1) Relates input (RAP) to output (CO)

2) Converts 1D length-tension curve into 3D- geometry serves as an amplifier: volume≈length³

3)Law of Laplace: tension controls muscle length

T≈P  T≈r  T≈1/H

1) End diastolic volume: atrial pressure=preload, when atrial and ventricular pressures are equal you get EDV and EDP: EDV vc EDP gives you  the ventricular diastolic pressure curve

2) End Systolic volume: arterial/aortic pressure=afterload,

3) Isovolumetric (Isometric) Systolic Pressure Curve: maximum isovolumetric pressure to EDV (Frank-Starling)

Combine diastolic and systolic curves to determine the amount of shortening/SV

↑preload=↑SV  ↓preload=↓SV

↑afterload=↓SV  ↓afterload=↑SV

↑contractility=↑SV  ↓contractility=↓SV

Compensatory changes to return SV towards normal in response to a change in EDV (preload), afterload, or contractility

Basis for compensation is a shift in blood volume between arterial and venous circulation, thereby altering preload and SV.  Compensation operates over several beats and is incomplete. (decreased contractility or increased afterload=increased preload)

Heart-lung prep: contractility, TPR, and HR are kept constant, afterload is allowed to vary as a function of flow (CO)

Because TPR is constant, increased SV causes an increased aortic pressure flow=ΔP/TPR

Curve is multiple PV loops connected

Steepest part of curve is between RAP=0 and 4, plateau at ≥7

the heart has transmural pressure

the intrapleural space has negative pressure, but pressures are measured relative to atmospheric pressure (0)

So, the heart still fills with blood when RAP is 0

1) The increased afterload offsets the increased preload.  We know the afterload increases for two reasons.  First, if TPR is constant and we know SV is increased by increased preload then afterload must also increase.  Second, the force-velocity relationship tells us a high EDV (preload) means the blood will be ejected faster and therefore increase afterload.

2) Pericardium is inelastic and limits the EDV.

1) Increased contractility increases both SV and CO (steeper slope and higher plateau), decreased contractility decreases both SV and CO (less steep and lower)

2) Increased TPR decreases SV and CO (less steep and lower), decreased TPR increases SV and CO (steeper and higher)

Under the condition used to obtain the cardiac function curve CO maxes out at a HR of 125.  So, increasing HR up to that point increases CO, but further increases cause a less than optimal curve.

A normal person continues ot improve function up to about 175 because we ↓TPR and ↑contractility to accomadate HR.

Atrial contraction plays a much bigger role in tachycardia than resting HR

The time for diastolic filling is inversely proportional to HR