Rapid Heart Rates
The most common cause of abnormal episodic or paroxysmal tachyarrhythmia in younger patients are supraventricular tachycardias (SVT), which originate in the atriae or AV-node above the two ventricles. Supraventricular tachycardias frequently recur incessantly and are often a disabiling nuisance, but are never life threatening. SVT is characterized by a rapid regular tachycardia with a narrow QRS that has a sudden onset and offset. Usually the tachycardia is 150 to 200 beats/min but may occasionally be slower. Typically the P-wave contour is similar to the contour of the sinus P-wave. Usually P-waves are buried within the QRS complex.
Paroxsymal Superventricular Tachycardia
PSVT is a rapid regular tachycardia with narrow QRS complexes, which begina and terminates abruptly. In this 4-second run of PRVT, the contours of the P-waves during the tachycardia differ from the contours of the P-waves during NSR. PSVT is oftern triggered by a premature atrial beat.
Supraventricular tachyarrhythmias, which are AV nodal reentrant tachycardias, commonly occur in younger patients with structurally normal hearts, starting from the second decade up to the fourth decade. The episodes of tachycardia occur sporadically and often result in symptoms of palpitations, generalized weakness, and anxiety. Usually the tachycardia terminates spontaneously after a few minutes or hours. Rarely, patients with an exceptionally rapid SV-tachycardia will experience a brief fainting spell. Very rarely, SV-tachycardia may last for weeks which can led to tachycardia-induced congestive heart failure.
Episodes of supraventricular tachycardia can occasionally be terminated if a patient holds their breath while placing their face in ice cold and bearing down. Alternatively, an injection of adenosine given intravenously in an emergency room terminates AV nodal reentry tachycardia successfully in most patients. Rarely, AV nodal reentry tachycardia is refractory to adenosine and causes cardiac decompensation and hypotension. For these patients, DC cardioversion with low electrical energy nearly always converts AVNRT.
If episodes of supraventricular tachycardia are well tolerated, brief, and infrequent occurring only a few times a year, no antiarrhythmic therapy is necessary. In patients with more frequent and prolonged episodes of SV-tachycardia, either a long-acting calcium antagonist or a long-acting betablocker and digoxin may be effective for preventing recurrences. Frequently, however, patients experience recurrences of supraventricular tachycardia despite preventive therapy with anti-arrhythmic medications or experience adverse side effects from these medications. For these patients, radiofrequency catheter ablation is a highly effective treatment that cures AVNRT in more than 95% of patients with a very low complication rate.
Atrial flutter is recognized by rapid regular saw tooth atrial waves on the electrocardiogram. During atrial flutter, the atrial rate is typically 250-350 beats/min, but the rate may be slower in patients treated with antiarrhythmic agents. Usually there is no isoelectric interval or horizontal flat line between flutter waves. Atrial flutter is frequently due to a reentrant circuit in the right atrium which causes the atrial impulse to circulate repeatedly in a circular fashion. Often the relationship of flutter waves to conducted QRS complexes is in a fixed ratio. The ventricular response to atrial flutter is often 2:1, resulting in a ventricular rate of approximately 150 beats/min. Rarely, 1:1 AV conduction occurs resulting in a very rapid ventricular rates of approximately 300 beats/min, which invariably makes patients highly symptomatic. Four to one atrial to ventricular conduction is less common and may result in normal ventricular rates.
Typically atrial flutter is characterized by rapid regular atrial rates ranging from 250 to 350 beats/minute. Atrial flutter waves have a sawtooth appearance.
Atrial flutter is an inherently unstable heart rhythm because the ratio of atrial-ventricular conduction may change at any time causing rapid ventricular rates and symptoms of palpitations, fatigue, and tachycardia. Atrial flutter is difficult to suppress with antiarrhythmic medications but is easily converted to normal sinus rhythm with low dose synchronized DC cardioversion.
Atrial flutter is more common in patients with right or left heart failure causing elevated right or left heart filling pressures resulting in dilatation of the atriae. Treatment of the underlying heart failure is often effective in preventing recurrences of atrial flutter. In patients with recurrent atrial flutter refractory to medical therapy, catheter ablation is often successful in terminating atrial flutter and has a high long-term success rate.
For patients with chronic atrial flutter, long-term anticoagulation is generally recommended because the risk of thromboembolism is elevated for these patients, although randomized controlled trials are not available regarding this issue.
Ventricular tachycardia can be recognized as a series of three or more consecutive wide QRS complexes with a wide range of rapid heart rates varying from 80 to 250 beats/min. Typically ventricualr tachycardia appears as a series of ventricular premature beats with the ST-segment vector pointing in the opposite direction to the QRS-wave. The QRS duration is always wide (> 120 milliseconds), and usually atrial ventricular dissociation is present. That is, the atriae and ventricles beat independently. As a result P-waves can often be seen superimposed on the QRS at a different rate from the ventricular tachycardia. Occasionally, retrograde VA conduction from the ventricles to the atriae occurs resulting in a 1:1 relationship between ventricular and atrial beats.
Ventricular tachycardia is a wide-complex QRS tachycardia, which is usually regular or slightly irregular. Typically, atrial contraction continues independently of ventricular tachycardia (AV dissociation). In this example, P-waves (arrows) are noted superimposed on the wide QRS complexes (designated V). The ventricular tachycardia spontaneously converts to normal sinus rhythm.
During ventricular tachycardia, the configuration of the QRS complexes is usually uniform or monomorphic. Occasionally beat-to-beat variations in QRS contours are noted resulting in multiform ventricular tachycardia. Brief episodes of ventricular tachycardia lasting less than 30 seconds are arbitrarily referred to as non-sustained V-tachycardia, and longer runs are referred to as sustained V-tachycardia.
Multifocal Atrial Tachycardia
MAT in a patient with respiratory failure due to chronic obstructive pulmonary disease. Note the wide variation in P-wave morphology, P-R intervals, and P-P intervals.
The cardiovascular prognosis of ventricular tachycardia is directly related to the extent of underlying structural heart disease, particularly the severity of LV-dysfunction. Patients with recurrent brief runs of non-sustained ventricular tachycardia and structurally normal hearts have an excellent cardiovascular prognosis; whereas, patients with congestive left heart failure from any cause and recurrent sustained ventricular tachycardia have a much higher risk of sudden cardiac death.
Although ventricular tachycardia can be associated with any type of structural heart disease, symptomatic recurrent VT is most common in patients with coronary heart disease and in patients with heart failure due to congestive or hypertrophic cardiomyopathy. Patients with sustained ventricular tachycardia and advanced congestive heart failure often experience generalized weakness, increasing shortness of breath, and lightheadedness. Sustained ventricular tachycardia in these patients may also cause hypotension, shock, loss of consciousness, angina, or worsening heart failure. In patients with very advanced heart disease, ventricular tachycardia may provoke ventricular fibrillation, resulting in sudden death.