy has not been shown to increase survival in such patients. If treatment is deemed necessary, a beta-blocker is again the agent of choice. It should be kept in mind that antiarrhythmic drugs are not benign and, in 5 to 10 percent of cases, may be associated with a proarrhythmic effect, in which they paradoxically exacerbate the arrhythmia. This is a major reason for the reluctance to treat PVCs in recent years.

Ventricular tachycardia. When short episodes of VT occur in a normal heart, they are usually benign. However, once VT is found, intensive cardiac evaluation is usually indicated to assess the patient for underlying heart disease. If heart disease is not present, no therapy may be needed.

On the other hand, when VT occurs with organic heart disease, the risk of VF is higher and, therefore, the risk of sudden cardiac death increases. Full evaluation with echocardiography, cardiac catheterization, and/or electrophysiologic studies should be strongly considered. Treatment options include amiodarone or other antiarrhythmic therapy or an implantable defibrillator, depending upon the LVEF and how inducible the VT is with electrophysiologic studies. For example, VT is much more likely to be inducible in a patient with ischemic cardiomyopathy compared to one with a nonischemic cardiomyopathy. In appropriately selected patients, use of an implantable cardioverterdefibrillator (ICD) may result in a greater than 90-percent survival rate at five years in those patients who otherwise would be at very high risk for sudden cardiac death.

Recently, the Multicenter Automatic Defibrillator Implantation Trial (MADIT) was completed, in which prophylactic implantation of an ICD appeared to benefit a select group of patients with nonsustained VT and impaired left ventricular function following myocardial infarction. Although additional data are needed to confirm these results, it would seem that  patients with sustained VT and underlying heart disease should be referred for extensive cardiac evaluation including electrophysiologic study. Management decisions are less clear at this time for patients with asymptomatic episodes of nonsustained ventricular tachycardia (NSVT) who have underlying heart disease. At the least, control of potentially exacerbating causes of ventricular arrhythmias (whenever possible) is essential in such patients, including correction of electrolyte abnormalities and treatment of ischemia, heart failure and/or hypoxia. Preference should be given to use of ACE inhibitors and beta-blockers when appropriate for treatment of these underlying conditions. Whether or not patients with asymptomatic NSVT and underlying heart disease hould be routinely referred for electrophysiologic study remains controversial at this time, and is a decision that should be individualized for each patient depending on specific circumstances of the particular case at hand.

Finally, for patients who develop either cardiac arrest from ventricular fibrillation and/or sustained ventricular tachycardia associated with hemodynamic compromise that is not the result of acute myocardial infarction, recent data suggest the superiority of treatment with an ICD over treatment with antiarrhythmic drugs. Patients with these presentations should be referred for electrophysiologic evaluation unless extenuating circumstances exist.

Read More