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

14. TACHYARRHYTHMIAS
CAUSE
ECTOPIC FOCI OF EXCITATION
RE ENTRY PHENOMENON

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

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

17. 1. EXTRA LONG PATHWAY

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

19. 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

22. 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

23. CONSQUENCES
 INADEQUATE
VENTRICULAR FILLING
 DEC. CARDIAC OUTPUT
 HEART FAILURE

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

25. RADIOFREQUENCY CATHETER
ABLATION

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

27. VENTRICULAR EXTRASYSTOLE

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

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

30. VENTRICULAR TACHYCARDIA

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

33. 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

34. VENTRIC. FIBRILLATION

35. VENTRIC. FIBRILLATION

37. DEFIBRILLATION

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

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

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

42. J POINT

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

46. (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

47. (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

48. (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

49. 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
DEPOLARISATI
ON
OUT OF
INFARCT
ST SEGMENT
ELEVATION

50. ST SEGMENT ELEVATION

52. ECG CHANGES IN M.I.

54. 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

55. POST M.I. CHANGES

57. ECG FEATURES
1.APPEARANCE OF Q WAVE
(WHERE EARLIER ABSENT)
2.INC. IN SIZE OF Q WAVE
(IF EARLIER PRESENT)
3.FAILURE OF PROGRESSION OF R
WAVE
4.INVERSION OF T WAVES

58. Q WAVE

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

61. HYPOKALEMIA
LONG PR INTERVAL
PROMINENT U WAVE
LATE T WAVE
INVERSION

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