01Core principlesThe concepts and mechanisms needed to understand the subject.
Haemodynamics starts with conservation. In a steady state, flow into a circuit must match flow out, although blood can be redistributed among parallel organ beds. The driving pressure is the difference between inlet and outlet, not the absolute arterial pressure alone. Resistance arises from viscosity, vessel length and especially radius. The idealised Poiseuille relationship is most useful for direction and sensitivity: small radius reductions greatly increase resistance under laminar conditions. Real blood is pulsatile and vessels are compliant and branching, so the equation is a model rather than a complete description.
The cardiac cycle coordinates electrical activation, pressure development, valve motion and volume change. Ventricular filling occurs while atrioventricular valves are open. Isovolumetric contraction begins after they close; ventricular pressure rises at constant volume until semilunar valves open. Ejection reduces ventricular volume, then semilunar closure starts isovolumetric relaxation. Stroke volume is end-diastolic minus end-systolic volume, and ejection fraction is stroke volume divided by end-diastolic volume. Ejection fraction can remain preserved despite impaired filling or low stroke volume, so it is not synonymous with total cardiac performance.
Preload describes myocardial fibre stretch before contraction and is approximated imperfectly by filling volume or pressure. Contractility changes force independent of initial fibre length, whereas afterload is the load opposing ejection and relates to pressure and wall stress. Laplace reasoning links wall stress to pressure and radius relative to wall thickness; a dilated thin-walled chamber bears greater stress for the same pressure. Venous return depends on circulating volume, venous tone, muscle and respiratory pumps and pressure between systemic veins and right atrium. At equilibrium, venous return and cardiac output must be equal.
Control operates over different times. Stretch-sensitive arterial baroreceptors alter afferent firing when pressure changes, producing rapid autonomic adjustments in rate, contractility, arteriolar resistance and venous capacitance. Local metabolites and endothelial signals match regional flow to tissue demand. Capillary movement depends on hydrostatic and oncotic forces plus permeability and lymphatic removal, but simple filtration equations are approximations in living tissues. Longer-term pressure control involves renal sodium-water balance and hormonal systems. In acute assessment, physiological trends and perfusion matter more than manipulating a single formula.
Key points
- Flow through a vascular bed equals its pressure difference divided by resistance; resistance is strongly influenced by vessel radius, while serial resistances add and parallel beds lower total resistance.
- Cardiac output equals heart rate multiplied by stroke volume; stroke volume reflects preload, contractility, afterload and the mechanical constraints of filling and ejection.
- The Frank–Starling mechanism increases force as ventricular filling stretches myocardium within the physiological range, helping match right and left ventricular outputs.
- Mean arterial pressure is approximated from diastolic pressure plus one-third pulse pressure at ordinary heart rates, and is related to cardiac output and systemic vascular resistance.
- Arterial compliance shapes pulse pressure: for a similar stroke volume, a less compliant arterial system produces a larger pressure swing.
- Baroreceptor reflexes rapidly buffer pressure through autonomic changes in heart, arterioles and veins; renal and hormonal mechanisms dominate longer-term volume and pressure control.
02Mechanisms and patternsImportant relationships and how to distinguish them.
For a fixed resistance, greater inlet-to-outlet pressure difference increases flow; for a fixed gradient, higher resistance reduces it.
Resistance changes steeply with radius under laminar-flow assumptions, explaining why arteriolar tone can redistribute flow efficiently.
More physiological filling can raise stroke volume through length-dependent activation until overdistension, disease or constraint limits the response.
An acute rise in opposing load tends to increase end-systolic volume and reduce stroke volume unless compensation alters contractility or filling.
For a given added volume, a less compliant chamber or artery experiences a larger pressure change.
Reduced arterial stretch tends to increase sympathetic and reduce parasympathetic activity, supporting pressure through cardiac, arteriolar and venous effects.
03Interpreting evidenceInformation, measurements and their limitations.
Consider the information, its meaning and its limitations before deciding what follows.
- 01
Cardiac-output calculation - Why
- Connect heart rate and stroke volume to systemic flow.
- Interpretation and limitations
- Multiply compatible units and test plausibility; tachycardia can raise output only until shortened filling or pathology reduces stroke volume.
- 02
Mean-pressure estimate - Why
- Approximate average arterial driving pressure from systolic and diastolic measurements.
- Interpretation and limitations
- Use diastolic pressure plus one-third pulse pressure at ordinary rates; altered cycle timing makes this approximation less accurate.
- 03
Resistance comparison - Why
- Predict flow changes after altered vessel radius or circuit arrangement.
- Interpretation and limitations
- State assumptions of laminar steady flow; series and parallel architecture may dominate the total response.
- 04
Pressure-volume loop analysis - Why
- Relate valve events, filling, ejection and ventricular work.
- Interpretation and limitations
- Width represents stroke volume and enclosed area reflects external stroke work; shifts require separate reasoning about preload, afterload and contractility.
- 05
Perfusion assessment - Why
- Relate calculated values to organ delivery and physiological adequacy.
- Interpretation and limitations
- Pressure alone does not guarantee flow or oxygen delivery; examine mental state, skin, urine output, lactate trend and the whole clinical context.
- 06
Dynamic-response reasoning - Why
- Distinguish immediate reflex change from slower volume regulation.
- Interpretation and limitations
- Baroreflex effects occur quickly, while renal retention and remodelling evolve over longer intervals and may sustain or maladapt the response.
04Applied reasoningWorked examples connecting principles to decisions.
01Worked exampleCalculate output and approximate mean pressureA model circulation has heart rate 80 beats/min, end-diastolic volume 130 mL, end-systolic volume 50 mL and arterial pressure 120/75 mmHg.+
- 1Calculate stroke volume as 130 minus 50, giving 80 mL per beat.
- 2Multiply 80 mL/beat by 80 beats/min to obtain 6400 mL/min, or 6.4 L/min cardiac output.
- 3Calculate pulse pressure as 120 minus 75, giving 45 mmHg; add one-third of 45 to diastolic pressure.
- 4The final approximate mean arterial pressure is 90 mmHg at an ordinary heart rate.
- 5Verify units and arithmetic, then check the physiological identity: output uses stroke volume rather than end-diastolic volume and the mean-pressure result lies between systolic and diastolic values.
02Ventricular reasoningIncrease afterload acutelyPreload and contractility are initially unchanged while arterial pressure opposing left ventricular ejection rises.+
- 1Recognise that the ventricle must generate a higher pressure before and during ejection.
- 2Predict less fibre shortening and more blood remaining at end systole during the first beat.
- 3Deduce a reduced stroke volume and increased end-systolic volume.
- 4Separate this immediate effect from later reflex, filling and remodelling responses.
03Circuit reasoningAdd a parallel vascular bedA new vascular pathway is opened in parallel with existing organ beds while individual bed resistances remain unchanged.+
- 1Recall that each parallel bed receives the same overall inlet-to-outlet pressure difference.
- 2Add conductances, or reciprocal resistances, rather than adding resistances directly.
- 3Conclude that total systemic resistance falls when another finite parallel conductance is added.
- 4Check whether cardiac output or pressure is specified as fixed before predicting the final flow distribution.
05Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.
- Verify every haemodynamic calculation with units and a range check before interpreting physiology.
- Redraw pressure-volume loops with valve events labelled to test whether a proposed shift is mechanically coherent.
- Separate first-beat effects from autonomic compensation and slower renal or structural responses.
- Check whether pressure, flow, resistance, compliance or oxygen content is actually being held constant in the question.
- Relate model predictions back to perfusion measures because identical mean pressure can coexist with different flow and distribution.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
Pressure is not flow
A high pressure may coexist with low output when resistance is high, while adequate flow can occur at lower pressure in a low-resistance circuit.
Ejection fraction can mislead
Because it is a ratio, ejection fraction may be preserved despite low end-diastolic volume and clinically inadequate stroke volume.
Veins govern reserve
Venous capacitance contains most blood volume and changes in venous tone can rapidly alter stressed volume and cardiac filling.
Coronary timing differs
Left ventricular coronary flow is constrained during systole by myocardial compression and is therefore strongly supported during diastole.
Models declare assumptions
Poiseuille flow, mean-pressure formulas and simple Starling forces are powerful when their steady-flow, geometry and timing limits are acknowledged.
07Common pitfallsFrequent interpretation and management errors.
- 01
Using arterial pressure as a direct synonym for cardiac output without considering systemic resistance.
- 02
Adding parallel vascular resistances as though they were arranged in series.
- 03
Calling end-diastolic pressure an exact measurement of preload in every ventricular condition.
- 04
Assuming tachycardia always raises cardiac output despite reduced filling time and rate-related dysfunction.
- 05
Reading preserved ejection fraction as proof that stroke volume, filling and tissue perfusion are normal.