Sinus rhythm, normal

Pirmenol. Pirmenol hydrochloride, a pyridine methanol derivative, is a racemic mixture. It has Class lA antiarrhythmic activity, ie, depression of fast inward sodium current, phase 0 slowing, and action potential prolongation. The prolongation of refractory period may be a Class III property. This compound has shown efficacy in converting atrial arrhythmias to normal sinus rhythm (34,35). 

Propranolol. Propranolol hydrochloride, considered the prototype of the P-adrenoceptor blocking agents, has been in use since 1964. It is a nonselective, highly Hpid-soluble P-adrenoceptor blocker having no ISA. It is a mixture of (+) and (—) enantiomers, and the (—) enantiomer is the active moiety. The local anesthetic effects of propranolol are equipotent to those of Hdocaine [137-58-6] C 4H22N20, (see Anesthetics). Therapeutic effects include termination of catecholamine-induced arrhythmias, conversion of SA nodal tachycardias (including flutter and fibrillation) and AV nodal tachyarrhythmias to normal sinus rhythm, digitahs-induced arrhythmias, and ventricular arrhythmias (1,2). The dmg also has cardioprotective properties (37,39). 

Normal sinus rhythm and a left atrial diameter >5.5 cm... 

A CarboMetrics bileaflet valve or Medtronic Hall tilting disk mechanical valve in the aortic position, with normal left atrial size and normal sinus rhythm... 

ECG normal sinus rhythm, PR 0.16 s, QRS 0.08 s, QTC 0.38 s, occasional polymorphic premature ventricular contractions, 3 mm ST-segment elevation anterior leads... 

The desired outcomes for treatment are to restore normal sinus rhythm and alleviate patient symptoms. 

Monitor the patient for termination of AV nodal blockade and restoration of normal sinus rhythm, heart rate, and alleviation of symptoms. 

Direct current cardioversion is the process of administering a synchronized electrical shock to the chest. The purpose of DCC is to simultaneously depolarize all of the myocardial cells, resulting in interruption and termination of the multiple reentrant circuits and restoration of normal sinus rhythm. The initial energy level of the shock is 100 joules (J) if the DCC attempt is unsuccessful, successive cardioversion attempts maybe made at 200,300, and 360 J.14 Delivery of the shock is synchronized to the ECG by the cardioverter machine, such that the electrical charge is not delivered during... 

TABLE 6-7. Drugs for Conversion of Atrial Fibrillation to Normal Sinus Rhythm... 

FIGURE 6-7. Decision algorithm for conversion of atrial fibrillation to normal sinus rhythm. 

Monitor patients for termination of PSVT and restoration of normal sinus rhythm. 

Electrocardiograph normal sinus rhythm Chest x-ray slightly enlarged heart Ventilation/perfusion (V/Q) scan high probability of PE... 

Within normal limits ECG Normal sinus rhythm... 

Direct current cardioversion The process of administering a synchronized electrical shock to the chest to simultaneously depolarize all of the myocardial cells, resulting in restoration of normal sinus rhythm. 

A 59-year-old male with a history of rheumatic heart disease is found to have atrial fibrillation (AF for which he is treated with digoxin. Treatment with digoxin converts his AF to a normal sinus rhythm and most likely results in a decrease in which of the following ... 

If sinus rhythm is to be restored, anticoagulation should be initiated prior to cardioversion because return of atrial contraction increases risk of thromboembolism. Patients with AF for longer than 48 hours or an unknown duration should receive warfarin (target international normalized ratio [INR] 2 to 3) for at least 3 weeks prior to cardioversion and continuing for at least 4 weeks after effective cardioversion and return of normal sinus rhythm. Patients with AF less than 48 hours in duration do not require warfarin, but it is recommended that these patients receive either IV unfractionated heparin or a low-molecular-weight heparin (subcutaneously at treatment doses) at presentation prior to cardioversion. 

For patients in normal sinus rhythm, effects on symptom reduction and quality-of-life improvement are evident in patients with mild to severe HF. Therefore, it should be used together with standard HF therapies (ACE inhibitors, /1-blockers, and diuretics) in patients with symptomatic HF to reduce hospitalizations. 

Ivabradine is used in the treatment of angina in patients in normal sinus rhythm. It acts on the sinus node resulting in a reduction of the heart rate. It is contraindicated in severe bradycardia (heart rate lower than 60 beats/ minute), cardiogenic shock, acute myocardial infarction, moderate-to-severe heart failure, immediately after a cerebrovascular accident, second and third-degree heart block and patients with unstable angina or a pacemaker. Side-effects include bradycardia, first-degree heart block, ventricular extrasystoles, headache, dizziness and visual disturbances, including blurred vision. 

Drugs of this group are calcium channel blockers that inhibit slow transmembrane calcium ion flow in the cell of the conductive system of the heart during depolarization, which causes a slowing of atrioventricular conductivity and increased effective refractive period of atrioventricular ganglia, which eventually leads to the relaxation of smooth muscle of heart musculature and restores normal sinus rhythm during supraventricular tachycardias. 

Atrial flutter Digitalis slows the heart normal sinus rhythm may appear. Often, flutter is converted to atrial fibrillation with a slow ventricular rate. 

Atrial fibrillation Peak digoxin body stores larger than the 8 to 12 mcg/kg required for most patients with heart failure and normal sinus rhythm have been used for control of ventricular rate in patients with atrial fibrillation. Titrate doses of digoxin used for the treatment of chronic atrial fibrillation to the minimum dose that achieves the desired ventricular rate control without causing undesirable side effects. Data are not available to establish the appropriate resting or exercise target rates that should be achieved. 

Rapid digitalization with a loading dose Peak digoxin body stores of 8 to 12 mcg/kg should provide therapeutic effect with minimum risk of toxicity in most patients with heart failure and normal sinus rhythm. Because of altered digoxin distribution and elimination, projected peak body stores for patients with renal insufficiency should be conservative (ie, 6 to 10 mcg/kg see Precautions). 

Transfer to Betapace AF from Betapace - Patients with a history of symptomatic atrial fibrillation/atrial flutter (AFIB/AFL) who are currently receiving Betapace for the maintenance of normal sinus rhythm should be transferred to Betapace AF because of the significant differences in labeling (ie, patient package insert for Sefapace AF, dosing, administration, and safety information). 

Tolerance Following 12 days of dronabinol, tolerance to the cardiovascular and subjective effects developed at doses 210 mg/day or less. An initial tachycardia induced by dronabinol was replaced successively by normal sinus rhythm and then bradycardia. A fall in supine blood pressure, made worse by standing, was also observed initially. Within days, these effects disappeared, indicating development of tolerance. Tachyphylaxis and tolerance did not, however, appear to develop to the appetite stimulant effect. 

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Although quinidine often is successful in producing normal sinus rhythm, its administration in the presence of a rapid atrial rate (flutter and possibly atrial fibrillation) can lead to a further and dangerous increase in the ventricular rate secondary to inhibition of basal vagal tone upon the A-V node. For this reason, digitalis should be used before quinidine when one is attempting to convert atrial flutter or atrial fibrillation to normal sinus rhythm... 

Because of the increase in A-V transmission observed with phenytoin administration, it should not be given to patients with atrial flutter or atrial fibrillation. Phenytoin will probably not restore normal sinus rhythm and may dangerously accelerate the ventricular rate. 

Mechanism of Action A cardiac agent that slows impulse formation in the SA node and conduction time through the AV node. Adenosine also acts as a diagnostic aid in myocardial perfusion imaging or stress echocardiography. Therapeutic Effect Depresses left ventricular function and restores normal sinus rhythm. 

Unlabeled Uses Control of hemodynamicallystableventriculartachycardia, control of rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias, conversion of atrial fibrillation to normal sinus rhythm, in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation, paroxysmal supraventricular tachycardia, polymorphic ventricular tachycardia or wide complex tachycardia of uncertain origin, prevention of postoperative atrial fibrillation... 

Temporary control of rapid ventricular rate in atrial flBrillation or flutter, rapid conversion of paroxysmal supraventricular tachycardia to normal sinus rhythm IV push Initially, 0.25 mg/kg actual body weight over 2 min. May repeat in 15 min at dose of 0.35 mg/kg actual body weight. Subsequent doses individualized. IV Infusion / fter initial bolus injection, may begin infusion at 5-10 mg/hr may increase by 5 mg/hr up to a maximum of 15 mg/hr. Infusion duration should not exceed 24 hr. 

Maintain normal sinus rhythm after conversion from atrial fibrillation or flutter PO Individualized using a seven-step dosing algorithm dependent upon calculated creatinine clearance and QT interval measurements. 

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