USMLE Step 1 - Cardiovascular Pathology & Hemodynamics Flashcards

Question 1

Describe the Frank-Starling mechanism.

Accepted Answer

States that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (end-diastolic volume) when all other factors remain constant. Greater stretch of myocardial fibers leads to a more forceful contraction, optimizing actin-myosin overlap.

Question 2

Describe the classic murmur of Aortic Stenosis (AS).

Accepted Answer

Crescendo-decrescendo systolic ejection murmur, best heard at the right upper sternal border (2nd intercostal space), radiating to the carotids. Often associated with a paradoxically split S2 and pulsus parvus et tardus.

Question 3

Describe the classic murmur of Mitral Regurgitation (MR).

Accepted Answer

Holosystolic (pansystolic) murmur, constant intensity throughout systole, best heard at the apex, radiating to the axilla. Often associated with a soft S1 and a loud P2 if pulmonary hypertension is present.

Question 4

Define Systolic Heart Failure (HFrEF) and its key characteristic.

Accepted Answer

Heart failure with reduced ejection fraction. Characterized by impaired ventricular contraction, leading to a reduced cardiac output and an ejection fraction (EF) typically $< 40-50\%$. Often caused by ischemic heart disease or dilated cardiomyopathy.

Question 5

Define Diastolic Heart Failure (HFpEF) and its key characteristic.

Accepted Answer

Heart failure with preserved ejection fraction. Characterized by impaired ventricular relaxation and/or increased stiffness, leading to elevated filling pressures despite a normal or near-normal EF ($> 50\%$). Often caused by hypertension, hypertrophy, or restrictive cardiomyopathy.

Question 6

What are the characteristic ECG findings in an acute ST-elevation myocardial infarction (STEMI)?

Accepted Answer

ST-segment elevation in $\ge 2$ contiguous leads (new LBBB can also indicate STEMI), often followed by Q-wave development and T-wave inversion. Reciprocal ST depression may also be present.

Question 7

What are the characteristic ECG findings in NSTEMI or Unstable Angina?

Accepted Answer

ST-segment depression, T-wave inversion, or non-specific ST-T changes. Unlike STEMI, there is no persistent ST elevation. NSTEMI has elevated cardiac biomarkers, while unstable angina does not.

Question 8

List major modifiable and non-modifiable risk factors for Coronary Artery Disease (CAD).

Accepted Answer

Modifiable: Hypertension, hyperlipidemia (high LDL, low HDL), diabetes mellitus, smoking, obesity, physical inactivity.
Non-modifiable: Age, male sex, family history of premature CAD.

Question 9

Briefly describe the key steps in the pathophysiology of atherosclerosis.

Accepted Answer

Endothelial injury/dysfunction $\rightarrow$ LDL oxidation $\rightarrow$ Macrophage uptake of oxidized LDL (foam cells) $\rightarrow$ Fatty streak formation $\rightarrow$ Smooth muscle cell migration/proliferation $\rightarrow$ Fibrous cap formation $\rightarrow$ Plaque growth and potential rupture.

Question 10

What is cardiac tamponade and what are its classic signs (Beck's Triad)?

Accepted Answer

Compression of the heart due to accumulation of fluid in the pericardial sac, impairing ventricular filling. Beck's Triad: 1. Hypotension, 2. Jugular venous distension (JVD), 3. Muffled heart sounds. Also pulsus paradoxus.

Question 11

Describe the characteristic ECG findings of Atrial Fibrillation (AFib).

Accepted Answer

Irregularly irregular rhythm, absence of distinct P waves (replaced by fibrillatory waves, 'f' waves), and a variable ventricular rate.

Question 12

Describe the characteristic ECG findings of Ventricular Fibrillation (VFib).

Accepted Answer

Chaotic, irregular deflections of varying amplitude and morphology, with no identifiable P waves, QRS complexes, or T waves. Represents disorganized electrical activity in the ventricles, leading to no effective cardiac output.

Question 13

Which valvular heart disease is most commonly associated with Rheumatic Fever?

Accepted Answer

Mitral Stenosis (MS). Rheumatic fever can cause chronic inflammation and fibrosis of the mitral valve leaflets, leading to narrowing of the valve orifice. Aortic valve can also be affected.

Question 14

Describe the murmur of Hypertrophic Cardiomyopathy (HCM) and how it changes with maneuvers.

Accepted Answer

Harsh systolic ejection murmur, best heard at the left sternal border, often radiating to the apex. Increases with maneuvers that decrease preload (e.g., Valsalva, standing) and decreases with maneuvers that increase preload/afterload (e.g., squatting, handgrip).

Question 15

What are the classic ECG findings in acute pericarditis?

Accepted Answer

Diffuse (widespread) ST-segment elevation (concave up) in most leads, PR-segment depression (especially in limb leads), and no reciprocal ST depression (except in aVR). T-wave inversions may follow.

Question 16

Define pulsus paradoxus and list conditions where it is observed.

Accepted Answer

An abnormally large decrease in systolic blood pressure ($>10$ mmHg) during inspiration. Occurs due to increased right ventricular filling and bowing of the interventricular septum into the left ventricle, reducing left ventricular filling. Seen in cardiac tamponade, severe asthma, COPD, and constrictive pericarditis.

Question 17

List common causes of Dilated Cardiomyopathy (DCM).

Accepted Answer

Idiopathic (most common), ischemic heart disease, alcohol abuse, viral myocarditis (e.g., Coxsackievirus B), peripartum cardiomyopathy, hemochromatosis, doxorubicin toxicity, genetic factors.

Question 18

List common causes of Restrictive Cardiomyopathy.

Accepted Answer

Amyloidosis, sarcoidosis, hemochromatosis, endomyocardial fibrosis, radiation fibrosis. Characterized by stiff, non-compliant ventricles leading to impaired diastolic filling.

Question 19

Describe the classic murmur of Aortic Regurgitation (AR).

Accepted Answer

High-pitched, blowing, decrescendo diastolic murmur, best heard at the left sternal border (3rd/4th intercostal space) with the patient leaning forward and exhaling. Can be associated with a wide pulse pressure and peripheral signs (e.g., water-hammer pulse).

Question 20

Describe the classic murmur of Mitral Stenosis (MS).

Accepted Answer

Low-pitched, rumbling diastolic murmur, best heard at the apex with the bell of the stethoscope, with the patient in the left lateral decubitus position. Often preceded by an opening snap. Intensity increases with exercise or left lateral decubitus position.

Question 21

What are the characteristic ECG findings in Wolff-Parkinson-White (WPW) Syndrome?

Accepted Answer

Short PR interval ($< 0.12$ s), a delta wave (slurring of the initial upstroke of the QRS complex), and widening of the QRS complex ($> 0.10$ s). Due to an accessory pathway (Bundle of Kent) bypassing the AV node.

Question 22

How do ACE inhibitors benefit patients with heart failure?

Accepted Answer

ACE inhibitors block the conversion of Angiotensin I to Angiotensin II. This leads to vasodilation (reduced preload and afterload), decreased aldosterone secretion (reduced sodium/water retention), and reduced cardiac remodeling (fibrosis and hypertrophy), improving symptoms and survival in HFrEF.

Question 23

How do beta-blockers benefit patients with chronic heart failure (HFrEF)?

Accepted Answer

Beta-blockers (e.g., carvedilol, metoprolol succinate, bisoprolol) block the effects of sympathetic nervous system activation. They reduce heart rate, improve myocardial oxygen demand, prevent arrhythmias, and reverse adverse cardiac remodeling, leading to improved ejection fraction and survival in stable HFrEF.

Question 24

Differentiate between Stable Angina and Unstable Angina.

Accepted Answer

Stable Angina: Chest pain/discomfort that is predictable, reproducible, and relieved by rest or nitroglycerin. Caused by fixed atherosclerotic plaque limiting blood flow during increased demand.
Unstable Angina: New-onset angina, angina that is increasing in frequency/intensity, or angina that occurs at rest. Not relieved by rest or nitroglycerin. Indicates plaque rupture with non-occlusive thrombus formation, a precursor to MI. No elevated cardiac biomarkers.

Question 25

Explain the pathophysiology of pulmonary edema in left-sided heart failure.

Accepted Answer

Impaired left ventricular function leads to increased left atrial pressure, which is transmitted back to the pulmonary veins and capillaries. This increases pulmonary capillary hydrostatic pressure, forcing fluid out of the capillaries into the interstitial space and alveoli, causing dyspnea and crackles.

USMLE Step 1 - Cardiovascular Pathology & Hemodynamics

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