Heart as a Pump (it up) Flashcards Preview

CVPR Unit 1 > Heart as a Pump (it up) > Flashcards

Flashcards in Heart as a Pump (it up) Deck (35):
1

Cardiac Output (CO) Definition and Equation

Volume of blood pumped per minute by left ventricle. CO = Stroke Volume (SV) * Heart Rate (HR). or CO = arterial pressure ÷ total peripheral resistance

2

CO is mainly affected by....?

Heart Rate. The HR can increase by a large percentage than SV can which causes larger increases in CO.

3

Stroke Volume Determinants and their effects

Afterload- Negative
Preload- Positive
Contractility (Inotropy)- Positive

4

Two factors that affect contraction strength

1) Length-Dependent intrinsic mechanism (Frank-Starling)
2) Length-Independent mechanism (Inotropy) - regulated via sympathetic nervous system stimulation

5

Edema results from....?

Unequal cardiac output from both sides of the heart.

6

Define Diastole

The atrium is full of oxygenated blood which is signaled to contract by the SA node. As the atrium contracts, the atrial pressure increases which opens the mitral valve and allows blood to fill the left ventricle.

7

Define Isovolumetric Expansion

As the left ventricle begins to contract, the mitral valve immediately closes as the pressure begins to rise. The pressure continues to rise with both valves closed as the ventricle contracts until the pressure in the ventricle is greater than that in the Aorta. It is at this point that the aortic valve opens and ejection begins.

8

Define Ejection Phase

Once the pressure in the left ventricle exceeds that of the aortic pressure, the aortic valve open and ejection occurs. Contraction continues to occur until the max systolic blood pressure at which point the ventricle begins to relax and pressure drops until it is below that of the aortic pressure and the aortic valve closes again.

9

Define Isovolumetric Relaxation

Once the aortic valve is closed, the pressure continues to fall rapidly while both valves are closed. The pressure will fall below that of the atrium and the mitral valve will open once again and this marks the end of isovolumetric relaxation.

10

Explain Pressure-Volume Graphs

The graph presents the end-diastolic and systolic pressures for a range of blood volumes. The systolic is the pressure at maximum ventricular contraction and the end-diastolic is the pressure of the ventricle full of that specific volume of blood. The difference between the two lines is the active tension.

11

Define a Starling Curve

It is a plot of cardiac performance as a function of preload. It is also based on the difference of the systolic and diastolic PV curves. All healthy hearts function on the ascending limb of the curve and ONLY hearts that are failing function in the descending portion.

12

End Diastolic Pressure-Volume Relationship (EDPVR) is determined by...?

The elastic properties of the ventricle. This is known as compliance which is defined as C = deltaV / deltaP, however, EDPVR plot is the inverse of C. The EDPVR represents the PRELOAD on the heart.

13

Define Preload

The length to which a muscle is stretched before shortening. For left ventricle, preload ~ end diastolic volume.

14

Define Afterload

The load against which a muscle contracts.
For left ventricle, afterload ~ aortic pressure.

15

Define Active Tension

Difference in force between peak systolic pressure and end diastolic pressure curves

16

Three ways to state Starling's Law

a) Heart responds to an increase in EDV by increasing the force of contraction.
b) Healthy heart always functions on the ascending limb of the ventricular function curve
c) What goes in, must come out. Cardiac output MUST equal venous return and cardiac output from left and right ventricles MUST match (on average).

17

Molecular basis for Starling’s law

a) Cardiac titin isoform is very stiff, resists stretch.
b) Ca2+ sensitivity of myofilaments increases as sarcomeres are stretched. So the same intracellular Ca2+ produces a greater force of contraction.
c) Closer lattice spacing – stretched sarcomeres have altered spacing between actin & myosin which results in more force generated per crossbridge.

18

Bainbridge Reflex

Stretch sinus node → increase in heart rate

19

Filling Phase (PV Loop Diagram)

A to C

20

Isovolumetric Contraction (PV Loop Diagram)

C to D

21

Ejection Phase (PV Loop Diagram)

D to F

22

Isovolumetric Relaxation (PV Loop Diagram)

F to A

23

What point is the diastolic blood pressure?

D

24

What point is the systolic blood pressure?

E

25

What two sets of lines define the stroke volume?

C to D minus F to A (or C minus A)

26

Point E minus Point D is what value?

Pulse Pressure!

27

Stroke Volume equals?

EDV - ESV

28

Ejection Fraction equals?

EF = SV/EDV or (EDV-ESV) / EDV

29

Stroke work is?

Energy per beat (joules) that corresponds to the integral of the PV loop diagram. NOT the same for both sides of the heart.

30

Factors that affect preload

o Blood volume (IV fluid, hemorrhage)
o filling pressure (venous blood pressure)
o filling time (reduced at high heart rates)
o resistance to filling (e.g. AV valve stenosis)
o resistance to emptying = afterload (e.g. hypertension)
o reduced inotropy (contractility)

31

Compliance volume to pressure relationship? Slope?

Increased compliance causes a decreased pressure for any given volume. This causes a decreased slope. The reverse is also true for decreased compliance.

32

Causes of increased and decreased compliance?

Decreased- Hypertrophy or diastolic heart failure
Increased- Dilated cardiomyopathy

33

Increased EDV (preload) results in what?

Immediate effect is an increase in stroke volume via Starling's Law. Ventricle matches increased EDV with increased stroke volume. Subsequent beats = SV returns to normal.

34

Increased Afterload results in what?

Decrease in SV on the next beat. (EDV unchanged, EF decreased, ESV increased and SV decreased). SV recovers on next beat due to the increased ESV with constant venous return means increased EDV → increased SV

35

Increased Inotropy results in what?

Results in a new Starling Curve. Increased systolic pressure at any given volume, increased stroke volume and ejection fraction and a decrease in end systolic volume. These effects last as long as the inotropy remains high.