Arrhythmias

ARRHYTHMIAS Dr. Rashad Siddiqi FCPS (Anaesthesiology), FCPS (Cardiothoracic Anaesthesia)

Associate Prof of Anaesthesiology CMH Lahore Medical College

Consultant Cardiac Anaesthetist Army Cardiac Center Lahore

Learning Objectives

  Etiology and recognition of common peri-operative arrhythmias

  Review management of cardiac arrhythmias, with a focus on the relevant recent literature

Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.

ECG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave

P wave is upright in lead II & downgoing in lead aVR

Normal Sinus Rhythm

Mechanisms of Arrhythmia

Arrhythmias

Altered Automaticity

Ectopic Foci

Reentry / Conduction

Block

Bradyarrhythmias

Sinus Bradycardia

Decreased Automaticity

Normal Sinus Bradycardia

  Occurs in normal children and adults (as low as 30/min during sleep)

  May also be seen in the absence of heart disease:   At rest, in 25 - 35% of asymptomatic individuals < 25 yrs

age   In well-conditioned athletes   In some elderly patients   As a manifestation of a rare familial syndrome (mutation

in HCN4, one of a family of pacemaker ion channel genes)

  Hypoxia, Hypothermia, Hypothyroidism   Intrinsic disease of the SA node (e.g. sick sinus syndrome)   Drugs:

  Digoxin   Beta-blockers   Quinidine   Adenosine   Calcium channel blockers

  Seizure (post-ictal)   Infection like Diphtheria, acute rheumatic fever, viral

myocarditis   Increased intracranial pressure (cushing’s reflex)   Electrolyte imbalance e.g., hyperkalemia

Sinus Bradycardia - Causes

Maintain airway; supplemental O2 (if hypoxic) IV access 12 lead ECG (if available)

Trea

tmen

t of B

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card

ia

Assess appropriateness for clinical condition HR typically less than 50 bpm

Hypotension? Acutely altered mental status? Signs of Shock? Ischemic chest discomfort? Acute Heart failure?

Atropine 0.5mg IV; or TransCutaneous Pacing; or Dopamine / Adrenaline infusion

Monitor & Observe

NO

YES

Bradycardia during Anaesthesia

•  Drugs -  inhalational agents -  suxamethonium -  induction agents -  neostigmine

•  Airway -  hypoventilation -  hypoxia

•  Vagal reflexes •  Regional anaesthesia

•  Surgical factors -  IVC compression -  pneumoperitoneum

•  Undetected blood loss •  Cardiac Event

-  tension pneumothorax -  haemothorax -  tamponade -  myocardial depression

Rhythms due to Conduction Block

1st Degree AV Block

ECG Characteristics: Prolongation of the PR interval, which is constant

All P waves are conducted

Usually benign but such patients are at higher risk of developing AF or CCF

Treatment not warranted except in rare cases of “Pacemaker Syndrome”

The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

Cheng S, et al. JAMA 2009 Magna. Circ Arrhythm Electrophysiol 2013

Crisel RK, et al Eur Heart J 2011

2nd Degree AV Block

Mobitz 1

(Wenckebach)

ECG Characteristics: Progressive prolongation of the PR interval until a P wave is not conducted.

As the PR interval prolongs, the RR interval actually shortens

Usually benign unless associated with underlying pathology, i.e. MI

Treatment: remove “reversible” causes

No treatment for asymptomatic patients

atropine / pacemaker for symptomatic

ECG Characteristics: Constant PR interval with intermittent failure to conduct

•  Rhythm is dangerous as the block is lower in the conduction system

•  May cause syncope or may deteriorate into complete heart block

•  Causes: drugs, anterioseptal MI

•  Treatment: permanent pacemaker

Mobitz 2

2nd Degree AV Block

Mobitz Type I vs Type II

  Mobitz type I & II can’t be differentiated in 2:1 blocks

  every other beat is non-conducted so no opportunity to observe PR prolongation   a long rhythm strip or a previous ECG examined

  PR > 300ms or narrow QRS means block at AV node (type I)

  response to atropine confirms type I block

  worsening by carotid sinus massage means type I block

3rd Degree (Complete) Block

ECG Characteristics: No relationship between P waves and QRS complexes

Constant PR intervals and RR intervals Block at AV node: 2/3rd narrow QRS Block at bundle of His: narrow QRS Trifascicular block: wide QRS complex

•  May be caused by inferior MI and its presence worsens the prognosis

•  May cause syncopal symptoms, angina, or CHF

•  Treatment: removing “reversible causes” / permanent pacemaker

Tachyarrhythmias

Increased/Abnormal Automaticity

Sinus tachycardia

Junctional tachycardia

Ectopic atrial tachycardia

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Ectopic Foci & Beats

Causes of Ectopic Foci & Generation of Arrhythmias

  Hypoxia: Lung disease

  Ischemia: CAD, Angina (local hypoxia)

  Sympathetic Stimulation: Anxiety, Exercise, CHF, hyperthyroidism

  Bradycardia: “Escape” rhythms…

  Electrolyte Disturbances: K+, Ca++, Mg++

  Drugs: Caffeine, stimulants, antiarrhyhtmic

  Stretch: CHF, hypertrophy, valve disease

normal ("sinus") beats

sinus node doesn't fire leading to a period of asystole (sick sinus syndrome)

p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria.

QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal

Atrial Escape Beats

  Causes   Mitral valve prolapse / MS

  Coronary heart disease

  exercise testing in IHD patients

  Toxins or chemicals — Smoking, alcohol, and coffee

  Miscellaneous - acute and chronic pulmonary disease

Atrial Escape Beats

Atrial Escape Beats

•  A single ectopic focus fires near the AV node, which then conducts normally to the ventricles (usually initiated by a PAC)

• The rhythm is always REGULAR

• Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter

•  May be terminated by carotid massage

•  Treatment: carotid massage, adenosine, Ca++ channel blockers, ablation

• Adenosine preferred in hypotension,

Rhythm usually begins with PAC

Note REGULAR rhythm in the tachycardia

Paroxysmal SVT

Paroxysmal SVT

•  Treatment –  vagal maneuvers –  adenosine –  if not effective

•  Ca++ channel blockers, beta blockers, digoxin •  cardioversion

–  Ca++ channel blockers, beta blockers, and primary antiarrhythmic agents should not be serially administered because of potential additive negative hypotensive, bradycardic, and proarrhythmic effects.

–  Class IIa antiarrhythmic drugs •  amiodarone, procainamide, sotalol, felcanide

–  in LV dysfunction •  digoxin, amiodarone, diltiazem

•  “wandering pacemaker”

•  Multiple ectopic foci fire in the atria, all of which are conducted normally to the ventricles

•  The rhythm is always IRREGULAR

•  P-waves of different morphologies (shapes) ± variable PR interval

• HR >100 (in COPD patients >90)

Note IRREGULAR rhythm in the tachycardia

Multifocal Atrial Tachycardia

(McCord et al, Chest 1998)

  Causes   Pulmonary disease (60%)

  COPD, Ac Resp Failure, Pneumonia, embolism

  Drugs for Resp Diseases (theophylline, salbutamol)

  Cardiac disease   coronary, valvular, hypertensive and other

  when associated with heart failure

  Other conditions:   Hypokalemia

Hypomagnesemia

  Chronic renal failure (15%) – cause unclear

  Sepsis


  Treatment   correction of electrolytes

  treatment of underlying disease

  removal of cause

  disappointing results with anti-arrhythmics

Ca++ channel blocker (verapamil)

  beta blockers



there is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV junction.

QRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normal

Junctional Escape Beats

  Causes   hypokalemia   digitalis toxicity   chronic lung disease   acute myocardial infarction

  Treatment   No therapy in asymptomatic   discontinue or control exposure to offending agents   persistent, limiting symptoms:

  beta blockers

Ca++ channel blockers

  class IA, IC, or III antiarrhythmic

Junctional Escape Beats

• a "retrograde” p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles

QRS is wide and much different looking than the normal beats. This indicates that the beat originated somewhere in the ventricles.

• no p wave, indicating that the beat did not originate anywhere in the atria

Ventricular Escape Beats

TREATMENT REQUIRED IN •  frequent (> 30% of complexes) or are increasing in frequency •  come close to or on top of a preceding T-wave (R on T) •  3 or more PVC's in a row (run of V-tach) •  Any PVC in the setting of an acute MI •  PVC's come from different foci ("multifocal" or "multiformed”) These may result in ventricular tachycardia or fibrillation.

sinus beats Unconverted V-tach to V-fib V-tach

“R on T phenomenon”

time

Re-entrant Rhythms

The Re-entry Mechanism

Fast Conduction Path Slow Recovery

Slow Conduction Path Fast Recovery

Electrical Impulse

Cardiac Conduction Tissue

Repolarizing Tissue (long refractory period)

Premature Beat Impulse



Electrical Impulse


Tissues with these type of circuits may exist:

•  in the SA node, AV node, or any type of heart tissue •  in a “macroscopic” structure such as an accessory pathway in WPW


Premature Beat Impulse

1. An arrhythmia is triggered by a premature beat

2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only




Repolarizing Tissue (long refractory period)


3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrograde (backwards) up the fast pathway





4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit





  AV nodal reentrant tachycardia (AVNRT)

  Supraventricular tachycardia

  AV reentrant tachycardia (AVRT)

  Wolf – Parkinson – White syndrome

  Atrial flutter

  Ventricular tachycardia

  Atrial fibrillation

  Ventricular fibrillation

The Re-entrant Rhythm

Atrio-Ventricular Nodal Re-entry •  supraventricular tachycardia

Atrial Re-entry •  atrial tachycardia •  atrial fibrillation •  atrial flutter

Atrio-Ventricular Re-entry •  Wolf Parkinson White Ventricular Re-entry

•  ventricular tachycardia •  ventricular fibrillation

Ventricular Re-entry •  ventricular tachycardia • ventricular fibrillation

Atrio-Ventricular Nodal Re-entry •  supraventricular tachycardia

Atrial Re-entry •  atrial tachycardia •  atrial fibrillation •  atrial flutter

Atrio-Ventricular Re-entry •  Wolf Parkinson White •  supraventricular tachycardia

Re-entry Circuits as Ectopic Foci

Rate 100-270 Normal QRS Aberrancy possible

Acute Rx: •  Vagal maneuvers •  Adenosine 6-12 mg IV push •  Ca++ channel blockers

AV Nodal Re-entrant Tachycardia

Atrial flutter is caused by a reentrant circuit in the wall of the atrium

ECG Characteristics: Typical: “sawtooth” flutter waves at a rate of ~ 300 bpm

Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle

There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75 bpm

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Atrial Flutter

Unmasking of flutter waves with adenosine.

Acute Rx: •  ventricular rate control can be difficult •  AV nodal blockers prevent 1:1 conduction •  Ibutilide 1-2mg rapid IV infusion – have paddles ready •  Rapid pacing or low voltage DC cardioversion is effective •  Anticoagulation as per atrial fibrillation

Atrial Flutter

Atrial fibrillation is caused by numerous waves of depolarization spreading throughout the atria, leading to an absence of coordinated atrial contraction Classifification •  Recurrent: when AF occurs on 2 or more occasions •  Paroxysmal: episodes that generally last 7 days or less (most last less than

24 hours) •  Persistent: AF that lasts more than 7 days •  Permanent: paroxysmal or persistent AF with failure to cardiovert or not

attempted

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Atrial Fibrillation

Atrial Fibrillation Causes

Treatment of Atrial Fib Haemodnamically Stable Patient:

Rate control therapy:   β blockers – esmolol, metoprolol, propranolol

Ca++ channel blockers – verapamil, diltiazem

Amiodarone   Digoxin - for AF with CHF, or LV dysfunction (not to be

given in patients with paroxysmal AF)

Conversion of rhythm:   Class I recommendation: flecainide, propafenone, ibutilide

  Class II a recommendations: amiodarone

  Class IIb: administration of quinidine/procainamide.

Anticoagulation therapy:

Treatment of Atrial Fib Haemodynamically Unstable Patient:

life-threatening - emergency electrical cardioversion (irrespective of the duration of AF)

non-life-threatening haemodynamic instability   where there is a delay in organising electrical cardioversion,

intravenous amiodarone should be used

  known permanent AF (caused mainly by a poorly controlled ventricular rate)   beta-blockers (esmolol, metoprolol, propranolol)   calcium channel blockers (verapamil, diltiazem)

amiodarone (where beta-blockers or calcium antagonists are contraindicated or ineffective)

Treatment of Atrial Fib

Haemodynamically Unstable Patient:

Antithrombotic therapy for acute-onset AF   emergency intervention should be performed ASAP

  initiation of anticoagulation should not delay any emergency intervention

  Heparin:

  heparin should be started at initial presentation

  continue heparin until full assessment made and appropriate antithrombotic therapy started

Treatment of Atrial Fib

Haemodynamically Unstable Patient:

Antithrombotic therapy for acute-onset AF   Oral Anticoagulation

  Needed in acute onset AF is uncertain

  Not needed in confirmed acute onset AF (<48 hours) if converted to sinus rhythm successfully

  Needed in confirmed acute onset AF if:

  stable sinus rhythm not successfully restored

  high risk of recurrence

  high risk of stroke

Treatment

•  Unstable – DC cardioversion •  Stable monomorphic – Adenosine, Amiodarone •  Stable polymorphic - treat underlying etiology

Rate 100-200 Wide QRS Monomorphic vs Polymorphic

Ventricular Tachycardia

Monomorphic   common in previous Q wave MI

  not caused by acute ischemia

Polymorphic (May have long QT interval)

  Medication

  Electrolyte imbalance

  Congenital predisposition

  Myocardial ischemia

Ventricular Tachycardia

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Ventricular fibrillation is caused by numerous waves of depolarization spreading throughout the ventricles simultaneously, leading to disorganized ventricular contraction and immediate loss of cardiac function.

ECG Characteristics: Absent P waves

Disorganized electrical activity

Deflections continuously change in shape, magnitude and direction

Ventricular Fibrillation

Questions

Question 1

A 25-year-old patient presenting with palpitations is noted to have a wide complex, irregular tachycardia at a rate of 260. The upstroke of the QRS is slurred. The blood pressure is normal, and the patient appears well. Most likely diagnosis is:

A.  Atrial fibrillation with WPW syndrome

B.  Unstable Ventricular Tachycardia

C.  Supraventricular Tachycardia

D.  Atrial Flutter

E.  Ventricular Fibrillation

Answer “A”

Question 2

A 50 years old gentleman is undergoing emergency exploratory laparatomy under GA. On ECG monitors, you notice wide-complexed ectopic beats occurring 3 to 4 times a minute. His heart rate remains 74 bpm and BP is 130/84mmHg. This arrhythmia is considered benign when the ectopic beats:

A. come on top of a preceding T-wave

B. occur three or more in a row

C. happen in an acute MI setting

D. are coming from same focus

E. are more than 30% of complexes

Answer “D”

Question 3

A 60-year-old man with a history of prior anterior myocardial infarction develops a monomorphic wide complex tachycardia after non-cardiac surgery. The differential diagnosis includes:

A. Ventricular Fibrillation B. Supraventricular Tachycardia C. Torse De Pointes D. Atrial Fibrillation E. SVT with aberrant conduction Answer “E”

Question 4

First line drug for rate control in atrial fibrillation is

A.  amiodarone

B.  digoxin

C.  esmolol

D.  verapamil

E.  quinidine

Answer “C”

Question 5

A 60 years old patient has arrived in emergency department with 6 days history of atrial fibrillation. This type of AF is classified as:

A. Chronic

B. Recurrent

C. Persistent

D. Paroxysmal

E. Permanent

Answer “D”

Thank you

Health & Medicine

Arrhythmias