Lecture Note 2 - Cardiovascular Physiology

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Transcript Lecture Note 2 - Cardiovascular Physiology

Cardiovascular Physiology
Definition of terms
 Cardiac cycle - Refers to the events of one complete heartbeat
during which both atria and ventricles contract and then relax.
 Systole - The time period when the heart contracting.
 Diastole - The time period when the heart in the state of relaxation.
 Systolic Pressure - Peak pressure in the arteries when ventricles
contract.
 Diastolic Pressure - Lowest pressure in the arteries when
ventricles relax.
 End-systolic Volume – Volume of blood in the left ventricle at the
end of contraction.
 End-diastolic Volume – Volume of blood in the left ventricle at the
end of filling.
Cardiovascular Physiology
Cardiovascular Physiology
Stroke Volume
 Volume of blood pumped by the heart in one contraction
SV = EDV – ESV
Where SV - stroke volume
EDV - end-diastolic volume
ESV - end-systolic volume
Stroke volume usually consider only volume of blood
pumped from the left side of the heart because that is
the amount of blood sent to all the tissues of our body.
Cardiovascular Physiology
 Stroke Volume can increase during exercise.
 Stroke volume depends on preload, afterload and
contractility.
Preload
 The pressure stretching the ventricular walls prior to
contraction.
 Depends on ventricular filling and venous return i.e.
return of blood back to the heart.
Afterload
 Pressure the ventricle must generate to eject blood into
aorta.
 Depends on arterial pressure
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Contractility (Inotropy)
 Force that muscle can create at given length.
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Cardiac Output
 Amount of blood in liter per minute pumped by the heart
particularly the left ventricle.
CO = SV x HR
Where CO – cardiac output (L/min)
SV – stroke volume (L)
HR – heart beat rate (beat/min)
Normal cardiac output is 5.0 L/min.
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Ejection Fraction
 Fraction of blood ejected by ventricle relative to enddiastolic volume
EF = (SV / EDV) x 100%
Normal EF is usually greater than 60%.
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Cardiac Cycle
 Events that occur in one heart beat.
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Atrial Contraction
 Semilunar valves close, AV valves open.
 Pressure within the atrial chambers increases, which forces
remaining blood in the chambers flow across the open
atrioventricular (AV) valves.
Isovolumetric Contraction
 All valves close.
 Pressure within ventricles increases.
Ventricular Ejection
 Semilunar valves open, AV valves close.
 Intraventricular pressure higher than pressure in large arteries.
 Semilunar valves forced to open, blood rushes out from ventricle.
Isovolumetric Relaxation
 All valves close.
 Intraventricular pressure falls causes all valves to close.
Cardiovascular Physiology
Ventricular Filling
 Semilunar valve close, AV valve open.
 Intraventricular pressure falls below arterial pressure.
 Blood flow through the atria into the ventricles.
 Intraventricular pressure continues to briefly fall because the
ventricles are still undergoing relaxation.
 Once the ventricles are completely relaxed, their pressures will
slowly rise as they fill with blood from the atria.
Cardiovascular Physiology
 Pressure-Volume Relationship
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 The P-V plot shown here is for left ventricle (LV)
 a, b, c and d indicate phases in cardiac cycle
- a : ventricular filling
- b : isovolumteric contraction
- c : ejection
- d : isovolumetric relaxation
 Point 1 : end-diastolic pressure (EDP) and end-diastolic
volume (EDV).
 Point 2 : LVP exceeds aortic diastolic pressure, the aortic valve
opens, ejection phase begins.
 Point 3 : aortic valve closes, ventricle relaxes isovolumetrically.
 Point 4 : LVP falls below left atrial pressure mitral valve opens,
ventricle begins to fill.
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


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ESV – end-systolic volume.
EDV – end-diastolic volume.
ESPVR – end-systolic pressure-volume relationship
EDPVR – end-diastolic pressure-volume relationship
SV – stroke volume
Stroke Work (SW)
 Work done by the ventricle to eject a volume of blood (i.e., stroke
volume) into the aorta.
 Basically SW is the area inside the P-V plot.
 Another term is Cardiac Work which is simply product of SW and
heart rate.
Cardiac Work = Stroke Work x Heart Rate
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Cardiovascular Physiology
HEMODYNAMICS
 The study of blood flow and blood pressure.
 Hemodynamics is essential to understand cardiovascular
dynamics system.
 Some basic relationships :
F = ΔP/R
Where F – blood flow (unit : ml/s)
Δ P – pressure difference along vessel (unit : mmHg)
R – resistance to flow (if it is not steady and change
with time we call it impedance) (unit mmHg/ml/s)
Cardiovascular Physiology
 To apply the concept in heart, suppose we know aortic
and intraventricular pressure ventricular ejection. To find
flow of blood :
F = (PIv - Pao)/R
 Factors that influence resistance to flow :
 - length and diameter of vessel
 - viscosity of blood
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VESSEL TYPE
Aorta
DIAMETER (mm)
25
FUNCTION
Pulse dampening and distribution
Large Arteries
1.0 - 4.0
Distribution of arterial blood
Small Arteries
0.2 - 1.0
Distribution and resistance
Arterioles
0.01 - 0.20
Capillaries
0.006 - 0.010
Venules
Veins
Vena Cava
0.01 - 0.20
0.2 - 5.0
35
Resistance (pressure & flow regulation)
Exchange
Exchange, collection, and capacitance
Capacitance function (blood volume)
Collection of venous blood
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VASCULAR COMPLIANCE
 ability of a blood vessel wall to expand with changes in
pressure.
C = ΔV/ΔP
C – vessel compliance
ΔV – change in blood volume
ΔP – change in pressure
 Reciprocal of compliance is elastance.
 What is the relationship between blood flow and volume?
Frank-Starling Mechanism
 The change of heart’s force of contraction in response to change in
venous return.
 During exercise, venous return i.e. blood that returns to the heart
increased which then causes increase to stroke volume.
 Frank-Starling mechanism tells how change in venous return will
alters the stroke volume.
 Increased venous return increases the ventricular filling (enddiastolic volume) and therefore preload, which is the initial stretching
of the cardiac myocytes prior to contraction. Myocyte stretching
causes an increase in force generation. This mechanism enables
the heart to eject the additional venous return, thereby increasing
stroke volume.
Frank-Starling Mechanism
Frank-Starling Mechanism