Western Governors University
4 TES• 511D
WGU College of Health Professions — Nursing Program
THE UNIVERSITY OF YOU
EST. 1997
WGU D115 — Cram Study Guide 4
C A R D I O VA S CU L A R , R E S P I R ATO R Y & R E N A L P H YS I O LO G Y
INSTITUTION Western Governors University — College COURSE CODE D115
of Health Professions
PROGRAM BSN Pre-Licensure / MSN Pathway ACADEMIC YEAR
EXAM TITLE Cram Study Guide 4 — Cardiovascular, TOTAL QUESTIONS 40 Questions
Respiratory & Renal
ACCREDITATION CCNE — Commission on Collegiate FORMAT Multiple Choice — Select the Single Best
Nursing Education Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on WGU D115 Advanced Pathophysiology content.
▸ Questions cover heart failure (left vs. right, cor pulmonale), cardiac anatomy/physiology (valves, conduction system,
cardiomyopathies), DVT (Virchow's triad), pneumothorax (primary, secondary, tension), pleural effusion, ARDS, lung cancer,
mechanical ventilation weaning, and renal physiology (nephron, ANP/BNP, EPO, acid-base).
▸ Correct answers and pathophysiological rationales appear below each question.
▸ All content aligns with WGU BSN curriculum and CCNE accreditation standards.
SECTION I — CRAM STUDY GUIDE 4: CARDIOVASCULAR, RESPIRATORY & Questions 1 –
RENAL 40
1. How does left-sided heart failure lead to right-sided heart failure?
A. Through systemic vasodilation decreasing afterload
B. Increased left ventricular filling pressure is reflected back into pulmonary circulation → increased pulmonary
pressure → increased resistance to right ventricular emptying → RV cannot compensate for increased afterload →
RV dilates and fails
C. Through direct mechanical compression of the right ventricle
D. Left and right heart failure never coexist
CORRECT ANSWER B — Increased LV filling pressure → pulmonary congestion → increased pulmonary pressure →
increased RV afterload → RV dilation and failure
RATIONALE Left-sided HF (most common type) causes blood to back up into the pulmonary circulation → increased
pulmonary venous pressure → increased pulmonary artery pressure → the right ventricle must pump against
this elevated afterload → initially compensates with hypertrophy → eventually dilates and fails. Right-sided
HF symptoms reflect systemic congestion: peripheral edema, leg swelling, hepatosplenomegaly, ascites, JVD.
Right-sided HF NOT associated with left HF (isolated right HF) is typically caused by pulmonary disease
(COPD, CF, ARDS) → pulmonary vasoconstriction → pulmonary hypertension → cor pulmonale. Other
causes: RV MI, cardiomyopathy, pulmonic valve disease. BNP >900 pg/mL indicates heart failure.
, 2. What makes heart valves close?
A. Active muscular contraction of the valve leaflets
B. Mostly passive — valves close due to pressure changes within the heart chambers; valves are forced shut when the
pressure behind them exceeds the pressure in front of them
C. Electrical signals from the SA node
D. Suction from the great vessels
CORRECT ANSWER B — Mostly passive; valves close due to pressure changes; forced shut when pressure behind exceeds
pressure in front
RATIONALE Heart valves operate passively based on pressure gradients — there are NO muscles in the valve leaflets. AV
valves (tricuspid and mitral/bicuspid): open when ventricular pressure is LOW (diastole — ventricles relaxed)
allowing atrial blood to fill ventricles. Close when ventricular pressure EXCEEDS atrial pressure (systole —
ventricles contract) preventing backflow into atria. Semilunar valves (pulmonary and aortic): open when
ventricular pressure exceeds pulmonary/aortic pressure (systole). Close when ventricular pressure falls below
great vessel pressure (diastole). Chordae tendineae ("heart strings") anchor AV valves to papillary muscles —
prevent prolapse/inversion. MI can rupture papillary muscle/chordae → acute mitral regurgitation. Ventricles
place the GREATEST oxygen demand during SYSTOLE (isovolumetric contraction) — LV must rapidly raise
pressure to overcome high afterload.
3. What is the pathophysiology of a DVT according to Virchow's triad?
A. Infection, inflammation, and immune response
B. Decreased flow rate of blood (stasis), damage to blood vessel wall (endothelial injury), and increased tendency to
clot (hypercoagulability)
C. Hypertension, hyperlipidemia, and smoking
D. Obesity, diabetes, and family history
CORRECT ANSWER B — Virchow's triad: venous stasis, endothelial injury, and hypercoagulability
RATIONALE Virchow's triad describes the three factors contributing to thrombus formation: (1) VENOUS STASIS —
decreased blood flow (prolonged immobility — long car ride, bed rest, surgery, paralysis); (2) ENDOTHELIAL
INJURY — damage to vessel wall (trauma, surgery, IV catheters, inflammation); (3) HYPERCOAGULABILITY —
increased clotting tendency (malignancy, pregnancy, oral contraceptives, inherited thrombophilias like Factor
V Leiden). A patient after a 12-hour car ride with sudden unilateral leg pain, edema, and a red, warm,
indurated vein likely has a DVT from venous stasis. Complications: pulmonary embolism (most serious), post-
thrombotic syndrome (chronic venous insufficiency). Treatment: anticoagulation (heparin → warfarin or
DOAC).
4 TES• 511D
WGU College of Health Professions — Nursing Program
THE UNIVERSITY OF YOU
EST. 1997
WGU D115 — Cram Study Guide 4
C A R D I O VA S CU L A R , R E S P I R ATO R Y & R E N A L P H YS I O LO G Y
INSTITUTION Western Governors University — College COURSE CODE D115
of Health Professions
PROGRAM BSN Pre-Licensure / MSN Pathway ACADEMIC YEAR
EXAM TITLE Cram Study Guide 4 — Cardiovascular, TOTAL QUESTIONS 40 Questions
Respiratory & Renal
ACCREDITATION CCNE — Commission on Collegiate FORMAT Multiple Choice — Select the Single Best
Nursing Education Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on WGU D115 Advanced Pathophysiology content.
▸ Questions cover heart failure (left vs. right, cor pulmonale), cardiac anatomy/physiology (valves, conduction system,
cardiomyopathies), DVT (Virchow's triad), pneumothorax (primary, secondary, tension), pleural effusion, ARDS, lung cancer,
mechanical ventilation weaning, and renal physiology (nephron, ANP/BNP, EPO, acid-base).
▸ Correct answers and pathophysiological rationales appear below each question.
▸ All content aligns with WGU BSN curriculum and CCNE accreditation standards.
SECTION I — CRAM STUDY GUIDE 4: CARDIOVASCULAR, RESPIRATORY & Questions 1 –
RENAL 40
1. How does left-sided heart failure lead to right-sided heart failure?
A. Through systemic vasodilation decreasing afterload
B. Increased left ventricular filling pressure is reflected back into pulmonary circulation → increased pulmonary
pressure → increased resistance to right ventricular emptying → RV cannot compensate for increased afterload →
RV dilates and fails
C. Through direct mechanical compression of the right ventricle
D. Left and right heart failure never coexist
CORRECT ANSWER B — Increased LV filling pressure → pulmonary congestion → increased pulmonary pressure →
increased RV afterload → RV dilation and failure
RATIONALE Left-sided HF (most common type) causes blood to back up into the pulmonary circulation → increased
pulmonary venous pressure → increased pulmonary artery pressure → the right ventricle must pump against
this elevated afterload → initially compensates with hypertrophy → eventually dilates and fails. Right-sided
HF symptoms reflect systemic congestion: peripheral edema, leg swelling, hepatosplenomegaly, ascites, JVD.
Right-sided HF NOT associated with left HF (isolated right HF) is typically caused by pulmonary disease
(COPD, CF, ARDS) → pulmonary vasoconstriction → pulmonary hypertension → cor pulmonale. Other
causes: RV MI, cardiomyopathy, pulmonic valve disease. BNP >900 pg/mL indicates heart failure.
, 2. What makes heart valves close?
A. Active muscular contraction of the valve leaflets
B. Mostly passive — valves close due to pressure changes within the heart chambers; valves are forced shut when the
pressure behind them exceeds the pressure in front of them
C. Electrical signals from the SA node
D. Suction from the great vessels
CORRECT ANSWER B — Mostly passive; valves close due to pressure changes; forced shut when pressure behind exceeds
pressure in front
RATIONALE Heart valves operate passively based on pressure gradients — there are NO muscles in the valve leaflets. AV
valves (tricuspid and mitral/bicuspid): open when ventricular pressure is LOW (diastole — ventricles relaxed)
allowing atrial blood to fill ventricles. Close when ventricular pressure EXCEEDS atrial pressure (systole —
ventricles contract) preventing backflow into atria. Semilunar valves (pulmonary and aortic): open when
ventricular pressure exceeds pulmonary/aortic pressure (systole). Close when ventricular pressure falls below
great vessel pressure (diastole). Chordae tendineae ("heart strings") anchor AV valves to papillary muscles —
prevent prolapse/inversion. MI can rupture papillary muscle/chordae → acute mitral regurgitation. Ventricles
place the GREATEST oxygen demand during SYSTOLE (isovolumetric contraction) — LV must rapidly raise
pressure to overcome high afterload.
3. What is the pathophysiology of a DVT according to Virchow's triad?
A. Infection, inflammation, and immune response
B. Decreased flow rate of blood (stasis), damage to blood vessel wall (endothelial injury), and increased tendency to
clot (hypercoagulability)
C. Hypertension, hyperlipidemia, and smoking
D. Obesity, diabetes, and family history
CORRECT ANSWER B — Virchow's triad: venous stasis, endothelial injury, and hypercoagulability
RATIONALE Virchow's triad describes the three factors contributing to thrombus formation: (1) VENOUS STASIS —
decreased blood flow (prolonged immobility — long car ride, bed rest, surgery, paralysis); (2) ENDOTHELIAL
INJURY — damage to vessel wall (trauma, surgery, IV catheters, inflammation); (3) HYPERCOAGULABILITY —
increased clotting tendency (malignancy, pregnancy, oral contraceptives, inherited thrombophilias like Factor
V Leiden). A patient after a 12-hour car ride with sudden unilateral leg pain, edema, and a red, warm,
indurated vein likely has a DVT from venous stasis. Complications: pulmonary embolism (most serious), post-
thrombotic syndrome (chronic venous insufficiency). Treatment: anticoagulation (heparin → warfarin or
DOAC).
