*6.5.2.2 Ventricular tachycardia (VT)*

VT is a severe, potentially life-threatening arrhythmia as the rhythm can degenerate into ventricular fibrillation, requiring emergent treatment. The ECG shows a rapid ventricular rhythm with broad abnormal QRS complexes. The ratio of P and QRS has no fixed relationship because of atrioventricular dissociation. Like other forms of arrhythmias, the correction of precipitating factors assumes great importance. It can be categorized into non-sustained and sustained ventricular tachycardia [24].

Non-sustained VT (NSVT) is defined as 3 or more PVCs that occur at a rate of more than 120 beats/min and lasting less than 30s without hemodynamic compromise. These arrhythmias are routinely seen in the absence of cardiac disease and may not require drug therapy. However, NSVT should be monitored carefully, as it can generate into a non-perfusing rhythm.

Sustained VT presents with a broad QRS complex that may be monomorphic or polymorphic. Timely termination of VT is desirable even if it is well-tolerated. Amiodarone is the first-line recommended therapy for patients with VT. The alternative pharmacological therapy includes lidocaine and procainamide. Patients may show signs of inadequate perfusion with or without a pulse. Pulseless VT should be treated immediately with defibrillation and initiation of cardiopulmonary resuscitation according to Advanced Cardiac Life Support (ACLS) algorithm, whereas VT with a pulse should be treated with synchronized cardioversion.

#### *6.5.2.3 Ventricular fibrillation (VF)*

This arrhythmia is characterized by very rapid, chaotic, grossly irregular, and disorganized broad complexes on the ECG with no mechanical effect, resulting either from rapid discharges of impulses from one or more ventricular foci or from multiple wandering re-enters circuits in the ventricles. On the ECG, the QRS is absent. It is a serious, life-threatening rhythm due to lack or no cardiac output during the arrhythmia. Clinically, pulses will be impalpable and there will be an acute drop in oxygen saturation on pulse oximetry.

VF during anesthesia and surgery is a critical event. The common causes are myocardial ischemia, hypoxia, hypothermia, metabolic electrolyte imbalance, and drug effects. Management includes prompt initiation of cardiopulmonary resuscitation. External defibrillation is the only effective method to convert VF to a viable rhythm. The most important factor affecting survival in patients experiencing VF is time to defibrillation. Survival is best if defibrillation occurs within 3–5 min of cardiac arrest.

As with any pulseless arrest, contributing factors must be investigated and addressed. When VF is refractory to electrical treatment, IV administration of adrenaline 1 mg or amiodarone 150–300 mg may improve the response to electrical defibrillation. Adjunctive therapy with amiodarone, lidocaine, or magnesium may be indicated. A precordial thump is occasionally effective in the termination of VF but should only be attempted if a defibrillator is not immediately available [25]. Standard ACLS algorithms should be followed for electrical, pharmacological, and adjunct therapy.

#### *6.5.2.4 Torsades de pointes (TdP)*

It is an atypical polymorphic form of VT characterized by a constantly changing/ twisting QRS axis around the baseline. A non-uniform delay in repolarization is the underlying electrophysiological derangement, manifested as prolonged QT interval on ECG. Tdp is usually short in duration and spontaneously reverts to sinus rhythm. However, rapidly recurring episodes may degenerate into VF and cardiac arrest [26]. The management of Tdp depends on hemodynamic stability and is initially aimed at correction of the precipitating factors and use of intravenous magnesium as cellular membrane stabilizer:


4.Pulseless arrhythmia: Follow VF treatment approach. Intravenous magnesium should be administered. Avoid amiodarone since it has a proarrhythmic effect because of the additional prolongation of the QTc interval but administer intravenous lidocaine instead.

Lidocaine is the preferred antiarrhythmic drug for TdP, though there is a lack of evidence to support its use. Other antiarrhythmic drugs such as amiodarone, procainamide, beta-blockers further prolong the QT interval and therefore worsen the condition. β-blockers will slow down the heart rate, increasing the risk of TdP.

#### *6.5.2.5 Pulseless electrical activity (PEA)*

PEA, previously known as electromechanical dissociation, is a life-threatening, non-shockable cardiac rhythm. It occurs when the electrical activity of the heart persists but does not usually follow sufficient ventricular response to produce a sufficient cardiac output to generate a pulse and supply blood to the organs in the body. While the absence of a pulse confirms a clinical diagnosis of cardiac arrest, PEA can only be differentiated from other causes of cardiac arrest by ECG. This means that PEA includes any pulseless waveform except for VF, VT, or asystole. PEA is often caused by a profound cardiovascular insult which weakens the cardiac contraction and is usually exacerbated by worsening acidosis, hypoxia, and increasing vagal tone (**Table 6**). Further compromise of the inotropic state of the cardiac muscle leads to inadequate mechanical activity, despite the presence of electrical activity and ultimately causing degeneration of the rhythm and death of the patient. Overall, the prognosis of PEA patients is poor and still shows a high mortality rate despite optimum CPR.

Prompt and good quality CPR according to ACLS guidelines to maintain cardiac output until the PEA can be corrected is the first step in the management of PEA, while potential underlying causes are identified and addressed [27]. Once a diagnosis is made, specific therapy to treat the cause should be commenced immediately. This process may involve the decompression of pneumothorax, pericardial drain for tamponade, fluids infusion for hypovolemia, correction of body temperature for hypothermia, administration of thrombolytics pulmonary embolism, and early coronary angiography with percutaneous coronary intervention (PCI) in patients with myocardial infarction. Where it is not possible to determine and/or reverse the underlying cause of PEA, the treatment of PEA is similar to that of asystole. The mainstay of drug therapy for PEA arrest is intravenous adrenaline 1 mg every 3–5 min. The routine use of sodium bicarbonate is not recommended, except in special situations (e.g., severe metabolic acidosis or hyperkalemia). Atropine is generally no longer recommended for PEA as it has not been shown to have a therapeutic benefit. Defibrillators cannot be used to correct this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses. Although PEA


#### **Table 6.**

*Factors contributing to the etiology of PEA that is widely thought as 4Hs and 4Ts include as following.*

and asystole are often considered fatal arrhythmias, PEA has a slightly better outcome than asystole. Previous data by the National Registry of Cardiopulmonary Resuscitation in 2003 revealed that 10% of hospital patients whose initial rhythm is PEA survive with good neurological outcomes [28].

### **7. Post resuscitation care**

Resuscitation of an intraoperative cardiac arrest victim does not end with ROSC and must be tailored to the needs of the individual patient.

Following ROSC after cardiac arrest, many patients suffer from post-cardiac arrest syndrome, which is a high inflammatory state characterized by brain injury, myocardial dysfunction, systemic ischemia and reperfusion injury, and persistent precipitating pathology [29]. The severity of this syndrome varies according to the duration and cause of cardiac arrest. Management of these patients is challenging and requires a structured approach including restoration of adequate hemodynamics and organ perfusion, optimizing ventilation, treatment of electrolyte abnormalities, glycemic control targeted temperature management, and multimodal prognostication to improve outcomes. Specific therapy is determined by the etiology of arrest and initiating treatment to prevent recurrence [30].

#### **Figure 4.**

*Summary of management of critical arrhythmias at any time in the operating room [26, 29]. CPR: cardiopulmonary resuscitation; OR: operating room; ROSC: return of spontaneous circulation.*

The flow diagram is designed as a step-by-step guide to critical arrhythmias management in the operating room, as shown in **Figure 4** [26, 31].
