Pathological Arrhythmias/ Tachyarrhythmias

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2 Pathological Arrhythmias/ Tachyarrhythmias caused by: 1.Ectopic focus: Extrasystole or premature beat. If discharge is occasional. Can be: Atrial Extrasystole Vevtricular Extrasystole

3 2.Cardiac Arrhythmia Caused by Ectopic focus discharging repetitively & rate is higher than SAN Circus movement

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5 Circus movement 1. Wave of excitation continue to travel indefinitely in myocardium 2. Retrograde conduction due to transient block in bundle of HIS 3. Wolff-Parkinson-White Syndrome

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8 CARDIAC ARRHYTHMIAS ATRIAL VENTRICULAR EXTRASYSTOLE HR 220 EXTRASYSTOLE FLUTTER HR V. Tachycardia FLUTTER FIBRILLATION HR FIBRILLATION

9 Atrial arrhythmias Following Atrial extrasystole atrial premature cont. are frequently present in healthy persons Paraoxysmal atrial Tachycardia Atrial flutter Atrial fibrillation

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11 Pulse deficit Definition - A deficit of pulse in relation to heart rate is called pulse deficit. Causes : Premature contraction Atrial fibrillation

12 Premature contration During premature contraction, heart contracts ahead of time & if ventricles are not filled properly stroke volume decreases & in such cond. pulse wave passing to periphery may be so weak that it is not felt at the radial artery.

13 Atrial fibrillation Irregular adequate filling of ventricles results in pulse deficit

14 Atrial Flutter SAW TOOTHED ECG

15 Atrial Fibrillation

16 Ventricular Arrhythmias Ventricular tachycardia Broad, bizarre QRS complex asystole Clinically ventricular Ventricular Flutter, Ventricular Fibrillation

17 Ventricular Tachycardia

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20 Fibrillatory waves

21 Paroxysmal Tachycardia Is a bout of tachycardia which begins & ends suddenly (paroxysm= a sudden outburst) A bout can last for several minutes

22 1.Paroxysmal Atrial (atrial rate= / min) Tachycardia 2.Atrioventricular junctional Tachycardia (atrial rate= / min) 3.Ventricular Tachycardia (ventricular rate= / min) Paroxysmal supraventricular Tachycardia includes Atrial & Junctional Tachycardia

23 Myocardial Ischemia Myocardial ischaemia -Is interruption in blood supply of heart. Irreversible changes & death of muscle cells

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25 ECG changes in MI Defect in infarcted Ecg changes in Cells over lying leads 1.Rapid Repolarization ST seg elevation 3.Delayed Depolarization

26 ECG findings in MI Findings in ant. Infarct: Time Changes Leads Hrs aft. Inf. ST ele. I,aVL & V3-6 ST dep. II,III& avf Hrs to days Q wave I,aVL,&V5-6

27 Weeks ---- Q wave & QS complex persists ST seg. becomes isoelectric T wave inverted Late years -- QS complex persists, T wave normal

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30 ECG Ionic Changes Hyperkalemia ( K+)-Dangerous & lethal Tall & peaked T wave Prolongation of QRS complex Paralysis of atria Vent. Arrhythmias RMP decreases

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32 ECG in hypokalemia Hypokalemia ( K+)-less dangerous PR interval prolonged U wave prominent T wave invertion in chest leads

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34 hypercalcemia Ca++) Hypercalcemia ( Enhances myocardial contractility Heart stops in systole (Clinically this level is not reached) ++ ) Hypocalcemia ( ST seg. prolonged

35 Effect of Sodium Sodium level has little effect Low voltage ECG

36 ECG: Uses Detection of HR Ectopic focus Heart block MI Axis deviation Electrolyte imbalance Research

37 ECG limitation False negative False positive

38 HIS Electrogram

39 Cardiac Cycle Includes various changes in heart from beat to beat Mechanical changes/cardiodynamics Electrical changes

40 Events during cardiac Cycle Atria & ven. are two separate units connected by conducting tissue only Main events are Atrial contraction Atrial relaxation Ventricular contraction Ventricular relaxation

41 Atrial cycle Total duration of one cycle is 0.8 sec (HR 75/mit) Atrial cycle Atrial systole sec Atrial diastole sec

42 Ventricular Diastole Diastole sec Protodiastolic phase sec Isovolumic relaxation sec First rapid filling sec Slow filling/ diastasis sec Last rapid filling sec

43 Changes during cardiac cycle Mechanical changes Valvular changes Pressure changes in Atria Ventricles & Aorta Volume changes in ventricles

44 IV HS Last Rapid Filling 0.1 Sec s Diastasis 0.18 Sec I HS AVC IMC 0.05 Sec SLV OPEN Max Ej. 0.1 First R.F Sec III HS AVO IMR 0.08 Sec Red. Ej Sec II HS SLV Cl. PD 0.04 Sec

45 IV HS Diastasis 0.18 Sec First R.F Sec III HS AVO IMR 0.08 Sec II HS SLV Cl. PD 0.04 Sec Last Rapid Filling 0.1 Sec I HS AVC IMC 0.05 Sec SLV OPEN Max Ej. 0.1 Red. Ej Sec

46 IV HS Diastasis 0.18 Sec First R.F Sec III HS AVO IMR 0.08 Sec II HS SLV Cl. PD 0.04 Sec Last Rapid Filling 0.1 Sec I HS AVC IMC 0.05 Sec SLV OPEN Max Ej. 0.1 Red. Ej Sec

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50 I heart Sound Produced EDV=135 ml

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53 Ventricular cycle - systole Ventricular cycle Systole sec Isometric/isovolumic contraction- 0.05sec Rapid/maximum ejection sec Reduced ejection sec

54 Changes are in AV valve (atrioventricular) Mitral (bicuspid) Tricuspid Semilunar valves Aortic Pulmonary

55 Heart sounds total 4 types I, II, III,& IV I & II heard by stethoscope III & IV picked by phonocardiography Period between I & II--Systolic period Diastolic period Heart Sounds Period between II & I

56 I & II Heart Sounds ECG SYSTOlic DIASTOLIC PERIOD

57 I H.S. First heart sound Mechanism of generation: Vibrations of closing valve Turbulance of blood Vibrations of ventricular wall Two components Mitral & Tricuspid

58 Characteristics I HS Are: Prolonged & soft-----lubb Duration sec Frequency Hz Auscultation- Best heard in Mitral & Tricuspid areas

59 Auscultation- I HS Mitral Area (near apex beat)-lt. V ICS slightly inside the mid clavicular line Tricuspid Area -Lt V ICS near sternal border

60 Significance Marks beginning of systole Duration & intensity indicates condition of myocardium & A-V valves. Proper closure of A-V valves Coincides with R wave of ECG

61 Abnormalities of I HS Faint sound- Weak myocardium PR interval prolonged Calcific mitral stenosis Mitral incompetence Intense sound- more force of contraction

62 Intense sound (loud) - more force of contraction Mitral stenosis Short PR interval

63 Splitting of Mitral & Tricuspid by 10 to 30 ms. is normal Split sound---- bundle branch block.

64 II HS Mechanism of generation; Closure of semilunar valves Oscillation of Aortic & Pulmonary walls Oscillation of blood column in Aorta & Pulmonary artery

65 Auscultation-II HS Duration sec Frequency Hz. Best at Aortic & Pulmonary Auscultation Areas Aortic Area--Rt. II ICS near the sternum Lt. II ICS near the sternum Pulm. Area

66 Splitting of -II HS It has two components Aortic & Pulmonary Normal splitting During inspiration sec During expiration sec

67 Signifance -II HS Marks end of systole & beginning of diastole Clear sound indicates perfect closure of semilunar valves & there is no (incompetence) Coincides with end of T wave of ECG

68 Applied aspects Intensified if Aortic or pulmonary press. Is high Splitting in Bundle branch block

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72 III HS Mechanism- Vibrations of ventricular wall caused by rapidly entering blood Characteristics- Short, soft & low pitched Duration- 0.1 sec Auscultation- Normally not heard with stethoscope, can be recorded Appears between T & P waves of ECG

73 IV HS Mechanism- Vibration caused by last rapid filling Characteristic- Short & low pitched Duration sec Recorded by phonocardiography Falls between end of P wave & onset of Q wave

74 Phonocardiogram A microphone is applied to precordium Sounds are amplified & recorded by oscillograph The record is called phonocardiogram

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78 Murmurs Definition- are abnormal heart sounds produced during cardiac cycle Type of murmur Abnormality Systolic - Aortic/pulmonary Stenosis Mitral/Tricuspid Insuffi. Diastolic - Aortic/Pulmonary Insuffi. Mitral/Tricuspid Stenosis

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