**4. Anesthetic agents and adjuvants related to arrhythmias**

Prolonged cardiac repolarization (represented as QT interval on ECG) induced by various anesthetic agents and adjuvant drugs may trigger the appearance of torsade de pointes (TdP), which in some patients degenerate towards malignant ventricular arrhythmias and sudden cardiac arrest [6, 7, 10]. The duration of QT interval, QT corrected for heart rate (QTc), JT interval, QT dispersion (QTd), QT variability index, and transmular dispersion of repolarization (TDR) are the commonly used ECG markers to check for the possibility of various degrees of TdP under different conditions [11]. All volatile anesthetics, especially isoflurane and desflurane cause QTC prolongation, while sevoflurane demonstrated no effects on TDR. Propofol is generally considered to be non-torsadogenic. The sympathomimetic properties of ketamine may promote the incidents of TdP [11]. Most opioids have no effect on QTc when used at clinically relevant doses. Succinylcholine has been shown to increase QTc, especially when used in conjunction with thiopental while most nondepolarizing muscle relaxants have no effect on the QT interval. Sugammadex at therapeutic doses has no effect on QTc whereas anticholinesteraseanticholinergic antagonism of neuromuscular blockade with neostigmine and glycopyrrolate or atropine causes clinically significant QTc prolongation. The commonly used local anesthetic agents are relatively safe; nevertheless, extensive central neuraxial blocks may increase the duration of QTc. Several antiemetic drugs, such as droperidol, domperidone, and most 5-HT3 antagonists, produce a significant prolongation of QT. The FDA's black box warning of fatal arrhythmias associated with the administration of droperidol leads to a decrease in the use of this medication in recent years. Midazolam seems to have no effect on QTc and TDR. Although dexmedetomidine may cause mild prolongation of QT interval, it is unlikely to cause TdP. It should also be prudent to use dexmedetomidine with caution, especially in patients with bradyarrhythmias tendencies where the risk of QT prolongation is increased [12–15].

### **5. Diagnostic evaluation**

During surgery, it is not always possible to get 12-lead ECG done. The anesthesiologists would have to make the diagnosis by looking at the continuous ECG monitor in the operating room. Changing the sweep speed on the ECG monitor (from 50 to 25 mm/s) may help with the identification of arrhythmias and their

management. Lead II and V5 are superior for arrhythmia detection and diagnosis. All available leads are displayed on the intraoperative monitor if arrhythmia develops and cannot be readily diagnosed. For non-cardiac surgery, 12-lead ECG can be obtained as soon as feasible [9, 16].

The blood pressure, arterial oxygen saturation, and temperature also need to be monitored. More advanced monitoring such as invasive arterial pressure, pulmonary artery catheterization, and transoesophageal echocardiography can provide additional clues when assessing the patient for causes of cardiovascular collapse. End-tidal carbon dioxide may help with the effectiveness of chest compressions during cardiopulmonary resuscitation. Estimation of serum electrolytes for verification of renal function is important in patients on medications for arrhythmias.

Adequate precautions should be taken during surgery to prevent the development of intraoperative arrhythmias:


Whenever an arrhythmia develops in the intraoperative period, the anesthesiologists should first be able to eliminate the possible causes of arrhythmia before instituting specific interventions. Attempts to correct them should be made while continuing to evaluate the arrhythmia.

#### **6. Specific intra-operative arrhythmias**

#### **6.1 Antiarrhythmic drugs**

Patients requiring oral antiarrhythmic should continue the medication until the time of surgery. Specific cardiologist consultation is advised for patients who require pacing-cardioverter devices to suppress or terminate tachyarrhythmias. With life-threatening circulatory compromise, prompt pacing or electroversion is required. Obvious electrolyte imbalance should be corrected, and management provided for underlying heart disease. Specific antiarrhythmic agents are used to suppress arrhythmias and prevent recurrences (**Table 3**).

The administration of antiarrhythmic drugs may paradoxically aggravate the arrhythmias that are being treated or cause new rhythm disorders. This is known as proarrhythmia generally occurs when the dosage of drugs does not exceed the therapeutic range [17]. Proarrhythmia is now considered omnipresent with all antiarrhythmic medications. Care should be taken when using antiarrhythmic drugs in patients with structural heart disease, as they are at higher risk of proarrhythmia with antiarrhythmic medications. These patients, such as heart failure or cardiomyopathy are not candidates for Class IC or Class III antiarrhythmics other than amiodarone or sotalol.

Antiarrhythmic agents, in general, have a narrow therapeutic index. As a result, they are often susceptible to drug interactions with anesthetic agents and can cause significant adverse effects (**Table 4**).


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

#### **Table 3.**

*The main intravenous agents useful in management of intraoperative arrhythmias.*


#### **Table 4.**

*Antiarrhythmics and its interaction with anesthetics agents.*
