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Atrioventricular node

Normal rhythmic activity is the result of the activity of the sinus node generating action potentials that are conducted via the atria to the atrioventricular node, which delays further conduction to the His-Tawara-Purkinje system. From the Purkinje fibres, action potentials propagate to the ventricular myocardium. Arrhythmia means a disturbance of the normal rhythm either resulting in a faster rhythm (tachycardia, still rhythmic) or faster arrhythmia (tachyarrhythmia) or slowed rhythm (bradycardia, bradyarrhythmia). [Pg.96]

Idiopathic degeneration of the atrioventricular node Myocardial ischemia or infarction Neurocardiac syncope Carotid-sinus hypersensitivity... [Pg.114]

Purkinje fibers Specialized myocardial fibers that conduct impulses from the atrioventricular node to the ventricles. [Pg.1575]

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. [Pg.1575]

Atrial natriuretic peptide (ANP), 5 186-187 Atrial tachycardia, 5 101, 104, 108 Atrioventricular node, 5 80 Atromid-S, 5 145-146... [Pg.78]

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. [Pg.1166]

IV Ibutilide Dofetilide Verapamil Diltiazem BepridiP Inhibit the slow inward calcium current, minimal effect (decrease) on ventricular action potential, major effects on the atrioventricular node to slow conduction velocity and increase the ERP. [Pg.170]

Moricizine depresses conduction and prolongs refractoriness in the atrioventricular node and in the in-franodal region. These changes are manifest in a prolongation of the PR interval on the electrocardiogram. [Pg.175]

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... [Pg.419]

Atrioventricular node Decrease in conduction velocity (negative dromotropy). Increase in refractory period... [Pg.136]

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. [Pg.137]

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. [Pg.184]

Cardiac muscle is highly dependent on calcium influx for normal function. Impulse generation in the sinoatrial node and conduction in the atrioventricular node—so-called slow-response, or calcium-dependent, action potentials—may be reduced or blocked by all of the calcium channel blockers. Excitation-contraction coupling in all cardiac cells requires calcium influx, so these drugs reduce cardiac contractility in a dose-dependent fashion. In some cases, cardiac output may also decrease. This reduction in cardiac mechanical function is another mechanism by which the calcium channel blockers can reduce the oxygen requirement in patients with angina. [Pg.262]

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. [Pg.262]

Class 4 action is blockade of the cardiac calcium current. This action slows conduction in regions where the action potential upstroke is calcium dependent, eg, the sinoatrial and atrioventricular nodes. [Pg.283]

Procainamide has direct depressant actions on sinoatrial and atrioventricular nodes that are only slightly counterbalanced by drug-induced vagal block. [Pg.285]

Amiodarone may produce symptomatic bradycardia and heart block in patients with preexisting sinus or atrioventricular node disease. [Pg.290]


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