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Cardiac & Vascular Function Curves

Name: Cardiac & Vascular Function Curves
Creator: Veli Bakalov, MD

Shift for volume, rotate for resistance, lift for contractility

Cardiovascular·Physiology·4 min read·8 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Steady-state cardiac output and right atrial pressure are set where the cardiac function (Frank-Starling) curve crosses the venous return curve.
Venous return = (MSFP − RAP) ÷ resistance to venous return; it reaches zero when RAP equals MSFP and levels off below an RAP of about 0 mmHg.
Mean systemic filling pressure (~7 mmHg) is the x-intercept; volume and venous tone move it, producing a parallel shift of the venous return curve.
Transfusion or venoconstriction shifts the curve right (↑CO, ↑RAP); hemorrhage or venodilation shifts it left (↓CO, ↓RAP).
A TPR change rotates the venous return curve without changing MSFP and also moves the cardiac curve via afterload; lower TPR raises CO with RAP about unchanged.
Positive inotropes (sympathetic stimulation, digoxin) lift the cardiac curve (↑CO, ↓RAP); HF and β-blockers lower it (↓CO, ↑RAP).
HF with fluid retention combines a lower cardiac curve with a right-shifted venous curve: CO partly recovers but RAP rises, causing congestion.
Exercise lifts the cardiac curve, raises MSFP and lowers TPR, so CO rises several-fold with little change in RAP.

Guyton's two-curve model

The idea. Guyton plotted cardiac output and venous return against the same x-axis, right atrial pressure (RAP). At steady state the heart pumps exactly what returns to it, so the operating point is where the two curves cross. At rest this is about 5 L/min at an RAP of a few mmHg.

Cardiac function curve. This is the Frank-Starling curve. As RAP (standing in for preload) rises, CO climbs steeply and then levels off. Contractility and afterload set its height.

Venous return curve. Venous return = (MSFP − RAP) ÷ resistance to venous return. A rising RAP shrinks the gradient, so venous return falls in a straight line and reaches zero when RAP equals MSFP. Below an RAP of about 0 mmHg the great veins collapse where they enter the thorax, and the curve levels off.

Mean systemic filling pressure

Definition. Mean systemic filling pressure (MSFP) is the pressure that would exist everywhere in the circulation if the heart stopped and all pressures equalized. It is about 7 mmHg and is the x-intercept of the venous return curve.

Stressed volume. MSFP reflects the stressed volume (blood that stretches vessel walls) divided by vascular compliance. Most of that compliance is venous, because veins are very distensible and hold about two-thirds of the blood. Venoconstriction turns unstressed volume into stressed volume, so MSFP rises even though no blood is added.

~7 mmHgmean systemic filling pressure

~2/3of the blood volume is held in the veins

~5 L/minresting CO at the normal intersection

MSFP up (curve shifts right): transfusion or IV fluid, renal salt and water retention (RAAS, ADH), sympathetic venoconstriction, skeletal muscle pump.
MSFP down (curve shifts left): hemorrhage, dehydration, venodilators such as nitrates, loss of sympathetic venous tone.

What moves each curve

Volume shifts the venous curve. A change in MSFP moves the venous return curve in parallel: the slope stays the same and the intercept moves. A right shift gives a higher CO and a higher RAP. A left shift gives a lower CO and a lower RAP.

Resistance rotates it. A change in TPR alters the slope, but the intercept stays where it is because MSFP does not depend on arteriolar tone. A lower TPR rotates the curve clockwise and makes it steeper; examples are exercising muscle, an AV fistula and hydralazine. A higher TPR rotates it counterclockwise and makes it flatter. TPR is also afterload, so the cardiac curve moves the same way: up when TPR falls and down when it rises. The result is a change in CO while RAP stays about the same.

Contractility raises or lowers the cardiac curve. Positive inotropes shift it up, giving a higher CO and a lower RAP; examples are sympathetic β1 stimulation, digoxin and dobutamine. Negative inotropy shifts it down, giving a lower CO and a higher RAP; causes include systolic HF, myocardium lost to MI, β-blockers and verapamil.

Primary changes and the new operating point

Change	Curve that moves	How it moves	CO	RAP
↑Volume or venoconstriction	Venous return	Parallel right shift (↑MSFP)	↑	↑
Hemorrhage or venodilation	Venous return	Parallel left shift (↓MSFP)	↓	↓
↓TPR (arteriolar dilation, AV fistula)	Both	Venous curve steeper (clockwise); cardiac curve up	↑	≈
↑TPR (arteriolar constriction)	Both	Venous curve flatter (counterclockwise); cardiac curve down	↓	≈
Positive inotrope	Cardiac function	Upward shift	↑	↓
Negative inotropy or HF	Cardiac function	Downward shift	↓	↑

Rule of thumb: volume moves CO and RAP in the same direction, inotropy moves them in opposite directions, and TPR changes CO while RAP stays about constant.

Combined changes and exam traps

Exercise. Sympathetic drive increases contractility and heart rate, which lifts the cardiac curve. Venoconstriction and the muscle pump raise MSFP, which shifts the venous curve right. Metabolic arteriolar dilation lowers TPR, which makes the venous curve steeper. CO rises several-fold and RAP barely changes.

Heart failure with fluid retention. The cardiac curve drops, so CO falls and RAP rises. Poor renal perfusion activates RAAS and ADH. The retained salt and water raise MSFP and shift the venous curve right. CO partly recovers along the flattened curve, but RAP climbs even higher, causing JVD, edema and congestion. Diuretics lower MSFP and RAP. CO falls only a little because the failing heart is working on the flat part of its curve.

Hemorrhage. Lower MSFP shifts the venous curve left, so both CO and RAP fall. Baroreflex venoconstriction partly restores MSFP and stronger contraction lifts the cardiac curve, bringing CO back toward normal.

Vasodilators. Hydralazine dilates arterioles. It lowers TPR and afterload, so CO rises. Nitroglycerin dilates veins. It lowers MSFP, which reduces RAP and preload and relieves congestion; in a normal heart CO dips slightly. Nitroprusside dilates both arterioles and veins. An AV fistula first acts as a fall in TPR and creates a high-output state. Over time the fistula also expands blood volume, which adds a right shift.

If the x-intercept moved, MSFP changed (volume or venous tone). If only the slope changed, TPR changed. If the cardiac curve moved alone, contractility changed. The classic distractor shifts the venous curve for a resistance change or rotates it for a transfusion.