Cardiac Function Curves

Edward Omron MD, MPH, FCCP

Pulmonary and Critical Care Service

Objectives

• Understand the Starling Curve

• Understand the Pressure Volume Curve

• 25 year old man presents to the ER in Shock

– BP 60/30, HR 150 bpm– Paleness– Cool Skin– Dilated Pupils– Semicomatose state– Low Urine Output

Starling Curve

Pressure Volume Curve

The Cardiac Output Curve relates cardiac output to right atrial pressure - The right atrial pressure (RAP) is a measure of RV end-diastolic fiber stretch or RV end-diastolic volume (Preload). It is the downstream end of the pressure gradient that drives venous return. - Knowledge of both the cardiac output / venous return curves are essential to determine the effects of an intervention or event on cardiac output and RAP

How does this relate to CVP as an indexOf preload?

The Normal Cardiac Output Curve - At any given point in time we operate only at one point on the two curves - Normal C.O. = 5L/min - Normal R.A.P. = 0 - Normal Mean Systemic Filling Pressure = 7 mm Hg (PMS) (pressure at which the venous return curve intersects the RAP at C.O. = 0) - The slope of venous return curve is the normal resistance to venous return - (PMS) acts as the hinge upon which the venous return curve rotates -- Clockwise for decreased resistance -- Counterclockwise for increased resistance

Effects of Interventions: Cardiac Output Curve - Must figure out how the intervention will affect both the cardiac output curve and the venous return curve at the same time

- FIRST: does the intervention cause the cardiac output curve to become: hyperdynamic, hypodynamic, or no effect?

1. Change in sympathetic tone2. Inotropic Agent3. Myocardial Infarct4. Septic Cardiomyopathy5. Valvular Heart Disease6 . Pericardial Effusion

Effects of Interventions: Venous Return Curve - Changes in PMS (Mean Systemic Pressure) - What happens to blood volume in relation to venous capacitance? -PMS is the hinge upon which the venous return curve rotates - Increase in blood volume increases PMS and moves the hinge to the right (Transfusion) - Decrease in blood volume decrease PMS (constant capacitance) and moves the hinge to the left (Hemorrhage)

Effects of Interventions: Venous Return Curve

- Increased sympathetic tone moves the hinge to the right (exercise) - Decreased sympathetic tone moves the hinge to the left (analgesia/anxiolysis)- Increased venous capacitance (venodilation) moves the hinge to the left (sepsis, cirrhosis, anaphylaxis via dysregulated NO synthase activity, NTP)- Decreased venous capacitance (venoconstriction )moves the hinge to the right (Epinephrine, Norepinephrine) - If the intervention does not change blood volume or capacitance then no change in PMS- graphically, where is the “hinge” and how does it change?

Effects of Interventions: Venous Return Curve - Resistance to venous return determines the slope of the venous return curve - After an intervention, the new PMS acts as a hinge upon which the venous return curve rotates clockwise or counterclockwise - A decrease in resistance, clockwise - An increase in resistance, counterclockwise

Decrease Rvr

Increase Rvr

- Resistance to venous return changes only when intervention changes total peripheral resistance -Vasodilation decreases Rvr, rotates clockwise (NTG) -Vasoconstriction (sympathetic tone, phenylephrine increases Rvr, rotates counterclockwise -Anemia decreases viscosity and decreases resistance, clockwise -Active venodilation and venoconstriction provides a rapid compensation for cardiovascular homeostasis

Mean systemic pressure is increased by an  increase in blood volume and/or a decrease in venous compliance (as shown below).  This will act to shift the vascular function curve to the right, illustrating an increase in both cardiac output and right atrial pressure.  Conversely, mean systemic pressure is decreased by a decrease in blood volume and/or an increase in venous compliance (not shown).  This will shift the vascular function curve to the left, illustrating a decrease in both C.O. and right atrial pressure.

Stroke VolumeCardiac OutputCardiac Index

Ventricular Preload or End diastolic Volume

preload-dependencepreload-dependence

preload-independencepreload-independence

The lower the ventricular preload, The lower the ventricular preload, the more likely the preload-dependency the more likely the preload-dependency

Starling Curve

Volume Responsive

Volume Unresponsive

Preload Augmentations/p fluid bolus

Preload RESPONSIVE

RVEDV or LVEDV

Stroke Volume

Normal

Abnormal (Cardiogenic or septic shock)

50 mL 100 mL 150 mL 200 mL

Preload Augmentations/p fluid bolus

Preload UNRESPONSIVE

RVEDV or LVEDV

Stroke Volume

Normal

Abnormal (Cardiogenic or septic shock)

50 mL 100 mL 150 mL 200 mL

.

Stroke volume

Ventricular preload

normal heart normal heart

failing heart failing heart

preload-dependencepreload-dependence

preload-independencepreload-independence

Starling Curve

Positive inotropic agents, such as digoxin, will increase contractility and therefore increase the cardiac output (as shown below).  This new equilibrium point now reflects an increased cardiac output and a lower right atrial pressure (more blood is now being ejected from the heart with each beat).Negative inotropic agents have the opposite effect, decreasing contractility and cardiac output, and increasing right atrial pressure (not shown).

An increase in TPR (shown above) will cause blood to be retained on the arterial side of circulation and will increase the aortic pressure against which the heart must pump.  This will act to shift both slopes downward.  As a result of this simultaneous change, both the cardiac output and the venous return are decreased, however the right atrial pressure remains the same .  A decrease in TPR (not shown) will allow more blood to flow to the venous side of circulation and will lower the aortic pressure against which the heart must pump.  This will shift both slopes upward.  Both cardiac output and venous return will be simultaneously increased; again, right atrial pressure will remain the same .         

NTG/ Beriberi/AV Fistula/Anemia Transfusion/ Fluid Bolus NTG+Trans

Phenylephrine/ PP ventilation Hypovolemia/ Sympath

Effects of Epinephrine on venous return curve

Effects of Epinephrine on Venous Return and Cardiac Output Curves

FIGURE 1  Time sequence of events during a single cardiac cycle. Pressures (P) in the aorta, left ventricle (LV), and left atrium (LA) are shown. The four phases of the cardiac cycle are also illustrated:isovolumic contraction (A), ejection (B), isovolumic relaxation (C), and filling (D). ECG = electrocardiogram; LVV = left ventricular volume.

FIGURE 50-3 The similar relationship between muscle length and force in isolated muscle and in the intact ventricle. A, Isolated muscle. When stretched from the slack length (the length at which no force is generated), both diastolic and systolic forces increase and result in the end-diastolic force-length relationship (EDFLR) and the end-systolic force-length relationship (ESFLR). The ESFLR increases much more steeply than the EDFLR does, so the force developed (difference between the two curves, indicated by the arrows) increases as the muscle is stretched. Pharmacologic agents that acutely increase contractile strength (contractility) have little effect on the EDFLR, but the ESFLR increases and consequently the force developed at any given length increases. B, The intact ventricle. Contractile properties are characterized by end-diastolic and end-systolic pressure-volume relationships (EDPVR and ESPVR). The slack length in muscle corresponds with V0, the volume at which no pressure is generated. The ESPVR is nearly linear and characterized by a slope, Ees, that varies in relation to contractility. The pressure-volume loop sits within the boundaries defined by the EDPVR and ESPVR. The four phases of the cardiac cycle are indicated by isovolumic contraction (A), ejection (B), isovolumic relaxation (C), and filling (D). DBP = diastolic aortic blood pressure; EDP = end-diastolic pressure; EDV = end-diastolic volume; ESV = end-systolic volume; LAP = left atrial pressure; SBP = peak systolic blood pressure; SV = stroke volume. 

The LV pressure-volume relationship during diastole(The End Diastolic Pressure Volume Relationship)

The slope of this curve is the ventricular elastance “Stiffness”The elastance increases at large end-diastolic volumes or becomes “stiffer”LVEDV < 140 mL, the ventricle is easy to fillLVEDV > 140 mL, the ventricle is harder to fillThe increase in pressure impedes additional filling

The Pressure Volume Loop of the Left Ventricle

Filling

IsovolemicContraction

Ejection

Isovolemic Relaxation

End Diastole

End Systole

The Effect of Increased Preload On LV Pressure Volume Loop

The Effect of Increased Afterload on LV Pressure Volume Loop

The Effect of Increased Contractility on LV Pressure Volume Loop

What Does the Area Within the Pressure Volume Loop Represent

Pressure x Volume = WorkPressure Volume Area (PVA) = Stroke Work (SW) + Potential Energy (PE)The area inside the loop represents external work performed by the LVfor that particular cycleThe total PVA is linearly related to myocardial oxygen consumption

Myocardial Infarction

• 25 year old man presents to the ER in Shock

– BP 60/30, HR 150 bpm– Paleness– Cool Skin– Dilated Pupils– Semicomatose state– Low Urine Output

Two Possible Causes of the Low Blood Pressure were Considered

• Inadequate Cardiac Output– Myocardial Infarction, Tamponade,

myocarditis,

• Severe internal blood loss

• What pressure measurement would distinguish between the two diagnosis?

Right Atrial PressureBlood Loss, Decreased Filling PressureHeart Failure, Increased Filling Pressure

Further examination confirmed that the problem was blood lossCardiac function was normal

Explain the Physical Findings– BP 60/30

• Hypovolemia, incomplete compensation

– Paleness• Peripheral vasoconstriction

– Cool Skin• Peripheral vasoconstriction

– Dilated Pupils• Sympathetic activation

– Semicomatose state• Hypotension and decreased CPP

– Low Urine Output• Renal compensation for hypovolemia

Starling Curve

Pressure Volume Curve

Final Points

• Resuscitation should be guided by 4 hemodynamic variables– Afterload– Preload– Mean Systemic Filling Pressure– Resistance to venous return