Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (3 page)

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-HT
₃
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 V
₁
or V
₂
≥30 mm
or
R in V
₅
or V
₆
≥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 V
₅
or V
₆
≥50 msec (1 point)

Sokolow-Lyon: S in V
₁
+ R in V
₅
or V
₆
≥35 mm or R in aVL ≥11 mm

Cornell: R in aVL + S in V
₃
>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 V
₁
or R in V
₁
≥7 mm, S in V
₅
or V
₆
≥7 mm, drop in R/S ratio across precordium

RAD ≥ +110° (LVH + RAD
or
prominent S in V
₅
or V
₆
→
biventricular
hypertrophy)

Ddx of dominant R wave in V1 or V2

• Ventricular enlargement: RVH (RAD, RAA, deep S waves in I, V
₅
, V
₆
); 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 (V
₁
–V
₃
); R wave in V
₃
≤3 mm

• Possible etiologies (nonspecific):

old anteroseptal MI (usually w/ R wave V
₃
≤1.5 mm, ± persistent ST ↑ or TWI V
₂
& V
₃
) cardiomyopathy

LVH (delayed RWP with prominent left precordial voltage), RVH, COPD (which may also have RAA, RAD, limb lead QRS amplitude ≤5, S
_I
S
_II
S
_III
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 V
₂
–V
₃
) or >25% height of R wave in that QRS complex

• Small (septal) q waves in I, aVL, V
₅
& V
₆
are nl, as can be isolated Qw in III, aVR, V
₁

• “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 V
₁
–V
₃
; typically associated TWI V
₁
–V
₄
, 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 V
₁
–V
₃
(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 V
₁
–V
₂
)

Hyperkalemia (↑ QRS duration, tall Ts, no Ps)

•
aVR
: STE >1 mm a/w ↑ mort in STEMI; STE aVR > V
₁
a/w left main disease

•
Early repolarization
: most often seen in V
₂
–V
₅
& 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 (V
₁
–V
₃
)

• 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 V
₅
, V
₆
, 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 V
₁
–V
₄
)

• Repolarization abnl in a/w LVH/RVH (“strain pattern”), BBB

• Posttachycardia or postpacing

• Electrolyte, digoxin, PaO
₂
, PaCO
₂
, pH or core temperature disturbances