APP - Cardiovascular system physiology

1. Which of the following correctly describes the sequence of ion movement during a cardiac contractile cell action potential?

A. Na⁺ influx → Ca²⁺ efflux → K⁺ influx

B. K⁺ efflux → Ca²⁺ influx → Na⁺ efflux

C. Na⁺ influx → Ca²⁺ influx → K⁺ efflux

D. Ca²⁺ influx → Na⁺ influx → K⁺ influx

Answer: C

Explanation: The cardiac action potential in contractile cells involves rapid Na⁺ influx (depolarization), followed by Ca²⁺ influx balanced by K⁺ efflux (plateau), then dominant K⁺ efflux (repolarization).

Reference: Tortora & Derrickson, 15th ed., p. 744

2. What is the primary ionic event responsible for the plateau phase of the cardiac contractile cell action potential?

A. Continued influx of sodium ions

B. Efflux of calcium ions

C. Simultaneous slow influx of Ca²⁺ and delayed efflux of K⁺

D. Sudden influx of potassium ions

Answer: C

Explanation: The plateau phase (phase 2) occurs due to slow Ca²⁺ influx through voltage-gated calcium channels while K⁺ exits at a slower rate, maintaining depolarization.

Reference: Tortora & Derrickson, 15th ed., p. 744

3. What characteristic of pacemaker (autorhythmic) cells allows them to generate spontaneous action potentials?

A. Stable resting membrane potential

B. Opening of fast Na⁺ channels

C. Gradual depolarization due to slow Na⁺ and Ca²⁺ inflow

D. Constant K⁺ efflux

Answer: C

Explanation: Pacemaker cells in the SA node have an unstable resting potential. Spontaneous slow Na⁺ inflow (funny currents) and Ca²⁺ influx gradually depolarize the membrane until threshold is reached.

Reference: Tortora & Derrickson, 15th ed., p. 743

4. Which of the following best explains why the SA node is the heart's natural pacemaker?

A. It is the only structure that conducts electrical impulses

B. It has the most stable resting membrane potential

C. It initiates action potentials at the fastest intrinsic rate

D. It directly stimulates ventricular muscle cells

Answer: C

Explanation: The sinoatrial (SA) node has the highest rate of spontaneous depolarization (~100 APs/min), making it the dominant pacemaker in the heart.

Reference: Tortora & Derrickson, 15th ed., p. 743

5. What effect would blocking calcium channels in cardiac muscle have on the action potential?

A. No effect, since sodium drives depolarization

B. Prolonged depolarization phase

C. Loss of plateau phase and weaker contractions

D. Enhanced pacemaker activity

Answer: C

Explanation: Calcium channel blockers reduce Ca²⁺ entry, shortening the plateau phase and diminishing the strength of cardiac muscle contraction.

Reference: Tortora & Derrickson, 15th ed., p. 744

6. During which phase of the cardiac action potential is the absolute refractory period maintained, and why is it essential?

A. Depolarization; prevents depolarization from spreading to atria

B. Plateau; prevents tetanus in cardiac muscle

C. Repolarization; allows re-excitation

D. Resting; stabilizes resting potential

Answer: B

Explanation: The plateau phase maintains the absolute refractory period, preventing another action potential from triggering during contraction, which ensures the heart doesn't enter tetany.

Reference: Tortora & Derrickson, 15th ed., p. 744

1. Which of the following cardiac structures has the slowest conduction velocity, and why is this physiologically significant?

A. Purkinje fibers - allows rapid ventricular contraction

B. Atrioventricular (AV) node - allows time for ventricular filling

C. Bundle of His - delays atrial repolarization

D. SA node - maintains the rhythm of contraction

Answer: B

Explanation: The AV node has the slowest conduction velocity (~0.05 m/s), which delays the impulse, giving the atria time to contract and push blood into the ventricles before ventricular contraction.

Reference: Tortora & Derrickson, 15th ed., p. 743

2. Which cardiac tissue has the fastest conduction velocity and what is its functional role?

A. SA node - initiates depolarization

B. AV node - coordinates atrial contraction

C. Purkinje fibers - ensures synchronous ventricular contraction

D. Ventricular myocardium - sustains contraction

Answer: C

Explanation: Purkinje fibers conduct impulses very rapidly (~4 m/s) to enable the near-simultaneous contraction of both ventricles for efficient blood ejection.

Reference: Tortora & Derrickson, 15th ed., p. 743-744

3. What best describes the absolute refractory period in cardiac muscle fibers?

A. The phase when muscle contraction is strongest

B. The phase when a stronger-than-normal stimulus can trigger another action potential

C. The period during which no stimulus, however strong, can initiate another action potential

D. The delay between atrial and ventricular contractions

Answer: C

Explanation: The absolute refractory period corresponds to phases 0, 1, 2, and part of 3 of the action potential. During this period, cardiac cells are completely unresponsive to new stimuli.

Reference: Tortora & Derrickson, 15th ed., p. 744

4. What is the functional significance of the long refractory period in cardiac muscle?

A. Allows rapid re-stimulation of the myocardium

B. Enables summation of contractions for stronger output

C. Prevents tetany, ensuring rhythmic contraction and relaxation

D. Increases conduction velocity for faster heart rate

Answer: C

Explanation: The long refractory period (~250 ms) in cardiac muscle prevents summation and tetanus, ensuring that each contraction is followed by relaxation to refill the chambers.

Reference: Tortora & Derrickson, 15th ed., p. 744

5. During which phase of the cardiac action potential is the relative refractory period observed?

A. Phase 0 - rapid depolarization

B. Phase 1 - partial repolarization

C. Phase 2 - plateau phase

D. Late phase 3 - repolarization

Answer: D

Explanation: The relative refractory period occurs during the latter part of repolarization (late phase 3), when a very strong stimulus may elicit a second action potential, although it may be abnormal.

Reference: Tortora & Derrickson, 15th ed., p. 744

1. What is the initial electrical event that leads to excitation-contraction coupling in cardiac muscle?

A. Opening of sarcoplasmic reticulum ryanodine receptors

B. Binding of calcium to troponin

C. Depolarization of the sarcolemma

D. ATP hydrolysis by myosin

Answer: C

Explanation: ECC begins with the depolarization of the cardiac muscle cell membrane (sarcolemma), which triggers downstream calcium signaling and contraction.

Reference: Tortora & Derrickson, 15th ed., p. 744-745

2. In cardiac muscle, what is the primary source of calcium that initiates contraction during ECC?

A. Sarcoplasmic reticulum release only

B. Influx from interstitial fluid through voltage-gated Ca²⁺ channels

C. Mitochondrial calcium stores

D. Calcium bound to troponin

Answer: B

Explanation: Unlike skeletal muscle, cardiac muscle relies heavily on extracellular calcium entering through L-type voltage-gated Ca²⁺ channels, which then stimulates further Ca²⁺ release from the sarcoplasmic reticulum.

Reference: Tortora & Derrickson, 15th ed., p. 744-745

3. What role does calcium-induced calcium release (CICR) play in cardiac ECC?

A. It inhibits further calcium influx

B. It activates Na⁺ channels

C. It triggers ryanodine receptors to release Ca²⁺ from the SR

D. It opens L-type calcium channels

Answer: C

Explanation: The small amount of Ca²⁺ that enters the cell during depolarization activates ryanodine receptors on the SR, triggering a larger release of stored Ca²⁺ in a process called CICR.

Reference: Tortora & Derrickson, 15th ed., p. 745

4. Which protein does calcium bind to in cardiac myocytes to allow cross-bridge cycling and contraction?

A. Actin

B. Myosin

C. Troponin C

D. Tropomyosin

Answer: C

Explanation: Calcium binds to the troponin C subunit, which induces a conformational change in tropomyosin, exposing actin binding sites for myosin cross-bridge formation.

Reference: Tortora & Derrickson, 15th ed., p. 745

5. What mechanism is primarily responsible for relaxation of cardiac muscle after contraction?

A. Closure of sodium channels

B. Removal of calcium via Na⁺/K⁺ ATPase

C. Reuptake of calcium into the sarcoplasmic reticulum by SERCA and extrusion by Na⁺/Ca²⁺ exchanger

D. Dephosphorylation of ATP

Answer: C

Explanation: Relaxation is achieved by active reuptake of Ca²⁺ into the SR by the SERCA pump and extrusion from the cell by the sodium-calcium exchanger (NCX).

Reference: Tortora & Derrickson, 15th ed., p. 745

6. What would be the most direct consequence of a mutation that impairs L-type calcium channel function in cardiac cells?

A. Increased heart rate

B. Weakened myocardial contraction

C. Shortened refractory period

D. Enhanced CICR

Answer: B

Explanation: L-type calcium channels are crucial for initiating calcium-induced calcium release. If impaired, less Ca²⁺ enters the cell, resulting in reduced CICR and weaker myocardial contraction.

Reference: Tortora & Derrickson, 15th ed., p. 744-745

1. Which event marks the beginning of the cardiac cycle?

A. Atrial systole

B. Ventricular systole

C. Atrial diastole

D. Ventricular diastole

Answer: A

Explanation: The cardiac cycle begins with atrial systole, where atrial contraction tops off ventricular filling just before ventricular systole begins.

Reference: Tortora & Derrickson, 15th ed., p. 749

2. During which phase of the cardiac cycle are all heart valves closed and ventricular pressure is increasing?

A. Atrial systole

B. Isovolumetric contraction

C. Ventricular ejection

D. Isovolumetric relaxation

Answer: B

Explanation: Isovolumetric contraction occurs after AV valves close but before semilunar valves open. Ventricular pressure rises rapidly with no change in volume.

Reference: Tortora & Derrickson, 15th ed., p. 749-750

3. The second heart sound ("dup") corresponds to which mechanical event?

A. AV valve opening

B. Semilunar valve closing

C. AV valve closing

D. Atrial contraction

Answer: B

Explanation: The second heart sound ("S2") occurs with the closure of the aortic and pulmonary (semilunar) valves at the beginning of ventricular diastole.

Reference: Tortora & Derrickson, 15th ed., p. 750

4. What happens to ventricular volume during isovolumetric contraction?

A. It increases

B. It decreases

C. It stays the same

D. It is maximal

Answer: C

Explanation: During isovolumetric contraction, all valves are closed so no blood enters or leaves the ventricles; thus, volume remains constant.

Reference: Tortora & Derrickson, 15th ed., p. 749-750

5. Which phase corresponds to rapid ejection of blood from the ventricles?

A. Atrial systole

B. Isovolumetric contraction

C. Ventricular ejection

D. Isovolumetric relaxation

Answer: C

Explanation: Once ventricular pressure exceeds aortic and pulmonary pressure, semilunar valves open, and blood is ejected during the ventricular ejection phase.

Reference: Tortora & Derrickson, 15th ed., p. 749-750

6. What is the typical end-diastolic volume (EDV) in a resting adult heart?

A. 30 mL

B. 60 mL

C. 100 mL

D. 130 mL

Answer: D

Explanation: EDV is the volume of blood in each ventricle at the end of ventricular diastole, usually about 130 mL.

Reference: Tortora & Derrickson, 15th ed., p. 750

7. Which factor is responsible for opening the atrioventricular valves during the cardiac cycle?

A. Atrial pressure falling below ventricular pressure

B. Ventricular pressure exceeding aortic pressure

C. Atrial pressure exceeding ventricular pressure

D. Contraction of papillary muscles

Answer: C

Explanation: The AV valves open when atrial pressure exceeds ventricular pressure, allowing passive ventricular filling.

Reference: Tortora & Derrickson, 15th ed., p. 749

8. Which phase immediately follows closure of the semilunar valves?

A. Atrial systole

B. Ventricular systole

C. Isovolumetric relaxation

D. Isovolumetric contraction

Answer: C

Explanation: After semilunar valves close, and before AV valves reopen, ventricles enter isovolumetric relaxation with all valves closed.

Reference: Tortora & Derrickson, 15th ed., p. 749-750

1. Which formula correctly defines cardiac output (CO)?

A. CO = Stroke Volume × End-Diastolic Volume

B. CO = Stroke Volume ÷ Heart Rate

C. CO = Heart Rate × Stroke Volume

D. CO = Heart Rate ÷ Blood Pressure

Answer: C

Explanation: Cardiac Output is the volume of blood ejected by each ventricle per minute and is calculated as CO = HR × SV.

Reference: Tortora & Derrickson, 15th ed., p. 751

2. If a person has a heart rate of 70 bpm and a stroke volume of 70 mL/beat, what is their cardiac output?

A. 140 mL/min

B. 490 mL/min

C. 4.9 L/min

D. 49 L/min

Answer: C

Explanation: CO = 70 bpm × 70 mL = 4900 mL/min = 4.9 L/min.

Reference: Tortora & Derrickson, 15th ed., p. 751

3. Which of the following would most likely increase cardiac output?

A. Parasympathetic stimulation

B. Decreased venous return

C. Increased sympathetic activity

D. Decreased preload

Answer: C

Explanation: Sympathetic stimulation increases both heart rate and contractility, leading to increased cardiac output.

Reference: Tortora & Derrickson, 15th ed., p. 752-753

4. What is the term for the degree of stretch on the heart before it contracts?

A. Afterload

B. Preload

C. Contractility

D. Ejection fraction

Answer: B

Explanation: Preload refers to the initial stretching of cardiac muscle fibers (related to end-diastolic volume) and is a key determinant of stroke volume.

Reference: Tortora & Derrickson, 15th ed., p. 752

5. Which factor would most directly decrease stroke volume?

A. Increased venous return

B. Increased afterload

C. Increased preload

D. Sympathetic activation

Answer: B

Explanation: Afterload is the resistance the ventricles must overcome to eject blood. A high afterload (e.g., in hypertension) reduces stroke volume.

Reference: Tortora & Derrickson, 15th ed., p. 752

6. Which of the following best describes the Frank-Starling Law of the Heart?

A. The more the heart fills during diastole, the weaker the next contraction

B. Stroke volume increases with increased heart rate

C. Increased end-diastolic volume leads to a stronger contraction

D. Cardiac output is independent of venous return

Answer: C

Explanation: The Frank-Starling mechanism states that a greater preload (stretch) increases the force of contraction, thereby increasing stroke volume.

Reference: Tortora & Derrickson, 15th ed., p. 752

7. Which of the following will directly decrease cardiac output?

A. Increased blood volume

B. Vasoconstriction

C. Beta-1 adrenergic receptor blockade

D. Increased calcium influx in cardiac cells

Answer: C

Explanation: Beta-blockers reduce heart rate and contractility by inhibiting sympathetic activity on beta-1 receptors, lowering cardiac output.

Reference: Tortora & Derrickson, 15th ed., p. 753

1. Which of the following best describes intrinsic regulation of cardiac output?

A. Activation of sympathetic nerves to increase stroke volume

B. Increased end-diastolic volume leading to increased stroke volume

C. Release of norepinephrine from cardiac nerves

D. Inhibition of the SA node by vagus nerve

Answer: B

Explanation: Intrinsic regulation refers to the Frank-Starling law, where the heart automatically adjusts its force of contraction in response to changes in venous return (preload).

Reference: Tortora & Derrickson, 15th ed., p. 752

2. According to the Frank-Starling law, which of the following conditions would lead to increased cardiac output?

A. Decreased venous return

B. Decreased preload

C. Increased stretch of ventricular walls due to higher EDV

D. Increased afterload

Answer: C

Explanation: Greater stretch of the myocardial fibers (preload) increases the force of contraction, enhancing stroke volume and cardiac output.

Reference: Tortora & Derrickson, 15th ed., p. 752

3. Which branch of the autonomic nervous system decreases heart rate and contractility?

A. Sympathetic

B. Parasympathetic

C. Somatic

D. Enteric

Answer: B

Explanation: Parasympathetic innervation (via the vagus nerve) reduces heart rate and has a minimal effect on ventricular contractility.

Reference: Tortora & Derrickson, 15th ed., p. 753

4. Which neurotransmitter and receptor combination is primarily responsible for increasing heart rate during sympathetic stimulation?

A. Acetylcholine - muscarinic receptor

B. Epinephrine - alpha-1 receptor

C. Norepinephrine - beta-1 adrenergic receptor

D. Dopamine - D2 receptor

Answer: C

Explanation: Sympathetic stimulation releases norepinephrine which binds to beta-1 adrenergic receptors on the SA node, increasing heart rate and contractility.

Reference: Tortora & Derrickson, 15th ed., p. 753

5. How does parasympathetic stimulation affect the SA and AV nodes?

A. Increases conduction velocity

B. Enhances pacemaker activity

C. Slows depolarization, reducing heart rate

D. Causes calcium influx, increasing contractility

Answer: C

Explanation: Acetylcholine released from the vagus nerve binds muscarinic receptors, opening K⁺ channels and hyperpolarizing pacemaker cells, which slows the heart rate.

Reference: Tortora & Derrickson, 15th ed., p. 753

6. A patient has a heart transplant and lacks autonomic innervation. Which mechanism will still regulate their cardiac output?

A. Sympathetic tone

B. Parasympathetic vagal reflexes

C. Hormonal reflexes only

D. Frank-Starling mechanism

Answer: D

Explanation: The transplanted heart cannot receive neural input, but intrinsic mechanisms like the Frank-Starling law still adjust output in response to venous return.

Reference: Tortora & Derrickson, 15th ed., p. 752

1. Which blood vessels are primarily responsible for regulating systemic vascular resistance (SVR)?

A. Veins

B. Capillaries

C. Arteries

D. Arterioles

Answer: D

Explanation: Arterioles are known as resistance vessels. They regulate blood flow and blood pressure through vasoconstriction and vasodilation, adjusting total peripheral resistance.

Reference: Tortora & Derrickson, 15th ed., p. 755-756

2. What is the main function of capillaries in the circulatory system?

A. Carry blood under high pressure

B. Act as blood reservoirs

C. Exchange nutrients and gases between blood and tissues

D. Prevent backflow of blood

Answer: C

Explanation: Capillaries are thin-walled vessels composed of a single endothelial layer, optimized for diffusion of oxygen, nutrients, and waste between blood and tissue fluid.

Reference: Tortora & Derrickson, 15th ed., p. 758-759

3. Which of the following vessels contains valves to prevent blood backflow, particularly in the limbs?

A. Arteries

B. Arterioles

C. Capillaries

D. Veins

Answer: D

Explanation: Veins, especially in the lower limbs, contain valves that prevent backflow and assist in venous return against gravity.

Reference: Tortora & Derrickson, 15th ed., p. 757

4. Which vessels act as the primary site of filtration and reabsorption in tissues?

A. Arteries

B. Arterioles

C. Capillaries

D. Venules

Answer: C

Explanation: Capillaries allow fluid exchange through hydrostatic and osmotic pressure gradients, facilitating filtration at the arterial end and reabsorption at the venous end.

Reference: Tortora & Derrickson, 15th ed., p. 759

5. Which circulatory components serve as blood reservoirs and contain the largest percentage of blood volume at rest?

A. Arteries and arterioles

B. Capillaries

C. Pulmonary arteries

D. Veins and venules

Answer: D

Explanation: Veins and venules hold about 60-70% of total blood volume at rest and serve as capacitance vessels.

Reference: Tortora & Derrickson, 15th ed., p. 756

6. What is the primary role of arterioles in local tissue perfusion?

A. Reducing blood velocity

B. Increasing blood oxygenation

C. Controlling blood distribution via vasomotion

D. Facilitating gas exchange

Answer: C

Explanation: Arterioles regulate local blood flow into capillary beds via vasoconstriction and vasodilation in response to neural, hormonal, or local metabolic signals.

Reference: Tortora & Derrickson, 15th ed., p. 756

7. In a capillary bed, what is the function of precapillary sphincters?

A. Increase capillary pressure

B. Maintain arterial blood flow

C. Control entry of blood into true capillaries

D. Act as a barrier to immune cells

Answer: C

Explanation: Precapillary sphincters are smooth muscle rings at the capillary entrance that open or close in response to local tissue demand, regulating perfusion.

Reference: Tortora & Derrickson, 15th ed., p. 759

1. What is the primary factor that causes blood to flow through the circulatory system?

A. Cardiac contractility

B. Autonomic innervation

C. Pressure gradient between arteries and veins

D. Capillary permeability

Answer: C

Explanation: Blood flows from areas of higher pressure (arteries) to lower pressure (veins). The pressure gradient is the driving force for circulation.

Reference: Tortora & Derrickson, 15th ed., p. 762

2. Which of the following best explains why veins are called "capacitance vessels"?

A. They have thicker walls than arteries

B. They actively pump blood to the heart

C. They contain smooth muscle that generates pressure

D. They can accommodate large volumes of blood with little change in pressure

Answer: D

Explanation: Veins are highly compliant and can store large blood volumes (up to 60% of total) at low pressure, functioning as a reservoir.

Reference: Tortora & Derrickson, 15th ed., p. 756, 762

3. Which vessel type experiences the greatest drop in pressure in the systemic circulation?

A. Arteries

B. Arterioles

C. Capillaries

D. Venules

Answer: B

Explanation: Arterioles are resistance vessels that cause the most significant pressure drop due to their small diameter and ability to constrict.

Reference: Tortora & Derrickson, 15th ed., p. 762

4. What is the approximate average pressure in large systemic arteries such as the aorta?

A. 10 mmHg

B. 25 mmHg

C. 60 mmHg

D. 100 mmHg

Answer: D

Explanation: Mean arterial pressure (MAP) in large arteries like the aorta is around 100 mmHg under resting conditions.

Reference: Tortora & Derrickson, 15th ed., p. 762

5. Which physiological mechanism helps maintain venous return against gravity in upright posture?

A. Arterial dilation

B. Capillary exchange

C. Venous valves and skeletal muscle pump

D. Pulmonary recoil

Answer: C

Explanation: Venous valves prevent backflow, and contraction of surrounding skeletal muscle compresses veins, propelling blood back toward the heart.

Reference: Tortora & Derrickson, 15th ed., p. 762-763

6. What is the compliance of a blood vessel defined as?

A. Resistance per unit length

B. Volume change per unit pressure change

C. Pressure gradient across its length

D. Velocity of flow through it

Answer: B

Explanation: Compliance = ΔV / ΔP. Veins are more compliant than arteries, allowing large volume changes with small pressure shifts.

Reference: Tortora & Derrickson, 15th ed., p. 756, 763

7. If arterial compliance decreases (e.g., in aging), what happens to systolic blood pressure (SBP)?

A. SBP decreases

B. SBP remains unchanged

C. SBP increases

D. SBP fluctuates randomly

Answer: C

Explanation: With reduced arterial compliance (stiffer arteries), the same stroke volume causes a greater rise in pressure, increasing SBP.

Reference: Tortora & Derrickson, 15th ed., p. 763

1. Which region of the brain contains the cardiovascular center that regulates heart rate and blood vessel diameter?

A. Cerebral cortex

B. Cerebellum

C. Medulla oblongata

D. Thalamus

Answer: C

Explanation: The cardiovascular center located in the medulla oblongata regulates blood pressure by adjusting heart rate and vessel tone.

Reference: Tortora & Derrickson, 15th ed., p. 765

2. Which of the following describes the function of the vasomotor center within the cardiovascular control center?

A. Regulates blood volume via kidney filtration

B. Controls skeletal muscle contraction

C. Adjusts peripheral resistance by altering vessel diameter

D. Inhibits sympathetic stimulation of the heart

Answer: C

Explanation: The vasomotor center controls sympathetic output to vascular smooth muscle, affecting arteriolar diameter and hence total peripheral resistance.

Reference: Tortora & Derrickson, 15th ed., p. 765

3. Which receptors detect blood pressure changes and send signals to the cardiovascular center?

A. Proprioceptors

B. Baroreceptors

C. Nociceptors

D. Chemoreceptors

Answer: B

Explanation: Baroreceptors in the carotid sinus and aortic arch sense stretch due to pressure changes and relay information to the medulla.

Reference: Tortora & Derrickson, 15th ed., p. 766

4. What happens when baroreceptors detect a rise in arterial pressure?

A. Sympathetic output increases, causing vasoconstriction

B. Parasympathetic output increases, reducing heart rate

C. ADH secretion increases

D. Epinephrine release is stimulated

Answer: B

Explanation: Elevated pressure stimulates baroreceptors, leading to parasympathetic activation (via vagus nerve) and inhibition of sympathetic tone to lower heart rate and vessel tone.

Reference: Tortora & Derrickson, 15th ed., p. 766

5. Which hormone causes vasoconstriction and stimulates aldosterone secretion, thus raising blood pressure?

A. Atrial natriuretic peptide (ANP)

B. Epinephrine

C. Angiotensin II

D. Antidiuretic hormone (ADH)

Answer: C

Explanation: Angiotensin II is a potent vasoconstrictor and promotes aldosterone release, which increases sodium (and water) retention to raise BP.

Reference: Tortora & Derrickson, 15th ed., p. 767-768

6. How does antidiuretic hormone (ADH) contribute to blood pressure regulation?

A. Causes vasodilation in skeletal muscle

B. Stimulates water loss via the kidneys

C. Promotes vasoconstriction and water retention

D. Enhances atrial natriuretic peptide release

Answer: C

Explanation: ADH increases water reabsorption in the kidneys and causes mild vasoconstriction, raising blood pressure and volume.

Reference: Tortora & Derrickson, 15th ed., p. 767

7. Which hormone lowers blood pressure by promoting vasodilation and sodium excretion?

A. Angiotensin II

B. ADH

C. Aldosterone

D. Atrial natriuretic peptide (ANP)

Answer: D

Explanation: ANP is released by atrial cells in response to stretch (high BP) and works to reduce blood volume and pressure through vasodilation and natriuresis.

Reference: Tortora & Derrickson, 15th ed., p. 767-768

8. Autoregulation of blood flow is primarily driven by:

A. Neural reflexes in the medulla

B. Hormonal fluctuations in plasma volume

C. Local changes in O₂, CO₂, pH, and temperature

D. Baroreceptor signaling to the hypothalamus

Answer: C

Explanation: Autoregulation ensures constant tissue perfusion by responding to local metabolic conditions—such as hypoxia, hypercapnia, or acidosis—by dilating or constricting arterioles.

Reference: Tortora & Derrickson, 15th ed., p. 768

1. How do the kidneys contribute to long-term regulation of arterial blood pressure?

A. By adjusting cardiac output via sympathetic stimulation

B. Through regulation of red blood cell production

C. By controlling extracellular fluid volume through filtration and reabsorption

D. By controlling heart rate via baroreceptors

Answer: C

Explanation: The kidneys regulate blood pressure over the long term by adjusting blood volume through control of sodium and water reabsorption, which determines extracellular fluid volume.

Reference: Tortora & Derrickson, 15th ed., p. 769

2. What is pressure diuresis?

A. Increased urine formation due to increased oncotic pressure

B. Increased urine output in response to decreased blood pressure

C. Increased excretion of water by kidneys in response to elevated arterial pressure

D. Decreased filtration rate due to renal artery stenosis

Answer: C

Explanation: Pressure diuresis is the process by which elevated arterial pressure increases renal excretion of water, thereby reducing blood volume and pressure.

Reference: Tortora & Derrickson, 15th ed., p. 769

3. Which statement best describes pressure natriuresis?

A. The excretion of potassium in response to low pressure

B. The reabsorption of sodium in response to dehydration

C. The loss of sodium in the urine in response to increased arterial pressure

D. A hormonal response mediated by aldosterone

Answer: C

Explanation: Pressure natriuresis is the increase in sodium excretion that occurs with elevated arterial pressure, contributing to a reduction in extracellular fluid volume and BP.

Reference: Tortora & Derrickson, 15th ed., p. 769

4. What is the initiating event in the renin-angiotensin-aldosterone system (RAAS)?

A. Increased blood sodium

B. Stimulation of baroreceptors

C. Decreased renal perfusion pressure sensed by juxtaglomerular cells

D. Increased atrial stretch

Answer: C

Explanation: Low blood pressure or decreased sodium delivery to the distal tubule prompts juxtaglomerular cells in the kidney to secrete renin.

Reference: Tortora & Derrickson, 15th ed., p. 767

5. Which hormone in the RAAS is a potent vasoconstrictor that raises blood pressure?

A. Aldosterone

B. Renin

C. Angiotensin II

D. Atrial natriuretic peptide

Answer: C

Explanation: Angiotensin II constricts blood vessels, increases total peripheral resistance, and stimulates aldosterone and ADH release to raise BP.

Reference: Tortora & Derrickson, 15th ed., p. 767

6. How does aldosterone increase blood pressure?

A. Stimulates vasodilation of systemic arteries

B. Increases sodium and water reabsorption in the kidneys

C. Promotes calcium reabsorption

D. Increases potassium secretion into the blood

Answer: B

Explanation: Aldosterone, released from the adrenal cortex, promotes sodium and water reabsorption in the renal tubules, increasing blood volume and pressure.

Reference: Tortora & Derrickson, 15th ed., p. 767-768

7. Which of the following contributes to hypertension via impaired renal pressure-natriuresis mechanism?

A. Increased baroreceptor sensitivity

B. Decreased renal sodium excretion despite elevated blood pressure

C. Enhanced atrial natriuretic peptide release

D. Lowered sympathetic tone

Answer: B

Explanation: If kidneys fail to excrete enough sodium and water in response to high pressure, extracellular fluid volume remains elevated, contributing to chronic hypertension.

Reference: Tortora & Derrickson, 15th ed., p. 769

1. What immediate cardiovascular response occurs at the onset of moderate exercise?

A. Decrease in stroke volume

B. Increase in parasympathetic activity

C. Increase in heart rate and stroke volume

D. Decrease in cardiac output

Answer: C

Explanation: Exercise stimulates sympathetic activity and suppresses parasympathetic tone, resulting in increased heart rate and stroke volume, thereby increasing cardiac output.

Reference: Tortora & Derrickson, 15th ed., p. 772

2. During sustained aerobic exercise, which of the following increases the most in terms of contribution to cardiac output?

A. Coronary blood flow

B. Renal blood flow

C. Skin blood flow

D. Skeletal muscle blood flow

Answer: D

Explanation: Blood is preferentially redirected toward active skeletal muscles during exercise, where metabolic demand is highest.

Reference: Tortora & Derrickson, 15th ed., p. 772

3. How does regular aerobic training affect resting heart rate?

A. Increases it due to greater cardiac demand

B. Decreases it due to increased vagal tone and stroke volume

C. Causes erratic fluctuations due to overtraining

D. Has no long-term effect

Answer: B

Explanation: Chronic aerobic training increases parasympathetic tone and stroke volume, which allows the heart to maintain adequate output at a lower rate.

Reference: Tortora & Derrickson, 15th ed., p. 772

4. What is the primary cardiovascular benefit of long-term endurance training?

A. Reduction in end-diastolic volume

B. Decrease in venous return

C. Improved oxygen delivery due to increased cardiac output and capillary density

D. Increase in systemic vascular resistance

Answer: C

Explanation: Regular exercise improves myocardial efficiency, increases stroke volume, and promotes angiogenesis, all of which improve oxygen delivery.

Reference: Tortora & Derrickson, 15th ed., p. 772

5. What happens to systolic and diastolic blood pressure during moderate dynamic exercise in a healthy individual?

A. Both increase significantly

B. Systolic increases, diastolic remains unchanged or slightly decreases

C. Diastolic increases, systolic remains constant

D. Both decrease due to vasodilation

Answer: B

Explanation: Systolic pressure rises due to increased cardiac output, while diastolic pressure remains the same or slightly decreases due to vasodilation in active muscles.

Reference: Tortora & Derrickson, 15th ed., p. 772

6. Which mechanism allows trained athletes to have a higher cardiac output during exercise compared to untrained individuals?

A. Higher resting heart rate

B. Enhanced stroke volume due to cardiac hypertrophy

C. Increased sympathetic stimulation only

D. Reduced blood volume

Answer: B

Explanation: Athletes develop physiological hypertrophy, which increases stroke volume and cardiac output without needing a very high heart rate.

Reference: Tortora & Derrickson, 15th ed., p. 772

7. Why is venous return important during exercise?

A. It triggers baroreceptor reflexes

B. It determines arterial oxygen levels

C. It increases preload, thereby enhancing stroke volume via the Frank-Starling mechanism

D. It causes vasoconstriction in coronary vessels

Answer: C

Explanation: Increased venous return during exercise stretches the ventricles, improving contractility and stroke volume via the Frank-Starling mechanism.

Reference: Tortora & Derrickson, 15th ed., p. 772

1. A patient experiences a sudden drop in arterial pressure due to blood loss. Which of the following integrated responses is most likely to occur first to maintain perfusion?

A. Renin-angiotensin-aldosterone activation causing sodium retention

B. Reflex bradycardia to conserve cardiac output

C. Decreased sympathetic output to reduce afterload

D. Baroreceptor-mediated sympathetic activation increasing heart rate and vasoconstriction

Answer: D

Explanation: Baroreceptors quickly detect the drop in pressure and increase sympathetic output to restore cardiac output and systemic vascular resistance. RAAS is slower and not immediate.

Reference: Tortora & Derrickson, 15th ed., p. 766-768

2. An elite athlete has a resting heart rate of 48 bpm and a high stroke volume. Which of the following best explains how their cardiac output is maintained?

A. Increased preload and decreased venous return

B. Reduced afterload and elevated blood pressure

C. Enhanced parasympathetic tone and increased end-diastolic volume

D. Depressed contractility with high resting heart rate

Answer: C

Explanation: Athletes have higher vagal tone (parasympathetic dominance), leading to lower HR but a higher stroke volume due to increased EDV and myocardial efficiency.

Reference: Tortora & Derrickson, 15th ed., p. 772

3. A patient with left-sided heart failure has elevated pulmonary capillary hydrostatic pressure. Which of the following physiological changes would be expected as a result?

A. Decreased filtration into alveoli

B. Increased reabsorption of fluid into pulmonary capillaries

C. Pulmonary edema due to excessive filtration

D. Systemic vasodilation

Answer: C

Explanation: Increased hydrostatic pressure in pulmonary capillaries promotes excess fluid filtration into alveolar spaces, leading to pulmonary edema.

Reference: Tortora & Derrickson, 15th ed., p. 749

4. Which statement best describes the expected change in vascular compliance in a 75-year-old hypertensive patient, and how does this affect systolic pressure?

A. Increased compliance; systolic pressure decreases

B. Decreased compliance; systolic pressure increases

C. Unchanged compliance; no effect on systolic pressure

D. Increased compliance; diastolic pressure increases

Answer: B

Explanation: Aging and hypertension decrease arterial compliance (more stiffness), resulting in a greater pressure rise during systole, raising systolic BP.

Reference: Tortora & Derrickson, 15th ed., p. 763

5. A patient is infused with a large volume of isotonic saline. Which mechanism will most directly help normalize their blood pressure in the long term?

A. Increased sympathetic tone

B. Pressure natriuresis and diuresis

C. Atrial natriuretic peptide inhibition

D. Vasoconstriction of renal afferent arterioles

Answer: B

Explanation: The kidneys respond to elevated arterial pressure by increasing sodium and water excretion (pressure natriuresis/diuresis), reducing blood volume and pressure.

Reference: Tortora & Derrickson, 15th ed., p. 769

6. In a patient with renal artery stenosis, which of the following would be most consistent with early physiological compensation?

A. Decreased systemic vascular resistance

B. Decreased renin release from the juxtaglomerular cells

C. Increased angiotensin II levels causing systemic vasoconstriction

D. Elevated atrial natriuretic peptide secretion

Answer: C

Explanation: Narrowing of the renal artery reduces perfusion to the kidney, triggering renin release, leading to elevated angiotensin II, vasoconstriction, and hypertension.

Reference: Tortora & Derrickson, 15th ed., p. 767-768

7. A patient has a resting end-diastolic volume (EDV) of 140 mL and an end-systolic volume (ESV) of 60 mL. What is the ejection fraction, and what does it indicate?

A. 60%; normal systolic function

B. 40%; mildly reduced systolic function

C. 50%; diastolic dysfunction

D. 80%; hyperdynamic state

Answer: A

Explanation: EF = (SV/EDV) × 100 = ((140-60)/140) × 100 = 57%. Normal range is ~55-70%, indicating normal systolic function.

Reference: Tortora & Derrickson, 15th ed., p. 750