TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU 题-Circulation
TMU Cardiac practice paper
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.
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).
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.
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.
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).