Junctional arrhythmias

When specialized pacemaker cells in the atrioventricular junction take over as the dominant pacemaker of the heart, several events can occur  

These illustrations show the various locations of P waves in junctional arrhythmias, depending on the direction of depolarization. 

If the atria are depolarized first, the P wave will appear before the QRS complex. 

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Therapeutic uses Lidocaine is useful in treating ventricular arrhythmias arising during myocardial ischemia, such as that experienced during a myocardial infarction. The drug does not markedly slow conduction and thus has little effect on atrial or AV junction arrhythmias. 

Street drugs sometimes contain adulterants added to increase the volume of drug perceived to be purchased. A case study reports atrioventricular junctional arrhythmia caused by quinine/quinidine added to heroin which was subsequently intravenously injected [24 ]. The authors report that a normal urine toxicological screening assay would not detect the adulteration, and that physicians should be aware of common adulterants. 

Short PR intervals (less than 0.12 second) signify impulses originating somewhere other than the SA node, as in junctional arrhythmias or preexcitation syndromes. 

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. 

The major therapeutic uses of the cholinomimetics are for diseases of the eye (glaucoma, accommodative esotropia), the gastrointestinal and urinary tracts (postoperative atony, neurogenic bladder), the neuromuscular junction (myasthenia gravis, curare-induced neuromuscular paralysis), and very rarely, the heart (certain atrial arrhythmias). Cholinesterase inhibitors are occasionally used in the treatment of atropine overdosage. Several newer cholinesterase inhibitors are being used to treat patients with Alzheimer s disease. 

The most common cardiac manifestations of digitalis toxicity include atrioventricular junctional rhythm, premature ventricular depolarizations, bigeminal rhythm, and second-degree atrioventricular blockade. However, it is claimed that digitalis can cause virtually any arrhythmia. 

Succinylcholine Agonist at nicotinic acetylcholine (ACh) receptors, especially at neuromuscular junctions depolarizes may stimulate ganglionic nicotinic ACh and cardiac muscarinic ACh receptors Initial depolarization causes transient contractions, followed by prolonged flaccid paralysis depolarization is then followed by repolarization that is also accompanied by paralysis Placement of tracheal tube at start of anesthetic procedure t rarely, control of muscle contractions in status epilepticus Rapid metabolism by plasma cholinesterase normal duration, 5 min Toxicities Arrhythmias hyperkalemia transient increased intraabdominal, intraocular pressure postoperative muscle pain... 

Vomiting is common in patients with digitalis overdose. Hyperkalemia may be caused by acute digitalis overdose or severe poisoning, whereas hypokalemia may be present in patients as a result of long-term diuretic treatment. (Digitalis does not cause hypokalemia.) A variety of cardiac rhythm disturbances may occur, including sinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias. 

What is the role of the gap junctions By coupling the myocardial cells in both directions (longitudinal and transverse) they are responsible for the biophysical properties of the tissue. A reduction in gap junction distribution or a closure of the gap junction channels causes nonuniformities and discontinuities which alter the biophysical properties of the tissue and make it more prone to nonuniform anisotropic reentry. According to the model proposed by Krinsky [1966], a reduction in gap junctions or a closure of gap junction channels will lead to local slowing of conduction, thereby allowing smaller perimeters of reentrant arrhythmia. In addition, slowing of conduction is generally believed to be a risk factor for initiation of reentry. Since in many... 

In the following paragraphs several types of arrhythmia will be discussed with regard to the underlying mechanisms. Since it would be out of the scope of this book on gap junction channels to discuss all possible mechanisms of arrhythmia in detail, readers interested in a complete detailed review of the pathophysiology and clinics of arrhythmia are referred to the reviews by Janse and Wit [1989] and Pogwizd and Corr [1987, 1990] and to the specialized literature. 

Furthermore, synchronization of contraction is facilitated by gap junctional communication as well as synchronization of electrical activation. The electrical coupling between cardiomyocytes mitigates differences in the membrane potential between these cells, for example in the course of an action potential if both cells repolarize at different timepoints. This results in smaller differences in the repolarization times thereby causing a reduction in the dispersion of the action potential duration. Since increased dispersion is known to make the heart more prone to reentrant arrhythmia, sufficient gap junctional communication can be considered as an endogenous arrhythmia-preventing mechanism. For a detailed discussion of the role of gap junctional communication in the biophysics of cardiac activation as related to anisotropy, nonuniformity and stochastic phenomena, see chapter 1 for a discussion of their role in arrhythmia, see chapter 6, and for a possible pharmacological intervention at the gap junctions for suppression of arrhythmia, refer to chapter 7. 

Besides these, type-lb arrhythmia can occur at 12-30 min after the onset of ischemia with a peak at 15-20 min. These type-lb arrhythmias are either due to a partial recovery of the cell excitability (partial recovery of dU/dt and of the action potential duration), which may be ascribed to the release of catecholamines [for review see, Janse and Wit, 1989] or are due to gap junctional... 

Another cardiac disease often associated with cardiac arrhythmias is heart failure. Many factors including high catecholamine levels, dilated tissue geometry, changes in the [3-adrenoceptor population, impairment of the regulation of the intracellular (diastolic) calcium concentration, possibly enhanced endo-thelin levels and many more contribute to altered cardiac function and make the heart more prone to arrhythmia. However, the question was whether, in addition to the well-known structural changes, gap junction alterations may also partially form the arrhythmogenic substrate. Thus, researchers were interested in whether in the course of heart failure gap junctional alterations may occur. 

From these experiments in rats and goats described above it was concluded that chronic arrhythmia may represent a state in which the distribution pattern of gap junctions can be altered by a yet unknown mechansim. This change in the gap junction pattern may then form the basis for chronification of the arrhythmia. 

The immunohistochemical findings were correlated with reduced intercellular coupling indicating a possible role of disturbed Cx43 expression and gap junction function in the pathogenesis of Chagas disease and the arrhythmias associated with that disease. 

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