Basic Electrocardiography

an on-line introduction to EKG

Objectives

Given the CCC EKG Interpretation Worksheet and a standard EKG, the student should be able to:


General Principles and Definitions

Depolarization: Electrical activation of the myocardium.

Repolarization: Restoration of the electrical potential of the myocardial cell.

Sequence: Depolarization occurs in the sinoatrial (SA) node; current travels through internodal tracts of the atria to the atrioventricular (AV) node; then through Bundle of His, which divides into right and left bundle branches; left bundle branch divides into left anterior and posterior fascicles.

ECG: A galvanometer and electrodes with six limb leads and six chest leads. Gives a graphic recording of the electric forces generated by the heart during depolarization and repolarization. The electrocardiogram is recorded on graph paper with divisions.

P wave: ECG deflection representing atrial depolarization. Atrial repolarization occurs during ventricular depolarization and is obscured.

QRS wave: ECG deflection representing ventricular depolarization.

T wave: ECG defection representing ventricular repolarization.

ECG Electrodes: Two arrangements, bipolar and unipolar leads.

Bipolar Lead: One in which the electrical activity at one electrode is compared with that of another. By convention, a positive electrode is one in which the ECG records a positive (upward) deflection when the electrical impulse flows toward it and a negative (downward) deflection when it flows away from it.

Unipolar Lead: One in which the electrical potential at an exploring electrode is compared to a reference point that averages electrical activity, rather than to that of another electrode. This single electrode, termed the exploring electrode, is the positive electrode.

Limb Leads: I, II, III, aVR, aVL, aVF explore the electrical activity in the heart in a frontal plane; i.e., the orientation of the heart seen when looking directly at the anterior chest.

Standard Limb Leads: I, II, III; bipolar, form a set of axes 60° apart

Lead I: Composed of negative electrode on the right arm and positive electrode on the left arm.

Lead II: Composed of negative electrode on the right arm and positive electrode on the left leg.

Lead III: Composed of negative electrode on the left arm and positive electrode on the left leg.

Augmented Voltage Leads: aVR, aVL aVF; unipolar ; form a set of axes 60° apart but are rotated 30° from the axes of the standard limb leads.

aVR: Exploring electrode located at the right shoulder.

aVL: Exploring electrode located at the left shoulder.

aVF: Exploring electrode located at the left foot.

Reference Point for Augmented Leads: The opposing standard limb lead; i.e., that standard limb lead whose axis is perpendicular to the particular augmented lead.

Chest Leads: Vl, V2, V3, V4, V5, V6, explore the electrical activity of the heart in the horizontal plane; i.e., as if looking down on a cross section of the body at the level of the heart. These are exploring leads.

Reference Point for Chest Leads: The point obtained by connecting the left arm, right arm, and left leg electrodes together.

Vl: Positioned in the 4th intercostal space just to the right of the sternum.

V2: Positioned in the 4th intercostal space just to the left of the sternum.

V3: Positioned halfway between V2 and V4.

V4: Positioned at the 5th intercostal space in the mid-clavicular line.

V5: Positioned in the anterior axillary line at the same level as V4.

V6: Positioned in the mid axillary line at the same level as V4 and V5.

Vl and V2*: Monitor electrical activity of the heart from the anterior aspect, septum, and right ventricle.

V3 and V4*: Monitor electrical activity of the heart from the anterior aspect.

V5 and V6*: Monitor electrical activity of the heart from the left ventricle and lateral aspect.

Normal R Wave Progression: Vl Consists of a small R wave and a large S wave, whereas V6 consists of a small Q wave and a large R wave. Since V3 and V4 are located midway between Vl and V6, the QRS complex would be expected to be nearly isoelectric in one of these leads; i.e., the positive and negative deflections will be about equal.
 
 

Normal ECG:

The time required is proportional to the heart rate. The faster the heart rate, the faster the repolarization, and therefore the shorter the Q-T interval. With slow heart rates, the Q-T interval is longer. The Q-T interval represents about 40% of the total time between the QRS complexes (the R-R interval). In most cases, the Q-T interval lasts between 0.34 and 0.42 seconds.

Dimensions of Grids on ECG Paper: Horizontal axis represents time. Large blocks are 0.2 seconds in duration, while small blocks are 0.04 seconds in duration. Vertical axis represents voltage. Large blocks are 5mm, while small blocks represent 1mm.

Estimation of Heart Rate

Heart Rates of 50 to 300 beats/min.: Can be estimated from the number of large squares in an R-R interval. Because there are 300 large blocks in one minute, the number of blocks between R-R intervals can be divided into 300 to approximate the rate. For example, one large block between R-R intervals would be determined thusly:

Heart Rates of <50 beats/minute: Can be estimated with the aid of markings at 3-second intervals along the graph paper. To calculate the rate, the cycles on a 6-second interval (two 3-second markings) are multiplied by 10 (to give the rate per 60 seconds; i.e., per minute).

Sinus Rhythm Disturbances

Background: Sinus rhythms originate in the sinoatrial node. Diagnosis of sinus rhythms requires examining leads II and aVR for the correct polarity of the P waves. The P wave is always positive in lead II and negative in lead aVR. A P wave will precede each QRS complex, and the P-R interval should be constant.

Sinus Tachycardia: Sinus rhythm with a rate >100 beats per minute. With fast rates, P waves may merge with preceding T waves and be indistinct. Can originate from the sinoatrial node, atrial muscle, or atrioventricular junction. Often referred to as supraventricular tachycardia without specifying site of origin.

Sinus Bradycardia: Sinus rhythm with a rate <60 beats per minute

Sinoatrial Block: Refers to failure of the sinus node to function for one or more beats. In this condition, there are simply one or more missing beats; i. e., there are no P waves or QRS complexes seen. Fortunately, when the sinus fails to function for a significant period of time (sinus arrest), another part of the conduction system usually assumes the role of pacemaker. These pacing beats are referred to as escape beats and may come from the atria, the atrioventricular junction, or the ventricles.

Sick Sinus Syndrome: In elderly people, the sinus node may undergo degenerative changes and fail to function effectively. Periods of sinus arrest, sinus tachycardia, or sinus bradycardia may occur.
 
 

Atrial Arrhythmias

Background: Include premature atrial beats, paroxysmal atrial tachycardia, multi-focal atrial tachycardia, atrial flutter, and atrial fibrillation. Because the stimuli arise above the level of the ventricles, the QRS pattern usually is normal.

Premature Atrial Contraction (PAC): An ectopic beat arising somewhere in either atrium but not in the sinoatrial node. Occurs before the next normal beat is due, and a slight pause usually follows. The P wave may have a configuration different from the normal P wave and may even be of opposite polarity.

Occasionally, the P wave will not be seen because it is lost in the preceding T wave. The P-R interval may be shorter then the normal. If the premature atrial depolarization wave reaches the AV node before the node has had a chance to repolarize, it may not be conducted, and what may be seen is an abnormal P wave without a subsequent QRS complex. These premature atrial depolarization waves may be conducted to ventricular tissue before complete repolarization has occurred, and in such cases, the subsequent ventricular depolarization may take place by an abnormal pathway, generating a wide, bizarre QRS complex.

Paroxysmal Atrial Tachycardia (PAT): Defined as three or more consecutive PACs. PAT usually occurs at a regular rate, most commonly between 150 and 250 beats per minute. P waves may or may not be seen and may be difficult to differentiate from sinus tachycardia.

Multi-Focal Atrial Tachycardia (MFAT): Results from the presence of multiple, different atrial pacemaker foci. This rhythm disturbance is characterized by a tachycardia with beat-to-beat variation of the P wave morphology.

Atrial Flutter: An ectopic atrial rhythm. Instead of P waves, characteristic sawtooth waves are seen. The atrial rate in atrial flutter is usually about 300 beats per minute. However, the AV junction is unable to contract at this rapid rate, so the ventricular rate is less-usually 150, 100, 75, and so on, beats per minute. Atrial flutter with a ventricular rate of 150 beats per minute is called a two-for-one flutter because of the ratio of the atrial rate (300) to the ventricular rate (150).

Atrial Fibrillation: Here the atria are depolarized at an extremely rapid rate, greater then 400 beats per minute. This produces a characteristic wavy baseline pattern instead of normal P waves. Because the AV junction is refractory to most of the impulses reaching it, it only allows a fraction of them to reach the ventricles. The ventricular rate, therefore, is only 110-180 beats per minute. Also characteristic of atrial fibrillation is a haphazardly irregular ventricular rhythm.
 
 

Junctional Rhythms

Background: The three types of junctional rhythms are premature junctional contractions, junctional tachycardia, and junctional escape rhythms. Junctional rhythms arise in the AV junction. P waves, when seen, are opposite their normal polarity. They are called retrograde P waves. These P waves may precede, be buried in, or follow the QRS complex. Since the stimulus arises above the level of the ventricles, the QRS complex is usually of normal configuration.

Premature Junctional Contractions: Can occur since the AV junction may also serve as an ectopic pacemaker. These are similar to PACs, in that they occur before the next beat is due and a slight pause follows the premature beat.

Atrioventricular Junctional Tachycardia: A run of 3 or more premature junctional beats. Has about the same rate as PAT and often cannot be distinguished from it. The difference is not clinically significant.

Atrioventricular Junctional Escape Beat: An escape beat that occurs after a pause in the normal sinus rhythm. Atrial pacing usually resumes after the junctional beat. A junctional escape rhythm, defined as a consecutive run of atrioventricular junctional beats, may develop if the SA node does not resume the pacemaker role. Junctional escape rhythm has a rate between 40 and 60 beats per minute.
 
 

Atrioventricular Heart Blocks

Background: Heart block occurs in 3 forms: first degree. second degree, and third degree. Second degree heart block is divided into two types: Mobitz type 1 and Mobitz type 2.

First Degree Heart Block: The ECG abnormality is simply a prolonged P-R interval to greater than 0.2 seconds.

Second Degree Heart Block, Mobitz Type 1: The characteristic ECG is progressive lengthening of the P-R interval until finally a beat is dropped. The dropped beat is seen as a P wave that is not followed by a QRS complex.

Second Degree Heart Block, Mobitz Type 2: A more severe form of second degree block, since it often progresses to complete heart block. The characteristic ECG picture is that of a series of non-conducted P waves; e.g., 2:1, 3:1, 4:1, block.

Third Degree Heart Block: Also known as: Complete Heart Block. The atrioventricular junction does not conduct any stimuli from the atria to the ventricles. Instead, the atria and the ventricles are paced independently. The characteristic ECG picture is: (1) P waves are present and occur at a rate faster than the ventricular rate; (2) QRS complexes are present and occur at a regular rate, usually <60 beats per minute; and (3) the P waves bear no relationship to the QRS complexes. Thus, the P-R intervals are completely variable. The QRS complex may be of normal or abnormal width, depending on the location of the blockage in the AV junction.
 
 

Pre-Excitation Syndromes

Background: Pre-excitation syndromes refer to clinical Conditions in which the wave of depolarization bypasses the atrioventricular node as it passes from the atria to the ventricles. The time required for the wave to leave the sinoatrial node and arrive at ventricular muscle (P-R interval) is, therefore, shortened. Two pre-excitation syndromes exist (1) the Wolff-Parkinson-White syndrome, and (2) the Lown-Ganong-Levine syndrome.

Wolff-Parkinson-White Syndrome (WPW): Patients with WPW possess an accessory pathway of depolarization, the bundle of Kent. Three electrocardiographic criteria for WPW are: (1) a short P-R interval, (2) a wide QRS complex, and (3) a delta wave.

The QRS complex is widened by the delta wave in exactly the same amount as the P-R interval is shortened. The delta wave is a slurring of the initial portion of the QRS complex produced by early depolarization. The major clinical manifestation of WPW is recurrent tachycardia.

Lown-Ganong-Levine Syndrome (LGL): LGL is the result of some of the internodal fibers' (James fibers) bypassing the major portion of the atrioventricular node and terminating in the bundle of His. The three criteria for LGL are: (1) a short P-R interval without a delta wave, a) a normal QRS, and (3) recurrent paroxysmal tachycardia. It should be noted that, unlike in WPW, episodes of tachycardia are required for the diagnosis of LGL.
 
 

Intraventricular Conduction Disturbances

Background: In the normal process of ventricular depolarization, the electrical stimulus reaches the ventricles by way of the atrioventricular (AV)junction. Then the depolarization wave spreads to the main mass of the ventricular muscle by way of the right and left bundle branches. The right bundle branch is undivided, while the left divides into anterior and posterior fascicles. Normally the entire process of ventricular depolarization occurs in less than 0.1 seconds. Any process that interferes with normal depolarization of the ventricles may prolong the QRS width.

Right Bundle Branch Block (RBBB): Septal depolarization results in a small R wave in V1. Left ventricular depolarization results in an S wave. Right ventricular depolarization produces a second R wave. The delayed depolarization of the right ventricle causes an increased width of the QRS complex to at least 0.12 seconds. Hence, RBBB is characterized by an R-R1 configuration in lead V1 with a QRS complex > 0.12 seconds. RBBB occasionally can be seen in normal subjects.

Incomplete RBBB: This shows the same QRS pattern as a complete RBBB; however, the QRS duration is between 0.1 and 0.12 seconds.

Left Bundle Branch Block (LBBB): Blockage of conduction in the left bundle branch prior to its bifurcation results primarily in delayed depolarization of the left ventricle. In LBBB, the septum depolarizes from right to left, since its depolarization now is initiated by the right bundle branch. Next the right ventricle depolarizes, followed by delayed depolarization of the left ventricle, giving an R-R1 configuration in lead V6 and a QRS interval 0.12 seconds. Hence, LBBB is characterized by an R-R1 configuration in lead V6 and a QRS interval > 0.12 seconds. Unlike RBBB, LBBB always is a sign of organic heart disease.

Incomplete LBBB: This shows the same QRS pattern as a complete LBBB; however, the QRS duration is between 0.1 and 0.12 seconds.

Fascicular Blocks (hemi-blocks): These are blockages of transmission that also may occur in the anterior or posterior branches (fascicles) of the left bundle branch. The main effect of a fascicular block is to markedly change the QRS axis without changing the shape or duration of the QRS wave form.

Left Anterior Hemiblock:* This results in left axis deviation (-30 degrees or more).

Left Posterior Hemiblock:* This results in right axis deviation (+90 degrees or more).

Ventricular Arrhythmias

Background: Ventricular tissue is capable of spontaneous depolarization. When this occurs, a premature ventricular contraction (PVC) is initiated. Because the depolarization wave arises in the myocardium, it usually does not follow the normal path of ventricular depolarization. Therefore, the QRS complex is prolonged and bizarre in shape. In addition to PVCs, ectopic ventricular beats produce ventricular tachycardia and sometimes ventricular fibrillation. Ventricular escape rhythms also occur.

Premature Ventricular Contractions (PVC): PVCs are premature beats arising from the ventricles, and are analogous to premature atrial contractions and premature junctional contractions. PVCs have two major characteristics: (1) they are premature and arise before the next normal beat is expected (a P wave is not seen before a PVC), and (2) they are aberrant in appearance. The QRS complex always is abnormally wide; the T wave and the QRS complex usually point in opposite directions. The PVC usually is followed by a compensatory pause. PVCs may be unifocal or multifocal. Unifocal PVCs arise from the same ventricular site, and as a result have the same appearance on a given ECG lead. Multifocal PVCs arise from different foci and give rise to different QRS patterns.

Ventricular Tachycardia: This is defined as a run of 3 or more PVCs and may occur in bursts or paroxysmally. They may be persistent until stopped by intervention. The heart rate is usually 120 to 200 beats per minute. Ventricular tachycardia is a life-threatening arrhythmia.

Ventricular Fibrillation: This occurs when ventricles fail to beat in a coordinated fashion and, instead, twitch asynchronously. The beats are sometimes divided into coarse and fine rhythms.

Ventricular Escape Beats: A ventricular focus may initiate depolarization when a faster pacemaker does not control the rate. They occur after a pause in the regular rhythm. If a higher focus fails to pick up the rhythm, ventricular escape beats may continue. When this occurs, the rhythm is called idioventricular and has a rate usually less than 100 beats per minute. The QRS complex is wide and bizarre; P waves will not be present. Idioventricular rhythms are usually of short duration and require no intervention.

Aberrant Ventricular Depolarization: Here the depolarization wave is initiated above the ventricular level and, because it is premature, reaches the ventricles when they are in a partially depolarized state, resulting in a wide QRS complex. The following rules can be used to determine aberrant ventricular depolarization: (1) the beat is aberrant if a P wave precedes the wide QRS complex, (2) the preceding R-R interval usually is longer than the other ones, (3) most aberrant beats are conducted via the left bundle branch, giving the appearance of right bundle branch block in lead V1, and (4) the initial deflection of the wide QRS is in the same direction as that of the normal QRS complex.
 


Determination of Axis

Axis: Defined as the mean vector of ventricular depolarization.

Normal Axis: A mean vector between +90 and 0 degrees.

"Gray Zone": A mean vector between 0 and -30 degrees. Equals normal.

Right Axis Deviation: A mean vector of > +90 degrees.

Left Axis Deviation: A mean vector more negative than -30 degrees.

Determining the axis of the mean vector:

  • if lead I is positive, axis is normal.
  • if lead II is positive, it is in the gray zone.
  • if lead II is negative, there is left axis deviation.
Atrial Enlargement

Background: To evaluate atrial enlargement, look at the P waves in leads II and V1. The right atrium generates the left portion of the P wave, the left atrium generates the right as you view the ECG.

Lead II: Generally parallel to the axis of the atrial depolarization vector force. Would expect the P wave configuration to be a positive deflection from the baseline that is symmetric to its return to the baseline.

Lead V1: Generally closest to the atria and perpendicular to the axis of the atrial depolarization vector force. Would expect first a positive deflection and then a negative deflection from the baseline, resulting in a sinusoidal curve.

Right Atrial Enlargement: Generates an accentuated left-sided portion of the P wave.

Left Atrial Enlargement: Results in an accentuated right-sided portion of the P wave.
 


Ventricular Hypertrophy

Background: The ECG normally reflects left ventricular depolarization because left ventricular mass is much greater than right ventricular mass.

Right Ventricular Hypertrophy (RVH): When right ventricular muscle mass become great enough, it causes alterations in the positivity of the right chest leads. In the absence of myocardial infarction or right bundle branch block, the diagnosis of RVH can be made when right axial deviation is present and when R > S in lead V1 or S > R in lead V6.

Left Ventricular Hypertrophy (LVH): Hypertrophy of the left ventricle causes an increase in the height and depth of the QRS complexes. LVH is present when the sum of the S wave in V1 and the R wave in V5 or V6 (whichever is larger) > 35 mm. Accuracy in diagnosing LVH can be improved by considering limb lead criteria; i.e., if the sum of the R wave in lead I and the S wave in lead III > 25 mm., LVH is said to be present when either the chest lead criteria or limb lead criteria is met.

RVH with Strain (systolic overload): In addition to RVH criteria, T wave inversion and usually ST segment depression are present in the right chest leads. (ST segment T wave changes are not present in diastolic overload.)

LVH with Strain (systolic overload): In addition to criteria for LVH, T wave inversion and ST segment depression occur in the left chest leads. (ST segment and T wave changes are not present in diastolic overload.)
 
 

Myocardial Ischemia

Background: Due to insufficient oxygen supply to the ventricular muscle. It may be transient, causing angina pectoris, or more severe, causing the death of a portion of heart muscle (myocardial infarction).

Subendocardial Ischemia: Produces classic angina and subendocardial myocardial infarction. Involves the inner layer of ventricular muscle.

Transmural Ischemia: Produces Prinzmetal's angina and transmural myocardial infarction.

Involves the entire thickness of the ventricular wall.

Classic Angina: Produces transient ST segment depression (except in lead aVR, which may show reciprocal ST segment elevation). Not all patients with coronary artery disease show ST segment depression during chest pain.

Prinzmetal's Angina: Atypical angina that occurs at rest or at night and results in ST segment elevation. Thought to be caused by transient transmural ischemia due to vasospasm. May occur in individuals with otherwise normal coronary arteries.
 
 

Myocardial Infarction

Transmural Infarction: The infarcted area remain in a depolarized (negative) state. A normal variant - early repolarization - often occurs in younger individuals and may be confused with myocardial infarction. With early repolarization, however, the T wave is distinct from the elevated ST segment, whereas with myocardial infarction, it is incorporated into it. The loss of positivity in the infarcted area is responsible for the characteristic Q waves that develop in the leads exploring the infarcted area. Keep in mind that a normal ECG may exhibit small Q waves in leads I, V5, and V6 that represent only normal septal depolarization. Q waves, to be considered diagnostic of acute myocardial infarction, must (1) have a duration of at least 0.04 seconds or (2) have a depth equal to 25% or more of the height of the R wave.

Time sequence of myocardial infarctions: 3 stages:

(1) acute phase-ST segment elevations generally appear within a few minutes and may last 3 to 4 days. During this period of time, Q waves appear in the leads showing the ST segment elevations.
(2) evolving phase-ST segments begin returning to their baseline, and the T waves become inserted.
(3) resolving phase-In the weeks to months that follow, the T waves again return to the upright position. In most cases, the abnormal Q waves persist for months or even years.
Localization of Myocardial Infarction: MIs tend to be localized to left ventricular areas supplied by particular branches of the coronary arteries. They are described by their locations: anterior, inferior, and posterior.

Anterior Infarction: Subdivided into strictly anterior, anteroseptal, and anterolateral infarctions.

Strictly Anterior Infarction: Diagnostic changes in V3 and V4.

Anteroseptal Infarction: Results in loss of the normal small septal R waves in V1 and V2 as well as diagnostic changes in V3 and V4.

Anterolateral Infarction: Results in changes in more laterally situated chest leads (V5, V6), as well as left lateral limb leads (I, aVL).

Inferior Infarction: Produces changes in the leads that explore the heart from below: leads II, III, aVF.

Posterior Infarction: Does not generate Q wave formation or ST segment deviation in the conventional 12-lead ECG since there are no posterior exploring electrodes. Instead, subtle reciprocal changes in the magnitude of R waves in V1 and V2 may occur. In posterior infarction, the R waves in V1 and V2 become taller than or equal to the S waves (R/S >1) Unlike RVH, right axis deviation is not present. ST segment depression also may occur in these leads.

Subendocardial Infarction: Affects only repolarization (ST-T complex) and not depolarization (QRS complex). Hence, Q waves are not characteristic of subendocardial infarction. When subendocardial infarction occurs, the ECG may show persistent ST segment depression instead of the transient depression seen with classic angina. Persistent T wave inversion without ST segment depression may occur. The ST-T change slowly returns to normal as the infarction resolves. ECG findings must be combined with the clinical circumstance and cardiac enzymes to make the diagnosis of subendocardial infarction.

Pseudo Infarction Syndromes: LBBB and Wolff-Parkinson-White usually have significant Q waves. Left ventricular aneurysm after extensive infarction may show persistent ST segment elevation. Pericarditis may show ST segment elevation and subsequent T wave inversion; however, there is no Q wave formation. Patients with idiopathic hypertrophic subaortic stenosis often may have significant Q waves due to distortion of the normal pattern of depolarization. Dramatic alterations of ST segments and T waves may occur with increased intracranial pressure.
 
 

Patterns Caused by Drug and Electrolyte Effects

Background: The drugs digitalis and quinidine produce major effects on an ECG that have considerable clinical significance. Two electrolytes-potassium and calcium-also produce significant ECG effects.

Digitalis: Changes include modification of the ST-T contour, slowing of AV conduction, and enhancement of ectopic automaticity. Digitalis may produce characteristic scooping of the ST-T complex. The ST segment and T wave are fused together, and it is impossible to tell where one ends and the other begins. This may occur when digitalis is in the therapeutic range. With toxicity, digitalis can cause virtually any arrhythmia and all degrees of atrioventricular block.

Quinidine: Increases repolarization time and, hence, prolongs the Q-T interval. In toxic doses, may widen the QRS complex and cause ST segment depression.

Potassium: Hyperkalemia produces tall, peaked T waves, widening of the QRS complex, and prolongation of the P-R interval. Hypokalemia produces flattening of the T waves, which may unmask U waves. T waves may become inverted, and ST segment depression may occur.

Calcium: Hypercalcemia shortens ventricular repolarization time, resulting in a shortened Q-T interval. Hypocalcemia prolongs the Q-T interval.
 
 

Non-specific ST-T Wave Abnormalities

Background: Non-specific abnormalities of the ST-T wave segment are diagnosed when the repolarization complex is abnormal but does not indicate a particular diagnosis. Factors such as temperature, hyperventilation, and anxiety can influence the ST-T complex.
 
 

Low Voltage Complexes

Background: Can be caused by pericardial effusion, obesity, diffuse myocardial fibrosis, infiltration of the heart muscle by substances such as amyloid, and hypothyroidism.

Bibliography

Dubin, Dale: Rapid Interpretation of EKG’s, Third Edition. Cover Publishing Company, Tampa, FL, 1981.

Grauer, Ken: 12 Lead EKGs A “Pocket Brain” for Easy Interpretation. KG/EKG Press, Gainsville, FL.

Marriott, Henry JL: Practical Electrocardiography, Sixth Edition. Waverly Press, Inc, Baltimore, MD. 1981.

Milhorn, Jr., HT: Electrocardiology for the Family Physician: Parts 1-5. Family Practice Recertification. Vol 5, No’s 2,3,4,5 & 6. Months Feb, Mar, Apr, May & June, respectively, 1983.


R. Richter, MD
updated 6/29/05


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