EKg Added 2.pptx - Electrocardiogram (ECG) PDF

Electrocardiogram(ECG )  William Einthoven, a Dutch physiologist, originally developed the technique of electrocardiography. He was awarded the Nobel prize in 1924 for his contribution and is called the father of modern electrocardiography ECG refers to extracellular recording...

Electrocardiogram(ECG )  William Einthoven, a Dutch physiologist, originally developed the technique of electrocardiography. He was awarded the Nobel prize in 1924 for his contribution and is called the father of modern electrocardiography ECG refers to extracellular recording of the summed-up electrical events of all the cardiac muscle fibres generated with each heart beat. Electrically, heart behaves as a dipole, i.e. a two terminal battery in which the excited part (depolarized segment) forms a negative pole and the non excited part forms the positive pole The record of the potential fluctuations during the cardiac cycle is called the electrocardiography Electrocardiograph is the recording device  If electrodes are placed on the skin on opposite sides of the heart, electrical potentials generated by the current can be recorded; the recording is known as an electrocardiogram (ECG) In bipolar recording, both the electrodes are active and one of the active electrodes is connected to the negative terminal of the ECG machine and the other to the positive  In bipolar recording, both the electrodes are active and one of the active electrodes is connected to the negative terminal of the ECG machine and the other to the positive terminal  In unipolar recording, one electrode is active or the exploring electrode and the other is an indifferent electrode at zero potential Two types of unipolar leads are used Unipolar chest leads(precordial leads) Unipolar limb leads  Lead V1: In the right fourth intercostal space, just near the sternum. Lead V2: In the left fourth intercostal space, just near the sternum. Lead V3: Halfway between V2 and V4. Lead V4: In the left fifth intercostal space at midclavicular line. Lead V5: In the left fifth intercostal space at anterior axillary line. Lead V6: In the left fifth intercostal space at mid axillary line. Augmented limb leads Zero potential In these leads, one limb carries a positive electrode, while a central terminal represents the negative pole which is actually at zero potential. Lead aVR: Active electrode is from right arm (RA) and indifferent electrode is from left arm (LA) + left leg (LF). Lead aVL: Active electrode is from LA and indifferent electrode is from RA + LF. Lead aVF: Active electrode is from LF and indifferent electrode is from RA + LA.  Einthoven’s assumption that the body is like an electrically homogeneous plate in which the right and left shoulders and the pubic region form the corners of an equilateral triangle with heart in its centre (Einthoven’s triangle) and that two active electrodes need to be placed at the two corners of this triangle P wave ECG, composed of a P wave, a QRS complex, and a T wave. P wave is the positive, It is produced by the depolarization of atrial musculature, duration P wave is not more than 0.1 s.; P wave amplitude is from 0.1 to 0.12 mV In mitral stenosis the left atrium is hypertrophied and P wave becomes larger and prolonged. In tricuspid stenosis right atrium is hypertrophied and P wave becomes tall (0.5 mV) and peaked with normal duration.  QRS complex The Q wave is not visible in all ECG leads. Physiological Q waves may be observed in leads LI, aVL, V5 and V6 where they represent initial activation of the interventricular septum in a direction opposite to the direction of activation of the main left ventricular mass. A physiological Q wave meets the following criteria: Less than 0.04 sec in width. Less than 25 percent of R wave  QRS complex The QRS complex is caused by ventricular depolarization QRS Complex is Normally less than 0.08s(0.06-0.1s) And is measure of Intraventricular Conduction Time. Q Wave is 0.1–0.2 mV, R wave is 1.0 mV, and S wave is 0.4 mV Deep Q wave (more than 0.2mV) along with other changes is an important sign of myocardial infarction (MI) Tall R wave (more than 1.3 mV) is seen in ventricular hypertrophy. Low-voltage QRS complex (total sum less than 1.5 mV) is seen in hypothyroidism and pericardial effusion QRS complex The S wave is the negative deflection that follows the R wave, representing the terminal portion of ventricular depolarization QRS complex is prolonged in bundle branch block. QRS complex T wave The T wave is a large rounded wave produced by the rapid phase of ventricular repolarization. The T wave is normally upright in most leads with certain exceptions. It is invariably inverted in lead aVR along with inversion of the P wave and QRS complex  T wave In old age, T wave is flattened. Exercise increases its amplitude in healthy hearts. Inverted T wave is an important sign of myocardial ischaemia or infarction. Tall and peaked T wave occurs in hyperkalaemia Digitalis toxicity – Digitalis is a drug used for increasing the strength of cardiac muscle (glycoside). Nonspecific changes in T wave (inversion of T wave, biphasic T wave) may occur, biphasic T wave is the earliest sign of digitalis toxicity. T wave the greatest portion of ventricular muscle mass to repolarize first is the entire outer surface of the ventricles, especially near the apex of the heart. Normal U Wave The U wave is a small rounded wave produced by slow and late repolarization of the intraventricular Purkinje system (The repolarization of the papillary muscle), after the main ventricular mass has been repolarized It becomes prominent in hypokalemia Atrial depolarization Ventricular n depolarizatio n Ventricular repolarizatio Vectorcardiogram Point 5 is the zero reference point, and this point is the negative end of all the successive vectors. While the heart muscle is polarized between heartbeats, the positive end of the vector remains at the zero point because there is no vectorial electrical potential. However, as soon as current begins to flow through the ventricles at the beginning of ventricular depolarization, the positive end of the vector leaves the zero reference point. When the septum first becomes depolarized, the vector extends downward toward the apex of the ventricles, but it is relatively weak, thus generating the first portion of the ventricular vectorcardiogram, as shown by the positive end of vector 1. As more of the ventricular muscle becomes depolarized, the vector becomes stronger and stronger, usually swinging slightly to one side. After another 0.02 second, vector 3 represents the potential, and vector 4 occurs in another 0.01 second. Finally, the ventricles become totally depolarized, and the vector becomes zero once again, as shown at point 5. The elliptical figure generated by the positive ends of the vectors is called the QRS vectorcardiogram.  PR interval It is measured from the onset of P wave to the onset of the QRS complex. Actually it is PQ interval but Q wave is frequently absent therefore it is called P–R interval. It measures the AV conduction time, including the AV nodal delay. Its duration varies from 0.12 to 0.20 sec depending on the heart rate. It is prolonged at slow heart rates and shortened at fast heart rates  PR interval Clinical significance. Prolonged PR interval indicates AV conduction block. First degree block is produced when PR interval is between 0.2 and 0.3 s and second degree block is produced when PR interval is increased (0.3–0.45 s).  J point refers to the point on ECG J point which coincides with the end of depolarization and start of repolarization of ventricles, i.e. it occurs at the end of QRS complex At J point all parts of the ventricles are depolarized no current flows around the heart. The potential of ECG is exactly zero voltage.  QT interval It is the time from the start of the QRS complex to the end of T wave. It indicates total systolic time of ventricles, i.e. ventricular depolarization and repolarization Duration of QT interval is about 0.4 s Clinical significance. Ischaemia and any ventricular conduction defects prolong the QT interval. In hypocalcaemia also QT interval is prolonged. The Q-T interval shortens at fast heart rates and lengthens at slow heart rates  It is an isoelectric period between the end of QRS complex and ST segment beginning of T wave. Its duration is about 0.32 s. Clinical significance. ST segment is elevated in patients with MI. In fact, whenever there is current of injury the TP segment shifts away from the zero and so it does not remain at the same potential level as ST segment.  Cardiac rithym The normal heart rate varies from 60 to 100 beats per minute. Normal rate (HR 60-100) Bradycardia (HR < 60) Tachycardia (HR > 100) 1 2 3 4 5 1500 :  Electrical axis three standard limb leads LI, LII and LIII form an equilateral triangle with the heart at its center, which is called the Einthoven triangle. The Einthoven triangle can be redrawn in such a way that the three leads pass through a common central point. This constitutes a triaxial reference system with each axis separated from the other by 60°. Also the three augmented limb leads can constitute another triaxial reference system When these two triaxial systems are superimposed on each other, we can derive a hexaxial reference system in a 360° circle, with each axis separated from the other by 30° The QRS axis is expressed as a degree on the hexaxial system and represents the direction of electrical forces in the frontal plane The net deflection in any lead is the algebraic sum of the positive and negative deflections. For instance, if in any lead the positive deflection (R) is +6 and the negative deflection (S) is –2, the net deflection is +4. Electrical axis EINTHOVEN TRIANGLE Dl + Dlll = Dll  DETERMINATION OF QRS AXIS Normal QRS axis –30o to + 90o Right axis deviation + 90o to + 180o Causes Thin tall body Chronic lung disease Pulmonary embolism Ostium secondum Atrial Septal Defect Right ventricular hypertrophy Lateral wall infarction Right bundle branch block  DETERMINATION OF QRS AXIS Normal QRS axis –30o to + 90o Left axis deviation –30o to –90o Causes WPW: Wolff-Parkinson-White syndrome Obese stocky body WPW syndrome (an extra electrical pathway between the heart's upper chambers and lower chambers causes a fast heartbeat) Cardiac pacing Ostium primum ASD (Atrial septal defect. These defects are often associated with trisomy 21.) Left ventricular hypertrophy Left anterior hemiblock Inferior wall infarction Left bundle block  DETERMINATION OF QRS AXIS Normal QRS axis –30o to + 90o North-West QRS axis –90o to –180o Causes Congenital heart disease Left ventricular aneurysm  DETERMINATION OF QRS AXIS The cause of high-voltage QRS complexes is usually increased muscle mass of the heart, which ordinarily results from hypertrophy of the muscle One of the most common causes of decreased voltage of the QRS complex is a series of old myocardial infarctions with resultant diminished muscle mass and it causes prolongation of the QRS complex Another cause is excessive fluid in the pericardium (pericardial effusion “short-circuits”), pulmonary emphysema(air collection) Bundle Branch Block (commonly occurs in coronary artery disease)  Bundle Branch Block the potentials generated by the two ventricles (on the two opposite sides of the heart) almost neutralize each other. However, if only one of the major bundle branches is blocked, the cardiac impulse spreads through the normal ventricle before it spreads through the other ventricle. As a result, axis deviation occurs Vectorial Analysis of Left Axis Deviation in Left Bundle Branch Block Much of the left ventricle remains polarized for as long as 0.1 second after the right ventricle has become totally depolarized vector projects from the right ventricle toward the left ventricle. Intense left axis deviation of about −50 degrees occurs the duration of the QRS complex is also greatly prolonged as a result of extreme slowness of depolarization in the affected side of the heart This extremely prolonged QRS complex differentiates bundle branch block from axis deviation caused by hypertrophy.  Bundle Branch Block With prolonged QRS complex  Bundle Branch Block Vectorial Analysis of Right Axis Deviation in Right Bundle Branch Block When the right bundle branch is blocked, the left ventricle depolarizes far more rapidly than the right ventricle, and thus the left side of the ventricles becomes electronegative as long as 0.1 second before the right Vector negative end toward the left ventricle and its positive end toward the right ventricle. Intense right axis deviation occurs.  VENTRICULAR FIBRILLATION When the normal cardiac impulse in the normal heart has traveled through the extent of the ventricles, it has no place to go because all the ventricular muscle is refractory and cannot conduct the impulse farther. Sometime can initiate re-entry and lead to what is referred to as circus movements, which in turn cause ventricular fibrillation Different conditions can cause this impulse to continue to travel around the circle  VENTRICULAR FIBRILLATION 1. If the pathway around the circle is much longer than normal, by the time the impulse returns to the 12 o’clock position, the originally stimulated muscle will no longer be refractory, and the impulse will continue around the circle again and again. 2. If the length of the pathway remains constant but the velocity of conduction becomes decreased enough, an increased interval of time will elapse before the impulse returns to the 12 o’clock position. By this time, the originally stimulated muscle might be out of the refractory state, and the impulse can continue around the circle again and again. 3. The refractory period of the muscle might become greatly shortened. In this case, the impulse could also continue around and around the circle.  VENTRICULAR FIBRILLATION All these conditions occur in different pathological states of the human heart: 1- a long pathway typically occurs in dilated hearts; 2- a decreased rate of conduction frequently results from blockage of the Purkinje system, ischemia of the muscle, high blood potassium levels, or many other factors; 3- a shortened refractory period commonly occurs in response to various drugs, such as epinephrine, or after repetitive electrical stimulation.  VENTRICULAR FIBRILLATION The most serious of all cardiac arrhythmias is ventricular fibrillation, which, if not stopped within 1 to 3 minutes, is almost invariably fatal re-excite the same ventricular muscle over and over, never stopping many small portions of the ventricular muscle will be contracting at the same time there is no coordinated contraction of all the ventricular muscle at once After fibrillation begins, unconsciousness occurs within 4 to 5 seconds because of lack of blood flow to the brain, and irretrievable death of tissues begins to occur throughout the body within a few minutes initiater fibrillation are sudden electrical shock of the heart, ischemia of the heart muscle, or ischemia of the specialized conducting system Ventricular fibrillation Occurs when small segments of ventricular myocardium show rapid, irregular ineffective contractions. In this condition, cardiac output is zero and so the peripheral pulse is absent Causes. Ventricular fibrillation is very common during electric shock and during ischaemia of conductive system. Other causes are coronary occlusion, trauma to heart, chloroform anaesthesia and improper handling of heart during cardiac surgery. ECG appearance Undulating waves of varying frequency and amplitude. The voltage of the ECG waves in ventricular fibrillation is about 0.2-0.5 mV or less Significance. Ventricular fibrillation is the most common cause of sudden death in patients with myocardial infarcts. Premature ventricular contractions are caused by action potentials initiated by and propagated away from an ectopic focus in the ventricle. As a result, the ventricle depolarizes and contracts before it normally would. A premature ventricular contraction is often followed by a missed beat (called a compensatory pause) because the ventricular cells are still refractory when the next normal impulse emerges from the SA node  Atrial FIBRILLATION Cells in different areas of the atria depolarize, repolarize, and are excited again randomly. Consequently, no P waves appear in the electrocardiogram although there may be rapid irregular small waves apparent throughout diastole. The ventricular rate is often very irregular in atrial fibrillation because impulses enter the AV node from the atria at unpredictable times The real danger with atrial fibrillation lies in the tendency for blood to form clots in the atria in the absence of the normal vigorous coordinated atrial contraction Cardiovascular physiology Chapter 5: Cardiac abnormalities Atrial fibrillation ECG appearance is characterized by: Small irregular oscillations called F waves. There are no recognizable P waves R–R interval is irregular QRS complex and T wave are normal because the impulses that are transmitted through the AV node are conducted normally through the ventricles. Causes. Atrial fibrillations are frequently associated with enlarged atria secondary to AV valve diseases.  Atrial FIBRILLATION A frequent cause of atrial fibrillation is atrial enlargement, which can result, for example, from heart valve lesions that prevent the atria from emptying adequately into the ventricles or from ventricular failure with excess damming of blood in the atria. The dilated atrial walls provide ideal conditions of a long conductive pathway Ganong WF., S:542 Cardiovascular physiology Chapter 5: Cardiac abnormalities Atrial fibrillation is characterized by a totally irregular, rapid rate (350– 500 beats/min). In it, there occurs contraction of only small portion of the atrial musculature at one time because large portion of the atria are still in refractory period. Ventricular rate is completely irregular because only a fraction of the atrial impulses that reach the AV node are transmitted to the ventricles. Atrial flutter is said to occur with atrial rates of 220–350 beats/min. During atrial flutter, AV node is unable to transmit all of the atrial impulses and therefore the ventricular rate may be half, one-third or one-fourth of the atrial rates. Atrial flutter may result either from a single ectopic focus or a re-entry phenomenon. ECG appearance in atrial flutter: the P wave is strong and QRS-T complex follows once after two P waves or three P waves (2:1 or 3:1 rhythm).  AV block Cardiovascular physiology Chapter 5: Cardiac abnormalities 1.1. degree AV Derece AV block blok Usually AV block is caused by drugs that prolong AV conduction; these are digoxin, calcium channel blockers and beta blockers.  2. degree DegreeAV block (Type l)(MOBITZ I or WENCKEBACH) AVblock PR intervals gradually become longer until a P wave is completely blocked and does not produce a QRS complex. After a pause during which the AV node recovers, this cycle is repeated. This rhythm is accompanied by drugs such as beta blockers, digoxin and calcium channel blockers.. Ischemia involving the right coronary artery is another cause. 2. Degree AV block (MOBITZ II) Conduction ratio (from P waves to QRS complexes) is usually 2:1, 3:1, 4:1 or variable The resulting bradycardia can compromise cardiac output and It may cause AV block. This rhythm usually occurs with cardiac ischemia or an MI.  3. Degree AV block Conduction between the atria and ventricles is completely absent due to complete electrical block at or below the AV node. Third-degree AV block may be associated with ischemia involving the left coronary arteries. Myocardial Infarction Diagrammatic illustration of serial electrocardiographic patterns in anterior infarc A) Normal tracing. B) Very early pattern (hours after infarction): ST segment eleva in I, aVL, and V3–6; reciprocal ST depression in II, III, and aVF.. Diagrammatic illustration of serial electrocardiographic patterns in anterior infar A) Normal tracing. C) Later pattern (many hours to a few days): Q waves have ap in I, aVL, and V5–6. QS complexes are present in V3–4. This indicates that the major transmural infarction is underlying the area recorded by V3–4; ST segment changes persist but are of lesser degree, and the T waves are beginning to invert in the leads in which t ST segments are elevated. D) Late established pattern (many days to weeks): Q waves and QS complexes persist, the ST segme are isoelectric, and the T waves are symmetric and deeply inverted in leads that had ST elevation and in leads that had ST depression. This pattern may persist for the remainder of the patient’s life. E) Very late pattern: This may occur many months years after the infarction. The abnormal Q waves and QS complexes persist. The T waves have gradually returned to normal.  Ischemia, injury, and infarction are three stages that cardiac tissue goes through when a complete blockage occurs in a coronary artery. Q T Q T Q LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'. Anatomic Groups (Summary)  Leads II, III, and aVF provide a view of the right coronary artery or distal circumflex artery. Primary changes on ECG involving these three leads suggests a problem in the right coronary. On the other hand, leads I, aVL, and V5 - V6 provide information about the proximal circumflex artery Anteroseptal infarcts are highly specific indicators of disease of the left anterior descending (LAD) artery  Occlusion of the left coronary artery––left anterior descending branch ECG changes: ST segment elevation with tall T waves and taller-than-normal R waves in leads V 3 and V4.;MI frequently involves a large area of Anterior the myocardium and can present with cardiogenic shock, second-degree AV block Type II, or third- degree AV block. Occlusion of the right coronary artery––posterior descending branch ECG changes: ST segment elevation in leads II, III, and aVF Occlusion of the left coronary artery–– circumflex Branch ECG changes: ST segment elevation in leads I, aVL, V5, and V6 Acute posterior wall infarction Hypertrophy- ECG When one ventricle hypertrophies greatly, the axis of the heart shifts toward the hypertrophied ventricle There is more muscle on the hypertrophied side of the heart generate more potential More time is required for the depolarization wave to travel Consequently, the normal ventricle becomes depolarized considerably in advance of the hypertrophied ventricle, and this situation causes a strong vector from the normal side of the heart toward the hypertrophied side, which remains strongly positively charged. Thus, the axis deviates toward the hypertrophied ventricle. Hypertension, aortic valvular stenosis, aortic valvular regurgitation, or congenital heart conditions in which the left ventricle enlarges Right ventricle Hypertrophy- ECG hypertrophy of the right ventricle as a result of congenital pulmonary valve stenosis, Tetralogy of Fallot and interventricular septal defect. Ionic changes Plasma level of sodium Low plasma (ECF) levels of Na+ may be associated with low voltage ECG complexes. Plasma levels of potassium Depending upon the levels of plasma K+ following ECG changes are seen: 1. With normal plasma levels of K+ (4–5.5 mEq/L). The normal ECG tracings are produced with PR interval = 0.16 s; QRS interval = 0.06 s, QT interval = 0.4 s. 2. Hyperkalaemia, i.e. increase in plasma K+ is very dangerous and potentially lethal condition because of its effects on heart. Hyperkalaemia with plasma K+ ± 7.0 mEq/L The T wave become tall and peaked Ionic changes In hyperkalaemia with plasma K+ levels, 8.5 mEq/L the ECG shows Broad and slurred QRS complex with a QRS interval of 0.2 s occurs due to paralysis of atria T wave remains tall and slender A further increase in plasma K+ levels may result in ventricular tachycardia and ventricular fibrillation As the extracellular K+ concentration increases, eventually the fibres become unexcitable, and the heart stops in diastole Ionic changes Hypokalaemia, i.e. decrease in the plasma levels of potassium is a serious condition but it is not as rapidly fatal as hyperkalaemia. It PR interval is prolonged, produces U waves thebecome following changes in ECG prominent, ST segment is depressed, Late T wave inversion may occur in the precordial leads and If the T and U waves merge, the apparent QT interval is often prolonged, but if the T and U waves are separated, the true QT interval is of normal duration. Ionic changes Long QT syndrome. Long QT syndrome occurs due to genetic abnormality which blocks one type of K+ channels KVLQT1 resulting in slow K+ efflux, prolonging cardiac action potential and hence QT interval. The incidence of ventricular arrhythmia and sudden death is more with prolonged QT interval In this syndrome patients are also predispose to ventricular arrhythmia “twisting of the points.” Ionic changes Hypercalcaemia, increased in extracellular Ca2+, clinically is rare if ever high enough to affect the heart. However, when large amounts of calcium are infused into experimental animals, the heart relaxes less during diastole and eventually stops in systole (calcium rigor). Hypocalcaemia, decreased plasma level of Ca2+ produces prolongation of the ST segment and consequently the QT interval is also increased.