Tricia pauses a heart animation just before blood leaves the left ventricle. The wall is already moving. The chamber is already developing force. Yet its outlet remains closed. Alicia calls this a delay between beats. Kai Kai disagrees: the beat has begun, but ejection has not. Their disagreement contains the central problem of learning the cardiac cycle. We often use one word, heartbeat, for several events that do not happen at the same instant.
The cardiac cycle is the repeating sequence through which a ventricle accepts blood, develops pressure, ejects part of its contents and becomes ready to accept blood again. Valves change state as conditions on either side change. Electrical activation initiates a molecular sequence, but the resulting force, chamber pressure and blood movement follow their own related timelines. Understanding the cycle means following those relationships rather than memorising four coloured regions.
This support pillar sits beneath How the Heart Works | Rhythm, Pressure, Valves and Flow. It owns the mechanics of one cycle. The companion How the Heartbeat Works explains electrical recruitment and calcium in greater detail. The three students are fictional learning companions, and every numerical problem below is an invented teaching model. None is a patient record, diagnostic threshold or instruction for changing an individual’s health care.
1. A cycle has no privileged beginning
A circle can be described from any point. Some textbooks begin with atrial contraction; others begin with ventricular filling or the onset of ventricular systole. These choices need not conflict. They are different starting positions on the same recurring route. What matters is whether the sequence reconnects correctly and whether the conditions at the end can generate the stated beginning.
We will start when ventricular filling begins. This makes the dependence on returning blood visible. A pump cannot repeatedly deliver a volume that never reaches its inlet. Starting with filling also prevents the quiet-looking portion of the animation from becoming mentally optional. The next pressure pulse depends on the volume, relaxation state and timing established before it.
The terms systole and diastole require a chamber reference. Atrial systole is not ventricular systole. When the terms are used alone, they commonly refer to ventricular contraction and relaxation. The OpenStax overview introduces this coordination. Treat any fixed duration or volume in an introductory diagram as an illustrative case, not a schedule that every heart follows. A useful sequence can remain recognisable while its timing changes.
2. Draw three compartments before drawing four phases
For the left ventricular cycle, draw the left atrium, left ventricle and aorta. Place the mitral valve between atrium and ventricle and the aortic valve between ventricle and aorta. Now give each compartment a pressure that can change independently. The relevant questions become comparisons: is atrial pressure above ventricular pressure, and is ventricular pressure sufficient relative to aortic pressure?
The corresponding right-sided arrangement uses the right atrium, tricuspid valve, right ventricle, pulmonary valve and pulmonary artery. The NHLBI circulation guide locates these connections. The names are necessary, but connectivity alone does not explain valve state. An anatomical line between two compartments is not evidence that blood can pass freely through it at every moment.
This three-compartment model deliberately leaves out many details. It does not yet show wall thickness, electrical propagation, coronary vessels or regional motion. Its limited job is to make the boundary conditions explicit. A small model that correctly exposes the relevant pressure comparisons can explain more than a beautiful complete anatomy drawing whose arrows never change. Add detail when it answers a question the simpler model cannot.
3. A valve is a mechanically responsive boundary
Heart valves do not receive a private command to open at a numbered stage. Their leaflets move under changing pressure and flow forces. A useful first approximation is that a valve permits forward flow when the upstream condition favours it and closes as the relationship reverses. Real transitions include fluid inertia, leaflet deformation and three-dimensional flow, so the rule is a starting model rather than a perfect instantaneous equation.
Suppose atrial pressure exceeds ventricular pressure while the aortic side remains at a higher pressure. The inlet can be open while the outlet is closed. Later, ventricular pressure rises above atrial pressure but remains below aortic pressure. Both valves can then be closed. The two valves do not have to change state together because they compare the ventricle with different neighbouring compartments.
That simple observation generates the isovolumetric phases. There are intervals between losing one permissive pressure relationship and gaining the next. The valve sequence is not an arbitrary four-step choreography imposed on the pump. It emerges because pressure must cross different boundaries before blood can move along the next route. Remembering this is more reliable than remembering which flap looked open in one animation frame.
4. Early filling depends on a receiving ventricle
After the previous ejection, ventricular pressure falls. When conditions favour forward movement from atrium to ventricle, the mitral valve opens and filling begins. Blood enters because of a pressure difference, not because the ventricle has been declared empty. It still contains the volume remaining after its preceding systole. Filling adds to that residual volume rather than starting from zero.
The receiving chamber is not an inert bag. Its active relaxation changes pressure, and its mechanical recoil and passive properties influence how it expands. The atrium also brings a changing reservoir of blood and pressure. Filling therefore results from interaction between two evolving compartments. Saying that the atrium pushes or the ventricle draws blood captures only part of that relationship unless the pressure conditions are specified.
Imagine two otherwise similar model ventricles connected to the same atrial source. One lowers its active tension more quickly. Their early filling patterns can differ even before any difference in eventual passive stiffness is introduced. This thought experiment isolates relaxation timing. It does not claim that every observed difference in early filling has that cause; it shows why the receiving chamber’s state belongs in the explanation.
5. Atria act as reservoirs, conduits and contributors
During ventricular systole, blood continues returning to the atria while the atrioventricular valves are closed. The atria can therefore act as reservoirs. Once the valves open, they provide a route into the ventricles. Atrial contraction then contributes to late filling. These are three related functions, not three separate anatomical structures.
Do not assign atrial contraction one universal percentage of filling. Its relative contribution changes with rate, age, atrial function and ventricular mechanical conditions. A number useful in an introductory resting example is not a biological contract. The stronger understanding is relational: an appropriately timed atrial pressure rise can add volume before ventricular pressure rises enough to close the inlet.
Alicia asks whether removing the active atrial contribution from a model would stop every drop of filling. Tricia follows the earlier open-valve interval and sees why it need not. Kai Kai then asks whether the lost contribution must be unimportant. That does not follow either. A process can supply less than the entire volume and still matter greatly under particular conditions. Avoiding an all-or-nothing explanation makes the role of the atria easier to understand.
6. End-diastolic volume records an outcome, not a single cause
End-diastolic volume is the ventricular volume near the end of filling. It reflects available venous return, the driving pressure, valve properties, filling time, relaxation and chamber mechanics. It is not identical to end-diastolic pressure, and neither measurement is automatically identical to myocardial fibre stretch. Volume, pressure and preload are connected concepts with different definitions.
In an invented model, Chamber A receives an extra 18 mL for a pressure rise of 3 mmHg. Chamber B requires 9 mmHg for the same added volume. Their average incremental compliances over those tested intervals are 6 and 2 mL/mmHg. Equal added volume has therefore produced different pressure changes. The model contains no contradiction because the receiving walls have different pressure-volume relationships.
Now allow incomplete relaxation during the measurement. The observed pressure can include residual active tension as well as passive resistance to expansion. A single volume-pressure pair cannot uniquely separate those influences. To explain a measurement, ask what state the tissue was in, which pressures were referenced and whether the comparison held other conditions constant. Naming the endpoint is the beginning of an explanation, not its completion.
7. Isovolumetric contraction prepares the outlet condition
Ventricular electrical activation initiates calcium-dependent force development. As ventricular pressure rises relative to atrial pressure, the inlet closes. The aortic valve can remain closed because aortic pressure is still higher. During the intervening period, the ventricular cavity contains approximately the same volume while its pressure increases. This is isovolumetric contraction.
The word isovolumetric applies to cavity volume. It does not mean every myocardial fibre remains at the same length or that the chamber cannot change shape. Regional tissue motion, wall thickening and force development can occur without a large change in the total enclosed volume. A statement about the integral volume is not a statement about every point in the wall.
Consider a sealed flexible pouch containing nearly incompressible fluid. Its shape can change while its contained volume changes little. The heart differs because the wall itself actively generates force, but the comparison separates geometry from total volume. This is why a moving ventricular wall does not prove that blood is already being ejected. The outlet must become permissive before the contraction can create substantial forward arterial flow.
8. Papillary muscles stabilise closure rather than opening the inlet
The mitral and tricuspid valve leaflets are supported by chordae tendineae attached to papillary muscles. During ventricular contraction, that support helps keep the leaflets from prolapsing backward into the atria. The muscular support system does not open the valve by pulling its leaflets apart. Opening follows the changing pressure and flow relationship.
A rope attached to a door can limit how far the door moves without being the force that opens it. That restricted analogy captures the supporting role, but real valves deform in fluid and have more complicated attachments. The aortic and pulmonary valves use a different geometry and do not have the same chordal apparatus. Learning one generic flap model for all four valves loses that distinction.
The useful question is not simply whether a structure is present. Ask which force it resists and during which phase it becomes important. A support may contribute little to producing the forward pressure gradient yet be essential for preventing an unwanted route under that gradient. In a pump, maintaining the correct boundary can matter as much as generating the driving force.
9. Ejection begins into an artery that already contains pressure
The aorta does not return to zero pressure whenever the ventricle relaxes. Its elastic behaviour and the resistance of downstream vessels help maintain pressure between ejections. The next ventricular contraction therefore starts against an existing receiving condition. Aortic-valve opening requires the evolving ventricular pressure to create suitable forward forces at that boundary.
In a controlled model, raise the initial aortic pressure while leaving ventricular filling and the activation programme unchanged. More pressure must be developed before the outlet opens. This can alter the ejection trajectory. It does not establish the eventual response after multiple beats, because changes in residual volume, venous return and regulation can subsequently change the starting conditions.
Tricia calls the aorta an obstacle. Alicia calls it a store. Both descriptions contain a useful feature. The receiving circulation presents a load during ejection while its elasticity helps maintain downstream delivery afterward. A structure can oppose one immediate movement and support the larger cyclic function. The heart cannot be understood by ranking every resistance as bad and every reduction in resistance as good without asking which system-level job is being performed.
10. Pressure can rise while cavity volume falls
Once the outlet opens, ventricular volume decreases as blood leaves. Early in ejection, pressure can nevertheless continue rising because the myocardium is still developing active force. A passive container with one fixed pressure-volume relationship would not adequately describe this behaviour. The ventricle changes its mechanical state while the fluid is moving.
Classic experiments by Suga and Sagawa in supported canine hearts investigated instantaneous pressure-volume relationships. Their historical importance is that they examined pressure and volume together through time, rather than treating pressure as a fixed consequence of volume alone. Such models remain abstractions with assumptions; an experimental relationship in an animal preparation is not a universal equation for every human beat.
The causal lesson can be tested without specialist mathematics. Select one cavity volume that the ventricle passes during filling and again during ejection. It can have a low pressure in the first passage and a much higher pressure in the second. The missing variable in a simple pressure-equals-function-of-volume story is active state, along with the other conditions of the wall. The same amount of blood does not require the same pressure at every moment.
11. End-systolic volume is not leftover work the heart forgot to do
The ventricle normally finishes ejection with blood remaining inside. End-systolic volume is that residual amount near the end of systole. Stroke volume is the difference between end-diastolic and end-systolic volumes under the usual simplified intact-valve model. The normal operating pattern is movement between two nonzero volumes, not a cycle from completely full to completely empty.
Take an invented chamber that begins at 126 mL and finishes at 54 mL. Its cavity-volume change is 72 mL. Its ejection fraction is 72/126, about 57.1%. Neither number says what percentage of the myocardium is alive or how much reserve remains. The first is an amount; the second compares that amount with the initial volume.
Now change the outlet load while preserving the same starting volume and activation programme in the model. The remaining volume can change. A residual amount is therefore not a pure measure of intrinsic contractile quality. It reflects interaction between muscle and load. Observing the endpoint tells us where the cycle arrived; explaining why it arrived there requires the path and conditions as well.
12. Valve closure marks a transition in a moving fluid
As ventricular force development subsides and ejection decelerates, the ventricular-aortic relationship changes. The aortic valve closes as the forces favour reversal. A small transition in the aortic pressure waveform accompanies closure and the associated fluid and wall dynamics. This is often shown as the dicrotic notch in a central arterial tracing.
Do not turn a simplified diagram into the claim that blood instantaneously stops whenever two pressures become equal. Blood has inertia, and both the valve and receiving vessel deform. During rapid transitions, a steady resistance equation omits relevant dynamics. It can still be useful for suitable averaged flow, but it is not a complete description of acceleration and deceleration.
A moving trolley can continue briefly even when the applied forward push falls because its motion depends on more than the present push. The analogy illustrates inertia, not the exact forces inside the aorta. Its purpose is to explain why transition events require care. The robust starting rule is to compare pressure conditions; the more complete account includes the history and momentum of the fluid moving through the boundary.
13. Isovolumetric relaxation creates the next receiving state
After aortic closure, ventricular pressure can still exceed atrial pressure. Both main valves remain closed while active tension declines, so cavity volume changes little. Only when the ventricle becomes a suitable lower-pressure receiver does the mitral valve open. Relaxation therefore begins before filling, just as contraction begins before ejection.
Weiss, Frederiksen and Weisfeldt studied pressure decline in isolated canine ventricular preparations. They characterised the fall over a defined interval with a time constant and investigated how experimental conditions changed it. The study illustrates that relaxation has a measurable time course, not merely an on–off label. Its numerical values should not be borrowed as universal human limits.
Suppose two models begin relaxation at the same pressure and volume. One reduces active tension faster. The time at which its pressure falls below the same atrial pressure can be earlier. That can alter when filling begins even if both eventually reach the same fully relaxed pressure-volume relationship. The thought experiment separates speed of recovery from passive stiffness, two properties often mistakenly combined into one vague description of a difficult-to-fill chamber.
14. Relaxation, compliance and recoil are not synonyms
Relaxation describes the decline of active force. Compliance describes how volume changes with pressure under specified conditions. Recoil describes a mechanical return toward a less-deformed configuration. These processes interact during early filling, but substituting one word for all three makes it impossible to locate the mechanism responsible for a change.
Ventricular contraction includes twisting and longitudinal deformation rather than simple uniform squeezing. Imaging studies such as Notomi and colleagues’ observations from infancy to adulthood examine age-related differences in torsional mechanics. The important boundary is that a feature observed in one age group or measurement method should not be assumed identical in every heart. Geometry and timing are physiological variables.
A spring analogy can help explain stored mechanical energy but cannot replace the active calcium-removal process. A soft-bag analogy can help explain compliance but does not represent coordinated untwisting. Use several limited models rather than forcing one object to explain every property. The heart is living tissue whose activation, material behaviour and shape all change through the cycle.
15. A Wiggers-style diagram puts different measurements on one clock
A combined cardiac-cycle diagram can place atrial pressure, ventricular pressure, aortic pressure, ventricular volume, an ECG and heart sounds above one shared time axis. Its value is alignment: it lets the reader compare when different events occur. The curves do not become measurements of the same thing merely because they share horizontal positions.
Begin by naming the unit of every vertical axis. Electrical voltage, pressure and volume cannot be compared by height as though they share one scale. Then locate valve transitions from the pressure relationships and check whether the volume trajectory agrees. During a closed-valve interval, the idealised cavity volume should be nearly constant. During ejection, it should fall.
Alicia initially uses the largest ECG deflection as the point of maximum pumping. Tricia traces the following pressure rise and sees the mistake. Electrical activation precedes the mechanical sequence; its peak is not automatically the peak of force or flow. The repair is not to memorise a different vertical line. It is to keep each signal attached to the physical process it records.
16. Heart sounds help mark events but do not measure stroke volume
The first heart sound is associated chiefly with atrioventricular-valve closure and vibrations of the connected cardiac structures and blood. The second is associated chiefly with semilunar-valve closure. The NHLBI heartbeat guide introduces these recurring sounds. The familiar door-slamming comparison is incomplete because a vibrating fluid–tissue system produces the sound.
Listening can identify timing information, but sound amplitude is not a calibrated reading of litres per minute. Transmission through tissue, recording position and the source of vibration affect what is heard. A louder signal is not automatically a stronger pump, and a quiet recording does not by itself quantify low output. Clinical interpretation requires context beyond this educational model.
Imagine marking two sounds on the same time axis as pressure curves. The marks can help locate transitions, but they do not provide all the missing pressure and volume values between them. A landmark is useful precisely because it anchors part of a journey. It does not tell us the speed or distance of every segment that follows. This distinction prevents auscultation from being treated as an all-purpose mechanical measurement.
17. A pressure-volume loop removes time from the axes
Plot ventricular volume horizontally and ventricular pressure vertically. Follow the cycle counterclockwise: filling moves rightward at relatively low pressure; isovolumetric contraction moves upward; ejection moves leftward; isovolumetric relaxation moves downward. Time is represented by progression around the path, not by either coordinate.
The loop makes the two pressure states at the same volume especially clear. It also reveals why the topmost pressure and the width of the loop answer different questions. Width records cavity-volume change. Height records a pressure range. The enclosed area represents net pressure-volume work for the chamber under the selected convention. None of these automatically specifies how quickly the loop was traversed.
Two model pumps can follow the same loop at different rates. Their work per cycle is the same, but their work per minute differs. Conversely, two cycles can take equal time while tracing different loops. A time graph and a pressure-volume plot are complementary representations. Switching between them should change which relationships are easy to see, not erase the physical definitions of the variables.
18. Work per cycle is an area, not a pressure peak
For an intentionally rectangular model loop, suppose ejection occurs at 95 mmHg, filling at 5 mmHg and the volume change is 68 mL. The enclosed area is (95 − 5) × 68 = 6,120 mmHg·mL. Using the physical unit conversion, that is approximately 0.816 joules of net model pressure-volume work.
Now compare a second loop with a higher ejection pressure of 115 mmHg, the same filling pressure and a smaller volume change of 48 mL. Its area is 5,280 mmHg·mL, approximately 0.704 joules. The higher peak belongs to the loop doing less work per cycle in this example. Maximum pressure and accumulated mechanical work are not the same ranking.
Real loops are not rectangles, so a real calculation integrates changing pressure over displacement. Nor does external pressure-volume work equal total metabolic energy use. Calcium handling, ion maintenance and other cellular processes consume energy. These exercises explain a mechanical quantity and its units; they do not calculate the heart’s complete oxygen requirement or provide an efficiency score for a person.
19. Higher rate compresses time, but not every phase equally
At 75 beats per minute, a regular model cycle lasts 0.8 seconds. At 120, it lasts 0.5 seconds. Those values follow directly from 60 divided by rate. They do not tell us that each named phase is shortened by the same proportion. The heart can change the durations and dynamics of its phases differently.
To make the distinction concrete, assign 0.3 seconds of the first model to ventricular systole and 0.5 to diastole. In a second invented state, assign 0.25 to each. Total cycle duration fell by 37.5%, whereas systole fell by about 16.7% and diastole by 50%. These are chosen arithmetic examples, not a normal timing table. Their purpose is to show why total shortening does not determine each component’s shortening.
Filling also depends on the rate of inflow during the available time, not duration alone. Faster relaxation, changed atrial pressure and altered venous return can change that rate. Therefore neither more time always means more output nor faster rate always means less filling is sufficient without conditions. A time budget matters, but the processes using it matter too.
20. The two ventricles share a circulation, not identical waveforms
Right and left ventricular outputs must be closely matched over a sufficiently stable interval because the circuits are connected in series. Otherwise, blood volume would progressively accumulate between them. This conservation constraint does not require identical instantaneous pressure curves or identical opening times of corresponding valves.
The pulmonary circulation ordinarily presents a lower pressure burden than the systemic circulation. The right ventricle therefore operates with a different pressure-volume pattern and geometry from the left. A lower peak pressure is not evidence that it has failed to achieve the left ventricle’s job; it has a different receiving load. Matching useful flow to that load is the relevant function.
Breathing and changes in venous return can also alter short-term timing and storage. A single instant need not show equal flows at every location. The stronger rule is input minus output equals change in stored volume across a defined interval. This allows transient differences without abandoning conservation, while ruling out a permanent mismatch with no changing storage and no additional route.
21. Pressure across the wall differs from pressure inside the chamber
The distending pressure across a chamber wall depends on the difference between internal and external pressure. If a model chamber contains a pressure of 14 units while its surroundings are at 4, the transmural difference is 10. If its surroundings rise to 9 while internal pressure remains 14, the difference becomes 5. The inside reading is unchanged; the distending condition is not.
This does not let us calculate fibre stretch without knowing geometry and material behaviour. It simply repairs the mistake of treating one absolute-looking reading as the entire loading condition. The heart is surrounded by other tissues and shares mechanical relationships between its chambers. It is not a pressure vessel suspended in a permanent zero-pressure environment.
Alicia now labels every pressure with a location and reference. Tricia adds whether it is instantaneous, a maximum or an average. Kai Kai asks which boundary the pressure difference acts across. Their labels look less elegant than one large number on an animation, but the explanation becomes more reliable. Scientific clarity often requires keeping the reference visible instead of hiding it behind a familiar unit.
22. One pressure snapshot can describe two opposite journeys
In an idealised left-heart snapshot, atrial pressure is 8 units, ventricular pressure is 35 and aortic pressure is 85. Both main valves are closed. Can you decide whether the ventricle is contracting or relaxing? Not from those values alone. The ventricle can pass through 35 on its way upward before ejection and again on its way downward after ejection.
The discriminating observation is the direction of change. A sequence 25, 35, 45 supports rising pressure; 45, 35, 25 supports falling pressure. The same present state can occur along different trajectories. A second appropriately timed observation can therefore answer a question that a more elaborate static picture cannot.
This exercise is about identifiability. Ask which alternatives remain compatible with the supplied evidence and what smallest extra observation separates them. Guessing a phase because one pressure value looks familiar replaces mechanism with association. The cycle becomes genuinely useful when it lets you explain why the information is insufficient and exactly what would make it sufficient.
23. Measurements must describe the same beat and the same question
Imaging estimates chamber shape and volume; electrical recordings describe voltage patterns; pressure sensors describe local mechanical conditions. Combining them requires compatible timing. An end-diastolic frame from one kind of beat and an end-systolic frame from a different kind may not form a valid stroke-volume estimate. Correct subtraction cannot repair incompatible inputs.
The NIBIB ultrasound explanation describes how returning sound signals become images. A two-dimensional image is a selected view of a three-dimensional chamber, and acquisition geometry matters. A clear-looking boundary is not proof that the image includes the true full extent of the cavity. Measurement quality includes choosing the right view and phase, not only drawing an outline precisely.
Imagine repeatedly measuring the same incorrectly selected view. The results may be highly consistent while systematically missing volume. Repetition improves some forms of random uncertainty but does not automatically correct a wrong geometry. To understand a reported cycle, inspect the measurement chain: what was observed, how it was transformed, which assumptions were used and whether the observations belong to a compatible physiological state.
24. Build a four-state model, then test its assumptions
Begin with four labels: filling, isovolumetric contraction, ejection and isovolumetric relaxation. For each label, record inlet state, outlet state and whether cavity volume is rising, falling or approximately constant. Then add the pressure change that permits entry into the next state. This produces an event-driven model rather than a clock that changes phases regardless of conditions.
Test it with a counterfactual. Hold the outlet closed while the ventricle develops force. Pressure may rise without forward ejection. Now leave a backward route available during contraction. The usual cavity-volume difference no longer necessarily equals useful forward arterial delivery. These altered models show which assumptions support the familiar four-phase description. They are not invitations to diagnose abnormal valves from a simple animation.
Finally, require conservation. Any fall in cavity volume must correspond to flow through a route permitted by the model; any sustained inflow–outflow mismatch must change storage. A simulation that displays blood disappearing with every valve closed has violated its own bookkeeping. Testing these constraints is a more powerful learning activity than watching a visually convincing animation without asking whether its state transitions are physically coherent.
25. The cardiac cycle is a chain of readiness conditions
Filling requires an available inlet and a receiving pressure relationship. Ejection requires sufficient ventricular pressure and an available outlet. The transition between them requires changing muscle activation. The return requires active recovery and a new pressure relationship. Each phase creates conditions that the next phase needs. The apparent pauses are not omissions; they are intervals in which those conditions are being established.
Tricia restarts the animation. This time she names the changing variable rather than saying the heart is doing nothing. Alicia watches cavity volume. Kai Kai compares the pressures on both sides of each valve. The same animation now supplies three related stories: what the wall does, what the fluid experiences and which route is available. Their understanding has improved because the questions have become more precise.
The compact explanation is therefore not squeeze, rest, repeat. It is receive, develop pressure, meet the outlet condition, eject, reduce active tension, meet the inlet condition and receive again. Keeping pressure, volume, flow and time separate makes their connections visible. That is what turns the cardiac cycle from a diagram to memorise into a mechanism that can answer unfamiliar questions.
Evidence trail and return paths
For anatomical connections, consult NHLBI: How Blood Flows through the Heart. OpenStax: Cardiac Cycle supplies an introductory phase map. Original experimental routes include Suga and Sagawa’s pressure-volume work, Weiss and colleagues’ relaxation study, and Notomi and colleagues’ torsional-mechanics observations. Read the species, preparation and measurement conditions before transferring a research result beyond its original setting.
Return to the main article: How the Heart Works, including its four support pillars. Continue outward to How the Human Body Works, How Science Works | Physiology and the How X Works library. This guide explains physiology; personal symptoms and clinical test results require qualified assessment.