**6.2 Pacing and cardiac electroversion**

Both cardiac pacing and electroversion provide a more prompt therapeutic effect and easier dose titration (i.e., pacing mode, rate, current) than with drugs [8, 18]. They have advantages over drugs for the management of intraoperative arrhythmias.

Pacing is considered in patients with symptomatic bradycardia when a pulse is present but not responded to atropine or second-line drugs (e.g., adrenaline and dopamine) [19]. Temporary cardiac pacing is used in cardiac surgery to increase heart rate, suppress bradycardia dependent tachycardia, overdrive escape rhythms, suppress atrial or ventricular extrasystoles, and terminate re-entrant SVT or atrial flutter. Transcutaneous pacing is used if invasive pacing is not feasible or is impractical.

Cardiac electroversion includes cardioversion (synchronized shocks) or defibrillation (nonsynchronized shocks) of hemodynamically unstable patients, which use high-energy capacitor discharges to simultaneously depolarize all excitable myocardium to terminate arrhythmias. It is highly effective and avoids the potential complications of drug therapy [20]. Defibrillation or unsynchronized cardioversion is indicated in any patients with pulseless ventricular tachycardia or ventricular fibrillation whereas synchronized cardioversion is utilized for the treatment of persistently unstable tachyarrhythmias in patients without loss of pulse. In synchronized cardioversion, the direct current electrical discharge is synchronized with the R or S wave of the QRS complex, avoiding the energy delivery near the apex of T wave, which coincides with a vulnerable period of induction of ventricular fibrillation. The recent use of biphasic cardioversion has shown that less energy is required to convert an arrhythmia to a sinus rhythm. It results in fewer delivered shocks to the patient, less cumulative energy delivered, and less myocardial tissue damage than is found with higher voltage shocks.

### **6.3 Management of arrhythmias during anesthesia and surgery**

Cardiac arrhythmias may not always require treatment. However, the distinction between benign and malignant arrhythmias which carry the risk of sudden death is fundamental [21]. **Figure 2** provides an algorithm for the evaluation and management of rhythm disturbances.

**Figure 2.**

*Management of arrhythmias developed during anesthesia and surgery.*


**Table 5.** *Classification of bradyarrhythmia and tachyarrhythmia.*

Arrhythmias are broadly classified as bradyarrhythmia and tachyarrhythmia (**Table 5**).

Strategies for clinical care of a patient with bradyarrhythmia (**Figure 3A**) and tachyarrhythmia (**Figure 3B**).

#### **6.4 Bradyarrhythmia**

#### *6.4.1 Conduction defects*

AV conduction block can occur in the settings of intrinsic cardiac disease, acute myocardial ischemia, general anesthetics, electrolyte abnormalities, and excessive vagal tone. In cardiac surgery, high-grade AV block is not so uncommon complication and thus, a temporary epicardial pacing system is necessary. AV block is classified as first, second, and third-degree (complete). First-degree AV block is generally benign, often needs no treatment apart from careful observation for progression to a higher degree of the block that requires prompt treatment. The second-degree AV block is divided into Mobitz type I and II. In Mobitz type I, the block is often transient and asymptomatic. In Mobitz type II, the block is often symptomatic and has a less favorable prognosis because there is a potential risk of progression to third-degree heart block. Pacing is required if there is severe bradycardia with hemodynamic insufficiency. Third-degree AV block is characterized by electrical instability and may evolve towards asystole. There is no apparent relationship exists between the P waves and QRS complexes. Pacing is typically required because no conduction to ventricles occurs with atrial activity more rapid than ventricular activity (approximately 20–40 beats/min). These bradyarrhythmia (Mobitz type II and third-degree heart block) are not likely to be responsive to atropine and should be treated with transcutaneous pacing or isoproterenol infusion acting as a "chemical pacemaker" while the patient is prepared for transvenous pacing.

Intraventricular conduction defects are generally classified as LBBB, RBBB, or Hemiblock. Intraventricular blocks may be of a His bundle branch block pattern, a fascicular block pattern, or both and result from significant slowing or interruption

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

of conduction. They are frequently seen in those with and without cardiac disease. In the vast majority of cases, RBBB may be a normal variant with little or no impact on cardiovascular prognosis. LBBB is a more serious conduction disturbance and is always associated with significant heart disease. In the presence of LBBB, acute myocardial infarction is difficult to diagnose. When the LBBB occurs in myocardial infarction, a complete heart block may develop. The anatomical or functional block in a fascicle causes a fascicular block. The left anterior hemiblock is common, while the left posterior hemiblock is uncommon. The combination of RBBB with left anterior or posterior hemiblock is called bifascicular block. Trifascicular block refers to a block of both the left and right bundles or to first- or second-degree AV block with additional bifascicular block. Patients with bifascicular and trifascicular blocks are at risk of a slow progression to an advanced or complete AV block.

#### **6.5 Tachyarrhythmia**

Tachyarrhythmias are classified into two categories (narrow complex supraventricular tachycardia and wide complex tachycardia), based on the appearance of QRS complex, heart rate, and regularity.

#### *6.5.1 Supraventricular arrhythmias*

#### *6.5.1.1 Premature atrial contractions (PACs)*

PACs are a common kind of arrhythmia characterized by early (premature) ectopic beats originating in the atria, which may be seen in patients with heart and chronic lung diseases, sepsis, shock, use of volatile agents, sympathetic stimulation, and excessive alcohol, nicotine, or caffeine. PAC is usually hemodynamically insignificant and self-limiting. But when they are in excess or compromise the cardiovascular function, β-blockers, digitalis or calcium channel blockers can be used after excluding the underlying causes.

#### *6.5.1.2 Paroxysmal supraventricular tachycardia (PSVT)*

PSVT is due to the rapid electrical discharge from an ectopic atrial focus, causing regular and consecutive atrial extrasystoles or may be caused by reentry in the AV node by the accessory pathway (AVNRT). It occurs most commonly in normal individuals, who may show no clinical evidence of heart disease. Less common causes of PSVT are rheumatic valvular heart disease, pulmonary embolism, cardiac surgery, thyrotoxicosis, and coronary artery disease. PSVT is characterized by rapid regular atrial rhythm at a rate of 160–220 beats/min, usually with a narrow QRS complex and lacking the P wave. It is typically rapid in onset and conclusion. The majority of patients who develop intraoperative PSVT maintain hemodynamic stability and do not require electrical direct current (DC) cardioversion. For this reason, heart rate control is the mainstay of the therapy that does not require immediate cardioversion [19]. PSVT can be confused with sinus tachycardia, atrial fibrillation, atrial flutter, and ventricular tachycardia. Carotid sinus massage can abruptly terminate the arrhythmia by activation of baroreceptors in the carotid sinus, resulting in increased vagal activity and transient AV nodal conduction block. This aids differentiation between PSVT, atrial flutter, and fibrillation. The Valsalva maneuver can also be used. If these vagal maneuvers are unsuccessful, then rapid intravenous adenosine in a dose of 6–12 mg is the drug of choice for terminating the re-entrant variety of PSVT arrhythmia. Adenosine slows the sinoatrial and AV nodal conduction and prolongs refractoriness, which is very effective in terminating PSVT. Its

ultrashort duration of action (10 s) and very rapid onset of action (15–30 s) make it desirable over other intravenous drugs. However, atrial flutter and atrial fibrillation do not respond to adenosine. Other intravenous drugs that are useful for terminating PSVT are verapamil, diltiazem, and β-blockers. Intravenous digoxin is not clinically useful in the acute control of PSVT because of its delayed peak effect and a narrow therapeutic index. DC cardioversion is indicated for PSVT unresponsive to drug therapy or PSVT associated hemodynamic deterioration. Radiofrequency ablation is the preferred approach for patients with persistent symptomatic reentry PSVT.

#### *6.5.1.3 Atrial flutter*

Atrial flutter is due to electrical impulse re-entry into the atria, often giving an atrial rate of 250–350 beats/min with a ventricular rate of 150 beats/min. It is usually associated with varying degrees of AV block, manifesting 2:1–4:1 AV conduction. The rapid P waves create a classic saw tooth appearance on ECG (best seen in leads II, III, aVF, and V1) and are called flutter waves (F waves). Normal T waves are lost in F waves. Atrial flutter often occurs in association with other arrhythmias such as AF. It usually signifies the presence of underlying severe heart disease and exacerbation of a chronic condition such as pulmonary disease, thyrotoxicosis, or after cardiac surgery. In many instances, treatment of the underlying disease process restores sinus rhythm. Intraoperative management of atrial flutter depends on the hemodynamic stability of the patient. Synchronized cardioversion using a low energy current (50–100 J) is the treatment of choice if the hemodynamic deterioration is present. If vital signs are stable, intravenous amiodarone, diltiazem or verapamil may convert the flutter to normal sinus rhythm.

#### *6.5.1.4 Atrial fibrillation (AF)*

AF is much commoner than an atrial flutter, and is one of the most common of all arrhythmias, especially in the elderly population [20, 22]. It accounts for more than 90% of supraventricular arrhythmia in the perioperative setting. AF has an irregularly irregular rhythm. The absence of P waves and variable QRS complexes on ECG is diagnostic of AF. AF is due to excessively rapid and disorganized atrial electrical activation without effective atrial contraction at a higher ventricular rate. The loss of atrial contraction may lead to a decrease in cardiac output and blood pressure that is often hemodynamically clinically significant. Other complications of AF include heart failure, pulmonary and systemic thromboembolism, and a significant risk of cerebrovascular events. Patients with ischemic heart disease, rheumatic heart disease, hypertension, thyrotoxicosis, and pneumonia are more prone to develop AF. The immediate intraoperative management of AF should begin with an assessment of hemodynamic status and correction of precipitating factors. The onset of AF or faster rates of chronic AF during the intraoperative period may be precipitated by acid-base and electrolyte abnormalities, hypovolemia, myocardial ischemia, sepsis, and surgical manipulation in the thoracic cavity. The goal of management is directed towards the control of ventricular response rate with pharmacological agents that slow AV node conduction. IV β-blockers or calcium channel blockers produce rapid control of rate. In the acute setting, the usefulness of digoxin is limited due to slow onset and low efficacy in high adrenergic states such as surgery. Amiodarone is a good choice for rate and rhythm control in patients with AF in the operating room. This agent also suppresses atrial ectopy and thus, recurrent AF and improves the success rate of electrical cardioversion. In cardiovascular compromised patients, synchronized DC cardioversion at 100–200 J (biphasic) is the most reliable method of converting AF to sinus rhythm. However, it should not be used in AF of more than 48-h duration without at least 3 weeks of anticoagulation, attempts to restore sinus rhythm may increase the risk of atrial blood clot formation and systemic thromboembolism.
