Lab 1 · The beating heart

Chambers, valves and conduction

A frontal section of a living heart model. Deoxygenated blood (blue) and oxygenated blood (red) flow as the valves open and close at the right moments. Click any structure, switch to the conduction or coronary views, choose a rhythm, or zoom into the valves.

FROM BODY TO LUNGS FROM LUNGS TO BODY PATIENT'S RIGHTPATIENT'S LEFT
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Lab 2 · Monitor

ECG and the Wiggers diagram

The same model, plotted against time: the ECG (electrical), aortic, left-ventricular and left-atrial pressures, left-ventricular volume and the heart sounds. The sweep line is "now"; coloured bands mark the phases of the cycle.

Lab 3 · Two circulations

Systemic and pulmonary circuits

The right heart pumps blood through the lungs at low pressure; the left heart pumps it to every organ at high pressure. The flow speed follows the heart rate set above; the share of cardiac output each organ receives at rest is shown.

CircuitPressure (mmHg)ResistanceBlood volume
SystemicAorta ≈ 120/80, mean ≈ 93High (≈ 1 mmHg·s/mL)≈ 84 %
PulmonaryPulmonary artery ≈ 25/10, mean ≈ 15About one-tenth of systemic≈ 9 %

Both ventricles pump the same volume per minute: in the steady state the outputs of the right and left heart must match, or blood would pile up in one circuit. That is why left heart failure causes pulmonary congestion (breathlessness) and right heart failure causes swollen ankles and a congested liver.

Organ (at rest)Share of CO≈ mL/min at 5 L/min
Liver & gut (splanchnic)25 %1250
Kidneys20 %1000
Skeletal muscle20 %1000
Brain15 %750
Skin5 %250
Heart (coronary)5 %250
Other10 %500

During heavy exercise cardiac output can rise four- to five-fold and skeletal muscle may receive over 80 % of it.

For learning only, not a clinical tool. Drug doses and energies on this page are teaching examples: always follow current national guidelines, your hospital's protocols and your supervisor.

Key facts to remember

  • Normal adult at rest: HR 60–100 bpm, BP below 120/80 mmHg, SV ≈ 70 mL, CO = HR × SV ≈ 5 L/min, EF 55–70 %.
  • MAP ≈ DBP + ⅓(SBP − DBP). A MAP of at least about 65 mmHg is needed to perfuse the brain, kidneys and gut.
  • Hypertension (Kenya CVD guidelines): ≥ 140/90 mmHg on two or more visits; stage 2 ≥ 160/100; ≥ 180/120 is a hypertensive crisis (an emergency if organs are being damaged).
  • Valve areas: aortic 2nd right intercostal space (ICS) at the sternal edge; pulmonary 2nd left ICS; tricuspid 4th–5th left ICS at the lower sternal edge; mitral at the apex, 5th left ICS mid-clavicular line.
  • S1 = mitral and tricuspid closing (start of systole); S2 = aortic and pulmonary closing (start of diastole). Time a murmur against the carotid pulse.
  • Rheumatic heart disease follows repeated group A streptococcal sore throats and rheumatic fever; the mitral valve is affected in over 90 %. Mitral stenosis: low-pitched mid-diastolic rumble at the apex after an opening snap, loud S1; listen with the bell, patient turned to the left.
  • Secondary prophylaxis for RHD: benzathine penicillin G by deep IM injection every 3–4 weeks for years (WHO).
  • Arrest rhythms: VF and pulseless VT are shockable; asystole and PEA are not. CPR at once; children 15 : 2, 4 J/kg per shock, adrenaline 10 mcg/kg (RCUK paediatric ALS).
  • ECG at 25 mm/s: one large square = 0.2 s, one small square = 0.04 s. HR = 300 ÷ large squares (or 1500 ÷ small squares) between R waves.

Sources: Kenya National Guidelines for Cardiovascular Diseases Management; WHO fact sheet on rheumatic heart disease; Resuscitation Council UK paediatric ALS algorithm (2025); standard physiology texts.

Structure and the path of blood

Deoxygenated blood returns through the superior and inferior venae cavae to the right atrium, passes the tricuspid valve into the right ventricle, and is pumped through the pulmonary valve into the pulmonary trunk and arteries to the lungs. Oxygenated blood returns in four pulmonary veins to the left atrium, crosses the mitral valve into the thick-walled left ventricle, and is ejected through the aortic valve into the aorta. The atrioventricular (AV) valves are held by chordae tendineae and papillary muscles so they cannot evert; the semilunar valves close passively when arterial pressure exceeds ventricular pressure.

The cardiac cycle

  1. Atrial systole (after the P wave): tops up ventricular filling by about 20 % at rest.
  2. Isovolumetric contraction (starts just after the QRS): ventricular pressure rises above atrial pressure, closing the AV valves (S1, "lub"); all valves are shut and volume is constant.
  3. Ejection: when LV pressure exceeds aortic pressure (≈ 80 mmHg) the aortic valve opens; pressure peaks at ≈ 120 mmHg.
  4. Isovolumetric relaxation (after the T wave): LV pressure falls below aortic pressure, the aortic valve closes (S2, "dub", with the dicrotic notch on the aortic trace).
  5. Ventricular filling: when LV pressure falls below LA pressure the mitral valve opens; rapid then slow filling (diastasis).

Cardiac output, stroke volume and ejection fraction

$$SV = EDV - ESV, \qquad CO = HR \times SV, \qquad EF = \frac{SV}{EDV}\times 100\%$$
$$MAP \approx DBP + \tfrac13\,(SBP - DBP), \qquad MAP \approx CO \times SVR$$

Typical adult values at rest: HR 60–100 bpm, SV ≈ 70 mL, CO ≈ 5 L/min, EF 55–70 %. Stroke volume depends on preload (filling; the Frank–Starling law: a more stretched ventricle contracts more strongly), afterload (the pressure it ejects against) and contractility. At very high heart rates diastole shortens so much that filling, and therefore stroke volume, falls.

The model behind the labs

The left ventricle is a time-varying elastance: $P_{LV}(t) = E(t)\,[V_{LV}(t) - V_0]$, where $E(t)$ rises from a diastolic value $E_{min}$ to a systolic peak $E_{max}$ after each ventricular activation (a normalised "double-Hill" activation curve). The left atrium is a smaller elastance with its own contraction, fed from the pulmonary veins. Valves are one-way resistors, and the arteries are a three-element Windkessel (characteristic impedance, compliance $C$ and systemic resistance $R$): $C\,\dfrac{dP}{dt} = Q_{AV} - \dfrac{P}{R}$. The right heart is assumed to move the same volume with the same timing. The model has no baroreflex or autonomic control, so it shows the direct mechanical effect of each rhythm.

Electrical conduction and the ECG

The sinoatrial (SA) node fires spontaneously (≈ 60–100/min). The impulse spreads across the atria (P wave), is delayed ≈ 0.1 s in the atrioventricular (AV) node so the atria can empty, then races down the bundle of His, the left and right bundle branches and the Purkinje fibres (QRS complex, < 0.12 s). Ventricular repolarisation gives the T wave. Normal PR interval 0.12–0.20 s; normal QRS duration < 0.12 s; heart rate from a standard ECG at 25 mm/s is $300 \div$ (number of large squares between R waves).

RhythmECGMechanical effect
Sinus tachycardia (> 100)Normal P–QRS–T, short RRShort diastole, smaller SV
Sinus bradycardia (< 60)Normal complexes, long RRLarge SV, but CO may fall
Atrial fibrillationNo P waves, fibrillatory baseline, irregularly irregular RRNo atrial kick; beat-to-beat SV varies; stroke risk from clots in the left atrial appendage
Ventricular tachycardiaWide (> 0.12 s) regular complexes, AV dissociationLittle filling time, low output: may cause collapse; can degenerate to VF
First-degree AV blockPR > 0.20 s, every P conductedUsually none
Third-degree AV blockP waves and QRS complexes independent; slow escape rhythm (narrow if junctional, wide if ventricular)Low rate and output; atria sometimes contract against closed AV valves (cannon waves); needs pacing
Ventricular fibrillationChaotic waves of varying size and shape; no P, QRS or TVentricles quiver without pumping: no pulse, CO = 0. Shockable
AsystoleFlat line (check leads and gain), sometimes P waves onlyNo electrical or mechanical activity. Not shockable

Clinical relevance

Rheumatic heart disease (RHD) is the commonest acquired heart disease in people under 25 and the leading cardiac cause of complications in pregnancy (WHO). A group A streptococcal sore throat, untreated, can trigger rheumatic fever; repeated attacks scar the valves. Children and adolescents usually have mitral regurgitation (pansystolic murmur at the apex radiating to the axilla); adults more often develop mitral stenosis. A narrowed mitral valve needs a high left atrial pressure to fill the ventricle: the left atrium dilates (atrial fibrillation, clots and stroke) and the high pressure backs up into the lungs (breathlessness, haemoptysis, pulmonary hypertension). The murmur comes in diastole because that is when blood crosses the mitral valve; try the valves view in Lab 1 and watch the mitral valve open after S2. Treating sore throats with penicillin (primary prevention) and giving benzathine penicillin every 3–4 weeks after rheumatic fever (secondary prophylaxis) stop the disease progressing.

Hypertension is often silent: measure BP with the right cuff size, after 5 minutes' rest, arm supported at heart level, and confirm on at least two occasions. The Kenya guidelines suggest a calcium-channel blocker (e.g. amlodipine) or a thiazide-type diuretic first for most Black African adults without diabetes or kidney disease, with two drugs from the start in stage 2. Raised afterload thickens the left ventricle (left ventricular hypertrophy) and in time it fails.

Cardiac arrest. In the monitor, choose ventricular fibrillation or asystole: the pressure trace collapses and the stats show no pulse. In adults sudden arrest is often VF from a heart attack, and early defibrillation saves lives. In children (ETAT+) arrest is usually the end of hypoxia or shock, giving bradycardia then asystole: open the airway and ventilate first, then compressions at 15 : 2.

Blood pressure and output calculator

Type in a patient's numbers or pick a preset. The working is shown step by step so you can copy the method in an exam.

Practice drill

Randomised questions with instant feedback. Pick a topic; get five right in a row to complete the challenge.

Worked examples

1. Cardiac output and ejection fraction

  1. EDV = 130 mL, ESV = 55 mL: $SV = 130 - 55 = 75$ mL.
  2. HR = 72 bpm: $CO = 72 \times 75 = 5400$ mL/min $= 5.4$ L/min.
  3. $EF = 75/130 = 58\%$: normal. Compare the live values in Lab 2.

2. Mean arterial pressure and resistance

  1. BP 120/80: $MAP \approx 80 + (120-80)/3 = 93$ mmHg.
  2. With CO = 5.4 L/min = 90 mL/s and right atrial pressure ≈ 0: $SVR = 93/90 = 1.03$ mmHg·s/mL (≈ 1380 dyn·s·cm⁻⁵ after multiplying by 1333).

3. Why tachycardia does not raise output for ever

  1. At 72 bpm each beat lasts 0.83 s; systole ≈ 0.3 s, diastole ≈ 0.53 s.
  2. At 180 bpm each beat lasts 0.33 s; systole shortens only to ≈ 0.2 s, leaving ≈ 0.13 s to fill.
  3. In the model SV falls from about 80 mL to about 32 mL, so CO stays near 5.7 L/min even though the rate has more than doubled (set 180 bpm and see). In a real heart, sympathetic drive also shortens systole, speeds relaxation and raises contractility and venous return, so output keeps rising up to about 150–170 bpm; the model has no autonomic control, so it shows only the filling-time limit.

4. Heart rate from an ECG

  1. At 25 mm/s one large square (5 mm) = 0.2 s.
  2. R–R = 4 large squares = 0.8 s: $HR = 60/0.8 = 75$ bpm (or 300 ÷ 4).
  3. PR = 1.5 large squares = 0.30 s > 0.20 s: first-degree AV block (try the preset).

5. Classifying a blood pressure

  1. A 52-year-old man has 168/104 mmHg on two visits a week apart, with no chest pain, breathlessness or confusion.
  2. Classify by the higher category of either number: systolic 168 ≥ 160 and diastolic 104 ≥ 100, so stage 2 hypertension (below 180/120, so not a crisis).
  3. $MAP = 104 + (168 - 104)/3 = 104 + 21.3 = 125$ mmHg; pulse pressure $= 64$ mmHg.

6. Adrenaline in a paediatric arrest (teaching example)

  1. Dose 10 mcg/kg IV or IO. A 14 kg child: $10 \times 14 = 140$ mcg $= 0.14$ mg.
  2. Adrenaline 1 in 10,000 contains 1 mg in 10 mL $= 0.1$ mg/mL $= 100$ mcg/mL.
  3. $\text{Volume} = \dfrac{D}{H}\times V = \dfrac{140}{100}\times 1\text{ mL} = 1.4$ mL, i.e. 0.1 mL/kg of 0.1 mg/mL (1 in 10,000). Repeat every 3–5 minutes during CPR (RCUK paediatric ALS).
Practice cases for learning. They are simplified; real patients need full assessment and current national and hospital protocols.

Clinical scenarios

Work through each patient one step at a time. Where a case has a lab button, open the simulator to see the rhythm or pressures for yourself.

OSCE station: precordial examination and blood pressure

A timed station of the kind used in clinical practical exams (OSCEs). Read the instructions, start the clock and work through the tasks; the examiner's mark sheet with the correct answers appears at the end.

Challenges check themselves as you use the labs.