This chapter includes criteria for the diagnosis of basic electrocardiographic waveforms and cardiac arrhythmias. It is intended for use as a reference and assumes a basic understanding of the electrocardiogram (ECG) * .
Electrocardiographic interpretation is a “stepwise” procedure, and the first steps are to study and characterize the cardiac rhythm.
Categorize what you see in the 12-lead ECG or rhythm strip, using the three major parameters that allow for systematic analysis and subsequent diagnosis of the rhythm:
Step 2 consists of examining and characterizing the morphology of the cardiac waveforms.
Most electrocardiograph machines display 10 seconds of data in a standard tracing. A rhythm is defined as three or more successive P waves or QRS complexes.
Categorize the patterns seen in the tracing according to a systematic method. This method proceeds in three steps that lead to a diagnosis based on the most likely rhythm producing a particular pattern:
|Narrow QRS duration|| Sinus tachycardia |
Atrial flutter (2:1 AV conduction)
| Sinus rhythm |
Ectopic atrial rhythm
Atrial flutter (4:1 conduction)
Accelerated junctional rhythm
| Sinus bradycardia |
Ectopic atrial bradycardia
|Wide QRS duration||All rhythms listed above under narrow QRS duration, but with BBB or IVCD patterns|
| Ventricular tachycardia |
|Accelerated ventricular rhythm||Ventricular escape rhythm|
|Narrow QRS duration|| Atrial fibrillation |
Atrial flutter (variable AV conduction)
Multifocal atrial tachycardia
Atrial tachycardia with AV block (rare)
| Atrial fibrillation |
Atrial flutter (variable AV conduction)
Multiform atrial rhythm
Atrial tachycardia with AV block (rare)
| Atrial fibrillation |
Atrial flutter (variable AV conduction)
Multiform atrial rhythm
Sinus rhythm with 2° AV block
|Wide QRS duration||All rhythms listed above under narrow QRS duration, but with BBB or IVCD patterns|
| Torsade de pointes |
Rarely, anterograde conduction of atrial fibrillation over an accessory pathway in patients with WPW syndrome
The sinus node is the primary pacemaker for the heart. Because the sinus node is located at the junction of the superior vena cava and the right atrium, in sinus rhythm the atria are activated from “right to left” and “high to low.” The P wave in sinus rhythm is upright in lead II and inverted in lead aVR. In lead VI, the P wave is usually biphasic with a small initial positive deflection due to right atrial activation and a terminal negative deflection due to left atrial activation.
The normal sinus rate is usually between 60 and 100 bpm but can vary significantly. During sleep, when parasympathetic tone is high, sinus bradycardia (sinus rates <60 bpm) is a normal finding, and during conditions associated with increased sympathetic tone (exercise, stress), sinus tachycardia (sinus rates >100 bpm) is common. In children and young adults, sinus arrhythmia (sinus rates that vary by more than 10% during 10 seconds) due to respiration is frequently observed.
In some situations, the atria are activated by an ectopic atrial focus rather than the sinus node. In this case, the P wave will have an abnormal shape depending on where the ectopic focus is located. For example, if the focus arises from the left atrium, the P wave is inverted in leads I and aVL. If the depolarization rate of the ectopic focus is between 60 and 100 bpm, the patient has an ectopic atrial rhythm. If the rate is <60 bpm, the rhythm is defined as an ectopic atrial bradycardia.
In atrial flutter, the atria are activated rapidly (usually 300 bpm) owing to a stable reentrant circuit. Most commonly, the reentrant circuit rotates counterclockwise around the tricuspid valve. Because the left atrium and interatrial septum are activated low-to-high, “sawtooth” flutter waves that are inverted in the inferior leads (II, III, and aVF) are usually observed. If every fourth atrial beat is conducted to the ventricles (owing to slow conduction in the atrioventricular [AV] node), a relatively normal ventricular rate of 75 bpm is observed.
It is common to have isolated premature QRS activity that leads to mild irregularity of the heart rhythm. A premature narrow QRS complex is most often due to a normally conducted premature atrial complex (PAC) or more rarely a premature junctional complex (PJC). A premature wide QRS complex is usually due to a premature ventricular complex (PVC) or to a premature supraventricular complex (PAC or PJC) that conducts to the ventricle with aberrant conduction due to block in one of the bundle branches. Premature supraventricular complexes (with or without aberrant conduction) are commonly observed phenomena that are not associated with cardiac disease. Although PVCs are observed in normal individuals, they are usually associated with higher risk in patients with cardiac disease.
Tachycardias are normally classified by whether the QRS complex is narrow or wide and whether the rhythm is regular or irregular. A narrow QRS tachycardia indicates normal activation of the ventricular tissue regardless of the tachycardia mechanism. Narrow QRS tachycardias are frequently grouped together as supraventricular tachycardia (SVT) and can be due to a number of mechanisms described in the following text. This grouping also has clinical usefulness because SVTs are not usually life-threatening. In addition to QRS width, it is useful to consider the anatomic site from which the tachycardia arises: atrium, atrioventricular junction, ventricle, or utilization of an accessory pathway (Figure 7–1).
The most common cause of wide QRS complex tachycardia with a regular rhythm (WCT-RR) is sinus tachycardia with either right bundle branch block (RBBB) or left bundle branch block (LBBB). However, if a patient with structural heart disease presents with WCT-RR, one assumes a worst-case scenario and the presumptive diagnosis becomes ventricular tachycardia (VT). Most commonly, VT originates from a rapid reentrant circuit located at the border of infarcted and normal myocardium. Because the ventricles are not activated via the bundle branches or the Purkinje system, an abnormally wide QRS complex is observed. Any atrial or junctional tachycardias associated with aberrant conduction can also cause a WCT-RR. Finally, in very rare circumstances, patients with accessory pathways present with antidromic AVRT in which the ventricles are activated via the accessory pathway (leading to a wide and bizarre QRS complex) and the atria are activated retrogradely via the His bundle-AV node ( anti is Greek for against).
The ECG differentiation between regular SVTs with aberrant conduction (sinus tachycardia, atrial tachycardia, atrial flutter, junctional tachycardia, orthodromic AVRT) and VT can sometimes be difficult. Accurate diagnosis of VT is critical because this rhythm is frequently life-threatening. The two principal techniques for identifying VT are the presence of AV dissociation and abnormal QRS morphology.
The most important reason to identify AV dissociation is in wide complex tachycardia for the differentiation of SVT with aberrancy from VT. In VT, the rapid ventricular rate is often associated with retrograde block within the His-Purkinje system (ventriculoatrial block). This leads to P waves (from sinus node depolarization) that are not associated in 1:1 fashion with the QRS complexes (Figure 7–5). The presence of AV dissociation makes VT the most likely diagnosis in a patient with a regular wide complex tachycardia. In some circumstances, AV dissociation can be identified by the presence of capture beats or fusion beats. Occasionally, a properly timed P wave conducts to the ventricles and a portion (fusion beat) or all (capture beat) of ventricular tissue is activated by the His-Purkinje tissue for one QRS complex. It is always easier to identify AV dissociation rather than AV association; T waves can often be confused with P waves. Always examine the entire ECG for unexpected deflections in the QRS complex, ST segment, and T waves that are dissociated P waves. The P waves are usually most obvious in the inferior leads (II, III, and aVF) or V1.
This method derives from an analysis of typical waveforms of RBBB or LBBB as seen in leads I, V1, and V2. If the waveforms do not conform to either the common or uncommon typical morphologic patterns, the diagnosis defaults to VT.
Determine the morphologic classification of the wide QRS complexes (RB type or LB type), using the criteria below.
Apply criteria for common and uncommon normal forms of either RBBB or LBBB, as described below. The waveforms may not be identical, but the morphologic descriptions must match. If the QRS complexes do not match, the rhythm is probably VT.
(Requires all six precordial leads.)
Brugada and coworkers reported on a total of 554 patients with WC-TRR whose mechanism was diagnosed in the electrophysiology laboratory. Patients included 384 (69%) with VT and 170 (31%) with SVT with aberrant ventricular conduction.
This method derives from an analysis of typical waveforms of RBBB or LBBB as seen in both leads V1 and V6. If the waveforms do not conform to the typical morphologic patterns, the diagnosis defaults to VT.
Determine the morphologic classification of the wide QRS complexes (RB type or LB type), using the criteria above.
Apply criteria for normal forms of either RBBB or LBBB, as described below. A negative answer to any of the three questions is inconsistent with either RBBB or LBBB, and the diagnosis defaults to VT.
Sinus node dysfunction is manifested in a number of ECG findings. Most commonly, there is a sinus pause with a junctional escape beat. Alternatively, sinus bradycardia can be associated with sinus node dysfunction.
In rare circumstances, accelerated junctional rhythms between 60 and 100 bpm are observed due to more rapid depolarization of AV nodal cells. If the junctional rate is faster than the sinus rate, the sinus node will be suppressed by retrograde atrial activation because of repetitive depolarization from the junction. Accelerated junctional rhythms can be present in digitalis toxicity, rheumatic fever, and after cardiac surgery.
Because AV conduction normally occurs along a single axis, the AV node and His bundle, atrioventricular (AV) block most commonly is due to block at one of these two sites. Block within the His bundle is associated with a worse prognosis and should be suspected in any form of AV block associated with a wide QRS complex. Electrocardiographically, AV block is usually described as first-degree, second-degree, or third-degree AV block. In first-degree (1°) AV block, every P wave is conducted to the ventricles, but there is an abnormal delay between atrial activation and ventricular activation (PR interval >0.2 second). In 1° AV block, the ventricular rate is not slow unless sinus bradycardia is also present.
In second-degree (2°) AV block, some but not all P waves are conducted to the ventricles. This leads to an irregular ventricular rhythm. Second-degree AV block is usually subclassified as Mobitz type I block, Wenckebach block or Mobitz type II block. In type I 2° AV block, progressive prolongation of the PR interval is observed; in type II 2° AV block, the PR interval remains relatively constant before the blocked P wave. The importance of this distinction is this: type I 2° AV block usually indicates that conduction is blocked within the AV node, whereas type II AV block suggests that conduction is blocked within the His bundle (regardless of the width of the QRS complex). The simplest way to differentiate between type I and type II 2° AV block is to compare the PR intervals before and after the blocked P wave. In type I 2° AV block, the PR interval after the blocked P wave is shorter than the PR interval before the blocked P wave; in type II 2° AV block, the PR intervals are the same.
In third-degree (3°) or complete AV block, no P waves are conducted to the ventricles. The P-to-P and QRS-to-QRS intervals are constant and unrelated (AV dissociation). The QRS rate and morphology depend on the site of the subsidiary intrinsic pacemaker. If the block is within the AV node, a lower AV nodal pacemaker often takes over and the rate is 40–50 bpm with a normal-appearing QRS complex (junctional rhythm). If the block is within the His bundle, a ventricular pacemaker with a rate of 20–40 bpm and a wide QRS will be noted (ventricular escape rhythm).
The most common pattern is illustrated below and is usually seen in leads I or II and V6. There is a small “septal” Q wave <30 ms in duration. The T wave is upright. The normal ST segment, which is never normally isoelectric except sometimes at slow rates (<60 bpm), slopes upward into an upright T wave, whose proximal angle is more obtuse than the distal angle. The normal T wave is never symmetric.
The pattern seen in the right precordial leads, usually V1–3, is shown below. There is a dominant S wave. The J point—the junction between the end of the QRS complex and the ST segment—is usually slightly elevated, and the T wave is upright. The T wave in V1 may occasionally be inverted as a normal finding in up to 50% of young women and 25% of young men, but this finding is usually abnormal in adult males. V2 usually has the largest absolute QRS and T-wave magnitude of any of the 12 electrocardiographic leads.
Diagnostic criteria include a positive component of the P wave in lead V1 or V2 ≥1.5 mm. Another criterion is a P-wave amplitude in lead II >2.5 mm.
Note: A tall, peaked P in lead II may represent RAE but is more commonly due to either chronic obstructive pulmonary disease (COPD) or increased sympathetic tone.
Clinical correlation: RAE is seen with right ventricular hypertrophy (RVH).
The most sensitive lead for the diagnosis of LAE is lead V1, but the criteria for lead II are more specific. Criteria include a terminal negative wave ≥1 mm deep and ≥40 ms wide (one small box by one small box in area) for lead V1 and > 40 ms between the first (right) and second (left) atrial components of the P wave in lead II, or a P-wave duration >110 ms in lead II.
Clinical correlations: left ventricular hypertrophy (LVH), coronary artery disease, mitral valve disease, or cardiomyopathy.
The normal QRS duration in adults ranges from 67–114 ms (Glasgow cohort). If the QRS duration is ≥120 ms (three small boxes or more on the electrocardiographic paper), there is usually an abnormality of conduction of the ventricular impulse. The most common causes are either RBBB or LBBB (see below). However, other conditions may also prolong the QRS duration.
RBBB is defined by delayed terminal QRS forces that are directed to the right and anteriorly, producing broad terminal positive waves in leads V1 and aVR and a broad terminal negative wave in lead I.
LBBB is defined by delayed terminal QRS forces that are directed to the left and posteriorly, producing wide R waves in leads that face the left ventricular free wall and wide S waves in the right precordial leads.
The diagnosis of uncomplicated complete RBBB is made when the following criteria are met:
In uncomplicated RBBB, the ST–T segment is depressed and the T wave inverted in the right precordial leads with an R′ (usually only in lead V1 but occasionally in V2). The T wave is upright in leads I, V5, and V6.
The diagnosis of uncomplicated complete LBBB is made when the following criteria are met:
In uncomplicated LBBB, the ST segments are usually depressed and the T waves inverted in left precordial leads V5 and V6 as well as in leads I and aVL. Conversely, ST-segment elevations and positive T waves are recorded in leads V1 and V2. Only rarely is the T wave upright in the left precordial leads. As a general rule, ST–T changes in LBBB are usually in the direction opposite the direction of the QRS complex (inverted T waves and ST-segment depression if the QRS is upright).
The waveforms are similar to those in complete LBBB, but the QRS duration is <120 ms. Septal Q waves are absent in I and V6. Incomplete LBBB is synonymous with LVH and commonly mimics a delta wave in leads V5 and V6.
The waveforms are similar to those in complete RBBB, but the QRS duration is <120 ms. This diagnosis suggests RVH. Occasionally, in a normal variant pattern, there is an rSr′ waveform in lead V1. In this case, the r′ is usually smaller than the initial r wave; this pattern is not indicative of incomplete RBBB.
If the QRS duration is ≥120 ms but typical waveforms of either RBBB or LBBB are not present, there is an intraventricular conduction delay or defect (IVCD). This pattern is common in dilated cardiomyopathy. An IVCD with a QRS duration of ≥170 ms is highly predictive of dilated cardiomyopathy.
Clinical correlations: hypertensive heart disease, coronary artery disease, or idiopathic conducting system disease.
Clinical correlations: LPFB is a diagnosis of exclusion. It may be seen in the acute phase of inferior myocardial injury or infarction or may result from idiopathic conducting system disease.
The mean electrical axis is the average direction of the activation or repolarization process during the cardiac cycle. Instantaneous and mean electrical axes may be determined for any deflection (P, QRS, ST–T) in the three planes (frontal, transverse, and sagittal). The determination of the electrical axis of a QRS complex is useful for the diagnosis of certain pathologic cardiac conditions.
Arzbaecher developed the hexaxial reference system that allowed for the display of the relationships among the six frontal plane (limb) leads, which is shown on the following diagram.
The normal range of the QRS axis in adults is –30 degrees to +90 degrees.
It is rarely important to precisely determine the degrees of the mean QRS. However, the recognition of abnormal axis deviations is critical because it leads to a presumption of disease. The mean QRS axis is derived from the net area under the QRS curves. The most efficient method of determining the mean QRS axis uses the method of Grant, which requires only leads I and II (see below). If the net area under the QRS curves in these leads is positive, the axis falls between –30 degrees and +90 degrees, which is the normal range of axis in adults. (The only exception to this rule is in RBBB, in which the first 60 ms of the QRS is used. Alternatively, one may use the maximal amplitude of the R and S waves in leads I and II to assess the axis in RBBB.) The following diagram shows abnormal axes.
The four main causes of left axis deviation are as follows:
The four main causes of right axis deviation (RAD) are as follows:
This category is rare. Causes include RVH, apical myocardial infarction, VT, and hyperkalemia. Right superior axis deviation may rarely be seen as an atypical form of LAFB.
The ECG is very insensitive as a screening tool for LVH, but electrocardiographic criteria are usually specific. Echocardiography is the major resource for this diagnosis.
The best electrocardiographic criterion for the diagnosis of LVH is the Cornell voltage, the sum of the R-wave amplitude in lead aVL and the S-wave depth in lead V3, adjusted for sex:
Typical repolarization abnormalities in the presence of LVH are an ominous sign of end-organ damage. In repolarization abnormalities in LVH, the ST segment and T wave are directed opposite to the dominant QRS waveform in all leads. However, this directional rule does not apply either in the transitional lead (defined as a lead having an R-wave height equal to the S wave depth) or in the transitional zone (defined as leads adjacent to the transitional lead) or one lead to the left in the precordial leads.
The waveforms, as in the following illustration, usually seen in leads I, aVL, V5, and V6 but more specifically in leads with dominant R waves, represent hypothetical stages in the progression of LVH.
The ECG is insensitive for the diagnosis of RVH. In 100 cases of RVH from one echocardiography laboratory, only 33% had RAD because of the confounding effects of LV disease. Published electrocardiographic criteria for RVH are listed below, all of which have ≥97% specificity.
With rare exceptions, right atrial enlargement is synonymous with RVH.
Recommended criteria for the electrocardiographic diagnosis of RVH are as follows:
A variant of RVH (type C loop) may produce a false-positive sign of an anterior myocardial infarction.
The morphology of repolarization abnormalities in RVH is identical to those in LVH, when a particular lead contains tall R waves reflecting the hypertrophied RV or LV. In RVH, these typically occur in leads V1–2 or V3 and in leads aVF and III. This morphology of repolarization abnormalities due to ventricular hypertrophy is illustrated earlier. In cases of RVH with massive dilation, all precordial leads may overlie the diseased RV and may exhibit repolarization abnormalities.
Defined as peak-to-peak QRS voltage <5 mm in all limb leads.
Defined as peak-to-peak QRS voltage <5 mm in all limb leads and <10 mm in all precordial leads. Primary myocardial causes include multiple or massive infarctions; infiltrative diseases such as amyloidosis, sarcoidosis, or hemochromatosis; and myxedema. Extracardiac causes include pericardial effusion, COPD, pleural effusion, obesity, anasarca, and subcutaneous emphysema. When there is COPD, expect to see low voltage in the limb leads as well as in leads V5 and V6.
The normal R-wave height increases from V1 to V5. The normal R-wave height in V5 is always taller than that in V6 because of the attenuating effect of the lungs. The normal R-wave height in lead V3 is usually >2 mm.
The term “poor R-wave progression” (PRWP) is a nonpreferred term because most physicians use this term to imply the presence of an anterior myocardial infarction, although it may not be present. Other causes of small R waves in the right precordial leads include LVH, LAFB, LBBB, cor pulmonale (with the type C loop of RVH), and COPD.
Reversed R-wave progression is defined as a loss of R-wave height between leads V1 and V2 or between leads V2 and V3 or between leads V3 and V4. In the absence of LVH, this finding suggests anterior myocardial infarction or precordial lead reversal.
Causes of tall R waves in the right precordial leads include the following:
The following pages contain a systematic method for the electrocardiographic diagnosis of myocardial injury or infarction, arranged in seven steps. Following the steps will achieve the diagnosis in most cases.
Identify presence of and areas of myocardial injury.
The GUSTO study of patients with ST-segment elevation in two contiguous leads defined four affected areas as set out in Table 7–3.
|Area of ST-Segment Elevation||Leads Defining This Area|
|Lateral (Lat)||I, aVL|
|Inferior (Inf)||II, aVF, III|
Two other major areas of possible injury or infarction were not included in the GUSTO categorization because they do not produce ST elevation in two contiguous standard leads. These are:
Identify the primary area of involvement and the culprit artery.
ST elevation in two contiguous V1–4 leads defines a primary anterior area of involvement. The left anterior descending coronary artery (LAD) is the culprit artery. Lateral (I and aVL) and apical (V5 and V6) areas are contiguous to anterior (V1–4), so ST elevation in these leads signifies more myocardium at risk and more adverse outcomes.
ST-segment elevation in two contiguous leads (II, aVF, or III) defines a primary inferior area of involvement. The right coronary artery (RCA) is usually the culprit artery. Apical (V5 and V6), posterior (V1–3 or V7–9), and right ventricular (V4R) areas are contiguous to the inferior (II, aVF, and III) area, so ST elevation in these contiguous leads signifies more myocardium at risk and more adverse outcomes.
In the GUSTO trial, 98% of patients with ST-segment elevation in any two contiguous V1–4 leads, either alone or with associated changes in leads V5–6 or I and aVL, had LAD obstruction. In patients with ST-segment elevation only in leads II, aVF, and III, there was RCA obstruction in 86%.
Acute occlusion of the LAD produces a sequence of changes in the anterior leads (V1–4).
A patient who presents to the emergency department with chest pain and T-wave inversion in leads with pathologic Q waves is most likely to be in the evolutionary or completed phase of infarction. Successful revascularization usually causes prompt resolution of the acute signs of injury or infarction and results in the electrocardiographic signs of a fully evolved infarction. The tracing below shows QS complexes in lead V2.
A primary inferior process usually develops after acute occlusion of the RCA, producing changes in the inferior leads (II, III, and aVF).
The earliest findings are of acute injury (ST-segment elevation). The J point may “climb up the back” of the R wave (a), or the ST segment may rise up into the T wave (b).
ST-segment elevation decreases and pathologic Q waves develop. T-wave inversion may occur in the first 12 hours of an inferior myocardial infarction—in contrast to that in anterior myocardial infarction.
With right ventricular injury, there is ST-segment elevation, best seen in lead V4R. With right ventricular infarction, there is a QS complex.
For comparison, the normal morphology of the QRS complex in lead V4R is shown below. The normal J point averages +0.2 mm.
Posterior injury or infarction is commonly due to acute occlusion of the left circumflex coronary artery, producing changes in the posterior leads (V7, V8, V9) or reciprocal ST-segment depression in leads V1–3.
Acute posterior injury or infarction is shown by ST-segment depression in V1–3 and perhaps also V4, usually with upright (often prominent) T waves.
Chronic posterior injury or infarction is shown by pathologic R waves with prominent tall T waves in leads V1–3.
Identify the location of the lesion within the artery to risk stratify the patient.
Aside from an acute occlusion of the left main coronary artery, occlusion of the proximal LAD conveys the most adverse outcomes. Four electrocardiographic signs indicate proximal LAD occlusion:
If the occlusion occurs in a more distal portion of the LAD (after the first diagonal branch and after the first septal perforator), ST-segment elevation is observed in the anterior leads, but the four criteria described above are not seen. In patients with occlusion of the left main coronary artery, diffuse endocardial injury leads to ST-segment elevation in aVR, because this is the only lead that “looks” directly at the ventricular endocardium, and diffuse ST-segment depression is observed in the anterior and inferior leads.
Nearly 50% of patients with inferior myocardial infarction have distinguishing features that may produce complications or adverse outcomes unless successfully managed:
ST depressions in leads remote from the primary site of injury are felt to be a purely reciprocal change. With successful reperfusion, the ST depressions usually resolve. If they persist, patients more likely have significant three-vessel disease and so-called ischemia at a distance. Mortality rates are higher in such patients.
The 12-lead ECG shown below contains numbers corresponding to pathologic widths for Q waves and R waves for selected leads (see Table 7–4 for more complete criteria).
|Infarct Location||ECG Lead||Criterion||Sensitivity||Specificity||Likelihood Ratio (+)||Likelihood Ratio (–)|
|Inferior||II||Q ≥ 30 ms||45||98||22.5||0.6|
|aVF||Q ≥ 30 ms||70||94||11.7||0.3|
|Q ≥ 40 ms||40||98||20.0||0.6|
|R/Q ≤ 1||50||98||25.0||0.5|
|V2||Any Q, or R ≤ 0.1 mV and R ≤ 10 ms, or RV2 ≤ RV1||80||94||13.3||0.2|
|V3||Any Q, or R ≤ 0.2 mV, or R ≤ 20 ms||70||93||10.0||0.3|
|V4||Q ≥ 20 ms||40||92||5.0||0.9|
|R/Q ≤ 0.5, or R/S ≤ 0.5||40||97||13.3||0.6|
|I||Q ≥ 30 ms||10||98||5.0||0.9|
|R/Q ≤ 1, or R ≤ 2 mm||10||97||3.3||0.9|
|aVL||Q ≥ 30 ms||7||97||0.7||1.0|
|R/Q ≤ 1||2|
|Apical||V5||Q ≥ 30||5||99||5.0||1.0|
|R/Q ≤ 2, or R ≤ 7 mm, or R/S ≤ 2, or notched R||60||91||6.7||0.4|
|R/Q ≤ 1, or R/S ≤ 1||25||98||12.5||0.8|
|V6||Q ≤ 30||3||98||1.5||1.0|
|R/Q ≤ 3, or R ≤ 6 mm, or R/S ≤ 3, or notched R||40||92||25.0||0.7|
|R/Q ≤ 1, or R/S ≤ 1||10||99||10.0||0.9|
|V1||R/S ≤ 1||15||97||5.0||0.9|
|R ≥ 6 mm, or R ≥ 40 ms||20||93||2.9||0.9|
|S ≤ 3 mm||8||97||2.7||0.9|
|V2||R ≥ 15 mm, or R ≥ 50 ms||15||95||3.0||0.9|
|R/S ≥ 1.5||10||96||2.5||0.9|
|S ≤ 4 mm||2||97||0.7||1.0|
One can memorize the above criteria by mastering a simple scheme of numbers that represents the durations of pathological Q waves or R waves. Begin with lead V1 and repeat the numbers in the box below in the following order. The numbers increase from “any” to 50.
Haisty and coworkers studied 1344 patients with normal hearts documented by coronary arteriography and 837 patients with documented myocardial infarction (366 inferior, 277 anterior, 63 posterior, and 131 inferior and anterior) (Table 7–4). (Patients with LVH, LAFB, LPFB, RVH, LBBB, RBBB, COPD, or WPW patterns were excluded from analysis because these conditions can give false-positive results for myocardial infarction.) Shown below are the sensitivity, specificity, and likelihood ratios for the best-performing infarct criteria. Notice that leads III and aVR are not listed: lead III may normally have a Q wave that is both wide and deep, and lead aVR commonly has a wide Q wave.
Conditions that can produce pathologic Q waves, ST-segment elevation, or loss of R-wave height in the absence of infarction are set out in Table 7–5.
|WPW pattern||Any, most commonly inferoposterior or lateral|
|Hypertrophic cardiomyopathy||Lateral apical (18%), inferior (11%)|
|LBBB||Anteroseptal, anterolateral, inferior|
|RBBB||Inferior, posterior (using criteria from leads V1 and V2), anterior|
|LAFB||Anterior (may cause a tiny Q in V2)|
|COPD||Inferior, posterior, anterior|
|RVH||Inferior, posterior (using criteria from leads V1 and V2), anterior, or apical (using criteria for R/S ratios from leads V4-6)|
|Acute cor pulmonale||Inferior, possibly anterior|
|Cardiomyopathy (nonischemic)||Any, most commonly inferior (with IVCD pattern), less commonly anterior|
|Left pneumothorax||Anterior, anterolateral|
|Normal hearts||Posterior, anterior|
An acute infarction manifests ST-segment elevation in a lead with a pathologic Q wave. The T waves may be either upright or inverted.
An old or age-indeterminate infarction manifests a pathologic Q wave, with or without slight ST-segment elevation or T-wave abnormalities.
Persistent ST-segment elevation ≥1 mm after a myocardial infarction is a sign of dyskinetic wall motion in the area of infarct. Half of these patients have ventricular aneurysms.
There are two possibilities for the major electrocardiographic diagnosis: myocardial infarction or acute injury. If there are pathologic changes in the QRS complex, one should make a diagnosis of myocardial infarction—beginning with the primary area, followed by any contiguous areas—and state the age of the infarction. If there are no pathologic changes in the QRS complex, one should make a diagnosis of acute injury of the affected segments—beginning with the primary area and followed by any contiguous areas.
Table 7–6 summarizes major causes of ST-segment elevations. Table 7–7 summarizes major causes of ST-segment depressions or T-wave inversions. The various classes and morphologies of ST–T waves as seen in lead V2 are shown in Table 7–8.
In many normal hearts, low-amplitude positive U waves <1.5 mm tall that range from 160–200 ms in duration are seen in leads V2 or V3. Leads V2 and V3 are close to the ventricular mass and small-amplitude signals may be best seen in these leads.
Abnormal U waves have increased amplitude or merge with abnormal T waves and produce T–U fusion. Criteria include an amplitude ≥1.5 mm or a U wave that is as tall as the T wave that immediately precedes it.
Causes: Hypokalemia, digitalis, antiarrhythmic drugs.
These are best seen in leads V4–6.
Causes: LVH, acute ischemia.
Table 7–9 summarizes various classes and morphologies of ST–T–U abnormalities as seen in lead V4.
A prolonged QT interval conveys adverse outcomes. The QT interval is inversely related to the heart rate. QT interval corrections for heart rate often use Bazett’s formula, defined as the observed QT interval divided by the square root of the R–R interval in seconds. A corrected QT interval of ≥440 ms is abnormal.
Measure the QT interval in either lead V2 or V3, where the end of the T wave can usually be clearly distinguished from the beginning of the U wave. If the rate is regular, use the mean rate of the QRS complexes. If the rate is irregular, calculate the rate from the immediately prior R–R cycle, because this cycle determines the subsequent QT interval. Use the numbers you have obtained to classify the QT interval using the nomogram below. Or remember that at heart rates of ≥40 bpm, an observed QT interval ≥480 ms is abnormal.
The four major causes of a prolonged QT interval are as follows:
The five causes of a short QT interval are hypercalcemia, digitalis, thyrotoxicosis, increased sympathetic tone, and genetic abnormality.
This error should not occur but it does occur nevertheless. It produces a “far field” signal when one of the bipolar leads (I, II, or III) records the signal between the left and right legs. The lead appears to have no signal except for a tiny deflection representing the QRS complex. There are usually no discernible P waves or T waves. RL–RA cable reversal is shown here.
Hypothermia is usually characterized on the ECG by a slow rate, a long QT, and muscle tremor artifact. An Osborn wave is typically present.
There is usually widespread ST-segment elevation with concomitant PR-segment depression in the same leads. The PR segment in aVR protrudes above the baseline like a knuckle, reflecting atrial injury.
Only lead V6 is used. If the indicated amplitude ratio A/B is ≥25%, suspect pericarditis (shown on left side). If A/B <25%, suspect early repolarization (shown on right side).
The WPW pattern is most commonly manifest as an absent PR segment and initial slurring of the QRS complex in any lead. The lead with the best sensitivity is V4.
The P-wave amplitude in the inferior leads is equal to that of the QRS complexes.
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