Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (4 page)

• Intracranial bleed (“cerebral T waves,” usually w/ ↑ QT)

• Normal variant in children (V
₁
–V
₄
) 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

CHEST PAIN

Initial approach

•
Focused history
: quality & severity of pain; location & radiation; provoking & palliating factors; intensity at onset; duration, frequency & pattern; setting in which it occurred; associated sx; cardiac hx and risk factors

•
Targeted exam
: VS (including BP in both arms), cardiac gallops, murmurs or rubs; signs of vascular disease (carotid or femoral bruits, ↓ pulses), signs of heart failure; lung & abdominal exam; chest wall exam for reproducibility of pain

•
12-lead ECG
: obtain w/in 10 min; c/w priors & obtain serial ECGs; consider posterior leads (V
₇
–V
₉
) to reveal posterior MI if hx c/w ACS but ECG unrevealing or ST ↓ V
₁
–V
₄

•
Cardiac biomarkers (Tn
±
CK-MB)
: ✓ Tn at baseline & 3–6 h after sx onset
troponin
: >95% Se, 90% Sp; level >99th %ile w/ rise & fall in approp. setting is dx of MI detectable 1–6 h after injury, peaks 24 h, may remain elevated for 7–10 d in STEMI
high-sens. Tn
: 98% Se, 90% Sp w/in 3 h of admit, 90% Se w/in 1 h (
 JAMA
2011;306:2684)

Causes for ↑ Tn other than ACS (= “type 1 MI”): (1) Supply-demand mismatch not due to Δ in CAD (= “type 2 MI”; eg, ↑↑ HR, shock, HTN crisis, spasm, HCM, severe AS), (2) non-ischemic injury (myocarditis/toxic CMP, cardiac contusion) or (3) multifactorial (PE, sepsis, severe HF, renal failure, Takotsubo, infilt dis.) (
Circ
2012;126:2020)

CK-MB
: less Se & Sp (skel. muscle, tongue, diaphragm, intestine, uterus, prostate), useful for dx of post-PCI/CABG MI or MI if Tn already elevated

•
CXR
; other imaging (echo, PE CTA, etc.) as indicated based on H&P and initial testing

• If low prob of ACS (eg,
ECG & Tn) & stable → noninvasive fxnal or imaging test

• Coronary CT angio (CCTA): NPV 98% for signif CAD, but PPV 35% for ACS; helpful to r/o CAD if low-intermed prob of ACS. CCTA vs. noninv. fxnal test for ischemia → ↓ time to dx & LOS, but ↑ prob of cath/PCI, contrast exposure & ↑ radiation (
NEJM
2012;366:1393 & 367:299;
JACC
2013;61:880). “Triple r/o” CT angiogram for CAD, PE, AoD.

NONINVASIVE EVALUATION OF CAD

Stress testing (
Circ
2007;115:1464;
JACC
2012;60:1828)

•
Indications
: dx CAD, evaluate Δ in clinical status in Pt w/ known CAD, risk stratify s/p ACS, evaluate exercise tolerance, localize ischemia (imaging required) •
Contraindications
(
Circ
2002;106:1883; & 2012;126:2465)

Absolute
: AMI w/in 48 h, high-risk UA, acute PE, severe sx AS, uncontrolled HF, uncontrolled arrhythmias, myopericarditis, acute aortic dissection

Relative
: left main CAD, mod valvular stenosis, severe HTN, HCMP, high-degree AVB, severe electrolyte abnl

•
Exercise
: standard Bruce (↑ speed & incline q3min), modified Bruce (begins w/o treadmill incline), submax (if <3 wk post-MI) or sx-limited; hold nitrates/βB/CCB/ranolazine if trying to dx CAD, but give when assessing if Pt ischemic on meds •
Pharmacologic
: if unable to exer., low exer. tol, or recent MI. Se & Sp
exercise. Preferred if LBBB (requires imaging since ECG not interpretable).
Coronary vasodilators
(will reveal CAD, but
not
tell you if Pt
ischemic
): regadenoson, dipyridamole or adenosine (may precipitate bradycardia and bronchospasm).
Chronotropes/inotropes
(more physiologic): dobutamine (may precipitate tachyarrhythmias).

•
Imaging
: used if uninterpretable ECG (paced, LBBB, resting ST ↓ >1 mm, dig., LVH, WPW), after indeterminate ECG test, pharmacologic tests, or localization of ischemia

SPECT
(eg,
^99m
Tc-sestamibi),
PET
(rubidium-82; usually w/ pharm test),
echo
,
MRI

Test results

•
HR
(must achieve ≥85% of max pred HR [220-age] for
exer
. test to be dx),
BP
response, peak
double product
(HR × BP; nl >20k), HR recovery (HR
_peak
– HR
_{1
min later}
; nl >12) •
Max exercise capacity
achieved (METS or min) • Occurrence of
symptoms
(at what level of exertion and similarity to presenting sx) •
ECG
Δ
s
:
downsloping
or
horizontal
ST ↓ (≥1 mm) 60–80 ms after QRS predictive of CAD (but does
not
localize ischemic territory); however, STE highly predictive & localizes • Duke treadmill score = exercise min – (5 × max ST dev) – (4 × angina index) [0 none, 1 nonlimiting, 2 limiting]; score ≥5 → <1% 1-y mort; –10 to + 4 → 2–3%; ≤ –11 → ≥5%

•
Imaging
: radionuclide defects or echocardiographic regional wall motion abnormalities

reversible defect = ischemia; fixed defect = infarct; transient isch dilation = severe CAD

false
: breast → ant “defect” and diaphragm → inf “defect”

false
may be seen if balanced (eg, 3VD) ischemia (global ↓ perfusion w/o regional Δs)

High-risk test results (PPV ~50% for LM or 3VD, ∴ consider coronary angio)

• ECG: ST ↓ ≥2 mm
or
≥1 mm in stage 1
or
in ≥5 leads
or
≥5 min in recovery; ST ↑;  VT

• Physiologic: ↓ or fail to ↑ BP, <4 METS, angina during exercise, Duke score ≤ –11; ↓ EF