USMLE Step 1 - Cardiovascular Pathology & Electrocardiography (ECG) Interpretation Flashcards

Question 1

ECG Findings: Hyperkalemia vs. Hypokalemia

Accepted Answer

**Hyperkalemia**:
- Tall, peaked T waves (earliest sign)
- PR interval prolongation and QRS widening
- Flattening of P waves
- Progresses to a sine wave pattern and ventricular fibrillation

**Hypokalemia**:
- Prominent U waves (following T wave)
- T-wave flattening or inversion
- ST-segment depression
- Prolonged QT/QU interval (predisposing to Torsades de Pointes)

Question 2

STEMI vs. NSTEMI Key Differences

Accepted Answer

**STEMI (ST-Elevation Myocardial Infarction)**:
- Transmural (full-thickness) myocardial ischemia
- ST-elevation $\ge 1	ext{ mm}$ in $\ge 2$ contiguous leads (or new LBBB)
- Positive cardiac biomarkers (Troponin I/T, CK-MB)

**NSTEMI (Non-ST-Elevation Myocardial Infarction)**:
- Subendocardial (partial-thickness) ischemia
- ST depression and/or T-wave inversion (no ST elevation)
- Positive cardiac biomarkers

Question 3

First-Degree AV Block

Accepted Answer

**ECG Pattern**: Constant, prolonged PR interval ($>200	ext{ ms}$ or $>5$ small boxes) without dropped QRS complexes.

**Pathophysiology**: Delayed conduction through the AV node.

**Clinical Significance**: Usually benign and asymptomatic; no treatment required.

Question 4

Second-Degree AV Block: Mobitz Type I (Wenckebach)

Accepted Answer

**ECG Pattern**: Progressive lengthening of the PR interval until a QRS complex is dropped ("longer, longer, longer, drop").

**Location**: AV node level.

**Clinical Significance**: Usually benign, often due to increased vagal tone or AV-node blocking agents; typically asymptomatic.

Question 5

Second-Degree AV Block: Mobitz Type II

Accepted Answer

**ECG Pattern**: Constant PR intervals with unpredictable, intermittent dropped QRS complexes (e.g., $2:1$ or $3:1$ block).

**Location**: Below the AV node (His-Purkinje system).

**Clinical Significance**: Pathological; high risk of progression to Third-Degree AV block. Requires cardiac pacemaker.

Question 6

Third-Degree (Complete) AV Block

Accepted Answer

**ECG Pattern**: Complete AV dissociation where P waves and QRS complexes fire independently. Atrial rate ($>P	ext{ waves}$) is faster than ventricular rate ($>QRS$).

**Pathophysiology**: Absence of conduction between atria and ventricles. Ventricular escape rhythm generated by AV junction ($40	ext{--}60	ext{ bpm}$) or ventricles ($20	ext{--}40	ext{ bpm}$).

**Treatment**: Definite pacemaker insertion.

Question 7

Atrial Fibrillation vs. Atrial Flutter

Accepted Answer

**Atrial Fibrillation**:
- "Irregularly irregular" rhythm with no discrete P waves; fibrillatory baseline waves ($300	ext{--}600	ext{ bpm}$).
- Risk of mural thrombi in left atrial appendage $ightarrow$ embolic stroke.

**Atrial Flutter**:
- Rapid, regular atrial rhythm ($250	ext{--}350	ext{ bpm}$) with characteristic "sawtooth" flutter waves ($F$ waves).
- Commonly presents with fixed conduction ratios (e.g., $2:1$ or $4:1$ AV block).

Question 8

Pressure-Volume Loop: Increased Preload

Accepted Answer

**Changes on Loop**:
- Rightward shift of the End-Diastolic Volume (EDV) point.

**Hemodynamic Outcomes**:
- Increased End-Diastolic Volume ($EDV$)
- Increased Stroke Volume ($SV = EDV - ESV$)
- Unchanged End-Systolic Volume ($ESV$)

Question 9

Pressure-Volume Loop: Increased Afterload

Accepted Answer

**Changes on Loop**:
- Taller and narrower loop due to higher aortic pressure during ejection.

**Hemodynamic Outcomes**:
- Increased Peak Systolic Pressure
- Increased End-Systolic Volume ($ESV$)
- Decreased Stroke Volume ($SV = EDV - ESV$)

Question 10

Pressure-Volume Loop: Increased Inotropy (Contractility)

Accepted Answer

**Changes on Loop**:
- Leftward/upward shift of the End-Systolic Pressure-Volume Relationship (ESPVR) line.

**Hemodynamic Outcomes**:
- Decreased End-Systolic Volume ($ESV$)
- Increased Stroke Volume ($SV$)
- Increased Ejection Fraction ($EF = \frac{SV}{EDV}$)

Question 11

Aortic Stenosis (AS) - Murmur & Hemodynamics

Accepted Answer

**Murmur**: Crescendo-decrescendo systolic ejection murmur, loudest at the right upper sternal border, radiating to carotids. Associated with *pulsus parvus et tardus* (weak and delayed carotid pulse).

**Pathophysiology**: Obstruction of LV outflow leads to high pressure overload and concentric Left Ventricular Hypertrophy (LVH).

Question 12

Mitral Regurgitation (MR) - Murmur & Hemodynamics

Accepted Answer

**Murmur**: Holosystolic, high-pitched "blowing" murmur, loudest at the apex with radiation to the left axilla.

**Dynamic Maneuvers**: Intensity increases with increased afterload (handgrip, squatting).

**Pathophysiology**: Retrograde blood flow into the Left Atrium during systole $\rightarrow$ LA enlargement and eccentric LV hypertrophy.

Question 13

Aortic Regurgitation (AR) - Murmur & Physical Exam Signs

Accepted Answer

**Murmur**: High-pitched, early diastolic, decrescendo blowing murmur at the left sternal border. Loudest when patient sits up and leans forward in full expiration.

**Physical Exam Signs**:
- Wide pulse pressure ($PP = SBP - DBP$)
- "Water-hammer" pulse
- Head bobbing with systole (De Musset sign)
- Quincke capillary pulsations in fingernails

Question 14

Mitral Stenosis (MS) - Murmur & Dynamic Characteristics

Accepted Answer

**Murmur**: Opening snap (OS) followed by a mid-to-late diastolic rumbling murmur, loudest at the apex in the left lateral decubitus position.

**Key Concept**: A shorter interval between $S_2$ and the Opening Snap ($S_2	ext{--}OS$ interval) correlates with **more severe** stenosis (indicates higher left atrial pressure).

Question 15

$S_3$ vs. $S_4$ Heart Sounds

Accepted Answer

**$S_3$ Sound**:
- Occurs in early diastole during rapid ventricular filling.
- Caused by fluid overload or dilated ventricles (e.g., Heart Failure, MR).
- Normal in children and young adults/pregnant women.

**$S_4$ Sound**:
- Occurs in late diastole during atrial contraction ("atrial kick").
- Caused by high ventricular stiffness (e.g., LVH, hypertensive heart disease).
- Always pathological.

Question 16

Systolic vs. Diastolic Heart Failure

Accepted Answer

**Systolic Failure (HFrEF)**:
- Reduced Ejection Fraction ($EF < 40\%$)
- Increased EDV with eccentric remodeling
- Caused by MI, dilated cardiomyopathy

**Diastolic Failure (HFpEF)**:
- Preserved Ejection Fraction ($EF \ge 50\%$)
- Normal EDV with decreased compliance and concentric hypertrophy
- Caused by chronic hypertension, amyloidosis

Question 17

Hypertrophic Cardiomyopathy (HCM) - Maneuver Dynamics

Accepted Answer

**Pathophysiology**: Autosomal dominant mutations in sarcomeric proteins (most commonly $\beta$-myosin heavy chain or myosin-binding protein C) causing asymmetric septal hypertrophy.

**Murmur**: Harsh systolic ejection murmur along left sternal border.

**Effect of Maneuvers**:
- **Increases intensity**: Decreased preload or afterload (Valsalva strain, standing up) $\rightarrow$ smaller LV cavity size increases outflow tract obstruction.
- **Decreases intensity**: Increased preload or afterload (squatting, handgrip) $\rightarrow$ larger LV cavity size separates anterior mitral leaflet from septum.

Question 18

Myocardial Infarction: Microscopic Timeline

Accepted Answer

- **0–4 hours**: No light microscopic changes; wavey fibers under electron microscopy.
- **4–12 hours**: Early coagulative necrosis, edema, hemorrhage, contraction bands.
- **1–3 days**: Dense neutrophilic infiltrate, extensive coagulative necrosis.
- **3–7 days**: Macrophage phagocytosis of necrotic tissue (**highest risk for free wall rupture, papillary muscle rupture, or VSD**).
- **1–2 weeks**: Granulation tissue and neovascularization.
- **>2 weeks**: Dense collagenous scar tissue formation.

Question 19

Cardiac Biomarkers: Troponin I/T vs. CK-MB

Accepted Answer

**Cardiac Troponin I/T**:
- Gold standard diagnostic test
- Rises within $2	ext{--}4$ hours, peaks at $24$ hours, stays elevated for $7	ext{--}10$ days.

**CK-MB**:
- Rises within $4	ext{--}6$ hours, peaks at $24$ hours, returns to baseline in $48	ext{--}72$ hours.
- Clinical utility: Diagnosing **re-infarction** occurring shortly after initial MI.

Question 20

Acute Pericarditis - ECG & Clinical Diagnosis

Accepted Answer

**Clinical Presentation**: Sharp, retrosternal chest pain that decreases when leaning forward; pericardial friction rub on auscultation.

**ECG Findings**:
- Widespread, diffuse ST-segment elevation
- PR-segment depression in multiple leads
- Lead aVR shows reciprocal ST depression and PR elevation.

Question 21

Ventricular Tachycardia (VT) vs. Ventricular Fibrillation (VF)

Accepted Answer

**Ventricular Tachycardia (VT)**:
- Wide QRS complexes ($>120	ext{ ms}$) at a rapid rate ($>100	ext{ bpm}$).
- Monomorphic or polymorphic (e.g., Torsades de Pointes).
- May produce pulse or hemodynamic instability; can degenerate to VF.

**Ventricular Fibrillation (VF)**:
- Completely chaotic, irregular ventricular rhythm with no recognizable P waves, QRS complexes, or T waves.
- Fatal arrhythmia causing absent cardiac output; requires immediate CPR and electrical defibrillation.

Question 22

Pathophysiology of Atherosclerotic Plaque Formation

Accepted Answer

1. **Endothelial injury** due to hypertension, smoking, or hyperlipidemia.
2. **LDL entry and oxidation** ($oxLDL$) in the subendothelial tunica intima.
3. **Monocyte recruitment** and transmigration into the intima, differentiating into macrophages.
4. **Foam Cell formation**: Macrophages phagocytose $oxLDL$ via scavenger receptors.
5. **Smooth muscle migration**: Vascular smooth muscle cells proliferate from tunica media to intima, depositing collagen to form a **fibrous cap**.

USMLE Step 1 - Cardiovascular Pathology & Electrocardiography (ECG) Interpretation

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