Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Diltiazem tachycardia

Nifedipine, verapamil, and diltiazem are all efficacious in the treatment of mild and moderate hypertension, but nifedipine is more efficacious than diltiazem and verapamil in the control of severe hypertension. Nifedipine does not cause significant reflex tachycardia or orthostatic hypotension. Nifedipine benefits the older and black patients and patients with low PRA. [Pg.142]

Closely monitor heart rate in patients treated with drugs that have negative chronotropic effects (e.g., fi-blockers, verapamil, or diltiazem) or drugs that may cause reflex tachycardia (e.g, nitrates or dihydropyridine CCBs). [Pg.81]

Diltiazem reduces transmembrane influx of calcium ions into cardiac muscle cells and vascular smooth musculature. It causes widening of coronary and peripheral vessels. It increases coronary blood flow, thus, preventing the development of coronary artery spasms. It lowers elevated blood pressure and reduces tachycardia. [Pg.303]

Fig. 3. Haemodynamic effects of different types of calcium antagonists. Drawn lines nifedipine and other rapidly an short-acting dihydropyridines. Dotted lines verapamil and diltiazem. MAP = mean arterial pressure HR = heart rate CO = cardiac output TPR = total peripheral resistance UE = urinary excretion of Na and H2O. Note the reflex tachycardia, provoked by nifedipine. Fig. 3. Haemodynamic effects of different types of calcium antagonists. Drawn lines nifedipine and other rapidly an short-acting dihydropyridines. Dotted lines verapamil and diltiazem. MAP = mean arterial pressure HR = heart rate CO = cardiac output TPR = total peripheral resistance UE = urinary excretion of Na and H2O. Note the reflex tachycardia, provoked by nifedipine.
Diltiazem Paroxysmal supraventricular tachycardia Atrial fibrillation... [Pg.183]

The prominent depressant action of verapamil and diltiazem at the SA and A-V nodes finds use in specific arrhythmias. They are of proven efficacy in acute control and long-term management of paroxysmal supraventricular tachycardia (see Chapter 16).Their ability to inhibit conduction at the A-V node is employed in protecting ventricles from atrial tachyarrhythmias, often in combination with digitalis or propranolol. [Pg.221]

Nifedipine is just one of many 1,4-dihydropyridines in contrast, the remaining three classes have only one representative agent. Nifedipine is selective for vascular smooth muscle and is therefore an excellent hypotensive. However, it can cause tachycardia (i.e., an excessive increase in heart rate), and is therefore prescribed with [3-adrenergic blockers. Verapamil and diltiazem have a direct effect on the heart, do not cause tachycardia, and are therefore the ideal antianginal agents. Phenylalkylamines need a 1- to 2-week lag period until their antianginal effect is evident. Bepridil has a relatively non-selective action. [Pg.427]

Class IV drugs are calcium-entry blockers of the phenylalkylamine (verapamil) and benzothiazepine (diltiazem) type. They slow atrioventricular conduction, and are used to treat supraventricular and sinus tachycardia. [Pg.159]

The short-acting cholinesterase inhibitor edrophonium was used to treat supraventricular tachyarrhythmias, particularly paroxysmal supraventricular tachycardia. In this application, edrophonium has been replaced by newer drugs (adenosine and the calcium channel blockers verapamil and diltiazem). [Pg.145]

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]

During the acute phase of thyrotoxicosis, B-adrenoceptor blocking agents without intrinsic sympathomimetic activity are extremely helpful. Propranolol, 20-40 mg orally every 6 hours, will control tachycardia, hypertension, and atrial fibrillation. Propranolol is gradually withdrawn as serum thyroxine levels return to normal. Diltiazem, 90-120 mg three or four times daily, can be used to control tachycardia in patients in whom blockers are contraindicated, eg, those with asthma. Other calcium channel blockers may not be as effective as diltiazem. Adequate nutrition and vitamin supplements are essential. Barbiturates accelerate T4 breakdown (by hepatic enzyme induction) and may be helpful both as sedatives and to lower T4... [Pg.868]

Verapamil and diltiazem are prototypic calcium channel blockers. As indicated previously, these drugs influence cardiac function by blocking inward calcium movement through L channels. In so doing they block conduction velocity in SA and AV node cells. They are used therapeutically to treat reentry arrhythmias through the AV node as well as paroxysmal supraventricular tachycardias. In fact, verapamil has been reported to terminate 60-80 percent of paroxysmal supraventricular tachycardias within several minutes. However, because of their potent effect on AV conduction, these drugs are contraindicated in patients with preexisting conduction problems since they may produce complete AV block. [Pg.261]

Therapeutic uses Verapamil and diltiazem are more effective against atrial than ventricular dysrhythmias. They are useful in treating reentrant supraventricular tachycardia and reducing ventricular rate in atrial flutter and fibrillation. In addition, these drugs are used to treat hypertension (see p. 187) and angina (see p. 177). [Pg.184]

CALCIUM CHANNEL BLOCKERS DOXORUBICIN t serum concentrations and efficacy of doxorubicin when co-administered with verapamil, nicardipine and possibly diltiazem and nifedipine however, no cases of doxorubicin toxicity have been reported Uncertain however, verapamil is known to inhibit intestinal P-gp, which may t the bioavailability of doxorubicin Watch for symptoms/signs of toxicity (tachycardia, heart failure and hand-foot syndrome)... [Pg.81]

In 33 patients with sjmptomatic and inducible supraventricular tachycardias single doses of placebo, flecainide 3 mg/kg, or dUtiazem 120 mg plus propranolol 80 mg were used to terminate the dysrhythmia (5). Conversion to sinus rhythm was achieved within 2 hours in 17 patients with placebo, in 20 with flecainide, and in 31 with diltiazem plus propranolol. Time to conversion was shorter with diltiazem plus propranolol (32 minutes) than with flecainide (74 minutes) or placebo (77 minutes). Of those who were given flecainide, two had hypotension and one had sinus bradycardia. [Pg.1370]

Myoclonic dystonia has been described in a 70-year-old man who took verapamil for supraventricular tachycardia for 10 months the abnormal movements disappeared within 3 weeks of substituting diltiazem, but rechaUenge was not attempted (13). [Pg.3618]

Most side effects of the calcium channel blockers are related to their mechanism of action. Verapamil and diltiazem can both cause sinus bradycardia and may worsen CHF. Constipation has been associated with verapamil use. The dihydropyridines often cause symptoms associated with vasodilatation, such as facial flushing, peripheral edema, hypotension, and headache. Because dihydropyridines are potent vasodilators, they can cause reflex tachycardia, which may precipitate palpitations, worsening angina, or Ml. Lastly, all calcium channel blockers can cause Gl complaints and fatigue. [Pg.21]

Although -blockers and calcium chaimel blockers have taken a more prominent role in acutely controlling rate in patients with rapid atrial fibrillation or flutter, a cautionary note must be made. That is, most patients with these tachycardias also have concomitant symptoms of heart failure, and these two forms of drug therapy may worsen the situation initially. Usually, a prompt decline in rate and increase in stroke volume balances the decrease in contractility seen with p blockers or calcium chaimel blockers such that heart failure symptoms remain unchanged. However, occasionally, severe reactions and hypotension may occur one study implies that diltiazem may be safer than verapamil. ... [Pg.333]

Of the CCBs, the nondihydropyradines (verapamil and dilti-azem) are the most effective because they lower heart rate in addition to lowering blood pressure. Nifedipine, because of its strong vasodilator properties, tends to cause hypotension and reflex tachycardia. In addition, nifedipine causes peripheral edema. These characteristics make it less useful in DHR Amlodipine is also effective because it reduces blood pressure. Initial doses are verapamil 120 to 240 mg/day, diltiazem 90 to 120 mg/day, and amlodipine 2.5 mg/day. [Pg.364]


See other pages where Diltiazem tachycardia is mentioned: [Pg.299]    [Pg.308]    [Pg.378]    [Pg.578]    [Pg.220]    [Pg.237]    [Pg.263]    [Pg.263]    [Pg.869]    [Pg.378]    [Pg.312]    [Pg.312]    [Pg.249]    [Pg.279]    [Pg.280]    [Pg.281]    [Pg.899]    [Pg.243]    [Pg.182]    [Pg.318]    [Pg.202]    [Pg.299]    [Pg.1026]    [Pg.642]    [Pg.10]    [Pg.370]    [Pg.208]    [Pg.328]   
See also in sourсe #XX -- [ Pg.7 , Pg.8 ]




SEARCH



Diltiazem

Tachycardia

© 2024 chempedia.info