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Cardiac arrhythmias conduction system

Halogenated hydrocarbons depress cardiac contractility, decrease heart rate, and inhibit conductivity in the cardiac conducting system. The cardiac-toxicity of these compounds is related to the number of halogen atoms it increases first as the number of halogen atoms increases, but decreases after achieving the maximum toxicity when four halogen atoms are present. Some of these compounds, e.g., chloroform, carbon tetrachloride, and trichloroethylene, sensitize the heart to catecholamines (adrenaline and noradrenaline) and thus increase the risk of cardiac arrhythmia. [Pg.297]

Some metals, such as cadmium, cobalt, and lead, are selectively car-diotoxic. They depress contractivity and slow down conduction in the cardiac-system. They may also cause morphological alterations, e.g., cobalt, which was once used to prevent excessive foam formation in beers, caused cardiomyopathy among heavy beer drinkers. Some of the metals also block ion channels in myocytes. Manganese and nickel block calcium channels, whereas barium is a strong inducer of cardiac arrhythmia. [Pg.297]

Parenteral therapy The dangers of parenteral use of quinidine are increased in the presence of AV block or absence of atrial activity. Administration is more hazardous in patients with extensive myocardial damage. Use of quinidine in digitalis-induced cardiac arrhythmia is extremely dangerous because the cardiac glycoside may already have caused serious impairment of intracardiac conduction system. Too rapid IV administration of as little as 200 mg may precipitate a fall of 40 to 50 mm Hg in arterial pressure. [Pg.425]

Cardiovascular System. Atropine is sometimes used to block the effects of the vagus nerve (cranial nerve X) on the myocardium. Release of acetylcholine from vagal efferent fibers slows heart rate and the conduction of the cardiac action potential throughout the myocardium. Atropine reverses the effects of excessive vagal discharge and is used to treat the symptomatic bradycardia that may accompany myocardial infarction.4 Atropine may also be useful in treating other cardiac arrhythmias such as atrioventricular nodal block and ventricular asystole. [Pg.270]

Although cardiac arrhythmias involve the electrical conduction system of the heart including the sinus node, atrioventricular... [Pg.549]

Uhley HN. The quadrifascicular nature of the peripheral conduction system in cardiac arrhythmias. In Dreifus L, Likoff W (eds) Cardiac Arrhythmias. Grune - Stratton. New York 1973. [Pg.323]

During Amy Lloyd s evalnation, she developed a cardiac arrhythmia that was refractory to treatment. The extensive amyloid deposits in her heart had disrupted conduction of electrical impulses in the heart muscle, ultimately resulting in cardiac arrest. On autopsy, amyloid deposits were found within the heart, tongue, liver, adipose tissue, and every organ examined except the central nervous system, which had been protected by the blood-brain barrier. [Pg.111]

Six helpful appendices are included Quick guide to cardiac arrhythmias summarizes the details of 20 arrhythmias Cardiac drug overview covers commonly used cardiac drugs Best monitoring leads shows the most beneficial leads to monitor for the most challenging arrhythmias Depolarization-repolarization cycle explains the five phases of this cardiac cycle Action potential curves reviews the cellular changes that occur during the depolarization-repolarization cycle and Cardiac conduction system reviews how electrical impulses affect heart function. [Pg.303]

Mechanism of Action An antiarrhythmic that increases the electrical stimulation threshold of the ventricles and His-Purkinje system. Decreases myocardial excitability and conduction velocity and depresses myocardial contractility Exerts direct cardiac effects. Therapeutic Effect Suppresses arrhythmias. [Pg.1029]

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. [Pg.326]


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See also in sourсe #XX -- [ Pg.322 , Pg.323 , Pg.323 ]




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