2.4.2 Myocardial Performance Flashcards
Peak ventricular systolic pressure?
maximal pressure achieved during ejection
What is reduced in ventricular hypertrophy? What is a common cause?
Ventricular compliance (increased contractility w/ decreased filling)
Common cause: chronic systemic HTN
What would you expect to be altered in ventricular hypertrophy that isn’t altered by SYM firing?
Diastolic filling curve
Both affect the contractility
On Starling’s curve, stroke volume will increase as EDV increases up to a point. Then, the SV will decrease as EDV continues to increase. Why is this?
This is due to overstretching which causes the overlap of thick and thin filaments to become suboptimal.
What is the equation for SV?
EDV - ESV
Describe how decreased inotropic state would change a P-V loop.
Same aortic DP
Same EDV
Decreased contractile force
Decreased SV (increased ESV)
Reduced ejection fraction (EF)
Where do the components of an EKG and heart sounds match up to points on a pressure-volume loop?
What is the difference b/t the ionotropic reserve and Starling reserve?
Starling reserve: maximal increase in SV that can be achieved by increasing EDV
Inotropic reserve: the extent that increased contractility can raise SV
B
How do changes in inotropic state alter the Starling curve?
Increased inotropy: upward shift of curve
Decreased inotropy: downward shift of curve
What are some ways that TPR is decreased due to systemic ateriolar dilation (altered afterload)?
- Vasodilator administration
- Anaphylactic shock
What is true about intracellular calcium contrations at all points along a single Starling curve?
It is the same at all points
The area within the P-V loop represents what?
Stroke work
How can parasympathetic innervation of the heart affect CO?
Decrease HR by decreasing # of sodium funny channels
B
How can sympathetic innervation of the heart change CO?
- Increase HR (increase sodium funny channels)
- Increase preload (increases SV)
- Increase afterload (decreases SV)
- Increase inotropic state (increases SV)
Summarize the effects that changes in inotropy, afterload, HR, and venous return can have on the Starling curve.
Describe how decreased afterload would affect a P-V loop.
Same inotropic state
Same EDV
Decreased aortic DP
Decreased systolic pressure
Increased SV (decreased ESV)
What does inotropic state refer to?
The force of contraction (contractility)
What is a third way to alter afterload despite no change in TPR?
Aortic stenosis
C
A
What are the two main determinants of preload?
- Filling Time (HR)
- Rate of venous return (venous tone, blood volume, gravity)
What are some measures or variables related to preload?
EDV
Venous return
End-diastolic pressure
What is afterload?
Defined as ventricular wall tension during ejection. It is the resistance that must be overcome to eject blood.
Describe the process in which venous pressure is increased in both types of heart failure (systolic and diastolic dysfunction)
What are some of the indices of afterload?
Aortic diastolic pressure (when aorta opens) or aortic systolic pressure
What are the two reasons that ventricular filling is impaired in diastolic dysfunction?
Increased stiffness of the ventricular wall
Reduced ventricular relaxation during diastole
What are some ways to decrease inotropy? (4)
- Decrease SYM firing
- Beta antagonist
- Ca Channel blocker
- Heart failure
What is preload?
Defined as stretch on the myocardial fibers before contraction
Related to ventricular filling
What is represented by the isovolumic curve?
Maximal pressure that can be developed at any ventricular volume (same shape as the Starling curve)
What might be responsible for the shifts from 1 to 3 and 1 to 2 along the starling curve?
1 to 3: Increased HR or decreased venous return
1 to 2: Decreased HR or increased venous return
What are the three key components seen in a P-V loop due to L ventricular systolic dysfunction?
The P0 curve is shifted downwards
Same passive filling curve
Increased EDV
Distinguish b/t preload and afterload.
Preload: ventricular filling which occurs prior to contraction
Afterload: force the ventricle has to overcome during ejection, so it involves factors after ventricular contraction begins
How do skeletal muscle and cardiac muscle differ in regards to their inotropic state?
Skeletal muscle: cytosolic Ca++ levels are supramaximal during contraction
Cardiac muscle: cytosolic Ca++ levels are subramaximal for cross-bridge activation (Thus, altering Ca++ levels in contracting myocytes will result in formation of more cross bridges and increased contractile force)
What are some ways that TPR is increased due to systemic ateriolar constriction (altered afterload)?
- Administer a vasocontrictor
- Some forms of HTN (chronic)
What are two ways that force of contraction is enhanced?
Sympathetic nerves and cardiac glycosides (these block Na/K ATPase causing the sodium/calcium exchanger to pump Na out while pumping in Ca causing increased contractility)
Describe how increased inotropic state would change a P-V loop.
Same aortic DP
Same EDV
Increased contractile force
Increased SV (decreased ESV)
Increased SP
If aortic DP was increased (everthing else remains the same), how would the ejection rate change?
The ejection rate would decrease b/ there would be a smaller difference in P0 - DP
What two curves are used to to contruct a pressure-volume loop?
End-systolic pressure volume curve, Po, and Diastolic filling curve
aka isovolumic and filling curves, respectively
D
What differentiates systolic dysfunction from diastolic dysfunction
Systolic dysfunction decreases EF compared to normal
What is the ventricular end-diastolic pressure?
Pressure at the end of filling at the time that the QRS complex occurs
Decribe how increased preload would change P-V loop.
Same inotropic state
Same aortic diastolic pressure
Increased EDV
Increased systolic pressure
Increased SV
Draw out a pressure-volume loop and label its key elements.
Describe how diastolic dysfunction would alter a P-V loop.
Where is edema located in each of the forms of heart failure? (R and L)
R: edema in the systemic organs
L: pulmonary edema due to increased pulmonary venous pressure
Describe how decreased preload would change a P-V loop.
Same inotropic state
Same aortic DP
Decreased sytolic pressure
Decreaed EDV
Decreased SV
What are some ways to increase inotropy?
- SYM nerve firing
- Beta agonist
- Cardiac glycoside
What can used to determine the rate of ejection?
P0 - Aortic DP
Why is looking at a starling curve in terms of SV versus EDV limiting as compared to stroke work versus EDV?
In a SV v. EDV curve, increased inotropy cannot be distinguished from decreased afterload.
The stoke work versus EDV curve is unaffected by afterload, so it can distinguish b/t an inotropic change and a change in afterload.
Why does contractile force increase at greater preloads?
The stretch results in more favorable overlap of thin and thick filaments.
What does Starling’s Law of the heart state?
Stoke volume increases when preload is increased.
D
Describe how increased afterload would change a P-V loop.
Same inotropic state
Same EDV
Increased Aortic DP
Decreased SV (increased end-systolic volume)
Describe how ventricular hypertrophy would change a P-V loop.
Increase inotropy
Increase aortic DP
Decrease EDV
Increase EDP
How do changes in inotrophy shift a Starling curve that is based off stroke work verses EDV?
It is the same as looking at SV vs. EDV
How do changes in afterload affect the Starling curve?
Decreased afterload: Shift Starling curve up (increased SV)
Increased afterload: Shift Starling curve downward (decreased SV)
