BIOS 255 / BIOS255 EXAM 2
2026-2027 | Anatomy &
Physiology III Complete Guide |
100% Correct Q&A |
Chamberlain | Pass Guaranteed
- A+ Graded
ART A – MULTIPLE CHOICE (Q1‑55)
P
Q1 (Cardiovascular – Cardiac Muscle Action Potential): A cardiac pacemaker cell in the SA
node spontaneously depolarizes during phase 4 due to which ion channel opening?
A. Fast voltage-gated Na⁺ channels
B. Funny (HCN) channels allowing Na⁺ influx
C. Voltage-gated K⁺ channels
D. L-type Ca²⁺ channels
[CORRECT] B
Rationale: Pacemaker cells lack stable resting membrane potential; funny (HCN) channels open
in response to hyperpolarization, allowing Na⁺ influx and gradual depolarization during phase 4.
Fast Na⁺ channels (A) are found in contractile cells, not pacemaker cells. K⁺ channels (C) cause
repolarization, not depolarization. L-type Ca²⁺ channels (D) open during phase 0 of pacemaker
action potentials, not phase 4. Clinical pearl: HCN channel blockers like ivabradine reduce heart
rate by inhibiting phase 4 depolarization—know this drug mechanism for clinical applications.
Q2 (Cardiovascular – ECG): During which ECG interval does the ventricular myocardium
remain in an absolute refractory state?
A. P wave duration
B. PR interval
C. QRS complex duration
D. QT interval
[CORRECT] C
Rationale: The QRS complex represents ventricular depolarization; during this period and
immediately following, Na⁺ channels are inactivated, creating an absolute refractory period
preventing tetany. The P wave (A) represents atrial depolarization, not ventricular. The PR
,interval (B) includes atrial depolarization and AV nodal delay but not the absolute refractory
period of ventricles. The QT interval (D) includes both depolarization and repolarization but
extends beyond the absolute refractory period into relative refractoriness. Clinical pearl: A
prolonged QT interval increases risk for torsades de pointes; always check electrolytes (K⁺,
Mg²⁺, Ca²⁺) in patients with QT prolongation.
Q3 (Cardiovascular – Cardiac Cycle): During isovolumetric ventricular contraction, which valve
status is correct?
A. AV valves open; semilunar valves open
B. AV valves closed; semilunar valves closed
C. AV valves open; semilunar valves closed
D. AV valves closed; semilunar valves open
[CORRECT] B
Rationale: Isovolumetric contraction begins when ventricular pressure exceeds atrial pressure
(closing AV valves) but before ventricular pressure exceeds aortic/pulmonary pressure
(semilunar valves remain closed), creating a brief period of constant volume. Option A describes
the ejection phase, C describes ventricular filling, and D describes isovolumetric relaxation.
Clinical pearl: The "lub" (S1) heart sound occurs at the beginning of isovolumetric contraction
when AV valves close; understanding this timing helps distinguish systolic from diastolic
murmurs.
Q4 (Cardiovascular – Cardiac Output): A 68-year-old patient has a stroke volume of 70 mL/beat
and a heart rate of 72 bpm. What is the patient's cardiac output?
A. 4.2 L/min
B. 5.04 L/min
C. 6.3 L/min
D. 7.56 L/min
[CORRECT] B
Rationale: Cardiac output (CO) = Stroke Volume (SV) × Heart Rate (HR) = 70 mL × 72 bpm =
5,040 mL/min = 5.04 L/min. Option A incorrectly uses 60 bpm instead of 72. Option C uses 90
mL SV. Option D uses 90 mL SV and 84 bpm. Clinical pearl: Normal CO is 4–8 L/min; in heart
failure, both SV and CO decrease, while compensatory tachycardia initially maintains CO but
increases myocardial oxygen demand.
Q5 (Cardiovascular – Frank-Starling Law): According to the Frank-Starling law of the heart,
increased venous return results in:
A. Decreased stroke volume due to overstretching
B. Increased stroke volume due to greater sarcomere stretch
C. Decreased heart rate via vagal stimulation
D. Increased afterload on the ventricles
[CORRECT] B
Rationale: The Frank-Starling mechanism states that increased ventricular preload
(end-diastolic volume) stretches cardiac muscle fibers, optimizing actin-myosin overlap and
increasing contractile force, thereby increasing stroke volume. Option A describes the
descending limb of the curve, which rarely occurs physiologically. Option C confuses
Frank-Starling with Bainbridge reflex. Option D confuses preload with afterload. Clinical pearl: In
, eart failure, the Frank-Starling curve shifts downward; diuretics reduce preload to prevent
h
pulmonary congestion, while positive inotropes improve contractility.
Q6 (Cardiovascular – Blood Pressure): Which formula correctly calculates mean arterial
pressure (MAP)?
A. MAP = Systolic BP + Diastolic BP ÷ 2
B. MAP = Diastolic BP + ⅓(Systolic BP − Diastolic BP)
C. MAP = Systolic BP − Diastolic BP
D. MAP = (Systolic BP × 2 + Diastolic BP) ÷ 3
[CORRECT] B
Rationale: MAP = Diastolic BP + ⅓(Systolic BP − Diastolic BP), or equivalently (2 × Diastolic +
Systolic) ÷ 3, because diastole lasts approximately twice as long as systole at normal heart
rates. Option A averages the pressures equally, ignoring the longer diastolic period. Option C
calculates pulse pressure, not MAP. Option D weights systolic pressure incorrectly. Clinical
pearl: MAP must be ≥65 mmHg for adequate tissue perfusion; in shock, vasopressors are
titrated to maintain MAP ≥65 mmHg to preserve organ perfusion.
Q7 (Cardiovascular – Baroreceptor Reflex): A patient experiences acute hemorrhage, causing
decreased arterial pressure. Which baroreceptor-mediated response occurs first?
A. Decreased sympathetic outflow to the heart
B. Increased parasympathetic outflow to the SA node
C. Increased sympathetic outflow to arterioles causing vasoconstriction
D. Decreased ADH secretion from the posterior pituitary
[CORRECT] C
Rationale: Baroreceptors in the carotid sinus and aortic arch detect decreased stretch, reducing
inhibitory signals to the medulla, which increases sympathetic outflow to arterioles
(vasoconstriction), increasing total peripheral resistance to maintain BP. Option A is incorrect
because sympathetic outflow increases, not decreases. Option B is wrong because
parasympathetic tone decreases, allowing heart rate to increase. Option D is incorrect because
ADH secretion increases, not decreases. Clinical pearl: The baroreceptor reflex responds within
seconds; if BP remains low after 10–20 seconds, chemoreceptors and hormonal mechanisms
(RAAS, ADH) are activated.
Q8 (Cardiovascular – RAAS): In the renin-angiotensin-aldosterone system (RAAS), angiotensin
II directly causes all of the following EXCEPT:
A. Vasoconstriction of arterioles
B. Stimulation of aldosterone secretion from the adrenal cortex
C. Increased thirst via hypothalamic stimulation
D. Decreased sodium reabsorption in the proximal tubule
[CORRECT] D
Rationale: Angiotensin II promotes Na⁺ and water retention by stimulating aldosterone (which
acts on distal tubule/collecting duct) and directly enhancing Na⁺-H⁺ exchange in the proximal
tubule, increasing Na⁺ reabsorption—not decreasing it. Options A, B, and C are all correct
actions of angiotensin II. Clinical pearl: ACE inhibitors block angiotensin II formation, causing
vasodilation and reduced aldosterone; however, they can cause hyperkalemia due to decreased
aldosterone-mediated K⁺ secretion—monitor electrolytes closely.
, 9 (Cardiovascular – Capillary Exchange): At the arterial end of a capillary, net filtration occurs
Q
primarily because:
A. Hydrostatic pressure is less than oncotic pressure
B. Hydrostatic pressure exceeds oncotic pressure
C. Oncotic pressure exceeds hydrostatic pressure
D. Interstitial fluid pressure exceeds capillary pressure
[CORRECT] B
Rationale: At the arterial end, capillary hydrostatic pressure (≈35 mmHg) exceeds plasma
oncotic pressure (≈25 mmHg), creating a net outward force that filters fluid into interstitial
spaces. At the venous end, oncotic pressure exceeds hydrostatic pressure, promoting
reabsorption. Options A, C, and D describe conditions favoring reabsorption, not filtration.
Clinical pearl: In liver disease (decreased albumin synthesis) or nephrotic syndrome (albumin
loss), decreased oncotic pressure causes edema because less fluid is reabsorbed at the
venous end.
Q10 (Cardiovascular – Shock): A patient presents with hypotension, warm flushed skin, and
bounding pulses after a severe allergic reaction. This describes which type of shock?
A. Hypovolemic shock
B. Cardiogenic shock
C. Anaphylactic (distributive) shock
D. Obstructive shock
[CORRECT] C
Rationale: Anaphylactic shock is a form of distributive shock characterized by massive
vasodilation (warm, flushed skin), increased capillary permeability, and hypotension due to
histamine and other mediators. Hypovolemic shock (A) presents with cold, clammy skin due to
compensatory vasoconstriction. Cardiogenic shock (B) shows signs of pump failure (cool
extremities, JVD). Obstructive shock (D) results from physical obstruction (tamponade, tension
pneumothorax). Clinical pearl: First-line treatment for anaphylactic shock is epinephrine IM
(0.3–0.5 mg of 1:1000), which causes α₁-mediated vasoconstriction and β₂-mediated
bronchodilation.
Q11 (Cardiovascular – ECG Intervals): A prolonged PR interval (>0.20 seconds) on ECG
indicates:
A. Delayed conduction through the AV node
B. Bundle branch block
C. Ventricular hypertrophy
D. Atrial fibrillation
[CORRECT] A
Rationale: The PR interval represents the time from atrial depolarization onset to ventricular
depolarization onset, primarily reflecting AV nodal conduction; prolongation indicates
first-degree AV block. Bundle branch block (B) widens the QRS complex, not the PR interval.
Ventricular hypertrophy (C) alters QRS amplitude and axis. Atrial fibrillation (D) shows absent P
waves and irregular rhythm, not PR prolongation. Clinical pearl: First-degree AV block is often
benign and asymptomatic; however, if it progresses to second- or third-degree block, a
pacemaker may be indicated—monitor progression.
2026-2027 | Anatomy &
Physiology III Complete Guide |
100% Correct Q&A |
Chamberlain | Pass Guaranteed
- A+ Graded
ART A – MULTIPLE CHOICE (Q1‑55)
P
Q1 (Cardiovascular – Cardiac Muscle Action Potential): A cardiac pacemaker cell in the SA
node spontaneously depolarizes during phase 4 due to which ion channel opening?
A. Fast voltage-gated Na⁺ channels
B. Funny (HCN) channels allowing Na⁺ influx
C. Voltage-gated K⁺ channels
D. L-type Ca²⁺ channels
[CORRECT] B
Rationale: Pacemaker cells lack stable resting membrane potential; funny (HCN) channels open
in response to hyperpolarization, allowing Na⁺ influx and gradual depolarization during phase 4.
Fast Na⁺ channels (A) are found in contractile cells, not pacemaker cells. K⁺ channels (C) cause
repolarization, not depolarization. L-type Ca²⁺ channels (D) open during phase 0 of pacemaker
action potentials, not phase 4. Clinical pearl: HCN channel blockers like ivabradine reduce heart
rate by inhibiting phase 4 depolarization—know this drug mechanism for clinical applications.
Q2 (Cardiovascular – ECG): During which ECG interval does the ventricular myocardium
remain in an absolute refractory state?
A. P wave duration
B. PR interval
C. QRS complex duration
D. QT interval
[CORRECT] C
Rationale: The QRS complex represents ventricular depolarization; during this period and
immediately following, Na⁺ channels are inactivated, creating an absolute refractory period
preventing tetany. The P wave (A) represents atrial depolarization, not ventricular. The PR
,interval (B) includes atrial depolarization and AV nodal delay but not the absolute refractory
period of ventricles. The QT interval (D) includes both depolarization and repolarization but
extends beyond the absolute refractory period into relative refractoriness. Clinical pearl: A
prolonged QT interval increases risk for torsades de pointes; always check electrolytes (K⁺,
Mg²⁺, Ca²⁺) in patients with QT prolongation.
Q3 (Cardiovascular – Cardiac Cycle): During isovolumetric ventricular contraction, which valve
status is correct?
A. AV valves open; semilunar valves open
B. AV valves closed; semilunar valves closed
C. AV valves open; semilunar valves closed
D. AV valves closed; semilunar valves open
[CORRECT] B
Rationale: Isovolumetric contraction begins when ventricular pressure exceeds atrial pressure
(closing AV valves) but before ventricular pressure exceeds aortic/pulmonary pressure
(semilunar valves remain closed), creating a brief period of constant volume. Option A describes
the ejection phase, C describes ventricular filling, and D describes isovolumetric relaxation.
Clinical pearl: The "lub" (S1) heart sound occurs at the beginning of isovolumetric contraction
when AV valves close; understanding this timing helps distinguish systolic from diastolic
murmurs.
Q4 (Cardiovascular – Cardiac Output): A 68-year-old patient has a stroke volume of 70 mL/beat
and a heart rate of 72 bpm. What is the patient's cardiac output?
A. 4.2 L/min
B. 5.04 L/min
C. 6.3 L/min
D. 7.56 L/min
[CORRECT] B
Rationale: Cardiac output (CO) = Stroke Volume (SV) × Heart Rate (HR) = 70 mL × 72 bpm =
5,040 mL/min = 5.04 L/min. Option A incorrectly uses 60 bpm instead of 72. Option C uses 90
mL SV. Option D uses 90 mL SV and 84 bpm. Clinical pearl: Normal CO is 4–8 L/min; in heart
failure, both SV and CO decrease, while compensatory tachycardia initially maintains CO but
increases myocardial oxygen demand.
Q5 (Cardiovascular – Frank-Starling Law): According to the Frank-Starling law of the heart,
increased venous return results in:
A. Decreased stroke volume due to overstretching
B. Increased stroke volume due to greater sarcomere stretch
C. Decreased heart rate via vagal stimulation
D. Increased afterload on the ventricles
[CORRECT] B
Rationale: The Frank-Starling mechanism states that increased ventricular preload
(end-diastolic volume) stretches cardiac muscle fibers, optimizing actin-myosin overlap and
increasing contractile force, thereby increasing stroke volume. Option A describes the
descending limb of the curve, which rarely occurs physiologically. Option C confuses
Frank-Starling with Bainbridge reflex. Option D confuses preload with afterload. Clinical pearl: In
, eart failure, the Frank-Starling curve shifts downward; diuretics reduce preload to prevent
h
pulmonary congestion, while positive inotropes improve contractility.
Q6 (Cardiovascular – Blood Pressure): Which formula correctly calculates mean arterial
pressure (MAP)?
A. MAP = Systolic BP + Diastolic BP ÷ 2
B. MAP = Diastolic BP + ⅓(Systolic BP − Diastolic BP)
C. MAP = Systolic BP − Diastolic BP
D. MAP = (Systolic BP × 2 + Diastolic BP) ÷ 3
[CORRECT] B
Rationale: MAP = Diastolic BP + ⅓(Systolic BP − Diastolic BP), or equivalently (2 × Diastolic +
Systolic) ÷ 3, because diastole lasts approximately twice as long as systole at normal heart
rates. Option A averages the pressures equally, ignoring the longer diastolic period. Option C
calculates pulse pressure, not MAP. Option D weights systolic pressure incorrectly. Clinical
pearl: MAP must be ≥65 mmHg for adequate tissue perfusion; in shock, vasopressors are
titrated to maintain MAP ≥65 mmHg to preserve organ perfusion.
Q7 (Cardiovascular – Baroreceptor Reflex): A patient experiences acute hemorrhage, causing
decreased arterial pressure. Which baroreceptor-mediated response occurs first?
A. Decreased sympathetic outflow to the heart
B. Increased parasympathetic outflow to the SA node
C. Increased sympathetic outflow to arterioles causing vasoconstriction
D. Decreased ADH secretion from the posterior pituitary
[CORRECT] C
Rationale: Baroreceptors in the carotid sinus and aortic arch detect decreased stretch, reducing
inhibitory signals to the medulla, which increases sympathetic outflow to arterioles
(vasoconstriction), increasing total peripheral resistance to maintain BP. Option A is incorrect
because sympathetic outflow increases, not decreases. Option B is wrong because
parasympathetic tone decreases, allowing heart rate to increase. Option D is incorrect because
ADH secretion increases, not decreases. Clinical pearl: The baroreceptor reflex responds within
seconds; if BP remains low after 10–20 seconds, chemoreceptors and hormonal mechanisms
(RAAS, ADH) are activated.
Q8 (Cardiovascular – RAAS): In the renin-angiotensin-aldosterone system (RAAS), angiotensin
II directly causes all of the following EXCEPT:
A. Vasoconstriction of arterioles
B. Stimulation of aldosterone secretion from the adrenal cortex
C. Increased thirst via hypothalamic stimulation
D. Decreased sodium reabsorption in the proximal tubule
[CORRECT] D
Rationale: Angiotensin II promotes Na⁺ and water retention by stimulating aldosterone (which
acts on distal tubule/collecting duct) and directly enhancing Na⁺-H⁺ exchange in the proximal
tubule, increasing Na⁺ reabsorption—not decreasing it. Options A, B, and C are all correct
actions of angiotensin II. Clinical pearl: ACE inhibitors block angiotensin II formation, causing
vasodilation and reduced aldosterone; however, they can cause hyperkalemia due to decreased
aldosterone-mediated K⁺ secretion—monitor electrolytes closely.
, 9 (Cardiovascular – Capillary Exchange): At the arterial end of a capillary, net filtration occurs
Q
primarily because:
A. Hydrostatic pressure is less than oncotic pressure
B. Hydrostatic pressure exceeds oncotic pressure
C. Oncotic pressure exceeds hydrostatic pressure
D. Interstitial fluid pressure exceeds capillary pressure
[CORRECT] B
Rationale: At the arterial end, capillary hydrostatic pressure (≈35 mmHg) exceeds plasma
oncotic pressure (≈25 mmHg), creating a net outward force that filters fluid into interstitial
spaces. At the venous end, oncotic pressure exceeds hydrostatic pressure, promoting
reabsorption. Options A, C, and D describe conditions favoring reabsorption, not filtration.
Clinical pearl: In liver disease (decreased albumin synthesis) or nephrotic syndrome (albumin
loss), decreased oncotic pressure causes edema because less fluid is reabsorbed at the
venous end.
Q10 (Cardiovascular – Shock): A patient presents with hypotension, warm flushed skin, and
bounding pulses after a severe allergic reaction. This describes which type of shock?
A. Hypovolemic shock
B. Cardiogenic shock
C. Anaphylactic (distributive) shock
D. Obstructive shock
[CORRECT] C
Rationale: Anaphylactic shock is a form of distributive shock characterized by massive
vasodilation (warm, flushed skin), increased capillary permeability, and hypotension due to
histamine and other mediators. Hypovolemic shock (A) presents with cold, clammy skin due to
compensatory vasoconstriction. Cardiogenic shock (B) shows signs of pump failure (cool
extremities, JVD). Obstructive shock (D) results from physical obstruction (tamponade, tension
pneumothorax). Clinical pearl: First-line treatment for anaphylactic shock is epinephrine IM
(0.3–0.5 mg of 1:1000), which causes α₁-mediated vasoconstriction and β₂-mediated
bronchodilation.
Q11 (Cardiovascular – ECG Intervals): A prolonged PR interval (>0.20 seconds) on ECG
indicates:
A. Delayed conduction through the AV node
B. Bundle branch block
C. Ventricular hypertrophy
D. Atrial fibrillation
[CORRECT] A
Rationale: The PR interval represents the time from atrial depolarization onset to ventricular
depolarization onset, primarily reflecting AV nodal conduction; prolongation indicates
first-degree AV block. Bundle branch block (B) widens the QRS complex, not the PR interval.
Ventricular hypertrophy (C) alters QRS amplitude and axis. Atrial fibrillation (D) shows absent P
waves and irregular rhythm, not PR prolongation. Clinical pearl: First-degree AV block is often
benign and asymptomatic; however, if it progresses to second- or third-degree block, a
pacemaker may be indicated—monitor progression.
