Unit 04 — Cardiovascular · Question Bank

TMU Physiology · Circulation · Guyton 14e Ch 9–20
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Q1
The sinoatrial (SA) node is a:
TMU 题-Circulation
A. slow-response rhythmic cell
B. fast-response rhythmic cell
C. fast-response non-rhythmic cell
D. slow-response non-rhythmic cell
✅ Answer: A. slow-response rhythmic cell
SA node phase 0 uses the L-type Ca²⁺ channel (slow) and it is self-firing (rhythmic). Purkinje cells are fast-response rhythmic.
Q2
In the SA node pacemaker (P) cell, phase 0 is caused by:
TMU 题-Circulation
A. the fast voltage-gated Na⁺ channel
B. the L-type Ca²⁺ channel
C. the T-type Ca²⁺ channel
D. the funny current I_f
✅ Answer: B. the L-type Ca²⁺ channel
Pacemaker upstroke is carried by L-type Ca²⁺ channels (no fast Na⁺). I_f and T-type Ca²⁺ drive the phase-4 slow depolarization.
Q3
The effective refractory period of cardiac muscle is mainly caused by:
TMU 题-Circulation
A. inactivation of Ca²⁺ channels
B. inactivation of K⁺ channels
C. inactivation of Na⁺ channels
D. activation of K⁺ channels
✅ Answer: C. inactivation of Na⁺ channels
During the long plateau the Na⁺ channels stay inactivated, so no propagated AP can fire — the basis of the very long refractory period.
Q4
Which autorhythmic tissue has the fastest intrinsic rhythm?
TMU 题-Circulation
A. AV node
B. bundle branches
C. Purkinje fibres
D. SA node
✅ Answer: D. SA node
Intrinsic rates: SA (~100) > AV (~50) > Purkinje (~25–40). The fastest (SA) is the normal pacemaker; the rest are latent.
Q5
Which is NOT an electrophysiological property of myocardium?
TMU 题-Circulation
A. contractility
B. excitability
C. conductivity
D. autorhythmicity
✅ Answer: A. contractility
Contractility is the MECHANICAL property. The electrophysiological properties are excitability, autorhythmicity and conductivity.
Q6
During which cardiac-cycle phase does the intraventricular pressure rise to its maximum?
TMU 题-Circulation
A. isovolumic contraction
B. rapid ejection
C. isovolumic relaxation
D. rapid filling
✅ Answer: B. rapid ejection
Ventricular pressure peaks during rapid ejection (when LV pressure exceeds and tracks the aortic pressure).
Q7
At a heart rate of 75/min, the longest period of the cardiac cycle is:
TMU 题-Circulation
A. isovolumic contraction
B. isovolumic relaxation
C. ventricular filling
D. ventricular ejection
✅ Answer: C. ventricular filling
Diastolic filling is the longest phase at normal heart rate — and it is the part that shortens most when the heart speeds up.
Q8
The intraventricular pressure drops most rapidly during:
TMU 题-Circulation
A. isovolumic contraction
B. rapid ejection
C. rapid filling
D. isovolumic relaxation
✅ Answer: D. isovolumic relaxation
With all valves shut and the ventricle relaxing, pressure falls steeply during isovolumic relaxation.
Q9
The first heart sound (S₁) is mainly caused by:
TMU 题-Circulation
A. closure of the AV valves
B. closure of the semilunar valves
C. opening of the AV valves
D. opening of the semilunar valves
✅ Answer: A. closure of the AV valves
S₁ = closure of the AV (mitral + tricuspid) valves, marking the start of systole. S₂ = closure of the semilunar valves (start of diastole).
Q10
Contraction of the atria accounts for about what fraction of ventricular filling?
TMU 题-Circulation
A. 40–50%
B. 20–30%
C. 60–70%
D. 70–80%
✅ Answer: B. 20–30%
Most filling is passive; the 'atrial kick' adds only ~20–30% at rest (more important during tachycardia).
Q11
For an intact heart, the preload is usually considered to be the:
TMU 题-Circulation
A. venous return only
B. end-systolic volume
C. end-diastolic volume
D. stroke volume
✅ Answer: C. end-diastolic volume
Preload = the end-diastolic volume (the stretch on the ventricle just before contraction), set by venous return.
Q12
The afterload of the left ventricle is the:
TMU 题-Circulation
A. atrial pressure
B. ventricular pressure during isovolumic contraction
C. end-diastolic volume
D. aortic (arterial) pressure
✅ Answer: D. aortic (arterial) pressure
Afterload = the resistance the ventricle ejects against = the aortic/arterial pressure.
Q13
Stroke volume is changed through the Frank–Starling mechanism by altering:
TMU 题-Circulation
A. preload
B. afterload
C. myocardial contractility
D. heart rate
✅ Answer: A. preload
Frank–Starling (heterometric regulation) works through preload (initial fibre length). Contractility changes are homometric (length-independent).
Q14
A very rapid heart rate (>170–180/min) reduces cardiac output mainly because:
TMU 题-Circulation
A. the rapid-ejection period shortens
B. the filling period shortens
C. the slow-ejection period shortens
D. isovolumic relaxation shortens
✅ Answer: B. the filling period shortens
Excessive tachycardia cuts diastolic filling time → ↓EDV → ↓stroke volume → ↓cardiac output.
Q15
The peripheral resistance is formed mainly by the:
TMU 题-Circulation
A. large and middle arteries
B. large and middle veins
C. small arteries and arterioles
D. capillaries
✅ Answer: C. small arteries and arterioles
Small arteries and arterioles are the resistance vessels — also the site of the greatest pressure drop.
Q16
Which substance is a vasodilator?
TMU 题-Circulation
A. endothelin
B. angiotensin II
C. thromboxane A₂
D. nitric oxide
✅ Answer: D. nitric oxide
Nitric oxide (and PGI₂) dilate vessels; endothelin, angiotensin II and thromboxane A₂ constrict them.
Q17
The systemic veins are best described as:
TMU 题-Circulation
A. capacitance (volume) vessels holding ~60% of the blood
B. resistance vessels
C. exchange vessels
D. cushioning vessels
✅ Answer: A. capacitance (volume) vessels holding ~60% of the blood
Thin, compliant veins are the capacitance vessels, holding roughly 60% of total blood volume at any moment.
Q18
The major factor for LONG-TERM regulation of arterial pressure is:
TMU 题-Circulation
A. the baroreceptor reflex
B. blood volume (renal control of salt and water)
C. blood flow
D. nerve reflexes
✅ Answer: B. blood volume (renal control of salt and water)
Long-term pressure control depends on blood volume via the kidneys (pressure natriuresis); the baroreceptor reflex is short-term.
Q19
When arterial baroreceptors increase their firing rate (rising BP), the result is:
TMU 题-Circulation
A. increased sympathetic outflow to the heart
B. increased sympathetic outflow to arterioles
C. increased parasympathetic (vagal) outflow to the heart
D. increased sympathetic outflow to veins
✅ Answer: C. increased parasympathetic (vagal) outflow to the heart
↑Baroreceptor firing → ↑vagal + ↓sympathetic outflow → ↓HR, ↓contractility, vasodilation → BP falls (negative feedback).
Q20
Purkinje fibres are best classified as:
TMU Cardiac practice paper
A. slow-response rhythmic cells
B. fast-response non-rhythmic cells
C. slow-response non-rhythmic cells
D. fast-response rhythmic cells
✅ Answer: D. fast-response rhythmic cells
Purkinje cells use the fast voltage-gated Na⁺ channel for phase 0 (fast-response) AND show spontaneous phase-4 depolarization (rhythmic) — they are latent pacemakers if the SA node fails.
1Cardiac cycle+
One complete sequence of atrial and ventricular systole (contraction) and diastole (relaxation), ~0.8 s at HR 75. One-way blood flow is enforced by the AV and semilunar valves.
TMU 题-Circulation
2Stroke volume (SV)+
The volume of blood ejected by one ventricle in a single beat (end-diastolic minus end-systolic volume), ~70 mL. Determined by preload, afterload and contractility.
TMU 题-Circulation
3Cardiac output (CO)+
The volume of blood pumped by one ventricle per minute = stroke volume × heart rate ≈ 5 L/min at rest. The cardiac reserve (max ÷ resting CO) is about 400%.
TMU 题-Circulation
4Ejection fraction (EF)+
The ratio of stroke volume to ventricular end-diastolic volume (SV/EDV), normally ~55–65%. It is a clinical index of myocardial contractility; a low EF indicates systolic heart failure.
TMU 题-Circulation
5Central venous pressure (CVP)+
The pressure in the right atrium and great thoracic veins, normally close to zero (can be slightly negative; ~4–12 cmH₂O clinically). It reflects the balance of venous return and cardiac pumping and guides IV fluid therapy; it rises in heart failure/overload.
TMU 题-Circulation
6Cardiac reserve+
The maximum percentage that cardiac output can rise above its resting value. In a healthy young adult CO can rise from ~5 L/min at rest to ~25 L/min during severe exercise — a reserve of about 400–500%. Falls in valvular disease, heart failure or coronary disease; the shrinking reserve is what limits exercise tolerance.
TMU Cardiac practice paper
Essay 1
Explain the ionic mechanism of the action potential of a ventricular working cell.
10 marks

Phase 0 — depolarization

Rapid upstroke caused by opening of fast voltage-gated Na⁺ channels → Na⁺ influx.

Phase 1 — early repolarization

Na⁺ channels inactivate + transient K⁺ efflux (a small notch).

Phase 2 — plateau (the hallmark)

Sustained depolarization: inward Ca²⁺ (L-type) is balanced by outward K⁺. This long plateau gives the prolonged refractory period and supplies Ca²⁺ for contraction.

Phase 3 — repolarization

Ca²⁺ channels close while K⁺ efflux increases → return to rest.

Phase 4 — resting

−90 mV maintained by the Na⁺/K⁺-ATPase and Na⁺-Ca²⁺ exchange restoring the gradients.

Marking guide (10 marks): phase 0 Na⁺ influx 2 · phase 1 transient K⁺ 1 · phase 2 plateau = Ca²⁺ in / K⁺ out 3 · phase 3 K⁺ efflux 2 · phase 4 pump-maintained −90 mV 2
Essay 2
Explain the ionic mechanism of the action potential of a pacemaker (SA node) cell.
10 marks

No stable resting potential

The maximum diastolic potential (~−60 mV) is unstable and slowly drifts upward.

Phase 4 — slow (diastolic) depolarization

The funny current I_f (Na⁺ inward, activated by hyperpolarization) plus T-type Ca²⁺ influx slowly depolarise the cell to threshold → this gives automaticity and sets the heart rate.

Phase 0 — upstroke

Slow, carried by the L-type Ca²⁺ channel (not fast Na⁺) → slow conduction.

Phase 3 — repolarization

K⁺ efflux repolarises the cell, then the cycle repeats.

Pacemaker hierarchy

SA (fastest) drives the heart; AV and Purkinje are latent pacemakers suppressed by overdrive. Sympathetic stimulation steepens phase 4 (↑rate); vagal stimulation flattens it (↓rate).

Marking guide (10 marks): unstable max diastolic potential 1 · phase 4 = I_f (Na⁺) + T-Ca²⁺ slow depolarization → automaticity 4 · phase 0 = L-type Ca²⁺ 2 · phase 3 K⁺ efflux 1.5 · pacemaker hierarchy/autonomic modulation 1.5
Essay 3
What factors influence the cardiac output?
10 marks

Basic relation

Cardiac output = stroke volume × heart rate (~70 mL × 75/min ≈ 5 L/min). Stroke volume itself has three determinants:

Preload

= end-diastolic volume (set by venous return). Via the Frank–Starling (heterometric) mechanism, more stretch → stronger contraction → larger SV.

Afterload

= aortic/arterial pressure the ventricle ejects against. ↑Afterload → ↓SV.

Contractility (inotropy)

Length-independent (homometric) regulation — increased by sympathetic stimulation, adrenaline and Ca²⁺.

Heart rate

↑HR raises CO, but >170–180/min shortens filling → ↓EDV → ↓CO.

Marking guide (10 marks): CO = SV × HR 1 · preload (EDV / Frank–Starling) 2.5 · afterload (aortic pressure) 2 · contractility (homometric) 2.5 · heart rate (and the upper-limit effect) 2
Essay 4
Describe the mechanical events of the cardiac cycle.
10 marks

Atrial systole

AV valves open, semilunar closed; LA > LV; the atrial 'kick' adds ~20–30% of filling.

Isovolumic contraction

All valves shut; LA < LV < aorta; pressure rises fastest at constant volume; S₁ begins.

Ventricular ejection (rapid then slow)

Semilunar valves open; LV > aorta in rapid ejection (ventricular pressure peaks; SBP = aortic pressure); flow continues by momentum in slow ejection.

Isovolumic relaxation

Semilunar valves close (S₂); all valves shut; pressure falls fastest.

Ventricular filling (rapid then slow)

AV valves open at the end of isovolumic relaxation; LA > LV; the longest phase at normal heart rate.

Marking guide (10 marks): atrial systole + ~20–30% filling 1.5 · isovolumic contraction (all valves shut, S₁) 2 · ejection (peak pressure, semilunar open) 2 · isovolumic relaxation (S₂, fastest pressure fall) 2 · filling (AV open, longest) 2.5
Essay 5
Describe the baroreceptor reflex and its role in regulating arterial blood pressure.
10 marks

Receptors

Stretch (pressure) receptors in the carotid sinus and aortic arch; their firing rate increases with arterial pressure and pulse pressure.

Centre

The medullary cardiovascular (vasomotor) centre — in the medulla, NOT the cortex.

Response to a rise in BP

↑Baroreceptor firing → ↑parasympathetic (vagal) outflow to the heart + ↓sympathetic outflow to heart/arterioles/veins → ↓HR, ↓contractility, vasodilation, venodilation → BP falls.

Response to a fall in BP (e.g. haemorrhage)

The reverse: ↑HR, ↑contractility, vasoconstriction, ↑total peripheral resistance → BP restored.

Nature

It is a rapid, SHORT-TERM regulator (buffer) of arterial pressure; long-term control rests with blood volume (RAAS/kidney).

Marking guide (10 marks): receptors (carotid sinus + aortic arch, stretch) 2 · centre = medulla 1.5 · response to ↑BP (↑vagal/↓sympathetic → ↓BP) 3 · response to ↓BP/haemorrhage 2 · short-term buffer vs long-term volume 1.5