Cardiovascular System

Compare the systemic and pulmonary circuits

- Pulmonary circulation: RV pumps deoxygenated blood through the pulmonary trunk to the lungs for gas exchange. Oxygenated blood returns via the pulmonary veins to the LA. Low pressure ~27 mmHg.

- Systemic circulation: LV pumps oxygenated blood through the aorta to body organs. Deoxygenated blood returns via the venae cavae to the RA. High pressure ~120 mmHg.

- Equal blood flow: Both pumps move the same blood volume, approx 7,000 L/day.

What is unusual about venous drainage of the gut?

Blood travels via the hepatic portal vein to the liver sinusoids (second capillary bed) before draining through the hepatic veins → IVC → right atrium. Portal veins drain into another capillary bed, not directly to the heart.

Why are the organs arranged in parallel in systemic circuits, not series?

Each organ gets full-pressure arterial blood (35 mmHg at the capillary start) and its flow can be adjusted independently. In series, pressure would fall after each organ.

Why does BP homeostasis matter?

Maintains capillary perfusion to deliver O₂ and nutrients and remove wastes. The brain is most vulnerable to reduced BP due to its high metabolic rate and gravity.

Great vessels and the chamber each enters or leaves.

- RA receives blood from the SVC, IVC and coronary sinus: These vessels bring deoxygenated blood into the RA.

- RV pumps blood into the pulmonary trunk: The pulmonary trunk carries deoxygenated blood towards the lungs.

- LA receives blood from the four pulmonary veins: These veins bring oxygenated blood from the lungs into the LA and form the posterior base of the heart.

- LV pumps blood into the aorta: The aorta carries oxygenated blood to the rest of the body.

Trace blood through the heart, naming each valve.

Vena cavae → RA → tricuspid → RV → pulmonary valve → pulmonary trunk → lungs → pulmonary veins → LA → mitral → LV → aortic valve → aorta.

Orientation and borders of the heart

About ⅓ of its mass lies right of midline, ⅔ left. Apex points inferiorly, anteriorly, left (LV). Right border: right atrium. Inferior: right ventricle. Left: left ventricle (and part of LA/auricle). Superior: great vessels = base. Posterior base: mostly LA.

Atrium versus auricle?

Atrium: thin-walled low-pressure reservoir that fills the ventricle quickly. Auricle: appendage that adds atrial capacity. No valves guard the pulmonary vein entry.

Surface landmarks between chambers.

Anterior and posterior interventricular sulci mark the septum between ventricles; the coronary (atrioventricular) sulcus separates atria from ventricles. Coronary vessels run in them.

Fetal remnants in the adult heart.

Fossa ovalis (former foramen ovale, in the interatrial septum) and ligamentum arteriosum (former ductus arteriosus, aortic arch to pulmonary trunk).

Layers of the heart wall and pericardium, outside in

• Heart wall and pericardium (outside in): Fibrous pericardium → parietal serous pericardium → pericardial cavity (serous fluid reduces friction) → visceral pericardium (epicardium) → myocardium → endocardium.

• Serous layers: Single-layer squamous mesothelium.

• Heart sits within the pericardial sac, with the visceral layer covering its surface.

What is cardiac tamponade?

Blood or fluid collects in the pericardial space under pressure, compressing the heart and limiting filling, so CO falls. Remedy: drain it (pericardiocentesis).

Fibrous skeleton: functions and features.

• Dense connective tissue that anchors valve cusps and cardiac myocytes.

• Supports and stabilises heart valves.

• Electrical function: Insulates atria from ventricles, so the AV node and AV bundle provide the normal conducting route.

• Features: Aortic and mitral rings are fibrous; tricuspid ring is incomplete; pulmonary ring is absent (fatty connective tissue fills gaps).

Inlet (AV) valves: structure and how they hold blood.

Tricuspid (R, 3 cusps) and mitral/bicuspid (L, 2 cusps): flat fibrous flaps whose free edges are tethered by chordae tendineae to papillary muscles, preventing prolapse into the atrium in systole. They hold blood like a parachute holds air. LV has 2 papillary muscles; RV has 3.

Outlet (semilunar) valves: structure.

Aortic and pulmonary: 3 pocket-shaped cusps, no cords. Back-pressure fills the pockets and the edges meet; strength comes from 3D shape. Coronary arteries open just above the aortic valve. Oxygenated blood passes the aortic valve.

When do papillary muscles/chordae first work, and what supplies them?

During isovolumetric contraction, as ventricular pressure rises (they hold the cusps closed). Supplied by Purkinje fibres.

Why are inlets wide and outlets narrow?

Inlets admit blood at low pressure (large diameter); outlets eject at high pressure (small diameter). Blood takes a V-shaped path through each ventricle.

Ventricle shape, wall thickness and pressure.

LV: hollow cone, thick wall, peak 120 mmHg. RV: crescent (“hip pocket”) on the LV, thinner wall, peak 27 mmHg. Pressure ratio ≈ 4:1. Atria are thin with low pressures.

S1 and S2: cause and timing

S1 “lub”: mitral and tricuspid close at start of isovolumetric contraction.

S2 “dub”: aortic and pulmonary close at start of isovolumetric relaxation. Aortic closes first, pulmonary last (split S2).

Conduction pathway, speed and result.

SA node (pacemaker, RA) → atrial muscle: fast (P wave); causes atrial contraction.

AV node (RA): slow; delays conduction to allow ventricular filling. Only electrical pathway through the cardiac skeleton.

AV bundle → bundle branches → Purkinje fibres: very fast; causes coordinated ventricular contraction from apex to base.

SA node pacemaker potential.

Unstable resting potential: spontaneous progressive depolarisation between action potentials until threshold, then an AP starts the beat. Gives auto-rhythmicity (heart beats outside the body).

Ventricular myocyte action potential: 3 phases.

1 Rapid depolarisation: voltage-gated fast Na⁺ in.

2 Plateau (~0.3 s total AP): slow Ca²⁺ in balances some K⁺ out; triggers contraction.

3 Repolarisation: Ca²⁺ channels inactivate, delayed-rectifier K⁺ out.

Why does the long plateau matter?

Prolongs the refractory period, preventing re-excitation and tetanus. Ensures one-way conduction and allows the heart to relax and refill between contractions.

ECG waves and what they mean.

• P wave: Atrial depolarisation → atrial systole.

• QRS complex: Ventricular depolarisation → ventricular systole begins.

• T wave: Ventricular repolarisation → ventricular relaxation.

• PR interval: AV node delay.

• ST segment: Ventricular plateau phase.

Somatic versus autonomic nervous system.

• Sensory: Somatic – somatic/special senses; autonomic – interoceptors.

• Control: Somatic – voluntary (cortex); autonomic – involuntary (brainstem, hypothalamus, limbic system, spinal cord).

• Effectors: Somatic – skeletal muscle; autonomic – smooth/cardiac muscle and glands.

• Pathway: Somatic – 1 motor neuron; autonomic – 2 neurons (pre- and postganglionic).

• Neurotransmitters: Somatic – ACh; autonomic – ACh (all preganglionic, PSNS postganglionic) and noradrenaline (SNS postganglionic).

Parasympathetic versus sympathetic wiring.

PSNS: long pre-ganglionic fibres (vagus, CN X to the heart), ganglia at the organ, short post-ganglionic, ACh.

SNS: short pre-ganglionic, ganglia in chain near the cord, long post-ganglionic, noradrenaline.

How does the ANS change heart rate?

The SA node receives both inputs: at rest, PSNS (vagal tone) dominates (50–70 bpm vs intrinsic ~100); withdrawing PSNS increases HR to ~100, while SNS can increase it to ~200 bpm, as noradrenaline steepens the pacemaker potential (HR ↑) and ACh slows it (HR ↓).

Phases of the cardiac cycle (left & right heart), with valves.

LEFT

1 Ventricular filling - mitral open, aortic closed (~80% of filling).

2 Atrial contraction (after P wave) - tops up the rest.

3 Isovolumetric contraction - both closed, S1, LVP rises.

4 Ejection - LVP > aortic pressure, aortic opens.

5 Isovolumetric relaxation - both closed, S2, dicrotic notch. Mitral reopens when LVP < LAP.

Right

1. Ventricular filling - Tricuspid open, pulmonary closed (~80%).

2. Atrial contraction - Tops up the remaining blood.

3. Isovolumetric contraction - Both valves closed; tricuspid closes (S1), RVP rises.

4. Ejection - RVP > pulmonary artery pressure; pulmonary valve opens.

5. Isovolumetric relaxation - Both valves closed; pulmonary valve closes (S2). Tricuspid reopens when RVP < RAP.

Typical pressures and volumes.

LV pressure: near 0 in diastole to ~120 peak.

Aorta: ~80 to ~120. EDV ~120–140 mL, ESV ~50–70 mL.

Volume is greatest at end of atrial contraction, lowest at end of ejection. Pressure in LV is the highest of any chamber just before isovolumetric relaxation.

Why is the atrial pressure rise small during atrial contraction?

Thin atrial muscle, and no valves at the pulmonary vein entry, so some blood can flow backwards.

CO, SV and EF formulas with values.

CO = HR × SV (rest 4–7 L/min; e.g. 70 × 70 mL = 5 L/min). SV = EDV − ESV (50–100 mL). EF = SV/EDV (normal 55–70%). Exercise example: 200 bpm × 0.1 L = 20 L/min.

Preload and the Frank–Starling law.

Preload = stretch of fibres at end of diastole (EDV). More venous return → more filling → stronger contraction → higher SV (“more in, more out”), matching CO to venous return. Preload changes with venous return, blood volume, filling time, respiratory pump, compliance. Atrial fibrillation loses the atrial boost, lowering preload.

Contractility (inotropy).

Force at a given preload, set by Ca²⁺ available. SNS, noradrenaline/adrenaline, glucagon, thyroid hormone and ↑Ca²⁺ = positive inotropy: ↑SV, ↓ESV. PSNS = negative inotropy. No immediate change on standing.

Afterload.

Pressure the ventricle must beat to open the aortic valve. Hypertension, aortic stenosis or plaques ↑ afterload → ↑ESV → ↓SV. Lower afterload ↑SV.

Which factors raise heart rate?

↑SNS/↓PSNS, catecholamines, thyroid hormones, ↑Ca²⁺, higher body temperature; also infants/elderly, low fitness (higher resting HR).

BP, MAP and where pressure drops.

BP = CO × TPR. ↑CO → ↑BP; arteriolar dilation → ↓TPR → ↓BP. Typical 120/80 mmHg; MAP ≈ diastolic + ⅓ pulse pressure. Pressure is highest in elastic arteries and falls most across arterioles/capillaries; veins and vena cavae are near 0–10 mmHg.

Blood volume distribution.

Systemic veins and venules 64% (reservoirs), arteries/arterioles 13%, pulmonary vessels 9%, heart 7%, capillaries 7%.

Arterial baroreceptors: where, what, how.

Stretch receptors in carotid sinus and aortic arch. Stretch opens ion channels; tonically active, so firing rises and falls with BP. Afferents run in cranial nerves (IX, X) to the CV centre in the medulla. The carotid site guards brain blood supply.

Baroreflex when BP falls (negative feedback).

↓Stretch → ↓firing → medulla: ↓PSNS, ↑SNS. • Heart: ↑HR and contractility (↑SV, ↑CO). Arterioles: vasoconstriction (↑TPR). Veins: venoconstriction (↑venous return). Adrenal medulla: adrenaline/noradrenaline. • BP = CO × TPR rises back to normal. Reverse when BP rises.

Standing up suddenly: sequence and reflex response.

Circle answers (2023/2024): blood volume in lower body ↑; venous return ↓; contractility no change (strictly; the lecture slide says force of contraction ↓ via Starling, so check the mark scheme); SV ↓; CO ↓; BP ↓ (BP = CO × TPR, no compensation). Reflex = arterial baroreflex. HR rise: ↓PSNS and ↑SNS to the SA node. • Other effectors (organ / SNS / effect): arterioles / SNS / vasoconstriction, ↑TPR; veins / SNS / venoconstriction, ↑venous return and preload; adrenal medulla / SNS / adrenaline release.

Lying down: why doesn’t BP rise?

Venous return rises → ↑preload, ↑SV, ↑CO → ↑BP → baroreceptors fire more → ↓SNS, ↑PSNS → ↓HR, vasodilation, ↓TPR → BP restored.

How can chronic stress raise heart attack risk?

Sustained SNS/adrenaline: ↑HR, contractility, vasoconstriction, ↑BP (↑afterload) → more work and O₂ demand, plus endothelial damage and atheroma → coronary narrowing → ischaemia and infarction. Acute stress: SNS → ↑HR, SV, CO, TPR → ↑BP.

Elastic and muscular arteries.

Elastic: many elastin sheets in tunica media; expand in systole and recoil in diastole, smoothing pulsatile flow. • Muscular: many smooth muscle layers; distribute blood, radius adjusts flow (flow ∝ r⁴). Coronary arteries are muscular arteries.

Arterioles and capillaries.

Arteriole: 1–3 smooth muscle layers, thickest wall relative to size; biggest resistance and pressure drop; sets TPR and thus BP; controls flow into capillary beds. • Capillary: one endothelial layer plus basement membrane, no muscle; diameter fits one RBC; slow flow; exchange; leaky to plasma, not cells.

Venules and veins.

Venule: endothelium ± little connective tissue (larger ones have one muscle layer); where white cells leave blood. • Vein: thin, compliant, low pressure, reservoir; valves (especially legs) prevent backflow; skeletal muscle and respiratory pumps return blood to the RA. Portal veins drain to another capillary bed.

Coronary arteries and coronary disease.

Left and right arteries arise from the aorta just above the aortic valve and supply myocardium. Atheroma narrowing to ~20% of cross-section blocks flow: exercise ischaemia (angina), then infarction. Anastomoses may widen to supply ischaemic muscle. Cardiac veins return blood to the RA.

Three ways substances cross the capillary wall.

Transcytosis: vesicles carry large lipid-insoluble molecules (e.g. insulin). Diffusion: solutes and gases down gradients. Bulk flow: passive fluid movement driven by hydrostatic versus osmotic pressure, much faster than diffusion.

Net filtration pressure calculation.

NFP = (BHP + IFOP) − (BCOP + IFHP). Values: BHP 35 (arterial) / 16 (venous), BCOP 26, IFOP 1, IFHP 0. • Arterial: (35+1) − (26+0) = +10 mmHg, filtration. Venous: (16+1) − 26 = −9 mmHg, reabsorption. • (2023 variant: BHP 36, IF pressures negligible → +10 and −10.)

Is filtration balanced with reabsorption? What happens to the excess?

Not quite: ~20 L/day filtered, ~17 L/day reabsorbed (~85%). The ~3 L/day remainder, with leaked proteins, returns via lymph vessels, which also clear interstitial fluid and support immune responses.

Causes of oedema (filtration imbalance).

Hypertension: ↑arterial BHP → ↑filtration (lymph flow rises to compensate locally). • Kidney disease: protein loss → ↓BCOP. • Heart failure, long-haul travel, standing: ↑venous BHP → less reabsorption. • Inflammation: ↑permeability → ↑IFOP.

2024 flight scenario: venous BHP +5 mmHg.

Arterial end unchanged (+10). Venous end becomes (21+1) − 26 = −4 (was −9), so reabsorption falls, net filtration rises and fluid accumulates in the legs (oedema).

Why is capillary flow slow, and why does it help?

Velocity ∝ 1/total cross-sectional area. Capillaries have the largest total area, so the slowest flow, giving time for diffusion, filtration and reabsorption.

Pressure, radius and flow (Poiseuille relationships).

Flow ∝ ΔP and Flow ∝ r⁴ (know the relationships, not the equation). Halve the radius → flow ÷16. Vessel diameter, not pressure, is how the body redirects flow.

How are supply and demand matched?

Raise CO (↑HR or SV), and/or redirect existing CO by vasoconstriction in some organs and dilation in others (e.g. exercise: gut flow cut, muscle flow up). Precapillary sphincters open → blood through the capillary bed; closed → shunt via thoroughfare channel.

Explain or draw the inlet and outlet valves open and closed. (Lecture 1 ILO 3)

Inlet (mitral/tricuspid): OPEN in filling (atrial P > ventricular P, cusps hang into ventricle); CLOSED in systole (ventricular P > atrial P, cusps meet, chordae taut). • Outlet (aortic/pulmonary): OPEN in ejection (ventricular P > arterial P, cusps flattened to wall); CLOSED in filling (backflow fills the pockets, free edges meet).

2024 diagram, period just after S1. Name the phase, the previous phase, LV pressure trend, LV volume, and the function of the cords/papillary muscles.

Phase: isovolumetric ventricular contraction. Previous: atrial contraction. LV pressure: increasing. LV volume: ≈ EDV, ~120–140 mL. Cords and papillary muscles: stop AV valve cusps being forced back into the atrium. Conduction at the apex: Purkinje fibres. AV valves differ by cusps: mitral 2, tricuspid 3.

2023 labelling questions: one-line answers.

Thickest wall relative to size: arteriole. ‘Lub’: mitral + tricuspid close. Slowest conduction (AV node) begins in the right atrium. Two papillary muscles: LV. Bulk flow to organs: muscular artery. Exchange: capillary. Series of valves: vein. Right border: right atrium. Coronary arteries: muscular arteries. Valve with 3 cusps carrying oxygenated blood: aortic. Highest pressure before isovolumetric relaxation: LV. Peak LV − RV ≈ 120 − 27 ≈ 93 mmHg. External layer of a ventricle: epicardium.

Link ECG events to mechanical events. (Lecture 2 ILO 5, Lecture 4 ILO 5)

P wave → atrial systole. QRS → onset of ventricular systole (isovolumetric contraction, S1, then ejection). T wave → ventricular repolarisation, relaxation (isovolumetric relaxation, S2, then filling). Flat PR segment = AV node delay.

Compare two vessel classes (e.g. artery vs vein, arteriole vs capillary). (Lecture 3 ILO 1)

Artery vs vein: thicker, more muscle and elastin, high pressure, no valves, resistance/distribution vs thin, compliant, low pressure, valves, 64% of blood volume reservoir. • Arteriole vs capillary: 1–3 muscle layers, controls resistance and TPR vs endothelium only, no muscle, exchange, slowest flow.

Describe or draw the two coronary arteries.

Right and left coronary arteries arise from the aortic root above the aortic valve and run in the coronary (AV) groove. Left divides into the anterior interventricular and circumflex branches; right runs around the right border and supplies the inferior/posterior heart. Blockage causes ischaemia in the region supplied.

What determines vascular resistance, and what are the units of blood flow?

Resistance rises with smaller radius (the key variable, ∝ 1/r⁴), longer vessel and higher blood viscosity. Flow = volume per time (mL/min or L/min); Flow = ΔP / R.

Fill in the blanks (guide knowledge checks).

↓Venous return → ↓ventricular filling, ↓preload, ↓SV. • SNS ↑ inotropy; PSNS ↓ inotropy; positive inotrope ↑ Ca²⁺ inflow, ↑ force, ↑ SV. • Hypertension: ↑ aortic pressure, ↑ afterload, ↓ SV. • ↑CO → ↑BP; arteriolar dilation → ↓BP.

2025 short answer: sensors, stimulus, afferent target, two end organs.

Sensors: carotid sinus and aortic arch. Stimulus: decrease in arterial BP (less wall stretch). Afferents project to the CV centre in the medulla. • Heart: SNS ↑HR and contractility → ↑SV → ↑CO. Arterioles: SNS vasoconstriction → ↑TPR. BP = CO × TPR. • Greatest impact: vasoconstriction (justify via ↑TPR and venous return).

Peak pressure in each structure (2023 Q140, 2024 Q54, 2025 Q26).

LV ~120 mmHg. Aorta ~120 systolic / 80 diastolic. RV ~27 mmHg; pulmonary trunk peaks at about the same (~25–27). Atria: LA 6–12 mmHg (lecture normal values). Vena cavae/large veins: ~0–5 mmHg. Capillary: 35 (arterial end) falling to 16 (venous end).

Pressure crossover questions (2023 Q141).

LV pressure falls below aortic pressure at the end of ejection → aortic valve closes → isovolumetric relaxation begins (S2). • LV pressure rises above aortic pressure → aortic opens → ejection. • LV pressure rises above atrial pressure → mitral closes (S1, isovolumetric contraction). • LV pressure falls below atrial pressure → mitral opens → filling.

Label the capillary schematic (2023 Q145–147, 2024 Q67).

Arterial end: high BHP (35–36), left side, BHP > BCOP → net filtration (fluid out). Venous end: low BHP (16), right side, BHP < BCOP → net absorption (fluid in). BHP = the sloping line; BCOP = the flat ~26 line. The lines cross mid-capillary.

Vein question (2024 Q52–54): classify, key feature, pressure.

Vessel at K (vena cava): vein. Key features: thin, compliant wall with a large lumen, so it acts as a blood reservoir; valves in limb veins stop backflow. Peak pressure about 0–5 mmHg (low).

Acute stress and the heart: pathway and formulae (2024 Q56–63).

Stress → limbic system/hypothalamus → medulla CV centre → ↑SNS (cardiac accelerator nerves; adrenal medulla releases adrenaline/noradrenaline). SA node: ↑HR. Myocytes: ↑contractility → ↑SV. CO = HR × SV ↑. Arterioles constrict → ↑TPR. BP = CO × TPR ↑.

Previous exam (12 marks): inversion therapy. Explain (i) the rapid rise in arterial pressure and (ii) the later fall in heart rate.

(i) Gravity shifts blood from the legs to the central circulation → ↑venous return → ↑preload/EDV → Frank–Starling ↑SV → ↑CO → ↑BP (BP = CO × TPR). • (ii) ↑BP stretches carotid sinus and aortic arch baroreceptors → ↑firing via cranial nerves to the medulla CV centre → ↑PSNS (vagus), ↓SNS → ACh slows SA node depolarisation → ↓HR (also vasodilation, ↓TPR) → negative feedback restores BP. • Name the principle, sensor and reflex, and give the direction of each step.

Normal values from the lectures.

HR 60–100 bpm (SA node intrinsic 90–100; rest 50–70 from vagal tone). SBP 100–120, DBP 60–80, MAP 80–100 mmHg. SV 50–100 mL. CO 4–8 L/min. LA pressure 6–12 mmHg. LV pressure 0 to 120 mmHg; LV end-diastolic pressure 2–12 mmHg. EF 55–70%. • Exercise example: rest 50 bpm × 70 mL = 3.5 L/min; exercise 150 bpm × 120 mL = 18 L/min.

How is BP regulated intrinsically, neurally and hormonally? (Lecture 7 guide questions)

Intrinsic: Frank–Starling (more venous return → more SV, matching CO to venous return). Neural: arterial baroreflex via medulla CV centre, SNS/PSNS to heart, arterioles and veins. Hormonal: adrenal medulla adrenaline/noradrenaline (↑HR, contractility, vasoconstriction) and angiotensin (vasoconstriction, ↑TPR).

Which events lower or raise BP, and how does the baroreflex respond?

↓BP: standing (postural hypotension), haemorrhage (↓blood volume → ↓venous return → ↓CO). Reflex: ↑SNS, ↓PSNS → ↑HR, contractility, vasoconstriction. • ↑BP: lying down (supine), exercise, inversion. Reflex: ↑PSNS, ↓SNS → ↓HR, vasodilation.

Three tunics of a vessel wall, and where each vessel class differs.

Tunica interna (intima: endothelium), tunica media (smooth muscle and/or elastin; thick in arteries, thin in veins) and tunica externa (outer connective tissue). Elastic arteries: elastin in media. Muscular arteries and arterioles: smooth muscle in media. Capillaries: endothelium + basement membrane only.