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Appendix
Horizontal axis represents time. Large squares are 0.2 seconds in duration, while small squares are 0.04 seconds in duration. Vertical axis represents voltage. Large squares are 5 mm (0.5 mV), while small squares represent 1mm (0.1 mV). Paper speed is 25 mm/second. Calibration = 10 mm (full standard) or 5 mm (half standard).
Conduction System of the Heart
Depolarization originates 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.
Deflections, Intervals, and Segments
P wave. EKG deflection representing atrial depolarization. Atrial repolarization occurs during ventricular depolarization and is obscured. Normally largest in lead II. Upright in all leads except aVR. Less than 0.11 seconds long and 2.5 mV high. QRS complex. EKG deflection representing ventricular depolarization. T wave. EKG defection representing ventricular repolarization. Normally upright in all leads except aVR and less than 2.5 mm high. U Wave. Second wave following T wave. Normally less than 1/3 of height of T wave. Significance unknown. Low voltage deflections. Error occurs if interpreting EKG at full standard when it was recorded at half standard. Present in some normal individuals as well as pathological states that decrease the magnitude of the signal. P-R interval. Time required for the depolarization wave to complete atrial depolarization: be conducted through the AV node, bundle of His, and bundle branches: and arrive at the ventricular myocardial cells. Beginning of P wave to beginning of QRS. Normally 0.12 to 0.2 seconds QRS interval. Time required for the ventricular cells to depolarize. Normal duration 0.06 to 0.10 seconds. Q-T interval. Inversely proportional to heart rate. The faster the heart rate, the shorter the Q-T interval. The Q-T interval represents about 40 percent of the total time between QRS complexes (the R-R interval). In most cases, the Q-T interval lasts between 0.34 and 0.42 seconds. PR segment. Portion of the tracing falling between the end of the P wave and the beginning of the R wave. ST segment. Portion of the tracing falling between the QRS complex and the T wave. The ST segment is normally even with the baseline. ST-T Complex. Repolarization complex. The most sensitive part of the electrocardiogram. Consists of the ST segment and the T wave. Can be influenced by many nonpathological factors, including temperature, hyperventilation, and anxiety. The diagnosis of nonspecific ST-T abnormality is made when the repolarization complex is abnormal, but not suggestive of a specific diagnosis. The most common ST-T abnormalities are low T-wave voltages with slight sagging or flattening of the ST segment. J Point. Intersection between the end of the QRS complex and the onset of the ST segment.
Leads
Limb Leads
Leads I, II, III, aVR, aVL, aVF explore the electrical activity in the heart in a frontal plane; that is, the orientation of the heart seen when looking directly at the anterior chest.
Standard Limb Leads. Leads I, II, III form a set of axes 60° apart.
· Lead I. Negative electrode on the right arm and positive electrode on the left arm. · Lead II. Negative electrode on the right arm and positive electrode on the left leg. · Lead III. Negative electrode on the left arm and positive electrode on the left leg.
Augmented Voltage Leads. Leads aVR, aVL aVF 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 arm or shoulder. Negative “electrode” is formed by connecting the left arm and left foot electrodes together. · aVL. Exploring electrode located at the left arm or shoulder. Negative “electrode” is formed by connecting the right arm and left foot electrodes together. · aVF. Exploring electrode located at the left foot (leg). Negative “electrode” is formed by connecting the electrodes of the two arms together.
Right arm and left arm electrodes may be placed on the right shoulder and left shoulder, respectively.
Chest Leads
Leads Vl, V2, V3, V4, V5, V6 explore the electrical activity of the heart in the horizontal plane; that is, as if looking down on a cross section of the body at the level of the heart.
· 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.
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 in a normal EKG is nearly isoelectric in one of these leads; that is, the positive and negative deflections are about equal.
Lead Combinations
· Lateral leads. I, aVL, V4-6 · Inferior leads. II, III, aVF · Anteroseptal leads. V1-V4 (right side of heart), V1-V2 (septum), V3-V4 (anterior area of heart)
Normal EKG
Mean Electrical Activity.
Mean Electrical Activity can be represented by a vector. The length of the vector represents the magnitude of the activity (positive QRS deflection minus negative QRS deflection) and the angle represents the mean direction of the vector. A normal mean vector lies between 0 and 90 degrees, averaging 58 degrees.
Criteria for Normality
1. Pulse rate is between 60 and 100 bpm. 2. Rhythm is regular except for minor variations with respiration, usually no more than 10 percent. 3. P waves precede every QRS complex. 4. P waves are normally positive or biphasic in all leads, except aVR, and sometimes V1. 5. P waves in lead II should be upright. Otherwise sinus rhythm is not present. 6. P-R interval is the time required for completion of atrial depolarization; conduction through the AV note, bundle of His, and bundle branches; and arrival at the ventricular myocardial cells. The normal P-R interval is 0 12 to 0.20 seconds. 7. The QRS interval represents the time required for ventricular cells to depolarize. The normal duration is 0.06 to 0.10 seconds. 8. The Q-T interval is the time required for depolarization and repolarization of the ventricles. The time required is inversely proportional to the heart rate. The faster the heart rate the shorter the Q-T interval. With slow heart rates, the Q-T interval is longer. The Q-T interval represents about 40 percent 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. 9. Lead I is mirror image of aVR. 10. The QRS deflections in leads I and III approximately equal that of lead II. Similarly, the sum of The QRS deflections in aVR, aVL, and aVF should approximately equal zero. When this is not true, there is reason to suspect the electrodes were placed incorrectly or that recordings were mixed up during mounting. 11. R-wave progression occurs in the chest leads, with the transition zone (point of equal positive and negative voltages) occurring somewhere between V3 and V4.
Estimation of Heart Rate
Rates of 50 to 300 bpm. Estimated from the number of large squares in an R-R interval. Because there are 300 large squares in one minute, the number of squares between R-R intervals can be divided into 300 to approximate the rate. Rates of < 50 bpm. Estimated with the aid of markings at 3-second intervals along the graph paper. To calculate the rate, the cycles and partial cycles in a 6-second interval (two 3-second markings) are multiplied by 10.
Determination 0f Axis
Axis. Defined as the mean vector of ventricular depolarization. Normal Axis. A mean vector between 0 and 90 degrees. Average = 58 degrees.
· Right Axis Deviation (RAD). A mean vector greater than 90 degrees. · Gray Zone. A mean vector between 0 and -30 degrees. Usually considered normal. · Left Axis Deviation (LAD). A mean vector more negative than -30 degrees. · Northwest axis (no man’s land). A mean vector between -90 and +180 degrees. Right axis deviation or left axis deviation can occur in this zone, although left axis deviation is more common.
Determining the Axis of the Mean Vector
Check lead aVF.
Atrial Enlargement
Normal P wave is < 2.5 high and 0.08-0.1 seconds in duration. 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 portion.
· Lead V1. Normally closest to the atria and perpendicular to the axis of the atrial depolarization vector force. A positive deflection and then a negative deflection from the baseline, resulting in a sinusoidal appearing curve. · Lead II. Normally parallel to the axis of the atrial depolarization vector force. P wave configuration is positive deflection from baseline.
Right Atrial Enlargement (RAE). Generates an accentuated left-sided portion of the P wave. P > 2.5 mm in lead II and or greater than 1.5 mm in lead V1. Biphasic P in V1 with initial portion greater in amplitude than terminal portion. Left Atrial Enlargement (LAE). Results in an accentuated right-sided portion of the P wave > 2.5 mm in any lead. P is double humped in any lead. Negative deflection of terminal portion of P in V1.
Biatrial Enlargement
Features of both RAE and LAE. The P wave in lead II is greater than 2.5 mm tall and greater than or equal to 0.12 seconds in duration. The initial positive component of the P wave in V1 is greater than 1.5 mm tall and a prominent terminal P component is present.
Ventricular Hypertrophy
The EKG 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 (R/S > 1) or S > R in lead V6 (R/S < 1) . Left Ventricular Hypertrophy (LVH). Hypertrophy of the left ventricle causes an increase in the height and depth of the QRS complexes. LVH may be present when the sum of the S wave in V1 or V2 (whichever is larger) and the R wave in V5 or V6 (whichever is larger) > 35 mm (SV1 + RV5-6 > 35). Accuracy in diagnosing LVH can be improved by considering limb lead criteria; that is, if the sum of the R wave in lead I and the S wave in lead III equal or greater than 25 mm (RI + SIII > 25). Other criteria include R wave in aVL is > 11mm and RaVL + SV3 > 28 (M) or 20 (F). Criteria apply to individuals 35 years of age and older. Diagnosis is best made by echocardiography. 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. LVH with Strain (systolic overload). In addition to criteria for LVH, T wave inversion and ST segment depression occur in the left chest leads.
Biventricular Hypertrophy
Biventricular Hypertrophy is a difficult EKG diagnosis to make. In the presence of LAE any one of the following suggests this diagnosis: R/S ratio in V5 or V6 < 1, S in V5 or V6 > 6 mm, or RAD is present. Other suggestive EKG findings include: Criteria for LVH and RVH are both met and LVH criteria is met and RAD or RAE is present.
Intraventricular Conduction Disturbances
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 (R′). 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-R′ configuration in lead V1 with a QRS complex of 0.12 seconds or greater. 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-R′ configuration in lead V6 and a QRS interval 0.12 seconds or greater. 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 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 (LAH). Results in left axis deviation (-30 degrees or more). · Left Posterior Hemiblock (LPH). Results in right axis deviation (+90 degrees or more).
RBBB plus Hemiblock (bifascicular block). Blockage of right bundle branch plus LAH or LPH. Potentially significant since the presence of either means the ventricles are being depolarized via only on fascicle of the left bundle branch and subject to complete heart block.
· RBBB plus LAH. Produces EKG picture of RBBB plus LAD. · RBBB plus LPH. Produces EKG picture of RBBB plus RAD.
Nonspecific Intraventricular Conduction Defects. QRS duration greater than 0.10 seconds. Criteria for specific bundle branch or fascicular block not met.
Myocardial Ischemia
Myocardial ischemia is 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. Unstable Angina. Chest pain may occur while resting or even sleeping (nocturnal angina), and the discomfort may last longer and be more intense than that of stable angina. Unstable angina may be a sign of impending myocardial infarction. 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 remains in a depolarized (negative) state. The loss of positivity in the infarcted area is responsible for the characteristic Q waves that develop in the leads exploring the infarcted area. A normal EKG may exhibit small Q waves in leads I, V5, and V6 that represent 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 percent or more of the height of the R wave.
Time sequence of myocardial infarction
· 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. · Evolving phase. ST segments begin returning to their baseline, and the T waves become inserted. · 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. Myocardial infarctions 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 results in 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 (II, III, aVF). · Posterior Infarction. Does not generate Q wave formation or ST segment deviation in the conventional 12-lead EKG since there are no posterior exploring electrodes. Instead, subtle reciprocal changes in the magnitude of R waves in V1 and V2 may occur. 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.
Silent Myocardial Infarction. Incidental finding of Q waves where they shouldn’t be without a history of having had a prior myocardial infarction. 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 EKG 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. Pseudoinfarction Syndromes. Some medical conditions may show EKG characteristics that can be confused with myocardial infarction:
· Complete or incomplete LBBB (QS waves or poor R wave progression in leads V1-3). · Dramatic alterations of ST segments and T waves may occur with increased intracranial pressure due to changes in re-polarization that result from enhanced sympathetic nervous system activity. · LAH (may see small Q waves in anterior chest leads) · Left ventricular aneurysm after extensive infarction may show persistent ST segment elevation. · LVH (may have QS pattern or poor R-wave progression in leads V1-3). · Patients with hypertrophic cardiomyopathy may have significant Q waves on their electrocardiograms due to distortion of the normal pattern of depolarization because of the asymmetrical hypertrophied ventricular muscle. · Pericarditis may show ST segment elevation and subsequent T-wave inversion. However, with pericarditis there is no Q-wave formation. · Pneumothorax (loss of right precordial R waves) · Pulmonary emphysema and cor pulmonale may show loss of R waves in V1-3 and/or inferior Q waves with right axis deviation. · RVH (tall R waves in V1 or V2 may mimic true posterior MI).
Rhythm Disturbances
Sinus Rhythms. 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 relatively constant, varying no more than 10 percent with respiration.
Categories of Arrhythmias
· Regular. R-R interval constant (except for minor variation with respiration). · Basically regular. Regular except for occasional premature beats or escape beats. · Regularly irregular. R-R interval variable but with a definite pattern. (normal beats and ectopic beats grouped together and repeating over and over). · Irregularly irregular. R-R interval variable with no pattern (totally irregular).
Sinus Arrhythmias. Initiated by SA node. Rhythm is irregular or varies more than 10 percent with respiration.
· Sinus Tachycardia. Defined as sinus rhythm with a rate > 100 bpm. With fast rates, P waves may merge with preceding T waves and be indistinct. · Sinus Bradycardia. Defined as sinus rhythm with a rate < 60 bpm. · Sinoatrial Block. Refers to failure of the sinus node to function for one or more beats. In this condition, there are one or more missing beats; that is, there are no P waves or QRS complexes seen during this period of time. · 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.
Non-sinus Atrial Arrhythmias. Non-sinus atrial arrhythmias 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 also 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 bpm. P waves may or may not be seen and the condition 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 bpm. However, the AV junction is unable to contract at this rapid rate, so the ventricular rate is less-usually 150, 100, 75 bpm and so on. Atrial flutter with a ventricular rate of 150 bpm is called a two-for-one flutter because of the ratio of the atrial rate to the ventricular rate, a ventricular rate of 100 bpm is a three-to-one flutter because of the ratio of the atrial rate to the ventricular rate, and so on. · Atrial Fibrillation (AF). With AF the atria are depolarized at an extremely rapid rate, greater then 400 bpm. 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 bpm. Also characteristic of atrial fibrillation is a haphazardly irregular ventricular rhythm (variable R-R intervals).
Junctional Rhythms. Three types of junctional rhythms occur: 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. · Junctional Tachycardia. A run of three 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. · 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 bpm.
Ventricular Rhythm Disturbances. 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 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. A 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 EKG lead. Multifocal PVCs arise from different foci and give rise to different QRS patterns. · Ventricular Tachycardia (V-tach). This is defined as a run of three 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 bpm. Ventricular tachycardia is a life-threatening arrhythmia. Torsades de pointes is a form of V-tach in which the QRS complexes swing up and down around the baseline in a chaotic pattern. The disorder is related to a prolonged Q-T interval. Some medications and electrolyte imbalances may precipitate this in susceptible individuals. · Ventricular Fibrillation (V-fib). 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. It occurs 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 bpm. The QRS complex is wide and bizarre; P waves will not be present. Idioventricular rhythms are usually of short duration and require no intervention.
Supraventricular Beat with Aberration. 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 resembling a PVC. 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. Atrioventricular Heart Block. Heart block occurs in three 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 EKG abnormality is simply a prolonged P-R interval to greater than 0.2 seconds. · Second Degree Heart Block, Mobitz Type 1. The characteristic EKG 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 EKG picture is that of a series of non-conducted P waves; that is, 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 EKG 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 bpm; 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 (high or low). Trifascicular heart block is a form of third-degree heart block in which The right bundle and both branches of the left are blocked.
Bigeminy. Bigeminy is an alternating pattern of combinations of atrial-atrial, atrial-ventricular, and ventricular-ventricular beats. Trigeminy and even quadrigeminy also can occur.
Preexcitation Syndromes
Preexcitation syndromes refer to clinical conditions in which the wave of depolarization partially 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 important pre-excitation syndromes are (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 (bundle of Kent). The 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 with either normal or wide and bizarre QRS complexes depending on whether reentry via the AV node is antegrade or retrograde, respectively. Tachycardia is not required to make the diagnosis of WPW. 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, (2) 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.
Early Repolarization
Early repolarization is characterized by concave ST segment elevation in lateral leads (V5, V6, I, aVL). It is a benign condition that is more common in young, healthy, black men.
Pulmonary Embolus
The EKG is abnormal in more than two thirds of the cases, but findings are not sensitive, nor specific; and classic findings are seen in under 20 percent of the cases. The most common abnormal findings are sinus tachycardia and nonspecific ST-segment and T-wave changes. The S1Q3T3 pattern is a classic finding (S Wave in Lead I, Q Wave in Lead III, T Wave Inversion in Lead III). Other common findings include (1) atrial fibrillation or other atrial arrhythmia (new onset), (2) findings that mimic myocardial infarction (ST segment and T wave changes), (3) right axis deviation, (4) right bundle branch block (transient), (4) right sided strain pattern, and (5) T-wave inversion in precordial leads V1 through V4 The EKG is a really poor diagnostic test for pulmonary embolism. The greatest utility of the procedure in the patient with suspected pulmonary embolism is ruling out other potential life-threatening diagnoses such as myocardial infarction.
Pericarditis
The EKG in acute viral pericarditis typically shows changes that evolve over a period of three to four weeks through four stages, although only about 50 percent of patients with pericarditis demonstrate all four phases.
· Stage I. Characterized by an onset of one to two days and a duration of up to two weeks. Electrocardiographic changes include (1) diffuse, concave ST segment elevation without a distinct J point; (2) ST segment depression in leads aVR or V1 with concordant T wave changes; and (3) PR segment depression in leads II, aVF, and V4 to V6. There are no T-wave inversions at this stage. · Stage II. Characterized by a duration of days to weeks. During this period of time the ST segments return toward baseline and the T waves flatten. · Stage III. Characterized by an onset by week two or three and a duration of two to three weeks. Electrocardiographic findings include a return of ST segments to baseline and deep T wave inversion in leads II, aVF and V4 to V6. · Stage IV. Characterized by a duration of up to three months, with gradual resolution of T wave inversion and return to normal.
Athletic Heart Syndrome
Resting sinus bradycardia is the most frequent abnormal finding in EKGs of well-conditioned athletes. Marathon runners may have a heart rate as low as 35 bpm. Athletes also have a considerably higher incidence of first and second degree atrioventricular block, more premature atrial beats, and slightly more premature ventricular beats. Increased QRS complex height may be present, giving the appearance of left or right ventricular hypertrophy. Widened QRS complexes may indicate incomplete right bundle branch block. Repolarization changes may include ST segment elevation indicative of early repolarization. Flipped T waves may also occur. Despite these Findings, athletic heart syndrome is a benign condition.
Ventricular Pacemaker
The electrocardiogram of someone with a ventricular pacemaker shows a spike at the time the pacemaker fires, followed by a wide QRS complex.
Drug Effects
The drugs, digitalis and quinidine, produce major effects on an EKG that have considerable clinical significance. · 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 even 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.
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