Pathological Arrhythmias/ Tachyarrhythmias caused by: 1.Ectopic focus: Extrasystole or premature beat. If discharge is occasional. Can be: Atrial Extrasystole Vevtricular Extrasystole
2.Cardiac Arrhythmia Caused by Ectopic focus discharging repetitively & rate is higher than SAN Circus movement
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
CARDIAC ARRHYTHMIAS ATRIAL VENTRICULAR EXTRASYSTOLE HR 220 EXTRASYSTOLE FLUTTER FIBRILLATION HR 200-350 HR 300-500 V. Tachycardia FLUTTER FIBRILLATION
Atrial arrhythmias Following Atrial extrasystole atrial premature cont. are frequently present in healthy persons Paraoxysmal atrial Tachycardia Atrial flutter Atrial fibrillation
Pulse deficit Definition - A deficit of pulse in relation to heart rate is called pulse deficit. Causes : Premature contraction Atrial fibrillation
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.
Atrial fibrillation Irregular adequate filling of ventricles results in pulse deficit
Atrial Flutter SAW TOOTHED ECG
Atrial Fibrillation
Ventricular Arrhythmias Ventricular tachycardia Broad, bizarre QRS complex asystole Ventricular Flutter, Ventricular Fibrillation Clinically ventricular
Ventricular Tachycardia
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Fibrillatory waves
Paroxysmal Tachycardia Is a bout of tachycardia which begins & ends suddenly (paroxysm= a sudden outburst) A bout can last for several minutes
1.Paroxysmal Atrial (atrial rate= 160-220/ min) Tachycardia 2.Atrioventricular junctional Tachycardia (atrial rate= 120-200/ min) 3.Ventricular Tachycardia (ventricular rate= 140-220/ min) Paroxysmal supraventricular Tachycardia includes Atrial & Junctional Tachycardia
Myocardial Ischemia Myocardial ischaemia -Is interruption in blood supply of heart. Irreversible changes & death of muscle cells
ECG changes in MI Defect in infarcted Ecg changes in Cells over lying leads 1.Rapid Repolarization ST seg elevation 3.Delayed Depolarization
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
Weeks ---- Q wave & QS complex ST seg. becomes isoelectric T wave inverted persists Late years -- QS complex persists, T wave normal
ECG Ionic Changes Hyperkalemia ( K+)-Dangerous & lethal Tall & peaked T wave Prolongation of QRS complex Paralysis of atria Vent. Arrhythmias RMP decreases
ECG in hypokalemia Hypokalemia ( K+)-less dangerous PR interval prolonged U wave prominent T wave invertion in chest leads
hypercalcemia Hypercalcemia ( Ca++) Enhances myocardial contractility Heart stops in systole (Clinically this level is not reached) Hypocalcemia ( ST seg. prolonged ++ )
Effect of Sodium Sodium level has little effect + ----Low voltage ECG
ECG: Uses Detection of HR Ectopic focus Heart block MI Axis deviation Electrolyte imbalance Research
ECG limitation False negative False positive
HIS Electrogram
Cardiac Cycle Includes various changes in heart from beat to beat Mechanical changes/cardiodynamics Electrical changes
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
Atrial cycle Total duration of one cycle is 0.8 sec Atrial cycle Atrial systole-------0.1 sec Atrial diastole------0.7 sec (HR 75/mit)
Ventricular Diastole Diastole----0.5 sec Protodiastolic phase---------0.04 sec Isovolumic relaxation--------0.08 sec First rapid filling--------------0.10 sec Slow filling/ diastasis--------0.18 sec Last rapid filling--------------0.10 sec
Changes during cardiac cycle Mechanical changes Valvular changes Pressure changes in Atria Ventricles & Aorta Volume changes in ventricles
s Diastasis 0.18 Sec IV HS Last Rapid Filling 0.1 Sec I HS AVC IMC 0.05 Sec SLV OPEN First R.F. 0.10 Sec Max Ej. 0.1 III HS AVO IMR 0.08 Sec Red. Ej. 0.15 Sec II HS SLV Cl. PD 0.04 Sec
IV HS Last Rapid Filling 0.1 Sec Diastasis 0.18 Sec I HS AVC IMC 0.05 Sec SLV OPEN Max Ej. 0.1 First R.F. 0.10 Sec III HS AVO IMR 0.08 Sec Red. Ej. 0.15 Sec II HS SLV Cl. PD 0.04 Sec
IV HS Last Rapid Filling 0.1 Sec Diastasis 0.18 Sec I HS AVC IMC 0.05 Sec SLV OPEN Max Ej. 0.1 First R.F. 0.10 Sec III HS AVO IMR 0.08 Sec Red. Ej. 0.15 Sec II HS SLV Cl. PD 0.04 Sec
I heart Sound Produced EDV=135 ml
Ventricular cycle - systole Ventricular cycle Systole---------0.3 sec Isometric/isovolumic contraction- 0.05sec Rapid/maximum ejection---------- 0.10 sec Reduced ejection-------------------- 0.15 sec
Changes are in AV valve (atrioventricular) Mitral (bicuspid) Tricuspid Semilunar valves Aortic Pulmonary
Heart Sounds Period between II & I Heart sounds total 4 types I & II heard by stethoscope III & IV picked by phonocardiography Period between I & II--Systolic period Diastolic period I, II, III,& IV
I & II Heart Sounds ECG SYSTOlic DIASTOLIC PERIOD
I H.S. First heart sound Mechanism of generation: Vibrations of closing valve Turbulance of blood Vibrations of ventricular wall Two components Mitral & Tricuspid
Characteristics I HS Are: Prolonged & soft-----lubb Duration-------0.15 sec Frequency ---25---45 Hz Auscultation- Best heard in Mitral & Tricuspid areas
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
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
Abnormalities of I HS Faint sound- Weak myocardium PR interval prolonged Calcific mitral stenosis Mitral incompetence Intense sound- more force of contraction
Intense sound (loud) - more force of contraction Mitral stenosis Short PR interval
Splitting of Mitral & Tricuspid by 10 to 30 ms. is normal Split sound---- bundle branch block.
II HS Mechanism of generation; Closure of semilunar valves Oscillation of Aortic & Pulmonary walls Oscillation of blood column in Aorta & Pulmonary artery
Auscultation-II HS Duration------0.12 sec Frequency----50 Hz. Auscultation Best at Aortic & Pulmonary Areas Aortic Area--Rt. II ICS near the sternum Pulm. Area Lt. II ICS near the sternum
Splitting of -II HS It has two components Aortic & Pulmonary Normal splitting During inspiration-----0.04 sec During expiration------0.02 sec
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
Applied aspects Intensified if Aortic or pulmonary press. Is high Splitting in Bundle branch block
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
IV HS Mechanism- Vibration caused by last rapid filling Characteristic- Short & low pitched Duration-0.03 sec Recorded by phonocardiography Falls between end of P wave & onset of Q wave
Phonocardiogram A microphone is applied to precordium Sounds are amplified & recorded by oscillograph The record is called phonocardiogram
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
Ca