ATRIAL RHYTHM DISTURBANCES



Premature atrial complexes (PAC’s) are char­acterized by a premature P wave, usually of dif­fering morphology from the sinus P wave. PAC’s occurring very early in diastole may be followed by either aberrantly conducted QRS complexes or no QRS complexes (nonconducted PAC). In gen­eral, the shorter the interval from the last QRS to the P wave, the longer the PR interval after the PAC. PAC’s are less likely to be followed by a fully compensatory pause than are PVC’s (see discus­sion below). PAC’s are common in normal people but may occur in a variety of situations, for ex­ample, infection, inflammation, myocardial is­chemia, psychological stress, tobacco or alcohol use, or caffeine ingestion. PAC’s can be the fore­runner of a sustained supraventricular tachyar­rhythmia. They do not require therapy unless they produce symptoms or precipitate tachyarrhyth­mias.

In atrial flutter, the atrial rate is usually 250 to 350 per minute. Ordinarily, the ventricular rate is half of the atrial rate. If AV block is greater than 2:1 in the absence of drugs, abnormal AV con­duction is suggested. In children, patients with pre-excitation syndrome, or patients with hyper­thyroidism, 1:1 AV conduction can occasionally occur. Drugs such as quinidine, procainamide, or disopyramide may reduce the atrial rate to the range of 200 per minute, raising the danger of 1:1 AV conduction. The atrial activity appears as reg­ular sawtooth waves without an isoelectric inter­val between flutter waves. Flutter waves are com­monly inverted in leads 2,3, and aVF. Ventricular response to atrial flutter may be irregular, gener­ally of a Wenckebach nature, or regular. Chronic atrial flutter is usually associated with underlying heart disease, but paroxysmal atrial flutter may occur in patients without organic heart disease. Toxic and metabolic conditions such as thyrotox­icosis, alcoholism, or pericarditis may be asso­ciated with atrial flutter. There are fewer systemic emboli in patients with atrial flutter than in pa­tients with atrial fibrillation, presumably because of the atrial contraction. Carotid sinus massage may decrease the ventricular response but does not terminate the arrhythmia. Cardioversion (less than 50 joules) usually restores sinus rhythm. If atrial fibrillation ensues, a second shock of higher energy may be necessary. Rapid atrial pacing also terminates atrial flutter, although some patients develop atrial fibrillation instead of sinus rhythm; however, atrial fibrillation is usually an easier ar­rhythmia in which to control the ventricular re­sponse.
Intravenous verapamil, beta blockers, or digi­talis may slow the ventricular response to atrial flutter, and in a few patients may restore sinus rhythm. Type 1 antiarrhythmic drugs such as quinidine, procainamide, or disopyramide may terminate atrial flutter in some patients and are often useful to prevent recurrences. These drugs should not be administered unless AV nodal block has been previously achieved, since slow­ing the atrial flutter rate combined with the va­golytic effects of disopyramide or quinidine may lead to 1:1 AV conduction.
Atrial fibrillation is characterized by totally disorganized atrial activation without effective atrial contraction. The electrocardiogram shows small, irregular baseline undulations of variable amplitude. The ventricular response is irregularly irregular, usually between 100 and 160 beats per minute in the untreated patient with normal AV conduction. It is easier to slow the ventricular re­sponse with drugs in patients with atrial fibril­lation than in patients with atrial flutter because of the greater number of atrial impulses reaching the AV node and decreasing the overall number of impulses that conduct to the ventricles. Chronic atrial fibrillation is usually associated with underlying heart disease, whereas paroxys­mal atrial fibrillation may occur in apparently normal hearts. Atrial fibrillation commonly re­sults from rheumatic heart disease (especially with mitral valve involvement], cardiomyopathy, hypertensive heart disease, pulmonary emboli, pericarditis, coronary heart disease, thyrotoxi­cosis, or heart failure from any cause. Episodes of atrial fibrillation may cause decompensation of patients with borderline cardiac function, espe­cially those with mitral or aortic stenosis. Patients with chronic atrial fibrillation are at a greatly in­creased risk of developing systemic emboli, par­ticularly if mitral valve disease is also present. Left atrial diameter tends to be smaller in patients with paroxysmal atrial fibrillation or in patients whose atrial fibrillation is easily terminated with cardioversion. Physical findings in patients with atrial fibrillation include a variation in the inten­sity of the first heart sound, absence of a waves in the jugular venous pulse, and an irregularly ir­regular ventricular rhythm. A pulse deficit may appear with faster ventricular rates; that is, the auscultated apical rate exceeds the palpable radial rate due to failure of many of the ventricular con­tractions to generate a palpable peripheral pulse. Although atrial fibrillation with a very rapid ven­tricular response can sometimes seem regular, it is always irregularly irregular upon careful mea­surement, and true regularization of the ventric­ular rhythm in patients with atrial fibrillation should suggest development of sinus rhythm, atrial flutter, junctional rhythm, or ventricular tachycardia (the latter two may be manifestations of digitalis intoxication).

It is important to correct any precipitating causes of atrial fibrillation such as thyrotoxicosis, mitral stenosis, pulmonary emboli, or pericardi­tis. If the onset of atrial fibrillation is associated with acute hemodynamic decompensation, DC cardioversion should be employed (usually re­quires 100 to 200 joules}. In the absence of de­compensation, the patient should be treated with digitalis to maintain a resting apical rate of 60 to 80 beats per minute that does not exceed 100 beats per minute after mild exercise. At times, the ad­dition of a beta- or calcium-blocker may be useful to slow the ventricular rate. Quinidine or other type 1 antiarrhythmic drugs may be useful either to convert atrial fibrillation to sinus rhythm or to maintain sinus rhythm once it is restored with electrical cardioversion. Patients with atrial fi­brillation of less than 12 months duration or with­out markedly enlarged left atria are more likely to remain in sinus rhythm after cardioversion. The role of anticoagulation is controversial, but anti­coagulation prior to drug or electrical cardiover­sion is definitely indicated in patients at high risk of emboli, i.e., those with mitral stenosis, pre­vious emboli, a prosthetic mitral valve, or car-diomegaly. Anticoagulation therapy should be ad­ministered two weeks prior to cardioversion and continued for about two weeks afterward. Rapid atrial pacing does not terminate atrial fibrillation.

In atrial tachycardia with AV block, the atrial rate is usually 150 to 200 beats per minute, and variable degrees of AV conduction are present. This rhythm is often associated with digitalis ex­cess and occurs most commonly in patients with significant organic heart disease, such as coronary heart disease, cor pulmonale, and digitalis intox­ication. Isoelectric intervals are present between P waves in contrast to atrial flutter. Carotid sinus massage should be performed with caution in pa­tients suspected of having digitalis toxicity. If the patient is not receiving digitalis, the rhythm may be treated with digitalis to slow the ventricular response, and subsequently quinidine, disopyr­amide, or procainamide may be added. If atrial tachycardia occurs in a patient receiving digitalis, digitalis toxicity should be suspected. Usually the ventricular response is not rapid and withholding digitalis is sufficient therapy.
Chaotic or multifocal atrial tachycardia is char­acterized by atrial rates between 100 and 130 beats per minute with marked variation in P wave mor­phology and irregular PP intervals. It occurs com­monly in patients with pulmonary disease and in diabetics or older patients who eventually may develop atrial fibrillation. Digitalis is usually not helpful in this arrhythmia. Therapy is directed to­ward the underlying disease.