HESI RN Advanced Pathophysiology
Study Questions and verified answers
Graded A+
CARDIOVASCULAR PATHOPHYSIOLOGY
1. What is the primary pathophysiological mechanism in systolic heart
failure?
Answer: Decreased contractility of the left ventricle leading to reduced ejection fraction
(<40%). The heart cannot pump blood effectively, causing backup into pulmonary
circulation.
2. Which compensatory mechanism in heart failure leads to increased
preload?
Answer: Activation of the renin-angiotensin-aldosterone system (RAAS), causing sodium
and water retention, increasing blood volume and venous return.
3. What causes the S3 gallop sound in heart failure?
Answer: Rapid ventricular filling during diastole due to increased preload and decreased
ventricular compliance, creating turbulent blood flow.
4. In myocardial infarction, what is the difference between STEMI and
NSTEMI?
,Answer: STEMI involves complete coronary artery occlusion with full-thickness myocardial
damage and ST elevation. NSTEMI involves partial occlusion with subendocardial damage
and no ST elevation.
5. What is the Frank-Starling mechanism?
Answer: The relationship between ventricular stretch (preload) and contractile force.
Increased preload stretches myocardial fibers, leading to stronger contraction up to an
optimal point.
6. Why does hypertension cause left ventricular hypertrophy?
Answer: Chronic increased afterload forces the left ventricle to work harder, causing
compensatory muscle fiber thickening to maintain cardiac output.
7. What causes the murmur in aortic stenosis?
Answer: Turbulent blood flow through the narrowed aortic valve during systole, creating a
harsh, crescendo-decrescendo murmur.
8. How does atherosclerosis develop?
Answer: Endothelial injury → lipid accumulation → inflammatory response → plaque
formation with fibrous cap → potential rupture and thrombosis.
9. What is the pathophysiology of atrial fibrillation?
Answer: Multiple chaotic electrical impulses in the atria cause irregular, rapid atrial
contraction without effective pumping, leading to irregular ventricular response.
, 10. Why are patients with atrial fibrillation at risk for stroke?
Answer: Ineffective atrial contraction causes blood stasis, particularly in the left atrial
appendage, promoting thrombus formation and potential embolization.
RESPIRATORY PATHOPHYSIOLOGY
11. What is the primary pathophysiological change in COPD?
Answer: Chronic inflammation leading to airway obstruction, alveolar destruction
(emphysema), and mucus hypersecretion (chronic bronchitis).
12. How does emphysema affect gas exchange?
Answer: Alveolar wall destruction reduces surface area for gas exchange and causes loss of
elastic recoil, leading to air trapping and impaired ventilation.
13. What causes the barrel chest appearance in emphysema?
Answer: Loss of lung elasticity and air trapping cause chronic hyperinflation, forcing the
chest into an expanded position.
14. What is the pathophysiology of asthma?
Answer: Chronic airway inflammation with bronchial hyperresponsiveness, leading to
bronchoconstriction, mucus production, and airway edema.
15. Why do asthma patients develop wheezing?
Study Questions and verified answers
Graded A+
CARDIOVASCULAR PATHOPHYSIOLOGY
1. What is the primary pathophysiological mechanism in systolic heart
failure?
Answer: Decreased contractility of the left ventricle leading to reduced ejection fraction
(<40%). The heart cannot pump blood effectively, causing backup into pulmonary
circulation.
2. Which compensatory mechanism in heart failure leads to increased
preload?
Answer: Activation of the renin-angiotensin-aldosterone system (RAAS), causing sodium
and water retention, increasing blood volume and venous return.
3. What causes the S3 gallop sound in heart failure?
Answer: Rapid ventricular filling during diastole due to increased preload and decreased
ventricular compliance, creating turbulent blood flow.
4. In myocardial infarction, what is the difference between STEMI and
NSTEMI?
,Answer: STEMI involves complete coronary artery occlusion with full-thickness myocardial
damage and ST elevation. NSTEMI involves partial occlusion with subendocardial damage
and no ST elevation.
5. What is the Frank-Starling mechanism?
Answer: The relationship between ventricular stretch (preload) and contractile force.
Increased preload stretches myocardial fibers, leading to stronger contraction up to an
optimal point.
6. Why does hypertension cause left ventricular hypertrophy?
Answer: Chronic increased afterload forces the left ventricle to work harder, causing
compensatory muscle fiber thickening to maintain cardiac output.
7. What causes the murmur in aortic stenosis?
Answer: Turbulent blood flow through the narrowed aortic valve during systole, creating a
harsh, crescendo-decrescendo murmur.
8. How does atherosclerosis develop?
Answer: Endothelial injury → lipid accumulation → inflammatory response → plaque
formation with fibrous cap → potential rupture and thrombosis.
9. What is the pathophysiology of atrial fibrillation?
Answer: Multiple chaotic electrical impulses in the atria cause irregular, rapid atrial
contraction without effective pumping, leading to irregular ventricular response.
, 10. Why are patients with atrial fibrillation at risk for stroke?
Answer: Ineffective atrial contraction causes blood stasis, particularly in the left atrial
appendage, promoting thrombus formation and potential embolization.
RESPIRATORY PATHOPHYSIOLOGY
11. What is the primary pathophysiological change in COPD?
Answer: Chronic inflammation leading to airway obstruction, alveolar destruction
(emphysema), and mucus hypersecretion (chronic bronchitis).
12. How does emphysema affect gas exchange?
Answer: Alveolar wall destruction reduces surface area for gas exchange and causes loss of
elastic recoil, leading to air trapping and impaired ventilation.
13. What causes the barrel chest appearance in emphysema?
Answer: Loss of lung elasticity and air trapping cause chronic hyperinflation, forcing the
chest into an expanded position.
14. What is the pathophysiology of asthma?
Answer: Chronic airway inflammation with bronchial hyperresponsiveness, leading to
bronchoconstriction, mucus production, and airway edema.
15. Why do asthma patients develop wheezing?
