Arrhythmias (2)


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Arrhythmias (2)

  1. 1. WELCOME
  2. 2. arrhythmiasBasil
  3. 3. arrhythmias
  4. 4. Properties of cardiac cellsAutomaticity• Ability to initiate an impulse spontaneously andcontinuously.Excitability.• Ability to be electrically stimulated.Conductivity• Ability to transmit an impulse along a membrane inan orderly manner.Contractility• Ability to respond mechanically to an impulse.
  5. 5. Pacemakers of the Heart• SA Node - Dominant pacemaker with anintrinsic rate of 60 - 100 beats/minute.• AV Node - Back-up pacemaker with anintrinsic rate of 40 - 60 beats/minute.• Ventricular cells - Back-up pacemaker withan intrinsic rate of 20 - 45 bpm.
  6. 6. Impulse Conduction & the ECGSinoatrial nodeAV nodeBundle of HisBundle BranchesPurkinje fibers
  7. 7. The “PQRST”• P wave - Atrialdepolarization• T wave - Ventricularrepolarization• QRS - Ventriculardepolarization
  8. 8. The PR IntervalAtrial depolarization+delay in AV junction(AV node/Bundle of His)(delay allows time forthe atria to contractbefore the ventriclescontract)
  9. 9. The ECG Paper• Horizontally– One small box - 0.04 s– One large box - 0.20 s• Vertically– One large box - 0.5 mV
  11. 11. Criterias of a normal heart rhythm1. Presence of one upright and consistent-appearing P wave before each QRScomplex.2. P-R interval between 0.12-0.20 seconds3. A consistent appearing QRS complex ofless than 0.12 seconds.4. Consistent R-R interval5. A heart rate between 60-100 beats/minute6. The ST segment should be isoelectrical
  12. 12. Arrhythmias• It is a disturbance in therhythmic patterns of the heart.Results from abnormalimpulse initiation, abnormalconduction or both mechanismtogether.
  13. 13. Four Steps to Identify Arrhythmias1- Begin by labeling the P wave, QRScomplex, T wave, PR interval, and QTinterval.2- Calculate the atrial and ventricular heartrates.3- Determine if the rhythm is regular orirregular.4- Evaluate the waveform of the ECG indetail for additional clues:
  14. 14. Mechanisms Of ArrhythmiasArrhythmias result from1-Abnormal impulse initiation and2-Abnormal impulse conduction.
  15. 15. Mechanisms Of ArrhythmiasThe major mechanisms of arrhythmias areABNORMAL IMPULSE INITIATIONEnhanced normal automaticityAbnormal automaticityTriggered activity due to afterdepolarizationABNORMAL IMPULSE CONDUCTIONConduction blocksReentry12
  16. 16. Enhanced normal automaticity• Automaticity is defined as the ability of a cellto independently initiate an action potential.
  17. 17. Classification Of Arrhythmias• Disorders of ImpulseGeneration• Disorders of ImpulseConduction
  18. 18. II. Disorder of impulse conduction• S.A. Block• First degree AV Block• Second Degree A.V.Block» Mobitz type I» Mobitz type II• Third Degree or Complete A.V Block
  19. 19. Common causes• Underline cardiac disease• Sympathetic stimulation• Vagal stimulation• Electrolyte imbalance• Hypoxia
  20. 20. Mechanism responsible for phase 4depolarization1. Decreased outward permeability topotassium2. Increased inward permeability to sodium3. Reduced sodium pump activity4. Increased inward permeability to calcium
  21. 21. Rhythms Originating in SA NodeSINUS BRADYCARDIA• It is characterized by atrial and ventricular ratesof less than 60 beats/minutes.• It occur gradually or suddenly for a brief period.• It is usually a benign dysrhythmias and iscommon among general population• It is commonly seen in athletes and also beassociated with sleep
  22. 22. Sinus BradycardiaCAUSES StimulationCarotid Sinus MassageIncreased vagal tone vomiting suctioning severe pain extreme emotionsDecreased sympathetic toneIntra Occular PressureValsalva maneuver
  23. 23. Disease ProcessMIUremiaRaised ICPAnorexia NervosaHypothermiaHypothyroidism
  24. 24. • Right and left Vagus nerve fibers of theparasympathetic nerve system plays animportant role in the rate of impulse formation,the speed of conduction and the strength ofcardiac contraction.• Stimulation of the Vagus nerve causes adecrease rate of firing of the SA node, slowedimpulse conduction of the AV node, anddecreased force of cardiac muscle contraction.
  25. 25. • Stimulation of the sympathetic nervesystem that supply the heart has essentiallythe opposite effect on the heart.
  26. 26. Valsalva maneuver• The Valsalva maneuver or Valsalvamanoeuvre is performed by moderately forcefulattempted exhalation against a closed airway,usually done by closing ones mouth andpinching ones nose shut.
  27. 27. • Variations of the maneuver can be used either inmedical examination as a test of cardiac functionand autonomic nervous control of the heart, or to"clear" the ears and sinuses (that is, to equalizepressure between them) when ambient pressurechanges, as in diving, hyperbaric oxygen therapy,or aviation.• The technique is named after Antonio MariaValsalva
  28. 28. The normal physiological responseconsists of 4 phases• Initial pressure rise: On application ofexpiratory force, pressure rises inside the chestforcing blood out of the pulmonary circulationinto the left atrium. This causes a mild rise instroke volume.
  29. 29. • Reduced venous return and compensation:Return of systemic blood to the heart is impededby the pressure inside the chest. The output of theheart is reduced and stroke volume falls. Thisoccurs from 5 to about 14 seconds in theillustration. The fall in stroke volume reflexivelycauses blood vessels to constrict with some rise inpressure (15 to 20 seconds).
  30. 30. • This compensation can be quite markedwith pressure returning to near or evenabove normal, but the cardiac output andblood flow to the body remains low. Duringthis time the pulse rate increases.
  31. 31. • Pressure release: The pressure on the chest isreleased, allowing the pulmonary vessels andthe aorta to re-expand causing a further initialslight fall in stroke volume (20 to 23 seconds)due to decreased left ventricular return andincreased aortic volume, respectively. Venousblood can once more enter the chest and theheart, cardiac output begins to increase.
  32. 32. • Return of cardiac output: Blood return tothe heart is enhanced by the effect of entryof blood which had been dammed back,causing a rapid increase in cardiac output(24 seconds on). The stroke volume usuallyrises above normal before returning to anormal level. With return of blood pressure,the pulse rate returns towards normal.
  33. 33. DrugsDigitalisMorphine sulfateSedativesBeta-BlockersCa-Channel BlockersAmiodarone
  34. 34. 30 bpm• Rate?• Regularity? regularnormal0.10 s• P waves?• PR interval? 0.12 s• QRS duration?Interpretation? Sinus Bradycardia
  35. 35. Sinus Bradycardia• Deviation from NSR- Rate < 60 bpm
  36. 36. Sinus Bradycardia• Etiology: SA node is depolarizing slowerthan normal, impulse is conducted normally(i.e. normal PR and QRS interval).
  37. 37. ManagementInj Atropine Sulphate is administered ifpresented with hypotension, restless, chestpain, other signs of hemodynamic changesDecrease the Vagal stimulationAvoid drugs which causes BradycardiaTranscutaneous pacingDopamineEpinephrineIsoproterenol
  38. 38. Sinus Tachycardia• It is characterized by an atrial and ventricularrate of 100 beats/minute or more.• Generally the upper limit of sinus tachycardiais 160 beats/ minute.
  39. 39. Sinus TachycardiaCauses• Increased Sympathetic Stimulation Exercise Emotions/ excitement Fever Fear Acute painAny condition that require a higherbasal metabolism
  40. 40. Causes……..• Hyper metabolic States• Blood Loss• Consumption of alcohol, caffeine and tobacco.• Drugs likeAtropineDopamineDobutamineNor epinephrineamphetamines
  41. 41. • It can be a short term compensatory responseto heart failure, anemia, hypovolemia, andhypotension.• HyperthyroidismCauses……..
  42. 42. Sinus Tachycardia
  43. 43. 130 bpm• Rate?• Regularity? regularnormal0.08 s• P waves?• PR interval? 0.16 s• QRS duration?Interpretation? Sinus Tachycardia
  44. 44. Sinus Tachycardia• Deviation from NSR- Rate > 100 bpm
  45. 45. Sinus Tachycardia• Etiology: SA node is depolarizing fasterthan normal, impulse is conductednormally.• Remember: sinus tachycardia is a responseto physical or psychological stress, not aprimary arrhythmia.
  46. 46. Management• Treatment is directed at the cause• Digitalis• Beta-blockers• Diltiazem• Carotid Sinus Massage
  47. 47. Sinus Arrest/Sinus Pause• Sinus node automaticity is depressed• Impulses are not formed when expected• No P wave or no QRS complex is generated• Patient may feel palpitation from theincreased stroke volume that accompaniesthe next beet after the pause.
  48. 48. Etiology• Vagal Stimulation• Hypoxia• Myocardial ischemia• Injury to SA node• Carotid sinus sensitivity• MI• Drugs:- Digitalis, Beta-Blocker and Ca-Channel Blockers
  49. 49. ECG Characteristics• Rate- Normal unless sinus node fails toform impulse• Rhythm-Irregular• P_waves- present when SA Node Initiates• PR interval –normal if P waves present• QRS –present, absent when arrest
  50. 50. Management• Treatment is directed to the Cause• Discontinue/withheld offending drugs• Minimize Vagal Stimulation• Inj Atropine sulphate• Insertion of a permanent pacemaker
  51. 51. Sick Sinus Syndrome• The term sick sinus syndrome is used todescribe the rhythm in which there ismarked sinus bradycardia, sinus pause orperiods of sinus arrest alternating withparoxysms of rapid atrial arrhythmias.• The term brady- tachy syndrome iscommonly used to describe the samearrhythmias.
  52. 52. Causes• Inflammatory cardiac disease.• Cardiomyopathy• Sclerodegenerative process involving boththe SA and AV node• Drugsbeta-blockerscalcium-channel blockersdigitalis, amiodarone, and adenosine.
  53. 53. Etiologies of Sick Sinus SyndromeMore CommonSinus node fibrosisAtherosclerosis of theSA arteryCongenital heartdiseaseExcessive vagal toneDrugsLess CommonFamilial SSS (due tomutations in SCN5A)Infiltrative diseasesPericarditisLyme diseaseHypothyroidismRheumatic fever
  54. 54. ECG characteristics• Rate :varies from bradycardiac to tachycardiacrates depending on sinus node function andpresence of atrial tachy dysrhythmias• Rhythm: irregular• P waves : normal during sinus rhythm• PR interval : may be normal depend upon thestate of AV conduction• QRS complex: usually normal
  55. 55. Sinus bradycardia (rate of ~43 bpm) witha sinus pause
  56. 56. Abrupt termination of atrial flutter with variable AV block,followed by sinus arrest with a junctional escape beat.
  57. 57. Clinical manifestations• Patients are usually elderly and present withlightheadedness and/or syncope,• but it can also manifest as• angina,• dyspnea,• and palpitations.
  58. 58. Treatment• Ing.Atropine sulphate for brady arrhythmias• Atntiarrhyhmics like quinidine orprocainamide• Permanent pacemaker insertion
  59. 59. Rhythms originating in atria
  60. 60. Atrial TachycardiaIt is rapid atrial rhythm at a rate of 120 to 250b/min. It is due to rapid firing of an ectopicfoci present in the atriaAtrial tachycardia frequently occurs inparoxysms.
  61. 61. Possible mechanisms of atrial Tachyarrhythmias.• Two groups of fundamentally differentmechanisms are responsible for producingTachy arrhythmias• 1- those mechanisms based on some form ofabnormal impulse formation• 2- based on a disorder of impulse conduction,leading to circulating excitation or reentry.
  62. 62. Pathophysiology• The spontaneous depolarization in the fibersin the center of the sinus node is normallythe fastest, and therefore this depolarizationbrings these fibers to a discharge beforeothers. Thus under normal conditions,automaticity of the dominant pacemaker inthe center of the sinus node suppress thesubsidiary pacemakers in the atria.
  63. 63. • Abnormal impulse formation may bedefined as the generation of impulses byfibers other than the dominant pacemakerfibers in the centre of the sinus noderegardless of whether the abnormalimpulse is generated spontaneously orinduced by foregoing normal or abnormalactivities.
  64. 64. • Normal impulse formation is the occurrenceof a spontaneous depolarization before theonset of an action potential, the so- calleddiastolic depolarization.• If depolarization occurs either duringrepolarization or under special conditionsdirectly after repolarization the termabnormal impulse formation may be used.
  65. 65. • There are some muscle fibers in the rightatrium close to the crista terminalis that have asome characteristics of purkinje fibers (ie.Relatively low resting potential and developsspontaneous depolarization under certainconditions)
  66. 66. Etiology• RHD• COPD• Mitral valve Disease• Acute MI• Digitalis Toxicity• Caffeine• Tobacco• Alcohol
  67. 67. ECG Characteristics• Rate- 140-250/min,• Rhythm- regular unless there is block• P-wave- differ in configuration• PR interval- may be shorter and difficult tomeasure• QRS- Usually normal
  68. 68. Signs and Symptoms• Palpitation• Light headedness• Angina• Syncope
  69. 69. Management• Sedation to terminate the rate• Carotid sinus massage• Cardioversion if severe symptoms occurs• Beta-blockers• Radiofrequency catheter ablation of theectopic focus
  70. 70. Atrial FlutterA rapid well-organized contraction of the atriumat a rate of 200-350 contractions per minutewhich is fired by ectopic foci present in theatria.Atrial flutter can be classified in to two typestype-1 which is the commonest one has anatrial rate of 240-340 beats/ minute
  71. 71. Causes• Mitral valve disease• Pulmonary embolism• Thoracic surgery• Myocardial hypoxia• Electrolyte disturbances• Hypercalcaemia
  72. 72. ECG Characteristics• Rate- Atrial 250 to 350b/minVentricular 150 to 200b/min• Rhythm- Atrial Rhythm is regularVentricular may be irregular• P waves- saw tooth appearance• QRS- usually normal• PR Interval not measurable
  74. 74. 2:1 Atrial flutter
  75. 75. Signs and Symptoms• Palpitation• Chest pain• Dizziness• Blurred vision
  76. 76. Management• Carotid Sinus Massage• Digitalis• Ca Channel Blockers• Beta Blockers• Synchronized Cardioversion if 1:1
  77. 77. ATRIAL FIBRILLATION• Atrial fibrillation is an extremelyrapid and disorganized pattern ofdepolarization in the atria where therate is 400 to 600b/min.
  78. 78. Atrial fibrillationShowing multiple ectopicsFiring erratically
  79. 79. Causes• Coronary Artery Diseases• Atrial enlargement• Valve diseases• Sick sinus syndrome• Pericarditis• Lung disease• Congenital heart defects• Thyrotoxicosis
  80. 80. ECG Characteristics• Rate- atrial- 400 to 600b/minventricular- 110 to160b/min• Rhythm- irregular• P wave- not present. Atrialactivity is chaotic.• PR Interval- not measurable• QRS- Usually normal
  82. 82. Management• Cardioversion ifHemodynamically unstable• Inj DilitiazemVerapmilBeta-blockers• Anticoagulation if fibrillation ischronic
  83. 83. Complication• Mural Thrombi• Pulmonary Emboli• CHF
  85. 85. Premature Ventricular Contraction• Premature contraction that isgenerated by the ectopic focipresent in the ventricles. Whichfires independently.
  86. 86. Premature ventricular contraction
  87. 87. Etiology• Ischemia or MI• Hypoxia• Hypokalemia• Digitalis toxicity• Acidosis• Hyper metabolic states
  89. 89. • After each normal QRS complex there is oneEctopic appear
  90. 90. • After two QRS complex whichare from normal sinus rhythmthen the ectopic foci fires calledTrigeminy
  91. 91. • When 2 ectopic appearssequentially in a row or pairscalled Couplets
  92. 92. • When 3 ectopic occurssequentially in one row iscalled Triplets
  93. 93. ECG Characteristics• Rate- 60-100b/min• Rhythm- Irregular• P-waves usually present in sinusrhythm not related to PVC• QRS- wide and bizarre, greaterthan 0.12sec
  94. 94. Management• Treatment is directed to the cause• If PVCs are associated with heartdisease can be treated• Inj lidocaine bolus followed bytitrated drip
  95. 95. Ventricular Tachycardia• It is repetitive firing of theventricular ectopic foci at a ratemore than 100 to 200b/min, whichmay cause the heart to beatinefficiently.
  96. 96. Etiology• Ischemia• Acute MI• Hypoxia• Hypokalemia• Digitalis toxicity• Acidosis• Hypermetabolic states
  97. 97. ECG Characteristics• Rate- ventricular rate 100 to200b/min• Rhythm- usually regular• P-waves present if S.A.Node firesmay be buried in QRS or T• PR Interval- not measurable• QRS- wide, bizarre and greaterthan 0.12sec
  98. 98. V-TACH
  99. 99. Management• Cardioversion• Defibrillation can be done when thepatient is pulseless• Inj Lidocaine bolus and drip asmaintenance dose• Antiarrhythmic like inj Amidaroneor inj MgSo4• Resuscitative measures to keptready
  100. 100. Ventricular Fibrillation• An erratic, disorganized firing ofimpulses from the ventricles.
  101. 101. Etiology• Myocardial Infarction• V-Tach• Drug toxicity• Electrocution• Drowning
  102. 102. ECG Characteristics• Rate- rapid, uncoordinated, ineffective• Rhythm- Chaotic, irregular• P waves- not seen• PR interval- none• QRS – no formed QRS complex
  103. 103. Management• Defibrillation• CPR must be performed• Anti-arrhythmic likeinj Lidocaineinj Procainmideinj MgSo4 most commonlyused• Beta-Blockers
  104. 104. Disorders of impulse Conduction• S.A. Block• First degree AV Block• Second Degree A.V.Block» Mobitz type I» Mobitz type II• Third Degree or Complete A.V Block• Bundle Branch Block» RBBB» LBBB
  105. 105. First Degree A.V.Block• It is defined as prolonged AVconduction time of supraventricularimpulses into the ventricles.
  106. 106. Etiology• Congestive Heart Disease• Rheumatic Heart Disease• Vagal Stimulation• Digitalis• Beta-Blockers• Ca-channel Blockers
  107. 107. ECG Characteristics• Rate- 60 to 100b/min• Rhythm- Regular• P waves- normal, precede every QRS• PR Interval- Greater than 0.20 sec• QRS complex- usually normal
  108. 108. Management• Usually does not require treatment• It should be observed for progression
  109. 109. Second Degree A.V.Block• It occurs when one atrial impulseat a time fails to be conducted tothe ventricles.It is classified into two• Mobitz type I• Mobitz type II
  110. 110. Type I Second degree A.V.Block• It is a progressive increase inconduction times of consecutive atrialimpulses into the ventricles until oneimpulse fail to conduct or is ‘dropped’
  111. 111. Etiology• Aortic Valve Disease• Congestive Heart Failure• Inferior Wall MI• ASD• Drugs• Mitral Valve Prolapse
  112. 112. ECG Characteristics• Rate- usually normal• Rhythm- irregular unless 2:1conduction present• P waves- normal. Some p waves arenot conducted to the ventricle, butonly one at time fails.• PR Interval- gradually lengthens inconsecutive beats.• QRS- normal unless BBB
  113. 113. IInd Degree type I
  114. 114. Management• Treatment depends on theconduction ratio, ventricular rate• If the ventricular rate slow giveinj Atropine Sulphate• Removal of precipitating factor• Temporary pacing can be done.
  115. 115. Type II Second degree A.V.Block• It is sudden failure of conduction ofan atrial impulse to the ventricleswithout progressive increase inconduction time.
  116. 116. ECG Characteristics• Rate- normal• Rhythm- irregular• P waves- usually regular andprecede QRS.Periodically a Pwave is not followed by aQRS• PR interval- constant unless thereis block• QRS- usually normal
  117. 117. IInd Degree type II
  118. 118. Management• Pacemaker therapy because it isoften permanent and progress tocomplete block
  119. 119. Third Degree A.V. Block(Complete Block)• It is complete failure of conductionof all atrial impulses to theventricles.
  120. 120. Etiology• Congestive Heart Disease• MI• Lenegre’s disease• Cardiac Surgery• Congenital Heart Disease• Digitalis Toxicity
  121. 121. ECG Characteristics• Rate- atrial normal, Ventricularrate is less that 45/min• Rhythm- Regular• P waves- independent• PR Interval- no consistent PRinterval• QRS- Normal If ventriclescontrolled by Junctionalpacemaker, may be wide
  122. 122. Management• Onset is sudden or associated withMI pacing can be done without delay• CPR should performed if the cardiacout put severly diminished
  123. 123. Ventricular Asystole• It refers to the absence of anyventricular rhythm; there is no QRScomplex, no pulse and no cardiacoutput.
  124. 124. Management• Cardio Pulmonary Resuscitation• Endotracheal Intubation immediately• Obtain IV Access• Confirm Asystole in more than one lead• Consider immediate TranscutaneousPacing• Epinephrine 1 mg IV push q3-5 minutes– Consider Vasopressin as alternative• Atropine 1 mg IV q3-5 minutes
  125. 125. The P wave is caused by atrialdepolarization. The P wave duration isnormally less than 0.12 sec. The P wave isusually smooth and positive.The QRS complex represents ventriculardepolarization. The normal QRS intervalrange is from 0.04 sec - 0.12 sec, measuredfrom the first deflection to the end of theQRS complexThe T wave due to ventricularrepolarization The wave is normallyrounded and positive.
  126. 126. • The PR interval is the beginning of the P wave tobeginning of QRS complex. It is normally 0.12 -0.20 seconds. (onset of atrial depolarization to onset ofventricular depolarization)• The QT interval begins at the onset of the QRScomplex and to the end of the T wave.• The ST Segment represents the period ofventricular muscle contraction beforerepolarization.
  127. 127. • The ECG below illustrates primary ST-T wave abnormalities (leadsI, II, aVR, V5, V6) in a patient with RBBB. ST-T waveabnormalities such as these may be related to ischemia, infarction,electrolyte abnormalities, medications, CNS disease, etc.
  128. 128. • In the above ECG the ST-T waves are "normal" forLBBB; i.e., they are secondary to the change in theventricular depolarization sequence.
  129. 129. Wolff-Parkinson-White Preexcitation• Early ventricular activation in region of the accessory AV pathway• Short PR interval (<0.12s)• Initial slurring of QRS complex (delta wave) representing early ventricularactivation through normal ventricular muscle in region of the accessorypathway• Prolonged QRS duration (usually >0.10s)• Secondary ST-T changes due to the altered ventricular activation sequence
  130. 130. The ectopic atrial rate is 150 bpm. Some of the ectopic P waves are easily seen and indicated by thearrows. Other P waves are burried in the T waves and not so easily identified. Atrial tachycardia with AVblock is often a sign of digitalis intoxication. 3:2 and 2:1 AV block is seen in this example.
  131. 131. Premature Atrial ContractionsWhen an irritable focus in the atriafires before the next sinus impulseis due
  132. 132. Premature atrial contractions
  133. 133. Thank You