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Arrhythmia abnormal impulse conduction

O Cardiac arrhythmias may be caused by abnormal impulse formation (automaticity), abnormal impulse conduction (reentry), or both. [Pg.107]

In general, cardiac arrhythmias are caused by (1) abnormal impulse formation (2) abnormal impulse conduction or (3) both. [Pg.110]

The mechanism of abnormal impulse conduction is traditionally referred to as reentry. Reentry is often initiated as a result of an abnormal premature electrical impulse (abnormal automaticity) therefore, in these situations, the mechanism of the arrhythmia is both abnormal impulse formation (automaticity) and abnormal impulse conduction (reentry). In order for reentry to occur, three conditions must be present. There must be (1) at least two pathways down which an electrical impulse may... [Pg.110]

The procedure causes immediate depolarization, interrupting reentry circuits (abnormal impulse conduction that occurs when cardiac tissue is activated two or more times, causing reentry arrhythmias) and allowing the SA node to resume control. [Pg.113]

Hypersensitivity or idiosyncrasy to quinidine or other cinchona derivatives manifested by thrombocytopenia, skin eruption or febrile reactions myasthenia gravis history of thrombocytopenic purpura associated with quinidine administration digitalis intoxication manifested by arrhythmias or AV conduction disorders complete heart block left bundle branch block or other severe intraventricular conduction defects exhibiting marked QRS widening or bizarre complexes complete AV block with an AV nodal or idioventricular pacemaker aberrant ectopic impulses and abnormal rhythms due to escape mechanisms history of drug-induced torsade de pointes history of long QT syndrome. [Pg.424]

Many factors can precipitate or exacerbate arrhythmias ischemia, hypoxia, acidosis or alkalosis, electrolyte abnormalities, excessive catecholamine exposure, autonomic influences, drug toxicity (eg, digitalis or antiarrhythmic drugs), overstretching of cardiac fibers, and the presence of scarred or otherwise diseased tissue. However, all arrhythmias result from (1) disturbances in impulse formation, (2) disturbances in impulse conduction, or (3) both. [Pg.279]

Arrhythmias are caused by abnormal pacemaker activity or abnormal impulse propagation. Thus, the aim of therapy of the arrhythmias is to reduce ectopic pacemaker activity and modify conduction or refractoriness in reentry circuits to disable circus movement. The major mechanisms currently available for accomplishing these goals are (1) sodium channel blockade, (2) blockade of sympathetic autonomic effects in the heart, (3) prolongation of the effective refractory period, and (4) calcium channel blockade. [Pg.281]

Most arrhythmias arise either from aberrations in impulse generation (abnormal automaticity) or from a defect in impulse conduction. [Pg.176]

In some types of rhythm disorders, antiar-rhythmics of the local anesthetic, Na+-channel blocking type are used for both prophylaxis and therapy. These substances block the Na+ channel responsible for the fast depolarization of nerve and muscle tissues. Therefore, the elicitation of action potentials is impeded and impulse conduction is delayed. This effect may exert a favorable influence in some forms of arrhythmia, but can itself act arrhythmogenically. Unfortunately, antiarrhythmics of the local anesthetic, Na+-channel blocking type lack suf -cient specificity in two respects (1) other ion channels of cardiomyocytes, such as K1 and Ca+ channels, are also affected (abnormal QT prolongation) and (2) their action is not restricted to cardiac muscle tissue but also impacts on neural tissues and brain cells. Adverse effects on the heart include production of arrhythmias and lowering of heart rate, AV conduction, and systolic force. CNS side effects are manifested by vertigo, giddiness, disorientation, confusion, motor disturbances, etc. [Pg.136]

Cardiac arrhythmias or dysrhythmias are disturbances of the normal regular rhythm which may be caused by an abnormality in the site of impulse generation, its rate or regularity, or its propagation or conduction (1,2). The more commonly encountered cardiac arrhythmias are... [Pg.112]

Normal cardiac contraction depends on the conduction of electrical impulses through the myocardium in a highly coordinated fashion. Any abnormality of the initiation or propagation of the impulse is referred to as an arrhythmia. These disorders are the most common clinical problem encountered by a cardiologist. There is a wide range of types of arrhythmias with multiple etiologies and a variety of symptoms. In this section, two types of cardiac tachyarrhythmias are discussed. The most common treatment for these conditions is drug therapy. [Pg.176]

Inhalation of certain hydrocarbons, including some anesthetics, can make the mammalian heart abnormally sensitive to epinephrine, resulting in ventricular arrhythmias, which in some cases can lead to sudden death (Reinhardt et al. 1971). The mechanism of action of cardiac sensitization is not completely understood but appears to involve a disturbance in the normal conduction of the electrical impulse through the heart, probably by producing a local disturbance in the electrical potential across cell membranes. The hydrocarbons themselves do not produce arrhythmia the arrhythmia is the result of the potentiation of endogenous epinephrine (adrenalin) by the hydrocarbon. [Pg.160]

Cardiac arrhythmias is a group of disorder characterized by an abnormal cardiac rhythm and arise as a result of disorders of impulse formation or conduction or both. [Pg.189]

The primary cause of death in acute diazinon poisoning is a depression of the neurons in the brainstem (medulla), collectively known as the respiratory center, resulting in loss of respiratory drive or, in the case of managed treatment, cardiac failure due to electrical impulse or beat conduction abnormalities in cardiac muscles (fatal arrhythmias). Other effects, such as bronchoconstriction, excessive bronchial secretions, and paralysis of the respiratory muscles (intercostal muscles and diaphragm) may also contribute to respiratory insufficiency and death. Thus, death results from loss of respiratory drive and paralysis of the respiratory muscles, or cardiac failure, or both, with attendant asphyxia or cardiac arrest (Klaassen et al. 1986 Shankar 1967, 1978 Williams and Burson 1985). [Pg.93]

Simultaneous abnormalities of impulse generation and conduction. A combination of both previously listed factors may cause cardiac arrhythmias. [Pg.323]

Altered rate of automatic discharge or abnormality of the mechanism by which an impulse is generated from a centre in the nodes or conducting tissue, is one cause of cardiac arrhythmia, e.g. atrial fibrillation, flutter or tachycardia. [Pg.498]

P-ARK An enzyme that phosphoylates the occupied form of a G-protein coupled receptor, e.g. the 6-adrenoceptor, leading to uncoupling of that receptor and desensitization. ARMI age-related memory impairment, arrhythmia (dysrhythmia) An abnormality of heart rhythm or rate of heartbeat, usually caused by disturbance of the electrical impulses and their conduction within the heart. They include ectopic beats (isolated irregular beats), tachycardias (too fast a heartbeat), bradycardias (too slow a heartbeat) and atrial flutter and ventricular fibrillation. Arthus reaction A severe local inflammatory response, a skin reaction characterized by erythema, oedema, necrosis, local haemorrhage. A type III hypersensitivity reaction. Arunlakshana and Schild plot See Schild plot, ascites fluid The fluid that accumulates in the peritoneal cavity during certain pathological conditions, aspiration The withdrawal of fluid or tissue from the body by suction. [Pg.301]

Reentrant arrhythmia Arrhythmia of abnormal conduction involves the repetitive passage of an impulse through tissue previously excited by the same impulse... [Pg.130]


See other pages where Arrhythmia abnormal impulse conduction is mentioned: [Pg.420]    [Pg.318]    [Pg.256]    [Pg.176]    [Pg.89]    [Pg.889]    [Pg.117]    [Pg.599]    [Pg.256]    [Pg.174]    [Pg.174]    [Pg.477]    [Pg.56]    [Pg.154]   
See also in sourсe #XX -- [ Pg.11 , Pg.110 ]




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