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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 !!navigator!!

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.

Rhythm !!navigator!!

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. 124 Bradyarrhythmias and 125 Tachyarrhythmias.

Mean Axis !!navigator!!

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. 113-1. Electrocardiographic Lead Systems: The Hexaxial Frontal Plane Reference System to Estimate Electrical Axis). 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) !!navigator!!

PR (0.12-0.20 S) !!navigator!!

Qrs (0.06-0.10 S) !!navigator!!

Widened: (1) ventricular premature beats, (2) bundle branch blocks: right (RsR' in V1, deep S in V6) and left (RR' in V6 [Fig. 113-2. Intraventricular Conduction Abnormalities]), (3) toxic levels of certain drugs (e.g., flecainide, propafenone, quinidine), (4) severe hypokalemia.

QT (<50% of RR interval; corrected QT 0.45 s in men, 0.46 s in women)!!navigator!!

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

Hypertrophy !!navigator!!

Infarction

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 113-1 Leads with Abnormal Q Waves in MI; acute non-ST-segment elevation MI shows ST-T changes in these leads without Q-wave development (Fig. 113-4. Sequence of Depolarization and Repolarization Changes). A number of conditions (other than acute MI) can cause Q waves (Table 113-2 Differential Diagnosis of Q Waves (with Selected Examples)).

ST-T Waves !!navigator!!

  • ST elevation: Acute MI, coronary spasm, pericarditis (concave upward) (see Fig. 118-1 Electrocardiogram in Acute Pericarditis and Table 118-2 ECG in Acute Pericarditis vs Acute ST-Elevation MI), LV aneurysm, Brugada pattern (RBBB with ST elevation in V1-V2).
  • 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).

Outline

Section 8. Cardiology