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Normally, voltage standardization is 1.0 mV per 10 mm, and paper speed is 25 mm/s (each horizontal small box = 0.04 s).

Heart Rate

Beats/min = 300 divided by the number of large boxes (each 5 mm apart) between consecutive QRS complexes. For faster heart rates, divide 1500 by number of small boxes (1 mm apart) between each QRS.


Sinus rhythm is present if every P wave is followed by a QRS, PR interval ≥0.12 s, every QRS is preceded by a P wave, and the P wave is upright in leads I, II, and III. Arrhythmias are discussed in Chaps. 122 and 123.

Mean Axis

If QRS is primarily positive in limb leads I and II, then axis is normal. Otherwise, find limb lead in which QRS is most isoelectric (R = S). The mean axis is perpendicular to that lead (Fig. 111-1). If the QRS complex is positive in that perpendicular lead, then mean axis is in the direction of that lead; if negative, then mean axis points directly away from that lead.

Left-axis deviation (more negative than –30°) occurs in diffuse left ventricular disease, inferior MI, and in left anterior hemiblock (small R, deep S in leads II, III, and aVF).

Right-axis deviation (>90°) occurs in right ventricular hypertrophy (R > S in V1) and left posterior hemiblock (small Q and tall R in leads II, III, and aVF). Mild right-axis deviation is common in thin, healthy individuals (up to 110°).

FIGURE 111-1

Electrocardiographic lead systems: The hexaxial frontal plane reference system to estimate electrical axis. Determine leads in which QRS deflections are maximum and minimum. For example, a maximum positive QRS in I which is isoelectric in aVF is oriented to 0°. Normal axis ranges from −30° to +90°. An axis > +90° is right-axis deviation and <30° is left-axis deviation.


PR (0.12–0.20 s)

  • Short: (1) preexcitation syndrome (look for slurred QRS upstroke due to “delta” wave), (2) nodal rhythm (inverted P in aVF).
  • Long: first-degree atrioventricular (AV) block (Chap. 122).

QRS (0.06–0.10 s)

Widened: (1) ventricular premature beats, (2) bundle branch blocks: right (RsR′ in V1, deep S in V6) and left (RR′ in V6 [Fig. 111-2]), (3) toxic levels of certain drugs (e.g., flecainide, propafenone, quinidine), (4) severe hypokalemia.

FIGURE 111-2

Intraventricular conduction abnormalities. Illustrated are right bundle branch block (RBBB); left bundle branch block (LBBB); left anterior hemiblock (LAH); right bundle branch block with left anterior hemiblock (RBBB + LAH); and right bundle branch block with left posterior hemiblock (RBBB + LPH).

QT (<50% of RR interval; corrected QT ≤0.44 s)

Prolonged: congenital, hypokalemia, hypocalcemia, drugs (e.g., class IA and class III antiarrhythmics, tricyclics).


  • Right atrium: P wave ≥2.5 mm in lead II.
  • Left atrium: P biphasic (positive, then negative) in V1, with terminal negative force wider than 0.04 s.
  • Right ventricle: R > S in V1 and R in V1 > 5 mm; deep S in V6; right-axis deviation (Fig. 111-3).
  • Left ventricle: S in V1 plus R in V5 or V6 ≥35 mm or R in aVL >11 mm (Fig. 111-3).
FIGURE 111-3

Left ventricular hypertrophy (LVH) increases the amplitude of electrical forces directed to the left and posteriorly. In addition, repolarization abnormalities may cause ST-segment depression and T-wave inversion in leads with a prominent R wave. Right ventricular hypertrophy (RVH) may shift the QRS vector to the right; this effect usually is associated with an R, RS, or qR complex in lead V1. T-wave inversions may be present in the right precordial leads.


Following acute ST-segment elevation MI without successful reperfusion: Pathologic Q waves (≥0.04 s and ≥25% of total QRS height) in leads shown in Table 111-1; acute non-ST-segment elevation MI shows ST-T changes in these leads without Q-wave development (Fig. 111-4). A number of conditions (other than acute MI) can cause Q waves (Table 111-2).

Leads with Abnormal Q WavesSite of Infarction
I, aVL, V5–V6Anterolateral
II, III, aVFInferior
V1–V2 (tall R, not deep Q)True posterior

Physiologic or positional factors

  1. Normal “septal” Q waves
  2. Left pneumothorax or dextrocardia

Myocardial injury or infiltration

  1. Acute processes: myocardial infarction, myocarditis, hyperkalemia
  2. Chronic processes: cardiomyopathy, amyloid, sarcoid, scleroderma, myocardial tumor

Ventricular hypertrophy/enlargement

  1. Left ventricular (poor R-wave progression)a
  2. Right ventricular (reversed R-wave progression)
  3. Hypertrophic cardiomyopathy

Conduction abnormalities

  1. Left bundle branch block
  2. Wolff-Parkinson-White patterns

aSmall or absent R waves in the right to midprecordial leads.
Source: Modified from AL Goldberger: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby-Year Book, 1991.
FIGURE 111-4

Sequence of depolarization and repolarization changes with A. acute anterior and B. acute inferior ST-elevation infarctions (in the absence of successful early reperfusion). With anterior infarcts, ST elevation in leads I, aVL, and the precordial leads may be accompanied by reciprocal ST depressions in leads II, III, and aVF. Conversely, acute inferior (or posterior) infarcts may be associated with reciprocal ST depressions in leads V1–V3. (Modified from AL Goldberger et al: Goldberger’s Clinical Electrocardiography: A Simplified Approach, 8th ed. Philadelphia Elsevier, 2013.)


  • ST elevation: Acute MI, coronary spasm, pericarditis (concave upward) (see Fig. 116-1 and Table 116-2), LV aneurysm, Brugada pattern (RBBB with ST elevation in V1V2).
  • ST depression: Digitalis effect, strain (due to ventricular hypertrophy), ischemia, or nontransmural MI.
  • Tall peaked T: Hyperkalemia; acute MI (“hyperacute T”).
  • Inverted T: Non-Q-wave MI, ventricular “strain” pattern, drug effect (e.g., digitalis), hypokalemia, hypocalcemia, increased intracranial pressure (e.g., subarachnoid bleed).

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