CARDIOLOGY
ELECTROCARDIOGRAPHY
Approach (a systematic approach is vital)
• Rate (? tachy, brady) and rhythm (? relationship between P and QRS)
• Intervals (PR, QRS, QT) and axis (? LAD or RAD)
• Chamber abnormality (? LAA and/or RAA, ? LVH and/or RVH)
• QRST changes (? Q waves, poor R-wave progression V1–V6, ST ↑/↓ or T-wave Δs)
Figure 1-1 QRS axis
Left axis deviation (LAD)
• Definition: axis beyond –30° (S > R in lead II)
• Etiologies: LVH, LBBB, inferior MI, WPW
• Left anterior fascicular block: LAD (–45 to –90°) and qR in aVL and QRS <120 msec and no other cause of LAD (eg, IMI)
Right axis deviation (RAD)
• Definition: axis beyond +90° (S > R in lead I)
• Etiologies: RVH, PE, COPD (usually not > +110°), septal defects, lateral MI, WPW
• Left posterior fascicular block: RAD (90–180°) and rS in I & aVL and qR in III & aVF and QRS <120 msec and no other cause of RAD
Prolonged QT interval (NEJM 2008;358:169; www.torsades.org)
• QT measured from beginning of QRS complex to end of T wave (measure longest QT)
• QT varies w/ HR → correct w/ Bazett formula: QTc = QT/√RR (in sec), formula inaccurate at very high and low HR (nl QTc <440 msec and <460 msec )
• QT prolongation a/w ↑ risk TdP (esp. >500 msec); perform baseline/serial ECGs if using QT prolonging meds, no estab guidelines for stopping Rx if QT prolongs
• Etiologies:
Antiarrhythmics: class Ia (procainamide, disopyramide), class III (amiodarone, sotalol)
Psych drugs: antipsychotics (phenothiazines, haloperidol, atypicals), Li, ? SSRI, TCA
Antimicrobials: macrolides, quinolones, azoles, pentamidine, atovaquone, atazanavir
Other: antiemetics (droperidol, 5-HT3 antagonists), alfuzosin, methadone, ranolazine
Electrolyte disturbances: hypoCa (nb, hyperCa a/w ↓ QT), ? hypoK, ? hypoMg
Autonomic dysfxn: ICH (deep TWI), stroke, carotid endarterectomy, neck dissection
Congenital (long QT syndrome): K, Na, Ca channelopathies (Circ 2013;127:126)
Misc: CAD, CMP, bradycardia, high-grade AVB, hypothyroidism, hypothermia, BBB
Left ventricular hypertrophy (LVH) (Circ 2009;119:e251)
• Etiologies: HTN, AS/AI, HCMP, coarctation of aorta
• Criteria (all w/ Se <50%, Sp >85%; accuracy affected by age, sex, race, BMI)
Romhilt-Estes point-score system: 4 points = probable, 5 points = definite ↑ Amplitude (any of the following): largest R or S in limb leads ≥20 mm or S in V1 or V2 ≥30 mm or R in V5 or V6 ≥30 mm (3 points)
ST displacement opposite to QRS deflection: w/o dig (3 points); w/ dig (1 point)
LAA (3 points); LAD (2 points); QRS duration ≥90 msec (1 point)
Intrinsicoid deflection (QRS onset to peak of R) in V5 or V6 ≥50 msec (1 point)
Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm or R in aVL ≥11 mm
Cornell: R in aVL + S in V3 >28 mm in men or >20 mm in women
If LAD/LAFB, S in III + max (R+S) in precordium ≥30 mm
Right ventricular hypertrophy (RVH) (Circ 2009;119:e251)
• 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 in V1 or R in V1 ≥7 mm, S in V5 or V6 ≥7 mm, drop in R/S ratio across precordium
RAD ≥ +110° (LVH + RAD or prominent S in V5 or V6 → biventricular hypertrophy)
Ddx of dominant R wave in V1 or V2
• Ventricular enlargement: RVH (RAD, RAA, deep S waves in I, V5, V6); HCMP
• Myocardial injury: posterior MI (anterior Rw = posterior Qw; often with IMI)
• Abnormal depolarization: RBBB (QRS >120 msec, rSR′); WPW (↓ PR, Δ wave, ↑ QRS)
• Other: dextroversion; Duchenne muscular dystrophy; lead misplacement; nl variant
Poor R wave progression (PRWP) (Am Heart J 2004;148:80)
• Definition: loss of anterior forces w/o frank Q waves (V1–V3); R wave in V3 ≤3 mm
• Possible etiologies (nonspecific):
old anteroseptal MI (usually w/ R wave V3 ≤1.5 mm, ± persistent ST ↑ or TWI V2 & V3) cardiomyopathy
LVH (delayed RWP with prominent left precordial voltage), RVH, COPD (which may also have RAA, RAD, limb lead QRS amplitude ≤5, SISIISIII w/ R/S ratio <1 in those leads)
LBBB; WPW; clockwise rotation of the heart; lead misplacement; PTX
Pathologic Q waves
• Definition: ≥30 msec (≥20 msec V2–V3) or >25% height of R wave in that QRS complex
• Small (septal) q waves in I, aVL, V5 & V6 are nl, as can be isolated Qw in III, aVR, V1
• “Pseudoinfarct” pattern may be seen in LBBB, infiltrative dis., HCMP, COPD, PTX, WPW
ST elevation (STE) (NEJM 2003;349:2128; Circ 2009;119:e241 & e262)
• Acute MI (upward convexity ± TWI) or prior MI with persistent STE
• Coronary spasm (Prinzmetal’s angina; transient STE in a coronary distribution)
• Myopericarditis (diffuse, upward concavity STE; a/w PR ↓; Tw usually upright)
• HCMP, Takotsubo CMP, ventricular aneurysm, cardiac contusion
• Pulmonary embolism (occ. STE V1–V3; typically associated TWI V1–V4, RAD, RBBB)
• Repolarization abnormalities
LBBB (↑ QRS duration, STE discordant from QRS complex)
dx of STEMI in setting of LBBB: ≥1 mm STE concordant w/ QRS (Se 73%, Sp 92%), STD ≥1 mm V1–V3 (Se 25%, Sp 96%) or STE ≥5 mm discordant w/ QRS (Se 31%, Sp 92%) (“Sgarbossa criteria,” NEJM 1996;334:481)
LVH (↑ QRS amplitude); Brugada syndrome (rSR′, downsloping STE V1–V2)
Hyperkalemia (↑ QRS duration, tall Ts, no Ps)
• aVR: STE >1 mm a/w ↑ mort in STEMI; STE aVR > V1 a/w left main disease
• Early repolarization: most often seen in V2–V5 & in young adults (Ann Emerg Med 2012;60:45)
J point ↑ 1–4 mm; notch in downstroke of R wave; upward concavity of ST; large Tw;
ratio of STE / T wave amplitude <25%; pattern may disappear with exercise
? early repol in inf leads may be a/w ↑ risk of VF (NEJM 2009;361:2529; Circ 2011;124:2208)
ST depression (STD)
• Myocardial ischemia (± Tw abnl) or acute true posterior MI (V1–V3)
• Digitalis effect (downsloping ST ± Tw abnl, does not correlate w/ dig levels)
• Hypokalemia (± U wave)
• Repolarization abnl in a/w LBBB or LVH (usually in leads V5, V6, I, aVL)
T wave inversion (TWI; generally ≥1 mm; deep if ≥5 mm) (Circ 2009;119:e241)
• Ischemia or infarct; Wellens’ sign (deep early precordial TWI) → proximal LCA lesion
• Myopericarditis; CMP (Takotsubo, ARVC, apical HCM); MVP; PE (esp. if TWI V1–V4)
• Repolarization abnl in a/w LVH/RVH (“strain pattern”), BBB
• Posttachycardia or postpacing
• Electrolyte, digoxin, PaO2, PaCO2, pH or core temperature disturbances
• Intracranial bleed (“cerebral T waves,” usually w/ ↑ QT)
• Normal variant in children (V1–V4) and leads in which QRS complex predominantly
Low voltage
• QRS amplitude (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