Premature atrial complexes

Common supraventricular tachycardias requiring drug treatment are atrial fibrillation (AF) or atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and automatic atrial tachycardias. Other common supraventricular arrhythmias that usually do not require drug therapy are not discussed in this chapter (e.g., premature atrial complexes, wandering atrial pacemaker, sinus arrhythmia, sinus tachycardia). 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

Premature atrial complexes are benign. However, when frequent, they can be premonitory of atrial flutter and, especially, of atrial fibrillation. 

Indeca.inide. Indecainide hydrochloride is a po active antiarrhythmic agent that received PDA approval in 1989, but it has not been marketed as of this writing. Chemically, it is 9-[3-(isopropylamino)propyl]fiuorine-9-carboxamide [74517-78-5]. The dmg has potent activity against premature ventricular complexes (PVCs) and ventricular tachycardias. Indecainide has no effect on sinus node function, atrial or ventricular effective refractory periods (32,33). 

Cardiac glycosides have a small ratio of toxic to therapeutic concentration. Possible adverse effects are nausea, vomiting, abdominal pain, diarrhoea, fatigue, headache, drowsiness, colour vision disturbances, sinus bradycardia, premature ventricular complexes, AV-block, bigeminy, atrial tachycardia with AV-Block, ventricular fibrillation. There are several mechanisms relevant for their toxic action (Table 2). 

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. 

Nonconducted No QRS complex follows premature atrial contraction (PAC). 

An isolated nonconducted P wave (a P wave not followed by a QRS complex, as shown in the shaded areas below) may result from second-degree atrioventricular (AV) block type 11 or a nonconducted premature atrial contraction (RAQ. Thinking a patient has nonconducted PACs when he really has AV block can have serious consequences. The former is usually benign, but the latter can be life-threatening. 

Lead II or the best lead that clearly shows P waves and the QRS complex may be used for sinus node arrhythmias, premature atrial contractions, and atrioventricular block... 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

In the AAI mode, atrial pacing will occur when the atrial rate falls below the programmed atrial rate (Fig. 3.1). When no intrinsic atrial activity has occurred within a specified interval (lower rate limit, LRL), atrial pacing occurs. The letter P is commonly used to indicate an atrial sensed event and the letter A is commonly used to indicate an atrial paced event. The intervals used in the AAI timing intervals are PP, AA, AP, and PA. Ventricular events such as a conducted QRS complex or a premature ventricular beat are not sensed in the AAI mode. The AAI mode is only appropriate in patients with intact... 

Fig. 3.23 Pacemaker mediated tachycardia (PMT). In this case, a premature ventricular contraction (second QRS complex) leads to retrograde ventriculo-atrial (VA) conduction. The atrial activity occurs after the PVARP has expired, is sensed, and leads to ventricular pacing, which again is associated with VA conduction. An incessant tachycardia can be initiated and sustained in this way.

Similarly, some systems identify an event sensed on the ventricular channel of the pacemaker which is not preceded by an atrial event, either paced or sensed, as a premature ventricular contraction (PVC). PVC s have a very definite implication for the clinician. The pacemaker s definition is far more specific as the pacemaker cannot analyze the morphology of the complex. Hence, nonphysiologic make-break electrical potentials associated with an internal insulation failure or conductor fracture will also be identified as PVCs as will accelerated junctional rhythms or episodes of atrial undersensing but with intact AV nodal conduction. Some systems may also identify runs of ventricu-... 

Ventricular bigeminy in contrast consists of alternating normal (intrinsic) QRS complexes followed by a regular repeating ventricular premature beat (Fig. 6.14). Ventricular trigeminy like atrial trigeminy occurs after every second QRS complex... 

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