USMLE STEP 1 • PDF COMMAND MAP

High-Yield Cardio

Tap, compare, and pressure-test the facts most likely to become vignette traps.

Tap a node

RHF, LHF, and shock separate cleanly when you anchor them to pressure and backup location.

Preload dial

Normal volumeBaseline murmur intensity

Low preload exception
HOCM and MVP get louder; most others soften.

Maneuver compass

Valsalva / stand ↓ preload

↑ HOCM, ↑ MVP
↓ most other murmurs

Squat / leg raise ↑ preload

Usually reverses the low-preload pattern; squatting also ↑ afterload.

Handgrip ↑ afterload

↑ MR, AR, VSD; ↓ AS and HOCM. PDF trap: may intensify MS.

Inspiration → right

TR, TS, PR, PS intensify. Expiration favors left-sided sounds.

Sound → lesion

AS
Crescendo–decrescendo → carotids
SAD: syncope, angina, dyspnea

MR
Holosystolic → axilla
Often louder with handgrip

MS
Opening snap + diastolic rumble
Rheumatic fever, AF risk

AR
Early diastolic decrescendo
Wide pulse pressure

ASD
Fixed split S2 ± flow murmur

VSD
Holosystolic at LLSB; late Eisenmenger

Checkpoint: murmur louder on standing?

Standing lowers preload, shrinking the LV cavity and worsening dynamic outflow obstruction.

The infarct clock

0–24 h

Coagulative necrosis; markers may initially be normal. ECG drives acute recognition.

1–3 d

Neutrophils dominate. Fibrinous pericarditis can appear.

3–14 d

Macrophages digest tissue → rupture risk peaks. Yellow, soft myocardium by ~10–14 d.

≥2 wk

Granulation then collagen scar; old infarcts become white.

Free-wall rupture
Tamponade → Beck triad.

Papillary rupture
Acute MR + pulmonary edema.

Septal rupture
New harsh holosystolic murmur.

Markers
Troponin: longest. CK-MB: reinfarction.

ECG anchor

ST elevation = transmural acute injury pattern. Reperfusion is beneficial despite free-radical injury. Adenosine accumulates with ATP depletion and contributes to ischemic pain.

Shunt logic

Early: pressure drives L→R flow, so oxygen “steps up” in the receiving right-sided chamber.

Chronic: excess pulmonary flow → pulmonary hypertension → RV hypertrophy.

Late: reversal to R→L = Eisenmenger → cyanosis and clubbing.

ASD
O₂ step-up in RA; fixed S2; paradoxical embolus.

VSD
O₂ step-up in RV; loud after PVR falls; LLSB murmur.

PDA
O₂ step-up in PA; continuous machinery murmur; rubella.

TOF
PROVe; severity follows pulmonic stenosis; squatting ↑ SVR.

Ductus control

PGE₁ keeps open

Indomethacin closes

A duct-dependent neonate who becomes cyanotic days after birth may have deteriorated when the ductus closed.

Loop

NKCC2 block, thick ascending limb. Strong diuresis, hypokalemia, ototoxicity, ↑ urinary Ca²⁺.

Thiazide

NaCl block, early DCT. ↓ urinary Ca²⁺, hypercalcemia, gout risk.

ENaC blockers

Amiloride/triamterene: potassium-sparing; useful add-on for edema with loop therapy.

Aldosterone blockers

Spironolactone/eplerenone: K⁺-sparing and remodeling benefit; gynecomastia with spironolactone.

ACE inhibitor

↓ Ang II, ↓ aldosterone, ↑ bradykinin. Cough, hyperkalemia, angioedema; avoid pregnancy and bilateral renal artery stenosis.

Pulmonary HTN

↑ endothelin-1, ↓ NO signaling. Bosentan blocks endothelin receptors.

Fast discriminator: edema relief is not the same as mortality benefit. Diuretics improve congestion; ACEi, selected β-blockers, and aldosterone antagonists oppose remodeling.

HY Cardio Command Map