1. dr. Sri Lestari Sulistyo Rini, MSc
CARDIAC PUMP
dr. Sri Lestari Sulistyo Rini, MSc

2. Phases of the Cardiac Cycle
Figure 20–16

3. 8 Steps in the Cardiac Cycle
Atrial systole:
atrial contraction begins
right and left AV valves are open
Atria eject blood into ventricles:
filling ventricles
Atrial systole ends:
AV valves close
ventricles contain maximum volume
end-diastolic volume (EDV)
Ventricular systole:
isovolemic ventricular contraction
pressure in ventricles rises
AV valves shut

4. 8 Steps in the Cardiac Cycle
Ventricular ejection:
semilunar valves open
blood flows into pulmonary and aortic trunks
Stroke volume (SV) = 60% of end-diastolic volume
Ventricular pressure falls:
semilunar valves close
ventricles contain end-systolic volume (ESV), about 40% of end-diastolic volume

5. cardiac cycle

6. 8 Steps in the Cardiac Cycle
Ventricular diastole:
ventricular pressure is higher than atrial pressure
all heart valves are closed
ventricles relax (isovolumetric relaxation)
Atrial pressure is higher than ventricular pressure:
AV valves open
passive atrial filling
passive ventricular filling
cardiac cycle ends

7. 3 Factors that Affect ESV
Preload:
ventricular stretching during diastole
Contractility:
force produced during contraction, at a given preload
Afterload:
tension the ventricle produces to open the semilunar valve and eject blood

8. 1. Preload
The degree of ventricular stretching during ventricular diastole
Directly proportional to EDV
Affects ability of muscle cells to produce tension

9. Frank-Starling Mechanism
The amount of blood pumped by the heart is determined by the rate of blood flow from the veins (venous return).
The intrinsic ability of the heart to adapt to increasing volumes of blood is the Frank-Starling mechanism.
With the extra delivery of blood, the cardiac muscle contracts with greater force because of improved actin/myosin interaction.

10. Frank-Starling Mechanism
Allows the heart to readily adapt to changes in venous return.
The Frank-Starling Mechanism plays an important role in balancing the output of the 2 ventricles.
In summary: Increasing venous return and ventricular preload leads to an increase in stroke volume.

11. Stroke Volume Cont., Preload
The degree of ventricular stretch at end-diastole
The Frank-Starling Law of the Heart
 Preload =  Contractility (to a point)
Factors Affecting Preload
Circulating volume
Body positioning
Atrial systole
Medications
Diuretics (i.e. Lasix)
ACE Inhibitors
I.V. Fluids
Starling Curve

12. Physical Limits Ventricular expansion is limited by:
myocardial connective tissue
the fibrous skeleton
the pericardial sac
End-Systolic Volume (ESV)
The amount of blood that remains in the ventricle at the end of ventricular systole is the ESV

13. Factors Affecting Heart Rate and Stroke Volume
Autonomic nervous system:
sympathetic and parasympathetic
Circulating hormones
Venous return and stretch receptors
Figure 20–24

16. 2. Contractility
The inherent capacity of the myocardium to contract independently of changes in afterload or preload.
Changes in contractility are caused by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length.
Alternate name is inotropy.

17. Contractility Force of contraction
Increased rate and/or quantity of Calcium delivered to myofilaments during contraction
Heart functions at lower end-systolic volume and lower end-diastolic volume

18. Stroke Volume Cont., Contractility Positive inotropic agents
 Force of contraction
Negative inotropic agents
 Force of contraction
Factors that affect contractility
Autonomic nervous system (ANS)
Medications:
Digoxin (Lanoxin)
Beta-adrenergic blockers (i.e. metoprolol )
Calcium channel blockers (i.e. verapamil )

19. Contractility is affected by: autonomic activity & hormones :
Sympathetic stimulation:
NE released by postganglionic fibers of cardiac nerves
epinephrine and NE released by adrenal medullae
causes ventricles to contract with more force
increases ejection fraction and decreases ESV
Parasympathetic activity:
acetylcholine released by vagus nerves
reduces force of cardiac contractions

20. Hormones and Contractility
Many hormones affect heart contraction
Pharmaceutical drugs mimic hormone actions:
stimulate or block beta receptors
affect calcium ions e.g., calcium channel blockers

21. 3. Afterload
More precisely defined in terms of ventricular wall stress:
LaPlace’s Law: Wall stress = Pr/h
P = ventricular pressure
R = ventricular radius
h = wall thickness

22. Afterload is better defined in relation to ventricular wall stress
LaPlace’s Law
Wall Stress
Wall Stress P r h

23. Afterload
Is increased by any factor that restricts arterial blood flow
As afterload increases, stroke volume decreases

24. Stroke Volume Cont., Afterload
Resistance to ventricular ejection during systole
Factors that affect afterload
Outflow impedance
Left side
High systemic blood pressures (SVR)
Aortic valve stenosis
Right side
High pulmonary blood pressures (PVR)
Pulmonary valve stenosis
Diameter of arterial vessels
Blood characteristics
Medications:
ACE (angiotension converting enzyme) inhibitors

25. EDV, Preload, and Stroke Volume
At rest:
EDV is low
myocardium stretches less
stroke volume is low
With exercise:
EDV increases
myocardium stretches more
stroke volume increases
As EDV increases, stroke volume increases

27. Factors Involved in Regulation of Cardiac Output

28. STROKE WORK
Stroke work (SW) refers to the work done by the ventricle to eject a volume of blood (i.e., stroke volume) into the aorta. 
Stroke work is sometimes used to assess ventricular function.
Cardiac work is the product of stroke work and heart rate, which is the equivalent of the triple produce of stroke volume, mean aortic pressure and heart rate.
Analyze the stroke work using Left Ventricular Pressure Volume Loop
To generate a PV loop for the left ventricle, the left ventricular pressure (LVP) is plotted against left ventricular (LV) volume at multiple time points during a complete cardiac cycle. 

29. Work Output of the Heart
Understand how the systolic and diastolic pressure curves are derived.
By combining the end diastolic and systolic curves, the volume-pressure diagram can be defined.
The area inside the VP diagram is the EW.

30. Ventricular Function Curve
The dependancy of stroke volume on preload was described more than 100 years ago by Otto Frank and E.H. Starling and since then has been called the Frank-Starling mechanism. Using this relationship between preload and stroke volume or stroke work, a ventricular function curve can be consructed by plotting stroke work at various levels of preload.

32. Point 1 on the PV loop is the pressure and volume at the end of ventricular filling (diastole), and therefore represents the end-diastolic pressure and end-diastolic volume (EDV) for the ventricle.
As the ventricle begins to contract isovolumetrically (phase b), the LVP increases but the LV volume remains the same, therefore resulting in a vertical line (all valves are closed).
Once LVP exceeds aortic diastolic pressure, the aortic valve opens (point 2) and ejection (phase c) begins.
When the aortic valve closes (point 3), ejection ceases and the ventricle relaxes isovolumetrically - that is, the LVP falls but the LV volume remains unchanged, therefore the line is vertical (all valves are closed). The LV volume at this time is the end-systolic (i.e., residual) volume (ESV).
When the LVP falls below left atrial pressure, the mitral valve opens (point 4) and the ventricle begins to fill.
The width of the loop represents the difference between EDV and ESV, which is by definition the stroke volume (SV).
The area within the loop is the ventricular stroke work.

33. Left Ventricular Pressure Volume Loop
120
Left Ventricular Pressure
(mmHg) SV 6
ESV
EDV 70
130
Volume (ml)

34. Left Ventricular Pressure
Effects of an Increase in Preload on Left Ventricular Pressure Volume Loop
Ejection Pressure
120
Left Ventricular Pressure
(mmHg) SV
EDV 6 70
130
Volume (ml)

35. VENTRICULAR COMPLIANCE
As the ventricle fills with blood, the pressure and volume that result from filling are determined by the compliance of the ventricle.
Is determined by the physical properties of the cardiac muscle and other tissues making up the ventricular wall as well as by the state of ventricular contraction and relaxation.

36. VENTRICULAR COMPLIANCE
in ventricular hypertrophy the ventricular compliance is decreased
ventricular end-diastolic pressure (EDP) is higher at any given end-diastolic volume (EDV) (see Figure).
in some forms of heart failure, ventricular relaxation is impaired
at a given EDP, a less compliant ventricle would have a smaller EDV

37. In a disease state such as dilated cardiomyopathy, the ventricle becomes very dilated without appreciable thickening of the wall.
This dilated ventricle will have increased compliance as shown in the figure; therefore, although the EDV may be very high, the EDP may not be greatly elevated.

38. VENTRICULAR COMPLIANCE

39. PRELOAD EFFECTS

40. Left Ventricular Pressure
Effects of an Increase in Afterload on Left Ventricular Pressure Volume Loop
Left Ventricular Pressure
(mmHg)
120
d SV 6 40
140
Volume (ml)

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