**4. Types of arrhythmias**

The conduction system of the heart has to be intact anatomically and physiologically for synchronized contraction of the heart in a regular and coordinated fashion. Arrhythmias are caused when there is disturbance in the working of the conduction system for any reason. The accepted mechanisms include abnormality of conduction (i.e. blocking or Re-entry of the impulse), abnormality of impulse initiation (i.e. altered automaticity or triggered activity). The underlying causes can include ischemia, electrolyte imbalances, scarring or fibrosis of atrial and ventricular tissue, increased or decreased excitability for various reasons including changes in autonomic nervous system, action of drugs and others.

Disturbances of the normal cardiac rhythm can be of many types. A universal hierarchical classification which can encompass all the salient arrhythmias is difficult to conceive. Arrhythmias are usually classified based on morphology, rate or origin. They can be divided into fast or slow based on the rate- Tachyarrhythmias when heart rate is faster than 100 bpm and bradyarrhythmias when rate is slower than 60 bpm. The QRS duration which defines the ventricular depolarization is usually less than 0.12 seconds (or 3 small boxes on the ECG at 25 mm/sec paper speed). If it is more than 0.12 seconds it represents delayed depolarization and can be used as a feature to divide the tachyarrhythmias into narrow complex and wide complex tachycardia. Another classification of arrhythmias describes regular versus irregular rhythms. Finally arrhythmias can generally be classified based on various anatomical substrates of the heart, which initiate these rhythm changes like atrial (or supraventricular) or ventricular arrhythmias. As mentioned above these classifications are an attempt, far from perfect, to distinguish normal from abnormal and define categories with different underlying pathophysiology and treatment options.

The following chapter will discuss Atrial Fibrillation (AF) after cardiac surgery initially as this seems to be the most common and most extensively studied arrhythmia.

### **5. Postoperative AF**

#### **Incidence:**

The incidence of any arrhythmia postoperatively can be up to 85% (5). The Multi center anesthesia outcomes study quotes that postoperative arrhythmias can complicate about 70% of the operations. (6) AF seems to be the most common arrhythmia in the post operative period (7). Goldman concluded as early as 1978 utilizing a prospective registry that the incidence of postoperative AF was nearly 3% after non-cardiac surgeries. (8) While AF is certainly more frequent after cardiac surgery, incidence varies between studies. Reasons for these variations seem to be different ascertainment methods between studies (12 lead ECG vs. continuous telemetry monitoring etc). Mathew et al document an incidence of up to 34% with similar incidences in North America and Europe but lower incidence in Asia at 16 %. (13) The incidence also varies depending on the type of cardiac surgery undertaken. AF seems to occur 60% of the time post mitral valve surgery, 36% of the time post aortic valve surgery, (10) and 25% post cardiac transplants. (11) The combination of coronary artery bypass graft surgery (CABG) with valve surgery seems to increase the risk for AF as well. (12) Often times the

If the answer to any of questions 1-3 is yes or to question 4 is no, the rhythm is probably ventricular tachycardia. There are several additional ways to distinguish between supra

The conduction system of the heart has to be intact anatomically and physiologically for synchronized contraction of the heart in a regular and coordinated fashion. Arrhythmias are caused when there is disturbance in the working of the conduction system for any reason. The accepted mechanisms include abnormality of conduction (i.e. blocking or Re-entry of the impulse), abnormality of impulse initiation (i.e. altered automaticity or triggered activity). The underlying causes can include ischemia, electrolyte imbalances, scarring or fibrosis of atrial and ventricular tissue, increased or decreased excitability for various

Disturbances of the normal cardiac rhythm can be of many types. A universal hierarchical classification which can encompass all the salient arrhythmias is difficult to conceive. Arrhythmias are usually classified based on morphology, rate or origin. They can be divided into fast or slow based on the rate- Tachyarrhythmias when heart rate is faster than 100 bpm and bradyarrhythmias when rate is slower than 60 bpm. The QRS duration which defines the ventricular depolarization is usually less than 0.12 seconds (or 3 small boxes on the ECG at 25 mm/sec paper speed). If it is more than 0.12 seconds it represents delayed depolarization and can be used as a feature to divide the tachyarrhythmias into narrow complex and wide complex tachycardia. Another classification of arrhythmias describes regular versus irregular rhythms. Finally arrhythmias can generally be classified based on various anatomical substrates of the heart, which initiate these rhythm changes like atrial (or supraventricular) or ventricular arrhythmias. As mentioned above these classifications are an attempt, far from perfect, to distinguish normal from abnormal and define categories

The following chapter will discuss Atrial Fibrillation (AF) after cardiac surgery initially as

The incidence of any arrhythmia postoperatively can be up to 85% (5). The Multi center anesthesia outcomes study quotes that postoperative arrhythmias can complicate about 70% of the operations. (6) AF seems to be the most common arrhythmia in the post operative period (7). Goldman concluded as early as 1978 utilizing a prospective registry that the incidence of postoperative AF was nearly 3% after non-cardiac surgeries. (8) While AF is certainly more frequent after cardiac surgery, incidence varies between studies. Reasons for these variations seem to be different ascertainment methods between studies (12 lead ECG vs. continuous telemetry monitoring etc). Mathew et al document an incidence of up to 34% with similar incidences in North America and Europe but lower incidence in Asia at 16 %. (13) The incidence also varies depending on the type of cardiac surgery undertaken. AF seems to occur 60% of the time post mitral valve surgery, 36% of the time post aortic valve surgery, (10) and 25% post cardiac transplants. (11) The combination of coronary artery bypass graft surgery (CABG) with valve surgery seems to increase the risk for AF as well. (12) Often times the

ventricular and ventricular arrhythmias, which exceed the objectives of this review.

reasons including changes in autonomic nervous system, action of drugs and others.

with different underlying pathophysiology and treatment options.

this seems to be the most common and most extensively studied arrhythmia.

**4. Types of arrhythmias** 

**5. Postoperative AF** 

**Incidence:** 

definition for postoperative AF includes the need of medical treatment or electrical cardioversion (14) or confirmation on a 12 lead ECG (13) altering the incidence rates further. The peak incidence of postoperative AF (POAF) has been consistently described on day 2 and 3 after surgery. (10) It usually is transient with 80% of the patients converting to sinus rhythm within 24 hours. The recurrence rate has been quoted to be as much as 50% but still only 10% of patients are still in AF at 6 weeks post operation. (13) Late Postoperative AF is less frequent but was seen in nearly 5% of the postoperative patients after discharge from the hospital. This was found when patients were being followed for cardiac rehabilitation and documented in the ISYDE and ICAROS registries in Italy. (15) Despite better coordinated postoperative care and advances in cardiothoracic surgical and anesthetic practices, the incidence of AF seems stable with no reduction over the last 2 decades.

### **Pathophysiology of Postoperative AF:**

AF is generally due to reentry of multiple wavelets circling the atria. It is likely that a preexisting substrate is needed to allow peri-operative triggers to initiate AF. It is thus a specific interaction of preexisting and perioperative risk factors which can lead to AF.

### **Preexisting factors:**

Age is the most consistent risk factor seen in past studies. Advancing age increases the risk with each decade. The incidence of POAF is around 6% when less than 40y of age, 18% in less than 60y olds and increasing to as much as 50% in patients older than 80 years. (13,14,16) Other risk factors include male gender, history of prior AF, heart valve disease (especially if the mitral valve is affected), prior cardiac surgery, prior cardiac structural changes like increased left atrial size and left ventricular hypertrophy. Preexisting medical conditions like obesity, chronic lung disease, peripheral vascular disease, hypertension, prior stroke are associated with increased incidence of POAF. However certain other morbid factors like preexisting diabetes, chronic kidney disease, hyperlipidemia, smoking have not been shown to be individual risk factors for POAF in some studies. (17) Pericarditis which is usually a consequence of the cardiac surgery itself is mechanistically involved. Other unique factors such as preoperative use of Digoxin or Dopamine, raised Brain natriuretic peptide (BNP) and right-sided coronary artery disease have been associated as well. ECG features like increased P wave duration of more than 140 ms, which is suggestive of atrial conduction delay can increase the susceptibility to AF. (18) Withdrawal of preoperative Angiotensin converting enzyme inhibitor (ACE I) or Beta blocker therapy is also contributory if not immediately initiated after the surgery. (13)

### **Intraoperative factors:**

Certain operative features like aortic cross clamping, pulmonary venting, bicaval venous cannulation, increased length of cardiopulmonary bypass time and mitral valve surgery can increase the propensity for POAF. It has also been noted that at times cardioplegia via coronary sinus does not stun the atria completely and may be associated with occurrence of POAF(19) Direct cardiac injury due to operative techniques causing inflammation is perceived as plausible cause as well.

### **Postoperative features:**

The postoperative period is a critical stage as the body is yet to recover from the operative stress completely. Many proarrhythmic features such as pericardial inflammation, acute blood pressure or volume changes, acute cardiac ischemia, electrolyte imbalances,

Post Operative Arrhythmias 247

(33). It can reduce postoperative AF by 50% - 70% and evidence suggests that ventricular arrhythmias are also reduced. However, there is concern about possible complications including proarrhythmia, sudden respiratory distress or bradycardia requiring pacing following Amiodarone prophylaxis or treatment. Therefore, Amiodarone therapy needs to

Digoxin has also been studied but seems to be better only when used along with beta

Magnesium has been studied as a preventive strategy and while hypomagnesaemia does definitely portend arrhythmias (20) supplementation does not seem to be helpful in reducing rhythm disturbances. One meta analysis (35) has shown a positive outcome but another study (36) has cast a doubt on the utility of Magnesium supplementation in

Sotalol which has beta blocker as well as potassium channel blocking properties has been shown in certain studies (37) to be useful in preventing AF with relative risk reduction of up to 90%. However, studies generally involved small sample sizes. (29) There may not be an

Angiotensin Converting Enzyme inhibitor (ACE I) therapy did not consistently reduce POAF, but incidence may be increased if the ACE inhibitor therapy is withdrawn in patients

Statins appear to have a beneficial effect in preventing AF. The ARMYDA 3 trial showed that taking a statin two weeks prior to surgery significantly reduces the incidence of POAF, although

Various other agents like Non steroidal anti inflammatory agents (NSAID), Ascorbic acid, N-acetyl cysteine, Nitroprusside, Glucocorticoids, Fish oil have been tried on the premise that they reduce the oxidative stress and help modify the inflammatory process that seems to be present postoperatively and thereby contributing to lower the risk of POAF. However despite positive results in small trials, larger randomized controlled trials are necessary to

Pacing via epicardial wires introduced at the time of the surgery has been recognized as an effective method in controlling AF in as much as 63% of the cases. (40) Pacing is done either at the sinus rate or faster with overdrive pacing. Studies have showed that bi atrial pacing (BAP) seems to be better than pacing in only one atrium. The American College of Chest Physicians (ACCP) guide recommends BAP over either right or left single atrial pacing. (41) Beta blockers seem to provide additive benefits along with pacing in preventing POAF. The odds ratios of various agents used in POAF prevention are given below: (21)

The ACC/AHA/ESC 2006 guidelines recommend using a beta blocker routinely to prevent POAF and using Amiodarone or pacing only if the patient is intolerant of beta blockers or in high risk cases such as when the patient is undergoing mitral valve surgery or if they have

incremental effect of Sotalol along with Beta blocker therapy to prevent POAF.

there were concerns about the relatively high incidence of AF in the control group. (38)

be closely monitored.

preventing POAF.

blockers and is currently not recommended. (34)

who were receiving it before surgery.

ascertain any true benefit. (39)

Beta blockers – 0.35 Sotalol – 0.36 Amiodarone – 0.54 Pacing – 0.57 Potassium – 0.53 NSAID – 0.49

ACE inhibition – 0.62

had prior history of AF. (32)

hypothyroidism are present at this juncture. (20, 21, 22) Increased sympathetic activation causing exaggerated adrenergic responses could be a factor as well. (23)

The assumption is that non-uniform disruption of the electric conduction properties leads to changes in the resistance between adjacent cells in the atria. This causes decreased atrial conduction and creation of micro reentry loops causing AF. (24) Various factors mentioned above change the atrial refractoriness/transmembrane potentials causing increased local reentry and subsequent AF. (25) The suggestion that expression of connexin 40, a gap junction protein in the atria is altered during the postoperative period lends credence to the theory that the gap junction function in the atria is altered. (26)

### **Clinical Significance:**

POAF is usually transient as the underlying mechanical and metabolic changes are usually reversible and not long lasting. However it is associated with significant morbidity and mortality even when it occurs briefly. POAF can increase the risk of stroke by 3-4 folds. (27) Cresswell et al noted that the occurrence of stroke postoperatively with AF was at 3.3 vs.1.2% without AF. (12) However, other features such as increased age, prior stroke, length of cardiac bypass time seem to be playing additional role in the additive risk of stroke postoperatively.

AF has been shown to increase overall health care cost. The hospitalization time is increased by an average of 2 to 5 days. (13, 14) The costs were higher by as much as \$10,000 per patient if AF occurred postoperatively. The chances that the patient will suffer infection, renal failure, and mechanical ventilation also seem to be higher when AF is present. There has been suspicion that cognition of the patients can be affected as evidenced by a fall in the Mini Mental Score postoperatively when AF occurred. (10, 17, 28)

AF remains the leading cause for readmission after hospital discharge following cardiac surgery. It is estimated that AF contributed to nearly 23% of readmissions in one series. (9) So it would seem AF is a problem even after discharge and it would argue for continued monitoring of the patient as an outpatient preferably in a cardiac rehabilitation program.

AF seems to be associated with increased mortality both early and late after operation even after correction for many important confounding variables. It is estimated that the mortality associated with postoperative AF is around 5% compared to around 2% without AF. (13)

### **Management:**

Given the morbidity and mortality associated with POAF it has long been a target for preventive as well as suppressive therapy. A variety of interventions have been studied and validated. We would like to clarify that our list does not claim to be complete, but only gives an overview of some of the most important therapies available. In most cases consultation with a Cardiologist is recommended. Multiple studies (29) have shown that AF can be suppressed in the postoperative period and various meta analyses confirmed their findings. Incidence of AF was reduced by as much as 50%. (30, 31) We categorize preventative measures into preoperative, operative and postoperative measures.

### **Preoperative measures:**

The main thrust has been to reduce the sympathetic drive and Beta blockers seem to be the mainstay of this preventive approach. The 2004 ACC/AHA guidelines give a class I recommendation for preoperative and early postoperative beta blockade to prevent POAF. (32) Amiodarone which blocks Potassium and Calcium ion channels, and has both alpha and beta blockade properties has been assessed in various trials such as AFIST, ARCH, AFIST 2, GAP and PapaBear for prevention of POAF and has been summarized in a meta analysis

hypothyroidism are present at this juncture. (20, 21, 22) Increased sympathetic activation

The assumption is that non-uniform disruption of the electric conduction properties leads to changes in the resistance between adjacent cells in the atria. This causes decreased atrial conduction and creation of micro reentry loops causing AF. (24) Various factors mentioned above change the atrial refractoriness/transmembrane potentials causing increased local reentry and subsequent AF. (25) The suggestion that expression of connexin 40, a gap junction protein in the atria is altered during the postoperative period lends credence to the

POAF is usually transient as the underlying mechanical and metabolic changes are usually reversible and not long lasting. However it is associated with significant morbidity and mortality even when it occurs briefly. POAF can increase the risk of stroke by 3-4 folds. (27) Cresswell et al noted that the occurrence of stroke postoperatively with AF was at 3.3 vs.1.2% without AF. (12) However, other features such as increased age, prior stroke, length of cardiac bypass time seem to be playing additional role in the additive risk of stroke postoperatively. AF has been shown to increase overall health care cost. The hospitalization time is increased by an average of 2 to 5 days. (13, 14) The costs were higher by as much as \$10,000 per patient if AF occurred postoperatively. The chances that the patient will suffer infection, renal failure, and mechanical ventilation also seem to be higher when AF is present. There has been suspicion that cognition of the patients can be affected as evidenced by a fall in the

AF remains the leading cause for readmission after hospital discharge following cardiac surgery. It is estimated that AF contributed to nearly 23% of readmissions in one series. (9) So it would seem AF is a problem even after discharge and it would argue for continued monitoring of the patient as an outpatient preferably in a cardiac rehabilitation program. AF seems to be associated with increased mortality both early and late after operation even after correction for many important confounding variables. It is estimated that the mortality associated with postoperative AF is around 5% compared to around 2% without AF. (13)

Given the morbidity and mortality associated with POAF it has long been a target for preventive as well as suppressive therapy. A variety of interventions have been studied and validated. We would like to clarify that our list does not claim to be complete, but only gives an overview of some of the most important therapies available. In most cases consultation with a Cardiologist is recommended. Multiple studies (29) have shown that AF can be suppressed in the postoperative period and various meta analyses confirmed their findings. Incidence of AF was reduced by as much as 50%. (30, 31) We categorize preventative

The main thrust has been to reduce the sympathetic drive and Beta blockers seem to be the mainstay of this preventive approach. The 2004 ACC/AHA guidelines give a class I recommendation for preoperative and early postoperative beta blockade to prevent POAF. (32) Amiodarone which blocks Potassium and Calcium ion channels, and has both alpha and beta blockade properties has been assessed in various trials such as AFIST, ARCH, AFIST 2, GAP and PapaBear for prevention of POAF and has been summarized in a meta analysis

causing exaggerated adrenergic responses could be a factor as well. (23)

theory that the gap junction function in the atria is altered. (26)

Mini Mental Score postoperatively when AF occurred. (10, 17, 28)

measures into preoperative, operative and postoperative measures.

**Clinical Significance:** 

**Management:** 

**Preoperative measures:** 

(33). It can reduce postoperative AF by 50% - 70% and evidence suggests that ventricular arrhythmias are also reduced. However, there is concern about possible complications including proarrhythmia, sudden respiratory distress or bradycardia requiring pacing following Amiodarone prophylaxis or treatment. Therefore, Amiodarone therapy needs to be closely monitored.

Digoxin has also been studied but seems to be better only when used along with beta blockers and is currently not recommended. (34)

Magnesium has been studied as a preventive strategy and while hypomagnesaemia does definitely portend arrhythmias (20) supplementation does not seem to be helpful in reducing rhythm disturbances. One meta analysis (35) has shown a positive outcome but another study (36) has cast a doubt on the utility of Magnesium supplementation in preventing POAF.

Sotalol which has beta blocker as well as potassium channel blocking properties has been shown in certain studies (37) to be useful in preventing AF with relative risk reduction of up to 90%. However, studies generally involved small sample sizes. (29) There may not be an incremental effect of Sotalol along with Beta blocker therapy to prevent POAF.

Angiotensin Converting Enzyme inhibitor (ACE I) therapy did not consistently reduce POAF, but incidence may be increased if the ACE inhibitor therapy is withdrawn in patients who were receiving it before surgery.

Statins appear to have a beneficial effect in preventing AF. The ARMYDA 3 trial showed that taking a statin two weeks prior to surgery significantly reduces the incidence of POAF, although there were concerns about the relatively high incidence of AF in the control group. (38)

Various other agents like Non steroidal anti inflammatory agents (NSAID), Ascorbic acid, N-acetyl cysteine, Nitroprusside, Glucocorticoids, Fish oil have been tried on the premise that they reduce the oxidative stress and help modify the inflammatory process that seems to be present postoperatively and thereby contributing to lower the risk of POAF. However despite positive results in small trials, larger randomized controlled trials are necessary to ascertain any true benefit. (39)

Pacing via epicardial wires introduced at the time of the surgery has been recognized as an effective method in controlling AF in as much as 63% of the cases. (40) Pacing is done either at the sinus rate or faster with overdrive pacing. Studies have showed that bi atrial pacing (BAP) seems to be better than pacing in only one atrium. The American College of Chest Physicians (ACCP) guide recommends BAP over either right or left single atrial pacing. (41) Beta blockers seem to provide additive benefits along with pacing in preventing POAF. The odds ratios of various agents used in POAF prevention are given below: (21)

Beta blockers – 0.35 Sotalol – 0.36 Amiodarone – 0.54 Pacing – 0.57 Potassium – 0.53 NSAID – 0.49 ACE inhibition – 0.62

The ACC/AHA/ESC 2006 guidelines recommend using a beta blocker routinely to prevent POAF and using Amiodarone or pacing only if the patient is intolerant of beta blockers or in high risk cases such as when the patient is undergoing mitral valve surgery or if they have had prior history of AF. (32)

Post Operative Arrhythmias 249

Stroke, transient ischemic attack (TIA) or thrombo embolism are given 2 points each. Factors including Hypertension, Congestive heart failure, Diabetes, Ages 65-74y, female Sex and co existent Vascular disease are scored 1 point each. Anticoagulation is indicated if the combined score is > 2. (48) Newer agents like Dabigatran are available on the market but studies will need to be done to assess its value specifically in the postoperative period. Not much significant data is available as to the management of patients after discharge. They are usually reassessed 4-6 weeks after discharge and often times Holter monitoring is employed. Most of the patients can stop their anti arrhythmic medications and anti coagulation if they are deemed to be in sinus rhythm without intermittent AF, 3-6 months

In spite of all studies and evidence regarding preventing and treating POAF, doubts still exist whether any real benefit is obtained. Some evidence suggests that AF prevention does not or only minimally reduces the length of stay or the overall cost. (50) It is also noted that there is no actual decrease in the stroke incidence post operatively even if the AF is suppressed. It is unclear if the mortality and morbidity are improved if the AF is indeed suppressed. (51) It seems that stroke may be an epiphenomenon and not directly related to the occurrence of POAF. However a large Meta analysis does seem to suggest some overall

These include the more common benign isolated ectopic beats or Non sustained ventricular tachycardia (NSVT) and the more dangerous ventricular tachycardia or ventricular fibrillation (VT/VF) which fortunately are less common. The incidence of sustained ventricular arrhythmias has been quoted at around 0.4 – 1.4% (53) to 0.7 – 3% (54). The benign rhythm changes including ectopic ventricular beats and NSVT can occur in up to 60% of patients (55) but are not known to portend the more malignant rhythms like VT/VF (56) nor do they portend any rise in mortality risk (55, 57) if no underlying structural heart disease is suspected. The mortality of sustained VT is high at around 50% in hospital and a

The risk factors for the occurrence of VT/VF seem to correlate with factors associated in general cardiology practice. Any underlying structural heart disease, prior myocardial infarction, reduced left ventricular ejection fraction or congestive heart failure increase the risk of life threatening ventricular arrhythmias. Immediate postoperative features which set off the rhythm disturbance include any hemodynamic instability, electrolyte or acid base disturbances, hypoxia, anemia, new onset ischemia etc. An occasional cause can be acute graft closure after bypass grafting. Any inotropes used in the postoperative phase can also

Even though frequent ectopics and NSVT are considered benign it would be prudent to look for any reversible factors mentioned before in the acute phase. Lidocaine and pacing have been studied to suppress these rhythm disturbances but no actual benefit was observed. (53, 58) Sustained Ventricular arrhythmia is invariably quite unstable and quick remedial measures need to be instituted to treat the patient. Electrical cardioversion with 200 – 360 Joules is usually the first line option to convert the arrhythmia. If Direct Current cardioversion is not an option or if medications are preferred as per the clinical situation, various drugs like Lidocaine, Amiodarone, Procainamide can be considered. Emergency

benefit with prophylaxis measures and prevention of POAF. (52)

**6. Post cardiac surgery ventricular arrhythmias** 

further 10% die within 2 years. (53)

be pro arrhythmic.

**Treatment:** 

after hospital discharge.
