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STANDARD APPROACH TO THE ECG
Normally, voltage standardization is 1.0 mV per 10 mm, and paper speed is 25 mm/s (each horizontal small box = 0.04 s).
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.
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°).
INTERVALS (NORMAL VALUES IN PARENTHESES)
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.
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).
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 Waves||Site of Infarction|
|I, aVL, V5–V6||Anterolateral|
|II, III, aVF||Inferior|
|V1–V2 (tall R, not deep Q)||True posterior|
Physiologic or positional factors
Myocardial injury or infiltration
- 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).