Dr. Faisal Rasool Dar( PG 3rd yr MD aneaesthesiology) GMC, srinagar

1. Perioperative Arrhythmias
and
ACLS Guidelines
Speaker: Dr. Faisal Rasool Dar
Moderator: Dr. Shakeel Ah. Siddique
Consultant,
Dept. of Anaesthesiology &critical care
GMC, Srinagar

2. Definition:
Abnormality of cardiac rate, rhythm or conduction
which can be either asymptomatic, symptomatic
(syncope ,near syncope, dizziness, or palpitations) or
lethal(sudden cardiac death).
Dysrhythmias represent an important cause of
perioperative complications because during this period
there are several clinical situations that may trigger
changes in cardiac rhythm.
Most perioperative dysrhythmias are benign, without
significant hemodynamic consequences.

3. Incidence:
Seen in 70.2% of patients subjected to general
anesthesia for various surgical procedures.
Varies from patients undergoing cardiac or
non-cardiac surgery.
In patients undergoing cardiac surgery
reported incidence is >90%

4. Electrophysiology of conduction
system:
 impulses are conducted through the heart by a process
of progressive depolarization.
 Cardiac muscle cells have a resting membrane
potential of −80 to −90 mV
 The resting gradient is maintained by membrane-
bound (Na+ K+-ATPase.)
 The membrane potential increases when the sodium
and calcium channels open.
 At the point at which the membrane potential reaches
+20 mV, an action potential (or depolarization) occurs.

5.  Transmembrane action potential &
corresponding events occurring in ECG:

6.  Transmembrane action potential &
corresponding events occuring in ECG(cont.):
 Phase 4:represents spontaneous depolarization from the
resting membrane potential (−90 mV) until the threshold
potential(broken line) is reached.
 Phase 0 : represents depolarization ncorresponds to the QRS
on ECG
 Phase 1 to 3: represents repolarization with phase 3
corresponding to T wave in ECG.
* Effective refractory period (ERP) is the time during which cardiac
impulses cannot be conducted, regardless of the intensity of the
Stimulus while as during the Relative refractory period (RRP), a strong
stimulus can initiate an action potential.

7. Normal ECG:

8. Pathogenesis:
1) Injury or damage(pathology) of the cardiac conduction systems.
2) Re-entry: accessory tracts can exist that can bypass AV node & normal
infranodal conduction tract. In a reentry circuit, there is anterograde
(forward) conduction over the slower normal conduction pathway and
retrograde (backward) conduction over a faster accessory pathway.
3) Automaticity: is a phenomenon in which SA node (fastest pacemaker) which
discharges @ 60-100BPM is overdriven by accelerated secondary pacemakers
and results in abnormal depolarizations.
4) Mutations in ion channels: since these ion channels are mainly responsible
for depolarization, their mutations can lead to arrhythmias.

10. Contributing factors and causes:
1) Patient related factors:
• Preexisting cardiac disease
• CNS disease
• Old age
2 )Anesthesia related factors:
• Tracheal intubation
• General anesthetics
• Regional anesthesia
• Electrolyte imbalance and abnormal blood gases
• central venous cannulation
3) Surgery related factors:
• Cardiac surgery ( surgical manipulation, release of aortic clamp etc.)
• Non-cardiac surgery ( vagal stimulation d/t traction on peritoneum, direct
pressure on vagus nerve etc.)

11.  Reversible causes of arrhythmias:
Hypoxemia
Hypercarbia
Hypotension
Acidosis
Light anesthesia
Proarrhythemic drugs
Electrolyte imbalance
Hypothermia
Mechanical irritation (e.g. central venous
catheter, chest tube etc.)

12.  Classification of cardiac arrhythmias:
Tachy arrhythmias : Brady arrhythmias:
1) Supraventricular arrhythmias
 Sinus Tachycardia
 Sinus Arrhythmia
 Premature atrial contractions(PAC)
 Supraventricular Tachycardia
 Atrial Flutter
 Atrial Fibrillation
1) Sinus bradycardia
2) Ventricular arrhythmias
 Premature ventricular contractions(PVC)
 Ventricular Tachycardia
 Ventricular Fibrillation
2) Various types of conduction blocks
 1st Degree AV heart block
 2nd Degree AV heart block
 3rd Degree AV heart block( complete
heart block)

13. TACHY ARRHYTHMIAS

14.  Sinus Tachycardia
 occurs at a heart rate of 100 to 160 beats per minute.
 ECG-Normal P wave before every QRS complex.
 PR interval is normal unless a co-existing conduction block exists.
 caused by acceleration of SA node discharge secondary to
sympathetic stimulation.
 without manifestations of hemodynamic instability is not life-
threatening.
 Since it increase s myocardial oxygen demand, it can contribute to
myocardial ischemia and congestive heart failure in susceptible
patients.
 most common supraventricular dysrhythmia associated with acute
myocardial infarction, occurring in 30% to 40% of these patients.

15. Perioperative management:
• Correcting any underlying cause of increased
sympathetic stimulation.
• Avoidance of vagolytic drugs, such as pancuronium.
• Supplemental oxygen should be administered to
increase oxygen supply in response to the increased
oxygen demand.
• β-blockers may be employed to lower the heart rate
and decrease myocardial oxygen demand.
 β-blockers must be used with caution as they can cause bronchospasm in
susceptible patients and can also lead toabrupt & dangerous drop in BP.

16. Sinus Arrhythmia
Normal variant of sinus rhythm .
ECG-Normal P wave before every QRS complex.
Rhythm is irregular
• Rate increases with inspiration
• Rate decreases with expiration
Rate is usually 60-100 BPM
It is a normal variant and carries no risk of deterioration into a more
dangerous rhythm.
Common in children and young and decreases with age.

17. Perioperative management:
• No treatment required

18. Premature Atrial Contractions
 arise from ectopic foci in the atria.
 ECG - early, abnormally shaped P waves, PR interval is variable. Most often
the corresponding QRS complex is normal.
 PACs is not a risk factor for progression to a life-threatening dysrhythmia.
 symptoms of PACs include an awareness of a "fluttering“ or a "heavy"
heart beat.
 Precipitating factors include excessive caffeine, emotional stress, alcohol,
nicotine, recreational drugs, and hyperthyroidism.
 Common in patients with chronic lung disease, ischemic heart disease, and
digitalis toxicity.

19. Perioperative management:
• Avoid precipitating drugs or toxins.
• Avoid excessive sympathetic stimulation.
• Pharmacologic treatment is required only
if the PACs trigger secondary arrhythmias.
• Usually suppressed by calcium channel
blockers or β-blockers.

20.  Supraventricular Tachycardia(SVT)
average heart rate of 160 to 180 beats per minute.
Initiated and sustained by tissue at or above the AV node.
SVT is usually paroxysmal.
AV nodal reentrant tachycardia (AVNRT) is the most common type of
SVT.
Common symptoms during an episode of SVT include light-
headedness, dizziness, fatigue, chest discomfort and dyspnea.
15% of patients with SVT experience overt syncope.
occurs most often in the absence of structural heart disease in
younger individuals .
M:F ratio = 1:3

21. Perioperative management:
• Monitoring of vital signs to detect any progression to hemodynamic instability is usually all that is needed
until an episode of SVT terminates.
• Avoid increased sympathetic tone, electrolyte imbalances, and acid base disturbances.
• In hemodynamically stable patients treatment of SVT consists of vagal maneuvers such as carotid sinus
massage or Valsalva's maneuver.
• If conservative treatment fails pharmacologic treatment directed at blocking AV nodal conduction is
indicated.
• adenosine, calcium channel blockers, and β-blockers are commonly used to terminate SVT.
• Adenosine has a very rapid onset (15 to 30 secs.) and very brief duration of action (10 secs.) & usually
single dose is enough to terminate SVT.
• Calcium channel blockers like verapamil and diltiazem have a longer duration of action than adenosine.
• Intravenous digoxin is not clinically useful in acute control of SVT
• Electrical cardioversion is indicated for SVT unresponsive to drug therapy or SVT associated with
hemodynamic instability.

22.  Atrial Flutter
 An organized atrial rhythm with an atrial rate of 250 to 350 beats per minute with varying degrees of AV
block.
 ECG- rapid P waves create a saw tooth appearance and are called flutter waves, particularly noticeable in
leads II, III, aVF, and V1.
 Ventricular rate- may be regular or irregular(depending on conduction rate)
 Most commonly patients have 2:1 AV conduction(e.g. an atrial rate of 300 BPM with 2:1 conduction
results in a ventricular rate of 150 BPM).
 Deterioration of atrial flutter into atrial fibrillation and then its reversal is common.
 Usually associated with structural heart disease.
 Usually associated with acute exacerbation of a chronic condition such as pulmonary disease,
acute MI, ethanol intoxication, thyrotoxicosis, or after cardiothoracic surgery.

23. Perioperative management:
• Before induction- surgery should be
postponed,if possible until control of the
arrhythmia has been achieved.
• Intraoperative management-
H/D unstable-Synchronized cardioversion starting at
50 J (monophasic)
H/D stable- Pharmacologic control of the ventricular
response with intravenous amiodarone, diltiazem, or
verapamil may be attempted( goal is to prevent
deterioration in AV conduction from 2:1 to 1:1)

24.  Atrial Fibrillation(AF)
 AF occurs when multiple areas of the atria continuously depolarize and contract in a disorganized
manner.
 No coordinated depolarization or contraction, only a quivering of the atrial walls.
 ECG-chaotic atrial activity with no discernible P waves the QRS complex is often wide.
 Rhythm is irregularly irregular.
 If HR is <100 it is cosidered controlled AF, if HR is >100 it is said to have a “ Rapid Ventricular
Response”.
 Av node acts as a “filter”, blocking out most atrial impulses in an attempt to control HR.
 Predisposing conditions-rheumatic heart disease (especially mitral valve disease), HTN,
hyperthyroidism, ischemic heart disease, COPD, alcohol intake (holiday heart syndrome), pericarditis,
pulmonary embolus, and ASD.
 Symptoms-may be identified on physical examination or ECG in a patient with no associated
symptoms or patient may come with symptoms like generalized weakness and fatigue, or
prominent, such as palpitations, angina pectoris, shortness of breath, orthopnea, and hypotension.

25. Perioperative management:
• Before induction- If new-onset atrial fibrillation occurs before induction of
anesthesia, surgery should be postponed if possible until ventricular rate
control or conversion to sinus rhythm has been achieved.
• Intraoperative management-
 H/D unstable-Synchronized cardioversion at 100 to 200 J (biphasic) is
indicated.
 H/D stable-
1)Pharmacologic conversion to sinus rhythm with IV amiodarone may be
attempted.
2) Rate control can be achieved with a β-blocker or calcium channel blocker.
 Patients with chronic atrial fibrillation should continue to receive their
antiarrhythmic drugs perioperatively with close attention to serum Mg+ and
K+ levels(esp. those on digoxin)
 Manage the transition on and off of IV and oral anticoagulation.

26.  Premature ventricular contractions(PVC)
 PVCs arise from single (unifocal) or multiple (multifocal) foci located below the AV node.
 ECG- premature and wide QRS complex, no preceding P wave, ST segment and T-wave deflection
opposite to the QRS deflection, and a compensatory pause before the next sinus beat.
 R-on-T phenomenon-PVCs that occur during relative refractory period of the cardiac action potential
or approximately the middle third of the T wave may initiate repetitive beats that can deteriorate into
a sustained rhythm such as ventricular tachycardia or ventricular fibrillation. This clinical situation is
known as the R-on-T phenomenon.
 PVCs short episodes with spontaneous termination or as a sustained period of bigeminy or trigeminy.
 The occurrence of more than three consecutive PVCs is considered ventricular tachycardia.
 symptoms associated with PVCs are palpitations, near syncope, and syncope.

27.  BIGEMINY
 R-on-T phenomenon

29. Perioperative management:
• During administration of an anesthetic, if a patient exhibits
six or more PVCs per minute and repetitive or multifocal
forms of ventricular ectopy, there is an increased risk of
development of a life-threatening arrhythmia.
• Immediate availability of a defibrillator should be
confirmed.
• elimination of as many of causative factors as possible.
• Antiarrhythmics are indicated only if the PVCs progress to
ventricular tachycardia or are frequent enough to cause
hemodynamic instability.
• β-Blockers are the most successful drugs in suppressing
ventricular ectopy.

30.  Ventricular Tachycardia(VT)
 Ventricular tachycardia(also called monomorphic ventricular tachycardia) is present
when three or more consecutive PVCs occur at a heart rate of more than 120 beats per
minute (usually 150 to 200 beats per minute).
 Torsade de pointes (TdP; also called polymorphic ventricular tachycardia) is a distinct
form of VT initiated by a PVC in the setting of abnormal ventricular repolarization
(prolongation of the QT interval).
 ECG- The rhythm is regular with wide QRS complexes and no discernible P waves
 VT is common after an acute myocardial infarction and in the presence of inflammatory
or infectious diseases of the heart. Digitalis toxicity may also present as VT.

31.  monomorphic ventricular tachycardia
 polymorphic ventricular tachycardia (Torsade de pointes )

32. Perioperative management:
• Patients with symptomatic or unstable monomorphic ventricular tachycardia or SVT should
undergo cardioversion immediately.
• Cardioversion can begin at an output of 100 J (monophasic) and increase in increments of 50
to 100 J.
• If vital signs are stable but the VT is persistent or recurrent after cardioversion, then
administration of amiodarone 150mg over 10 minutes is recommended & can be repeated as
needed to a maximum total dose of 2.2 g in 24 hours.
• Alternative drugs include procainamide, sotalol, and lidocaine.
• Pulseless ventricular tachycardia or polymorphic ventricular tachycardia under any
circumstances requires initiation of cardiopulmonary resuscitation (CPR) and immediate
defibrillation using 360 J (monophasic).
• In addition to electrical therapy and drug treatment, endotracheal intubation and evaluation
and correction of acid-base and electrolyte disturbances should be undertaken as clinically
appropriate.

33.  Ventricular Fibrillation(VF)
 VF is the most common cause of sudden cardiac death.
 Most victims have underlying ischemic heart disease.
 Ventricular tachycardia often precedes the onset of ventricular fibrillation.
 VF is a rapid, grossly irregular ventricular rhythm with marked variability in QRS cycle length,
morphology, and amplitude.
 VF is incompatible with life because there is no associated stroke volume or cardiac output.
 A pulse or blood pressure never accompanies VF.
 If a patient with presumed VF is awake or responsive, the ECG must be reevaluated before treatment
decisions are made.
 The gold standard for long-term treatment of recurrent episodic VT or VF is implantation of a
permanent automatic pacemaker cardioverter-defibrillator.

34. Perioperative management:
• Ventricular fibrillation during anesthesia is a critical event. CPR must be
initiated immediately.
• Electrical defibrillation is the only effective method to convert ventricular
fibrillation to a rhythm capable of generating a cardiac output.
 Biphasic: Manufacturer recommendation (eg, initial dose of 120-200 J); if unknown, use maximum
available. Second and subsequent doses should be equivalent or higher.
 Monophasic: 360 J
• Survival is best if defibrillation occurs within 3 to 5 minutes of cardiac
arrest.
• Drug therapy-
 Epinephrine IV/IO dose: 1 mg every 3-5 minutes
 Amiodarone IV/IO dose: First dose: 300 mg bolus. Second dose: 150 mg.
 Lidocaine IV/IO dose: First dose: 1-1.5 mg/kg. Second dose: 0.5-0.75 mg/kg
• contributing factors should be sought and treated.

36. Brady
ARRHYTHMIAS

37.  Sinus Bradycardia
 Bradycardia is defined as a heart rate of less than 60 beats per minute.
 ECG- regular rhythm with a normal-appearing P wave before each QRS complex and a
heart rate of 60 beats per minute or less.
 Trained athletes often exhibit resting bradycardia, as may normal individuals during
sleep.
 Inability to increase the heart rate adequately during exercise, symptomatic bradycardia
(such as syncope, dizziness, and chest pain), or a heart rate of less than 40 BPM in the
absence of physical conditioning or sleep is considered abnormal.
 Dysfunction of the SA node, also referred to as sick sinus syndrome, is a common cause
of bradycardia.( symptomatic SSS-most common cause for pacemaker placement)
 Bradycardia during neuraxial blockade can occur in patients of any age and any ASA
physical status class
 The risk of bradycardia and asystole may persist into the postoperative period even after
the sensory and motor blockade has diminished

39. Perioperative management:
• In asymptomatic patients with sinus bradycardia no treatment is required.
• In severely symptomatic patients i.e., those with chest pain or syncope
immediate transcutaneous or transvenous pacing is indicated.
• Atropine 1 mg IV every 3 to 5 minutes (to a maximum of 3 mg) may be given.
It should be noted that small doses of atropine (<0.5 mg IV) can cause a
further slowing of the heart rate.
• Epinephrine@ 2-10 mcg/ min. Or Dopamine@5-20 mcg/kg per min. Infusion
can be titrated awaiting pacing
 but these measures should not delay initiation of pacing.
• In bradycardia d/t β-blocker or calcium channel blocker overdose atropine is
ineffective. Glucagon @50 to 70 mcg/kg (3 to 5 mg in a 70-kg patient) every 3
to 5 minutes until clinical response is achieved or a total dose of 10 mg is
reached followed by continuous infusion @ 2 to 10 mg/hr. to maintain clinical
effect.

40.  1st Degree AV heart block
 First-degree AV block is defined as a PR interval of longer than 0.2 seconds.
 ECG- Each P wave is conducted and has a corresponding QRS complex of normal
duration.PR is prolonged d/t conduction delay through the AV node.
 First-degree AV block can be found in patients with and without structural heart disease.
 First-degree AV block is often a result of minor degenerative changes in the cardiac
conduction system that accompany normal aging.
 Other causes - myocardial ischemia (involving the blood supply to the AV node), inferior
wall MI, drugs affecting AV node conduction (digitalis and amiodarone), and processes that
enhance parasympathetic nervous system activity and vagal tone.
 Patients with first-degree AV block are usually asymptomatic and appear to have no
significant increase in mortality compared with matched controls.

41. Perioperative management:
• Anesthetic management should be aimed at avoiding any clinical situation
or drug that increases vagal tone or slows AV conduction.
• Atropine can speed conduction of cardiac impulses through the AV node.
However, in patients with significant heart disease, the increase in heart
rate produced by atropine may contribute to myocardial ischemia.
• In patients with risk factors such as coronary ischemia and systemic
infection, these clinical conditions should be treated and medically
optimized before surgery.
• In patients receiving digoxin-digoxin levels should be checked before
surgery & K+ levels should be monitored and maintained WNL.

42.  2nd Degree AV heart block
Second-degree AV block can be suspected
when a P wave is present without a
corresponding QRS complex.
Second-degree AV heart block can be
categorized as:
 Mobitz type I (Wenckebach) block.
 Mobitz type II block.

43. 2nd Degree AV heart block
→ Mobitz Type I (Wenckebach)
 Mobitz type I block shows progressive prolongation of the PR interval until a beat is
entirely blocked (dropped beat) followed by a repeat of this sequence.
 This type of block is often transient and asymptomatic.
 The prognosis is good, since reliable secondary pacemakers in the AV node usually take
over pacing duties and maintain adequate cardiac output.
 Causes –myocardial pathologies like ischemia , infarction, fibrosis , calcification etc.,
after cardiothoracic surgery. Certain drugs such as calcium channel blockers, β-blockers,
digoxin, and sympatholytic drugs.

44. Perioperative management:
• Mobitz type I block does not require treatment
unless the decreased ventricular rate results in
signs of hypoperfusion.
• Symptomatic patients may be treated with
atropine as needed. If atropine is unsuccessful,
pacing may be indicated.

45.  2nd Degree AV heart block
→ Mobitz Type II
 Mobitz type II block is characterized by sudden and complete interruption of conduction
(dropped QRS) without PR prolongation.
 Usually associated with permanent damage to the conduction system and may progress to
third-degree block.
 There is a complete interruption in the conduction of a cardiac impulse, usually at a point
below the AV node.
 Usually symptomatic, with palpitations and near syncope being common complaints.
 Less favorable prognosis because there is a substantial risk of progression to third-degree AV
block.
 Associated with serious disease involving the infranodal conduction system

46. Perioperative management:
• Mobitz type II block has a high rate of
progression to third degree heart block and
can manifest as a slow escape rhythm
insufficient to sustain an acceptable cardiac
output.
• Treatment for Mobitz type II block includes
transcutaneous or transvenous cardiac
pacing. Atropine is often ineffective.

47.  3rd Degree AV heart block
 Third-degree heart block, also known as complete heart block.
 There is complete interruption of AV conduction.
 Continued activity of the ventricles is due to impulses from an ectopic pacemaker distal to
the site of the conduction block.
 Heart rate-
• 45 to 55 BPM (if block is near the AV node)
• 30 to 40 BPM (if block is below the AV node)
 Common causes-
• fibrotic degeneration of the distal cardiac conduction system associated with aging
(Lenègre's disease).
• Degenerative and calcific changes in more proximal conduction tissue adjacent to the mitral
valve annulus can also interrupt cardiac conduction (Lev's disease).

48. Perioperative management:
• Treatment of third-degree AV block during anesthesia
consists of transcutaneous or transvenous cardiac pacing.
• If the block persists, placement of a permanent cardiac
pacemaker is indicated.
• Preoperative placement of a transvenous pacemaker or the
availability of transcutaneous cardiac pacing is necessary
before an anesthetic is administered for insertion of a
permanent cardiac pacemaker.
• Isoproterenol may be needed to maintain an acceptable
heart rate and act as a "chemical pacemaker" until a
permanent pacemaker is implanted and functional.

50.  Asystole
 Prolonged cardiac electrical inactivity is called Asystole.
 No P waves
 No QRS complexes
 No T waves.
 Incompatible with life as no cardiac output is present.

51. Perioperative management:
• Check patient
• Check ECG leads
• No pulse→ start CPR as per current ACLS
guidelines.

53. References
 Stoelting's Anesthesia and co-existing disease.
6th ed. Roberta L. Hines, Katherine E. Marschall.
 Advanced Cardiovascular Life Support: 2020
American Heart Association - Guidelines for
Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care.

54. thank
you