Venous return and cardiac function curves: where they cross
Right atrial pressure is not a free input: it is set by where the cardiac function curve and the venous return curve cross. Learn which curve each change moves.
Chapters (11)
Interpret the intersection of the venous return and cardiac function curves, and predict how blood volume, venoconstriction, arteriolar resistance and inotropy move it.
The short version
- Where the cardiac function curve and the venous return curve cross is the steady state; that one point sets both cardiac output and right atrial pressure.
- Blood volume and venous tone slide the venous return curve sideways: a rightward shift raises both cardiac output and right atrial pressure, a leftward shift lowers both.
- Arteriolar resistance changes the slope of the venous return curve with little change in mean circulatory filling pressure; raising it lowers cardiac output.
- Inotropy and heart failure shift the cardiac function curve, and they push cardiac output and right atrial pressure in opposite directions.
- Veins move the venous return curve sideways, arterioles tilt it, and the heart moves the cardiac curve: read the new crossing point from there.
Venous return and cardiac function curves: which caused which?
A 31-year-old man, three days after surgery, is given one litre of saline (illustrative values). His right atrial pressure climbs from 4 to 8 mm Hg. His cardiac output climbs too, from 4.8 to 6.1 L/min.
The pressure rose, and so did the output. So which one caused which? The answer comes from reading the point where the venous return and cardiac function curves cross, and from predicting how blood volume, venous tone, arteriolar resistance and contractility move that point.[1][2]
The cardiac function curve (Frank–Starling)
The first curve is the familiar one: the cardiac function curve plots cardiac output against right atrial pressure. It is the Frank–Starling relationship: more filling, more output.[1][2]
But the heart can only pump what comes back to it. In steady state, venous return equals cardiac output.[1][2][3]
The venous return curve and mean circulatory filling pressure
The second curve asks the opposite question: how much blood returns to the heart at each right atrial pressure? It slopes downward. The higher the pressure at the heart's entrance, the less blood returns.[1][2]
It reaches zero flow when right atrial pressure rises to the mean circulatory filling pressure (Pmc), about 8 mm Hg, measured with the heart stopped. Pmc is also called the mean systemic filling pressure.[1][3]
Venous return is a pressure gradient. Pmc is the zero-flow point of the curve. This is the classical Guyton model as taught for the exam.
Both curves are plotted against right atrial pressure on the x-axis, but the roles of the axes are reversed: for the cardiac function curve, right atrial pressure is the independent variable and cardiac output depends on it; for the venous return curve, venous return is the independent variable and right atrial pressure depends on it.[1]
The crossing point is the steady state
Where the two curves cross is the steady state. That one point sets both cardiac output and right atrial pressure.[1][2][3]
The lesson uses a simplified teaching model: venous return = (Pmc − RAP) / R, with a linear cardiac curve. At baseline, right atrial pressure is 2 mm Hg, cardiac output is 5 L/min and Pmc is 8 mm Hg. The resistance to venous return is 1.2 mm Hg per L/min, and the cardiac curve rises by about 0.8 L/min for each 1 mm Hg of right atrial pressure. Check the venous return: (8 − 2) / 1.2 = 5 L/min, the same as the cardiac output, so the curves cross there.
Move one: blood volume and venous tone
Adding blood volume, or tightening the veins (venoconstriction), raises the mean circulatory filling pressure (to 10 mm Hg in the model). The whole venous return curve slides to the right, parallel to itself.[1][3]
In the model, the crossing point moves to a right atrial pressure of about 3 mm Hg and a cardiac output of about 5.8 L/min. Both rise, as the heart moves up its own curve. That is the saline from the opening case.[1][3]
Losing blood or dilating the veins does the opposite: the curve slides left, and both cardiac output and right atrial pressure fall.[1]
Move two: arteriolar resistance tilts the curve
Tightening the arterioles barely changes the mean circulatory filling pressure, but it flattens the venous return curve: the slope falls.[1][3]
In the model, the resistance to venous return rises from 1.2 to 1.8. The crossing point slides to a right atrial pressure of about 1 mm Hg and a cardiac output of about 4 L/min. Both fall (the lower right atrial pressure follows from the geometry of the two curves). Dilating the arterioles reverses this. Arteriolar effects are shown with the heart held constant.[1][3]
Move three: the heart itself (inotropy and failure), and the rule for reading the crossing point
More inotropy lifts the cardiac function curve. The venous return curve stays put, so the crossing slides up and to the left along it. Output rises to about 5.8 L/min, but right atrial pressure falls to about 1 mm Hg.[1][3]
A failing heart does the opposite. The cardiac curve drops: output falls to about 4.3 L/min and right atrial pressure climbs to about 3 mm Hg.[1][3]
| Change | Curve moved | Cardiac output | Right atrial pressure |
|---|---|---|---|
| More blood volume or venoconstriction | Venous return, shifts right | Rises (about 5.8) | Rises (about 3) |
| Blood loss or venodilation | Venous return, shifts left | Falls | Falls |
| Arteriolar constriction | Venous return, slope falls | Falls (about 4) | Falls (about 1) |
| More inotropy | Cardiac function, lifts | Rises (about 5.8) | Falls (about 1) |
| Failing heart | Cardiac function, drops | Falls (about 4.3) | Rises (about 3) |
Veins move the venous return curve sideways, arterioles tilt it, and the heart moves the cardiac curve. Read the new crossing point from there.[1][3]
A useful consequence of the curve geometry: a change in the venous return curve moves right atrial pressure and cardiac output in the same direction, whereas a cardiac curve shift moves them in opposite directions.
Practice question
Original · USMLE styleA 66-year-old man is in the cardiac intensive care unit 2 days after an anterior myocardial infarction. A pulmonary artery catheter is in place. No intravenous fluids or vasoactive drugs have been given. Compared with measurements on admission:
| Right atrial pressure, admission | 3 mm Hg |
|---|---|
| Right atrial pressure, now | 9 mm Hg |
| Cardiac output, admission | 5.4 L/min |
| Cardiac output, now | 3.8 L/min |
Common questions
What is the steady state on the venous return and cardiac function curves?
It is the point where the two curves cross. Venous return equals cardiac output there, and that one point sets both cardiac output and right atrial pressure.
What is mean circulatory filling pressure?
It is the pressure measured with the heart stopped, about 8 mm Hg. It is the point where the venous return curve reaches zero flow, and it is also called the mean systemic filling pressure.
How does blood volume shift the venous return curve?
More blood volume, or venoconstriction, raises the mean circulatory filling pressure and slides the curve to the right, so cardiac output and right atrial pressure both rise. Blood loss or venodilation slides it left.
How does arteriolar resistance change the venous return curve?
Raising arteriolar resistance flattens the curve (the slope falls) with little change in mean circulatory filling pressure. The crossing point then has a lower cardiac output.
Why do inotropy and heart failure move cardiac output and right atrial pressure in opposite directions?
They shift the cardiac function curve, not the venous return curve. More inotropy raises output and lowers right atrial pressure; a failing heart lowers output and raises right atrial pressure.
Transcript
Read the full narration, by chapter702 words
0:00A saline bolus: which caused which?
A 31-year-old man, 3 days after surgery, is given one litre of saline. His right atrial pressure climbs from four to 8 mm Hg. And his cardiac output climbs too, from 4.8 to 6.1 litres per minute. The pressure rose, and so did the output. So which one caused which? By the end of this lesson, you'll read the point where two curves cross, and predict how blood volume, venous tone, arteriolar resistance and contractility move it.
0:32The cardiac function curve (Frank-Starling)
The first curve you know: Frank–Starling, cardiac output against right atrial pressure. More filling, more output. But the heart can only pump what comes back, so in steady state venous return equals cardiac output.
0:47The venous return curve and Pmc
So the second curve asks the opposite question: how much blood returns at each right atrial pressure? It slopes downward. The higher the pressure at the heart's entrance, the less blood returns. It reaches zero flow when right atrial pressure rises to the mean circulatory filling pressure, about 8 mm Hg, measured with the heart stopped.
1:11Venous return as a pressure gradient
Venous return is a pressure gradient: mean circulatory filling pressure minus right atrial pressure, divided by the resistance to venous return.
1:22The crossing point is the steady state
Where the two curves cross is the steady state. That one point sets both cardiac output and right atrial pressure. Baseline: right atrial pressure two, cardiac output five litres per minute, mean circulatory filling pressure eight.
1:39Move one: blood volume and venous tone
Move one: add blood volume, or tighten the veins. Both raise the mean circulatory filling pressure, so the whole venous return curve slides to the right, parallel to itself. In our model, the crossing point moves to a right atrial pressure of about three and a cardiac output of about 5.8. Both rise, as the heart moves up its own curve. That is the saline. Lose blood or dilate the veins, and the curve slides left. Both fall.
2:10Move two: arteriolar resistance tilts the curve
Move two: tighten the arterioles. The mean circulatory filling pressure barely changes, but the curve flattens. In our model, resistance to venous return rises from 1.2 to 1.8, and the crossing point slides to a right atrial pressure of about one and an output of about four. Both fall. Dilate the arterioles and the reverse happens.
2:35Move three: the heart (inotropy and failure)
Move three: the heart itself. More inotropy lifts the cardiac function curve. The venous return curve stays put, so the crossing slides up and to the left along it. Output rises to about 5.8, but right atrial pressure falls to about one. A failing heart does the opposite: output falls to about 4.3, and right atrial pressure climbs to about
3:02The rule for the three moves
three. The rule: veins move the venous return curve sideways, arterioles tilt it, and the heart moves the cardiac curve. Read the new crossing point from there.
3:14Practice question
Your turn. A 66-year-old man is in the cardiac intensive care unit 2 days after an anterior myocardial infarction. A pulmonary artery catheter shows his right atrial pressure has risen from three to nine millimetres of mercury, while his cardiac output has fallen from 5.4 to 3.8 litres per minute. No fluids or drugs were given. Which change best explains this new steady state? A, the cardiac function curve shifts up and to the left. B, the cardiac function curve shifts down and to the right. C, the venous return curve shifts to the right. D, the venous return curve shifts to the left. E, the venous return curve rotates downward. Pause here and decide. A is out: that gives more output and a lower pressure, the opposite of this patient. C is out: a rightward shift raises both, and output fell. D is out: a leftward shift lowers both, and pressure rose. E is out too: a flatter curve also lowers both. So the answer is B: the infarct weakened the heart, the cardiac curve dropped, output fell, and blood backed up, so right atrial pressure rose.
4:37Recap and next lesson
Three things to keep. One: where the cardiac function curve and the venous return curve cross sets cardiac output and right atrial pressure. Two: volume and venous tone shift the venous return curve sideways; arteriolar resistance changes its slope. Three: inotropy and failure shift the cardiac curve, and they push output and right atrial pressure in opposite directions. Next up: the baroreceptor reflex, which retunes these curves within seconds.
Sources
Numbers in the text, e.g. [1], point here- Klabunde RE. CV Physiology: Cardiac and Vascular Function Curves (CF027). cvphysiology.com/cardiac-function/cf027
- Klabunde RE. CV Physiology: Venous Return (CF016). cvphysiology.com/Cardiac%20Function/CF016
- Deranged Physiology. Cardiac output curves and vascular function curves. derangedphysiology.com/main/cicm-primary-exam/cardiovascular-system/Chapter-028/cardiac-output-curves-and-vascular-function-curves
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. All video diagrams, curves, charts and handwriting are drawn in code (original); no third-party artwork or 3D models are used in the video. Thumbnail plate: Servier Medical Art (smart.servier.com), "Heart (sagittal overview)", licensed under CC BY 4.0, recoloured and resized. Previous: EP 10 · Blood Pressure, Resistance and Poiseuille's Law · Next: EP 12 · The Baroreceptor Reflex
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-017.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01Pressure-volume loop explained: four phases, four valve events5:00
- EP 02Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR5:04
- EP 03Afterload on the pressure-volume loop4:49
- EP 04Contractility on the pressure-volume loop: the ESPVR explained5:17
- EP 05Wiggers diagram explained: the cardiac cycle step by step5:30
- EP 06The Frank-Starling curve: preload, inotropy and heart failure4:44
- EP 07Aortic stenosis vs mitral regurgitation on the pressure-volume loop5:41
- EP 08Fick principle: how to calculate cardiac output5:07
- EP 09HFrEF vs HFpEF on the pressure-volume loop5:33
- EP 10Poiseuille's law and vascular resistance: why arterioles matter5:15
- EP 11Venous return and cardiac function curves: where they cross5:11
- EP 12The baroreceptor reflex: from stretch to vagal and sympathetic output5:17
- EP 13Myocardial oxygen supply and demand: why tachycardia causes ischaemia4:50
- EP 14Unstable angina vs NSTEMI vs STEMI: from plaque to ACS4:50
- EP 15Antianginal drugs: nitrates, beta blockers, calcium channel blockers4:56
- EP 16Complications of myocardial infarction, by timeline4:59