(see Chap. 19)

The regular RR interval excludes atrial fibrillation. The presence of an organized atrial rhythm at a rate of 300 bpm, with no isoelectric segment between the typical “sawtooth” waves, best seen in inferior leads, suggests the diagnosis of typical atrial flutter.

The two-to-one conduction makes difficult to recognize the atrial waves superimposed on the QRS complex or T waves, but the cardiologist performed vagal maneuvers (carotid massage) to reveal atrial waves increasing AV block (Fig. 21.2).

The presence of AV block and the ineffectiveness of carotid massage to terminate the tachycardia exclude the hypothesis of supraventricular reentrant tachycardia. The atrial tachycardia may be excluded because of higher atrial rate and the absence of isoelectric baseline between regular atrial activations.

At the end, the cardiologist concluded a diagnosis of typical atrial flutter.

The routine laboratory did not show any reversible proarrhythmic trigger such as electrolyte imbalance, anemia, and thyroid dysfunction. The troponin I-hs value was slightly increased due to the tachyarrhythmia. The high myocardial rate may cause an imbalance between myocardial oxygen supply and demand by enhancing myocardial oxygen requirements and reduces the diastolic coronary filling time. Also the BNP value was slightly increased as a result of initial atrial increased filling pressure.

Both lung fields and costophrenic angles are clear. The mediastinum is within normal limits. Cardiac size and shape are normal.

In agreement with patient’s symptoms and physical examination, chest X-ray did not show radiographic signs of pulmonary stasis.

Normal trileaflet aortic valve and normal aorta dimension (aortic root dimension = 2.7 cm; ascending aorta = 3.1 cm; aortic arch = 3.1 cm; thoracic aorta = 2.8 cm; abdominal aorta = 1.8 cm). Mild enlarged left atrium (LA diameter M-mode 41 mm; LA indexed volume 36 ml/m²). Normal right atrium. No atrial septal defect. Mild left ventricular hypertrophy with normal systolic function (mass indexed volume 70 ml/m²; EF 0.65) in the absence of regional wall motion abnormalities. Normal right ventricle size with normal function. Mild mitral and tricuspid regurgitation with normal pulmonary arterial pressure (PAPs = 30 mmHg). No pericardial effusion. Slightly dilated inferior vena cava (24 mm) with >50 % respiratory collapse. Monophasic diastolic flow pattern with initial increase of estimated filling pressure.

The patient was a young active person and he had never had heart rhythm problems before; in fact this episode of arrhythmia was the first in his life. Furthermore it could be triggered by bronchitis.

For these reasons, and in consideration of the presence of only mild left atrium enlargement, the cardiologist chose a rhythm-control strategy. The patient was electrically cardioverted. Catheter ablation is indicated for recurrent, symptomatic, or drug-refractory arrhythmia and therefore was not performed in this case.

The exact duration of atrial flutter was unknown and lasted longer than 48 h. The patient had a CHA2DS2-VASc score of 2, suggesting a considerable risk of stroke.

Many risks and complications of cardioversion are associated with thromboembolic events, so effective anticoagulation for at least 3 weeks is mandatory for AFL of >48 h or AFL of unknown duration, unless the patient was hemodynamically unstable (LGAF).

At this point, the cardiologist proposed to perform a transesophageal echocardiography (TEE) as an alternative to 3 weeks of adequate pre-cardioversion anticoagulation.

In the meantime, a good control of ventricular rate was achieved by administrating a calcium-channel blocker (verapamil).

Transesophageal echocardiography was performed.

The patient was fully informed about the risk of cardioversion procedure.

He was sedated with a light anesthetic (midazolam). Two electrode paddles were placed on his chest: the anterior patch was placed under the right clavicle and the apical patch was placed at the apex (anterior-apical paddle position). Electrical cardioversion was performed during a close oxygen level, blood pressure, and heart rhythm monitoring. Atrial flutter was successfully converted to sinus rhythm after one synchronized biphasic electrical shock at 50 J, without complications (Figs. 21.3 and 21.4).

Atrial flutter (AFL) management includes antithrombotic and antiarrhythmic therapy, correction of possible underlying causes, and treatment of associated comorbidities. The patient had a considerable risk of thromboembolism (CHADS2VASc = 2) and a low risk of bleeding (HAS-BLED = 1). In this case, oral anticoagulant (OAC) therapy is indicated not only for 4 weeks after cardioversion (atrial stunning-related risk), but it should continue lifelong irrespective of an apparent maintenance of sinus rhythm. The cardiologist explained pros and cons of the OAC therapy and following the patient’s preferences prescribed a new oral anticoagulant (NOAC).

Catheter ablation and chronic prophylactic antiarrhythmic therapy were not recommended because it was the patient’s first episode of AFL and his AFL was probably due to a respiratory trigger (bronchitis). It was also well tolerated. Catheter ablation is indicated in case of poorly tolerated or recurrent symptomatic AFL.

Hypertension is a risk factor for atrial flutter and its related complications. The patient referred optimal blood pressure control with systolic blood pressure <140 mmHg and diastolic blood pressure <90 mmHg; the antihypertensive therapy was not changed.