4 - Ventricular Function

Question 1

Left Ventricular Pressure-Volume Loop: What parameters can be calculated?

Equations (or explanations)

Answer 1

Stroke Volume (SV): Amount of blood ejected

End Diastolic Volume (EDV) - End Systolic Volume (ESV)

Ejection Fraction (EF): % of end-diastolic volume ejected during systole

EF = SV / EDV x 100% (normal > 55%)

Question 2

Ejection Fraction (EF) Changes?

High, Normal, Low Values?

Answer 2

Direct relationship w/Contractility

Clinical Index for evaluating inotropic state of heart

- - -

Exercise = 90%

Normal = 55%

Heart Failure = 20%

Question 3

End Diastolic Pressure-Volume Relationship (EDPVR)

Answer 3

Relationship vetween Pressure and Volume in the Ventricle at the moment the ventricle is completely relaxed (End Diastole)

Descrives the passive filling curve of the ventricle depends on the passive properties of myocardium (stiffness of the heart)

Question 4

Definitions:

Compliance of Heart (C)

Elastance of Heart

Answer 4

The distensibility

recriprical of Compliance; stiffness

Question 5

Equation for Compliance (C) of heart?

Answer 5

The radio of a change in volume divided by a change in pressure

RUN / RISE

C = ΔV/ΔP

**Remember, the reciprocal is Elastance or stiffness of the heart; this is calculated RISE/RUN**

Question 6

What does Compliance measure?

Answer 6

Intrinsic property of Ventricle wall

Reflects the relative each which ventricle can fill with blood

Question 7

Clinical: Cardiac Hypertrophy (and Compliance)

Answer 7

Increased thickness of the ventricle decreases ventricular compliance

Heart will have smaller end-diastolic volume and given end-diastolic pressure than a normal heart

Question 8

Clincial: What can increase compliance in the heart? End Diastolic Pressure?

Answer 8

Dilation of Heart

Decreased EDP

Question 9

End Systolic Pressure-Volume Relationship (ESPVR)

What is this an index of?

Answer 9

Hypothetical suspension of heart at maximum activation and assessment of changes in pressure in respone to changes in pressure

Plot will (straight line) will be the ESPVR, upper left corner of pressure volume loop (end of systole) falls on ESPVR

- - -

Index of Myocardial Contractility, slope will shift with contractility

Question 10

What will happen to the ESPVR slope if contractility is increased or decreased?

How is ESPVR affected to changes in preload, afterload, or heart rate?

Answer 10

Increase = Left Shift (steeper)

Decrease = Right Shift (flatter)

Relatively insensitive to changes, so PV Loop should not cross over ESPVR when ventricular volume changes (e.g. more blood, less blood, change in HR, etc.)

Question 11

What graphical representation is a good method for visualizing ventricular performance?

What factors impact this assessment?

How are these changes related?

Answer 11

Pressure Volume (PV) Loop

Affected by preload, afterload, contractility

Under normal conditions, these are interdependent, e.g if you increase preload, you will further stretch myocardial tissue (contractility) thus increasing the afterload (arterial pressure)

Question 12

If you hold arterial pressure (afterload) and contractility constant, what variable are you measuring?

What is a good index of this situation?

What is the end result?

What will be the resultant change to end product of heart contraction?

Answer 12

Increased preload or increase in venous return

Produce a PV loop with higher end diastolic volume (EDV) and pressure

Thus, LVEDV and LVEDP are good indices of preload

Greater stretch from increased preload (more venous filling) results in increased stroke volume

Question 13

If you hold preload (venous filling or end diastolic volume) and contractility constant, what does an increase in afterload result it?

What is the result on the aortic pressure?

Answer 13

LV PV Loop with reduced stroke volume (you have put less blood in, stretching heart less, you get less blood out!)

Aortic pressure is increased, so the aortic valve (top right corner) opens at a higher pressure, and closes at higher pressure–there is greater blood in the left ventricle at end of systole

Question 14

What is the resulting PV loop if preload is increased while holding contractility constant? How is this hypothetically accomplished?

Answer 14

Arterial pressure will rise (preload increased)

Afterload increases from preload, less blood is being ejected

However–the two have competing stages, stroke volume is increased, but not as much as preload alone

This is hypothetically accomplished by increasing venous return

Question 15

What is the resulting PV loop if contractility is held constant and afterload is increased? (e.g. preload is allowed to adjust)

What is the clinical implication in this?

Answer 15

Blood will remain (stroke volume is reduced) and subsequent contraction will have increased stroke volume

Clinical: Decrease in stroke volume is offset, heart can easily adjust to transitory changes in blood pressure

Question 16

How does a PV loop change when contractility is increased and preload/afterload are held constant?

What is the affect on the mitral and aortic valves?

What is the effect on stroke volume?

Answer 16

ESPVR slope will become steeper, left portion of loop will shift left, right will remain unchanged

The ventricle will generate more pressure at any given preload

The mitral valve closes at the same P/V

The aortic valve opens at the same P/V

Stroke Volume is increased

Question 17

Frank Starling Curves

How is ventricular function often assessed?

How is preload often assessed?

Answer 17

Ventricular Function curves which relate preload and ventricular function

Ventricular Function: Stroke Volume , Cardiac Output (SV*HR)

Preload: End-Diastolic Volume, End Diastolic Pressure, Right Atrial Pressure`

Question 18

According to Frank Starling Curves, what does an increase of ventricular muscle result in?

Answer 18

An increase in end-diastolic volume, which induces a more forceful contraction, causing more blood to be ejected

Question 19

How do the following factors affect preload?

Total Blood Volume

Venous Tone

Atrial Contraction

Intrathoraci Pressure

Body Position

Skeletal Muscle Pump

Intrapercardia Pressure

Answer 19

Total Blood Volume: Direct relationship, increase = increas preload, decrease = decrease preload (dehydration, hemorrhage)

Venous Tone: Alter amount of blood stored in veins

Atrial Contraction: During exercise, atrial kick can increase preload (amount of blood entering ventricle)

Intrathoracic Pressure: Inspiration increases pressure gradient at RA, expiration decreases P gradiatent for return at RA–net effect is increase venous return (you breath heavy during exercise, increase SV)

Body Position: Standing = decrease, blood is fighting gravity

Skeletal Muscle Pump: More movement pushes more blood to heart via squeezing blood past one way valves

Intrapercardia Pressure: Pressure outside of heart can limit filling, decreasing preload thus decreasing SV

Question 20

How will contractility and afterload affect the Ventricular Performance curves?

Answer 20

Increase contractility will shift up, decrease shift down

Decrease in afterload will increase curve

Increase in afterload will decrease curve

***Your plotting stroke volume vs end diastolic volume or pressure, so your stroke volume will be decreased if afterload is increased and vise versa

Question 21

What is the most important physiological regulator of contractility of cardiac muscle?

What is their effect?

Answer 21

Circulating Catecholamines and sympathetic stimulation

Enhance contractility

Norepinephrine and epinephrin increase intracellular Ca²⁺

Question 22

What factors can affect inotropy on ventricular function curves?

Inotropic Drugs

Damaged Myocardium

Cardium Ischemia and Acidosis

B-Blockers / Calcium Channel Blockers

Answer 22

Inotropic Drugs - Digitalis, decrease Na+ gradient, intracellular Ca²⁺ levels stay elevated

Damaged Myocardium - Less forceful contraction produced, decrease SV

Cardium Ischemia and Acidosis - Decrease contractility, decrease SV

B-Blockers / Calcium Channel Blockers - Reduce contractility, decrease HR (thus SV)

Question 23

How do the following factors affect afterload?

Vascular Resistance

Decreased compliance of ventricles/great vessels

Semilunar Valve Stenosis

Angiotensin-Converting Enzyme Inhibitor

Answer 23

Vascular Resistance - major determinant, small muscular arteries and arterioles are major resistance, if pathologic, can decrease SV abnormally

Decreased compliance of ventricles/great vessels - Increase afterload, Impedes ejection of blood, decreases SV

Semilunar Valve Stenosis - Increased afterload, decreased SV

Angiotensin-Converting Enzyme Inhibitor - Reduce afterload, reduce SV

Question 24

How does an increase in HR affect SV?

So when you exercise, why do you not die?

Answer 24

As heart rate increases, less time spent in diastole

Less time available for ventricular filling

Mechanisms in place to counter this!

1. Sympathetic Stimulation - Atrial Kick increase, increase ventricular contractility
2. Venous return increase from skeletal muscle pump/respiration gradient
3. Enhanced venous constriction
4. Lusitropy - increase in cardiac muscle relaxation; Phospholambin in SERCA increases rat of myocardial relaxation