arrhythmias (2)

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2. arrhythmiasBasil 3. arrhythmias 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. 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. Impulse Conduction & the ECGSinoatrial nodeAV nodeBundle of HisBundle BranchesPurkinje fibers 7. The PQRST P wave - Atrialdepolarization T wave - Ventricularrepolarization QRS - Ventriculardepolarization 8. The PR IntervalAtrial depolarization+delay in AV junction(AV node/Bundle of His)(delay allows time forthe atria to contractbefore the ventriclescontract) 9. The ECG Paper Horizontally One small box - 0.04 s One large box - 0.20 s Vertically One large box - 0.5 mV 10. ECG Composed of Waves And ComplexesP- WAVE QT- INTERVALQRS- COMPLEX PR- INTERVALT- WAVE ST- SEGMENT 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. Arrhythmias It is a disturbance in therhythmic patterns of the heart.Results from abnormalimpulse initiation, abnormalconduction or both mechanismtogether. 13. Four Steps to Identify Arrhythmias1- 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. Mechanisms Of ArrhythmiasArrhythmias result from1-Abnormal impulse initiation and2-Abnormal impulse conduction. 15. Mechanisms Of ArrhythmiasThe major mechanisms of arrhythmias areABNORMAL IMPULSE INITIATIONEnhanced normal automaticityAbnormal automaticityTriggered activity due to afterdepolarizationABNORMAL IMPULSE CONDUCTIONConduction blocksReentry12 16. Enhanced normal automaticity Automaticity is defined as the ability of a cellto independently initiate an action potential. 17. Classification Of Arrhythmias Disorders of ImpulseGeneration Disorders of ImpulseConduction 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. Common causes Underline cardiac disease Sympathetic stimulation Vagal stimulation Electrolyte imbalance Hypoxia 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. 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. Sinus BradycardiaCAUSES StimulationCarotid Sinus MassageIncreased vagal tone vomiting suctioning severe pain extreme emotionsDecreased sympathetic toneIntra Occular PressureValsalva maneuver 23. Disease ProcessMIUremiaRaised ICPAnorexia NervosaHypothermiaHypothyroidism 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. Stimulation of the sympathetic nervesystem that supply the heart has essentiallythe opposite effect on the heart. 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. 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. 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. 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. 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. 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. 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. DrugsDigitalisMorphine sulfateSedativesBeta-BlockersCa-Channel BlockersAmiodarone 34. 30 bpm Rate? Regularity? regularnormal0.10 s P waves? PR interval? 0.12 s QRS duration?Interpretation? Sinus Bradycardia 35. Sinus Bradycardia Deviation from NSR- Rate < 60 bpm 36. Sinus Bradycardia Etiology: SA node is depolarizing slowerthan normal, impulse is conducted normally(i.e. normal PR and QRS interval). 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. 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. Sinus TachycardiaCauses Increased Sympathetic Stimulation Exercise Emotions/ excitement Fever Fear Acute painAny condition that require a higherbasal metabolism 40. Causes.. Hyper metabolic States Blood Loss Consumption of alcohol, caffeine and tobacco. Drugs likeAtropineDopamineDobutamineNor epinephrineamphetamines 41. It can be a short term compensatory responseto heart failure, anemia, hypovolemia, andhypotension. HyperthyroidismCauses.. 42. Sinus Tachycardia 43. 130 bpm Rate? Regularity? regularnormal0.08 s P waves? PR interval? 0.16 s QRS duration?Interpretation? Sinus Tachycardia 44. Sinus Tachycardia Deviation from NSR- Rate > 100 bpm 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. Management Treatment is directed at the cause Digitalis Beta-blockers Diltiazem Carotid Sinus Massage 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. Etiology Vagal Stimulation Hypoxia Myocardial ischemia Injury to SA node Carotid sinus sensitivity MI Drugs:- Digitalis, Beta-Blocker and Ca-Channel Blockers 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. Management Treatment is directed to the Cause Discontinue/withheld offending drugs Minimize Vagal Stimulation Inj Atropine sulphate Insertion of a permanent pacemaker 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. Causes Inflammatory cardiac disease. Cardiomyopathy Sclerodegenerative process involving boththe SA and AV node Drugsbeta-blockerscalcium-channel blockersdigitalis, amiodarone, and adenosine. 53. Etiologies of Sick Sinus SyndromeMore CommonSinus node fibrosisAtherosclerosis of theSA arteryCongenital heartdiseaseExcessive vagal toneDrugsLess CommonFamilial SSS (due tomutations in SCN5A)Infiltrative diseasesPericarditisLyme diseaseHypothyroidismRheumatic fever 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. Sinus bradycardia (rate of ~43 bpm) witha sinus pause 56. Abrupt termination of atrial flutter with variable AV block