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Then measure to the point where the isoelectric line following the P wave transitions into the Q or R wave in the absence of an S wave. This is considered the end of the PR interval. The line that follows the QRS complex and connects it to the T wave. ST segment Begins at the isoelectric line extending from the S wave until it gradually curves upward to the T wave.

Under normal circumstances, it appears as a flat T wave line neither positive nor negative , although it may vary by 0. Measure at a point 0. The ST segment is considered elevated if it is above the baseline and considered depressed if it is below it. T wave Larger, slightly asymmetrical waveform that follows the ST segment. Peak is closer to the end than the beginning, and the first half has a more gradual slope than the second half. Normally not more than 5 mm in height in the limb leads or 10 mm in any precordial lead.

Normally oriented in the same direction as the preceding QRS complex. Measures time of ventricular depolarization and repolarization. Normal duration of 0. U wave Small upright except in lead aVL waveform sometimes seen following the T wave, but before the next P wave. P waves seen with impulses that originate in the SA node but travel through altered or damaged atria or atrial conduction pathways appear tall and rounded or peaked, notched, wide and notched or biphasic.

Absent Present P waves appear different than sinus P waves when the impulse arises from the atria instead of the sinus node. Unusual Normal, Inverted looking round Sawtooth appearing waveforms flutter waves occur when an ectopic site in the atria fires rapidly. A chaotic-looking baseline no discernible P waves More P One for waves than every occurs when many ectopic atrial sites rapidly fire. Abnormal QRS complexes Abnormally tall due to ventricular hypertrophy or abnormally small due to obesity, hyperthyroidism, or pleural effusion.

Slurred delta wave due to ventricular preexcitation. Vary from being only slightly abnormal to extremely wide and notched due to bundle branch block, intraventricular conduction disturbance, or aberrant ventricular conduction. Wide due to ventricular pacing by a cardiac pacemaker. Wide and bizarre looking due to electrical impulses originating from an ectopic or escape pacemaker site in the ventricles. H Figure Types of QRS complexes: a tall, b low amplitude, c slurred, d wide due to intraventricular conduction defect, e wide due to aberrant conduction, f wide due to bundle branch block, g wide due to ventricular cardiac pacemaker, and h various wide and bizarre complexes due to ventricular origin.

Abnormal PR intervals Abnormally short or absent due to impulse arising from low in the atria or in the AV junction. Abnormally short due to ventricular preexcitation. Absent due to ectopic site in the atria firing rapidly or many sites in the atria firing chaotically. Absent due to impulse arising from the ventricles. Longer than normal due to a delay in AV conduction. Vary due to changing atrial pacemaker site. Progressively longer due to a weakened AV node that fatigues more and more with each conducted impulse until finally it is so tired that it fails to conduct an impulse through to the ventricles.

Absent due to the P waves having no relationship to the QRS complexes. Figure Types of PR intervals: a shortened, b absent, c longer than normal, d progressively longer in a cyclical manner, e varying, and f absent due to an absence in the relationship between the atrial impulses and ventricular impulses. What is in this chapter Normal sinus rhythm characteristics Sinus bradycardia characteristics. Sinus tachycardia characteristics Sinus dysrhythmia characteristics Sinus arrest characteristics. Arise from SA node.

Normal P wave precedes each QRS complex. PR intervals are normal at 0. QRS complexes are normal. Normal sinus rhythm arises from the SA node. Each impulse travels down through the conduction system in a normal manner. Sinus bradycardia arises from the SA node. Sinus tachycardia arises from the SA node.

It is regularly irregular patterned irregularity ; seems to speed up, slow down, and speed up in a cyclical fashion. Sinus dysrhythmia arises from the SA node. Typically 60 to beats per minute, but may be slower depending on frequency and length of arrest. It is irregular where there is a pause in the rhythm the SA node fails to initiate a beat.

What is in this chapter Premature atrial complexes PACs characteristics Wandering atrial pacemaker characteristics Atrial tachycardia characteristics. Multifocal atrial tachycardia characteristics Atrial flutter characteristics Atrial fibrillatrion characteristics. Characteristics common to atrial dysrhythmias Arise from atrial tissue or internodal pathways. P waves if present that differ in appearance from normal sinus P waves precede each QRS complex. PR intervals may be normal, shortened, or prolonged. QRS complexes are normal unless there is also an interventricular conduction defect or aberrancy.

May be occasionally irregular or frequently irregular depends on the number of PACs present. It may also be seen as patterned irregularity if bigeminal, trigeminal, or quadrigeminal PACs are seen. May be upright or inverted, will appear different than those of the underlying rhythm. Will be normal duration if ectopic beat arises from the upper- or middle-right atrium. It is shorter than 0. In some cases it can also be prolonged. The pause that follows a premature beat is called a noncompensatory pause if the space between the complex before and after the premature beat is less than the sum of two R-R intervals.

When the tip of the right caliper leg fails to line up with the next R wave it is considered a noncompensatory pause. Rotate or slide the calipers over until the left leg is lined up with the second R wave mark the point where the tip of the right leg falls. Rotate or slide the calipers over until the left leg is lined up with your first mark. When the tip of the right caliper leg lines up with the next R wave it is considered a compensatory pause.

Measure first R-R interval that precedes the early beat Rotate or slide the calipers over until the left leg is lined up with the second R wave mark the point where the tip of the right leg falls Rotate or slide the calipers over until the left leg is lined up with your first mark. Compensatory pauses are typically associated with premature ventricular complexes PVCs. Premature beats occurring in a pattern One way to describe PACs is how they are intermingled among the normal beats.

Regular PACs at greater intervals than every fourth beat have no special name. Chapter 4. Narrow complex tachycardia that has a sudden, witnessed onset and abrupt termination is called paroxysmal tachycardia. Narrow complex tachycardia that cannot be clearly identified as atrial or junctional tachycardia is referred to as supraventricular tachycardia.

P waves change in morphology appearance from beat to beat at least three different shapes. Ventricular rate may be slow, normal, or fast; atrial rate is between and beats per minute. May be regular or irregular depending on whether the conduction ratio stays the same or varies. Absent, instead there are flutter waves; the ratio of atrial waveforms to QRS complexes may be , , or An atrial-to-ventricular conduction ratio of is rare. Ventricular rate may be slow, normal, or fast; atrial rate is greater than beats per minute. What is in this chapter Premature junctional complexes PJCs characteristics Junctional escape rhythm characteristics.

Accelerated junctional rhythm characteristics Junctional tachycardia characteristics. Characteristics common to junctional dysrhythmias Arise from the AV junction, the area around the AV node, or the bundle of His. P wave may be inverted when they would otherwise be upright with a short PR interval less than 0. If present, PR intervals are shortened. QRS complexes are normal unless there is an interventricular conduction defect or aberrancy. May be occasionally irregular or frequently irregular depends on the number of PJCs present. It may also be seen as patterned irregularity if bigeminal, trigeminal, or quadrigeminal PJCs are seen.

What is in this chapter Premature ventricular complexes PVCs characteristics Idioventricular rhythm characteristics. Accelerated idioventricular rhythm characteristics Ventricular tachycardia characteristics. Arise from the ventricles below the bundle of His. QRS complexes are wide greater than 0. Ventricular beats have T waves in the opposite direction of the R wave. P waves are not visible as they are hidden in the QRS complexes. May be occasionally irregular or frequently irregular depends on the number of PVCs present.

It may also be seen as patterned irregularity if bigeminal, trigeminal, or quadrigeminal PVCs are seen. PVCs are followed by a compensatory pause. Sometimes, PVCs originate from only one location in the ventricle. These beats look the same and are called uniform also referred to as unifocal PVCs. Other times, PVCs arise from different sites in the ventricles. These beats tend to look different from each other and are called multiformed multifocal PVCs. Chapter 6 Ventricular Dysrhythmias Figure Couplet of PVCs.

It may be called a salvo, run, or burst of ventricular tachycardia. Figure Run of PVCs. Chapter 6. It appears as a PVC squeezed between two regular complexes. Figure Interpolated PVC. PVC that occurs on or near the T wave can precipitate ventricular tachycardia or fibrillation. Not preceded by a P wave if seen, they are dissociated and would therefore be a 3rd-degree heart block with an idioventricular escape.

Idioventricular rhythm arises from a single site in the ventricles s. Idioventricular rhythm arises from a single site in the ventricles. QRS complexes are wide and bizarre in appearance, have T waves in the opposite direction of the R wave. Ventricular tachycardia may be monomorphic, where the appearance of each QRS complex is similar, or polymorphic, where the appearance varies considerably from complex to complex. Ventricular tachycardia Idioventricular rhythm Accelerated idioventricular rhythm to beats per minute 20 to 40 beats per minute 40 to beats per minute.

Two other conditions to be familiar with: Ventricular fibrillation VF results from chaotic firing of multiple sites in the ventricles. This causes the heart muscle to quiver, much like a handful of worms, rather than contracting efficiently. On the ECG monitor it appears like a wavy line, totally chaotic, without any logic. Asystoleis the absense of any cardiac activity. It appears as a flat or nearly flat line on the monitor screen. Characteristics common to AV heart blocks P waves are upright and round. In 1st-degree AV block PR interval is longer than normal and constant.

In 3rd-degree block there is no PR interval. QRS complexes may be normal or wide. In 2nd-degree AV heart block, Type I Wenckebach , impulses arise from the SA node but their passage through the AV node is progressively delayed until the impulse is blocked. In 3rd-degree AV heart block there is a complete block at the AV node resulting in the atria being depolarized by an impulse that arises from the SA node and the ventricles being depolarized by an escape pacemaker that arises somewhere below the AV node. Direction of ECG waveforms Depolarization and repolarization of the cardiac cells produce many small electrical currents called instantaneous vectors.

The mean, or average, of all the instantaneous vectors is called the mean vector. When an impulse is traveling toward a positive electrode, the ECG machine records it as a positive or upward deflection. When the impulse is traveling away from a positive electrode and toward a negative electrode, the ECG machine records it as a negative or downward deflection. Chapter 8. The sum of all the small vectors of ventricular depolarization is called the mean QRS vector. Because the depolarization vectors of the thicker left ventricle are larger, the mean QRS axis points downward and toward the patients left side.

If an area of the heart is enlarged or damaged, specific ECG leads can provide a view of that portion of the heart. While there are several methods used to determine the direction of the patients electrical axis, the easiest is the four-quadrant method. The four-quadrant method works in the following manner: An imaginary circle is drawn over the patients. A Me an representing one of the six limb leads. Lead I Lead I is oriented at 0 located at the three oclock position.

If the QRS complex points down negative , then the impulses are moving from left to right; this is considered abnormal.

Pocket Guide for ECGs Made Easy: 1st SAE

Persons who are thin, obese, or pregnant can have axis deviation due to a shift in the position of the apex of the heart. Myocardial infarction, enlargement, or hypertrophy of one or both of the hearts chambers, and hemiblock can also cause axis deviation. Right atrial enlargement Right ventricular hypertrophy Right bundle branch block Left atrial enlargement Left ventricular hypertrophy.

Right atrial enlargement Leads II and V1 provide the necessary information to assess atrial enlargement. Indicators of right atrial enlargement include: An increase in the amplitude of the first part of the P wave. The P wave is taller than 2. If the P wave is biphasic, the initial component is taller than the terminal component. The width of the P wave, however, stays within normal limits because its terminal part originates from the left atria, which depolarizes normally if left atrial enlargement is absent.

Chapter 9. Figure Right atrial enlargement leads to an increase in the amplitude of the first part of the P wave. Left atrial enlargement Indicators of left atrial enlargement include: The amplitude of the terminal portion of the P wave may increase in V1. The terminal left atrial portion of the P wave drops at least 1 mm below the isoelectric line in lead V1.

There is an increase in the duration or width of the terminal portion of the P wave of at least one small square 0. Often the presence of ECG evidence of left atrial enlargement only reflects a nonspecific conduction irregularity. However, it may also be the result of mitral valve stenosis causing the left atria to enlarge to force blood across the stenotic tight mitral valve.

Figure Left atrial enlargement leads to an increase in the amplitude and width of the terminal part of the P wave. Key ECG indicators of left ventricular hypertrophy include: Increased R wave amplitude in those leads overlying the left ventricle. The S waves are smaller in leads overlying the left ventricle, but larger in leads overlying the right ventricle. Figure The thick wall of the enlarged right ventricle causes the R waves to be more positive in the leads that lie closer to lead V1.

Figure The thick wall of the enlarged left ventricle causes the R waves to be more positive in the leads that lie closer to lead V6 and the S waves to be larger in the leads closer to V1. Right bundle branch block The best leads for identifying right bundle branch are V1 and V2.

Right bundle block causes the QRS complex to have a unique shape its appearance has been likened to rabbit ears or the letter M. As the left ventricle depolarizes, it produces the initial R and S waves, but as the right ventricle begins its delayed depolarization, it produces a tall R wave called the R. In the left lateral leads overlying the left ventricle I, aVL, V5, and V6 , late right ventricular depolarization causes reciprocal late broad S waves to be generated. Figure In right bundle branch block, conduction through the right bundle is blocked causing depolarization of the right ventricle to be delayed; it does not start until the left ventricle is almost fully depolarized.

Left bundle branch block Leads V5 and V6 are best for identifying left bundle branch block. QRS complexes in these leads normally have tall R waves, whereas delayed left ventricular depolarization leads to a marked prolongation in the rise of those tall R waves, which will either be flattened on top or notched with two tiny points , referred to as an R, R wave.

True rabbit ears are less likely to be seen than in right bundle branch block. Leads V1 and V2 leads overlying the right ventricle will show reciprocal, broad, deep S waves. Figure In left bundle branch block, conduction through the left bundle is blocked causing depolarization of the left ventricle to be delayed; it does not start until the right ventricle is almost fully depolarized. Left anterior hemiblock With left anterior hemiblock, depolarization of the left ventricle occurs progressing in an inferior-to-superior and right-to-left direction.

This causes the axis of ventricular depolarization to be redirected upward and slightly to the left, producing tall positive R waves in the left lateral leads and deep S waves inferiorly. Figure With left anterior hemiblock, conduction down the left anterior fascicle is blocked resulting in all the current rushing down the left posterior fascicle to the inferior surface of the heart.

Hypertrophy, Bundle Branch Block, and Preexcitation Left posterior hemiblock In left posterior hemiblock, ventricular myocardial depolarization occurs in a superior-to-inferior and left-to-right direction. This causes the main electrical axis to be directed downward and to the right, producing tall R waves inferiorly and deep S waves in the left lateral leads. This results in right axis deviation.

In contrast to complete left and right bundle branch block, in hemiblocks, the QRS complex is not prolonged. Lead aVF Small Q Figure With left posterior hemiblock, conduction down the left posterior fascicle is blocked resulting in all the current rushing down the left anterior fascicle to the myocardium. P waves are normal. QRS complexes are widened due to a characteristic slurred initial upstroke, called the delta wave.

PR interval is usually shortened less than 0. Bundle of Kent Instead of the impulse traveling through the AV node, it travels down an accessory pathway to the ventricles. The QRS complex is widened due to premature activation of the ventricles. The PR interval is less than 0. The QRS complex is not widened. There is no delta wave. WPW and LGL are called preexcitation syndromes and are the result of accessory conduction pathways between the atria and ventricles.

James fibers Instead of traveling through the AV node, the impulse is carried to the ventricles by way of an intranodal accessory pathway. Figure In LGL, the impulse travels through an intranodal accessory pathway, referred to as the James fibers, bypassing the normal delay within the AV node. What is in this chapter ECG changes associated with ischemia, injury, and infarction Identifying the location of myocardial ischemia, injury, and infarction Anterior Septal Lateral Inferior Posterior.

Changes in the ST segment depression or elevation. Enlarged Q waves or appearance of new Q waves. ST segment elevation is the earliest reliable sign that myocardial infarction has occurred and tells us the myocardial infarction is acute. Pathologic Q waves indicate the presence of irreversible myocardial damage or past myocardial infarction. Myocardial infarction can occur without the development of Q waves.

Chapter Identifying the location of myocardial ischemia, injury, and infarction Leads V1, V2, V3, and V4 provide the best view for identifying anterior myocardial infarction. Leads V1, V2, and V3 overlie the ventricular septum, so ischemic changes seen in these leads, and possibly in the adjacent precordial leads, are often considered to be septal infarctions. Posterior infarctions can be diagnosed by looking for reciprocal changes in leads V1 and V2. What is in this chapter Pericarditis Pericardial effusion with lowvoltage QRS complexes Pericardial effusion with electrical alternans.

Pericarditis Initially with pericarditis the T wave is upright and may be elevated. During the recovery phase it inverts. The ST segment is elevated and usually flat or concave. While the signs and symptoms of pericarditis and myocardial infarction are similar, certain features of the ECG can be helpful in differentiating between the two: The ST segment and T wave changes in pericarditis are diffuse resulting in ECG changes being present in all leads.

In pericarditis, T wave inversion usually occurs only after the ST segments have returned to base line. In myocardial infarction, T wave inversion is usually seen before ST segment normalization. Figure Pericarditis and ST segment elevation. Chapter 11 Other Cardiac Conditions. The pericardial space is the space between the heart and the pericardial sac. Formation of a substantial pericardial effusion dampens the electrical output of the heart, resulting in low-voltage QRS complex in all leads. However, the ST segment and T wave changes of pericarditis may still be seen.

Figure Pericardial effusion with low-voltage QRS complexes. If a pericardial effusion is large enough, the heart may rotate freely within the fluid-filled sac. This can cause electrical alternans, a condition in which the electrical axis of the heart varies with each beat. A varying axis is most easily recognized on the ECG by the presence of QRS complexes that change in height with each successive beat. This condition can also affect the P and T waves. Figure Pericardial effusion with electrical alternans. This is called the S1 Q3 T3 pattern.

ST segment depression in lead II. Right bundle branch block usually subsides after the patient improves. The T waves are inverted in leads V1V4. Q waves are generally limited to lead III. Pacemakers A pacemaker is an artificial device that produces an impulse from a power source and conveys it to the myocardium. It provides an electrical stimulus for hearts whose intrinsic ability to generate an impulse or whose ability to conduct electrical current is impaired.

The power source is generally positioned subcutaneously, and the electrodes are threaded to the right atrium and right ventricle through veins that drain to the heart. The impulse flows throughout the heart causing the muscle to depolarize and initiate a contraction. Figure Pacemakers are used to provide electrical stimuli for hearts with an impaired ability to conduct an electrical impulse. Figure Location of pacemaker spikes on the ECG tracing with each type of pacemaker. Ventricular pacing Atrial pacing. An atrial pacemaker will produce a spike trailed by a P wave and a normal QRS complex.

With an AV sequential pacemaker, two spikes are seen, one that precedes a P wave and one that precedes a wide, bizarre QRS complex. With a ventricular pacemaker, the resulting QRS complex is wide and bizarre.

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Because the electrodes are positioned in the right ventricle, the right ventricle will contract first, then the left ventricle. This produces a pattern identical to left bundle branch block, with delayed left ventricular depolarization. Depressed depression. ST segment U wave Flattening of the T wave. Appearance of U waves. U wave becomes more prominent Prolongation of the QT interval. Figure ECG effects seen with hypokalemia. Flattened P waves. Prolonged PR interval 1stdegree AV heart block.

Deepened S waves and merging of S and T waves. Concave up and down slope of the T wave. Torsades de pointes, a variant of ventricular tachycardia, is seen Prolonged QT interval in patients with prolonged QT intervals.

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Figure ECG effects seen with hypocalcemia and hypercalcemia. Digoxin effects seen on the ECG Digoxin produces a characteristic gradual downward curve of the ST segment it looks like a ladle. The R wave slurs into the ST segment. Sometimes the T wave is lost in this scooping effect. The lowest portion of the ST segment is depressed below the baseline. When seen, the T waves have shorter amplitude and can be biphasic.

The QT interval is usually shorter than anticipated, and the U waves are more visible. Also, the PR interval may be prolonged. Index Accelerated idioventricular rhythm, Accelerated junctional rhythm, Atrial dysrhythmias, 68 Atrial fibrillation, Atrial flutter, Atrial tachycardia, Augmented limb leads, AV heart blocks, Bipolar leads, 11 Bradycardia, 25, 26 Caliper method, 29 Conduction system, hearts, 7 Counting the small squares method, Sinus rhythm, Sinus tachycardia, 6-second X 10 method, heart rate using, 21 ST segment, 47 T wave, 48 Tachycardia, 25, 26 Thin lines, to determine heart rate, 23 3rd-degree AV heart block, , , , 75, 60, 50 method, heart rate using, 22 U waves, 48 Ventricular dysrhythmias, 96 Ventricular tachycardia, Wandering atrial pacemaker, Waveforms, ECG, 8, , Wenckebach, Wolff-Parkinson-White syndrome, Read Free For 30 Days.

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Related titles. Carousel Previous Carousel Next. Essentials of Kumar and Clark's Clinical Medicine. Quick Management Guide in Emergency Medicine v1. Physical Examination of the Heart and Circulation 4th Jump to Page. Search inside document. Sinoatrial node Inherent rate beats per minute Left atrium 1 Atrioventricular node Inherent rate beats per minute Bundle of His Left and right bundle branches Inherent rate beats per minute Purkinje fibers Apex Figure Electrical conductive system of the heart.

The Electrocardiogram Impulses traveling toward a positive electrode produce upward deflections. Negative electrode Positive electrode Figure Direction of electrical impulses and waveforms. Bipolar leads Lead I Positive electrodeleft arm or under left clavicle. End point Figure , , , 75, 60, 50 method. Start point 75 94 60 72 88 58 68 84 63 43 48 56 65 79 50 42 47 54 52 38 37 41 45 44 33 36 40 39 35 34 Figure Identified values shown for each of the thin lines.

Figure Types of PR intervals: a shortened, b absent, c longer than normal, d progressively longer in a cyclical manner, e varying, and f absent due to an absence in the relationship between the atrial impulses and ventricular impulses. What is in this chapter Normal sinus rhythm characteristics Sinus bradycardia characteristics. Sinus tachycardia characteristics Sinus dysrhythmia characteristics Sinus arrest characteristics. Arise from SA node.

Normal P wave precedes each QRS complex. PR intervals are normal at 0. QRS complexes are normal. Normal sinus rhythm arises from the SA node. Each impulse travels down through the conduction system in a normal manner. Sinus bradycardia arises from the SA node. Sinus tachycardia arises from the SA node. It is regularly irregular patterned irregularity ; seems to speed up, slow down, and speed up in a cyclical fashion.

Sinus dysrhythmia arises from the SA node. Typically 60 to beats per minute, but may be slower depending on frequency and length of arrest. It is irregular where there is a pause in the rhythm the SA node fails to initiate a beat. What is in this chapter Premature atrial complexes PACs characteristics Wandering atrial pacemaker characteristics Atrial tachycardia characteristics. Multifocal atrial tachycardia characteristics Atrial flutter characteristics Atrial fibrillatrion characteristics.

Characteristics common to atrial dysrhythmias Arise from atrial tissue or internodal pathways. P waves if present that differ in appearance from normal sinus P waves precede each QRS complex. PR intervals may be normal, shortened, or prolonged. QRS complexes are normal unless there is also an interventricular conduction defect or aberrancy. May be occasionally irregular or frequently irregular depends on the number of PACs present. It may also be seen as patterned irregularity if bigeminal, trigeminal, or quadrigeminal PACs are seen. May be upright or inverted, will appear different than those of the underlying rhythm.

Will be normal duration if ectopic beat arises from the upper- or middle-right atrium. It is shorter than 0. In some cases it can also be prolonged. The pause that follows a premature beat is called a noncompensatory pause if the space between the complex before and after the premature beat is less than the sum of two R-R intervals. When the tip of the right caliper leg fails to line up with the next R wave it is considered a noncompensatory pause.

Rotate or slide the calipers over until the left leg is lined up with the second R wave mark the point where the tip of the right leg falls. Rotate or slide the calipers over until the left leg is lined up with your first mark. When the tip of the right caliper leg lines up with the next R wave it is considered a compensatory pause. Measure first R-R interval that precedes the early beat Rotate or slide the calipers over until the left leg is lined up with the second R wave mark the point where the tip of the right leg falls Rotate or slide the calipers over until the left leg is lined up with your first mark.

Compensatory pauses are typically associated with premature ventricular complexes PVCs.

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Premature beats occurring in a pattern One way to describe PACs is how they are intermingled among the normal beats. Regular PACs at greater intervals than every fourth beat have no special name. Chapter 4. Narrow complex tachycardia that has a sudden, witnessed onset and abrupt termination is called paroxysmal tachycardia. Narrow complex tachycardia that cannot be clearly identified as atrial or junctional tachycardia is referred to as supraventricular tachycardia. P waves change in morphology appearance from beat to beat at least three different shapes.

Ventricular rate may be slow, normal, or fast; atrial rate is between and beats per minute. May be regular or irregular depending on whether the conduction ratio stays the same or varies. Absent, instead there are flutter waves; the ratio of atrial waveforms to QRS complexes may be , , or An atrial-to-ventricular conduction ratio of is rare. Ventricular rate may be slow, normal, or fast; atrial rate is greater than beats per minute. What is in this chapter Premature junctional complexes PJCs characteristics Junctional escape rhythm characteristics. Accelerated junctional rhythm characteristics Junctional tachycardia characteristics.

Characteristics common to junctional dysrhythmias Arise from the AV junction, the area around the AV node, or the bundle of His. P wave may be inverted when they would otherwise be upright with a short PR interval less than 0. If present, PR intervals are shortened. QRS complexes are normal unless there is an interventricular conduction defect or aberrancy. May be occasionally irregular or frequently irregular depends on the number of PJCs present.

It may also be seen as patterned irregularity if bigeminal, trigeminal, or quadrigeminal PJCs are seen. What is in this chapter Premature ventricular complexes PVCs characteristics Idioventricular rhythm characteristics. Accelerated idioventricular rhythm characteristics Ventricular tachycardia characteristics. Arise from the ventricles below the bundle of His. QRS complexes are wide greater than 0. Ventricular beats have T waves in the opposite direction of the R wave. P waves are not visible as they are hidden in the QRS complexes. May be occasionally irregular or frequently irregular depends on the number of PVCs present.

It may also be seen as patterned irregularity if bigeminal, trigeminal, or quadrigeminal PVCs are seen. PVCs are followed by a compensatory pause. Sometimes, PVCs originate from only one location in the ventricle. These beats look the same and are called uniform also referred to as unifocal PVCs. Other times, PVCs arise from different sites in the ventricles. These beats tend to look different from each other and are called multiformed multifocal PVCs. Chapter 6 Ventricular Dysrhythmias Figure Couplet of PVCs.

It may be called a salvo, run, or burst of ventricular tachycardia. Figure Run of PVCs. Chapter 6. It appears as a PVC squeezed between two regular complexes. Figure Interpolated PVC. PVC that occurs on or near the T wave can precipitate ventricular tachycardia or fibrillation. Not preceded by a P wave if seen, they are dissociated and would therefore be a 3rd-degree heart block with an idioventricular escape. Idioventricular rhythm arises from a single site in the ventricles s.

Idioventricular rhythm arises from a single site in the ventricles. QRS complexes are wide and bizarre in appearance, have T waves in the opposite direction of the R wave. Ventricular tachycardia may be monomorphic, where the appearance of each QRS complex is similar, or polymorphic, where the appearance varies considerably from complex to complex. Ventricular tachycardia Idioventricular rhythm Accelerated idioventricular rhythm to beats per minute 20 to 40 beats per minute 40 to beats per minute. Two other conditions to be familiar with: Ventricular fibrillation VF results from chaotic firing of multiple sites in the ventricles.

This causes the heart muscle to quiver, much like a handful of worms, rather than contracting efficiently. On the ECG monitor it appears like a wavy line, totally chaotic, without any logic. Asystoleis the absense of any cardiac activity. It appears as a flat or nearly flat line on the monitor screen.

Characteristics common to AV heart blocks P waves are upright and round. In 1st-degree AV block PR interval is longer than normal and constant. In 3rd-degree block there is no PR interval. QRS complexes may be normal or wide. In 2nd-degree AV heart block, Type I Wenckebach , impulses arise from the SA node but their passage through the AV node is progressively delayed until the impulse is blocked. In 3rd-degree AV heart block there is a complete block at the AV node resulting in the atria being depolarized by an impulse that arises from the SA node and the ventricles being depolarized by an escape pacemaker that arises somewhere below the AV node.

Direction of ECG waveforms Depolarization and repolarization of the cardiac cells produce many small electrical currents called instantaneous vectors. The mean, or average, of all the instantaneous vectors is called the mean vector. When an impulse is traveling toward a positive electrode, the ECG machine records it as a positive or upward deflection. When the impulse is traveling away from a positive electrode and toward a negative electrode, the ECG machine records it as a negative or downward deflection.

Chapter 8. The sum of all the small vectors of ventricular depolarization is called the mean QRS vector. Because the depolarization vectors of the thicker left ventricle are larger, the mean QRS axis points downward and toward the patients left side. If an area of the heart is enlarged or damaged, specific ECG leads can provide a view of that portion of the heart.

While there are several methods used to determine the direction of the patients electrical axis, the easiest is the four-quadrant method. The four-quadrant method works in the following manner: An imaginary circle is drawn over the patients. A Me an representing one of the six limb leads.

Lead I Lead I is oriented at 0 located at the three oclock position. If the QRS complex points down negative , then the impulses are moving from left to right; this is considered abnormal. Persons who are thin, obese, or pregnant can have axis deviation due to a shift in the position of the apex of the heart. Myocardial infarction, enlargement, or hypertrophy of one or both of the hearts chambers, and hemiblock can also cause axis deviation. Right atrial enlargement Right ventricular hypertrophy Right bundle branch block Left atrial enlargement Left ventricular hypertrophy.

Right atrial enlargement Leads II and V1 provide the necessary information to assess atrial enlargement. Indicators of right atrial enlargement include: An increase in the amplitude of the first part of the P wave. The P wave is taller than 2. If the P wave is biphasic, the initial component is taller than the terminal component. The width of the P wave, however, stays within normal limits because its terminal part originates from the left atria, which depolarizes normally if left atrial enlargement is absent. Chapter 9. Figure Right atrial enlargement leads to an increase in the amplitude of the first part of the P wave.

Left atrial enlargement Indicators of left atrial enlargement include: The amplitude of the terminal portion of the P wave may increase in V1. The terminal left atrial portion of the P wave drops at least 1 mm below the isoelectric line in lead V1. There is an increase in the duration or width of the terminal portion of the P wave of at least one small square 0. Often the presence of ECG evidence of left atrial enlargement only reflects a nonspecific conduction irregularity.

However, it may also be the result of mitral valve stenosis causing the left atria to enlarge to force blood across the stenotic tight mitral valve. Figure Left atrial enlargement leads to an increase in the amplitude and width of the terminal part of the P wave. Key ECG indicators of left ventricular hypertrophy include: Increased R wave amplitude in those leads overlying the left ventricle. The S waves are smaller in leads overlying the left ventricle, but larger in leads overlying the right ventricle. Figure The thick wall of the enlarged right ventricle causes the R waves to be more positive in the leads that lie closer to lead V1.

Figure The thick wall of the enlarged left ventricle causes the R waves to be more positive in the leads that lie closer to lead V6 and the S waves to be larger in the leads closer to V1.

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Right bundle branch block The best leads for identifying right bundle branch are V1 and V2. Right bundle block causes the QRS complex to have a unique shape its appearance has been likened to rabbit ears or the letter M. As the left ventricle depolarizes, it produces the initial R and S waves, but as the right ventricle begins its delayed depolarization, it produces a tall R wave called the R.

In the left lateral leads overlying the left ventricle I, aVL, V5, and V6 , late right ventricular depolarization causes reciprocal late broad S waves to be generated. Figure In right bundle branch block, conduction through the right bundle is blocked causing depolarization of the right ventricle to be delayed; it does not start until the left ventricle is almost fully depolarized. Left bundle branch block Leads V5 and V6 are best for identifying left bundle branch block.

QRS complexes in these leads normally have tall R waves, whereas delayed left ventricular depolarization leads to a marked prolongation in the rise of those tall R waves, which will either be flattened on top or notched with two tiny points , referred to as an R, R wave. True rabbit ears are less likely to be seen than in right bundle branch block. Leads V1 and V2 leads overlying the right ventricle will show reciprocal, broad, deep S waves. Figure In left bundle branch block, conduction through the left bundle is blocked causing depolarization of the left ventricle to be delayed; it does not start until the right ventricle is almost fully depolarized.

Left anterior hemiblock With left anterior hemiblock, depolarization of the left ventricle occurs progressing in an inferior-to-superior and right-to-left direction. This causes the axis of ventricular depolarization to be redirected upward and slightly to the left, producing tall positive R waves in the left lateral leads and deep S waves inferiorly. Figure With left anterior hemiblock, conduction down the left anterior fascicle is blocked resulting in all the current rushing down the left posterior fascicle to the inferior surface of the heart.

Hypertrophy, Bundle Branch Block, and Preexcitation Left posterior hemiblock In left posterior hemiblock, ventricular myocardial depolarization occurs in a superior-to-inferior and left-to-right direction. This causes the main electrical axis to be directed downward and to the right, producing tall R waves inferiorly and deep S waves in the left lateral leads. This results in right axis deviation.


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  7. In contrast to complete left and right bundle branch block, in hemiblocks, the QRS complex is not prolonged. Lead aVF Small Q Figure With left posterior hemiblock, conduction down the left posterior fascicle is blocked resulting in all the current rushing down the left anterior fascicle to the myocardium. P waves are normal. QRS complexes are widened due to a characteristic slurred initial upstroke, called the delta wave. PR interval is usually shortened less than 0. Bundle of Kent Instead of the impulse traveling through the AV node, it travels down an accessory pathway to the ventricles.

    The QRS complex is widened due to premature activation of the ventricles. The PR interval is less than 0. The QRS complex is not widened. There is no delta wave. WPW and LGL are called preexcitation syndromes and are the result of accessory conduction pathways between the atria and ventricles. James fibers Instead of traveling through the AV node, the impulse is carried to the ventricles by way of an intranodal accessory pathway. Figure In LGL, the impulse travels through an intranodal accessory pathway, referred to as the James fibers, bypassing the normal delay within the AV node.

    What is in this chapter ECG changes associated with ischemia, injury, and infarction Identifying the location of myocardial ischemia, injury, and infarction Anterior Septal Lateral Inferior Posterior. Changes in the ST segment depression or elevation. Enlarged Q waves or appearance of new Q waves.

    ST segment elevation is the earliest reliable sign that myocardial infarction has occurred and tells us the myocardial infarction is acute. Pathologic Q waves indicate the presence of irreversible myocardial damage or past myocardial infarction. Myocardial infarction can occur without the development of Q waves. Chapter Identifying the location of myocardial ischemia, injury, and infarction Leads V1, V2, V3, and V4 provide the best view for identifying anterior myocardial infarction.

    Leads V1, V2, and V3 overlie the ventricular septum, so ischemic changes seen in these leads, and possibly in the adjacent precordial leads, are often considered to be septal infarctions.

    Posterior infarctions can be diagnosed by looking for reciprocal changes in leads V1 and V2. What is in this chapter Pericarditis Pericardial effusion with lowvoltage QRS complexes Pericardial effusion with electrical alternans. Pericarditis Initially with pericarditis the T wave is upright and may be elevated.

    During the recovery phase it inverts. The ST segment is elevated and usually flat or concave. While the signs and symptoms of pericarditis and myocardial infarction are similar, certain features of the ECG can be helpful in differentiating between the two: The ST segment and T wave changes in pericarditis are diffuse resulting in ECG changes being present in all leads. In pericarditis, T wave inversion usually occurs only after the ST segments have returned to base line. In myocardial infarction, T wave inversion is usually seen before ST segment normalization.

    Figure Pericarditis and ST segment elevation. Chapter 11 Other Cardiac Conditions. The pericardial space is the space between the heart and the pericardial sac. Formation of a substantial pericardial effusion dampens the electrical output of the heart, resulting in low-voltage QRS complex in all leads. However, the ST segment and T wave changes of pericarditis may still be seen. Figure Pericardial effusion with low-voltage QRS complexes. If a pericardial effusion is large enough, the heart may rotate freely within the fluid-filled sac.

    This can cause electrical alternans, a condition in which the electrical axis of the heart varies with each beat. A varying axis is most easily recognized on the ECG by the presence of QRS complexes that change in height with each successive beat. This condition can also affect the P and T waves. Figure Pericardial effusion with electrical alternans. This is called the S1 Q3 T3 pattern. ST segment depression in lead II.

    Right bundle branch block usually subsides after the patient improves. The T waves are inverted in leads V1V4. Q waves are generally limited to lead III. Pacemakers A pacemaker is an artificial device that produces an impulse from a power source and conveys it to the myocardium. It provides an electrical stimulus for hearts whose intrinsic ability to generate an impulse or whose ability to conduct electrical current is impaired.

    The power source is generally positioned subcutaneously, and the electrodes are threaded to the right atrium and right ventricle through veins that drain to the heart. The impulse flows throughout the heart causing the muscle to depolarize and initiate a contraction. Figure Pacemakers are used to provide electrical stimuli for hearts with an impaired ability to conduct an electrical impulse. Figure Location of pacemaker spikes on the ECG tracing with each type of pacemaker. Ventricular pacing Atrial pacing. An atrial pacemaker will produce a spike trailed by a P wave and a normal QRS complex.

    With an AV sequential pacemaker, two spikes are seen, one that precedes a P wave and one that precedes a wide, bizarre QRS complex. With a ventricular pacemaker, the resulting QRS complex is wide and bizarre. Because the electrodes are positioned in the right ventricle, the right ventricle will contract first, then the left ventricle. This produces a pattern identical to left bundle branch block, with delayed left ventricular depolarization. Depressed depression. ST segment U wave Flattening of the T wave.

    Appearance of U waves. U wave becomes more prominent Prolongation of the QT interval. Figure ECG effects seen with hypokalemia. Flattened P waves. Prolonged PR interval 1stdegree AV heart block. Deepened S waves and merging of S and T waves. Concave up and down slope of the T wave. Torsades de pointes, a variant of ventricular tachycardia, is seen Prolonged QT interval in patients with prolonged QT intervals.

    Pocket ECGs: A Quick Information Guide / Edition 1

    Figure ECG effects seen with hypocalcemia and hypercalcemia. Digoxin effects seen on the ECG Digoxin produces a characteristic gradual downward curve of the ST segment it looks like a ladle. The R wave slurs into the ST segment. Sometimes the T wave is lost in this scooping effect. The lowest portion of the ST segment is depressed below the baseline. When seen, the T waves have shorter amplitude and can be biphasic.

    The QT interval is usually shorter than anticipated, and the U waves are more visible. Also, the PR interval may be prolonged. Index Accelerated idioventricular rhythm, Accelerated junctional rhythm, Atrial dysrhythmias, 68 Atrial fibrillation, Atrial flutter, Atrial tachycardia, Augmented limb leads, AV heart blocks, Bipolar leads, 11 Bradycardia, 25, 26 Caliper method, 29 Conduction system, hearts, 7 Counting the small squares method, Sinus rhythm, Sinus tachycardia, 6-second X 10 method, heart rate using, 21 ST segment, 47 T wave, 48 Tachycardia, 25, 26 Thin lines, to determine heart rate, 23 3rd-degree AV heart block, , , , 75, 60, 50 method, heart rate using, 22 U waves, 48 Ventricular dysrhythmias, 96 Ventricular tachycardia, Wandering atrial pacemaker, Waveforms, ECG, 8, , Wenckebach, Wolff-Parkinson-White syndrome, Read Free For 30 Days.

    Description: electrocardiograma. Flag for inappropriate content. Related titles. Carousel Previous Carousel Next. Essentials of Kumar and Clark's Clinical Medicine. Quick Management Guide in Emergency Medicine v1. Physical Examination of the Heart and Circulation 4th Jump to Page. Search inside document. Sinoatrial node Inherent rate beats per minute Left atrium 1 Atrioventricular node Inherent rate beats per minute Bundle of His Left and right bundle branches Inherent rate beats per minute Purkinje fibers Apex Figure Electrical conductive system of the heart. The Electrocardiogram Impulses traveling toward a positive electrode produce upward deflections.

    Negative electrode Positive electrode Figure Direction of electrical impulses and waveforms. Bipolar leads Lead I Positive electrodeleft arm or under left clavicle. End point Figure , , , 75, 60, 50 method. Start point 75 94 60 72 88 58 68 84 63 43 48 56 65 79 50 42 47 54 52 38 37 41 45 44 33 36 40 39 35 34 Figure Identified values shown for each of the thin lines. Evaluating regularity Regular Slightly Sudden acceleration in heart rate Irregular Patterned Totally Variable conduction ratio Figure Algorithm for regular and irregular rhythms.

    Shorter Area where R-R interval it is irregular 21 15 25 Area where it is regular 21 21 21 Figure An occasionally irregular rhythm. Area where it is irregular Shorter R-R interval Area where it is regular Area where it is irregular Shorter R-R interval Shorter R-R interval Underlying rhythm against which the regularity of the rest of rhythm is measured. Figure A frequently irregular rhythm. Area where it is regular Area where it is slightly irregular Area where it is regular Figure A slightly irregular rhythm.

    Area where it is regular Area where the heart rate suddenly accelerates Figure A paroxsymally irregular rhythm. Area where it is patterned irregular Figure A patterned irregular rhythm. Entire tracing is irregular Figure An irregularly irregular rhythm. Areas where the conduction ratio changes Figure Variably irregular rhythm. This PR interval 0. Evaluate PR intervals Present Normal 0.

    Figure Normal sinus rhythm. Figure Sinus bradycardia. Figure Sinus tachycardia. Figure Sinus dysrhythmia. SA node fails to initiate impulse Figure Summary of characteristics of sinus arrest. Figure Wandering atrial pacemaker. P waves: May be upright or inverted, will appear different than those of the underlying rhythm QRS complexes: Normal PR interval: Will be normal duration if ectopic beat arises from the upper- or middle-right atrium. In some cases it can also be prolonged QT interval: Usually within normal limits but may vary Figure Summary of characteristics of premature atrial complexes.

    Figure Premature atrial complexes. When the tip of the right caliper leg fails to line up with the next R wave it is considered a noncompensatory pause Measure first R-R interval that precedes the early beat Rotate or slide the calipers over until the left leg is lined up with the second R wave mark the point where the tip of the right leg falls Rotate or slide the calipers over until the left leg is lined up with your first mark Figure Premature beats with a noncompensatory pause.

    Rate: to beats per minute Regularity: Regular unless the onset is witnessed thereby producing paroxysmal irregularity P waves: May be upright or inverted, will appear different than those of the underlying rhythm QRS complexes: Normal PR interval: Will be normal duration if ectopic beat arises from the upper- or middle-right atrium. Figure Summary of characteristics of atrial tachycardia. Figure Atrial tachycardia. Figure Multifocal atrial tachycardia. Figure Atrial flutter. Figure Atrial fibrillation. PJCs are typically followed by a non-compensatory pause.

    Figure Summary of characteristics of premature junctional complexes PJCs. Junctional escape rhythm 40 to 60 beats per minute Accelerated junctional rhythm 60 to beats per minute Junctional tachycardia to beats per minute Figure Junctional escape rhythm. Junctional escape rhythm 40 to 60 beats per minute Accelerated junctional rhythm 60 to beats per minute Junctional tachycardia to beats per minute Figure Accelerated junctional rhythm.

    Junctional escape rhythm 40 to 60 beats per minute Accelerated junctional rhythm 60 to beats per minute Junctional tachycardia to beats per minute Figure Junctional tachycardia.