Heart as a pump
The heart as a pump; dynamics of blood and lymph flow
Cardiac output is set by heart rate and stroke volume, and stroke volume by preload, afterload and contractility. Flow through vessels obeys simple physical laws that also explain Doppler ultrasound findings, and capillary Starling forces decide whether fluid stays in the vessels or forms oedema. CPSP expects quick calculations and the reasoning behind each law.
The cardiac cycle
| Phase | Valves | Key events |
|---|---|---|
| Isovolumetric contraction | All closed | Pressure rises; first heart sound at its start |
| Rapid ejection | Semilunar valves open at its start | Most of the stroke volume leaves |
| Reduced ejection | Semilunar open | T wave; ventricular systole spans roughly the QT interval |
| Isovolumetric relaxation | All closed | Second heart sound at its start |
| Rapid filling | AV valves open | Doppler E wave |
| Atrial systole | AV open | Doppler A wave: the "atrial kick", lost in atrial fibrillation (E waves only), poorly tolerated in a stiff hypertrophied ventricle |
Output and its determinants
- Cardiac output = stroke volume × heart rate. Ejection fraction = SV ÷ EDV.
- Worked examples: EDV 120 mL, ESV 50 mL gives SV 70 mL and EF 58%. CO 5.6 L/min at 70/min gives SV 80 mL; with EDV 145 mL, EF is about 55%. CO 6.6 L/min at 88/min gives SV 75 mL.
- Preload is best represented by end-diastolic volume. Frank–Starling law: stroke volume rises with EDV because stretched sarcomeres reach a better overlap and calcium sensitivity. A denervated transplanted heart raises output at the start of exercise this way, before its rate changes.
- Contractility (inotropes such as dobutamine) moves the curve upward: higher SV at the same EDV, so filling pressure falls.
- Afterload is ventricular wall stress during ejection (Laplace: stress ∝ pressure × radius ÷ wall thickness). Concentric hypertrophy in aortic stenosis keeps wall stress normal. A failing ventricle is very afterload-sensitive, so arterial vasodilators raise its SV.
- Athletes have a larger SV and a lower resting rate with the same resting output.
- Fluid responsiveness: a passive leg raise that increases SV by more than about 10% predicts a rise with fluid. High PEEP raises intrathoracic pressure and reduces venous return.
- In hypertrophic cardiomyopathy, reduced venous return (Valsalva strain) shrinks the cavity and worsens outflow obstruction.
- Pulse pressure reflects SV and arterial stiffness: wide in aortic regurgitation (large SV plus diastolic backflow) and thyrotoxicosis (large SV, low SVR).
- Output is measured by the Fick principle or indicator dilution (indocyanine green, thermodilution).
- An IVC under 2.1 cm that collapses by over 50% on sniffing means a normal right atrial pressure (about 3 mmHg).
Pregnancy and labour
- Cardiac output rises about 40%, from 4.5 to 6.5 L/min by mid-pregnancy, mainly from stroke volume, later also heart rate.
- Each contraction squeezes 300–500 mL of blood from the uterus into the circulation (output up a further 15–25%). The highest output and preload come just after placental delivery: the danger point in mitral stenosis.
- Uterine blood flow at term is about 500–750 mL/min, explaining rapid PPH from an atonic uterus. It is not autoregulated, so it follows maternal blood pressure (fetal bradycardia after spinal hypotension) and is reduced by catecholamines.
Physics of flow
| Law | Statement | Application |
|---|---|---|
| Ohm's law of flow | Flow = pressure difference ÷ resistance | Basis of blood pressure regulation |
| Poiseuille | Resistance ∝ viscosity × length ÷ radius⁴ | Halving radius raises resistance 16-fold; polycythaemia (high viscosity) lowers cerebral flow |
| Continuity | Velocity ∝ 1 ÷ cross-sectional area | Velocity rises through a stenosis (carotid Doppler grading) |
| Simplified Bernoulli | Pressure gradient = 4v² | 4 m/s across the aortic valve gives about 64 mmHg |
| Reynolds number | Turbulence ∝ velocity × diameter × density ÷ viscosity | Anaemia: low viscosity, high velocity, turbulent flow murmurs; helium–oxygen (low density) reduces turbulent resistance in croup |
- In fetal anaemia the middle cerebral artery peak systolic velocity rises (low viscosity, high output).
- Coronary flow: left coronary flow nearly stops in early systole because the left ventricular wall compresses its vessels; right coronary flow continues because right ventricular wall pressure is lower.
- Phase-contrast MRI measures flow: pulmonary 8 L/min with aortic 4 L/min is a Qp:Qs of 2:1 (left-to-right shunt).
Capillary exchange and oedema
- Net filtration pressure = (Pc − Pi) − (πc − πi). Filtration is favoured by capillary hydrostatic and interstitial oncotic pressure.
- Arterial end: (35 − 0) − (25 − 3) = 13 mmHg outwards. Venous end: (15 − 0) − (25 − 3) = 7 mmHg inwards.
| Mechanism of oedema | Example |
|---|---|
| Raised capillary hydrostatic pressure | Heart failure, venous obstruction |
| Low plasma oncotic pressure | Cirrhosis, nephrotic syndrome (low albumin) |
| Increased permeability | Inflammation, sepsis |
| Lymphatic obstruction | Tumour, filariasis, surgery |
- Safety factors: while interstitial pressure is negative the tissue is stiff (low compliance), lymph flow rises and protein is washed out. Once pressure rises above zero, compliance jumps and visible oedema appears suddenly.
- Lymph flow rises with capillary pressure and permeability, and falls if plasma oncotic pressure rises. Muscle contraction compresses lymphatics: patients walk during lymphoscintigraphy.
- Normal femoral vein Doppler is phasic with breathing; continuous non-phasic flow means proximal (iliac or IVC) obstruction.
- In the kidney, the same forces apply: obstruction raises Bowman's space pressure and lowers GFR.
Pulmonary venous pressure on the chest X-ray
| Wedge pressure | Radiograph |
|---|---|
| 13–18 mmHg | Upper lobe blood diversion |
| 18–25 mmHg | Interstitial oedema: Kerley B lines, peribronchial cuffing |
| Over 25 mmHg | Alveolar (bat-wing) oedema |
Remember Resistance depends on the fourth power of the radius: small changes in calibre dominate flow.
Exam trap Ejection fraction is SV divided by end-diastolic volume, not by end-systolic volume.
Exam trap The semilunar valves open at the start of the ejection phase, after isovolumetric contraction.
Test yourself on this topic
5 of the 56 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
After losing 1.5 L of blood in a road accident, a man's lymph flow from the tissues falls and interstitial fluid moves into his plasma. Which change explains this?
Answer: Fall in capillary hydrostatic pressure
Lymph flow equals the net fluid filtered from capillaries that is not reabsorbed. After haemorrhage, arteriolar constriction and low venous pressure lower capillary hydrostatic pressure, so filtration falls and absorption is favoured. Less fluid enters the interstitium, lymph flow falls, and fluid moves into the plasma (transcapillary refill), which later dilutes the haemoglobin. A rise in capillary pressure or permeability, or a fall in plasma proteins, does the opposite.
Lymph flow
- Lymph = net filtration
- Haemorrhage: capillary pressure falls
- Less filtration, less lymph
- Fluid refills plasma
Remember Low capillary pressure after bleeding pulls fluid back into vessels.
Exam trap Haemoglobin falls hours after a bleed because of this refill, not at once.
Why the other options are wrong
- Rise in interstitial oncotic pressure Would draw fluid out and raise lymph flow.
- Rise in capillary permeability Would increase filtration and lymph flow.
- Closure of lymphatic valves Valves direct flow; they do not stop it after bleeding.
- Fall in plasma oncotic pressure Would raise filtration and lymph flow; it falls only later as fluid refills.
At cardiac catheterisation, a 30-year-old woman with a secundum atrial septal defect has a pulmonary blood flow of 8 L/min and a systemic blood flow of 4 L/min. What is her pulmonary-to-systemic flow ratio, and which way is the shunt?
Answer: 2:1, left-to-right
Qp:Qs is pulmonary flow divided by systemic flow: 8 / 4 = 2. More blood goes through the lungs than the body, so the shunt is left to right, as expected in an atrial septal defect where left atrial pressure is higher. A ratio of 1.5 or more usually indicates a significant shunt with right heart volume overload. Flows are calculated by the Fick principle from oxygen saturations in each circulation.
Qp:Qs
- Qp:Qs = pulmonary / systemic flow
- > 1: left-to-right shunt
- < 1: right-to-left shunt
- ≥ 1.5: significant
Remember More lung flow than body flow: left-to-right shunt.
Exam trap Swapping the numerator and denominator reverses the shunt direction.
Why the other options are wrong
- 1:2, right-to-left Ratio and direction both reversed.
- 2:1, right-to-left Pulmonary flow exceeds systemic, so it is left-to-right.
- 1:2, left-to-right Ratio is reversed.
- 1:1, no shunt The flows are unequal.
Lymph flow from the legs rises several-fold when a person starts walking. What is the main reason?
Answer: Muscle contraction compresses lymphatics
Lymph moves forward by intrinsic rhythmic contraction of smooth muscle in lymphangion walls and by external compression from skeletal muscle, arterial pulsation and breathing. One-way valves between lymphangions ensure flow towards the nodes. Walking adds the skeletal muscle pump, increasing lymph flow several-fold. This is why immobile limbs swell more easily.
Lymph propulsion
- Intrinsic lymphangion contraction
- External muscle pump
- One-way valves
- Walking speeds lymph flow
Remember Lymph moves when muscles squeeze.
Exam trap Immobility slows lymph flow and worsens oedema.
Why the other options are wrong
- Walking raises arterial blood pressure Not the main driver of lymph flow.
- Exercise closes lymphatic valves Valves open forward and close to prevent backflow.
- Walking dilates the inguinal nodes Not the mechanism.
- Exercise lowers interstitial fluid Exercise increases interstitial fluid and lymph formation.
A 65-year-old man with long-standing severe aortic stenosis has concentric left ventricular hypertrophy with a normal cavity size and normal ejection fraction. How does the thickened wall help the ventricle?
Answer: It keeps systolic wall stress normal
By the law of Laplace, wall stress is proportional to pressure × radius / (2 × wall thickness). In aortic stenosis the ventricle must generate a very high systolic pressure. Adding sarcomeres in parallel thickens the wall, so the rise in pressure is balanced and wall stress, a key determinant of afterload and oxygen demand, stays near normal. The cost is a stiff ventricle with impaired relaxation and relatively reduced coronary reserve.
Law of Laplace
- Wall stress ∝ P × r / 2h
- Pressure load: concentric hypertrophy
- Thicker wall normalises stress
- Cost: stiff ventricle
Remember Pressure overload thickens the wall; volume overload dilates the cavity.
Exam trap Concentric hypertrophy preserves EF but causes diastolic dysfunction.
Why the other options are wrong
- It enlarges the stroke volume directly Stroke volume is maintained, not directly enlarged.
- It lowers the aortic valve gradient The gradient is set by the valve.
- It improves coronary perfusion Coronary reserve actually falls.
- It shortens ventricular relaxation Relaxation is slowed, not shortened.
A man with acute left ventricular failure has a chest radiograph showing upper lobe blood diversion, Kerley B lines and peribronchial cuffing, but no alveolar shadowing. Into which range does his pulmonary capillary wedge pressure most likely fall?
Answer: About 18–25 mmHg
Chest radiograph signs follow the rise in pulmonary venous pressure. Normal wedge pressure is about 5–12 mmHg. At about 13–18 mmHg, upper lobe vessels distend (diversion); at about 18–25 mmHg fluid enters the interstitium, giving Kerley B lines, peribronchial cuffing and fissural thickening. Above about 25 mmHg fluid floods the alveoli, causing bat-wing shadowing. Radiographic changes can lag behind pressure changes.
Wedge pressure and CXR
- 13–18: upper lobe diversion
- 18–25: interstitial oedema
- > 25: alveolar oedema
- Signs may lag behind pressure
Remember Kerley lines without alveolar shadowing: interstitial stage.
Exam trap Radiographic oedema can persist after the pressure has fallen with treatment.
Why the other options are wrong
- About 5–12 mmHg The normal range; no signs expected.
- About 13–17 mmHg Gives upper lobe diversion only.
- Above 30 mmHg Alveolar oedema would usually be present.
- Below 5 mmHg Below normal.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Cardiovascular, respiratory and renal physiology, Heart as a pump and its regulation; dynamics of blood and lymph flow