4 - Ventricular Function Flashcards
Left Ventricular Pressure-Volume Loop: What parameters can be calculated?
Equations (or explanations)
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%)
Ejection Fraction (EF) Changes?
High, Normal, Low Values?
Direct relationship w/Contractility
Clinical Index for evaluating inotropic state of heart
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Exercise = 90%
Normal = 55%
Heart Failure = 20%
End Diastolic Pressure-Volume Relationship (EDPVR)
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)
Definitions:
Compliance of Heart (C)
Elastance of Heart
The distensibility
recriprical of Compliance; stiffness
Equation for Compliance (C) of heart?
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**
What does Compliance measure?
Intrinsic property of Ventricle wall
Reflects the relative each which ventricle can fill with blood
Clinical: Cardiac Hypertrophy (and Compliance)
Increased thickness of the ventricle decreases ventricular compliance
Heart will have smaller end-diastolic volume and given end-diastolic pressure than a normal heart
Clincial: What can increase compliance in the heart? End Diastolic Pressure?
Dilation of Heart
Decreased EDP
End Systolic Pressure-Volume Relationship (ESPVR)
What is this an index of?
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
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Index of Myocardial Contractility, slope will shift with contractility
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?
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.)
What graphical representation is a good method for visualizing ventricular performance?
What factors impact this assessment?
How are these changes related?
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)
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?
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
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?
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
What is the resulting PV loop if preload is increased while holding contractility constant? How is this hypothetically accomplished?
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
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?
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
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?
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
Frank Starling Curves
How is ventricular function often assessed?
How is preload often assessed?
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`
According to Frank Starling Curves, what does an increase of ventricular muscle result in?
An increase in end-diastolic volume, which induces a more forceful contraction, causing more blood to be ejected
How do the following factors affect preload?
Total Blood Volume
Venous Tone
Atrial Contraction
Intrathoraci Pressure
Body Position
Skeletal Muscle Pump
Intrapercardia Pressure
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
How will contractility and afterload affect the Ventricular Performance curves?
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
What is the most important physiological regulator of contractility of cardiac muscle?
What is their effect?
Circulating Catecholamines and sympathetic stimulation
Enhance contractility
Norepinephrine and epinephrin increase intracellular Ca2+
What factors can affect inotropy on ventricular function curves?
Inotropic Drugs
Damaged Myocardium
Cardium Ischemia and Acidosis
B-Blockers / Calcium Channel Blockers
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)
How do the following factors affect afterload?
Vascular Resistance
Decreased compliance of ventricles/great vessels
Semilunar Valve Stenosis
Angiotensin-Converting Enzyme Inhibitor
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
How does an increase in HR affect SV?
So when you exercise, why do you not die?
As heart rate increases, less time spent in diastole
Less time available for ventricular filling
Mechanisms in place to counter this!
- Sympathetic Stimulation - Atrial Kick increase, increase ventricular contractility
- Venous return increase from skeletal muscle pump/respiration gradient
- Enhanced venous constriction
- Lusitropy - increase in cardiac muscle relaxation; Phospholambin in SERCA increases rat of myocardial relaxation
