The document discusses post-cardiac surgery arrhythmias, highlighting the prevalence and types, including atrial fibrillation and ventricular arrhythmias, along with their underlying mechanisms and etiologies. It outlines assessment protocols, treatment options for various arrhythmias, and the significance of monitoring and managing factors that may exacerbate these conditions post-surgery. Additionally, it emphasizes the importance of timely intervention and potential complications associated with arrhythmias in the postoperative setting.

1. Post Cardiac Surgery
Arrhythmia : Treatment
Rachata Mala. MD.
Cardiothoracic surgery
QSHC&SNH, KKU

2. Cardiac Arrhythmias
• The development of cardiac arrhythmias following open-heart surgery is fairly
common.
• Supraventricular arrhythmias, especially atrial fibrillation (AF), are about 25% of
patients.
•
• Ventricular arrhythmias are less common and usually reflect some degree of
myocardial injury.
• The mechanisms of most arrhythmias are altered automaticity (impulse
formation) and conductivity (impulse conduction).

3. Etiology
1. Cardiac problem
1. Underlying heart disease
2. Preexisting arrhythmias
3. Myocardial ischemia/infarction
4. Poor intraoperative myocardial protection
5. Pericardial inflammation

4. Etiology
2. Respiratory problems
1. Endotracheal tube irritation or misplacement
2. Hypoxia, hypercarbia, acidosis
3. Pneumothorax
3. Electrolyte imbalance (K, Mg)
4. Intracardiac monitoring lines (PA catheter)

5. Etiology
5. Surgical trauma (atriotomy, ventriculotomy,
dissection near the conduction system)
6. Drugs (vasoactive drugs, proarrhythmic effects
of antiarrhythmic medications)
7. Hypothermia
8. Fever, anxiety, pain
9. Gastric dilatation

6. Assessment
• 1. Check ABG, ventilator function, position of ET-tube, and CXR for mechanical
problems.
• 2. Check serum electrolytes (especially potassium).
• 3. Review a 12-lead ECG for ischemia and a more detailed examination of the
arrhythmia.

9. Sinus bradycardia
• Caused by persistent Beta-blocker and the use of narcotics, and result in atrial,
junctional, or ventricular escape rhythms
• Reduces cardiac output, the heart rate should be maintained around 80-90 bpm
following the termination of CPB.

10. Sinus bradycardia

11. Sinus bradycardia
Treatment
• Atrial pacing/Ventricular pacing
• Epinephrine 1–2 mg/min, dopamine 5–10 mg/kg/min, or isoproterenol 1–2
mg/min may be useful,
• Atropine 0.01 mg/kg IV (usually 0.5–1 mg IV) can be used for severe symptomatic
bradycardia on an emergency basis
• PPM

12. Conduction abnormalities and heart block
• Transient disturbances of conduction at the AV node, 25% post CABG receive cold
cardioplegia
• impair LV function, HT, severe CAD(especially involving the RCA in a right-dominant
system), long AOX periods, and extremely low myocardial temperatures. Although
most will resolve within 24–48 hours
• After aortic valve replacement (AVR) caused by
• hemorrhage, edema, suturing, or debridement near the AV node and His bundle.

14. Conduction abnormalities and heart block
• After MV surgery
• Exposure of the mitral valve by the biatrial transseptal approach involves division
of the sinus node artery and anterior internodal pathways.
• sinus node dysfunction with ectopic atrial rhythms, junctional rhythms, and varying
degrees of heart block.
• About 10% of patients require a PPM

23. Conduction abnormalities and heart block
Treatment
• First-degree AV block
• characterized by prolongation of the PR interval to greater than 200 ms and
usually does not require treatment.

24. Conduction abnormalities and heart block
Treatment
• Second-degree AV block
• i. Mobitz type I (Wenckebach)
• This usually does not require treatment unless the ventricular rate is slow. In this
situation, it can be treated by AV pacing (DVI) at a slightly faster rate. If the atrial
rate is too fast to overdrive, it can be treated by DDD pacing.

25. Conduction abnormalities and heart block
Treatment
• Second-degree AV block
• ii. Mobitz type II :. This reflects block in the His–Purkinje system and therefore is
associated with a wide QRS complex.
• If the ventricular rate is too slow, AV pacing in the DVI or DDD mode should be
used. If this rhythm persists, a permanent pacemaker should be implanted
because it is likely to progress to complete heart block.

26. Conduction abnormalities and heart block
Treatment
• iv. High-grade second-degree heart block is evident when there is a constant PR
interval but two or more consecutive atrial impulses do not conduct to the
ventricle. It is treated by AV pacing and may require permanent pacing if
persistent.

27. Conduction abnormalities and heart block
Treatment
• Third-degree (complete) heart block
• Requires AV pacing in the DDD or DVI mode.
• If the atrial rate is acceptable, the DDD mode should be used to track the atrial
rate and then provide a sequential ventricular contraction.
• If there is atrial inactivity or a slow atrial rate, either DDD or DVI pacing can be
used. Ventricular pacing should be used if atrial fibrillation/flutter is present.

28. Conduction abnormalities and heart block
Treatment
• Hold medication (beta-blockers, amiodarone, calcium channel blockers,
or digoxin)
• If complete heart block persists for more than a few days, a permanent
pacemaker system should be placed.

29. Sinus tachycardia
Etiology
1. Benign hyperdynamic reflex response related to sympathetic overactivity
1. Pain, fever, anxiety
2. Adrenergic rebound ( on B-blockers preoperative)
3. Drugs (Catecholamines, Pancuronium)
4. Gastric dilatation
5. Anemia
6. Hypermetabolic state (sepsis)

30. Sinus tachycardia
Etiology
2. Compensatory response to myocardial injury or impaired cardiorespiratory status
1. Hypoxia, hypercarbia, acidosis
2. Hypovolemia or low stroke volumes noted with small, stiff left ventricles with LVH and
diastolic dysfunction
3. Myocardial ischemia or infarction
4. Cardiac tamponade
5. Tension pneumothorax

32. Sinus tachycardia
Treatment
1. Correct cause
2. Sedation and analgesia in ICU setting
3. Beta blocker
• Esmolol 0.25–0.5 mg/kg IV over 1 minute followed by a continuous nfusion of 50–200
mg/kg/min. A trial bolus of 0.125 mg/kg is recommended to determine whether the patient
can tolerate esmolol.
• Metoprolol 5 mg IV increments every 5 minutes for three doses
4. Calcium channel blocker

33. Premature atrial complexes (PACs)
• PACs are premature beats arising in the atrium that generally have a different
configuration than the normal P wave and produce a PR interval that exceeds 120 ms.
• Magnesium sulfate may be beneficial in reducing the incidence of PACs in the
immediate postoperative period. The dose is 2 g in 100mL solution.

34. Premature atrial complexes (PACs)

35. Premature atrial complexes (PACs)
• Treatment
• PACs generally do not need to be treated
• Digoxin is useful in decreasing the frequency of PACs and slows conduction through
the AV node
• Temporary right atrial pacing at a faster rate (“overdrive pacing”) may suppress PACs
but it may also trigger atrial arrhythmias and induce AF

36. Atrial fibrillation or flutter
Most common arrhythmias after open-heart surgery, 25 – 30 %
• factors that increase the risk of AF
• older age
• a history of atrial arrhythmias
• Obesity
• COPD
• LVH
• right coronary artery disease
• valve surgery
• increased preoperative BNP levels

37. Atrial fibrillation or flutter
• Operative considerations include
• redo surgery
• inadequate myocardial protection
• Prolonged cross-clamp times
• atrial trauma
• useof lower systemic temperatures
• The efficacy of off-pump coronary surgery in reducing the incidence of AF
• Postoperative pericardial effusions may also increase the risk of AF

38. Atrial fibrillation or flutter
Etiology
• Enhanced sympathetic activity (“hyperadrenergic state”) or adrenergic rebound in
patients taking b-blockers preoperatively
• Atrial ischemia from poor myocardial preservation during aortic cross clamping
• Atrial distention from fluid shifts
• Surgical trauma or inflammation (pericarditis)
• Metabolic derangements (hypoxia, hypokalemia, hypomagnesemia)

41. Atrial fibrillation or flutter
Prevention
• Prophylactic therapy can reduce the risk of AF by approximately 50%, but cannot
eliminate its occurrence

42. Prophylaxis

43. Treatment

44. Management

45. supraventricular tachycardias (SVTs)
uncommon after cardiac surgery
tachycardia in the atrium (paroxysmal atrial tachycardia, PAT) or in the
AV nodal region (AV nodal reentrant tachycardia, AVNRT), or uses the AV
node as an integral part of the reentrant circuit (AV reentrant
tachycardia, AVRT)
rhythms usually occur at a rate of 150–250/min

47. supraventricular tachycardias (SVTs)
• Treatment
1. Rapid atrial overdrive pacing may capture the atrium and cause reversion to
sinus rhythm.
2. Cardioversion if there is evidence of hemodynamic compromise.
3. Vagal stimulation will often break a reentrant rhythm involving the AV node.
Carotid sinus massage must be used cautiously.
4. Adenosine It is given as a 6 mg rapid IV injection via a central line followed by a
saline flush. A repeat dose of 12 mg may be given 2 minutes later. The half-life of
adenosine is only 10 seconds.

48. supraventricular tachycardias (SVTs)
• Treatment
• Diltiazem (0.25 mg/kg IV over 2 minutes, followed 15 minutes later by 0.35 mg/kg,
if necessary) is effective in converting AVNRT to sinus rhythm in about 90% of
patients.
• Additional measures that can be used for AVNRT if the above fail include:
• Digoxin 0.5 mg IV in a patient not previously on digoxin
• Metoprolol 5 mg q5 min to a total dose of 15 mg
• Edrophonium 5 mg slow IV push, followed by a 10 mg dose

49. supraventricular tachycardias (SVTs)
• Treatment
• PAT with block is usually associated with digoxin toxicity and treatment should be
provided accordingly:
• Digoxin should be withheld and a digoxin level obtained
• Administration of potassium chloride (KCl)
• Digibind (digoxin immune Fab [ovine]) starting at a dose of 400 mg (10 vials) over 30 minutes if
severe digoxin toxicity
• Phenytoin (Dilantin) 250 mg IV over 5 minutes

50. AV junctional rhythm and non paroxysmal
AV junctional tachycardia
• An AV junctional rhythm occurs when junctional tissue has a faster intrinsic rate
than the sinus node. Heart rate less than 60 bpm and is termed a junctional escape
rhythm.
• Non paroxysmal AV junctional tachycardia occurs at a rate of 70–130/min and
usually results from enhanced automacity in the bundle of His. In the postoperative
patient, this rhythm may reflect digitalis toxicity, pericarditis, or an inferior
infarction.

53. AV junctional rhythm and non paroxysmal
AV junctional tachycardia
Treatment
• Slow junctional rhythm (junctional escape rhythm)
• Atrial pacing if AV conduction is normal.
• AV pacing if AV conduction is depressed.
• Use of a vasoactive drug with chronotropic B1 action to stimulate the sinus mechanism

54. AV junctional rhythm and non paroxysmal
AV junctional tachycardia
Treatment
• Non paroxysmal junctional tachycardia
• If the patient is receiving digoxin, it should be stopped. Severe digoxin toxicity may be treated
with digibind. Use of potassium, lidocaine, phenytoin, or a b-blocker may be helpful.
• Overdrive pacing at a faster rate
• If the patient is not on digoxin, it should be started. If the rhythm is not well tolerated, use of a
b-blocker or calcium channel blocker can be considered to slow the junctional focus, with use of
atrial or AV pacing to establish AV synchrony.

55. Premature ventricular complexes (PVCs)
• Etiology
• augmented sympathetic tone or increased levels of catecholamines (endogenous or
exogenous)
• irritation from a Swan-Ganz catheter or endotracheal tube
• Abnormal acid–base status
• Hypoxemia
• PVCs developing reflect poor intraoperative myocardial protection or myocardial
ischemia or infarction, and may herald malignant ventricular arrhythmias.

57. Premature ventricular complexes (PVCs)
• Treatment
• Correct the serum potassium with an IV KCl at a rate up to10–20 mEq/h through a
central line. Some patients require potassium levels between 4.5 and 5.0 mEq/L
• Atrial pace at a rate exceeding the current sinus rate (overdrive pacing)
• Magnesium sulfate (2 g in 100mL IV) administered at the termination of CPB
• in patients with impaired LV function, recent MI, ongoing ischemia, symptomatic PVCs,
and perhaps in the immediate perioperative period as the heart recovers from surgery,
use of drugs to control PVCs might be warranted.

58. Premature ventricular complexes (PVCs)
• Commonly used drugs include:
• Lidocaine 1 mg/kg with 1–2 repeat doses of 0.5 mg/kg 10 minutes apart. A continuous
infusion of 1–2 mg/min of a 1 g/250mL mix should be started. Do not exceed 4 mg/min
to avoid seizure activity.
• Amiodarone 150 mg IV load over 15 minutes, followed by a 60 mg/h infusion 6 hours,
then 30 mg/h 18 hours. Control of ventricular ectopy is an added benefit when
amiodarone is used prophylactically to prevent AF

59. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
Etiology
• VT/VF occur postoperatively in about 1–3% of patients undergoing open heart
surgery and carry a mortality rate of 20–30%.
• Reperfusion of zones of ischemia or infarction can trigger de novo malignant
ventricular arrhythmias.
• prior infarction, unstable angina, EF <40%, NYHA class III–IV CHF, pulmonary and
systemic hypertension, long CPB times, low cardiac output syndromes

60. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
Etiology
• The bypass grafts are placed to infarct zones or noncollateralized occluded vessels,
especially the left anterior descending artery.
• Potential triggers include residual ischemia or development of a perioperative
myocardial infarction secondary to incomplete revascularization, anastomotic
problems, or acute graft closure.

61. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Non sustained VT (NSVT) (VT lasting less than 30 seconds)
• Sustained monomorphic VT (VT lasting over 30 seconds) is
usually noted in patients with a previous myocardial infarction
and depressed LV function, often with formation of a left
ventricular aneurysm. The border zone between scar and
viable tissue

62. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Sustained polymorphic VT with a normal QT interval. Polymorphic VT may be
facilitated by perioperative phenomena such as ischemia, hemodynamic instability,
use of catecholamines or intrinsic sympathetic activity, withdrawal of b-blockers,
and other metabolic problems.
• Polymorphic VT with QT prolongation is called torsades de pointes.
• It may complicate the use of type IA and III antiarrhythmic agents, (Quinidine
Procainamide, Disopyramide, Amiodarone) especially if hypokalemia is present.
• Other medications that can contribute to torsades are metoclopramide, droperidol
(for nausea), and high-dose haloperidol (>35 mg/day) used for agitation in the ICU.

67. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Evaluation and treatment
• Any potential factors should be identified and managed.
• acid–base and electrolyte abnormalities,
• intracardiac catheters,
• myocardial ischemia or infarction,
• CHF,
• potentially proarrhythmic medications

68. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Evaluation and treatment
• Nonsustained VT (NSVT) with preserved LV function (EF >35%)
• lidocaine or amiodarone may be considered when this rhythm develops, b-blockers
alone should suffice
• NSVT in patients with depressed LV function (EF < 35%)
• an electrophysiology study and ICD placement should be considered if NSVT
develops after surgery in these patients

69. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Evaluation and treatment
• Sustained VT occurring without hemodynamic compromise can be managed by:
• i. Ventricular overdrive pacing to terminate the reentry circuit
• ii. Cardioversion if VT persists or hemodynamic compromise develops
• iii. Amiodarone 150 mg over 15 minutes, then 1 mg/min (60 mg/h) 6 hours, then
0.5 mg/min (30 mg/h) 18 hours
• Any patient developing VF or sustained VT that is pulseless or associated with
hemodynamic instability requires immediate defibrillation per ACLS protocol. If
unsuccessful, emergency resternotomy and open-chest massage are indicated

70. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Evaluation and treatment
• sustained VT and impaired LVEF (EF<35%)to improve the long-term prognosis. In
general, ICD placement can be justified
• Monomorphic VT is inducible in 80% spontaneous VT
• This usually requires antiarrhythmic therapy (usually amiodarone) as well as the
placement of an ICD.
• Polymorphic VT is usually associated with myocardial infarction, ischemia, or
reperfusion should coronary arteriography to identify potential graft occlusion or
an anastomotic stenosis which may a correctable problem.

71. Ventricular tachycardia (VT) and
ventricular fibrillation (VF)
• Evaluation and treatment
• Torsades de pointes
• Cardiovert immediately for hemodynamic compromise or prolonged episodes.
• Administer KCL, unless hyperkalemia is present, to shorten the QT interval.
• Ventricular pace at 90–100 beats/min or start an isoproterenol infusion at 1–4
mg/min.
• Magnesium 1–2 g and b-blockers may eliminate triggered activity to prevent
recurrence, but do not shorten the QT interval