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NROSCI/BIOSC 1070 & MSNBIO 2070

Determinants of Cardiac Output 2

September 18, 2013

cardiac function curve

During the last lecture, we considered the vascular function curve, which shows right atrial pressure as cardiac output is manipulated. Now we will look at the effects of manipulating right atrial pressure on cardiac output. In essence, this approach measures the effects of changing preload on cardiac output and blood pressure, and produces the cardiac function curve.

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In the experiments we will be discussing, cardiac contractile state and heart rate are maintained constant, as is arterial pressure (afterload).

The cardiac function curve is illustrated to the left.

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When right atrial pressure is low, cardiac output is 0, Drag picture to picture since there Drag is too littleto placeholder or in the placeholder blood cardiac or click icon to add click icon to add chambers to generate pressure during systole.

When right atrial pressure increases above ~4 mm Hg, cardiac output is maximum. This is because this right atrial pressure causes maximal filling of the ventricle (more on this later).

These cardiac function curves show the effect of increasing heart rate on cardiac output.

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Drag picture to increases Drag picture to Modest in heart placeholder or placeholder or rate facilitate cardiac click icon to add click icon to add

output, despite a shorter ventricular filling time, due to the Bowditch effect.

However, large increases in heart rate shorten filling time so much that cardiac output plummets.

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The cardiac output produced by a particular right atrial pressure is altered if the ventricle is hypereffective or hypoeffective. Drag picture to Drag picture to

placeholder or placeholder or A hypereffective ventricle click icon to add click icon to add

is present when sympathetic activity is high, or the ventricle is hypertrophied. In addition, the ventricle is hypereffective when afterload is low. A hypoeffective ventricle is present when there is no sympathetic stimulation, the ventricle is damaged, or

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The vascular function and cardiac function curves are plotted on the same axes in the diagram on the left. Drag picture to Drag picture to

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intersect at one point, called the equilibrium point. This point indicates the cardiac output, venous return, and right atrial pressure under this particular physiological condition.

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In the graph, point A shows the normal equilibrium point, when right atrial pressure is Drag picture to Drag picture to 0 and cardiac placeholder near or placeholder or output click andicon venous click icon to add to add return are near 5 L/min.

The dashed line indicates the effect of increasing blood The vascular function curve shifts but the cardiac volume by 20%. function curve doesnt. Note that Psf increases to about 16 mm Hg, right atrial pressure is near 8 mm Hg, and cardiac output is ~13 L/min.

Under most conditions, both the cardiac output and vascular function curves shift during a manipulation. For example, sympathetic nervous system activity causes the cardiac function curve to shift upwards and a bit to the left, while the vascular function curve shifts

The following effects are produced by the sympathetic nervous system: Increased cardiac contractility Increased heart rate Decreased venous compliance

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Increased total peripheral resistance. sympathetic stimulation, and this opposes a shift in the vascular function curve. Consequently, . cardiac output Note that afterload just rises to 10 L/min during sympathetic stimulation. increases during
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During exercise, the shift in the venous return curve is considerably different than during sympathetic stimulation. WHY?

Afterload decreases as arterioles in skeletal muscle dilate. Skeletal muscle pumping contributes to an increase in venous return. Cumulatively, these factors in addition to the actions of the sympathetic nervous system cause cardiac output to increase to ~20 L/min.

Using the Pressure Volume Relationship to Understand

We have already considered the functional pressurevolume curve, which shows the relationship between left ventricular volume and pressure

The functional pressure-volume curve shows what happens during one cardiac cycle. This is part of a larger relationship between left ventricular pressure and left ventricular volume, which predicts cardiac parameters under extreme conditions. The functional pressure-volume curve is shown in the area labeled by EW in the curve above (EW stands for external work).

The diastolic pressure curve shows the pressure pressure generated in the ventricle just before contraction occurs.

This curve is sometimes called the End Diastolic Pressure-Volume Relationship or EDPVR As the ventricle becomes overstretched, pressure increases tremendously as additional volume is added. Note that ventricular filling stops when diastolic

E D P V R

The End Systolic Pressure-Volume Relationship or ESPVR shows the pressure generated in the ventricle during contraction with different filling volumes.

Note that the curve is linear until the filling volume exceeds ~150 ml At very high filling volumes, the actin and myosin filaments of the cardiac muscle fibers are pulled apart far enough that the strength of each cardiac fiber contraction becomes less than optimal.

ES PV R

Experimental Generation of PRESSUREVOLUME CURVES

Pressure-volume curves can be measured experimentally in humans or animals. By overlapping curves generated during a variety of cardiac cycles, often while manipulating variables such as preload and afterload, a comprehensive analysis is possible.

End-Systolic Pressure-Volume Relationship (ESPVR)

VOLUME

A line is drawn connectin g the upper left corner of each

PRESSURE

ES PV R

VOLUME

The upper left corner of each curve demarks aortic valve closure, which occurs when aortic pressure is near mean arterial pressure. Hence, the

PRESSURE

ES PV R

End-Systolic Pressure-Volume Relationship (ESPVR) INCREASED

CONTRACTILITY

VOLUME

Increased contractility results in more pressure being generated at a particular endNORMAL diastolic volume.

PRESSURE

Effects of INCREASED CONTRACTILITY ON CARDIAC OUTPUT

An increase in contractility has a complex effect on cardiac output. This is because mean arterial pressure (and thus afterload) increases along with the

SV
PRESSURE

SV
VOLUME

If afterload increases, then pressure must rise higher before the aortic valve opens, and the valve shuts again sooner. As a consequence, stroke volume drops appreciably.

SV
PRESSURE

SV SV
VOLUME

The decrease in stroke volume with increased afterload can be offset if the slope of the ESPVR becomes steeper (i.e., contractility increases). Although the increase in contractility can preserve stroke volume, it comes at the cost of increased energy expenditure.

SV
VOLUME

As noted above, ventricular filling during diastole is limited by two major factors: 1. Filling time 2. Pressure developed in the ventricle during filling. This is due to the fluid volume pressing against the chamber wall EDPVR

PRESSURE

ES PV R

SV SV
VOLUME

In general, the ventricle will fill until the pressure in the chamber = atrial pressure. Hence, an increase in preload will result in higher atrial pressure, and thus more ventricular filling. EDPVR

PRESSURE

ES PV R

Factors that INCREASE PRELOAD INCLUDE:

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Decreased venous compliance (venoconstriction) Decreased resistance to venous return (RVR) Increased blood volume Negative intrathoracic pressure Decreased heart rate Decreased ventricular stiffness Supine posture Increased skeletal muscle pumping

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Why does cardiac output drop so much after a heart attack?

After a heart attack, muscle tissue dies and is replaced by scar tissue, that is not very elastic. This condition results in the EDPVR curve shifting upwards. As a result, pressure inside the ventricle increases quickly as fluid enters the chamber. Consequently, enddiastolic volume and stroke volume decrease.

Why does cardiac output drop so much after a heart attack?

In addition, ventricular contractility decreases (the slope of the ESPVR becomes less steep). These two factors result in a huge loss of stroke volume and cardiac output.

The area encompassed by the pressure-volume loop is defined as external work or stroke work, or the work performed by the ventricle to eject the stroke volume into the aorta. Stroke work can be estimated by the product of stroke volume and mean aortic pressure: SW = SV * MAP. In the graph to the left, the stroke work is the area labeled EW.

The graph also indicates the area that represents potential energy (PE). Potential energy is defined as the energy stored as a result of deformation of an elastic object. In the heart, the potential energy is the energy absorbed by the ventricular wall that does not result in a change in the pressure of the fluid in the chamber.

The term pressure-volume area (PVA) refers to the sum of potential energy and external work.

Correlations between cardiac work and Oxygen demand

There is a highly linear correlation between PVA and cardiac oxygen consumption per beat. This estimation of myocardial oxygen consumption (MVO2) is used to study the coupling of mechanical work and the energy requirement of the heart. MVO2 is also used in the calculation of cardiac efficiency, which is the ratio of cardiac stroke work to MVO2: Cardiac Efficiency = SW/MVO2