'Rate control of Atrial fibrillation c RVR' 왜 해야하는가?

음...

오늘은 혼자 공부하기도 아까우니 정리하면 맨날 까먹으니 이렇게 홈페이지를 이용해서 정리를 해야겠다는 생각이 들었습니다요. 

공부를 하는것도 중요한데요. 그만큼 중요한 것은 얼마나 궁금한것을 빨리 찾느냐이겠지요?

시간이 지나면 맨날 까먹으니 이제 정리를 해보려 합니다.

Aphasia 를 주소로 내원한 환자가 있습니다.

Stroke이 의심되는 환자입니다. 이런 경우 EKG가  Afib인 경우가 많은데요.

A fib c RVR 150회. vital은 안정적입니다만. Rate control을 해주어야 하는지 궁금해집니다.

그래서 찾아봤습니다. uptodate.

In patients with atrial fibrillation (AF), the ventricular rate is controlled by the conduction properties of the atrioventricular (AV) node. In the typical patient with untreated AF, the ventricular rate can reach 150 beats/min or higher.

There are two important reasons to prevent a rapid ventricular response in patients with AF:

• Avoidance of hemodynamic instability and/or symptoms. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm".)
• Avoidance of a tachycardia-mediated cardiomyopathy. (See "Tachycardia-mediated cardiomyopathy".)

The use of pharmacologic therapies to achieve rate control in AF will be reviewed here. Nonpharmacologic therapies for rate control in AF are discussed separately. (See "Control of ventricular rate in atrial fibrillation: Nonpharmacologic therapy".)

음.. 그렇군요. 혈역학적 불안성과, 증상을 피하기 위하여 조절을 한다. 그리고 cardiomyopathy가 발생하는 것을 막기 위해서 이군요.

그럼 당장 응급 협진을 진행 해야만 하는지 아니면 official 협진을 진행해도 되는지 궁금해 집니다. 

Atrial fibrillation (AF) can lead to a fall in cardiac output that is often clinically significant. Potential consequences include a fall in blood pressure, decreased exercise capacity, and pulmonary congestion, all of which are manifestations of heart failure (HF) (table 1). In addition, AF and HF often occur together, and each may predispose to the other [1].

The hemodynamic effects of AF and of cardioversion will be reviewed here. The clinical aspects and treatment of AF in patients with HF and cardiomyopathy are discussed separately. (See "Atrial fibrillation in patients with heart failure".)

음 그렇군요. 심실세동은 결국 cardiac output을 줄이게 되는군요. 그리고 심부전이 발생하게 되는군요. 그리고 폐부종이 발생합니다.  그리고 종종 심실세동과 심부전은 함께 일어나는군요.

아.. 그렇군요. 그래서 심부전환자가 심실세동이 많습니다. 그랬던것 같습니다.  이 경우에는 응급협진을 볼 수밖에 없는 것이군요.

ADVERSE HEMODYNAMICS IN AF

Many patients with AF develop a modest decline in left ventricular performance that typically returns to the previous baseline following reversion to sinus rhythm [2-5]. The magnitude of this effect and its reversibility were illustrated in a report of 15 patients with AF who were successfully cardioverted and maintained sinus rhythm for one month; 11 of these patients maintained sinus rhythm for three months [4]. The mean duration of AF was three months (range 5 to 254 days). The following findings were noted after cardioversion:

• The mean left ventricular ejection fraction (LVEF) increased from 47 percent at baseline to 55 percent immediately after cardioversion to 61 percent at one month; there was no further increase at three months. The improvement in LVEF occurred in all but one patient. The maximum improvement in LVEF by one month coincides with the time to full recovery of left atrial contractile function [6]. (See 'Atrial stunning' below.)
• The increase in LVEF was primarily due to enhanced diastolic filling resulting from two factors: (1) an increase in cycle length, which may involve both regularization of the heart rate and avoidance of short cycle lengths that impair ventricular contractility; and (2) the return of left atrial contractile function, as determined by peak A wave velocity, which increases the atrial contribution to ventricular filling [3,4].

The improvement in LVEF following reversion to sinus rhythm is associated with an increase in exercise capacity (table 1). (See 'Improved exercise capacity' below.)

심실세동에서 동율동으로 전환되는 경우에는 Cardiac output이 47% 에서 55%로 증가하는군요.

뭐 좋긴 합니다만 그래도 궁금한건 응급협진을 봐야 하는지 인데요.

Cardiomyopathies are a clinically heterogenous group of heart muscle disorders that are defined by the presence of abnormal myocardial structure and/or function in the absence of ischemic heart disease or abnormal loading conditions [1,2]. They are classified according to the phenotype, eg, hypertrophic, dilated, arrhythmogenic right ventricular cardiomyopathy. (See "Definition and classification of the cardiomyopathies" and "Causes of dilated cardiomyopathy".)

Long-standing tachycardia is well recognized for its potential to induce a dilated cardiomyopathy. The prognosis in patients with dilated cardiomyopathy is variable and dependent on the cause; importantly, there are some etiologies that may improve or resolve following treatment. One such cause is a tachycardia-mediated (or tachycardia-induced) cardiomyopathy, a relatively rare entity, though one that is readily treatable with a good prognosis in many patients [3]. While the exact incidence of tachycardia-mediated cardiomyopathy remains unclear, an association between tachycardia and cardiomyopathy has been recognized for some time [4-7]. Virtually every form of supraventricular tachyarrhythmia, including ectopic atrial tachycardia, nonparoxysmal junctional tachycardia, and atrial fibrillation (AF), has been associated with reversible left ventricular dysfunction or "cardiomyopathy." The development of a cardiomyopathy has also been documented with ventricular tachyarrhythmias and frequent ventricular premature beats [8-10]. (See"Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm"and 'Frequent ventricular ectopy' below and "Clinical significance and treatment of ventricular premature beats".)

A common clinical problem is determining whether the tachycardia is the primary cause of the patient's cardiomyopathy, or if the tachycardia is secondary to a cardiomyopathy of different etiology. This topic will discuss tachycardia-mediated cardiomyopathy as a primary cause of cardiomyopathy. Arrhythmias occurring in the setting of a specific cardiomyopathy are discussed separately. (See "Atrial fibrillation and other atrial tachyarrhythmias in hypertrophic cardiomyopathy" and "Ventricular arrhythmias and sudden cardiac arrest in hypertrophic cardiomyopathy" and "Clinical manifestations and diagnosis of arrhythmogenic right ventricular cardiomyopathy", section on 'Ventricular arrhythmias'.)

드디어 찾았습니다.

Long standing cardiomyopathy 가 확장성 심근병증을 일으킵니다.

음.. 그럼 응급협진을 봐야 할것은 아니군요.

A fib c RVR은 심부전이 동반되어 있으면, 응급협진을 보게 됩니다만..

vital 이 안정적인 경우에는 응급 협진을 보지 않아도 될것 같습니다.

물론 실제는 처음 발견된 심실세동은 응급협진을 봅니다만.. 기존에 있었던 심실세동일 경우 rate control을 해주면 좋지만 응급협진으로 하지 않아도 될것 같다는 생각을 해봅니다.