The patient has hemodynamically significant acute tachycardia. Further steps to diagnose the tachycardia are necessary, such as questioning the patient about possible causes (e.g., pain) and symptoms, pulmonary and cardiac auscultation, and a 12-lead ECG.

Dr. Ferdinand went to Mr. Gray’s bedside, where he was found to be calm and pain-free. He did say that he felt his heart racing, like he had never felt before. Auscultation of the lungs was unremarkable. Anesthesia tech Denise had finished the 12-lead ECG and presented it to Dr. Ferdinand (see Fig. 21.1).

The diagnosis is tachycardia due to atrial fibrillation (a-fib).

>> “Man!” said Dr. Ferdinand and asked the PACU nurse to measure the CVP stat, then to give 1,000 ml of crystalloid infusion. Afterwards he planned to….

An arterial blood gas is of utmost importance, in order to rule out electrolyte imbalance and acidosis as reversible causes for the occurrence of a-fib. A primary concern is a reduction in sympathetic tone. The patient should be questioned about other stress factors besides pain, such as fear. The epidural level should be checked as the patient might be worried about not being able to move his legs.

It is also important to increase the inspiratory oxygen concentration via face mask, to achieve an optimal cardiac oxygen supply.

Hypovolemia as a reversible cause of acute a-fib was considered and correctly treated by Dr. Ferdinand. The CVP should be measured before administrating fluids is also correct. It should be repeated. Volume overload must be avoided in CHF patients.

>> Dr. Ferdinand viewed the blood gas and electrolytes – both unremarkable, Hb 15.2 g/dl (reference 12–14 g/dl) and HCT 49 % (reference 37–47 %). He silently recapped the procedures. “Mr. Gray received fluids, without a cardiovascular effect. Acidosis and electrolyte imbalance are ruled out, he has no pain, he is receiving extra oxygen via face mask, and the atrial fibrillation is still there. Well, then I have no other choice but to…”

Acute a-fib is always an emergency situation. Possible causes are discussed in Sect. 21.​2.​3 in the Overview and in Table 25.​1. After ruling out reversible causes, attention focuses on therapy. In this case, only therapy for acute a-fib will be discussed (therapy of chronic a-fib, see Anderson et al. [2]).

The therapy has three goals:

The American Heart Association has developed guidelines which are regularly revised according to new medical knowledge [1, 2, 10]. The guidelines for therapy of a new-onset tachycardia are outlined in the algorithm in Fig. 21.2 (modified according to [1, 10]). An important prerequisite for the use of this algorithm is hemodynamic stability.

The antiarrhythmic therapies are determined from the stability of the patient. The most important symptoms of hemodynamic instability are listed in the Overview.

>> The most important symptoms of hemodynamic instability are:

In the presented case, moderate hemodynamic instability is present. A synchronized electrical cardioversion should be performed if the patient is symptomatic (e.g., chest pain, mental status changes, syncope, signs of shock), which can be repeated up to 3 times. If the arrhythmia is still present, 300 mg amiodarone should be given over 10–20 min. Afterwards, additional cardioversion may be attempted, and, if needed, 900 mg of amiodarone may be given over 24 h. The success rate is high. Up to 95 % of patients convert to a sinus rhythm with an applied energy of 360 J [2, 7].

In hemodynamically stable patients, the therapy is determined by the QRS morphology (broad or narrow complex). If acute a-fib is confirmed, and the patient has no symptoms, maintaining frequency control is the first priority because there is a high spontaneous conversion rate within the first 24 h. β-blockers or calcium antagonists (diltiazem, verapamil) are recommended. If these measures fail or are contraindicated, amiodarone should be given.

Typical risks of the electric cardioversion are:

Thromboembolism occurs in 1–7 % of patients who do not receive therapeutic anticoagulation. Cerebral infarction is most often encountered. But there are also cases of coronary emboli, myocardial infarction, and stroke after a left atrial thrombus was ruled out by echocardiography [6]. The cause is a transient mechanical dysfunction of the left atrium, also called “stunning”, which occurs during the electrical or pharmacological treatment, or spontaneously, and has a thrombogenic effect.

Return of the left atrium to normal function can take weeks and depends on the duration of a-fib. This explains the appearance of thromboembolism in patients with an a-fib duration of <48 h and no evidence of a thrombus in the left atrium. If the duration of an a-fib is over 48 h (or if the duration is unknown), anticoagulation is recommended (initial intravenous bolus followed by a continuous infusion to maintain activated partial thromboplastin time at 1.5–2 times the reference value) [2, 7].

Anticoagulation decisions must be made on an individual basis, especially in the perioperative situation – to weigh the risk of recurrent hemorrhage against the risk of a thromboembolism [2, 7]. The continuation of the therapeutic anticoagulation is not recommended postoperatively, if the a-fib was present for less than 48 h.

During cardioversion, arrhythmias of all forms may occur, which require appropriate therapy. To ensure a safe and effective cardioversion, the serum potassium level must not be below normal. Magnesium substitution does not increase the success of the electrical cardioversion [2], but can help to control rhythm <100/min, in combination with digoxin [16].