Atrioventricular

One of the remarkable features of the heart, which is about the size of a fist, is that the pumping action or contractions (- 70 times/min) of atria and ventricles are simultaneous. Deoxygenated blood is pumped out to the lungs from one side of the heart at the same time oxygenated blood is pumped out from the other side to the aorta and onward through the body. The entire process of blood flow between the atria, ventricles, and the principal vessels is in unison, controlled in part by four one-way valves. The atrioventricular valves, tricuspid on the right and mitral on the left, prevent blood from flowing... 

The properties of -adrenoceptor blockers that contribute to antiarrhythmic effects are antagonism of neural/humoral P-adrenergic activity, and antagonism of catecholamine-mediated electrophysiological properties, ie, increase refractory period and decrease in the rate of diastoHc depolarization, ie, decrease automaticity and slow atrioventricular conduction (1,2). 

Patients having high plasma renin activity (PRA) (>8 ng/(mLh)) respond best to an ACE inhibitor or a -adrenoceptor blocker those having low PRA (<1 ng/(mLh)) usually elderly and black, respond best to a calcium channel blocker or a diuretic (184). -Adrenoceptor blockers should not be used in patients who have diabetes, asthma, bradycardia, or peripheral vascular diseases. The thiazide-type diuretics (qv) should be used with caution in patients having diabetes. Likewise, -adrenoceptor blockers should not be combined with verapamil or diltiazem because these dmgs slow the atrioventricular nodal conduction in the heart. Calcium channel blockers are preferred in patients having coronary insufficiency diseases because of the cardioprotective effects of these dmgs. 

Adenosine is produced by many tissues, mainly as a byproduct of ATP breakdown. It is released from neurons, glia and other cells, possibly through the operation of the membrane transport system. Its rate of production varies with the functional state of the tissue and it may play a role as an autocrine or paracrine mediator (e.g. controlling blood flow). The uptake of adenosine is blocked by dipyridamole, which has vasodilatory effects. The effects of adenosine are mediated by a group of G protein-coupled receptors (the Gi/o-coupled Ai- and A3 receptors, and the Gs-coupled A2a-/A2B receptors). Ai receptors can mediate vasoconstriction, block of cardiac atrioventricular conduction and reduction of force of contraction, bronchoconstriction, and inhibition of neurotransmitter release. A2 receptors mediate vasodilatation and are involved in the stimulation of nociceptive afferent neurons. A3 receptors mediate the release of mediators from mast cells. Methylxanthines (e.g. caffeine) function as antagonists of Ai and A2 receptors. Adenosine itself is used to terminate supraventricular tachycardia by intravenous bolus injection. 

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). 

In the following, the cardiac action potential is explained (Fig. 1) An action potential is initiated by depolarization of the plasma membrane due to the pacemaker current (If) (carried by K+ and Na+, which can be modulated by acetylcholine and by adenosine) modulated by effects of sympathetic innervation and (3-adrenergic activation of Ca2+-influx as well as by acetylcholine- or adenosine-dependent K+-channels [in sinus nodal and atrioventricular nodal cells] or to dqjolarization of the neighbouring cell. Depolarization opens the fast Na+ channel resulting in a fast depolarization (phase 0 ofthe action potential). These channels then inactivate and can only be activated if the membrane is hyperpolarized... 

Not all cells in the heart express the fast sodium channel. Thus, sinus nodal and atrioventricular nodal cells lack the fast Na+ channel and instead generate their action potentials via opening of Ca2+ channels. This is the basis for their sensitivity to Ca2+ antagonists. 

Class II drugs are classical (3-adrenoceptor antagonists such as propranolol, atenolol, metoprolol or the short-acting substance esmolol. These drugs reduce sinus rate, exert negative inotropic effects and slow atrioventricular conduction. Automaticity, membrane responsiveness and effective refractory period of Purkinje fibres are also reduced. The typical extracardiac side effects are due to (3-adrenoceptor blockade in other organs and include bronchospasm, hypoglycemia, increase in peripheral vascular resistance, depressions, nausea and impotence. 

The antimuscarinic drug atropine, and its derivative ipratropiumbromide, can also be used for antiarrhyth-mic treatment. Muscarinic receptors (M2 subtype) are mainly present in supraventricular tissue and in the AV node. They inhibit adenylylcyclase via G proteins and thereby reduce intracellular cAMP. On the other hand, activation of the M2 receptor leads to opening of hyperpolarizing Ik.acii and inhibits the pacemaker current If probably via the (3y-subunit of the Gi protein associated with this receptor. The results are hyperpolarization and slower spontaneous depolarization. Muscarinic receptor antagonists like atropine lead to increased heart rate and accelerated atrioventricular conduction. There are no or only slight effects on the ventricular electrophysiology. 

Atrioventricular block in general is treated by implantation of an electrical pacemaker. A pharmacological alternative (although no longer used today) was atropine. However, atropine can be used for bridging the time between the onset of symptoms and the definitive implantation of a pacemaker. 

Class II antiarrhythmic drugs are (3-adrenoceptor antagonists such as propranolol, metoprolol or atenolol. (3-adrenoceptor antagonists slow sinus rate and atrioventricular conduction and exert negative inotropic effects. 

Class IV antiarrhythmic drugs are Ca2+ channel blockers, which predominantly slow sinus rate and atrioventricular conduction and thus are used in the treatment of supraventricular tachyarrhythmias. These drugs exert a pronounced negative inotropic effect. 

Sites of endothelin-receptor expression. ETA receptors are expressed in the smooth muscle cells of the vascular medial layer and the airways, in cardiac myocytes, lung parenchyma, bronchiolar epithelial cells and prostate epithelial cells. ETB receptors are expressed in endothelial cells, in bronchiolar smooth muscle cells, vascular smooth muscle cells of certain vessels (e.g. saphenous vein, internal mammary artety), in the renal proximal and distal tubule, the renal collecting duct and in the cells of the atrioventricular conducting system. 

Supraventricular tachycardia is a heart condition characterised by fast arrhythmias involving the atrioventricular (AV) node. 

Heart Blood vessels Increase in heart rate, heart muscle contractility, increase in speed of atrioventricular conduction P Decrease in heart rate, decrease in heart muscle contractility... 

Decreases the conduction velocity through the atrioventricular (AV) and sinoatrial (SA) nodes in the heart... 

Adverse events need to be coded consistently with respect to letter case. Problems can occur when there is discordant coding using all capital letters, all lower-case letters, or combinations thereof, as computer software will interpret these capitalization variations as different events. Letter case sensitivity can be important when two or more words are used to describe an adverse event. For example, some databases utilizing the Medical Dictionary for Regulatory Activities (MedDRA) coding dictionary employ a coding system in which only the first letter of the first word of an adverse event is capitalized (e.g., Atrioventricular block complete ). Failing to adhere to uniform letter case conventions across the data can result in severe errors in data analysis. 

Compare and contrast the risk factors for and the features, mechanisms, etiologies, symptoms, and goals of therapy of (1) sinus bradycardia (2) atrioventricular (AV) nodal blockade (3) atrial fibrillation (AF) (4) paroxysmal supraventricular tachycardia (PSVT) ... 

FIGURE 6-1. The cardiac conduction system. AV, atrioventricular. (Reprinted with permission from Cummins RO, (ed.) ACLS Provider Manual. Dallas American Heart Association 2003 253.)... 

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

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