Patients may also present with hemodynamic instability from the slow ventricular response (SVR). This was the case in our patient who had conduction pattern ranging from 2:1 to 6:1.Ītrial flutter with AV node blockade is a potentially life-threatening cause of bradycardia usually seen in patients with preexisting valvular or structural diseases and/or conduction system disease. Sometimes, variable conduction may occur with alternating or seemingly random patterns of 2:1, 3:1, 4:1, or other conduction patterns due to varying levels of block in the AV node. Odd ratios are thought to reflect a bilevel block in the AV node. Even input/output ratios in atrial flutter (e.g., 2:1 or 4:1 conduction) are more common than odd ratios (e.g., 3:1 or 5:1). It has been called a “slow response” tissue. The action potential of the AV node depends on calcium ions flowing through the kinetically slow channel. Thus, the clinical presentation of atrial flutter largely depends on the ventricular rate. However, the ventricular rate may be slower in the presence of atrial disease or antiarrhythmic drugs. In patients who are not taking atrioventricular (AV) nodal blockers, the atrial rate in atrial flutter typically ranges from 240 to 300 beats per minute with a regular ventricular rate of approximately 150 beats per minute. On arrival, ECG revealed atrial flutter with variable block ranging from 2:1 to 6:1, with a ventricular rate of 47 beats per minute and a right bundle branch block (RBBB). Initial labs and imaging workup were unremarkable except for a serum magnesium level of 1.7 mg/dL. On presentation, his vitals were unremarkable with a blood pressure of 146/56 mmHg and HR of 44 beats per minute. He denied any chest pain, palpitations, or dizziness.

He also reported chronic dyspnea, unchanged from his baseline. The patient stated that he had not taken his metoprolol for five days prior to the presentation. Home medications included amlodipine, aspirin, atorvastatin, clopidogrel, metoprolol, and sublingual nitroglycerin on an as-needed basis. Case PresentationĪ 77-year-old male with a history of coronary artery disease status post-percutaneous coronary intervention with two stents in-situ, hypertension, and type 2 diabetes mellitus was transferred from an outside facility on account of a one-week history of HRs ranging between 30 and 40 beats per minute. This paper was previously presented as a poster during the American College of Physicians West Virginia chapter meeting in 2020. Thus, clinicians need to always be aware of this and remember that bradycardia does not rule out a diagnosis of atrial flutter.

Less commonly, it may also be associated with a normal heart rate (HR) or even bradycardia, as seen in our patient. Atrial flutter typically causes tachycardia. It shows the characteristic negative sawtooth flutter waves in the inferior leads. Įlectrocardiography (ECG) remains the mainstay of diagnosis. When symptomatic, common presentations include palpitations, shortness of breath, fatigue, lightheadedness, as well as an increased risk of atrial thrombus formation that may cause cerebral and/or systemic embolization. It may represent a stable rhythm or a bridge arrhythmia between sinus rhythm and atrial fibrillation. Although less common, atrial flutter occurs in many of the same situations as atrial fibrillation.

Atrial flutter on ecg