Download Cardiovascular system

Cardiovascular system
Lectures in Medical Physiology
College of Dentistry/1st semester/ 2nd year
Dr. Entissar Mansour
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Cardiovascular system
Functional anatomy of the heart
The Cardiovascular System:
Transports blood to all parts of the body in two 'circulations': pulmonary
(lungs) & systemic (the rest of the body).
The heart
The heart is a muscular organ enclosed in a fibrous sac (the pericardium). The
pericardial sac contains watery fluid that acts as a lubricant as the heart moves
within the sac. The wall of the heart is composed of cardiac muscle cells,
termed the myocardium. The heart is actually two separate pumps separated
by septum. Each of these two pumps is consists of two chambers, an atrium
and a ventricle, separated by atrioventricular valve (left; mitral valve and
right; tricuspid valve).
It may be divided into 4 parts:
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The pumping organ →the heart.
The conducting and distributing vessels →the arteries and ventricles.
The exchanging parts →the capillaries.
The collecting vessels →the venules and veins.
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Systemic and Pulmonary Circulations
Pulmonary circulation: Pulmonary trunk carries deoxygenated blood
from the right ventricle to the lungs. Four pulmonary veins return
oxygenated blood from the lungs back to the left atrium.
Systemic circulation: Aorta carries oxygenated blood from left ventricle
to the body. Superior vena cava & inferior vena cava collect deoxygenated
blood from the body into the right atrium. Right and left coronary arteries
provide blood supply to the heart and coronary sinus drains blood from the
heart and pours into the right atrium (coronary circulation).
The heart beat originates in a specialized cardiac conduction system and
spreads via this system to all parts of the heart.
The structures that make up the conduction system are:
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Sinoatrial (SA) node Has the fastest rate of depolarization. Located
in right atrial wall.
Atrioventricular (AV) node . Depolarization wave initiated by SA
node reaches AV node. AV node is located in interatrial septum near
tricuspid valve. It slows impulse conduction to permit completion of
atrial contraction. Impulse passes to bundle of His.
Atrioventricular bundle (bundle of His) permits functional passage
of impulse from atria to ventricles. It is very short and branches to
form bundle branches right & left bundle branches .
Bundle branches(right&left) course interventricular septum toward
apex of heart
Purkinje fibers reach apex then branch superiorly into ventricular
walls.
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spread of cardiac excitation:
Depolarization initiated in the SA node spreads radially through the
atria, then converges on the AV node. Atrial depolarization is complete in
about 0.1 second .
The conduction in the AV node is slow(about 0.1 second)mainly
because of the small diameters of these cells. This AV nodal delay allows
the atria to contract and add additional blood to the ventricles before
ventricular contraction.
After leaving the AV node, the wave of excitation enters the ventricles
via the bundle of his and its branches. From the top of the septum, the wave
of depolarization spreads in purkinje fibers to all parts of the ventricles in
0.08-0.1 second.
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Function of pericardium
The pericardium sets a limit to the maximum size of the chambers of the
heart and prevents excessive stretching of the cardiac muscle fibers due to
overfilling with blood.
Types of valves:
There are two types of valves in the heart:
1- The atrioventricular valves: which separate the atria from the ventricles.
They prevent backflow of blood from the ventricles to the atria during
systole.
a- The bicuspid or mitral valve which separates the left atrium
from the left ventricle. It is composed of 2 flaps or cusps.
b-The tricuspid valve which separates the right atrium from the
right ventricle. It is composed of 3 flaps or cusps.
The free margins of the cusps are attached to the chordae tendineae. The
other ends of the chordae tendineae are attached to papillary muscles of the
ventricular walls contract, the chordae tendineae prevent the valve from
everting into the atrium when the ventricle contracts.
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2- The semilunar valves (the aortic and pulmonary artery valves) seen at
the origin of the aorta and pulmonary artery. They have three cusps and
prevent backflow from the aorta and pulmonary arteries into the ventricle
during diastole.
The Cardiac Cycle
The cardiac cycle is the sequence of events the heart during one heart
beat. Each cycle is initiated by spontaneous generation of an action potential
in the sinus node it is divided into a period of diastole( a period of relaxation
during which the heart fills with blood), and a period of systole(a period of
contraction).
Events in late diastole:
1-The mitral and tricuspid valves are opened.
2-The aortic and pulmonary valves are closed.
3-Blood flows into the heart, filling the atria and ventricles.
4-The rate of filling declines as the ventricles become distended.
5- The pressure in the ventricles remains low.
Atrial systole:
1-Contraction of the atria propels some additional blood into the ventricles.
2-Contraction of the atrial muscle that surrounds the orifices of the venae
cavae and pulmonary veins narrows their orifices.
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Ventricular systole:
A- Isovolumetric ventricular contraction:
1- At the start of ventricular systole, the mitral and tricuspid valves close.
2- Ventricular muscle initially shortens.
3- The intraventricular pressure rises sharply.
4- When the pressures in the left and right ventricle exceed the pressures
in the aorta(80 mmHg) and pulmonary artery(10 mmHg),the aortic and
pulmonary valves open.
B- Ventricular ejection:
1-Ventricular ejection is rapid at first and then slow.
2-The intraventricular pressure rises to amaximum (120mmHg in the L.V.
and 25mmHg in the R.V.) and then declines.
Early diastole:
A- Isovolumetric ventricular relaxation:
1- The pulmonary and aortic valves are closed.
2- The mitral and tricuspid valves are closed.
3- Ventricles are relaxed.
4- Blood flows into atria raising the atrial pressure.
5- The raised atrial pressure causes the opening of the mitral and
tricuspid valves.
B-Ventricular filling:
1- Blood flows rapidly into ventricles, then slow down.
2- Most of the ventriclular blood flows passively during this phase.
The total cycle takes about 0.8 second when the heart is beating at a rate of
75 times per minute.
Starts with :
1-Atrial systole lasts 0.1 s
2- then ventricular systole lasts 0.3 s
3- followed by atrial and ventricular relaxation lasts 0.4 s.
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Heart Sounds
They are caused by closures of heart valves. That is, heart sound does not
produced by the opening of the valve because this opening is a slow
developing process that makes no noise. The sounds occur in the following
sequence:
1. First heart sound(S1): It is a low, slightly prolonged "lub" caused
by closure of mitral and tricuspid valves at start of ventricular systole.
2. Second heart sound(S2): It is a shorter ,high pitched"dup" caused by
closure of aortic and pulmonary valves after end of ventricular systole.
3. Third heart sound(S3): It is a soft, low-pitched sound. Coincides with
the period of rapid ventricular filling and is probably due to vibrations set
up by the inrush of blood.
4. Fourth heart sound(S4): It can sometimes be heard immediately
before the first sound. This sound occurs when the atrial contraction
(rarely heard) and presumably it is caused by in rush of blood into the
ventricles, which initiates vibrations similar to those of the third heart
sound.
Phonocardiography:
It is the recording of heart sounds, usually by means of sensitive
microphones and electronic amplification.
The microphone is placed on the chest. The graphical recording of these
heart sounds is termed phonocardiogram.
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Murmurs:
Abnormal sound produced by turbulent blood flow through the valves.
The major cause of cardiac murmurs is disease of the heart valves. When a
valve is narrowed (stenosis),blood flow through it is turbulent. When a valve
is incompetent, blood leaks through it in the wrong direction (insufficiency).
The Normal Electrocardiogram(ECG OR EKG):
The ECG is a recording of differences of electrical potentials generated by
the waves of depolarization and repolarization traversing atria and
ventricles. Because the body fluids are good conductors, these electrical
potentials project to points on the surface of the body.
The system consists of:
1- Generator (heart).
2- Volume conductor (body fluids).
3- Wires connecting points on the body surface to the electrocardiograph
(leads).
4- Electrocardiograph ( galvanometer which detects ,amplifies, and
records voltage changes).
The normal ECG is characterized by the positive and negative deflections
occurring with each depolarization and repolarization of the myocardium.
These deflections are :P,Q,R ,S, and T waves.
1- P- wave: atrial depolarization.
2- QRS: ventricular depolarization.
3- T-wave: ventricular repolarization.
4- U-wave :it is believed to be due to slow repolarization of the papillary
muscles.
5_ P-R Interval: Interval from beginning of . P wave to the beginning of
QRS complex
6_ Q-T Interval: Interval from the beginning of QRS complex to the end
of T-wave.
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Cardiac output
The volume of blood pumped by each ventricle per minute.
The cardiac output is determined by multiplying the heart rate(HR) and stroke
volume(SV).
Co (L/MIN) = HR (Beats /min) X SV(L/beat)
Stroke volume
The volume of blood pumped by each ventricle per beat.
For example:
Heart rate = 72 beats/min
Stroke volume = 70 ml/beat
Co = 72 x 0.07 = 5L/min
Factors controlling cardiac output:
Variations in cardiac output can be produced by changes in heart rate or stroke
volume.
Heart rate:
1- The heart is supplied with sympathetic and parasympathetic(vagal) nerves.
Sympathetic stimulation increasing the heart rate and the parasympathetic
stimulation decreasing it.
2- Epinephrine (the main hormone liberated from the adrenal medulla)
speeds the heart rate.
3- The heart rate is also sensitive to changes in temperature, plasma
electrolyte concentrations and hormones. These are generally of lesser
importance, and the heart rate is primarily regulated by the cardiac
innervations.
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Stroke volume:
1- The stroke volume is also determined in part by neural input. Sympathetic
stimuli making the myocardial muscle fibers contract with greater
strength, and parasympathetic stimuli having the opposite effect.
2- Stroke volume varies with the length of the cardiac muscle fibers, and
this effect is independent of innervations.
Regulation of cardiac output due to changes in cardiac muscle fibers length is
sometimes called heterometric regulation, whereas regulation due to changes
in contractility independent of length is sometimes called homeometric
regulation
Changes in the force of contraction can be produced by changes in the enddiastolic volume (i.e. the volume of blood in the ventricles just prior to
contraction).
The increased diastolic volume stretches the ventricular muscle fibers and causes
them to contract more forcefully. The relationship between the diastolic volume
of the heart (i.e. the length of its muscle fibers) and the force of contraction is
referred to as Starlings law of the heart.
An increased flow of blood from the veins into the heart (venous return)
automatically forces an increase in cardiac output by distending the ventricle and
increasing stroke volume.
Blood flow
The flow of blood is governed by:
1- The dynamics of the pumping action of the heart.
2- The characteristic of the blood as fluid.
3- The characteristics of the blood vessels.
Blood always flows from areas to high pressure to areas of low pressure.
The flow of blood in the blood vessels is normally laminar (streamline).
Within the blood vessel, a thin layer of blood in contact with the wall of the
vessel does not move. The next layer within the vessel has a small velocity, the
next has a higher velocity and so forth, velocity being greatest in the center of
the stream.
Laminar flow occurs at velocities up to a certain critical velocity. At or above
this critical velocity, flow is turbulent. streamline flow is silent, but turbulent
flow creates sounds.
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The probability of turbulence is related to the diameter of the vessel and the
viscosity of the blood.
The average velocity of fluid movement at any point in a system of tubes is
proportionate to the total cross- sectional area. Therefore, the average velocity of
the blood is rapid in the aorta, declines in the smaller vessels, and is slowest in
the capillaries.
The average velocity of blood increases again in the veins and is relatively rapid
in the vena cava.
The resistance of blood flow is determined by the radius of the blood vessels and
the viscosity of the blood.
Viscosity depends for the most part on the hematocrit.
It is also affected by the composition of the plasma.
Blood pressure
It may be defined as the pressure blood exerts against the vessel walls.
The pressure of blood within the cardiovascular system depends upon:
1- The rate of output of blood by the heart (cardiac output) .
2- The resistance to flow of blood exerted by the vascular system.
Blood pressure = cardiac output X peripheral resistance
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Note:
Sources of resistance (PR):
1. Blood viscosity: Is the thickness related to formed elements
2.Diameter: Flow is inversely related to vessels diameter; larger diameter
results in less resistance. In healthy humans, smaller diameter is the greatest
source of resistance
The peripheral resistance to blood flow lies mainly in arterioles. An important
function of these vessels is to constrict or dilate and thus increase or decrease the
amount of resistance.
The pressure in the aorta and other large arteries in a young adult human rises to
a maximum value (systolic pressure) of about 120 mmHg &falls to a minimum
value (diastolic pressure) of about 70mmHg.
The arterial pressure is written as systolic pressure over diastolic pressure.
120
-------- mmHg.
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The pulse pressure is difference between the systolic and diastolic pressures
(about 50 mmHg).The mean pressure is the average pressure throughout the
cardiac cycle.
The pressure falls very slightly in the large and medium sized arteries because
their resistance to flow is small, but it falls rapidly in the small arteries and
arterioles, which are the main sites of the peripheral resistance.
Venous pressure is very low, it cannot promote adequate venous return. So, it
needs additional functional modifications. These functional modifications are:
a. Respiratory pump: During expiration, abdominal pressure increases squeeze
local veins while backflow is prevented by vein valves so, blood is forced toward
the heart.
b. Muscular pump(more important): Contraction of skeletal muscle surrounding
veins compress vein and, again, backflow is prevented by valves.So blood moves
in direction of heart.
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Cardiovascular regulatory mechanisms
Local regulatory mechanisms
Autoregulation:
It is the capacity of tissues to regulate their own blood flow. Most vascular beds
have an intrinsic capacity to compensate for moderate changes in pressure by
changes in vascular resistance, so that blood flow remains relatively constant.
Vasodilator metabolites:
The metabolic changes that produce vasodilatation include:
*Decreases in O2 tension and pH,
*Increases in CO2 tension , A rise in temperature , K +, lactic acid.
*Adenosine may play a vasodilator role in cardiac muscle but not in skeletal
muscle.
Local vasoconstrictions:
1-Injured arteries and arterioles constrict strongly.The constriction appears to be
due in part to the local release of serotonin from platelets.
2- A decrease in tissue temperature causes vasoconstriction.
3- Endothelial effects on vascular tone: Endothelin (polypeptide) has been
isolated from endothelial cells. It is one of the most potent vasoconstrictions.
The endothelium also play a role in vasodilation many stimuli act on the
endothelial cells to produce endothelium- derived relaxing factor(EDRF).
SYSTEMIC REGULATORY MECHANISMS
Kinins:
Two vasodilator peptides called kinins are found in the body:
1. Bradykinin.
2. Lysyl bradykinin (kallidin).
Kinins are formed from kininogens by the action of proteolytic enzymes called
kallikreins. kinins are converted to inactive peptides by 2 kininase (kininase I
and kininase II).
Actions of kinins:
1. They cause constriction of visceral smooth muscle.
2. They relax vascular smooth muscle, lowering blood pressure.
3. They increase capillary permeability.
4. They attract leukocytes and cause pain upon injection under the skin.
5. They appear to be formed during active secretion in sweat glands, salivary
glands, and they exocrine portion of the pancreas.
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Circulatory vasoconstrictions:
Norepinephrine, epinephrine, angiotensin II &vasopressin are vasoconstrictor
agents found in the circulation of normal individuals.
Norepinephrine produces vasoconstriction in most organs via α1 receptors, but
epinephrine dilates the blood vessels in skeletal muscle and the liver via β2
receptors.
Angiotensin II is formed from angiotensin I released by the action of rennin from
the kidney on angiotensinogen.
Angiotensinogen
Rennin
Angiotensin l
( kininase )
Angiotensin II
Innervations of the blood vessels
All blood vessels except capillaries and venules receive motor nerve fibers from
the sympathetic nervous system. The noradrenergic fibers are vasoconstrictor in
function are innervated by sympathetic, vasodilator fibers that are cholinergic .
Nerves containing peptides are found on many blood vessels. The peptides
released from these peptidergic nerves include vasoactive intestinal peptide VIP
,which produces vasodilatation.
Cardiac innervations
The heart is supplied with sympathetic and parasympathetic nerves. The
parasympathetic nerves are distributed mainly to the SA and AV nodes, to a
lesser extent to the atria and even less to the ventricles. The sympathetic nerves
are distributed to all parts of the heart.
Stimulation of the parasympathetic nerves (the vagi) causes release of Ach which
has 2 effects on the heart:
1- It decreases the rate of rhythm of the SA node.
2- It decreases the excitability of the fibers between atrial musculature and
AV node.
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Ach increases the permeability of the fiber membranes to potassium. This causes
increased negativity inside the fibers (hyperpolarization).
Sympathetic stimulation causes the release of NEwhich has the following effects:
1- It increases the rate of SA nodal discharge.
2- It increases the rate of conduction and the excitability in all parts of the
heart.
3- It increases the force of contraction.
NE increases the permeability of the fiber membrane to sodium and calcium.
Vasomotor center
It is a collection of neurons located in the medulla and lower third of Pons. This
center transmits impulses through the sympathetic vasoconstrictor fibers to
almost all the blood vessels of the body. The hypothalamus and different parts of
the cerebral cortex can excite or inhibit the vasomotor center.
Vasomotor center contains the following areas:
1- Vasoconstrictor area
The neurons of this area secrete NE. Their fibers excite the vasoconstrictor
neurons of the sympathetic nervous system. NE is secreted at the endings of the
vasoconstrictor nerves. It acts directly on the α- receptors of the vascular smooth
muscle to cause vasoconstriction.
2_Vasodilator area
The neurons of this area also secrete NE but their fibers project to the
vasoconstrictor area and inhibit the vasoconstrictor activity of that area, thus
causing vasodilatation.
3_ Sensory area
The neurons of this area receive nerve impulses from vagus& glossopharyngeal
nerves.The output impulses from the sensory area help control the activities of
the vasoconstrictor and vasodilator areas.
Functions of the vasomotor center:
1- It controls the degree of vascular constriction.
2- It controls heart activity.
The lateral portions of the vasomotor center transmit excitatory impulses through
the sympathetic nerves to the heart to increase heart rate and contractility, while
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the medial portion of the vasomotor center transmits impulses through the vagus
nerve to the heart to decrease heart rate.
Baroreceptors
The baroreceptors are stretch receptors found in the:
1- Carotid sinus.
2- Aortic arch.
3- Walls of the right and left atria at the entrance of the superior and inferior
vena cava and the pulmonary veins.
4- Wall of the left ventricle.
5- Pulmonary circulation.
The receptors are stimulated by distention of the structures in which they are
located. As the pressure rises the nerve impulse activity passing from
baroreceptors to the medulla increases. If the pressure falls, the impulse activity
decreases.
The afferent fibers pass via the glossopharyngeal & vagus nerves to the medulla.
Most of these fibers end in the nucleus of the tractus solitaries(NTS).
From the NTS, inhibitory interneuron's project to the vasoconstrictor area in the
medulla. Impulses generated in the baroreceptors inhibit the activity of the
vasoconstrictor nerves and excite the vagal innervations of the heart, producing
vasodilatation, venodilation, a drop in blood pressure, bradycardia, and a
decrease in cardiac output.
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