Bradyarrhythmias treatment

Dmgs that mimic or inhibit the actions of neurotransmitters released from parasympathetic or sympathetic nerves innervating the heart may also be used to treat supraventricular bradyarrhythmias, heart block, and supraventricular tachyarrhythmias. Those used in the treatment of arrhythmias may be found in Table 1. 

Isoproterenol. Isoproterenol hydrochloride is an nonselective P-adrenoceptor agonist that is chemically related to NE. It mimics the effects of stimulation of the sympathetic innervation to the heart which are mediated by NE. It increases heart rate by increasing automaticity of the SA and AV nodes by increasing the rate of phase 4 diastoHc depolarization. It is used in the treatment of acute heart block and supraventricular bradyarrhythmias, although use of atropine is safer for bradyarrhythmias foUowing MI (86). 

Treatment of sinus node dysfunction involves elimination of symptomatic bradycardia and possibly managing alternating tachycardias such as AF. Asymptomatic sinus bradyarrhythmias usually do not require therapeutic intervention. 

Propofol is very lipid soluble, has a large volume of distribution, and has a rapid onset of action. It has comparable efficacy to midazolam for refractory GCSE. It has been associated with metabolic acidosis, hemodynamic instability, and bradyarrhythmias that are refractory to treatment. 

Isoprenaline occasionally has a place in the management of cardiac conditions in which bradycardia is a feature, e.g. low cardiac output associated with slow heart rate after extracorporeal circulation in patients with excessive p-blocking therapy. It may also be used in the treatment of overdose with (3-adrenoceptor antagonists and for refractory bradyarrhythmias prior to cardiac pacing. Isoprenaline is used in the treatment of bronchial asthma on account of its 32 effects. 

Bradyarrhythmias (including asystole) and/or hypotension are frequent in CS, usually occur during balloon inflations and generally respond promptly to balloon deflation. Prevention is by adequate hydration, conservative balloon sizing, premedication with atropine and early ambulation. Although some advocate the routine prophylactic use of temporary transvenous pacemakers in CS (64,65), we consider the risks of this procedure to outweigh any potential benefit. In one series (n = I 14), a transvenous pacemaker was required in 9.6% (66), though in our experience this is needed far less frequently, Permanent pacemaker requirement is exceptionally rare, Occasionally, patients require short-term treatment... 

Scopolamine is an anticholinergic agent used for the treatment of spasmodic colic it has been shown to inhibit romifidine-induced bradyarrhythmias (Marques et al 1998). Unlike atropine, scopolamine does not induce an initial bradycardia (Grainger Smith 1983) and decreased gastrointestinal motility lasts only 20-30 min in horses (Roelvink et al 1991). The use of scopolamine in the face of life-threatening bradycardias in horses has not been established. 

The preceding sections reviewed the pathophysiology and treatment of tachyarrhythmias, and this section serves to briefly consider the bradyarrhythmias. For the most part, the symptoms of bradyarrhyth-... 

The incidence of phenytoin toxicity may be increased in the eideriy, or in those patients with hepatic or renal impairment, because of alterations in its pharmacokinetics. Plasma level determinations may be indicated in these cases. Although a role for P-glycoprotein transporter alleles in the development of phenytoin toxicity remains controversial, phenytoin is a robust substrate for the non-ABC efflux transporter RLIP76. Because RLIP76 has been found to be overexpressed in excised human epileptic foci, its action may account for treatment failures conversely, inhibition of transport may cause toxicity (34). There is a 2 to 3% increase in the risk of fetal epilepsy syndrome if the mother is taking phenytoin. Phenytoin is contraindicated in cardiac patients with bradyarrhythmias. Induction of CYP2C19 by ginkgo biloba may increase phenytoin clearance and precipitate serious seizures (35). 

Concurrent use is unquestionably valuable and uneventful in many patients, but severe adverse effects can develop. This is well established. A not dissimilar adverse interaction can occur with verapamil , (p.841). On the basis of 6 reports, the incidence of symptomatic bradyarrhythmia was estimated to be about 10 to 15%. It can occur with different beta blockers, even with very low doses, and at any time from within a few hours of starting treatment to 2 years of concurrent use. The main risk factors seem to be ventricular dysfunction, or sinoatrial or AV nodal conduction abnormalities. Note that these are usually contraindications to the use of diltiazem. Patients with normal ventricular function and no evidence of conduction abnormalities are usually not at risk. Concurrent use should be well monitored for evidence of adverse effects. Changes in the pharmacokinetics of the beta blockers may also occur, but these changes are probably not clinically important. 

As early as the late 1700s, Physicians speculated that electrical current could be used to stimulate the heart. In 1882, von Ziemssen used electrical current to directly stimulate the heart of a woman whose anterior chest wall had been removed after resection of a chest tumor. In 1952, ZoU used transthoracic current to pace the heart, and in 1958 the first implantable pacanaker was placed by Ake Senning and Rune Elmquist. At the same time, Furman and Robinson demonstrated the feasibility of transvenous cardiac pacing. In the late 1960s, Mirowski and colleagues pioneered the concept of an implantable device that could be used to defibrillate the heart. Over the last 50 years, implantable cardiac devices have become the primary treatment for bradyarrhythmias and ventricular tachyarrhythmias and have emerged as an important adjunctive therapy for patients with heart failure. It is currently estimated that almost 400,000 pacemakers and defibrillators are implanted annually in the United States. 

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