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Chapter 19. Basic ECG Reading

Basic ECG Reading: Introduction

The formal procedure for obtaining an ECG is given in Chapter 13, Electrocardiogram. Every ECG should be
approached in a systematic, stepwise way. Many automated ECG machines can give a preliminary
interpretation of a tracing; however, all automated interpretations require analysis and sign-o by a
physician. Determine each of the following:

Standardization. With the ECG machine set on 1 mV, a 10-mm standardization mark (0.1 mV/mm) is evident
(Figure 191).
Axis. If the QRS is upright (more positive than negative) in leads I and aVF, the axis is normal. The normal axis
range is 30 degrees to +105 degrees.
Intervals. Determine the PR, QRS, and QT intervals (Figure 192). Intervals are measured in the limb leads.
The PR should be 0.120.20 s, and the QRS, < 0.12 s. The QT interval increases with decreasing heart rate,
usually < 0.44 s. The QT interval usually does not exceed one half of the RR interval (the distance between two
R waves).
Rate. Count the number of QRS cycles on a 6-s strip and multiply that number by 10 to roughly estimate the
rate. If the rhythm is regular, you can be more exact in determining the rate by dividing 300 by the number of
0.20-s intervals (usually depicted by darker shading) and then extrapolating for any fraction of a 0.20-s
segment.
Rhythm. Determine whether each QRS is preceded by a P wave, look for variation in the PR interval and RR
interval (the duration between two QRS cycles), and look for ectopic beats.
Hypertrophy. One way to detect LVH is to calculate the sum of the S wave in V1 or V2 plus the R wave in V5 or
V6. A sum > 35 indicates LVH. Some other criteria for LVH are R > 11 mm in aVL or R in I + S in III > 25 mm.
Infarction or Ischemia. Check for ST-segment elevation or depression, Q waves, inverted T waves, and poor R-
wave progression in the precordial leads (see Myocardial Infarction).

Figure 191.
Examples of 10-mm standardization mark and time marks and standard ECG paper running at 25 mm/s.

Figure 192.

Diagram of the ECG complexes, intervals, and segments. The U wave is normally not well seen.

Basic Information
Equipment

Bipolar Leads
Lead I: Le arm to right arm
Lead II: Le leg to right arm
Lead III: Le leg to le arm

Precordial Leads:

V1 to V6 across the chest (see Figure 139).

ECG Paper:

With the ECG machine set at 25 mm/s, each small box represents 0.04 s, and each large box 0.2 s (see Figure
191). Most ECG machines automatically print a standardization mark.

Normal ECG Complex

Note: A small amplitude in the Q, R, or S wave is represented by a lowercase letter. A large amplitude is
represented by an uppercase letter. The pattern shown in Figure 192 can also be noted qRs.

P Wave. Caused by depolarization of the atria. With normal sinus rhythm, the P wave is upright in leads I, II,
aVF, V4, V5, and V6 and inverted in aVR.
QRS Complex. Represents ventricular depolarization
Q Wave. The first negative deflection of the QRS complex (not always present and, if present, may be
pathologic). To be significant, the Q wave should be > 25% of the QRS complex.
R Wave. The first positive deflection that sometimes occurs a er the S wave
S Wave. The negative deflection following the R wave
T Wave. Caused by repolarization of the ventricles and follows the QRS complex, normally upright in leads I,
II, V3, V4, V5, and V6 and inverted in aVR

Axis Deviation
Axis represents the sum of the vectors of the electrical depolarization of the ventricles and gives an idea of
the electrical orientation of the heart in the body. In a healthy person, the axis is downward and to the le
(Figure 193). The QRS axis is midway between two leads that have QRS complexes of equal amplitude, or the
axis is 90 degrees to the lead in which the QRS is isoelectric (ie, R amplitude wave equals S-wave amplitude).

Figure 193.
Graphic representation of axis deviation. ECG representations of each type of axis are shown in each
quadrant. Large arrow indicates normal axis.

Normal Axis. QRS positive in I and aVF (090 degrees). Normal axis is actually 30 to 105 degrees.
Le Axis Deviation (LAD). QRS positive in I and negative in aVF, 30 to 90 degrees
Right Axis Deviation (RAD). QRS negative in I and positive in aVF, +105 to +180 degrees
Extreme RAD. QRS negative in I and negative in aVF, +180 to +270 or 90 to 180 degrees

Clinical Correlations

RAD. Seen with RVH, RBBB, COPD, and acute PE (a sudden change in axis toward the right) and occasionally
in healthy persons
LAD. Seen with LVH, LAHB (45 to 90 degrees), LBBB, and in some healthy persons

Heart Rate
Bradycardia:

Heart rate < 50 beats/min

Tachycardia:

Heart rate > 100 beats/min

Rate Determination:
Figure 194, below

Method 1. Note the 3-s marks along the top or bottom of the ECG paper (15 large squares). The approximate
rate equals the number of cycles (ie, QRSs) in a 6-s strip 10.
Method 2 (for regular rhythms). Count the number of large squares (0.2-s boxes) between two successive
cycles. The rate equals 300 divided by the number of squares. Extrapolate if the QRS complex does not fall
exactly on the 0.2-s marks (eg, if each QRS complex is separated by 2.4 0.20-s segments, the rate is 120
beats/min. The rate between two 0.20-s segments is 150 beats/min, and between three 0.20-s segments is 100
beats/min). Each of the five smaller 0.04-s marks between the second and third 0.20 mark would be 10
beats/min (150 100 = 50 5). Because the rate is three of the 0.04-s marks from the third 0.20-s segment, the
rate is 100 + 30, or 130 beats/min. Remember that the number of beats per minute for each 0.04-s mark varies
depending on which two 0.20 marks they are associated with (eg, between the fi h and sixth 0.20-s mark
each 0.04 mark is 2 beats/min).

Figure 194.

Sample strip for rapid rate determination. In method 1, estimate the rate by counting the number of beats
(eight) in two 3-s intervals. The rate is 8 10, or 80 beats/min (method 1). In method 2, each beat is separated
from the next by four 0.20-s intervals, so divide 300 by 4, and the rate is 75 beats/min. Because the beats are
separated by exactly four beats, extrapolation is not necessary.

Rhythm
Sinus Rhythms

Normal:

Each QRS preceded by a P wave (which is positive in II and negative in aVR) with a regular PR and RR interval
and a rate between 60 and 100 beats/min (Figure 195)

Figure 195.
Normal sinus rhythm.

Sinus Tachycardia:

Normal sinus rhythm with a heart rate > 100 beats/min and < 180 beats/min (Figure 196)

Figure 196.

Sinus tachycardia. The rate is 120130 beats/min.

Clinical Correlations. Anxiety, exertion, pain, fever, hypoxia, hypotension, increased sympathetic tone
(secondary to drugs with adrenergic e ects [eg, epinephrine]), anticholinergic e ect (eg, atropine), PE, COPD,
AMI, CHF, hyperthyroidism, and others

Sinus Bradycardia:

Normal sinus rhythm with heart rate < 50 beats/min (Figure 197)

Figure 197.

Sinus bradycardia. Rate is approximately 38 beats/min.

Clinical Correlations. Well-trained athlete, normal variant, secondary to medications (eg, beta-blockers,
digitalis, clonidine, nondihydropyridine calcium channel blockers [verapamil, diltiazem]), hypothyroidism,
hypothermia, sick sinus syndrome (tachybrady syndrome), and others
Treatment

If asymptomatic (good urine output, adequate BP, and normal sensorium), no treatment.
If hypotension , support blood pressure

Sinus Arrhythmia:

Normal sinus rhythm with irregular heart rate. Inspiration causes a slight increase in rate; expiration
decreases rate. Normal variation between inspiration and expiration is 10% or less.

Atrial Arrhythmias

PAC:

Ectopic atrial focus firing prematurely followed by a normal QRS (Figure 198, below). The compensatory
pause following the PAC is partial; the RR interval between beats 4 and 6 is less than between beats 1 and 3
and beats 6 and 8.

Figure 198.

Premature atrial contraction (PAC). Fi h beat is PAC.

Clinical Correlations. Usually no clinical significance; caused by stress, ca eine, and myocardial disease

PAT:

A run of three or more consecutive PACs. The rate is usually 140250 beats/min. The P wave may not be
visible, but the RR interval is very regular (Figure 199). Falls under the more general category of
supraventricular tachycardia (SVT) because it is indistinguishable from AV nodal reentry tachycardia (AVNRT)
and paroxysmal junctional tachycardia and the treatments are similar.

Figure 199.
Paroxysmal atrial tachycardia.

Clinical Correlations. Some healthy persons; heart disease. Symptoms: palpitations, light-headedness, and
syncope

Treatment

Increase Vagal Tone. Valsalva maneuver or carotid massage

Medical Treatment. Can include adenosine, verapamil, digoxin, edrophonium, or beta-blockers (propranolol,
metoprolol, esmolol). Use verapamil and beta-blockers cautiously at the same time because asystole can
occur.
Cardioversion with Synchronized DC Shock. Particularly in patients in hemodynamically unstable condition
(see Chapter 21, Automatic External Defibrillation, Defibrillation, and Cardioversion)

MAT:

Originates from ectopic atrial foci; characterized by varying P-wave morphology and PR interval and irregular
(Figure 1910).

Figure 1910.

Multifocal atrial tachycardia.

Clinical Correlations. COPD, advanced age, CHF, diabetes, and theophylline use. Antiarrhythmics are o en
ine ective. Manage the underlying disease.

AFib:

Irregularly irregular rhythm, no discernible P waves. Ventricular rate varies 100180 beats/min (Figure 1911).
The ventricular response may be < 100 beats/min if the patient is taking digoxin, verapamil, or a beta-blocker
or has AV nodal disease.
Figure 1911.

Atrial fibrillation.

Clinical Correlations. Some healthy persons; organic heart disease (CAD, hypertensive heart disease, valve
disease), thyrotoxicosis, alcohol abuse, pericarditis, PE, and postoperative state

Treatment

Pharmacologic Therapy. IV adenosine, verapamil, diltiazem, digoxin, and beta-blockers (propranolol,

metoprolol, esmolol) can be used to slow the ventricular response. Quinidine, procainamide, propafenone,
ibutilide, and amiodarone can be used to maintain or convert to sinus rhythm (see individual agents in
Chapter 21, Emergencies)
DC-Synchronized Cardioversion. If associated with increased myocardial ischemia, hypotension, or
pulmonary edema (see Chapter 21, Automatic External Defibrillation, Defibrillation, and Cardioversion)

Atrial Flutter:

Sawtooth flutter waves with an atrial rate of 250350 beats/min; rate may be regular or irregular depending
on whether the atrial impulses are conducted through the AV node at a regular interval or at a variable
interval (Figure 1912).

Figure 1912.

Atrial flutter with varying atrioventricular (AV) block (3:1 to 5:1 conduction).

Example: One ventricular contraction (QRS) for every two flutter waves = 2:1 flutter. A flutter wave is buried
within each QRS complex so if you see two flutter waves before each QRS complex, that is 3:1 flutter; one
flutter wave before each QRS complex is 2:1 flutter (the second flutter is hidden in the QRS complex or the T-
wave).
Clinical Correlations. Valvular heart disease, pericarditis, ischemic heart disease; pulmonary disease,
including PE; alcohol abuse

Treatment. Do not use quinidine or procainamide (atrial conduction may decrease to the point where 1:1
atrial to ventricular conduction can occur, and the ventricular rate increases and causes hemodynamic
compromise); otherwise, similar to management of atrial fibrillation. Ibutilide (class III antiarrhythmic) or
radiofrequency ablation

Nodal Rhythm

AV Junctional or Nodal Rhythm:

Rhythm originates in the AV node. Associated with retrograde P waves that precede or follow the QRS. If the P
wave is present, it is negative in lead II and positive in aVR (opposite of normal sinus rhythm) (Figure 1913).
Three or more premature junctional beats in a row constitute junctional tachycardia, which has the same
clinical significance as PAT.

Figure 1913.

Junctional rhythm with retrograde P waves (inverted) following QRS complex.

Ventricular Arrhythmias

PVC:

A premature beat arising in the ventricle. P waves may be present but have no relation to the QRS of the PVC.
The QRS is usually > 0.12 s with an LBBB pattern. A compensatory pause follows a PVC that is usually longer
than a er a PAC (Figure 1914). The RR interval between beats 2 and 4 is equal to that between beats 4 and 6.
Thus the pause following the PVC (the third beat) is fully compensatory. The following patterns are
recognized:

Bigeminy. One normal sinus beat followed by one PVC in an alternating manner (Figure 1915)
Trigeminy. Sequence of two normal beats followed by one PVC
Unifocal PVCs. Arise from one site in the ventricle. Each has the same configuration in a single lead (see
Figure 1914).
Multifocal PVCs. Arise from di erent sites and therefore have various shapes (Figure 1916)

Figure 1914.
Premature ventricular contractions (PVCs). Third and seventh beats are PVCs.

Figure 1915.

Ventricular bigeminy.

Figure 1916.

Multifocal PVCs. Second, sixth, and seventh beats are PVCs. Second and sixth PVCs have the same
morphology.

Clinical Correlations. Healthy persons; excessive ca eine ingestion, anemia, anxiety; organic heart disease
(ischemic, valvular, or hypertensive); medications (epinephrine and isoproterenol; digitalis and theophylline
toxicity); predisposing metabolic abnormalities (hypoxia, hypokalemia, acidosis, alkalosis,
hypomagnesemia)

Criteria for Treatment.

No treatment if asymptomatic. Studies have shown increased mortality among patients treated for PVCs;
however, > 10 PVCs per hour does increase death risk in patients with heart disease.
If symptomatic, beta-blockers. Radiofrequency ablation for right ventricular outflow tract (RVOT) tachycardia
in structurally normal hearts.

Ventricular Tachycardia:
Three or more PVCs in a row (Figure 1917). A wide QRS usually with an LBBB pattern (vs narrow complex
seen with supraventricular tachycardia). May occur as short paroxysm or sustained run (> 30 s) with rate of
120250 beats/min. Can be life-threatening (hypotension and degeneration into ventricular fibrillation).
Management of nonsustained ventricular tachycardia is controversial.

Figure 1917.

Ventricular tachycardia.

Clinical Correlations. See PVCs. Patients with ventricular aneurysm are more susceptible to arrhythmias,
especially in the presence of cardiac disease.

Treatment. See Chapter 21, Automatic External Defibrillation, Defibrillation, and Cardioversion.

Ventricular Fibrillation:

Erratic electrical activity from the ventricles, which fibrillate or twitch asynchronously; no cardiac output
(Figure 1918).

Figure 1918.

Ventricular fibrillation.

Clinical Correlations. One of two patterns seen with cardiac arrest (the other is asystole/flat line)

Treatment. See Chapter 21, Automatic External Defibrillation, Defibrillation, and Cardioversion.

Heart Block

First-Degree Block:

PR interval > 0.2 s (or five small boxes). Usually not clinically significant (Figure 1919). Caused by drugs
(beta-blockers, digitalis, calcium channel blockers)
Figure 1919.

First-degree AV block. PR interval is 0.26 s.

Second-Degree Block

Mobitz Type I (Wenckebach). Progressive prolongation of PR interval until P wave is blocked and not followed
by a QRS complex (Figure 1920). Can occur as a 2:1, 3:2, or 4:3 block. The ratio of the atrial to ventricular
beats can vary. With 4:3 block, every fourth P wave is not followed by a QRS.

Figure 1920.

Second-degree AV block, Mobitz type I (Wenckebach) with 4:3 conduction.

Clinical Correlations. Acute myocardial ischemia such as inferior MI, ASD, valvular heart disease, rheumatic
fever, and digitalis or propranolol toxicity. Can be transient or rarely progress to life-threatening bradycardia.

Treatment. Usually expectant; if bradycardia occurs: atropine, isoproterenol, or a pacemaker

Mobitz Type II. A series of P waves with conducted QRS complexes followed by a nonconducted P wave. The
PR interval for the conducted beats remains constant. Can occur as 2:1, 3:2, or 4:3 block. The ratio of the atrial
to ventricular beats can vary. With 4:3 block, every fourth P wave is not followed by a QRS. (Note: 2:1 AV block
can be either Mobitz type I or Mobitz type II, which can be di icult to di erentiate. Mobitz I has a prolonged
PR with a narrow QRS; Mobitz II has a normal PR interval with an LBBB pattern [wide QRS]).

Clinical Correlations. Implies severe conduction system disease that can progress to complete heart block;
acute anterior MI and cardiomyopathy

Treatment. Temporary cardiac pacemaker, particularly when associated with acute anterior MI

Third-Degree Block:
Complete AV block with independent atrial and ventricular rates. The ventricular rate is usually 2040
beats/min (Figure 1921).

Figure 1921.

Third-degree AV block (complete heart block). Atrial rate is 100 beats/min; ventricular rate is 57 beats/min.

Clinical Correlations. Degenerative changes in conduction system in elderly persons, digitalis toxicity,
transient finding with an acute inferior MI (ischemia of the AV junction), a ermath of acute anterior MI (higher
probability of mortality than a er inferior MI); can result in syncope or CHF

Treatment. Placement of a temporary or permanent pacemaker

BBB:

Complete BBB is present when the QRS complex is > 0.12 s (or three small boxes on the ECG). Look at leads I,
V1, and V6. Degenerative changes and ischemic heart disease are the most common causes.

RBBB:

The RSR pattern seen in V1, V2, or both. Also a wide S in leads I and V6 (Figure 1922)

Figure 1922.

Leads I, V1, and V6 show right bundle branch block (RBBB) pattern.

Clinical Correlations. Healthy persons; diseases a ecting the right side of the heart (pulmonary hypertension,
ASD, ischemia); sudden onset associated with PE and acute exacerbation of COPD

LBBB:
RR' in leads I, V6, or both. QRS complex may be more slurred than double-peaked as in RBBB. A wide S wave
is seen in V1 (Figure 1923).

Figure 1923.

Leads I, V1, and V6 show le bundle branch block (LBBB) pattern.

Clinical Correlations. Organic heart disease (hypertensive, valvular, and ischemic), severe aortic stenosis.
New LBBB a er AMI can be an indication for inserting a temporary cardiac pacemaker. Consider new LBBB MI
until proven otherwise.

Cardiac Hypertrophy
Atrial Hypertrophy

P wave > 2.5 mm in height and > 0.12 s wide (three small boxes on the ECG)

RAE:

Tall (> 2.5 mm), slender, peaked P waves (P pulmonale pattern) in leads II, III, aVF (Figure 1924). Tall (> 1.5
mm) P may be present in V1 and V2.

Figure 1924.
Right atrial enlargement, leads II, III, aVF, and V1. Note tall P waves in II, III, and aVF and tall, slender P waves
in V1.

Clinical Correlations. Chronic di use pulmonary disease, pulmonary hypertension, congenital heart disease
(ASD)

LAE:

Notched P wave (P mitrale pattern) in leads I and II. Wide ( 0.11 s), slurred biphasic P in V1 with wider
terminal than initial component (negative deflection) (Figure 1925)

Figure 1925.

Le atrial enlargement.

Clinical Correlations. Mitral stenosis or mitral regurgitation or secondary to LVH with hypertensive
cardiovascular disease

Ventricular Hypertrophy

RVH:

Tall R wave in V1 (R wave > S wave in V1), persistent S waves in V5 and V6, progressively smaller R wave from
V1 to V6, slightly widened QRS intervals (Figure 1926), and strain pattern with ST-segment depression and T-
wave inversion in V1 to V3. Pattern of small R waves with relatively large S waves in V1 to V6 may be present.
Right axis deviation (> 105 degrees) invariably present.
Figure 1926.

Right ventricular hypertrophy, leads V1, V2, V5, and V6. Note the tall R waves in V1 and V2, greater than the R
waves in V5 and V6. Also note strain pattern in V1 and V2 with down-sloping ST-segment depression and T-
wave inversion.

Clinical Correlations. Mitral stenosis, chronic di use pulmonary disease, chronic recurrent PE, congenital
heart disease (eg, tetralogy of Fallot), Duchenne muscular dystrophy, biventricular hypertrophy (LVH and
RVH, LVH findings o en predominating)

LVH:

Voltage criteria (> age 35 y): S wave in V1 or V2 plus R wave in V5 or V6 > 35 mm, or R wave in aVL > 11 mm or R
wave in I + S wave in III > 25 mm, or R wave in V5 or V6 > 26 mm. QRS complex may be > 0.10 s wide in V5 or V6.
ST-depression and T-wave inversion in anterolateral leads (I, aVL, V5 or V6) suggest LVH with strain (Figure 19
27)

Figure 1927.
Le ventricular hypertrophy, leads V1, V2, V5, and V6. S wave in V2 + R wave in V5 is 55 mm. Note ST changes
and T-wave inversion in V5 and V6, suggesting strain.

Clinical Correlations. HTN, aortic stenosis, aortic insu iciency, long-standing CAD, some forms of congenital
heart disease

Myocardial Infarction
(See also Chapter 21, Acute Coronary Syndrome and Myocardial Infarction.)

Myocardial Ischemia:

Inadequate myocardial oxygen supply (coronary artery blockage or spasm). The ECG can show ST-segment
depression (subendocardial ischemia) (Figure 1928), ST elevation (transmural ischemia) (Figure 1929), or
symmetrically inverted (flipped) T waves (Figure 1930) in the area of ischemia (eg, inferior ischemia in II, III,
and F; anterior ischemia in V1 to V6; lateral ischemia in I, aVL; anterolateral ischemia in I, aVL, V5, and V6;
anteroseptal ischemia in V1, V2, V3, and V4.

Figure 1928.
ST segment depression in leads II, III, and aVF in a patient with acute subendocardial ischemia and infarction.

Figure 1929.

ST elevation in leads V4, V5, and V6 in a patient with acute anterolateral ischemia.

Figure 1930.

Inverted T waves.

MI:

Myocardial necrosis caused by severe ischemia. Can be transmural MI (ST elevation early, T-wave inversion, Q
waves late) or subendocardial MI (ST depression, T-wave inversion without evidence of Q waves). Table 191,
below, outlines the localization of MIs.

Acute Injury Phase (transmural). Hyperacute T waves, then ST-segment elevation. Hyperacute T waves return
to normal in minutes to hours. ST elevation usually regresses a er hours to days. Persistent ST elevation
suggests a le ventricular aneurysm.
Evolving Phase (transmural). Hours to days a er MI. Deep T-wave inversion occurs and then replaces ST-
segment elevation, and T wave may return to normal.
Q Waves (transmural). Hours to days a er transmural MI, a Q wave is the initial negative deflection of the QRS
complex. A significant Q wave is 0.04 s in duration and > 25% the height of the R wave (Figure 1931). May
regress to normal a er years.
 Table 191 Localization of Transmural Myocardial Infarction on ECG

Reciprocal ST
Location of MI Presence of Q Wave or ST-Segment Elevation
Depression

Anterior V1 to V6 (or poor R-wave progression in leads V1 to V6)a II, III, aVF

Lateral I, aVL, V5, V6 V1, V3

Inferior II, III, aVF I, aVL, possibly

anterior leads

Posterior Abnormally tall R and T waves in V1 to V3 V1 to V3

Subendocardial No abnormal Q wave. ST-segment depression in the anterior,

lateral, or inferior leads

aNormally in V to V , the R-wave amplitude gradually increases and the S wave decreases with a biphasic QRS (R = S) in V or V . With an
1 6 3 4
anterior MI, there will be a loss of R-wave voltage (instead of Q waves) and the biphasic QRS will appear more laterally in V4 to V6, hence the
term poor R-wave progression.

Figure 1931.

Q waves in leads V1, V2, and V3 in a patient with acute anteroseptal MI. Note ST elevation to determine acute
nature of infarction.

Electrolyte and Drug E ects

Electrolytes

Hyperkalemia:
Narrow, symmetrical, di use, peaked T waves. In severe hyperkalemia, PR prolongation occurs, the P wave
flattens and is lost, and the QRS widens and can progress to ventricular fibrillation (Figure 1932).

Figure 1932.

Di use tall T waves in leads V4, V6, and aVF with widened QRS and junctional rhythm (loss of P waves)
secondary to hyperkalemia.

Hypokalemia:

ST-segment depression with the appearance of U waves (positive deflection a er the T wave) (Figure 1933)

Figure 1933.

Leads II, V2, and V3 in a patient with hypokalemia. A U wave is easily seen in V2 and V3 but di icult to
distinguish from the T wave in II.

Hypercalcemia:

Short QT interval

Hypocalcemia:

Prolonged QT interval

Drugs

Digitalis E ect:

Down-sloping ST segment
Digitalis Toxicity

Arrhythmias. PVCs, bigeminy, trigeminy, ventricular tachycardia, ventricular fibrillation, PAT, nodal rhythms,
accelerated junctional tachycardia and sinus bradycardia
Conduction Abnormalities. First-degree, second-degree, and third-degree heart blocks

Quinidine and Procainamide:

With toxic levels, prolonged QT, flattened T wave, and QRS widening

Miscellaneous ECG Changes

Pericarditis:

Di use ST elevation concave upward, di use PR depression, di use T-wave inversion, or a combination of
these findings (Figure 1934)

Figure 1934.
Acute pericarditis.

Clinical Correlations. Idiopathic conditions; viral, bacterial, and fungal infections, such as TB; AMI,
postpericardiotomy syndrome, Dressler syndrome; collagenvascular diseases; uremia; cancer

Hypothermia:

Sinus bradycardia, AV junctional rhythm, ventricular fibrillation. Classically, J point (the end of the QRS
complex and the beginning of the ST segment) elevation, intraventricular conduction delay, and prolonged
QT interval possible (Figure 1935). Known as an Osborne wave.
Figure 1935.

Sinus bradycardia, Osborne wave. J-point elevation with ST-segment elevation and prolonged QT interval
(0.56 s) in patient with hypothermia.

WPW Pattern and Syndrome:

The WPW (Wol ParkinsonWhite) pattern is a short PR interval along with a delta wave (a delay in initial
deflection of the QRS complex) on the ECG (Figure 1936). WPW syndrome is the WPW pattern on ECG and
documented tachyarrhythmias, usually SVT or Afib. Tachyarrhythmia (preexcitation syndrome) due to
conduction from the SA node to the ventricle through an accessory pathway that bypasses the AV node
(bundle of Kent).

Figure 1936.

Short PR interval and delta waves in leads II, aVF, and V3 in a patient with Wol ParkinsonWhite syndrome.

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