BIOL 252 Human Anatomy & Physiology II w/Lab | Module 3 -
90 Questions and Answers Already Graded A+ Premium Exam
Tested And Verified
Subject Area Human Anatomy & Physiology II
Description Module 3 exam covering cardiovascular system: heart anatomy,
electrophysiology, cardiac cycle, hemodynamics, and regulation; blood vessels
and circulation; lymphatic system and immunity. Designed to test integrative
understanding of structure-function relationships, homeostatic regulation, and
clinical correlations.
Expected Grade A+
Total Questions 90
Duration 3 hours
Learning Outcomes 1. Analyze the sequence of electrical and mechanical events in the cardiac cycle.
2. Interpret pressure-volume loops and hemodynamic parameters.
3. Explain the regulation of blood pressure and flow through neural, hormonal,
and local mechanisms.
4. Differentiate between innate and adaptive immune responses.
5. Apply knowledge of cardiovascular physiology to clinical scenarios.
Accreditation This exam conforms to the standards of the American Association of Anatomists
and the Human Anatomy and Physiology Society (HAPS) for undergraduate
education.
Page 1
,1. During the cardiac cycle, the second heart sound (S2) is produced by the closure of
the semilunar valves. Which of the following conditions would cause a paradoxical
splitting of S2, where the aortic valve closure (A2) occurs after the pulmonary valve
closure (P2) during expiration?
A. Left bundle branch block
B. Right bundle branch block
C. Atrial septal defect
D. Aortic stenosis
Answer: A. Left bundle branch block
Paradoxical splitting of S2 occurs when A2 is delayed, causing it to follow P2 during
expiration. Left bundle branch block delays left ventricular activation and thus aortic
valve closure. Right bundle branch block delays pulmonary closure, causing wide
splitting that increases with inspiration. Atrial septal defect causes fixed splitting.
Aortic stenosis may delay A2 but typically causes a single S2 or paradoxical splitting
only in severe cases; however, left bundle branch block is the classic cause.
2. A researcher is investigating the effects of a novel drug on vascular smooth
muscle. The drug causes a rightward shift in the dose-response curve for
norepinephrine-mediated vasoconstriction without affecting the maximal response.
Which receptor mechanism is most likely involved?
A. Competitive antagonism of 1-adrenergic receptors
B. Noncompetitive antagonism of 1-adrenergic receptors
C. Partial agonism at 2-adrenergic receptors
D. Inhibition of phosphodiesterase type 5
Answer: A. Competitive antagonism of 1-adrenergic receptors
A rightward shift in the dose-response curve with no change in maximal response is
characteristic of competitive antagonism. The drug likely competes with
norepinephrine for 1-adrenergic receptors on vascular smooth muscle. Noncompetitive
antagonism would reduce the maximal response. Partial agonism would not shift the
curve rightward but would produce a submaximal response. PDE5 inhibition would
potentiate nitric oxide-mediated vasodilation, not affect norepinephrine.
Page 2
,3. In a patient with chronic hypertension, the left ventricular pressure-volume loop is
altered. Which of the following best describes the expected change in the end-systolic
pressure-volume relationship (ESPVR) and its physiological basis?
A. Increased slope of ESPVR due to increased contractility from compensatory hypertrophy
B. Decreased slope of ESPVR due to myocardial fibrosis and reduced contractility
C. Rightward shift of ESPVR due to increased preload
D. No change in ESPVR; the loop shifts rightward due to increased afterload
Answer: A. Increased slope of ESPVR due to increased contractility from
compensatory hypertrophy
Chronic hypertension increases afterload, leading to left ventricular hypertrophy.
Initially, the myocardium compensates with increased contractility, steepening the
ESPVR (increased slope). Over time, if heart failure develops, the ESPVR slope may
decrease. However, in compensated hypertension, the ESPVR slope is increased.
Rightward shift of the loop occurs with increased preload, but the ESPVR itself is a
measure of contractility, not preload.
4. A 45-year-old individual presents with lower extremity edema and jugular venous
distention. Echocardiography reveals a thickened, non-compliant pericardium.
Which phase of the cardiac cycle is most directly impaired by this condition, and
what is the resulting effect on ventricular filling?
A. Systole; reduced ejection fraction due to impaired contraction
B. Early diastole; rapid filling phase is restricted, leading to equalization of diastolic
pressures
C. Late diastole; atrial contraction becomes ineffective due to pericardial constraint
D. Isovolumetric relaxation; slowed relaxation due to pericardial stiffness
Answer: B. Early diastole; rapid filling phase is restricted, leading to equalization
of diastolic pressures
Constrictive pericarditis impairs ventricular filling, particularly during early diastole
(rapid filling phase). The non-compliant pericardium restricts expansion, causing a
rapid rise in ventricular pressure and equalization of diastolic pressures across all
chambers. Isovolumetric relaxation is not primarily affected. Systolic function is
typically preserved until late stages.
Page 3
, 5. In the context of the Frank-Starling mechanism, which of the following best
explains why an increase in venous return leads to an increase in stroke volume?
A. Increased end-diastolic volume stretches sarcomeres, optimizing actin-myosin overlap
B. Increased end-diastolic volume enhances calcium sensitivity of troponin C
C. Increased preload activates sympathetic nervous system, increasing contractility
D. Increased preload reduces afterload by decreasing peripheral resistance
Answer: A. Increased end-diastolic volume stretches sarcomeres, optimizing
actin-myosin overlap
The Frank-Starling mechanism states that increased venous return increases
end-diastolic volume (preload), which stretches the ventricular myocytes. This
stretching optimizes sarcomere length, allowing more cross-bridge formation and
increasing contractile force. Calcium sensitivity changes are not the primary
mechanism; sympathetic activation is separate. Afterload is not directly reduced by
preload.
6. A researcher measures the following in a subject at rest: heart rate 70 bpm, stroke
volume 70 mL, mean arterial pressure 93 mmHg, and central venous pressure 2
mmHg. What is the total peripheral resistance (in mmHg-min/L)?
A. 13.3
B. 16.0
C. 18.6
D. 20.0
Answer: C. 18.6
Total peripheral resistance (TPR) = (MAP - CVP) / CO. CO = HR × SV = 70 × 70 =
4900 mL/min = 4.9 L/min. MAP - CVP = 93 - 2 = 91 mmHg. TPR = .9 18.57
mmHg-min/L. Option C (18.6) is correct. The other options result from incorrect
calculations (e.g., using MAP alone or miscalculating CO).
Page 4
90 Questions and Answers Already Graded A+ Premium Exam
Tested And Verified
Subject Area Human Anatomy & Physiology II
Description Module 3 exam covering cardiovascular system: heart anatomy,
electrophysiology, cardiac cycle, hemodynamics, and regulation; blood vessels
and circulation; lymphatic system and immunity. Designed to test integrative
understanding of structure-function relationships, homeostatic regulation, and
clinical correlations.
Expected Grade A+
Total Questions 90
Duration 3 hours
Learning Outcomes 1. Analyze the sequence of electrical and mechanical events in the cardiac cycle.
2. Interpret pressure-volume loops and hemodynamic parameters.
3. Explain the regulation of blood pressure and flow through neural, hormonal,
and local mechanisms.
4. Differentiate between innate and adaptive immune responses.
5. Apply knowledge of cardiovascular physiology to clinical scenarios.
Accreditation This exam conforms to the standards of the American Association of Anatomists
and the Human Anatomy and Physiology Society (HAPS) for undergraduate
education.
Page 1
,1. During the cardiac cycle, the second heart sound (S2) is produced by the closure of
the semilunar valves. Which of the following conditions would cause a paradoxical
splitting of S2, where the aortic valve closure (A2) occurs after the pulmonary valve
closure (P2) during expiration?
A. Left bundle branch block
B. Right bundle branch block
C. Atrial septal defect
D. Aortic stenosis
Answer: A. Left bundle branch block
Paradoxical splitting of S2 occurs when A2 is delayed, causing it to follow P2 during
expiration. Left bundle branch block delays left ventricular activation and thus aortic
valve closure. Right bundle branch block delays pulmonary closure, causing wide
splitting that increases with inspiration. Atrial septal defect causes fixed splitting.
Aortic stenosis may delay A2 but typically causes a single S2 or paradoxical splitting
only in severe cases; however, left bundle branch block is the classic cause.
2. A researcher is investigating the effects of a novel drug on vascular smooth
muscle. The drug causes a rightward shift in the dose-response curve for
norepinephrine-mediated vasoconstriction without affecting the maximal response.
Which receptor mechanism is most likely involved?
A. Competitive antagonism of 1-adrenergic receptors
B. Noncompetitive antagonism of 1-adrenergic receptors
C. Partial agonism at 2-adrenergic receptors
D. Inhibition of phosphodiesterase type 5
Answer: A. Competitive antagonism of 1-adrenergic receptors
A rightward shift in the dose-response curve with no change in maximal response is
characteristic of competitive antagonism. The drug likely competes with
norepinephrine for 1-adrenergic receptors on vascular smooth muscle. Noncompetitive
antagonism would reduce the maximal response. Partial agonism would not shift the
curve rightward but would produce a submaximal response. PDE5 inhibition would
potentiate nitric oxide-mediated vasodilation, not affect norepinephrine.
Page 2
,3. In a patient with chronic hypertension, the left ventricular pressure-volume loop is
altered. Which of the following best describes the expected change in the end-systolic
pressure-volume relationship (ESPVR) and its physiological basis?
A. Increased slope of ESPVR due to increased contractility from compensatory hypertrophy
B. Decreased slope of ESPVR due to myocardial fibrosis and reduced contractility
C. Rightward shift of ESPVR due to increased preload
D. No change in ESPVR; the loop shifts rightward due to increased afterload
Answer: A. Increased slope of ESPVR due to increased contractility from
compensatory hypertrophy
Chronic hypertension increases afterload, leading to left ventricular hypertrophy.
Initially, the myocardium compensates with increased contractility, steepening the
ESPVR (increased slope). Over time, if heart failure develops, the ESPVR slope may
decrease. However, in compensated hypertension, the ESPVR slope is increased.
Rightward shift of the loop occurs with increased preload, but the ESPVR itself is a
measure of contractility, not preload.
4. A 45-year-old individual presents with lower extremity edema and jugular venous
distention. Echocardiography reveals a thickened, non-compliant pericardium.
Which phase of the cardiac cycle is most directly impaired by this condition, and
what is the resulting effect on ventricular filling?
A. Systole; reduced ejection fraction due to impaired contraction
B. Early diastole; rapid filling phase is restricted, leading to equalization of diastolic
pressures
C. Late diastole; atrial contraction becomes ineffective due to pericardial constraint
D. Isovolumetric relaxation; slowed relaxation due to pericardial stiffness
Answer: B. Early diastole; rapid filling phase is restricted, leading to equalization
of diastolic pressures
Constrictive pericarditis impairs ventricular filling, particularly during early diastole
(rapid filling phase). The non-compliant pericardium restricts expansion, causing a
rapid rise in ventricular pressure and equalization of diastolic pressures across all
chambers. Isovolumetric relaxation is not primarily affected. Systolic function is
typically preserved until late stages.
Page 3
, 5. In the context of the Frank-Starling mechanism, which of the following best
explains why an increase in venous return leads to an increase in stroke volume?
A. Increased end-diastolic volume stretches sarcomeres, optimizing actin-myosin overlap
B. Increased end-diastolic volume enhances calcium sensitivity of troponin C
C. Increased preload activates sympathetic nervous system, increasing contractility
D. Increased preload reduces afterload by decreasing peripheral resistance
Answer: A. Increased end-diastolic volume stretches sarcomeres, optimizing
actin-myosin overlap
The Frank-Starling mechanism states that increased venous return increases
end-diastolic volume (preload), which stretches the ventricular myocytes. This
stretching optimizes sarcomere length, allowing more cross-bridge formation and
increasing contractile force. Calcium sensitivity changes are not the primary
mechanism; sympathetic activation is separate. Afterload is not directly reduced by
preload.
6. A researcher measures the following in a subject at rest: heart rate 70 bpm, stroke
volume 70 mL, mean arterial pressure 93 mmHg, and central venous pressure 2
mmHg. What is the total peripheral resistance (in mmHg-min/L)?
A. 13.3
B. 16.0
C. 18.6
D. 20.0
Answer: C. 18.6
Total peripheral resistance (TPR) = (MAP - CVP) / CO. CO = HR × SV = 70 × 70 =
4900 mL/min = 4.9 L/min. MAP - CVP = 93 - 2 = 91 mmHg. TPR = .9 18.57
mmHg-min/L. Option C (18.6) is correct. The other options result from incorrect
calculations (e.g., using MAP alone or miscalculating CO).
Page 4
