Abnormal Electrocardiography

Cardiovascular Physiology

1. ABNORMAL ECG

2. SINUS BRADYCARDIA SINUS TACHYCARDIA

3. SICK SINUS SYNDROME MARKED BRADYCARDIA DIZZINESS SYNCOPE H.R < 50

4. A.V.NODE NODAL BLOCK PART OF NODE DISEASED REST OF A.V.N.TAKES OVER H.R.= 45/min INFRANODAL BLOCK DISORDER OF CONDUCTING SYSTEM BEYOND THE NODE VENTRICLES ACT AS PACEMAKER H.R. = 35/min

5. INCOMPLETE HEART BLOCK CONDUCTION BETWEEN ATRIA & VENTRICLES SLOWED BUT NOT COMPLETELY INTERRUPTED IST DEGREE ALL ATRIAL IMPULSES REACH THE VENTRICLE PR INTERVAL IS ABNORMALLY LONG

6. IST DEGREE HEART BLOCK

7. IIND DEGREE HEART BLOCK ALL ATRIAL IMPULSES NOT CONDUCTED TO THE VENTRICLES 2:1, 3:1 REGULARLY,IRREGULAR PULSE WENCKEBACH PHENOMENON PR INTERVAL LENGTHENS PROGRESSIVELY IN SEQUENTIAL BEATS TILL A VENTRICULAR BEAT IS DROPPED

8. IIND DEGREE HEART BLOCK

9. IIIRD DEGREE HEART BLOCK ATRIOVENTRICULAR CONDUCTION IS COMPLETELY INTERRUPTED VENTRICLES BEAT AT A SLOW PACE IDIOVENTRICULAR RHYTHM(40/ mt ) INDEPENDENT OF ATRIA (72/ mt ) ATRIOVENTRICULAR DISSOCATION ASYSTOLE + SYNCOPE STOKE’S ADAM SYNDROME

10. HEART BLOCK

11. BUNDLE BRANCH BLOCK EXCITATION PASSES DOWN THE BUNDLE ON NORMAL SIDE & THEN SWEEPS BACK THROUGH THE MUSCLE TO ACTIVATE VENTRICLE ON THE BLOCKED SIDE . VENTRICULAR RATE IS NORMAL LONG QRS COMPLEX (> 0.1 sec) RIGHT (RBBB) LEFT. (LBBB)

12. HEMIBLOCK BLOCKAGE IN ANTERIOR FASISCLE OF LEFT BUNDLE (LAH) BLOCKAGE IN POSTERIOR FASISCLE OF LEFT BUNDLE (LPH) BI /TRI FASISCULAR DIAGNOSIS – HIS BUNDLE ELECTROGRAM

13. TACHYARRHYTHMIAS CAUSE ECTOPIC FOCI OF EXCITATION RE ENTRY PHENOMENON

14. ECTOPIC FOCI OF EXITATION INCREASED AUTOMATICITY SINGLE DISCHARGE EXTRASYSTOLE (ATRIAL/ NODAL/VENTRICULAR) DISCHARGE RATE > S.A.NODE PAROXYSMAL TACHYCARDIA / ATRIAL FLUTTER

15. RE ENTRY CONTINUOUS PROPAGATION OF AN EXCITATION WAVE WITHIN A CLOSED CIRCUIT CIRCUS MOVEMENT

16. 1. EXTRA LONG PATHWAY

17. CIRCUS MOVEMENT 2. SLOW CONDUCTION VELOCITY 3. DECREASED REFRACTORY PERIOD

18. ATRIAL ARRHYTHMIAS FLUTTER RATE= 200 -350/min 2: 1 OR GREATER BLOCK “SAWTOOTH” PATTERN OF WAVES FIBRILLATION RATE= 350 - 500/min HIGHLY IRREGULAR CONTRACTION VENTRICULAR RATE = 80 -160/min

19. WOLFF PARKINSON-WHITE SYNDROME ACCELERATED A/V CONDUCTION VIA EXTRA BUNDLE OF KENT WHICH CONDUCTS FASTER THAN AVN NO A.V.NODAL DELAY SETS UP CIRCUS MOVEMENT SHORT PR INTERVAL PROLONGED QRS COMPLEX PREDISPOSES TO ATRIAL ARRYTHMIAS

20. CONSQUENCES INADEQUATE VENTRICULAR FILLING DEC. CARDIAC OUTPUT HEART FAILURE

21. TREATMENT INCREASE REFLEX VAGAL DISCHARGE OCULOCARDIAC REFLEX PRESSURE ON EYEBALL MASSAGING THE CAROTID SINUS

22. RADIOFREQUENCY CATHETER ABLATION

23. VENTRICULAR ARRYHTHMIAS QRS COMPLEX BIZARRELY SHAPED, PROLONGED AS SLOW SPREAD THROUGH THE VENTRICLE

24. VENTRICULAR EXTRASYSTOLE

25. LONG QT SYNDROME CONGENITAL (MUTATION IN K+ CHANNEL GENE) MYOCARDIAL ISCHEMIA DRUGS ELECTROLYTE ABNORMALITIES HIGH INCIDENCE OF VENTRIC. ARRYHTHMIAS & SUDDEN DEATH

26. PAROXYSMAL VENTRICULAR TACHYCARDIA CAUSE CIRCUS MOVEMENT RAPID,REGULAR VENTRICULAR DEPOLARISATION

27. VENTRICULAR TACHYCARDIA

28. LOWN-GANONG-LEVINE SYNDROME ATTACKS OF PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA SHORT PR INTERVAL NORMAL QRS DEFLECTION

29. VENTRICULAR FIBRILLATION VERY IRREGULAR,INEFFECTIVE CONTRACTION (BAG OF WORMS) STIMULUS IN “VULNERABLE PERIOD” MIDPORTION OF T WAVE MEDICAL EMERGENCY FATAL IF LASTS FOR > 3-5 MTS

30. VENTRIC. FIBRILLATION

31. VENTRIC. FIBRILLATION

32. DEFIBRILLATION

33. MYOCARDIAL ISCHEMIA DECREASED O2 INCREASED CO2 LACK OF NUTRIENTS ABNORMAL MEMBRANE POLARISATION

34. MYOCARDIAL ISCHEMIA PROLONGED A.P. IN APEX REPOLARISATION STARTS AT BASE. VECTOR POINTS FROM APEX TO BASE

35. MYOCARDIAL INFARCTION CURRENT FLOW BETWEEN INJURED AREA AND NORMAL AREA CONTINUES EVEN BETWEEN HEARTBEATS CURRENT OF INJURY

36. J POINT

37. MYOCARDIAL INFARCTION COMPLETE OBSTRUCTION OF BLOOD SUPPLY IRREVERSIBLE ISCHEMIC DAMAGE TO CARDIAC MUSCLE CELLS

38. (I) RAPID REPOLARISATION SECONDS AFTER STOPPAGE LASTS FOR A FEW MINUTES ACCELERATED OPENING OF K+ CHANNELS MEMB. POTENTIAL > NORMAL AREA HENCE, CURRENT FLOWS OUT OF INFARCTED AREA

39. (II) DECLINE IN RMP RISE IN INTERSTITIAL K+ CONC. DEPOLARISES THE INJURED AREA CURRENT FLOW INTO INFARCT FROM SURROUNDING AREAS OCCURS IN THE POLARISED STATE. DIASTOLIC CURRENT OF INJURY DISAPPEARS WHEN COMP. DEPOLARISED DEPRESSION OF TP SEGMENT OR ST SEGMENT ELEVATION

40. (III) DELAYED DEPOLARISATION ½ HOUR AFTER INFARCTION INFARCTED AREA BECOMES POSITIVE AS COMPARED TO THE HEALTHY TISSUE CURRENT FLOWS OUT OF INJURED AREA DURING SYSTOLE (DEPOL./REPOLARISATION) SYSTOLIC CURRENT OF INJURY DISAPPEARS WHEN COMP. REPOLARISED ST SEGMENT ELEVATION

41. DEFECT CURRENT FLOW ECG CHANGES RAPID RE POLARISATION OUT OF INFARCT ST SEGMENT ELEVATION DEC. RMP INTO INFARCT TQ SEGMENT DEPRESSION SEEN AS ST SEGMENT ELEVATION LATE DEPOLARISATION OUT OF INFARCT ST SEGMENT ELEVATION

42. ST SEGMENT ELEVATION

43. ECG CHANGES IN M.I.

44. AFTER DAYS / WEEKS DEAD AREA BECOMES ELECTRICALLY SILENT INJURY CURENT DISAPPEARS ST SEGMENT RETURNS TO NORMAL ALTERATION IN MAGNITUDE & DIRECTION OF CARDIAC VECTORS DURING CARDIAC CYCLE

45. POST M.I. CHANGES

46. ECG FEATURES APPEARANCE OF Q WAVE (WHERE EARLIER ABSENT) INC. IN SIZE OF Q WAVE (IF EARLIER PRESENT) FAILURE OF PROGRESSION OF R WAVE INVERSION OF T WAVES

47. Q WAVE

48. HYPERKALEMIA RMP DECREASES TALL PEAKED T WAVES ATRIAL PARALYSIS PROLONGATION OF QRS COMPLEXES VENTRICULAR ARRHYTHMIAS UNEXCITABLE HEART DIASTOLIC ARREST

49. HYPOKALEMIA LONG PR INTERVAL PROMINENT U WAVE LATE T WAVE INVERSION

50. HYPERCALCEMIA INC. MYOCARDIAL CONTRACTILITY SPEND LESS TIME IN DIASTOLE STOPS IN SYSTOLE SYSTOLIC ARREST RARELY SEEN