Harrison’s Manual of Medicine



Standard Approach to the ECG
Indications for Echocardiography
Normally, 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.
RHYTHM   Sinus rhythm is present if every P wave is followed by a QRS, PR interval ³0.12 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 Chap. 115.
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. 113-1). 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.

FIGURE 113-1. 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.

Left-axis deviation (£30°) occurs in diffuse left ventricular disease, inferior MI; also 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 seen in thin, healthy individuals (up to 110°).

Short: (1) preexcitation syndrome (look for slurred QRS upstroke due to “delta” wave), (2) nodal rhythm (inverted P in aVF).

Long: first-degree AV block (Chap. 115).
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. 113-2), (3) toxic levels of certain drugs (e.g., quinidine), (4) severe hypokalemia.

FIGURE 113-2. 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). (Reproduced from RJ Myerburg: HPIM-12.)

QT (£0.43 s; <50% of RR interval)

Prolonged: congenital, hypokalemia, hypocalcemia, drugs (quinidine, procainamide, tricyclics).

Right atrium: P wave ³2.5 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.

Left ventricle: S in V1 plus R in V5 or V6 ³ 35 mm or R in aVL > 11 mm.
INFARCTION (Fig. 113-3 and Fig. 113-4)   Q-wave MI: Pathologic Q waves (³0.04 s and ³25% of total QRS height) in leads shown in Table 113-1; acute non-Q-wave MI shows ST-T changes in these leads without Q wave development. A number of conditions (other than acute MI) can cause Q waves (Table 113-2).

FIGURE 113-3. Sequence of depolarization and repolarization changes with (A) acute anterior and (B) acute inferior wall Q-wave infarctions. 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 to V3. (After AL Goldberger, E Goldberger: Clinical Electrocardiography: A Simplified Approach, 6th ed. St. Louis, Mosby-Year Book, 1999.)

FIGURE 113-4. Acute inferior wall myocardial infarction. The ECG of 11/29 shows minor nonspecific ST-segment and T-wave changes. On 12/5 an acute myocardial infarction occurred. There are pathologic Q waves (1), ST-segment elevation (2), and terminal T-wave inversion (3) in leads II, III, and aVF indicating the location of the infarct on the inferior wall. Reciprocal changes in aVL (small arrow). Increasing R-wave voltage with ST depression and increased voltage of the T wave in V2 are characteristic of true posterior wall extension of the inferior infarction. (Reproduced from RJ Myerburg: HPIM-12.)

Table 113-1 Leads with Abnormal Q Waves in MI

Table 113-2 Differential Diagnosis of Q Waves (with Selected Examples)

ST-T Waves

ST elevation: Acute MI, coronary spasm, pericarditis (concave upward), LV aneurysm.

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).

FIGURE 113-5. A schematic presentation of the normal M-mode echocardiographic (Echo) recording of anterior (AML) and posterior mitral leaflet (PML) motion is shown in the center with the simultaneous ECG. Abnormal mitral echocardiograms which occur in (A) mitral stenosis, (B) left atrial myxoma, (C) mitral valve prolapse, and (D) obstructive hypertrophic cardiomyopathy are also depicted. In the ECHO, the A point represents the end of anterior movement resulting from left atrial contraction, the CD segment represents the closed position of both mitral leaflets during ventricular systole, and point E ends the anterior movement as the leaflet opens. The slope EF results from posterior motion of the AML during rapid ventricular filling. In obstructive hypertrophic cardiomyopathy, SAM represents systolic anterior movement. (Reproduced from J Wynne, RA O’Rourke, E Braunwald: HPIM-10, p. 1333.)

VALVULAR STENOSIS   Both native and artificial valvular stenosis can be evaluated, and severity can be determined by Doppler [peak gradient = 4 × (peak velocity)2].
VALVULAR REGURGITATION   Structural lesions (e.g., flail leaflet, vegetation) resulting in regurgitation may be identified. Echo can demonstrate whether ventricular function is normal; Doppler (Fig. 113-6) can identify and estimate severity of regurgitation through each valve.

FIGURE 113-6. Schematic presentation of normal Doppler flow across the aortic (A) and mitral valves (B). Abnormal continuous wave Doppler profiles are depicted in C. Aortic stenosis (AS) [peak transaortic gradient = 4 × Vmax2 = 4 × (3.8)2 = 58 mmHg] and regurgitation (AR). D. Mitral stenosis (MS) and regurgitation (MR).

VENTRICULAR PERFORMANCE   Global and regional wall motion abnormalities of both ventricles can be assessed; ventricular hypertrophy/infiltration may be visualized; evidence of pulmonary hypertension may be obtained.
CARDIAC SOURCE OF EMBOLISM   May visualize atrial or ventricular thrombus, intracardiac tumors, and valvular vegetations. Yield of identifying cardiac source of embolism is low in absence of cardiac history or physical findings. Transesophageal echocardiography is more sensitive than standard transthoracic study for this purpose.
ENDOCARDITIS   Vegetation visualized in more than half of pts (transesophageal echo has much higher sensitivity), but management is generally based on clinical findings, not echo. Complications of endocarditis (e.g., valvular regurgitation) may be evaluated.
CONGENITAL HEART DISEASE   Echo, Doppler, and contrast echo (rapid IV injection of saline) are noninvasive procedures of choice in identifying congenital lesions.
AORTIC ROOT   Aneurysm and dissection of the aorta may be evaluated and complications (aortic regurgitation, tamponade) assessed (Chap. 125).
HYPERTROPHIC CARDIOMYOPATHY, MITRAL VALVE PROLAPSE, PERICARDIAC EFFUSION   Echo is the diagnostic technique of choice for identifying these conditions.

For a more detailed discussion, see Goldberger AL: Electrocardiography, Chap. 226, p. 1262; and Nishimura RA, Gibbons RJ, Tajik AJ: Noninvasive Cardiac Imaging: Echocardiography and Nuclear Cardiology, Chap. 227, p. 1271, in HPIM-15.



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