Conventionally, sinus bradycardia is defined as HR < 60 beats/min, and sinus tachycardia is defined as HR > 100 beats/ min at resting state in adults. Generally, maximal HR is considered to be (220 − age) beats/min. Both arrhythmias have a regular rhythm, a ratio of P to QRS of 1 : 1, and a normal QRS, although severe sinus tachycardia is accompanied by ST depression. Because marked sinus bradycardia with HR < 40 beats/min may be poorly tolerated in healthy patients, the causes should be identified before treatment of the arrhythmia for maintenance of cardiac output. The treatments of sinus bradycardia are all attempts to increase HR, including pacing. If the patient is stable, despite marked sinus bradycardia, close observation may suffice. However, in cases with signs of inadequate systemic perfusion, such as hypotension or electrocardiographic evidence of ischemia, pharmacologic therapy or temporary percutaneous pacing may be necessary. Intravenous atropine of 0.5 mg is used as first-line therapy for the treatment of bradycardia, and may need to be repeated every 3 to 5 min up to a total of 3 mg. If bradycardia persists despite intravenous atropine, positive chronotropic agents such as isoproterenol, dopamine, dobutamine, and epinephrine may be needed to increase HR. In some cases, bradycardia degenerates into asystole, and thus, immediate cardiopulmonary resuscitation is necessary. This serious circumstance can be induced by vagal reflex with venipuncture or epidural puncture. The most common cause of sinus bradycardia is autonomic disturbance including vasovagal stimulation. Hypoxia, hypothermia, endotracheal suctioning, and increased intracranial pressure are also associated with sinus bradycardia. Con-versely, the causes of sinus tachycardia include pain, fever, and hypercarbia. Sinus tachycardia is the most common arrhythmia occurring in the perioperative period. The most common cause of sinus tachycardia is hypovolemia or inadequate anesthetic depth, and the correction of these conditions is the first step in the treatment of sinus tachyarrhythmia. The treatments of sinus tachycardia are all attempts to decrease HR.

Intraoperative AV block may occur in the settings of intrinsic cardiac disease, perioperative ischemia, electrolyte abnormalities, excessive vagal tone, or iatrogenic causes including surgical aortic valve replacement. Most cases of intraoperative AV block are transient and do not require pacing. However, this arrhythmia may be persistent or permanent, and thus, an epicardial pacing system is necessary when AV block develops in cardiac surgery, particularly in aortic or mitral valve surgery. AV block is classified as first, second, and third (complete) degree. First-degree AV block does not require treatment. In second-degree AV block, pacing may be required if bradycardia is severe or causes hemodynamic instability. Third-degree AV block is characterized by P waves that are discordant with QRS waves. Pacing is usually required because escape junctional or ventricular rhythm is usually very slow at < 40 beats/min. This information is shown in Fig. 2.

PSVT has a regular rhythm, and a ratio of P to QRS of 1 : 1 with normal QRS at HRs of 130–270 beats/min. It also shows an ischemic change in ECG such as sinus tachycardia. The P wave may often be hidden in the QRS complex or T wave. The mechanism of PSVT is different from that of sinus tachycardia. PSVT occurs as the result of excessive stimulation of the SA node; atrial excitation outside of the SA node; AV nodal re-entry; and re-entry through a bypass tract. To rule out or differentiate PSVT from sinus tachycardia or atrial flutter/fibrillation, carotid sinus massage or intravenous injection of edrophonium 5–10 mg is applied. Recently, intravenous adenosine (6 mg) was shown to rapidly slow AV nodal function, and has been easily used to differentiate or treat PSVT. Theoretically, AV nodal re-entrant tachycardia and AV re-entrant tachycardia are terminated by intravenous adenosine. Up to 80% of atrial tachycardias may be terminated by adenosine. However, atrial flutter or atrial fibrillation was not terminated by adenosine. If the response to adenosine fails, a double dose of adenosine should be tested. For treatment, adenosine is the drug of choice. Other agents that decrease HR or cardioversion are used for the treatment of PSVT. If PSVT persists with focal atrial impulses or atrioventricular re-entry electrical ablation with radiofrequency energy can be performed. This information is shown in Fig. 2.

Atrial flutter has a regular rhythm, regular rhythm, and a P and QRS ratio of 2 : 1 or 3 : 1, with normal QRS at HRs of 250–300 atrial beats/min with 150 ventricular beats/min. The mechanism of atrial flutter is macro re-entrant arrhythmia, circulating in a specific manner in the right atrium. Atrial flutter with very fast HR is usually accompanied by AV block, manifesting 2 : 1–4 : 1 AV conduction. Classic saw-tooth waves, so-called F waves, are usually present. T waves are lost in F waves. The treatment of atrial flutter should be started after consideration of the existence of thromboembolism. Pharmacologic or synchronized cardioversion is used for treatment of atrial flutter. Atrial fibrillation has an irregularly irregular rhythm, and normal QRS at HRs of 350–500 atrial beats/min and 60–170 ventricular beats/min. The P wave is absent and is replaced by F waves. The mechanism of atrial fibrillation has been suggested to involve multiple electrical wavelets caused by abnormal foci, micro or macro re-entrant, and so on. Atrial fibrillation causes an excessively rapid and irregular atrial contraction with no obvious atrial kick. It is called irregularly irregular and may be associated with a pulse deficit. The significance of atrial fibrillation is that the loss of atrial kick is associated with reduction of left ventricular filling and stroke volume. Consequently, hemodynamic instability occurs. The loss of obvious atrial kick can produce atrial thrombi, resulting in pulmonary and systemic thromboembolism. The treatment of atrial fibrillation is similar to the treatment of atrial flutter. It should be noted that, if atrial fibrillation is present for longer than 48 h, attempts to restore sinus rhythm may increase the risk of thromboembolism. This information is shown in Fig. 2.

PVC has an irregular rhythm. It has no associated P wave because PVC results from ectopic pacemaker activity arising below the AV node. PVC also has a wide (> 0.12 second) and bizarre QRS, because it originates in and spreads through the myocardium or ventricular conducting system. PVC is frequently observed during anesthesia. Its clinical significance is limited. However, a new onset of PVC should be considered a potentially serious event as it may lead to ventricular tachycardia/fibrillation. This information is shown in Fig. 3.

If three or more sequential PVCs are present, it is defined as VT. VT shows fusion, capture beats, and atrioventricular dissociation in an ECG. VT has a regular rhythm at HRs of 100–200 beats/min. The ratio of P and QRS has no fixed relationship because of atrioventricular dissociation. VT is a life-threatening state and needs emergent treatment. Amiodarone is recommended for treatment. Amiodarone is a type III anti-arrhythmic agent, but it also has the properties of I, II, and IV. Intravenous administration of amiodarone (150 mg) for longer than 10 min is used for a loading dose. After the loading dose, 1 mg/min for 6 h and 0.5 mg/min for 18 h is followed by dose reduction or administration by the oral route. Synchronized cardioversion is applied for hemodynamic instability. VF has an irregular and grossly disorganized HR, totally irregular rhythm, and no relationship between P and QRS. The QRS is absent. It means that no effective cardiac contraction with output exists. Immediate cardiopulmonary resuscitation is required. A non-synchronized defibrillation with 200–360 J is used. Biphasic shock reduces the required energy level and increases the efficacy of defibrillation. Magnesium sulfate may facilitate defibrillation. Epinephrine can be used to coarsen fibrillation just before defibrillation. It can also facilitate defibrillation. This information is shown in Fig. 3.

Torsade de pointes is usually invoked in the situation of prolonged QT interval or bradycardia. Therefore, the anesthesiologist should check the baseline QT interval and check for drugs that prolong QT interval before operation because prolongation of QT interval may increase the risk for torsade de pointes. Many anesthetic agents may cause mild prolongation of the QT interval, but are not likely to cause torsade de pointes, although some case reports of intraoperative torsade de pointes under specific anesthetic agents have been published [3738]. Therefore, anesthesiologists should pay special attention to the changes in QT interval and HR during anesthesia. If the patient is hemodynamically unstable, defibrillation should be delivered promptly. However, if the patient has recurrent non-sustained episodes of torsade de pointes in the perioperative period, first-line therapy is administration of magnesium sulfate 2 g as a slow intravenous bolus. This information is shown in Fig. 4.