dr hansraj (CARDIAC ARRHYTHMIAS)

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Dr. Hansraj verma Cardiac Arrhythmias senior resident (Anaesthesiology) SMS medical college , jaipur

Pacemakers of the Heart : 

Pacemakers of the Heart SA Node -Dominant pacemaker intrinsic rate -60 - 100 beats/minute AV Node -Back-up pacemaker intrinsic rate of 40 - 60 beats/minute Ventricular cells - Back-up pacemaker intrinsic rate of 20 - 45 bpm

Electrophysiology - Resting potential : 

Electrophysiology - Resting potential A transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell Caused by unequal distribution of ions inside vs. outside cell Na+ higher outside than inside cell Ca+ much higher “ “ “ “ K+ higher inside cell than outside Maintenance by ion selective channels, active pumps and exchangers

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-100 -80 -60 -40 -20 0 20 Phase 0 Phase 1 Phase 2 Phase 3 Phase 4 Na+ ca++ ATPase mv Cardiac Action Potential R.M.P Na+ m Na+ Na+ Na+ Na+ Na+ h K+ ca++ K+ K+ K+ ca++ ca++ (Plateau Phase) K+ K+ K+ Na+ K+ Depolarization Repolarization Phase 4 (only in pacemaker cells

PHASES OF ACTION POTENTIAL : 

PHASES OF ACTION POTENTIAL Phase 0 >Rapid depolarization >Opening fast Na+ channels→ Na+ rushes in →depolarization Phase 1 >Limited depolarization >Inactivation of fast Na+ channels→ Na+ ion conc equalizes >↑ K+ efflux & Cl- influx Phase 2 >Plateau Stage >Cell less permeable to Na+ >Ca++ influx through slow Ca++ channels >K+ begins to leave cell Phase 3 >Rapid repolarization >Na+ gates closed >K+ efflux >Inactivation of slow Ca++ channels Phase 4 >Resting Membrane Potential >High K+ efflux >Ca++ influx

Cardiac Action Potential : 

Cardiac Action Potential Divided into five phases (0,1,2,3,4) Phase 4 - resting phase (resting membrane potential) Phase cardiac cells remain in until stimulated Associated with diastole portion of heart cycle Addition of current into cardiac muscle (stimulation) causes Phase 0 – opening of fast Na channels and rapid depolarization Drives Na+ into cell (inward current), changing membrane potential Transient outward current due to movement of Cl- and K+ Phase 1 – initial rapid repolarization Closure of the fast Na+ channels Phase 0 and 1 together correspond to the R and S waves of the ECG

Cardiac Action Potential (con’t) : 

Cardiac Action Potential (con’t) Phase 2 - plateau phase sustained by the balance between the inward movement of Ca+ and outward movement of K + Has a long duration compared to other nerve and muscle tissue Normally blocks any premature stimulator signals (other muscle tissue can accept additional stimulation and increase contractility in a summation effect) Corresponds to ST segment of the ECG. Phase 3 – repolarization K+ channels remain open, Allows K+ to build up outside the cell, causing the cell to repolarize K + channels finally close when membrane potential reaches certain level Corresponds to T wave on the ECG

Normal Sinus Rhythm : 

Normal Sinus Rhythm Normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system. EKG 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

Arrhythmias : 

Arrhythmias Premature Beats Supraventricular Arrhythmias Ventricular Arrhythmias AV Junctional Blocks

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Supraventricular - Atrial Tachycardia - Paroxysmal Tachycardia Multifocal Atrial Tachycardia - Atrial Fibrillation - Atrial Flutter Ventricular Wolff-Parkinson-White (preexcitation syndrome) Ventricular Tachycardia Ventricular Fibrillation Premature Ventricular Contraction ARRHYTHMIAS

FACTORS PRECIPITATING CARDIAC ARRHYTHMIAS : 

FACTORS PRECIPITATING CARDIAC ARRHYTHMIAS 1. Ischemia pH & electrolyte abnormalities 80% – 90% asstd with MI 2. Excessive myocardial fiber stretch/ scarred/ diseased cardiac tissue 3. Excessive discharge or sensitivity to autonomic transmitters 4. Excessive exposure to foreign chemicals & toxic substances 20% - 50% asstd with General Anesthesia 10% - 20% asstd with Digitalis toxicity

Mechanisms of Cardiac Arrhythmias : 

Mechanisms of Cardiac Arrhythmias Result from disorders of impulse formation, conduction, or both Disorder of impulse formation- 1- no signal from pacemaker 2- development of ectopic pacemaker Disorder of impulse conduction- 1- Bradycardia (if AV block) 2-Tachycardia (if reentrant circuit)

Atrial Arrhythmias : 

Atrial Arrhythmias SINUS ARRYTHMIA- A condition in which the heart rate varies with breathing. This is usually a benign condition

PSVT : 

PSVT Paroxysmal Supraventricular tachycardia [HR 160-250/min]  Atrioventricular nodal re-entry tachycardia (AVNRT) It usually begins and ends rapidly, occurring in repeated periods. This condition can cause symptoms such as weakness, fatigue, dizziness, fainting, or palpitations if the heart rate becomes too fast. In AVNRT, there are two functionally and anatomically different pathways within the AV node: one is characterized by a short effective refractory period and slow conduction, and the other has a longer effective refractory period and conducts faster. In sinus rhythm, the atrial impulse that depolarizes the ventricles usually conducts through the fast pathway. If the atrial impulse (e.g. an atrial premature beat) occurs early when the fast pathway is still refractory, the slow pathway takes over in propagating the atrial impulse to the ventricles. It then travels back through the fast pathway which has already recovered its excitability, thus initiating the most common 'slow-fast', or typical, AVNRT.

AVNRT : 

AVNRT ECG - normal regular QRS complexes, usually at a rate of 140-240 per minute P waves are either not visible or are seen immediately before or after the QRS complex because of simultaneous atrial and ventricular activation.

PSVT (TREATMENT) : 

PSVT (TREATMENT) Acute Management- Haemodynamic instability - emergency cardioversion. Haemodynamically stable- vagal manoeuvres, including right carotid massage, Valsalva manoeuvre and facial immersion in cold water. If not successful, intravenous adenosine (up to 0.25 mg/kg) , verapamil 5-10 mg i.v. over 5-10 minutes, i.v. diltiazem, or beta-blockers should be tried. Long-term management- It includes ablation of an accessory pathway. Also, verapamil, diltiazem & β-blockers; are effective in 60-80% of patients.

Atrial Flutter : 

Atrial Flutter caused by a large reentrant circuit in the wall of the right atrium ECG : 1- Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm 2-Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle 3-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

Atrial flutter (TREATMENT) : 

Atrial flutter (TREATMENT) Symptomatic acute paroxysm - electrical cardioversion. atrial flutter more than 1-2 days - anticoagulated for 4 weeks prior to cardioversion. Recurrent paroxysms may be prevented by class Ic and class III agents The treatment of choice for patients with recurrent atrial flutter - radiofrequency catheter ablation

Atrial Fibrillation : 

Atrial Fibrillation Caused by numerous wavelets of depolarization spreading throughout the atria simultaneously, leading to an absence of coordinated atrial contraction. Atrial fibrillation is important because it can lead to: Hemodynamic compromise Systemic embolization Symptoms

Atrial Fibrillation : 

Atrial Fibrillation ECG:- Absent P waves Presence of fine “fibrillatory” waves which vary in amplitude and morphology Irregularly irregular ventricular response

(( ((Atrial fibrillation (TREATMENT) : 

(( ((Atrial fibrillation (TREATMENT) When atrial fibrillation is due to an acute precipitating event such as alcohol toxicity, chest infection or hyperthyroidism, the provoking cause should be treated. Acute management of AF – 1. ventricular rate control 2 cardioversion (± anticoagulation). Ventricular rate control - by drugs which block the AV node digoxin, b blockers or ca2+ channel blockers Cardioversion -electrically by DC shock or medically either by IV infusion of an anti-arrhythmic drug such as a class Ic or a class III agent Patients are anticoagulated ( warfarin) for 4 weeks before cardioversion. Anticoagulants are used to minimize the risk of thromboembolism associated with cardioversion unless atrial fibrillation is of less than 1-2 days' duration.

Rhythm : 

Rhythm 100 bpm Rate? Regularity? irregularly irregular none 0.06 s P waves? PR interval? none QRS duration? Interpretation? Atrial Fibrillation

Ventricular Arrhythmias : 

Ventricular Arrhythmias Ventricular tachycardia (VT)- electrical signal is sent from the ventricles at a very fast but often regular rate. ECG – 1- rapid ventricular rhythm with broad (often 0.14 s or more), abnormal QRS complexes 2- AV dissociation may result invisible P waves Treatment: Haemodynamically compromised patients - emergency DC cardioversion Hemodynamically stable patients- 1- class I drugs or amiodarone is usually used. 2- First-line drug treatment consists of lidocaine (50-100 mg i.v. over 5 minutes) followed by a lidocaine infusion (2-4 mg i.v. per minute). DC cardioversion is necessary if medical therapy is unsuccessful.

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Ventricular Tachycardia

What is this arrhythmia? : 

What is this arrhythmia? Ventricular tachycardia Ventricular tachycardia is usually caused by reentry, and most commonly seen in patients following myocardial infarction.

VENTRICLUAL FIBRILLATION (VF) : 

VENTRICLUAL FIBRILLATION (VF) Electrical signals are sent from the ventricles at a very fast and erratic rate. As a result, the ventricles are unable to fill with blood and pump. life-threatening because there is no pulse and complete loss of consciousness. ECG - shapeless, rapid oscillations no hint of organized complexes Treatment- prompt defibrillation to restore the normal rhythm and function of the heart. It may cause sudden cardiac death. Basic and advanced cardiac life support is needed Survivors of these ventricular tachyarrhythmias are, in the absence of an identifiable reversible cause (e.g. acute myocardial infarction, severe metabolic disturbance), at high risk of sudden death. Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management of these patients

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Ventricular Fibrillation

Premature ventricular contraction (PVC)s : 

Premature ventricular contraction (PVC)s Electrical signal originates in the ventricles and causes to contract before receiving the electrical signal from the atria. ECG -wide and bizarre QRS complex Early 'R-on-T' ventricular premature beats may induce ventricular fibrillation PVCs are not uncommon and often do not cause symptoms or problems. Treatment- only if symptomatic with beta-blockers.

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Premature ventricular contractions (PVCs)

Wolf Parkinson White Syndrome (WPW) : 

Wolf Parkinson White Syndrome (WPW) Abnormal band of atrial tissue connects the atria and ventricles Electrically bypass the normal pathways of conduction; a re-entry circuit can develop causing paroxysms of tachycardia. ECG : - Short PR interval - Delta wave on the upstroke of the QRS complex Treatment - flecainamide, amiodarone or disopyramide. Digoxin and verapamil are contraindicated. Treatment of choice- catheter radiofrequency ablation

WPW syndrome : 

WPW syndrome

Ventricular Arrhythmias : 

Ventricular Arrhythmias Torsades de pointes -  Short duration tachycardia that reverts to sinus rhythm spontaneously. It may be due to: - Congenital - Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia. - Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics. It may present with syncopal attacks and occasionally ventricular fibrillation. QRS complexes are irregular and rapid that twist around the baseline. prolonged QT interval. Treatment - correction of any electrolyte disturbances, stopping of causative drug, atrial or ventricular pacing, Magnesium sulphate 8 mmol (mg2+) over 10-15 min for acquired long QT, IV isoprenaline in acquired cases and B blockers in congenital types

Rhythms Produced by Conduction Block : 

Rhythms Produced by Conduction Block AV Block (relatively common) 1st degree AV block Type 1 2nd degree AV block Type 2 2nd degree AV block 3rd degree AV block SA Block (relatively rare)

1st Degree AV Block : 

1st Degree AV Block ECG Characteristics: 1- Prolongation of the PR interval, which 2- All P waves are conducted

Rhythm : 

Rhythm 60 bpm Rate? Regularity? regular normal 0.08 s P waves? PR interval? 0.36 s QRS duration? Interpretation? 1st Degree AV Block

2nd Degree AV Block : 

2nd Degree AV Block Mobiz Type 1 (Wenckebach) ECG Characteristics: 1-Progressive prolongation of the PR interval until a P wave is not conducted. 2- As the PR interval prolongs, the RR interval actually shortens ECG Characteristics: Constant PR interval with intermittent failure to conduct Mobiz Type 2

Rhythm : 

Rhythm 50 bpm Rate? Regularity? regularly irregular nl, but 4th no QRS 0.08 s P waves? PR interval? lengthens QRS duration? Interpretation? 2nd Degree AV Block, Type I

Rhythm : 

Rhythm 40 bpm Rate? Regularity? regular nl, 2 of 3 no QRS 0.08 s P waves? PR interval? 0.14 s QRS duration? Interpretation? 2nd Degree AV Block, Type II

3rd Degree (Complete) AV Block : 

3rd Degree (Complete) AV Block ECG Characteristics: 1- No relationship between P waves and QRS complexes 2- Relatively constant PP intervals and RR intervals 3- Greater number of P waves than QRS complexes

Rhythm : 

Rhythm 40 bpm Rate? Regularity? regular no relation to QRS wide (> 0.12 s) P waves? PR interval? none QRS duration? Interpretation? 3rd Degree AV Block

Bundle Branch Block (BBB) : 

Bundle Branch Block (BBB) Interruption of the right or left branch of the bundle of Hiss delays activation of the corresponding ventricle leading to broadening of the QRS complex Unlike right BBB, left BBB is always associated with an underlying heart disease. Both RT and LT BBB show wide deformed QRS complex. In RBBB there is rSR pattern in lead V1, while in LBBB there is a broad monophasic (or notched) R wave / M pattern in leads V5 and V6.

Bundle Branch Block (BBB)Block : 

Bundle Branch Block (BBB)Block Hemiblock Delay or block in the divisions of the left bundle branch produces a swing in the direction of depolarization (electrical axis) of the heart. When the anterior division is blocked (left anterior hemiblock), there is left axis deviation. Delay or block in the postero-inferior division causes(right axis deviation). Bifascicular block This is a combination of a block of any two of the following: the right bundle branch, the left antero-superior division and the left postero-inferior division. Block of the remaining fascicle will result in complete AV block.

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Phase 0 Phase 1 Phase 2 Phase 3 Phase 4 R.M.P (Plateau Phase) Class I: Na + channel blockers. Pacemaker potential Class III: K + channel blockers Class IV: Ca ++ channel blockers Class II: Beta blockers Classification of Anti-Arrhythmic Drugs

overview : 

overview Na+ channel blockade β-adrenergic receptor blockade K+Channel blocker (Prolong repolarization) Ca2+ channel blockade Miscellaneous: ADENOSINE- inhibits AV conduction & increases AV refractory period DIGITALIS GLYCOSIDES MAGNESIUM - Na+/K+ ATPase, Na+, K+, Ca++ channels POTASSIUM -normalize K+ gradients

Classification of Antiarrhythmic Drugs based on Drug Action : 

Classification of Antiarrhythmic Drugs based on Drug Action

Classification of antiarrhythmics(based on mechanisms of action) : 

Classification of antiarrhythmics(based on mechanisms of action) Class I – blocker’s of fast Na+ channels Subclass IA Cause moderate Phase 0 depression Prolong repolarization Increased duration of action potential Includes Quinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias, increases refractory period Procainamide - increases refractory period but side effects Disopyramide – extended duration of action, used only for treating ventricular arrthymias

Classification of antiarrhythmics(based on mechanisms of action) : 

Classification of antiarrhythmics(based on mechanisms of action) Subclass IB Weak Phase 0 depression Shortened depolarization Decreased action potential duration Includes Lidocane (also acts as local anesthetic) – blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmias Mexiletine - oral lidocaine derivative, similar activity Phenytoin – anticonvulsant that also works as antiarrhythmic similar to lidocane

Classification of antiarrhythmics(based on mechanisms of action) : 

Classification of antiarrhythmics(based on mechanisms of action) Subclass IC Strong Phase 0 depression No effect of depolarization No effect on action potential duration Includes Flecainide (initially developed as a local anesthetic) Slows conduction in all parts of heart, Also inhibits abnormal automaticity Propafenone Also slows conduction Weak β – blocker Also some Ca2+ channel blockade

Classification of antiarrhythmics(based on mechanisms of action) : 

Classification of antiarrhythmics(based on mechanisms of action) Class II – β–adrenergic blockers Based on two major actions 1) blockade of myocardial β–adrenergic receptors 2) Direct membrane-stabilizing effects related to Na+ channel blockade Includes Propranolol causes both myocardial β–adrenergic blockade and membrane-stabilizing effects Slows SA node and ectopic pacemaking Can block arrhythmias induced by exercise or apprehension Other β–adrenergic blockers have similar therapeutic effect Metoprolol Nadolol Atenolol Acebutolol Pindolol Stalol Timolol Esmolol

Classification of antiarrhythmics(based on mechanisms of action) : 

Classification of antiarrhythmics(based on mechanisms of action) Class III – K+ channel blockers Developed because some patients negatively sensitive to Na channel blockers (they died!) Cause delay in repolarization and prolonged refractory period Includes Amiodarone – prolongs action potential by delaying K+ efflux but many other effects characteristic of other classes Ibutilide – slows inward movement of Na+ in addition to delaying K + influx. Bretylium – first developed to treat hypertension but found to also suppress ventricular fibrillation associated with myocardial infarction Dofetilide - prolongs action potential by delaying K+ efflux with no other effects

Classification of antiarrhythmics(based on mechanisms of action) : 

Classification of antiarrhythmics(based on mechanisms of action) Class IV – Ca2+ channel blockers slow rate of AV-conduction in patients with atrial fibrillation Includes Verapamil – blocks Na+ channels in addition to Ca2+; also slows SA node in tachycardia Diltiazem

QUINIDINE : 

QUINIDINE Pharmacokinetics: Oral → rapid GI absorption 80% plasma protein binding 20% excreted unchanged in the urine → enhanced by acidity t½ = 6 hours Parenteral → hypotension Dosage: 0.2 to 0.6 gm 2-4X a day Therapeutic Uses: Atrial flutter & fibrillation Ventricular tachycardia IV treatment of malaria

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Toxicity: Antimuscarinic actions → inh. vagal effects Quinidine syncope (lightheadedness, fainting) Ppt. arrhythmia or asystole Depress contractility & ↓ BP Widening QRS duration Diarrhea, nausea, vomiting Cinchonism (HA, dizziness, tinnitus) Rare: rashes, fever, hepatitis, thrombocytopenia,etc QUINIDINE

Procainamide : 

Procainamide Loading infusion: 20 to 30 mg/min up to 12 to 17 mg/kg Maintenance infusion: 1 to 4 mg/min Precautions: Renal clearance. Watch for toxcity in patients with renal impairment. Administer the loading dose slowly to avoid hypotension.

Lidocaine (XYLOCARD) : 

Lidocaine (XYLOCARD) Preparation available--50ml vial (20mg / ml) Loading Bolus: 1.0 to 1.5 mg/kg (5ml) with supplemental boluses of 0.5 to 0.75 mg/kg every 5 to 10 min ( maximum 3 mg/kg ) Maintenance Infusion: 1 to 2 mg/min add 1 gm of xylocard in 1 liter solution (1ml=1mg) 16 macrodrops/minute Precautions: Hepatic clearance. Watch for toxicity in patients with hepatic dysfunction, CHF, hypotension, shock. Toxicity: Ppt. SA nodal standstill or worsen impaired conduction Exacerbates ventricular arrhythmias Hypotension in HF Neurologic: paresthesias, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions

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Only in serious ventricular arrhythmias MECHANISM of action - Very effective Na+ channel blocker Markedly lengthens AP by blocking also K+ channels Weak Ca++ channel blocker Noncompetetive inhibitor of beta adrenoceptors Powerful inhibitor of abnormal automaticity Slow sinus rate and AV conduction ↑ atrial, AV nodal & ventricular refractory periods Antianginal effects – due to noncompetetive α & β blocking property and block Ca++influx I n vascular sm.m Perivascular dilatation - α blocking property and Ca++ channel-inhibiting effects Improves ventricular function. Very low propensity to induce torsades des pointes. Can be combined with beta-blockers to augment its antiarrhythmic effects. O Amiodarone ( CORADRONE)

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Pharmacokinetics: > t½ = 13 to 103 days > effective plasma conc: 1-2 μg/l Dosage: Through central line whenever possible if concentration >2mg/ml Loading dose: 150 mg (1 amp) diluted in 100 ml D5W (15 mg/ml) given slow i.v over a period 10 minutes Sodium chloride is not suitable vechile Maintenance Infusion: 1.0 mg/min for 6 hours (360 mg over the NEXT 6 hours (1 mg/min). Add 18 mL of Cordarone I.V. (900 mg)/ 6 ampules to 500 mL D5W (conc = 1.8 mg/mL). =50 microdrops /minute then 0.5 mg/min ( 540 mg over the REMAINING 18 hours (0.5 mg/min) = 15 microdrops /minutes PREPARATION AVAILABLE - 1amp=3ml =150mg 1ml=50mg USE: Supraventricular & Ventricular arrhythmias resistant to electric defibrillation Amiodarone

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Toxicity: - pulmonary – alveolotis (pnueminitis) - Ocular -yellowish-brown microcrystals corneal deposits, - Dermatologic- grayish blue discoloration, photodermatitis - Neurologicologic-paresthesias, tremor, ataxia & headaches, peripheral neuropathy - Hypo - / hyperthyroidism - CVS- increase QT interval Symptomatic bradycardia or heart block - Ppt. heart failure - Constipation, hepatocellular necrosis, inflam’n, fibrosis, Amiodarone

Bretylium : 

Bretylium Loading infusion: 5 to 10 mg/kg Maintenance infusion: 1 to 2 mg/min Precautions: transient sinus tachycardia, hypotension

Esmolol : 

Esmolol Ultrashort acting β blocker 1 Vial =10ml=100mg 1ml=10mg Dose-.3-.5mg/kg for 1minute later .05mg/kg/minute for maintenance Treatment-PSVT, atrial flutter, atrial fibrillation

Ca2+channel blockers : 

Ca2+channel blockers Decrease AV conduction 2nd line treatment for PSVT Control ventricular rate in atrial flutter and AF NOT EFFECTIVE IN WPW SYNDROME- because increase conduction through accessory pathway VERAPAMIL- 1 amp=2ml=5mg 1ml =2.5 mg Doses-5-10 mg (.1-.15 mg/kg) over 1-3 minute repeated after 10 minutes if nedded then .005 mg /kg/minute in infusion DILTIAZAM ( CARDIZEM)- 1 amp= 5ml=25 mg 1 ml=5 mg Doses-.25 mg/kg (20 mg for average pt) over 2 minutes repeated after 15 minutes if inadequate response in dose .35 mg/kg (25 mg for average pt) over 2 minute if response occurs /heart rate falls start Infusion 10 mg/hour (add 25 ml/ 125 mg diltiazam in 100ml of D5W/NS that means 125 ml contains 125 mg drugs or 1ml=1mg Rate 10 ml/hour=( 10 ml/60 minutes) =(1ml/6 minutes)=60 microdrops/6 minutes) =(10 microdrops /minutes)

ADENOSINE : 

ADENOSINE A nucleoside that occurs naturally in the body Inhibits AV conduction Prolongs refractory period Decrease conduction through accessory pathway 1amp=10ml=30mg 1ml=3mg DOSE- 6mg IV if necessary 6-12 mg 3 minutes after t½ ≈ 10 seconds USES- PSVT—DOC for due to its high efficacy & very short duration of action WPW syndrome (conduction through accessory pathway) (NOT EFFECTIVE IN ATRIAL FLUTTER, ATRIAL FIBRILLATION AND VT} Toxicity: flushing, SOB or chest burning, atrial fibrillation, headache, hypotension, nausea, paresthesia

DIGITALIS(DIGOXIN) : 

DIGITALIS(DIGOXIN) Slow conduction through AV node due to vagolytic effect Dose-. Usual digitalization dose -1-1.5 mg oral in single or divided dose followed by 250-500 microgram 6 hourly Rapid digitalization-.5 -1 mg slow i.v 1amp=2ml=.5mg 1ml=.25mg NOT USED IN WPW SYNDROME-increase conduction through accessory pathway TOXICITY-M.C.- atrial tachycardia and block

Slide 64: 

Therapy directed toward normalizing K+ gradients & pools in the body Effects of increasing serum K+: 1. resting potential depolarizing action 2. membrane potential stabilizing action Hypokalemia: ↑ risk of early & delayed afterdepolarization ↑ ectopic pacemaker activity esp if (+) digitalis Hyperkalemia: Depression of ectopic pacemakers Slowing of conduction POTASSIUM

Questions to answer in order to identify an unknown arrhythmia: : 

Questions to answer in order to identify an unknown arrhythmia: 1. Is the rate slow (<60 bpm) or fast (>100 bpm)? Slow  Suggests sinus bradycardia, sinus arrest, or conduction block Fast  Suggest increased/abnormal automaticity or reentry 2. Is the rhythm irregular? Irregular  Suggests atrial fibrillation, 2nd degree AV block, multifocal atrial tachycardia, or atrial flutter with variable AV block 3. Is the QRS complex narrow or wide? Narrow  Rhythm must originate from the AV node or above Wide  Rhythm may originate from anywhere

Questions to answer in order to identify an unknown arrhythmia: : 

Questions to answer in order to identify an unknown arrhythmia: 4. Are there P waves? Absent P waves  Suggests atrial fibrillation, ventricular tachycardia, or rhythms originating from the AV node 5. What is the relationship between the P waves and QRS complexes? More P waves than QRS complexes  Suggests 2nd or 3rd degree AV block More QRS complexes than P waves  Suggests an accelerated junctional or ventricular rhythm 6. Is the onset/termination of the rhythm abrupt or gradual? Abrupt  Suggests reentrant rhythm Gradual  Suggests altered automaticity

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THANK YOU