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PERIOPERATIVE BRADYARRYTHMIAS- ANWESHA.pptx

The document discusses perioperative bradyarrhythmias, which are common cardiac abnormalities occurring during surgeries, particularly bradycardia, defined as a heart rate below 60 beats per minute. It outlines the causes, classifications, pathophysiology, and treatment options for various types of bradyarrhythmias, including sinus bradycardia, junctional rhythms, and various degrees of AV block. The management strategies include immediate pacing, the use of atropine, and monitoring for potential complications, especially in elderly patients.

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PERIOPERATIVE BRADYARRYTHMIAS Moderator- Dr. Surajit Moral Assistant Professor Department of Anaesthesiology and Critical Care, GMCH Presenter- Dr. Anwesha Bayan PGT- 3
INTRODUCTION • Arrhythmias are the most common perioperative cardiac abnormalities in patients undergoing both cardiac and non-cardiac surgery. • Bradycardia is the most common arrhythmias that occur during anesthesia. They result in significant causes of morbidity and mortality particularly in elderly patients • Bradycardia is defined as a heart rate less than 60 beats/min. • Relative Bradycardia – is used in explaining a HR which is not actually below 60bpm, is still considered too slow for individual’s current medical condition. • E.g – a HR of 70bpm is too slow for a patient with cardiogenic or septic shock • Symptomatic bradycardia, or high grade heart block (third degree heart block) warrants postponement of elective procedures to facilitate evaluation ,stabilisation and possible cardiology evaluation.
PATHOPHYSIOLOGY ACTION POTENTIAL OF CARDIAC MUSCLES Phase 4–spontaneous depolarization from RMP until threshold potential reached Phase 0 – depolarization occurs when the Threshold potential is reached and corres- ponds to QRS complex Phase 1-3 – represent repolarization, Phase 3 corresponds to T wave on ECG
ACTION POTENTIAL OF CARDIAC PACEMAKER CELLS
CONDUCTION OF CARDIAC IMPULSES
NORMAL ECG WAVES AND INTERVALS
CAUSES OF BRADYARRYTHMIAS INTRINSIC CAUSE • Systemic causes - hypoxia - hypercarbia - hypothermia < 34degree celsius - raised ICT (Cushings reflex) - drugs: opioids, volatile anesthetics, Succinyl choline, vecuronium, beta-blockers, CCBs, anticholinesterase inhibitors (neostigmine) • Cardiac causes - Sick sinus syndrome, sinus bradycardia - junctional rhythm - AV nodal block - Myocardial infarction
VAGAL RESPONSE - traction on extraocular muscles (oculocardiac reflex) oropharynx ( laryngoscopy , intubation and extubation) bronchus , peritoneum , bowel , rectum - right atrial distension - bladder distension DIRECT EFFECT - narcotics - volatile anesthetics - regional anesthesia - high spinal / spinal shock
DRUGS CAUSING BRADYARRYTHMIAS
CLASSIFICATION OF BRADYARRYTHMIAS • Sinus Bradycardia • Cardiac Conduction Defect Atrio-ventricular Conduction Defect - 1st degree heart block - 2nd degree heart block - 3rd degree heart block Intraventricular Conduction Defect - right bundle branch block - left bundle branch block
SINUS BRADYCARDIA • ECG demonstrates a regular rhythm with normal appearing P wave before each QRS complex and HR < 60bpm • common in athletes and many individuals during sleep. • It is due to decreased sympathetic stimulation or increased parasympathetic stimulation. • sinus bradycardia may be asymptomatic or symptomatic. Asymptomatic patients, no treatment is required • in symptomatic patients, experiencing chest pain or syncope immediate transcutaneous or transvenous pacing is indicated. • Atropine 0.5 mg i.v every 3- 5 minutes (to a maximum of 3 mg) may be given to increase heart rate but should not delay initiation of pacing. • If cardiac pacing is delayed or pacing capabilities are limited, an epinephrine or dopamine infusion maybe titrated to response while cardiac pacing is awaited.
• If bradycardia is due to beta-blockers or CCB overdose, or if unresponsive to atropine- Glucagon 50-70mcg/kg every 3- 5 minutes until clinical response is achieved or a total dose of 10 mg is reached. To maintain clinical effect, a continuous infusion at 2- 10 mg/ hour should be maintained. • Bradycardia during neuraxial blockade : incidence is approx. 1.5 per 10,000cases - can occur any time but most often occurs approx. 1hr after anesthetic administration - risk of bradycardia and asystole may extend into the postoperative period even after the sensory or motor blockade has diminished. - should be treated aggressively - in case of severe bradycardia , preparation should be made for management of asystole , which is treated with CPR (ACLS protocol) • Recalcitrant bradycardia necessitates transcutaneous / transvenous pacing.
JUNCTIONAL RHYTHM • occurs when the tissues around the AV node becomes the dominant pacemaker of the heart ( depressed SA node function, SA node block, delayed AV node conduction) • generates a rhythm with HR 40-60bpm • variable relation with P wave - absent P wave ( buried within QRS complex) - P wave may preceed the QRS complex ( short PR interval) - may follow the QRS complex • causes – myocarditis , myocardial ischaemia, digitalis toxicity • Atropine ( dose of 0.5mg iv) repeated every 5min , max dose 3mg – used to treat a slow junctional rhythm if it becomes hemodynamically significant
HEART BLOCKS • AVHB are broadly classified into 3 categories - first degree heart block - second degree heart block - third degree heart block • May be transient or permanent • Transient AVHB can be produced by acute MI and general anesthetics such as enflurane or halothane in patients using calcium channel blockers or amiodarone • Permanent AVHB – usually idiopathic , other causes – Levs or Lenegre disease , where fibrosis of the conducting system occurs
FIRST DEGREE AV BLOCK • Defined as a delay in the passage of the cardiac impulse through the AV node resulting in a PR interval of longer than 200 ms. • Each P wave has a corresponding QRS Complex of normal duration • considered generally benign, asymptomatic, accompanying normal ageing • other causes – myocardial ischemia, inferior wall MI, drugs affecting AV node conduction ( digoxin, amiodarone)
SECOND DEGREE AV BLOCK • Second-degree AV block can be suspected when a P wave is present without a corresponding QRS complex. • 1. Mobitz type 1 block (Wenckebach block) - characterized by progressive prolongation of the PR interval until a beat is dropped. - it is thought to occur because each successive depolarization produces a prolongation of the refractory period of the AV node. This process continues until an atrial impulse reaches the AV node during its absolute refractory period and conduction of that impulse is blocked completely. - more benign block, related to AV nodal delay - easily responsive to atropine and unlikely to progress to complete heart block - can be the result of myocardial ischemia/infarction, myocardial fibrosis or calcification, infiltrative or inflammatory disease of the myocardium, also seen after cardiothoracic surgery - can be associated with certain drugs – CCBs, beta-blockers, digoxin and sympatholytic drugs
2. Mobitz type 2 block - characterized by sudden and complete interruption of conduction (dropped QRS) without PR prolongation. - related to infranodal block, capable of progressing to complete heart block - usually symptomatic with palpitations and near syncope (common complaints) - placement of a cardiac pacemaker maybe necessary. - temporary treatment includes transcutaneous or transvenous cardiac pacing until a permanent pacemaker in place - atropine is unlikely to improve bradycardia, isoproterenol infusion ( chemical pacemaker) helpful as temporary measures
THIRD DEGREE AV BLOCK • complete dissociation between the atria and the ventricular beats (complete interruption of AV conduction) • can manifest as a slow escape rhythm insufficient to sustain an acceptable cardiac output • if conduction block near AV node:HR 45-55 and QRS Complex narrow if the conduction block is below AV node (infranodal) : HR 30-40, QRS Complex wide • Causes : - in anesthetized patients: cardiac ischaemia, metabolic or electrolyte abnormalities, infection or inflammation near the conduction system, reperfusion injury, stunned myocardium after cardiac surgery - in adults : fibrotic degeneration of the distal conducting system associated with ageing (Lenegre disease ) degenerative and calcific changes in more proximal conduction tissue adjacent to the mitral valve annulus can also interrupt cardiac conduction ( Lev disease)
• treatment : transcutaneous / transvenous cardiac pacing (during anaesthesia) IV isoproterenol infusion (acts as chemical pacemaker) • requires a pacemaker placement unless a reversible cause is identified
TRANSCUTANEOUS CARDIAC PACING -non–invasive pacing used on a temporary basis until a patient is stabilised and either an adequate intrinsic rhythm has returned or a transvenous pacemaker is inserted, whether temporary or permanent. 1. Place the pacing electrodes on the chest 2. Set the demand rate to 60-80/min . The rate can be adjusted 3. Set the current output 2mA above the dose at which consistent capture is observed. Transcutaneous pacing may be uncomfortable for the patient . Sedation should be considered
TCP stimulus doesnot work through normal cardiac conduction system but by a direct electical stimulus of the myocardium . Therefore a captured complex will resemble a PVC . Electrical capture is characterized by a wide QRS complex with the initial deflection and the terminal deflection always in the opposite direction.
QRS COMPLEX ABNORMALITIES • BUNDLE BRANCH BLOCK - RIGHT BUNDLE BRANCH BLOCK - LEFT BUNDLE BRANCH BLOCK • FASCICULAR BLOCK
RIGHT BUNDLE BRANCH BLOCK • Present in approximately 1% of hospitalized adult patients. • The conduction delay resulting from RBBB is seldom symptomatic and rarely progresses to advanced AV block. • It does not always imply cardiac disease and is often of no clinical significance in patients without structural heart disease. • RBBB is due to a disruption of the cardiac impulse as it travels over the RBB. • It is recognized by- - widened QRS complex >120ms - rSR configuration in lead V1 and V2 (M shaped QRS complex) - deep/ slurred S wave > 40ms in lead 1 and V6 * If the QRS is between 110 and 120 ms, with the other criteria for RBBB fulfilled, it is considered an incomplete RBBB. • Treatment: Observation and elimination of drugs or clinical factors known to contribute to conduction disturbance. Pacing capability should be available in the event of progression to complete heart block.
RBBB
LEFT BUNDLE BRANCH BLOCK • the LBB of the bundle of His composed of two components- LAF and LPF • A complete LBBB is recognized as - QRS complex > 120ms - absence of Q wave in lead 1 , V5 and V6 - broad notched or slurred R wave in lead 1, aVL ,V5 and V6 - S and T waves are usually opposite in direction to QRS • LAHB is the most common hemiblock. LPHB is uncommon because of larger and better perfused posterior fascicle. • left axis deviation associated with LAHB right axis deviation associated with LPHB
• the appearance of LBBB on ECG is often an indication of serious heart disease (e.g hypertension, coronary artery disease , aortic valve disease , cardiomyopathy) • The appearance of LBBB has been observed during anesthesia , particularly during hypertensive or tachycardic episodes and may be signs of myocardial ischaemia • The presence of LBBB has special implications if insertion of a pulmonary artery catheter is planned. Third degree heart block can occur if the catheter induces RBBB in a patient with preexisting LBBB. • RBBB (usually transient) occurs during insertion of a pulmonary artery catheter in approximately 2%- 5% of patients.
LBBB
FASCICULAR BLOCK • Bi fascicular heart block – when RBBB exist in combination with block of either the left anterior or left posterior fascicle of the LBB. RBBB+ LAHB is more common than than RBBB+ LPHB • concern in patients with bifascicular heart block is that , perioperative changes in BP , arterial oxygenation and serum electrolyte concentration might compromise impulse conduction in the remaining fascicles and lead to third degree heart block • Treatment : observation and elimination of drugs or clinical factors known to contribute to conduction disturbances
ALGORITHM FOR TREATMENT OF ADULT BRADYCARDIA
REFERENCES • Stoelting’s Anaesthesia and coexisting disease, 3rd SEA Edition. • Miller’s Anaesthesia, 9th edition