**1. Introduction**

## **1.1 Definition of cardiac arrhythmias**

Accelerated, slowed, or irregular heart rates caused by abnormalities in the electrical impulses of the myocardium*.*

Cardiac arrhythmias are very common in the general population and are a significant cause of morbidity and mortality of both cardiac and noncardiac surgical procedures during the perioperative period. While the incidence of perioperative arrhythmias is extremely high (the Multicenter Study of General Anesthesia reported a 70.2% incidence of Brady and tachyarrhythmias in 17,201 patients having general anesthesia for a variety of surgical procedures), only 1.6% of these required clinically significant management [1–3]. For cardiac surgery, the patients are more prone to develop arrhythmias with a reported incidence of greater than 90%, while incidence for patients undergoing non-cardiac surgery is lower and varies from 16.3 to 61.7% [4–6]. Patients with pre-existing cardiac disease for cardiac surgery are more prone to develop perioperative rhythm disturbances. It is obvious that arrhythmias that occur during surgery are clinically important as it can evolve to life-threatening malignant arrhythmias with severe hemodynamic instability and


**Table 1.**

*Choice of antiarrhythmic therapies based on Vaughan-Williams classification (classes I–IV).*

cardiovascular collapse, necessitating prompt initiation of adequate cardiopulmonary resuscitation (CPR) and defibrillation or electrical cardioversion. Hence, a thorough understanding and prompt diagnosis and intervention are critical for the anesthesiologist in order to reduce severe perioperative adverse outcomes.

An understanding of normal cardiac physiology is essential before rhythm disturbances can be understood. The normal cardiac electrical conduction system is responsible for the contraction of the heart muscle and is represented on the electrocardiogram.

Normal cardiac conduction begins with cardiac impulses coming from the sinoatrial node and travels to both atria. The atria depolarizes and generates the P wave. From here, the impulse propagates to the atrioventricular node, then reaches the his bundle and Purkinje fibers transforming into conduction, causing ventricular contraction and generates the QRS wave [6]. The resting sinus heart rate in adults is usually between 60 and 100 beats/min.

In the heart, electrical stimulation is created by a sequence of ion fluxes through specialized channels in the cardiomyocytes that generate action potential and lead to a coordinated cardiac contraction in systole. Each action potential corresponds to one beat of the heart and the inherent frequency of these cells is essential for maintaining proper rate control. Antiarrhythmic drugs act by modifying this action potential, which results from the alteration of ion channels (**Table 1**).

Five phases of cardiac action potential (as illustrated in **Figure 1**):


Damage to the normal conduction system of the heart can lead to rhythm disturbances which can be either benign or more serious in nature depending on the hemodynamic consequence of the arrhythmia and the possibility of evolving into a lethal arrhythmia.

*Life-Threatening Cardiac Arrhythmias during Anesthesia and Surgery DOI: http://dx.doi.org/10.5772/intechopen.101371*

**Figure 1.** *Cardiac action potential.*

Bradyarrhythmias result from decreased intrinsic pacemaker function or blocks in conduction, principally within the AV-node or the His-Purkinje system. Most tachyarrhythmias are caused by re-entry, some result from enhanced normal automaticity or from abnormal mechanisms of automaticity.
