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Supraventricular tachycardia treatment

Valproate overdose results in increasing sedation, confusion, and ultimately, coma. The patient may also manifest hyperreflexia or hyporeflexia, seizures, respiratory suppression, and supraventricular tachycardia. Treatment should include gastric lavage, electrocardiographic monitoring, treatment of emergent seizures, and respiratory support. [Pg.151]

Dlgltoxin. Digitoxin is a cardiac glycoside obtained from Digitalis purpurea. Digitoxin is indicated in the treatment of atrial flutter, atrial fibrillation, and supraventricular tachycardia. Its electrophysiologic and adverse effects are similar to those described for digoxin (87). [Pg.120]

Presently, only adenosine itself is approved for clinical use. It is used widely in the treatment of supraventricular tachycardia and in cardiac stress imaging to assess coronary artery disease [5]. Other agonists and antagonists and an allosteric modulator of the Ai receptor are in clinical trials for a variety of indications. [Pg.27]

PI (adenosine) receptors were explored as therapeutic targets before P2 receptors. Adenosine was identified early and is in current use to treat supraventricular tachycardia. A2a receptor antagonists are being investigated for the treatment of Parkinson s disease and patents have been lodged for the application of PI receptor subtype agonists and antagonists for myocardial ischaemia and reperfusion injury, cerebral ischaemia, stroke, intermittent claudication and renal insufficiency. [Pg.1052]

These dm are primarily used in the treatment of hypertension (see the Summary Drug Table Adrenergic Blocking Drugs also see Chap. 39) and certain cardiac arrhythmias (abnormal rhythm of the heart), such as ventricular arrhythmias or supraventricular tachycardia They are used to prevent reinfarction in patients with a recent myocardial infarction (1—4 weeks after MI). Some of these dm have additional uses, such as the use of propranolol for migraine headaches and nadolol for angina pectoris. [Pg.214]

Common supraventricular tachycardias requiring drug treatment are atrial fibrillation (AF) or atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and automatic atrial tachycardias. Other common supraventricular arrhythmias that usually do not require drug therapy are not discussed in this chapter (e.g., premature atrial complexes, wandering atrial pacemaker, sinus arrhythmia, sinus tachycardia). [Pg.73]

FIGURE 6-2. Algorithm for the treatment of acute (top portion) paroxysmal supraventricular tachycardia and chronic prevention of recurrences (bottom portion). Note For empiric bridge therapy prior to radiofrequency ablation procedures, calcium channel blockers (or other atrioventricular [AV] nodal blockers) should not be used if the patient has AV reentry with an accessory pathway. (AAD, antiarrhythmic drugs AF, atrial fibrillation AP, accessory pathway AVN, atrioventricular nodal AVNRT, atrioventricular nodal reentrant tachycardia AVRT, atrioventricular reentrant tachycardia DCC, direct-current cardioversion ECG, electrocardiographic monitoring EPS, electrophysiologic studies PRN, as needed VT, ventricular tachycardia.)... [Pg.83]

Gradual control For postoperative tachycardia and hypertension, the dosing schedule is the same as that used in supraventricular tachycardia. To initiate treatment, administer a loading dosage infusion of 500 mcg/kg/min for 1 minute followed by a 4-minute maintenance infusion of 50 mcg/kg/min. If an adequate therapeutic effect is not observed within 5 minutes, repeat the same loading dosage and follow with a maintenance infusion increased to 100 mcg/kg/min (see Supraventricular tachycardia). [Pg.512]

Verapamil and a few newer dmgs of this category are vasodilator agents, which in addition impair AV conduction, reduce heart rate and cardiac contractile force. Verapamil was initially developed for the treatment of supraventricular tachycardia and it continues to be an important drug for the management of this condition, also postoperatively. Verapamil is the CA of choice in the management of hypertrophic cardiomyopathy. Verapamil is also used in the treatment of stable angina and, less frequently, essential hypertension. [Pg.331]

Adenosine reduces heart rate and AV conduction, although it is not a calcium antagonist. It is administered intravenously for the acute treatment of paroxysmal supraventricular tachycardia. Adenosine displays a rapid onset and short duration of action. Apart from its antiarrhythmic activity it is also a vasodilator, in particular in the coronary system. [Pg.341]

Unlabeled Uses Prophylaxis and treatment of supraventricular tachycardia... [Pg.385]

It is a vasopressor agent with some structural similarity to adrenaline and has a powerful alpha receptor stimulant action. The pressor response is accompanied by reflex bradycardia. It is used as a nasal decongestant and mydriatic agent and also in the treatment of paroxysmal supraventricular tachycardia. [Pg.138]

Paroxysmal supraventricular tachycardia, atrial fibrillation and flutter. Not of benefit in treatment of ventricular arrhythmias Miscellaneous... [Pg.157]

This agent also has some class lA and class II effects. It is effective for the treatment of ventricular and supraventricular tachycardias (AV nodal and accessory pathway re-entry, atrial flutter and fibrillation). Propafenone is useful in converting recent-onset atrial fibrillation or flutter to sinus rhythm, and for terminating paroxysmal supraventricular tachycardia. Its pro-ariythmic and myocardial depressant effects limit its use, especially in patients with poor ventricular function. [Pg.159]

Supraventricular tachycardia is the major arrhythmia indication for verapamil. Adenosine or verapamil are preferred over older treatments (propranolol, digoxin, edrophonium, vasoconstrictor agents, and cardioversion) for termination. Verapamil can also reduce the ventricular rate in atrial fibrillation and flutter. It only rarely converts atrial flutter and fibrillation to sinus rhythm. Verapamil is occasionally useful in ventricular arrhythmias. However, intravenous verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. [Pg.292]

De Catte L, De Wolf D, Smitz J, Bougatef A, De Schepper J, Foulon W. Fetal hypothyroidism as a complication of amiodarone treatment for persistent fetal supraventricular tachycardia. Prenat Diagn 1994 14(8) 762-5. [Pg.660]

Verapamil s cardiotoxic effects are dose-related and usually avoidable. A common error has been to administer intravenous verapamil to a patient with ventricular tachycardia misdiagnosed as supraventricular tachycardia. In this setting, hypotension and ventricular fibrillation can occur. Verapamil s negative inotropic effects may limit its clinical usefulness in diseased hearts (see Chapter 12 Vasodilators the Treatment of Angina Pectoris). Verapamil can lead to atrioventricular block when used in large doses or in patients with atrio-ventricular nodal disease. This block can be treated with atropine and -receptor stimulants. In patients with sinus node disease, verapamil can precipitate sinus arrest. [Pg.339]

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. [Pg.260]

As noted above, the antiarrhythmic drugs can modify impulse generation and conduction. More than a dozen such drugs that are potentially useful in treating arrhythmias are currently available. However, only a limited number of these agents are clinically beneficial in the treatment of selected arrhythmias. For example, the acute termination of ventricular tachycardia by lidocaine or supraventricular tachycardia by adenosine or verapamil are examples in which antiarrhythmic therapy results in decreased morbidity. In contrast, many of the antiarrhythmic agents are now known to have lethal proarrhythmic actions, that is, to cause arrhythmias. [Pg.177]

When lack of therapeutic effect and toxicity may be difficult to distinguish. Digoxin is both a treatment for, and sometimes the cause of, cardiac supraventricular tachycardia a plasma digoxin measurement will help to distinguish whether an arrhythmia is due to too tittle or too much digoxin... [Pg.104]

An anaphylactic reaction has been reported in a 75-year-old woman who was given adenosine 12 mg for a supraventricular tachycardia. She developed bronchospasm and profound inspiratory stridor, her arterial blood pressure fell to 50/30 mmHg from an arterial systolic pressure of 70 mmHg, and she recovered with appropriate treatment (41). [Pg.38]

Pfammatter IP, Bauersfeld U. Safety issues in the treatment of paediatric supraventricular tachycardias. Drug Saf 1998 18(5) 345-56. [Pg.39]

Watt AH, Bernard MS, Webster J, Passani SL, Stephens MR, Routledge PA. Intravenous adenosine in the treatment of supraventricular tachycardia a dose-ranging study and interaction with dipyridamole. Br J Chn Pharmacol 1986 21(2) 227-30. [Pg.40]

Pfammatter JP, Stocker FP. Re-entrant supraventricular tachycardia in infancy current role of prophylactic digoxin treatment. Eur J Pediatr 1998 157(2) 101-6. [Pg.668]

D Souza D, MacKenzie WE, Martin WL. Transplacental flecainide therapy in the treatment of fetal supraventricular tachycardia. J Obstet Gynaecol 2002 22(3) 320-2. [Pg.1375]

Hypotension or hypertension, benign sinus or supraventricular tachycardia, and rarely distal cyanosis, have been reported within the first days of treatment in 5-15% of patients receiving high-dose interferon alfa (20). These adverse effects are usually benign, except in high-risk patients with a previous history of dysrhythmias, coronary disease, or cardiac dysfunction. [Pg.1794]

Laniado S, Kronzon I, Mehta SS. Pulmonary edema a complication of metaraminol treatment of paroxysmal supraventricular tachycardia. Isr J Med Sci 1974 10(5) 504-8. [Pg.2269]

Fassio T, Canobbio L, Gasparini G, VUlani F. Paroxysmal supraventricular tachycardia during treatment with cisplatin and etoposide combination. Oncology 1986 43(4) 219-20. [Pg.2866]


See other pages where Supraventricular tachycardia treatment is mentioned: [Pg.121]    [Pg.122]    [Pg.603]    [Pg.144]    [Pg.52]    [Pg.275]    [Pg.80]    [Pg.80]    [Pg.151]    [Pg.591]    [Pg.70]    [Pg.39]    [Pg.60]    [Pg.2092]    [Pg.2293]   
See also in sourсe #XX -- [ Pg.66 , Pg.78 , Pg.164 , Pg.172 ]




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