Download Physiology of cardiovascular system L5 Dr.Abdul

Physiology of cardiovascular system
Dr.Abdul-Aziz Ahmed
L5
The cardiac cycle
The cardiac cycle is described as the repetitive electrical and mechanical events
that occur with each beat of the heart. Each cardiac cycle has two phases: diastole,
the time during which cardiac muscle relaxes and ventricles fill with blood, and
systole, the time during which the cardiac muscle contracts and blood ejected by
ventricles. The duration of cardiac cycle a heart rate of 75 beat/min is about 0. 8
second, 0.5 second for diastole and 0. 0.3 second for systole. The long duration of
diatsole has two important physiologic and clinical implications.
 most of ventricular muscle perfusion occur during diastole.
 ventricular filling occur during diastole.
when heart increase the duration of both phases decrease but the major decrease
occur in diastole.
phases of cardiac cycle
The main phases of cardiac cycle are:
1. Filling Phase
2.Atrial Systole
3. Isovolumetric Contraction Phase
4. Rapid Ejection Phase
5. Reduced Ejection Phase
6. Isovolumetric Relaxation Phase
1.Filling Phase
ventricular pressure decreases below atrial, the A-V valves open and filling occurs
rapidly (rapid filling phase), the elastic recoil of the ventricle may aid in drawing
blood into the ventricle .As the ventricle fills intraventricular pressure increases
slowing the rate of filling(reduced filling phase) or diastasis. At large volumes, and
with ventricles with low compliance, the rapid reduction of filling at the end of this
phase may produce the third heart sound. About 70% of ventricular filling occur
in this phase.
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2.Atrial Systole
The sinoatrial pacemaker complex initiates excitation, which spreads across the
atria and is recognised in the ECG as the P-wave atrial contraction follows
increasing the pressure within both atria this increase in the RA pressure gives the
a-wave of the Jugular Venous pulse, or CVP trace. Atrial systole, force a small
extra amount of blood into the ventricles. atrial contraction is normally not
necessary for ventricular filling, however, at high heart rates diastasis is
abbreviated and the atrial contribution may be important similarly, in disease
states of the A-V valves, atrial contraction is important. NB: With reduced
ventricular compliance, atrial contraction may give rise to a fourth heart sound.
3.Isovolumetric Contraction Phase
Excitation of the ventricles occurs as the wave of excitation passes through the AV
node, bundle of His and Purkinje system. Ventricular contraction coinciding with
the peak of the R-wave of the ECG, in response to contraction of the muscle, the
ventricular pressure rises very rapidly this is not true isometric contraction, as
some fibers lengthen and others shorten as the ventricle changes shape. the
increasing intraventricular pressure lead to closure of the mitral and tricuspid
valves, producing the first heart sound. the rapid rise in ventricular pressure is
transmitted across the semilunar valves and appears as a small rise in the aortic
pressure trace.
figure1: ventricular pressure and volume curve.
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4.Rapid Ejection Phase
The intraventricular pressure rises rapidly until it exceeds the pressure in the great
arteries (aorta and pulmonary), leading to opening of
the outflow
(Aortic/Pulmonary) valves. There is then a rapid ejection period, where both
intraventricular and arterial pressure rise to a maximum. Because of the high
ventricular pressure, unless the papillary muscles perfectly compensate, there ,is a
tendency for the A-V valves to bulge into the atria producing the av-wave of the
JVP. Immediately after this the atrial pressure fall due to the descent of the base of
the heart and stretching of the atria, producing the x descent of the JVP. This
reduced atrial pressure aids the return of blood from the periphery.
5.Reduced Ejection Phase
both the contractile forces and the pressure within the ventricles are decreasing
during this phase and are less than those within the aorta by several mmHg .flow
continues due to the momentum of the bolus of blood into the aorta. This phase
coinciding with the Repolarisation of the myocardium occurs during ( T-wave of
the ECG). The ventricular pressure is decreasing very rapidly and there is reversal of
flow toward the heart, closing the valves and generating the second second heart
sound. The sudden increase in back-resistance to flow increases aortic pressure
giving rise to the incisura, or dicrotic notch in the aortic pressure trace .
6.Isovolumetric Relaxation Phase
both valve sets are closed, so pressure drops very rapidly as there is "no" change in
volume as this is occurring atrial pressure is increasing to its maximum, due to the:
1. movement of blood from the periphery
2. movement of the base of the heart back to its resting position ® v-wave of the
JVP
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Figure2: cardiac cycle
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Synchrony of Contraction
1.LV is first to start contraction and the last to start to fill. RV contraction lags due
to the anatomy of the conducting system by ~ 15 ms. The pulmonary valve opens
first, and pulmonary flow begins around 10 ms before aortic due to the lower
pressure in the pulmonary circuit
2. The isovolumetric period for the LV ~ 40 ms and RV ~ 15 ms
3. Because of higher systemic pressure LV outflow ends first with the total LVET
being shorter that the RVET
4. the mitral valve opens after the tricuspid due to the greater time for ventricular
pressure to drop below atrial pressure.
heart sounds and Murmurs
Normally, there are two audible heart sounds. The first (“lub”) is associated with
closure of the AV valves. The second (“dup”) is associated with closure of the
semilunar valves. Two additional heart sounds can be recorded :
 The third heart sound(S3), is a soft, low-pitched sound heard about one-third
of the way through diastole. It coincides with the period of rapid ventricular filling
and is probably due to vibrations set up by the inrush of blood. The third heart
sound is normal in children but is not heard in normal adults; in middle-aged or
older adults, the presence of S3 indicates volume overload, as in congestive heart
failure or advanced mitral or tricuspid regurgitation.

The fourth heart sound(S4),the fourth sound can sometimes be heard
immediately before the first sound. The sound is caused by the atrium contracting
against, and trying to fill, a stiffened ventricle. The fourth heart sound (S4) is not
audible in normal adults, it may be heard in ventricular hypertrophy, where
ventricular compliance is decreased.
Other abnormal heart sounds include clicking, caused by abnormal movement of
one of the valves, and murmurs, caused by the “whoosh” of blood leaking through
an incompletely closed or excessively narrowed (stenotic) valve. Murmurs due to
valve lesions may be heard during systole and called systolic murmur or heard
during diastole and called diastolic murmur:
 aortic or pulmonary stenosis causes systolic murmur.
 mitral or tricuspid insufficiency causes systolic murmur.
 Aortic or pulmonary insufficiency causes diastolic murmur.
 mitral or tricuspid stenosis causes diastolic murmur.
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Pressure-volume loops
Figure 3 shows the cardiac cycle of the left ventricle, represented by plotting
pressure against volume to produce a loop. At point A, the ventricle contains the
end-systolic blood volume, and the mitral valve opens. The ventricle fills until enddiastolic volume is achieved at point B, where the mitral valve is closed by the
onset of ventricular contraction. Isovolumic contraction increases pressure to
point C, which corresponds to diastolic blood pressure and opening of the aortic
valve. Ventricular ejection propels pressure through its peak value at point D,
corresponding to aortic systolic pressure, until the aortic valve closes at point E.
Pressure decreases back to point A during isovolumic relaxation, completing one
cardiac cycle. The width of the pressure-volume loop is the stroke volume (the
difference between end-diastolic volume and end-systolic volume).
Figure3:left ventricle pressure-volume loops
.
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Left atrial pressure
Left atrial pressure normally is no greater than 10 mm Hg at any time during the
cardiac cycle. Three small peaks, or waves, are identified as atrial pressure curve
and denoted as a, c, and v. The a wave is produced by atrial systole. The c wave
occurs when the mitral valve bulges into the left atrium during ventricular
contraction. The v wave reflects passive atrial filling during ventricular systole.
Figure4: atrial pressure waves.
Length-tension relationship in cardiac muscle
The maximal tension that can be developed by a myocardial cell depends on its
resting length. In myocardial cells, maximal tension development occurs at
sarcomeres lengths of about 2.2 μm, this length is called Lmax. The possible causes
of increase tension at Lmax muscle length are
1. increases the degree of overlap of thick and thin filaments.
2. increases troponin C sensitivity to Ca2+-.
3.increases Ca2+ release from the sarcoplasmic reticulum.
The relation between the initial length of the muscle fibers and the developed
force is given by Starling’s law of the heart, which states that, within limits, the
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force of ventricular contraction depends on the end-diastolic length of the cardiac
muscle; in the intact heart the latter relates closely to the ventricular end-diastolic
volume. The volume present at the end of diastole, in turn, depends on the
volume returned to the heart, or the venous return. Therefore, stroke volume and
cardiac output correlate directly with end-diastolic volume, which correlates with
venous return. The Frank-Starling relationship governs normal ventricular function
and ensures that the volume the heart ejects in systole equals the volume it
receives in venous return. Or, stated another way: Within physiologic limits, the
heart pumps all the blood that returns to it by the way of the veins. However,
when the returning blood does become more than the physiological limit of the
pumping capacity of the ,or when the pumping capacity of the heart is reduced
due to disease of the heart (heart failure), under such condition the heart
becomes the limiting factor that determines cardiac output.
Figure: Length-force relationships in the intact heart: A ventricular function curve is
the rise in ventricular performance as preload increases (Frank-Starling curve).
Cardiac output (CO)
The cardiovascular system consists of two pumps (left and right ventricles) and
two circuits (pulmonary and systemic) connected in series. Cardiac output (CO) is
the amount of blood pumped out by either the left or right ventricle, in 1 minute,
and because the left and right pump are connected in series, they CO are equal in
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both side. It is the product of heart rate (HR) and stroke volume (SV). The normal
value in adult is about 5 L/min. It is more in males than females.
CO = HR X SV
Using normal resting values for heart rate (75 beats/min) and stroke volume (70
ml/beat), the average adult cardiac output can be computed
CO= 75 X70 = 5250 ml/min
End diastolic volume
End diastolic volume (EDV), the amount of blood that collects in a ventricle during
diastole and just before contraction. It is normally about 120 ml.
End systolic volume
End systolic volume (ESV), the volume of blood remaining in a ventricle after it has
contracted. It is approximately 50 ml.
Stroke volume is defined as the volume of blood pumped out by one ventricle with
each beat. it is about 70 ml.
SV = EDV - ESV
SV= 120 - 50 = 70 ml.
Cardiac index
The adequacy of cardiac output should be considered in relation to tissue
metabolic demand, which varies by body size and activity. Therefore, cardiac
output is expressed relative to the body surface area (BSA) as the cardiac index
(CI):
CI = QT /BSA
Where:
CI = Cardiac index (L/min/m2)
QT = Cardiac output (L/min)
BSA = Body surface area (m2)
Example : A 24-year-old woman is found to have a resting cardiac output of 4.0
L/min. Her body surface area is 1.40 m2, determine her CI:
CI = 4.0 / 1.40 = 2.86 L/min/m2
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Measurement of cardiac output
Fick Principle , derived by Adolph Fick, a German physiologist, in 1870
Fick Principle, stated that the amount of O2 consumed by any organ = the A-V
[O2] difference x blood-flow. Therefore, pulmonary blood-flow, or CO, is equal to
the body O2-uptake divided by the arterial/mixed venous [O2] difference:
Factors controlling cardiac output
Cardiac output is The product of heart rate or stroke volume. Accordingly the
factors which effect heart rate or stroke volume will play important role in
controlling cardiac output.
I. Heart rate
Local factors such as temperature and tissue stretch can affect the discharge rate of
the SA node, however, under normal conditions the principal control of heart rate
is via the autonomic nervous system (ANS). Normal adults at rest HR ~ 70 bpm
during sleep the rate reduces by ~ 10-20 bpm, in well trained athletes the resting
HR may be 50-60 bpm. The SA node is usually under tonic influence of both
divisions of the ANS changes in rate being effected by reciprocal changes of tone in
both in normal adult at rest PNS tone is dominant over SNS with both divisions
blocked by drugs the intrinsic heart rate ~ 100 bpm. Although the heart rate is
controlled primarily by the cardiac innervation, sympathetic stimulation increasing
the rate and parasympathetic stimulation decreasing it, heart rate can also be
influenced by other factors:
 Hormones, epinephrine and norepinephrine released from the adrenal
medullae during exercise and stress increase both heart rate and contractility.
 Ions, elevated levels of sodium and potassium decrease heart rate and
contractility. A moderate increase in calcium ions increases heart rate.
 Body temperature, increased body temperature, as occurs during a fever or
strenuous exercise, increases heart rate.
 Age, newborns have higher heart rates (120 beats/ min) than adults. The heart
rate slows down graduallyduring childhood, until it reaches the adult rate of
around 72 beats/min.
 Gender,females tend to have higher resting heart rates than males.
 Physical fitness, regular exercise tends to slow the resting heart rate. Welltrained athletes have slower resting heart rates (40–60 beats/min) but have normal
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resting cardiac outputs because their hearts are enlarged, giving them larger stroke
volumes.
II.Factors effect Stroke volume
1.Preload
preload is the load or prestretch on ventricular muscle at the end of diastole. The
best indices of preload on ventricular are:
• Left ventricular end-diastolic volume (LVEDV)
• Left ventricular end-diastolic pressure (LVEDP)
Possibly somewhat less reliable indices of left ventricular preload are:
• Central venous pressure (CVP)
• Right atrial pressure (RAP)
• Pulmonary capillary wedge pressure (PCWP), it is measured from the tip of a SwanGanz catheter, which pass through the right heart, to small pulmonary artery where the
pressure is probably very close to left atrial pressure. A rise in pulmonary capillary
wedge pressure is evidence of an increase in preload on the left ventricle. In some
cases, like mitral stenosis, it is not a good index of left ventricular preload.
The preload determines the length of the sarcomeres at the onset of contraction. The
length of the sarcomeres associated with the most forceful contraction called resting
length which is about ~2.2 μm.
2.contractility
Contractility (lnotropic State)
contractility defined as a change in ventricular performance at a given preload and
afterload. Contractility increases as the amount of calcium available for contraction
increases. More calcium increases the availability of cross-link sites on the actin,
increasing cross-linking and the force of contraction during systole. Several
medications have important positive inotropic effects that can be exploited
clinically, including digoxin and the sympathomimetic amines (e.g., epinephrine,
norepinephrine, dopamine).
Indices of contractillty
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1.One way of quantitating contractility is as the ejection fraction (EF), defined as the
ratio of stroke volume (SV) to end-diastolic volume (EDV):
ejection fraction (EF)=stroke volume (SV) / end-diastolic volume (EDV)
Increased contractility causes an increased ejection fraction. A normal EF rate for
the ventricles is 50% to 70%. EF lower than 40% can confirm heart failure.
2. dp/dt (change in pressure vs. change in time) = rate of pressure development
during isovolumetric contraction.
3.afterload
Afterload is the force against which the ventricles must contract to eject blood.
The arterial pressure is often used as a practical measure of afterload, although, in
truth, afterload is determined by the intraventricular pressure, the size of the
ventricular cavity, and the thickness of the ventricular walls (Laplace's law). Thus,
afterload is increased in the setting of systemic hypertension or stenosis of the
aortic valve but may be equally increased in the setting of ventricular dilation or
ventricular hypertrophy.
Compliance
Compliance describes the distensibility of a structure. Compliance is defined as the
volume change produced by a given pressure change:
C = ΔV / ΔP
C = Compliance
ΔV = Volume change
ΔP = Pressure change
Low compliance is the central pathology in diastolic heart failure. Chronic
hypertension renders the left ventricle thickened and noncompliant, impairing
relaxation and diastolic filling. Ventricular compliance may be improved by
treatment with calcium channel blockers to aid relaxation of the cardiac myocytes
during diastole.
Return of Venous Blood to the Heart
By the time blood has passed from the capillaries into the venous system the pressure
has dropped significantly. The average blood pressure in the venous system is only 0-2
mmHg as compared to an average of 100 mmHg in the arterial system. The low venous
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pressure is barely adequate to drive blood back to the heart, particulary from the legs.
Other mechanisms are needed to aid in the return of blood to the heart.
The flow of venous blood back to the heart is increased by
(1) the sympathetic nervous system, Veins are enervated by sympathetic motor
neurons. Sympathetic input causes vasoconstriction, which increases pressure, which
drives blood back to the heart. When the body needs to mobilize more blood for
physical activity, the sympathetic nervous system induces vasoconstriction of veins.
(2) the skeletal muscle pump, Veins pass between skeletal muscles. The contraction of
skeletal muscle squeezes the vein, thus increasing blood pressure in that section of the
vein. Pressure causes the upstream valve (furthest from the heart) to close and the
downstream valve (the one closest to the heart) to open. Repeated cycles of
contraction and relaxation, as occurs in the leg muscles while walking, effectively
pumps blood back to the heart.
Figure: vein valves.
(3) the respiratory pump, While the contraction of skeletal muscle in the legs drives
venous blood out of the lower limbs, the act of breathing helps to drive venous blood
out of the abdominal cavity. As air is inspired, the diaphragm descends and abdominal
pressure increases. The increasing pressure squeezes veins and moves blood back
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toward the heart. The rhythmic movement of venous blood causes by the act of
breathing is called the respiratory pump.
Other factors effect venous return include, Right atrial pressure Total blood
volume.
Central venous pressure
Central venous pressure is the pressure of venous blood in the thoracic vena cava
and the right atrium. Low central venous pressure promotes venous return into
the central venous compartment, whereas high central venous pressure reduces
venous return. Central venous pressure has a strong influence on cardiac preload
and, through the Frank-Starling mechanism, determines ventricular SV.
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