Treatment

1. Atrial fibrillation with a rapid ventricular response and acute hemodynamic deterioration should be treated with synchronized cardioversion. Over 60 percent of patients can be converted with 100 J and over 80 percent with 200 J. Conversion to and retention in sinus rhythm is more likely when atrial fibrillation is of short duration and the atria are not greatly dilated. If initial cardioversion is unsuccessful, procainamide should be given intravenously to facilitate further cardioversion attempts. Oral quinidine or low-dose amiodarone can enhance maintenance of sinus rhythm. Metanalysis and decision analysis of postconversion antiarrhythmic treatment has found that the benefits of maintaining sinus rhythm with antiarrhythmics is partially offset by an increase in sudden death, presumably due to the proarrhythmic properties of these drugs. In the emergency department (ED) setting, all other causes of hypotension, such as acute blood loss, must be ruled out before concluding that the rate is causing the hemodynamic deterioration.

2. In the more stable patient, the first priority is to achieve ventricular rate control. Diltiazem 10 to 20 mg (0.125 to 0.25 mg/kg) given intravenously over 2 min is extremely effective in achieving ventricular rate control, with the peak response seen in 2 to 7 min. An infusion of 10 mg/h is usually started after the initial dose to maintain control and a second dose of 25 mg (0.35 mg/kg) can be given at 15 min if rate control is not achieved. Verapamil 5 to 10 mg IV is effective in slowing the ventricular response in 60 to 70 percent of patients with atrial fibrillation and converts 10 to 15 percent into sinus rhythm. Intravenous b-adrenergic blockers (e.g., esmolol and propranolol) are effective, especially in patients with thyrotoxicosis or rheumatic mitral stenosis, but the depressive effects on myocardial contractility make them poor agents to use in patients with ventricular failure. Intravenous digoxin is an effective agent for this purpose, although the onset of action is slow, with a mean time of over 11 h to achieve ventricular rate control.

3. Once ventricular rate control has been achieved, chemical conversion can be considered with procainamide, quinidine, or verapamil. Intravenous procainamide has also been used as a single agent to chemically convert atrial fibrillation of short duration into sinus rhythm; however, ibutilide is being touted as a better agent. Because of the risk of intraatrial thrombi and arterial embolization, patients with atrial fibrillation of more than 2 days' duration should be anticoagulated systemically for 1 to 3 weeks prior to attempts at either chemical or electrical conversion. More recent work indicates that there may be some increased risk of embolism even with AF of less than 2 days' duration. An alternative to anticoagulation is to exclude atrial thrombi by transesophageal echocardiography. Those without visible thrombi can be safely cardioverted without the need for preconversion oral anticoagulation.

4. Patients with a slow ventricular response not due to digitalis have AV node disease and probably a more generalized disorder of cardiac conduction (second- or third-degree AV block is seen in these patients when in sinus rhythm). These patients are at increased risk for profound bradycardias or asystole following cardioversion or antiarrhythmic drug therapy.

5. In some patients with a rapid ventricular response, conversion will reveal a very slow rate (tachy-brady syndrome) because of underlying disease of the pacemaker tissue (sick sinus syndrome).

SUPRAVENTRICULAR TACHYCARDIA (SVT) Supraventricular tachycardia is a regular, rapid rhythm that arises from either reentry or an ectopic pacemaker in areas above the bifurcation of the bundle of His. The reentrant variety is clinically the most common. These patients often present with acute, symptomatic episodes termed paroxysmal supraventricular tachycardia (PSVT).

Ectopic SVT usually originates in the atria with an atrial rate of 100 to 250 (most commonly 140 to 200) ( Fig 24-11). The regular P waves can be mistaken for atrial flutter, or, if there is a 2:1 AV block, sinus rhythm.

FIG. 24-11. Ectopic supraventricular, tachycardia (STV) with 2:1 AV conduction.

Reentrant SVT is seen in the majority of patients with SVT: about 60 percent of these patients have reentry within the AV node and 20 percent have reentry involving a bypass tract. The remainder have reentry in other sites. In the normal heart, reentrant SVT at the typical rates of 160 to 200 is often tolerated for hours or days. However, cardiac output is usually depressed—regardless of the blood pressure—and rapid rates may produce heart failure depending upon the health of the myocardium.

Reentrant SVT within the AV node usually is initiated when an ectopic atrial impulse encounters the AV node during the partially refractory period ( Fig.,24-12). There are two functionally different parallel conducting limbs within the AV node that are connected above at the atrial end and below at the ventricular end of the node. This circuit is capable of sustained reentry when properly stimulated. In AV nodal reentry, the P wave is usually buried in the QRS complex and not visible, there is 1:1 conduction, and the QRS complex is normal.

FIG. 24-12. Reentrant supraventricular tachycardia (SVT). Top: 2d (*) initiates run of PAT. Bottom: SVT, rate 286.

Patients with bypass tracts have two parallel limbs of the reentry circuit, the AV node and the bypass tract, with connections at the atrial and ventricular ends by myocardial cells. While reentry can occur in either direction, it usually occurs in a direction that goes down the AV node and up the bypass tract, producing a narrow QRS complex (orthodromic conduction). In the Wolff-Parkinson-White syndrome, about 85 percent of the reentrant SVTs have narrow QRS complexes. If the conduction is down the accessory bundle and up the AV node (antidromic conduction), the complexes are wide and are difficult to differentiate from ventricular tachycardia.

Clinical Significance Ectopic SVT may be seen in patients with acute myocardial infarction, chronic lung disease, pneumonia, alcohol intoxication, and digoxin toxicity [where it is often associated with AV block and termed paroxysmal atrial tachycardia (PAT) with block]. It is commonly held that a high percentage of SVT with block, as much as 75 percent, is due to digoxin toxicity. However, not all studies have found this to be the case. In the test situation, PAT with block is still pathognomonic for digitalis toxicity. The common dysrhythmias of digoxin toxicity are listed in T§ble.,2,4,-1,.

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