Pocket Medicine




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)

•  HCMPTakotsubo CMPventricular 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