Heart atrioventricular node

Radiofrequency catheter ablation Procedure during which radiofrequency energy is delivered through a catheter positioned at the atrioventricular node of the heart for the purpose of destroying one pathway of a reentrant circuit. 

Sympathetic (sympatholytic) Heart Sinus node Atrioventricular (AV node) Slowing Increased refractory period Bradycardia Dysrhythmias, conduction block... 

Cardiovascular conditions - Cholinesterase inhibitors have vagotonic effects on the sinoatrial and atrioventricular nodes, leading to bradycardia and AV block. These actions may be particularly important to patients with supraventricular cardiac conduction disorders or to patients taking other drugs concomitantly that significantly slow heart rate. Consider all patients to be at risk for adverse effects on cardiac conduction. 

Historically and romantically, the heartbeat is recognized as the quintessential hallmark of life. Normally, the heart beats at 60-100 beats per minute (bpm), with each beat yielding a ventricular contraction that ejects blood out to the body. Each heartbeat is an electrical event that originates from a collection of electrically excitable cells within the heart called the sinoatrial node (SA), anatomically located at the upper pole of the heart. The sinoatrial node is the primary pacemaker of the heart. The electrical impulse generated in the sinoatrial node spreads rapidly downward from the atria chambers of the heart and reaches the atrioventricular node (AV), a collection of electrically excitable cells that constitutes the electrical interface between the atria and ventricles of the heart. Erom the AV node, the impulse propagates throughout the ventricles via an electrical conduction system referred to as the His-Purkinje system. The electrical transmission... 

The primary cardiovascular effects of muscarinic agonists are reduction in peripheral vascular resistance and changes in heart rate. The direct effects listed in Table 7-3 are modified by important homeostatic reflexes, as described in Chapter 6 and depicted in Figure 6-7. Intravenous infusions of minimally effective doses of acetylcholine in humans (eg, 20-50 mcg/min) cause vasodilation, resulting in a reduction in blood pressure, often accompanied by a reflex increase in heart rate. Larger doses of acetylcholine produce bradycardia and decrease atrioventricular node conduction velocity in addition to hypotension. 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

Important differences between the available calcium channel blockers arise from the details of their interactions with cardiac ion channels and, as noted above, differences in their relative smooth muscle versus cardiac effects. Sodium channel block is modest with verapamil, and still less marked with diltiazem. It is negligible with nifedipine and other dihydropyridines. Verapamil and diltiazem interact kinetically with the calcium channel receptor in a different manner than the dihydropyridines they block tachycardias in calcium-dependent cells, eg, the atrioventricular node, more selectively than do the dihydropyridines. (See Chapter 14 for additional details.) On the other hand, the dihydropyridines appear to block smooth muscle calcium channels at concentrations below those required for significant cardiac effects they are therefore less depressant on the heart than verapamil or diltiazem. 

Amiodarone may produce symptomatic bradycardia and heart block in patients with preexisting sinus or atrioventricular node disease. 

FIGURE 23-2 Schematic representation of the conduction system of the heart. Conduction normally follows the pathways indicated by the dashed lines. Impulses originate in the sinoatrial node and are transmitted to the atrioventricular node. Impulses are then conducted from the atrioventricular node to the ventricles by the bundle of His and bundle branches. 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

The direct cardiac actions of muscarinic stimulants include the following (1) an increase in a potassium current (Ik(acii)) in atrial muscle cells and in the cells of the sinoatrial and atrioventricular nodes as well (2) a decrease in the slow inward calcium current (Ica) in heart cells and (3) a reduction in the hyperpolarization-activated current (If) that underlies diastolic depolarization. All of these actions are mediated by M2 receptors and contribute to slowing the pacemaker rate. Effects (1) and (2) cause hyperpolarization and decrease the contractility of atrial cells. 

Schematic representation of the heart and normal cardiac electrical activity (intracellular recordings from areas indicated and ECG). Sinoatrial node, atrioventricular node, and Purkinje cells display pacemaker activity (phase 4 depolarization). The ECG is the body surface manifestation of the depolarization and repolarization waves of the heart. The P wave is generated by atrial depolarization, the QRS by ventricular muscle depolarization, and the T wave by ventricular repolarization. Thus, the PR interval is a measure of conduction time from atrium to ventricle, and the QRS duration indicates the time required for all of the ventricular cells to be activated (ie, the intraventricular conduction time). The QT interval reflects the duration of the ventricular action potential.

In a healthy heart, the primary rhythm is generated by the sinuatrial node. If the latter is damaged or disconnected from the subsequent parts of conducting system, lower centers such as the atrioventricular node or the bundle of His can take over and supply a somewhat slower rhtythm. 

Figure 5.8. The conduction system of the heart, a Anatomy, b Electrical rhythm in the sinoatrial node (top), atrioventricular node (center), and the heart muscle (bottom). The dotted line inb (center) represents the own rhythm of the AV node that normally gets overridden by the faster sinoatrial rhythm (solid line).

The sinoatrial node (SA), consisting of spindle-shaped cells, initiates the electrical activity of the heart. From its location in the right atrium in proximity to the superior vena cava, the electrical activity spreads to the atria whose cells are larger than those of the SA. The pulse from the atria spreads to the atrioventricular node (AV), the gateway to the ventricles. The atria and the ventricles are electrically isolated. The AV node also slows down the electrical activity giving the atria time to fill. The bundle of His is the upper end of the electrical path, which through the Purkinje fibers allows the electrical signal to activate the ventricles and thus to pump the blood. 

Cardiac beta-1 stimulation results in increases in sinoatrial rate, myocardial contractility, and increased atrial, atrioventricular node, and ventricular conduction velocity. Beta blockers decrease heart... 

Cardiovascular Decreases heart rate, lowers blood pressure because of vasodilation, and slows conduction of atrioventricular node. Increases heart rate with large doses. Small doses can decrease heart rate. 

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