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Titlebook: Cardiac therapy; Michael R. Rosen,Brian F. Hoffman Book 1983 Martinus Nijhoff Publishers, Boston 1983 arrhythmia.atherosclerosis.cardiovas

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https://doi.org/10.1007/978-1-4613-9014-5he general points raised above. We will discuss the specific indications, clinical pharmacology, and toxicity of the various drugs currently employed in the United States and will consider the prophylactic use of antiarrhythmic drugs in order to prevent sudden cardiac death in populations at risk.
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Cardiac failurees (shortness of breath and fatigue), which relate to the primary physiologic derangements. As the contractile abilities of the myocardium decrease, the heart has difficulty ejecting the blood that returns to it. This results in an increase in the venous pressures filling the two sides of the heart.
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Alpha- and beta-adrenergic agonists and antagonistsn general the ..-preceptor appears to mediate vascular smooth muscle contraction whereas the ..-receptor mediates inhibition of neurotransmitter release from sympathetic neuron terminals, inhibition of renin release from the kidney, platelet aggregation, and central inhibition of sympathetic outflow
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Pharmacology of the antiarrhythmic drugsinitiation and conduction which cause cardiac arrhythmias. Until the early 1960s only two drugs, quinidine and procainamide, were used widely as antiarrhythmics in the United States. During the past 15 years there has been a continuous growth in the number of agents available. In this chapter we dis
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Cardiac pacing: role in diagnosis and treatment of disorders of cardiac rhythm and conductionred to the heart will evoke a propagated response provided the stimulus is of appropriate strength and duration and is delivered during a period when the cardiac tissue is capable of responding. External stimuli can be applied epicardially or endocardially to any of the cardiac chambers or, under sp
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