Approach (a systematic approach is vital)

• Intervals (PR. QRS. QT) and axis (? LAD or RAD)

• Chamber enlargement (> LAE and/or RAE. ? LVH and/or RVH)

• QRST changes (? Q waves, poor R wave progression. ST A. or T wave inversions)

Figure 1-1 QRS axil

Figure 1-1 QRS axil

Left axis deviation (LAD)

• Definition: axis beyond -30° (S > R in lead II)

• Etiologies: LVH. LBBB. inferior Ml. elevated diaphragm. WPW

and qR in I & rS in II. lll.aVF and QRS 120 msec and no other cause of LAD Right axis deviation (RAD)

septal defects, lateral Ml.WPW

and rS in I & qR in III and QRS 120 msec and no other cause of RAD

Bundle Branch Blocks


Initial depol. is left-to-right across septum (r In Vi & q in V^ nb. absent in LBBB) followed by LV S RV free wall, with LV dominating (nb. RV depol. later and visible in RBBB)


Aa V-

1 QRS -120 msec (100 119 incomplete)

2. rSR' in R precordial leads (Vi.Vj)

4 • STl or TWI in R precordial leads


1 QRS >120 msec (100 119 incomplete)

2. Broad, slurred, monophasic R in 1 & V. (r S if cardiomeg)

4. Displacement of ST &Tw opposite major QRS deflection

5. • PRWP. LAD. Q s in inferior leads

Bifaic.cular block: RBB8 • LAHB/LPHB; Trifascicular 1" AVB • RBB8 • LAHB/LPHB Prolonged QT interval (JAMA 2003:289:2120; Nf/M 2CX>4;3S0:1013: www.tonadej.ort)

• QT measured from beginning of QRS complex to end of T wave

• QT varies wI HR. correct w/ Bazett formula: QTc QT/VRR (nl QTc 440 msec)

Antiarrhythmics: class IA and class III

Psychiatric drugs: antipsychotics (phenothiazines, haloperidol. atypicals). lithium Antimicrobials: macrolides. quinolones. voriconazole, pentamidine, atovaquone.

chloroquine. amantadine, foscarnet Other drugs: antiemetics (droperidol. 5-HTj antagonists), alfuzosin. methadone Electrolyte disturbances: hypoCa. ? hypoK. ? hypoMg

Autonomic dysfxn: ICH (deep TWI). stroke, carotid endarterectomy. neck dissection Congenital (Long QT Syndrome): K/Na channelopathies. may be assoc w/ deafness Misc: CAD. CMP. bradycardia, high-grade AVB. hypothyroidism, hypothermia

Left Atrial Enlargement (LAE)

ECG P wave Criteria

Left Atrial Enlargement (LAE)

Left ventricular hypertrophy (LVH)

• Etiologies: HTN. AS/AI. HCMP. coarctation of aorta

Romhilt-Estes point-score system: 4 points probable. 5 points - definite T Amplitude (any of the following): largest R or S in limb leads ^20 mm or S in Vi orVj -30 mm or R inVs orV* ^30 mm (3 points)

ST displacement opposite to QRS deflection: w/o dig (3 points): w/ dig (1 point) LAE (3 points); LAD (2 points); QRS duration -90 msec (1 point) Intrinsicoid deflection (QRS onset to peak of R) inV$ orV6 -50 msec (1 point) Sokolow-Lyon: S in Vi - R in V* orV6 ^35 mm Cornell: R in aVL • S in V3 -28 mm in men or >20 mm in women Other: R in aVL -11 mm (or. if LAD. ^13 mm and S in III -15 mm) Right ventricular hypertrophy (RVH)

• Etiologies: cor pulmonale, congenital (tetralogy.TGA. PS. ASD.VSD). MS.TR

• Criteria (all tend to be insensitive, but highly specific, except in COPD)

R -S inVi or R inVi -7 mm.S lnV$ orV6 -7 mm. drop in R/S ratio across precordium RAD ♦110° (LVH • RAD - biventricular hypertrophy) Ddx of dominant R wave inVi orV2

• Ventricular enlargement: RVH (RAD. RAE. deep S waves in I. V5. V6); HCMP

• Myocardial injury:True posterior Ml (often IMI); Duchenne muscular dystrophy

• Abnormal depolarization: RBBB (QRS 120 msec. rSR'); WPW (i PR. ft wave. I QRS)

• Other: dextroversion; lead misplacement; normal variant Low voltage

• QRS amptitude (R *S) - 5 mm in all limb leads & 10 mm in all precordial leads

• Etiologies: COPD (precordial leads only), pericardial effusion, myxedema, obesity, pleural effusion, restrictive or infiltrative CMP. diffuse CAD

Pathologic Q waves

• Definition: ?40 msec or 25% height of the R wave in that complex

• Small (septal) q waves in I. aVL Vs & V6 are normal, as can be isolated Qw in III. aVR. Vi

• "Pseudo-infarct" pattern may be seen in LBB8. infiltrative disease. HCMP. COPD. PTX. WPW

Poor R wave progression (PRWP) 1982:142:1145)

• Definition: loss of anterior forces w/o frank Q waves (V1-V3); R wave in Vj ^3 mm

old anteroseptal Ml (usually R waveVj s1.5 mm. - persistent ST i orTWIVi &V3) cardiomyopathy

LVH (delayed RWP with prominent left precordial voltage) RVH/COPD (small R wave and prominent S wave in lead I) LBBB; WPW; clockwise rotation of the heart; lead misplacement ST elevation (STE) (nejm 2003:349:2128)

• Acute Ml (upward convexity • TWI) or prior Ml with persistent STE

• Coronary spasm (Prinzmetal's angina; transient STE in a coronary distribution)

• Pericarditis (diffuse, upward concavity STE; associated with PR l;Tw usually upright);

myocarditis; cardiac contusion; ventricular aneurysm

• Pulmonary embolism (occ. STE V, Vj; typically associated TWI V, V<. RAD. RBBB)

• Repolarization abnormalities

LBBB C QRS duration. STE discordant from QRS complex) dx of STEMI in setting of LBBB: 1 mm STE concordant w/ QRS (Se 73%. Sp 92%) or -5 mm discordant (Se 31%. Sp 92%) (Nejm 1996:334481) LVH (! QRS amplitude) Hyperkalemia (t QRS duration, tall Ts. no Ps) Brugada syndrome (rSR\ downsloping STE Vt Vj)

• Normal early repolarization: most often seen in leads Vj Vj and in young adults

J point r 1 4 mm; notch in downstroke of R wave; upward concavity of ST; large Tw. ratio of STE IT wave amplitude <25%; pattern may disappear with exercise ST depression

• Myocardial ischemia (• T wave abnormalities) or acute true posterior Ml (Vi Vj)

• Digitalis effect (downsloping ST • T wave abnormalities, does not correlate with dig levels)

• Repolarization abnl in association with LBBB or LVH (usually in leads Vj.V*, I. aVL) T wave inversion (TWI)

• Myocardial ischemia or infarct; peri/myocarditis: cardiomyopathy; mitral valve prolapse

• Repolarization abnl in association with LVH/RVH ("strain pattern"). BBB

• Post-tachycardia or post-pacing

• Electrolyte, digoxin. PaOj. PaC02. pH. or core temperature disturbances

• Intracranial bleed ("cerebral T waves." usually with T QT)

• Normal variant in children (Vi V«) and leads in which QRS complex predominantly

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