Antiarrhythmic drugs

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Arrhythmia and its treatment. (anti arrhythmic drugs)

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Antiarrhythmic drugs

  1. 1. ANTIARRHYTHMIC DRUGS
  2. 2. GROUP MEMBERS  Anum Aslam Khan  Bushra Rubab  Farah Ali Khan  Javeria Rahat  Najaf Farooq  Nameera Ahmed  Nida Ashraf  Rabia Khalid Nadeem  Urooba Iqbal
  3. 3. ANUM ASLAM KHAN INTRODUCTION
  4. 4. ARRHYTHMIA Abnormality in the origin, rate, rhythm, conduction velocity and sequence of heart activation. It may cause sudden death or syncope, heart failure, dizzines, palpitations, or no symptoms at all.
  5. 5. Normal Physiology of Heart  The cardiac muscles are specialised tissue with unique properties like excitability, contractility and automatcity  The myocardium has 2 types of cells, contracting and conducting cell.  The contracting cells participate in the pumping action of the heart, and the have the charachteristic property of Automaticity.
  6. 6.  Automaticity is the ability of the cell to generate electrical impulses spontaneously.  SA,AV and His-purkinje system comprises the conduction tissue system of heart. Normally the SA node act as a pace maker of the heart.  Excitability is the ability of the cell to undergo depolarization in response to a stimulus.  Contractility is he ability of he myocardium to adequately contract ad pump the blood out of the heart.
  7. 7. Cardiac Action Potential When the stimulus reach the cardiac cell, specific ions moves into and out of the eliciting the action potential cell. Such movement of ions is divided into following or phases:
  8. 8. Phases of Cardiac Action Potential
  9. 9.  Phase 0: rapid depolarization of cell membrane during which theirs is fast entry of Na ions into the cells through Na channels, this is followed by repolarization.  Phase 1: is short initial rapid repolarization due to Ka efflux  Phase 2:prolonged plateue phase due to slow Ca influx  Phases 3: rapid repolarization with Ka efflux  Phase 4: resting phase during which Ka ions return into the cell while Na and Ka move out of it and resting membrane potential is stored
  10. 10. Mechanism of Arrhythmia Abnormal heart pulse formation  Sinus pulse  Ectopic pulse  Triggered activity Abnormal heart pulse  Reentry  Conduction block
  11. 11. Two Main Features of Arrhythmia Site of origin  Atria  Atrioventricle node (AV node)h  Ventricles Affect on heart rate  Too slow heart rate (bradycardia : >60 beats/min)  Too fast heart rate (tachycardia : < 80 beats per min)
  12. 12. Classification of Arrhythmia Abnormal heart pulse formation Sinus arrythmia Atrial arythmia Atrio vetricular juctional arrythmia Ventricular arrythmia Abnormal heart pulse conduction Sinus-atrial block Intra-atrial block Atrio- ventricular block Intra-ventricular block
  13. 13. Symptoms
  14. 14. NAJAF FAROOQ CLASS I(A) ANTI ARRHYTHMIC DRUGS
  15. 15. CLASS I ANTI ARRHYTHMIC DRUGS  It is largest class of Anti arrhythmic drugs.  Class I anti arrhythmic drugs act by blocking voltage- sensitive sodium (Na+) channels.These drugs bind to sodium channels when the channels are open and in activated state and dissociate when the channels are in resting phase.  Inhibition of sodium channel decrease rate of rise of phase 0 of cardiac membrane action potential and a slowing of conduction velocity.  They also block K channels (class IA) thus, slows the repolarization in ventricular tissue.  These drugs have local anesthetic activity and may suppress myocardial contractile force, these affects are observed at a higher plasma concentration.
  16. 16. USE DEPENDENCE:  Class I drugs bind more rapidly to open or inactivated sodium channels than to channels that are fully repolarized following recovery from the previous depolarization cycle. Therefore, these drugs show a greater degree of blockade in tissues that are frequently depolarizing (for example, during tachycardia, when the sodium channels open often). This property is called use- dependence (or state-dependence) and it enables these drugs to block cells that are discharging at an abnormally high frequency, without interfering with the normal, low-frequency beating of the heart.
  17. 17. Class I anti arrhythmic drugs are classified into three sub classes: Class IA • Quinidine • Procainamide • Disopyramide Class IB • Lidocaine • Mexiletine • Tocainide Class IC • Flecanide • Propafenone Classification:
  18. 18. CLASS IA Blocking of the fast sodium channel interferes with rapid depolarization and decreases conduction velocity. This will increases the duration of the cardiac action potential . These drugs decrease rate of rise of phase 0 Block Na channels preferentially in open state ,so decrease the no. of available Na channels for membrane depolarization. Increase APD, and ERP
  19. 19. In addition to blocking the fast sodium channel (Phase 0) some class I agents also block the potassium channel (Phase 3) Potassium channel blockade directly affects the duration of the cardiac action potential and the effective refractory period All drugs have same effects but they differ in pharmacokinetics and adverse effect.
  20. 20. QUINIDINE • Quinidine is d-isomer of quinine obtained from cinchona tree. • Quinidine binds with sodium channel and prevent sodium influx, thus slowing the rapid upstroke during phase 0 • It also decreases the slope of phase 4 depolarization and inhibits potassium channels. Because of these action it decreases conduction velocity and increases refractoriness. • Additionally It has anti cholinergic activity (M receptor block) on SA and AV NODE which increases HR and AV conduction. • Inc: PR,QRS,QT interval
  21. 21. Therapeutic uses:  Quinidine is used in the treatment of a wide variety of arrhythmias, including:  atrial,AV-junctional, and ventricular tachyarrhythmias.  Quinidine is used to maintain sinus rhythm after direct-current cardioversion of atrial flutter or fibrillation and to prevent frequent ventricular tachycardia.
  22. 22. Adverse effects:  nausea, vomiting, diarrhoea.  large doses may produce cinchonism( tinnitus, ocular dysfunction, CNS excitation). hypotension,  prolongation of QRS and increase in QT interval associated with syncope( which is due to ventricular arrhythmia induced by quinidine),  Torsade de pointes.  Thrombocytopenia that disappear on drug withdrawal.  Enhances digoxin toxicity.
  23. 23. PROCAINAMIDE • It is a derivative of local anesthetic procaine. • Less M receptor blockade than quinidine, but more cardio depressant. • Orally effective, often substitution of quinidine. • Increase PR,QRS,QT interval • It Decreases re-entry by causing bidirectional block.
  24. 24. Indications:  effective in premature atrial contractions, PSVT,Atrial fibrillation.  It converts atrial flutter or atrial fibrillation to sinus rhythm although it has value in preventing reoccurrence of these arrhythmias once they have been terminated by DC cardio version.  Majority of patient of ventricular tachycardia respond to procainamide. Adverse effects: With chronic use, procainamide causes a high incidence of side effects, including  a reversible lupus erythematosus–like syndrome that develops in 25 to 30 percent of patients..
  25. 25.  Toxic concentrations of procainamide may cause asystole or induction of ventricular arrhythmias.  Central nervous system (CNS) side effects include depression, hallucination, and psychosis. With this drug, gastrointestinal intolerance is less frequent than with quinidine
  26. 26. DISOPYRAMIDE • It produces a negative ionotropic effect that is greater than the weak effect exerted by quinidine and procainamide, and unlike the latter drugs, disopyramide causes peripheral vasoconstriction • The drug may produce a clinically important decrease in myocardial contractility in patients with pre existing impairment of left ventricular function. • Disopyramide is used in the treatment of ventricular arrhythmias as an alternative to procainamide or quinidine.
  27. 27. Adverse effects:  Disopyramide shows effects of anticholinergic activity (for example, dry mouth, urinary retention, blurred vision, and constipation).
  28. 28. 31 ELECTROPHYSIOLOGICAL EFFECTS OF CLASS I A DRUGS DRUG CLASS ATRIA SA NOD E AV – NODE C-RP HIS PURKINJ E C-RP VENT MUSCLE C-RP APD ERP Quinidine I A DEC - D-0/I D-I DEC INC INC procainamide IA DEC - DEC DEC DEC INC INC Disopyramide IA DEC - DEC DEC DEC INC INC
  29. 29. UROOBA IQBAL CLASS I(B) ANTIARRHYTHMIC DRUGS
  30. 30. CLASS IB ANTIARRHYTHMIC DRUGS  These drugs have minimal effect on rate of depolarization and  They decrease APD and ERP. of purkinje fibers.  They block inactivated channels.  Examples are: Lidocaine, mexiletine, tocainide
  31. 31. LIDOCAINE  Lidocaine (xylocaine, or lignocaine ) is a common local anesthetic & a class IB anti arrhythmic drug.  It is used intravenously for the treatment of ventricular arrhythmias (for acute myocardial infarction, digoxin poisoning, cardioversion or cardiac catheterization).
  32. 32. Indications:  It is prescribed for ventricular arrhythmias (particularly in patients with Mayocardial Infarction). Adverse effects:  Drowsiness  Confusion  Irritability  Convulsions.
  33. 33. TOCAINIDE (Tonocord)  Tocainide (Tonocard) is a class IB antiarrhythmic drug. Mechanism of action:  It decreases His-purkinjie conduction.  Also it abolishes re-entry by causing bi- directional block.
  34. 34. Indications:  It is used in ventricular arrhythmia refractory to more conventional therapy. Adverse effects:  Light headedness  Dizziness  Nausea
  35. 35. MEXILETINE (Mexitil)  It is yet another class IB antiarrhythmic drug.  It is similar to lidocaine,tocainide in action but it produces greater effect in normal cardiac tissues than does lidocaine.
  36. 36. Mechanism of action:  It slows conduction in the heart and makes the heart tissue less sensitive. Indications:  It is used to treat arrhythmias within the heart or seriously irregular heart beats.
  37. 37. Adverse effects:  Dizziness  Heartburn  Nausea  Nervousness  Trembling  Unsteadiness  Widening of QRS wave  GI distress  Chest pain (rare)
  38. 38. ELECTROPHYSIOLOGICAL EFFECTS OF CLASS I B DRUGS DRUG CLASS ATRIA SA NODE AV NODE C-RP HIS – PURKIN JE C-RP VENTM USCLE C-RP APD ERP Lidocaine IB D - D-0/I D-I D DEC - Tocainide IB - - D D D DEC - Mexiletine IB - - D D D DEC DEC
  39. 39. FARAH ALI KHAN CLASS I(C) ANTIARRHYTHMIC DRUGS
  40. 40. CLASS IC ANTIARRHYTHMIC DRUGS Class IC antiarrhythmic medications are proarrhythmic, and their use should be limited to patients without structural heart disease. Class Ic does not significantly affect the action potential .It dec: QT interval b/c these drugs have less effect on K rectifier current. E.g. Moricizine, Flecainide, Propafenone
  41. 41. Potent blocker of Na & K channel with slow unblocking kinetics. Block K channel but does not prolong APD and QT interval. Slows conduction of the electrical impulse within the heart. Greatest effect is on the His-Purkinje system and ventricular myocardium. ventricular myocardium causes decreased contractility of the muscle. decrease in the ejection fraction. FLECAINIDE (TAMBOCOR): Mechanism of action:
  42. 42. Indication: •After digoxin it is 2nd line drug in the treatment of fetal arrhythmia, many types of supraventricular tachycardias, including AV nodal re-entrant tachycardia (AVNRT) and Wolff-Parkinson-White syndrome(WPW).This is because of the action of flecainide on the His-Purkinje system. •It is also used in ventricular tachyarrhythmias.
  43. 43. Contraindications: Flecainide is contraindicated in patients with pre- existing second- or third-degree AV block, or with right bundle branch block when associated with a left hemiblock (bifascicular block), unless a pacemaker is present to sustain the cardiac rhythm should complete heart block occur. Flecainide is also contraindicated in the presence of cardiogenic shock or known hypersensitivity to the drug.
  44. 44. Adverse effects:  visual disturbances, blurred vision, nausea, headache, dyspnea. Inc:PR ,QRS are likely to occur.  dizziness, fainting, or lightheadedness  fast, irregular, pounding, or racing heartbeat or pulse  tightness in the chest  wheezing
  45. 45. PROPAFENONE (Rythamol) Mechanism of Action:  Slowing the influx of sodium ions into the cardiac muscle cells, causing a decrease in excitability of the cells. it has additional activity as a beta-adrenergic blocker which can cause bradycardia and bronchospasm.
  46. 46. Indication: Contraindication:  hepatic or renal dysfunction  Asthma  CHF  bradycardia.  Life-threatening ventricular arrhythmias atrial fibrillation (AF) or in patients exclusively with atrial flutter
  47. 47. Adverse effects:  Lupus-like syndrome  Agranulocytosis  CNS disturbances such as dizziness, lightheadedness, gastrointestinal upset, a metallic taste  Bronchospasm  About 20% of patients treated with RYTHMOL have discontinued treatment because of adverse reactions.
  48. 48. MORICIZINE (Ethmozine) Indication:  Life threatening ventricular arrhythmias (eg, sustained ventricular tachycardia).  Used to treat irregular heartbeats (arrhythmias) and maintain a normal heart rate. Mechanism of action: Moricizine works by inhibiting the rapid inward sodium current across myocardial cell membranes. Ethmozine shortens Phase II and III repolarization, resulting in a decreased action potential duration and effective refractory period.
  49. 49. Contraindications: Ethmozine® (moricizine hydrochloride) is contraindicated in patients with pre- existing second- or third-degree AV block and in patients with right bundle branch block when associated with left hemiblock (bifascicular block) unless a pacemaker is present. Ethmozine® is also contraindicated in the presence of cardiogenic shock or known hypersensitivity to the drug.
  50. 50. Adverse effects:  Cardiac arrest  Heart failure  Sinus node dysfunction  Conduction block  Dizziness  Dyspnea  Headache  Visual disturbance
  51. 51. BUSHRA RUBAB CLASS II ANTIARRHYTHMIC DRUGS
  52. 52. CLASS II ANTIARRHYTHMIC DRUGS (BETA BLOCKERS)  It reduce sympathetic tone  Like propranolol exert anti arrhythmic effect due to blackade of cardiac beta receptor .They depress myocardial contractility ,automaticity and conduction velocity .
  53. 53. PROPRANOLOL  BRAND NAME : INDERAL  In all type of arrhythmias caused by enhance sympathetic stimulation  In SVT andVT. Mechanism of action : DIMINISH PHASE 4 DEPOLARIZATION DEPRESSED AUTOMATICITY GIVE NEGATIVE INOTROPIC EFFECT ,HEART RATE , CARDIAC OUTPUT CARDIAC AUTOMATICITY DECREASE PROLONG AV CONDUCTION AND INC AV NODAL RP
  54. 54. Adverse effects:  Bradycardia  Bronchospasm  Fatigue  Insomnia
  55. 55. JAVERIA RAHAT CLASS III ANTIARRHYTHMIC DRUGS
  56. 56. CLASS III ANTIARRYTHMIC DRUGS General Pharmacology:  The primary role of potassium channels in cardiac action potentials is cell repolarization.  In non-nodal tissue (see figure), action potentials are initiated when a cell is depolarized to a threshold potential by an adjacent cell.  This leads rapid opening of fast sodium channels and a slower opening of L-type calcium channels that permit calcium to enter the cell (phase 0 and 2, respectively).
  57. 57.  As these channels become inactivated, potassium channels open permitting potassium ions to leave the cell (K+ out), which causes repolarization of the membrane potential (phase 3). Potassium channels remain open until the next action potential is triggered.  There are also different potassium channels that are responsible for the initial repolarization (phase 1) that occurs as the fast sodium channels become inactivated. Potassium channels are also responsible for repolarizing slow-response action potentials in the sinoatrial and atrioventricular nodes.
  58. 58. POTASSIUM CHANNEL BLOCKER  Potassium-channel blockers comprise the Class III antiarrhythmic compounds according to the Vaughan- Williams classification scheme.  These drugs bind to and block the potassium channels that are responsible for phase 3 repolarization. Therefore, blocking these channels slows (delays) repolarization, which leads to an increase in action potential duration and an increase in the effective refractory period (ERP).
  59. 59.  On the electrocardiogram, this increases the Q- T interval.This is the common effect of all Class III antiarrhythmic drugs.The electrophysiological changes prolong the period of time that the cell is unexcitable (refractory) and therefore make the cell less excitable.
  60. 60.  By increasing the ERP, these drugs are very useful in suppressing tachyarrhythmia's caused by reentry mechanisms.  Reentry occurs when an action potential reemerges into normal tissue when that tissue is no longer refractory.  When this happens, a new action potential is generated prematurely (before normal activation) and a circular, repeating pattern of early activation can develop, which leads to a tachycardia. If the ERP of the normal tissue is lengthened, then the reemerging action potential may find the normal tissue refractory and premature activation will not occur.
  61. 61. CLASS III ANTIARYTHMIC DRUGS BRETYLIUM AMIODARONE SOTALOL
  62. 62. BRETYLIUM  Bretylium (also bretylium tosylate) is an antiarrhythmicagent.It blocks the release of noradrenaline from nerve terminals.  In effect, it decreases output from the peripheralsympathetic nervous system.  It also acts by blocking K+channels and is considered a class III antiarrhythmic
  63. 63.  It is used in emergency medicine, cardiology, and other specialties for the acute management of ventricular tachycardia and ventricular fibrillation.  It is contraindicated in patients with AV (atrioventricular)heart block or digoxin toxicity.  Bretylium should be used only in an ICU or Emergency Department setting and should not be used elsewhere due to its dramatic actions and its predominant side effect of hypotension.
  64. 64. Therapeutic uses:  In life-threatening ventricular tachycardia and fibrillation. Adverse effects:  nausea, hypotension, diarrhea Indications:  In treating life threatingVT, when lidocaine or procainamide become in effective.
  65. 65. NIDA ASHRAF CLASS III ANTIARRHYTHMIC DRUGS (CONTD.)
  66. 66.  Amiodarone is an antiarrhythmic agent used for various types of cardiac dysrhythmias, both ventricular and atrial. Mechanism of action:  Amiodarone is categorized as a class III antiarrhythmic agent, and prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability.  It is similar to those of antiarrhythmic classes I a, II, and IV. AMIODARONE
  67. 67. Amiodarone shows beta blocker-like and potassium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects
  68. 68. Indication:  tachyarrhythmia, including atrial fibrillation and ventricular tachycardia  patients at high risk of sudden cardiac death. Although amiodarone is effective, it is not generally recommended for minor rhythm disturbances because of its toxicity.
  69. 69. Contraindications: • Individuals who are pregnant or may become pregnant are strongly advised to not take amiodarone. • It is contraindicated in individuals with sinus nodal bradycardia, atrioventricular block, and second or third degree heart block who do not have an artificial pacemaker. • Individuals with baseline depressed lung function should be monitored closely if amiodarone therapy is to be initiated.
  70. 70. Adverse effects: Most common side effects are:  Cough  Dizziness, lightheadedness, or fainting  Fever (slight)  numbness or tingling in the fingers or toes  painful breathing  trouble with walking
  71. 71. Less common side effects are:  Blue-gray coloring of the skin on the face, neck, and arms  Blurred vision or blue-green halos seen around objects  Dry eyes  Fast or irregular heartbeat  Nervousness  Sensitivity of the eyes to light  Slow heartbeat  Sweating  Swelling of the feet or lower legs trouble with sleeping
  72. 72. SOTALOL • Sotalol is a drug used in individuals with rhythm disturbances (cardiac arrhythmias) of the heart, and to treat hypertension in some individuals. • It is a non-selective competitive β-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties by its inhibition of potassium channels. • Because of this dual action, Sotalol prolongs both the PR interval and the QT interval.
  73. 73. Mechanism of action: Sotalol hydrochloride has both beta-adrenoreceptor blocking and cardiac action potential duration prolongation antiarrhythmic properties. Sotalol hydrochloride is a racemic mixture of d- and l-Sotalol. Both isomers have similar Class III antiarrhythmic effects, while the I-isomer is responsible for virtually all of the beta-blocking activity.The beta- blocking effect of Sotalol is non-cardioselective. Sotalol does not have partial agonist or membrane stabilizing activity. In children, a Class III electro physiologic effect can be seen at daily doses of 210 mg/m2 body surface area (BSA).
  74. 74. Indications: Ventricular arrhythmias Like other beta-blockers, sotalol is an effective antihypertensive agent and it is also suited for combinations with other antihypertensive drugs. Because of the risk of hypokalemia, a combination with diuretics is better avoided
  75. 75. Adverse effects: More common side effects are:  Blurred vision  chest pain or discomfort  confusion  Diarrhea  lightheadedness, dizziness, or fainting  nausea and vomiting  shortness of breath  sweating  swelling of face, fingers, feet, or lower legs  tightness in chest  unusual tiredness or weakness  wheezing
  76. 76. Less common side effects are:  Abdominal pain or swelling  back pain  black, tarry stools  blood in eyes  blood in urine  body aches or pain
  77. 77. NAMEERA AHMED CLASS IV ANTIARRHYTHMIC DRUGS:
  78. 78. CLASS IV ANTIARRHYTHMIC DRUGS: •Class IV drugs are calcium channel blockers. •They decrease the inward current carried by Ca+2 resulting in a decreased rate of phase 4 spontaneous depolarization. •Also slow conduction in tissues that depend on calcium currents , such as AV node. •Major effect of CCBs is on vascular smooth muscles & on heart.
  79. 79. VERAPAMIL: •Verapamil is a prototype drug. •Shows greater action on heart than on vascular smooth muscle. Cardiac effects: •It usually slows the sinoatrial node by its direct action. •But its hypotensive action may occasionally result in a small reflex increase of sinoatrial nodal rate. •It can suppress both early & delayed after depolarizations & may antagonize slow responses arising in severly depolarized tissue.Verapamil blocks both activated & inactivated L-type calcium channels.
  80. 80. Extra-cardiac effects: •Verapamil cause peripheral vasodilation ,which may be beneficial in HTN & peripheral vasospastic disorders. •Its effects on smooth muscle produce a no. of cardiac effects. •Supra ventricular tachycardia is the major arrhythmia indication for verapamil. •It preferred over older treatments (propranolol ,digoxin ,etc)for termination. Therapeutic uses:
  81. 81. •Also reduce ventricular rate in atrial fibrillation or flutter. •Occasionally useful in ventricular arrhythmia. •IV verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. Adverse effects: • Verapamil have –ve inotropic properties. •May be contraindicated in patients with preexisting depressed cardiac function. • Verapamil can produce a decrease in BP b/c of peripheral vasodilation –an effect that is actually beneficial in treating HTN.
  82. 82. DILTIAZEM It is a class III antianginal drug, and a class IV antiarrythmic. Mechanism of action:  Diltiazem is a potent vasodilator, increasing blood flow and variably decreasing the heart rate via strong depression of AV node conduction. Its pharmacological activity is somewhat similar to verapamil.  It is a potent vasodilator of coronary and peripheral vessels, which reduces peripheral resistance and afterload.  Because of its negative inotropic effect, diltiazem causes a modest decrease in heart muscle contractility and reduces myocardium oxygen consumption. Its negative chronotropic effect results in a modest lowering of heart rate, due to slowing of the sinoatrial node. It results in reduced myocardium oxygen consumption.  Because of its negative dromotropic effect, conduction through the AV (atrioventricular) node is slowed, which increases the time needed for each beat. This results in reduced myocardium oxygen consumption.
  83. 83. Indications:  Hypertension  Angina pectoris  Arrhythmia Adverse effects:  Hypotension  Bradycardia  dizziness  flushing
  84. 84. Contraindications:  CHF  AV or Sa node disturbances  Low blood pressure  Bradycardia  Impaired left ventricle function  Peripheral artery occlusive disease  Chronic obstructive pulmonary disease
  85. 85. Drug interactions:  Beta blockers  Quinidine  Diltiazem inhibits hepatic cytochromes CYP3A4, CYP2C9 and CYP2D6, possibly resulting in drug interactions.
  86. 86. RABIA KHALID NADEEM OTHER DRUGS
  87. 87. DIGOXIN Mechanism of action:  Digoxin shortens the refractory period in atrial & ventricular myocardial cells while prolonging the ERF & diminishing conduction velocity in the AV node.  It is used to control the ventricular response rate in atrial fibrillation & flutter. OTHER DRUGS:-
  88. 88. Digoxin toxicity:  At toxic conc. it causes ectopic ventricular beats that may result in ventricular tachycardia & fibrillation.  [note: this arrhythmia is usually treated with Lidocaine]
  89. 89. Indications:  CHF  Atrial arrhythmia  Heart failure Adverse effects:  GI upset  Yellow vision  ECG will show increased RP interval  ST scooping  T-WAVE inversion
  90. 90. ADENOSINE Mechanism of action:  It is a naturally occurring nucleoside, but at high doses it decreases conduction velocity, prolongs the refractory period, & decreases automaticity in the AV node. Toxicity:  It has low toxicity, but causes flushing, chest pain, & hypotension.
  91. 91. We hope you liked our presentation. Thank you! 

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