Cardiovascular System ECG Lecture Notes PDF

CARDIOVASCULAR SYSTEM ECG LEC.5,6 By Dr. Zainab H.H.Alamily  The Electrocardiogram  The body is a good conductor of electricity because tissue fluids have a high concentration of ions that move (creating a current) in response to poten...

CARDIOVASCULAR SYSTEM ECG LEC.5,6 By Dr. Zainab H.H.Alamily  The Electrocardiogram  The body is a good conductor of electricity because tissue fluids have a high concentration of ions that move (creating a current) in response to potential differences.  Potential differences generated by the heart are conducted to the body surface, where they can be recorded by surface electrodes placed on the skin.  The recording thus obtained is called an electrocardiogram ( ECG or EKG ); the recording device is called an electrocardiograph.  Each cardiac cycle produces three distinct ECG waves, designated P, QRS, and T  The tracings are usually made at a standard recording speed of 25 mm/sec and amplification (1 mV = 1 cm deflection).  These tracings are made over the standard ECG paper.  This paper is divided into small squares.  Each small square on horizontal axis represents 0.04 sec. Five small squares represent 0.20 sec.  Horizontal axis determine the duration of waveform, segment or interval.  Each small square on vertical axis represents 0.1 mV. Five small squares represent 0.5 mV.  Vertical axis determine the amplitude of waveform, segment or interval.  The Electrocardiogram (ECG - EKG):  The names of the various waves and segments of the ECG in humans are:  P wave: is produced by atrial depolarization,  QRS complex by ventricular depolarization, and  T wave by ventricular repolarization.  The U wave is (inconstant) believed to be due to slow repolarization of the papillary muscles. Below, the intervals between the various ECG waves and the events that occur during them are shown:  The P wave, PR interval and PR segment  The P wave reflects atrial depolarization (activation).  The PR interval is the distance between the onset of P wave to the onset of QRS complex. F O  The PR interval is assessed to determine whether impulse O conduction from atria to ventricles is normal. T E  The flat line between end of P wave and onset of QRS complex R is called PR segment.  PR segment reflects slow impulse conduction through AV node.  It serves as baseline or reference line (isoeletrical line)  The QRS complex  It represents depolarization (activation) of the ventricles.  It always referred to as QRS complex, it may not always display all three waves.  Since the electrical vector generated of left ventricle is many times larger than that generated by right ventricle, the QRS complex is actually a reflection of left F venticular depolarization. O  QRS duration is the time interval between onset and end of QRS complex. O T  A short QRS complex is desirable as it proves that ventricles depolarized rapidly E which in turn implies that conduction system function properly. R  Wide QRS complex indicates the venticular depolarization is slow, which may be due to dysfunction in conductive system.  The ST Segment and The T Wave  It corresponds to plateau phase of cardiac muscle action potential  It must be studied carefully since it is altered in wide range of F conditions particularly in acute myocardial ischemia because O O ischemia causes deviation of ST segment T  The J point is the point where ST segment starts. E R  The T wave reflects a rapid repolarization of ventricles.  T wave changes occur in a wide range of conditions.  The U Wave and QT interval  Is seen occasionally, it is a positive wave occurring after T wave.  QT duration reflects a total duration of ventricular depolarization F and repolarization. O O  It is measured from onset of QRS complex to end of T wave. T E  QT duration is inversely related to heart rate. R  i.e. the QT interval increases at slower heart rate and decreases at higher heart rate.  Therefore to determine whether QT interval within normal limits, it is necessary to adjust for heart rate. F O O T E R Because the body fluids are good conductor “volume conductor”, the algebraic sum of APs of myocardial fibers can be recorded extracellularl.y. The record of these potential fluctuations during the cardiac cycle is the electrocardiogram (ECG - EKG). The ECG may be recorded by using two active or exploring electrodes (bipolar recording) or an active electrode connected to an indifferent electrode at zero potential (unipolar recording). In a volume conductor, the sum of the potentials at the angles of an equilateral triangle with a current source in the center is zero at all times. A triangle with the heart at its center (Einthoven's triangle) can be approximated by electrodes on both arms and on the left leg. These are the three standard limb leads used in ECG. If they are connected to a common terminal, an indifferent electrode that stays near zero potential is obtained. Leads  Is a graphic illustration of the electrical potential difference between two points on the skin surface that is being transmitted by the heart during the cardiac cycle.  Leads formation  Electrical activity is picked up on the skin surface by small disks called electrodes placed at various points on the body.  Two electrodes or one electrode and zero potential reference point (centre of the heart) are needed to determine the electrical potential difference between two points to produce a lead “ picture” on the ECG tracing.  Because each lead measures the heart´s electrical potential from different directions, each lead generates its own characteristic tracing.  In a volume conductor, depolarization moving toward an active electrode produces a positive deflection; whereas,depolarization moving in the opposite direction produces a negative deflection. By convention, an upward deflection is recorded when the active electrode becomes positive relative to the indifferent electrode, While, a downward deflection is recorded when the active electrode becomes negative. Bipolar (Standard Limb) Leads Bipolar (standard) limb leads were used before unipolar leads developed, recording potential differences between two limbs. Because current flows in the body fluids, the records would be obtained no matter where on the limbs the electrodes are placed. In lead I, electrodes are connected so that an upward deflection is written when the left arm becomes positive relative to the right (left arm positive). In lead II, electrodes are on the right arm and left leg, with left leg positive; In lead III, electrodes are on the left arm and left leg, with left leg positive.  Unipolar (V) Leads An additional nine unipolar leads are commonly used in clinical ECG. They record the potential difference between an exploring and an indifferent electrode, There are three unipolar limb leads: aVR (right arm), aVL (left arm), and aVF (left foot). The augmented limb leads are recordings between one limb and the other two limbs which increases the size of the potentials by 50%. There are six unipolar chest leads (precordial leads) designated V1–V6. Unipolar leads can also be inserted into the esophagus or heart. The ventricles are completely depolarized during which isoelectric portion of the electrocardiogram (ECG)? (A) PR interval (B) QRS complex (C) QT interval (D) ST segment (E) T wave Planes  Refers to a cross section of the heart being illustrated as a smooth flat surface.  Provide different perspectives of the same event (heart´s electrical activity) so more complete picture of the heart´s electrical activity can be obtained.  Frontal plane  Is a vertical cut made through the middle of the heart from top to bottom, dividing it into a front and back position.  The electrical activity is viewed from an anterior to posterior approach.  The six limb leads are viewed from the frontal plane. View of the heart  Lead I is a reflection of the lateral wall of the heart;  Leads II and III, the inferior wall.  Lead aVR provides no specific view of the heart.  Lead aVL is a reflection of electrical activity from the lateral heart wall  Lead aVF is a reflection of electrical activity from the inferior heart wall. Horizontal plane  Is a horizontal or transverse cut through the middle of the heart from side to side, dividing it into an upper and lower portion.  The electrical activity is viewed from a superior or inferior approach.  The six precordial leads are viewed from horizontal plane.  Leads V1 and V2 are called the right precordial leads; lead V3 and V4 the midprecordial leads; and leads V5 and V6 the left sided precordial leads.  An increase in the R wave with a decrease in the S wave is normally seen from V1 to V6.  More specifically lead V1 to V4 provide a view of the anteroseptal wall; leads V5 and V6 the anterolateral wall.  P wave is a small positive wave. It is small because the atria is small muscle mass. Under normal condition the P wave vector is directed downward and to the left in the frontal plane and yield a positive P wave in lead II FOOTER   Thus, aVR "looks at" the cavities of the ventricles, which means that atrial depolarization, ventricular depolarization, and ventricular repolarization move away from the exploring F electrode, and the P wave, QRS complex, and T wave are O therefore all negative (downward) deflections. O T E  aVL and aVF look at the ventricles, and the deflections are R therefore predominantly positive or biphasic.   There is no Q wave in V1 and V2, and the initial portion of the QRS complex is a small upward deflection because ventricular depolarization first moves across the midportion of the septum from left to right toward the exploring electrode. F O  The wave of excitation then moves down the septum and into the left O ventricle away from the electrode, producing a large S wave. Finally, it T moves back along the ventricular wall toward the electrode, producing E the return to the isoelectric line. R  Conversely, in the left ventricular leads (V4–V6) there may be an initial small Q wave (left to right septal depolarization), and there is a large R wave (septal and left ventricular depolarization) followed in V4 and V5 by a moderate S wave (late depolarization of the ventricular walls moving back toward the AV junction). Rate determination  In regular rhythm  Count the number of large squares between two consecutive R waves and divide 300 by this number.  Or count the number of small squares between two consecutive R waves and divide 1500 by this number  In irregular rhythm  Obtain 6 sec. or 30 large squares then count the R waves within these 30 large squares. Multiply this No. by 10. Determining the Electrical Axis from Standard Lead ECG:  Clinically, the electrical axis of the heart is estimated from two of the standard limb leads.  by determining the net potential and polarity of the recordings in leads I and III or I and II:  In lead I, the recording is positive, and in lead III, it is mainly positive but negative during part of the cycle.  Negative potential is subtracted from positive potential to determine the net potential for that lead. Each net potential is plotted on the axis of the respective lead, with the zero point at the meeting point of the leads. If net potential is positive, it is plotted in a positive direction along the lead axis. To determine the mean QRS vector, we draw perpendicular lines (dashed) from the apices of the respective lead potentials. The point of intersection of the perpendicular lines represents the apex of the mean QRS vector and the lead meeting point represents its base (zero end). Vector length represents the average QRS potential generated, while Vector direction represents the direction of the mean electrical axis. Thus, the mean electrical axis of the normal ventricles, is 59˚ positive (+59˚). Abnormal Ventricular Conditions That Cause Axis Deviation:  Mean electrical axis of the ventricles can swing even in the normal heart from about –30˚ to about +110˚.  Causes are mainly anatomical differences in the Purkinje distribution system or in musculature of different hearts. Abnormal Ventricular Conditions That Cause Axis Deviation:  Hypertrophy of One Ventricle:  When one ventricle greatly hypertrophies, the electrical axis shifts toward the hypertrophied ventricle for two reasons:  First: a greater quantity of muscle excitations, allowing for excess generation of electrical potential on that side.  Second: more time is required for the depolarization wave to travel through the hypertrophied muscle.  Consequently, the normal ventricle becomes depolarized considerably in advance of the hypertrophied ventricle,  A strong vector will point from the normal side of the heart toward the hypertrophied (strongly positively charged) side.  Thus, the axis deviates toward the hypertrophied ventricle. A  A typical ECG caused by hypertrophy of the left ventricle: It could be due to hypertension, which caused the left ventricle to hypertrophy. A similar picture occurs when the left ventricle hypertrophies as a result of aortic valvular stenosis, or regurgitation.  A typical ECG caused by hypertrophy of the right ventricle: It could be due to congenital pulmonary valve stenosis. also can occur in other congenital heart conditions that Abnormal Ventricular Conditions That Cause Axis Deviation:  Bundle Branch Block Causes Axis Deviation:  Ordinarily, both the left and the right bundle branches transmit the cardiac impulse to ventricular walls at almost same time (Left before right for fraction of a second).  If only one of the branches is blocked, the impulse spreads through the normal ventricle long before the other:  When the left bundle branch is blocked, depolarization wave spreads through the right ventricle two to three times more rapidly.  So, much of the left ventricle remain polarized (electropositive) after total depolarization of the right ventricle (electronegative).  Thus, a strong vector projects from the right toward the left ventricle, causing an intense left axis deviation.  Slowness of impulse conduction when the Purkinje system is blocked, greatly prolongs the duration of the QRS complex.  When the right bundle branch is blocked,  the left side of the ventricles becomes electronegative and  a strong vector projects from the left ventricle toward the right.  Cardiac Arrhythmias Normal Cardiac Rate:  In the normal human heart, each beat originates in the SA node (normal sinus rhythm, NSR).  The heart beats about 70 times a minute at rest.  The rate is slowed (bradycardia): - during sleep - in athletes  It is accelerated (tachycardia): - by emotion, - by exercise, - by fever, and many other stimuli. Sinus Arrhythmia:  In healthy young individuals, the heart rate accelerates during inspiration and decelerates during expiration.  It is primarily due to fluctuations in parasympathetic output to the heart; where impulses in the vagi from the lung stretch receptors inhibit the cardio- inhibitory area in the medulla.  The tonic vagal discharge that keeps the heart rate slow decreases and the heart rate rises.  Disease processes affecting the sinus node lead to marked bradycardia accompanied by dizziness (lightheadedness) and syncope (sick sinus syndrome).  Cardiac Arrhythmias:  When conduction between the atria and ventricles is slowed but not completely interrupted, incomplete heart block results:  First-degree heart block, all the atrial impulses reach the ventricles but the PR interval is abnormally long.  Second-degree heart block, not all atrial impulses are conducted.  So, ventricular beat may follow every second or third atrial beat (2:1 block, 3:1 block).  In another form, the PR interval lengthens progressively until a ventricular beat is dropped (Wenckebach phenomenon).  Sometimes one branch of the bundle of His is interrupted, causing bundle branch block.  Excitation passes normally down the intact bundle, then sweeps through muscle to activate the blocked side.  Block can also occur in the anterior or posterior fascicles (hemiblock or fascicular block).  Complete (third-degree) heart block results when conduction from atria to ventricles is completely interrupted,  the ventricles beat at a low rate (idioventricular rhythm) independently of the atria (P waves).  The block may be due to:  Disease in the AV node (AV nodal block), where the remaining nodal tissue becomes the pacemaker and the rate of the idioventricular rhythm is approximately 45 impulses/min.  Disease in the conducting system below the node (infranodal block), as in disease of the bundle of His, where the ventricular rate is lower; averaging 35 impulses/min,  In individual cases infranodal block can cause ventricular rates as low as 15 impulses/min.  There may also be periods of asystole, resulting cerebral ischemia causes dizziness and fainting (Stokes–Adams syndrome).  Ectopic Foci of Excitation:  In abnormal conditions, His–Purkinje fibers or myocardial fibers may discharge spontaneously. (increased automaticity of the heart).  If an ectopic focus discharges once, the result is an extrasystole or premature beat (atrial, nodal, or ventricular).  If the focus discharges repetitively at a higher rate than sinus rhythm, it produces rapid, regular tachycardia (atrial, ventricular, or nodal paroxysmal tachycardia). Atrial Arrhythmias:  Excitation spreading from an ectopic atrial focus stimulates the AV node prematurely (too early), produces an atrial extrasystole:  Abnormal P waves,  Usually normal QRST configurations.  A pause occurs between the extrasystole and next normal beat, i.e rhythm is "reset”,  Because, excitation may depolarize SA node which must repolarize before initiating next beat. In atrial flutter:  The atrial rate is 200 – 350 impulses/min.  There is the characteristic saw tooth pattern of flutter waves due to large counterclockwise circus movement in the right atrium.  It is almost always associated with 2:1 or greater AV block, because in adults, AV node cannot conduct more than 230 impulses/min. In atrial fibrillation:  the atria beat very rapidly (300–500/min) in a completely irregular and disorganized fashion.  Ventricles beat at a completely irregular rate, usually 80 - 160/min. (irregular AV node discharge).  Can be due to genetic predisposition, in some cases.  May be produced by one or more ectopic atrial foci.  Mostly, due to multiple circulating reentrant excitation waves in both atria.  Heart failure may complicate the picture.  Ventricular Arrhythmias:  Ventricular extrasystole: Ventricular premature beats are common and, usually benign:  Usually have bizarrely shaped prolonged QRS complexes.  Usually incapable of exciting the bundle of His, and retrograde conduction does not occur.  They are followed by a compensatory pause that is often longer than after an atrial extrasystole.  Ventricular premature beats do not interrupt or "reset" the regular sinus discharge.  As in atrial extrasystoles, they are not strong enough to produce a pulse at the wrist  They may not even open the aortic and pulmonary valves. Paroxysmal ventricular tachycardia:  A series of rapid regular ventricular depolarizations.  Usually due to “circus movement” in the ventricles.  Ventricular tachycardia is more serious. Ventricular Arrhythmias: Ventricular fibrillation:  The ventricular muscle fibers contract in a totally irregular and ineffective way,  Caused by the very rapid discharge of multiple ectopic foci or a circus movement.  The fibrillating ventricles, like the fibrillating atria, look like a quivering "bag of worms."  Ventricular fibrillation can be produced by an electric shock or an extrasystole during a “critical interval”;  the vulnerable period at the midportion of the T wave;  When some of the ventricular myocardium is depolarized, some incompletely repolarized, and some is completely repolarized.  The fibrillating ventricles cannot pump blood effectively, and circulation of the blood stops.  In absence of emergency treatment, VF that lasts more than a few minutes is fatal.  The most frequent cause of sudden death in patients with myocardial infarcts is VF. Effects of Changes in the Ionic Composition of the Blood  Changes in ECF concentration of different ions would be expected to affect the potentials of the myocardial fibers:  Clinically, a fall in the plasma Na+ level may be associated with low-voltage ECG complexes, but changes in the plasma K+ level produce severe cardiac abnormalities:  Hyperkalemia is a very dangerous and potentially lethal condition, effects on heart:  ↓RMP of the cardiac muscle fibers.  The first change in the ECG is the appearance of tall peaked T waves, a manifestation of altered repolarization.  At higher K+ levels, paralysis of the atria and prolongation of the QRS complexes and ventricular arrhythmias may develop.  The fibers eventually become unexcitable, and the heart stops in diastole. Effects of Changes in the Ionic Composition of the Blood  Hypokalemia: It is a serious condition, but it is not as fatal as hyperkalemia:  Here, conversely, there is prolongation of the PR interval,  prominent U waves, and,  occasionally, late T inversion in the precardial leads.  Hypercalcemia:  Increases in extracellular Ca+2 concentration enhance myocardial contractility.  The heart relaxes less during diastole and eventually stops in systole (calcium rigor).  Clinically in hypercalcemia, however, plasma Ca+2 level is rarely if ever high enough to affect the heart. A 30-year-old female patient’s electrocardiogram (ECG) shows two P waves preceding each QRS complex. The interpretation of this pattern is (A) decreased firing rate of the pacemaker in the sinoatrial (SA) node (B) decreased firing rate of the pacemaker in the atrioventricular (AV) node (C) increased firing rate of the pacemaker in the SA node (D) decreased conduction through the AV node (E) increased conduction through the HisPurkinje system