USMLE Step 1 - Cardiovascular Pathology & Pathophysiology Flashcards

Question 1

Cardiac Output (CO), Stroke Volume (SV), and Ejection Fraction (EF) Formulas

Accepted Answer

• **Stroke Volume (SV):** $SV = EDV - ESV$
• **Cardiac Output (CO):** $CO = HR 	imes SV = \frac{	ext{O}_2 	ext{ Consumption}}{	ext{Arteriovenous } 	ext{O}_2 	ext{ Difference}}$ (Fick Principle)
• **Ejection Fraction (EF):** $EF = \frac{SV}{EDV} = \frac{EDV - ESV}{EDV} 	imes 100\%$ (Normal $\ge 55\%$)

Question 2

Pressure-Volume (PV) Loop: Effects of Increased Preload

Accepted Answer

• **PV Loop Shift:** Widens to the right.
• **Changes:** Increased End-Diastolic Volume (EDV) and increased Stroke Volume ($SV = EDV - ESV$).
• **ESV & Contractility:** Unchanged.

Question 3

Pressure-Volume (PV) Loop: Effects of Increased Afterload

Accepted Answer

• **PV Loop Shift:** Taller and narrower.
• **Changes:** Increased aortic valve opening pressure and peak systolic pressure, increased End-Systolic Volume (ESV), and decreased Stroke Volume ($SV$).
• **EDV:** Unchanged.

Question 4

Pressure-Volume (PV) Loop: Effects of Increased Contractility

Accepted Answer

• **PV Loop Shift:** Shifts to the left; increases End-Systolic Elastance (steeper ESPVR slope).
• **Changes:** Decreased End-Systolic Volume (ESV) and increased Stroke Volume ($SV$).
• **EF Effect:** $EF$ increases significantly.

Question 5

Myocardial Infarction Timeline: 0 to 24 Hours

Accepted Answer

• **0-4 hours:** Grossly and light microscopically normal; risk of fatal ventricular arrhythmias (e.g., VFib).
• **4-12 hours:** Early coagulative necrosis, wave-front contraction band necrosis (if reperfused), edema, hemorrhage.
• **12-24 hours:** Coagulative necrosis becomes prominent, dark mottling, early neutrophilic infiltrate.

Question 6

Myocardial Infarction Timeline: 1 to 3 Days

Accepted Answer

• **Gross appearance:** Hyperemic border with central yellow-tan softening.
• **Histology:** Extensive coagulative necrosis with dense **neutrophilic infiltrate** and loss of cardiomyocyte nuclei/striations.
• **Complication:** Postinfarction **fibrinous pericarditis** (presents with sharp pleuritic chest pain and friction rub).

Question 7

Myocardial Infarction Timeline: 3 to 14 Days

Accepted Answer

• **Gross appearance:** Hyperemic border with central yellow-tan softening and maximal structural weakness.
• **Histology:** Macrophage infiltration clearing necrotic debris, followed by early granulation tissue formation.
• **Complications (Days 3-7):** Structural rupture due to tissue weakening: **free wall rupture** (cardiac tamponade), **papillary muscle rupture** (acute severe mitral regurgitation), or **interventricular septum rupture** (left-to-right shunt).

Question 8

Myocardial Infarction Timeline: > 2 Weeks

Accepted Answer

• **Histology:** Dense collagenous **fibrotic scar** replaces necrotic tissue; complete process by ~2 months.
• **Late Complications:** Ventricular aneurysm (risk of mural thrombus and embolization), heart failure, and **Dressler syndrome** (autoimmune pericarditis occurring 2-8 weeks post-MI).

Question 9

Valvular Pathology: Aortic Stenosis

Accepted Answer

• **Murmur:** Crescendo-decrescendo systolic ejection murmur heard best at the right upper sternal border; radiates to carotids.
• **Key Finding:** *Pulsus parvus et tardus* (weak and delayed carotid pulse).
• **Etiologies:** Age-related calcification (most common $>60$), calcification of bicuspid aortic valve ($<60$), or rheumatic heart disease.

Question 10

Valvular Pathology: Mitral Regurgitation

Accepted Answer

• **Murmur:** Holosystolic, high-pitched "blowing" murmur heard best at the apex; radiates to the left axilla.
• **Maneuvers:** Increases with increased afterload (handgrip, squatting).
• **Etiologies:** Post-MI papillary muscle rupture, MVP, dilated cardiomyopathy, rheumatic fever.

Question 11

Valvular Pathology: Mitral Stenosis

Accepted Answer

• **Murmur:** High-pitched **opening snap (OS)** followed by a mid-to-late diastolic rumbling murmur at the apex.
• **Severity Indicator:** A shorter interval between $S_2$ and the OS indicates more severe stenosis (higher left atrial pressure).
• **Complications:** Left atrial enlargement causing dysphagia (esophageal compression), Ortner syndrome (hoarseness from recurrent laryngeal nerve compression), and atrial fibrillation.

Question 12

Heart Failure: Compensatory Neurohormonal Mechanisms

Accepted Answer

Decreased cardiac output triggers compensatory responses that ultimately worsen heart failure long-term:
1. **Sympathetic NS:** $\uparrow$ HR and $\uparrow$ contractility, but increases cardiac workload and remodeling.
2. **RAAS Activation:** $\uparrow$ Aldosterone (salt/water retention $\rightarrow \uparrow$ preload) and $\uparrow$ Angiotensin II (vasoconstriction $\rightarrow \uparrow$ afterload).
3. **ANP/BNP:** Released due to atrial/ventricular stretch; promotes natriuresis and vasodilation (counter-regulatory).

Question 13

Antiarrhythmics: Class I Subclasses & Na+ Binding Strength

Accepted Answer

Block voltage-gated $Na^+$ channels (Phase 0 depolarization in non-pacemaker cells).
• **Binding Affinity:** Class $Ic > Ia > Ib$
• **Class Ia (Quinidine, Procainamide, Disopyramide):** Moderate $Na^+$ block; $\uparrow$ AP duration and $\uparrow$ QT interval.
• **Class Ib (Lidocaine, Mexiletine):** Weak $Na^+$ block; $\downarrow$ AP duration; selective for ischemic/depolarized tissues.
• **Class Ic (Flecainide, Propafenone):** Strong $Na^+$ block; no effect on AP duration; contraindicated post-MI due to proarrhythmic risk.

Question 14

Antiarrhythmics: Class II (Beta-Blockers) Mechanism

Accepted Answer

• **Drug Examples:** Metoprolol, Esmolol, Propranolol.
• **Mechanism:** Decrease $cAMP$ and $Ca^{2+}$ currents in SA and AV nodes.
• **ECG / Cardiac Effects:** Suppress **Phase 4 depolarization** in pacemaker cells; decrease SA node firing rate and prolong AV node conduction velocity ($\uparrow$ PR interval).

Question 15

Antiarrhythmics: Class III (K+ Channel Blockers) Mechanism & Risks

Accepted Answer

• **Drug Examples:** Amiodarone, Ibutilide, Dofetilide, Sotalol.
• **Mechanism:** Block outward $K^+$ currents during **Phase 3 repolarization**.
• **Effect:** Prolongs Action Potential Duration (APD) and Effective Refractory Period (ERP).
• **ECG Change & Risk:** Increases QT interval, increasing the risk of **Torsades de Pointes** (exception: Amiodarone has a lower risk of Torsades).

Question 16

Antiarrhythmics: Class IV (Calcium Channel Blockers) Mechanism

Accepted Answer

• **Drug Examples:** Verapamil, Diltiazem (non-dihydropyridines).
• **Mechanism:** Block L-type $Ca^{2+}$ channels in the nodal tissues.
• **Effect:** Prolong **Phase 0 depolarization** and **Phase 4 slope** in SA/AV nodes, slowing conduction velocity and increasing AV node refractory period ($\uparrow$ PR interval).

Question 17

Vasculitis: Giant Cell (Temporal) Arteritis

Accepted Answer

• **Demographics:** Elderly females ($>50$ years old); associated with **Polymyalgia Rheumatica**.
• **Presentation:** Unilateral headache, temporal artery tenderness, jaw claudication, and sudden irreversible vision loss (ophthalmic artery occlusion).
• **Pathology:** Granulomatous inflammation of the tunica media with multinucleated giant cells; fragmented internal elastic lamina.
• **Treatment:** Immediate high-dose corticosteroids prior to biopsy to prevent blindness.

Question 18

Vasculitis: Kawasaki Disease

Accepted Answer

• **Demographics:** Asian infants/children $< 4$ years old.
• **Presentation (CRASH and Burn):** **C**onjunctivitis, **R**ash, **A**denopathy (cervical), **S**trawberry tongue/oral mucositis, **H**and/foot changes (edema, desquamation), **Burn** (fever $>5$ days).
• **Complication:** **Coronary artery aneurysms** (may rupture or cause thrombosis/MI).
• **Treatment:** IVIG and high-dose Aspirin.

Question 19

Vasculitis: Granulomatosis with Polyangiitis (Wegener)

Accepted Answer

• **Classic Triad:**
  1. Upper respiratory tract: Chronic sinusitis, nasal septum perforation (saddle nose deformity).
  2. Lower respiratory tract: Hemoptysis, bilateral nodular cavitary infiltrates.
  3. Renal: Rapidly progressive glomerulonephritis (crescents).
• **Serology:** **PR3-ANCA / c-ANCA** positive.
• **Pathology:** Focal necrotizing granulomas and necrotizing vasculitis of small vessels.

Question 20

Vasculitis: Polyarteritis Nodosa (PAN)

Accepted Answer

• **Key Associations:** Strongly associated with **Hepatitis B virus (HBV)** infection.
• **Pathology:** Transmural necrotizing inflammation of medium-sized arteries with **fibrinoid necrosis**; lesions of different ages seen simultaneously.
• **Angiography:** Transmural weakness leads to microaneurysms forming a "string-of-beads" appearance.
• **Key Sparing:** Characteristically **spares the pulmonary arteries**.

Question 21

ECG Patterns: Subendocardial vs. Transmural Ischemia

Accepted Answer

• **Subendocardial Ischemia (NSTEMI / Unstable Angina):** Inner $1/3$ of myocardium is vulnerable to ischemia due to high endocardial pressure. Characterized by **ST-segment depression** and T-wave inversion.
• **Transmural Ischemia (STEMI):** Full-thickness ischemic necrosis across the ventricular wall. Characterized by **ST-segment elevation** and convex upwards Q waves.

USMLE Step 1 - Cardiovascular Pathology & Pathophysiology

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