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CARDIAC PUMP
dr. Sri Lestari Sulistyo Rini, MSc
Phases of the Cardiac Cycle
Figure 20–16
8 Steps in the Cardiac Cycle
1. Atrial systole:
–
–
atrial contraction begins
right and left AV valves are open
2. Atria eject blood into ventricles:
–
filling ventricles
3. Atrial systole ends:
–
–
–
AV valves close
ventricles contain maximum volume
end-diastolic volume (EDV)
4. Ventricular systole:
–
–
–
isovolemic ventricular contraction
pressure in ventricles rises
AV valves shut
8 Steps in the Cardiac Cycle
5. Ventricular ejection:
– semilunar valves open
– blood flows into pulmonary and aortic
trunks
•
Stroke volume (SV) = 60% of enddiastolic volume
6. Ventricular pressure falls:
– semilunar valves close
– ventricles contain end-systolic volume
(ESV), about 40% of end-diastolic volume
8 Steps in the Cardiac Cycle
7. Ventricular diastole:
– ventricular pressure is higher than atrial
pressure
– all heart valves are closed
– ventricles relax (isovolumetric relaxation)
8. Atrial pressure is higher than ventricular
pressure:
–
–
–
–
AV valves open
passive atrial filling
passive ventricular filling
cardiac cycle ends
3 Factors that Affect ESV
1. Preload:
– ventricular stretching during diastole
2. Contractility:
– force produced during contraction, at a given
preload
3. Afterload:
– tension the ventricle produces to open the
semilunar valve and eject blood
1. Preload
• The degree of ventricular stretching during
ventricular diastole
• Directly proportional to EDV
• Affects ability of muscle cells to produce
tension
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 FrankStarling mechanism.
• With the extra delivery of blood, the cardiac
muscle contracts with greater force because
of improved actin/myosin interaction.
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.
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
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
Factors Affecting Heart
Rate and Stroke Volume
Autonomic nervous
system:
sympathetic and
parasympath
etic
Circulating hormones
Venous return and
stretch receptors
Figure 20–24
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.
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
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 )
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
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
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
Afterload is better defined
in relation to ventricular wall stress
• LaPlace’s Law
Wall Stress
Wall Stress
Pr

h
P
r
h
Afterload
• Is increased by any factor that restricts
arterial blood flow
• As afterload increases, stroke volume
decreases
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
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
Nerve,Temperature
Ion, Hormon
Sinus Node
conducting
Tissues
Generation
Of impulse
synergistic
spread of
ventricular
mass
Number of activated
Sarcomeres
contractility
coronary
diastolic
diameter pressure
availability
of activator
Ca2+
O2
supply
anatomy blood
venous
volume
diameter
forward
movement
of blood
mitochondrial
metabolism
venous
return
filling
valves
compliance
arteriolar
of vasculature diameter (v.c)
depulsation
impedance
end diastolic pressure
metabolites
mass of contracting
myofibrils
ATP production
geometry
ventricular
dimension
FS
mechanism
Heart rate
preload
total load
Stroke Volume
Cardiac output
arterial pressure
Kinetic energy
pressure generation
External work of the heart
afterload
systemic
resistance
Factors Involved in Regulation of Cardiac Output
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.
Work Output of the Heart
 Understand how the
systolic and diastolic
pressure curves are
derived.
 By combining the end
diastolic and systolic
curves, the volumepressure diagram can
be defined.
 The area inside the
VP diagram is the EW.
• 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.
• 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.
Left Ventricular Pressure Volume Loop
Left
Ventricular
Pressure
120
SV
(mmHg)
6
EDV
ESV
70
130
Volume
(ml)
Effects of an Increase in Preload on Left
Ventricular Pressure Volume Loop
Ejection Pressure
Left
Ventricular
Pressure
120
SV
(mmHg)
EDV
6
70
130
Volume
(ml)
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.
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
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.
VENTRICULAR COMPLIANCE
PRELOAD EFFECTS
Effects of an Increase in Afterload on Left
Ventricular Pressure Volume Loop
Left
Ventricular
Pressure
120
d SV
(mmHg)
6
40
140
Volume
(ml)
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