Download Advance physiology Cardiovascular system

Advance physiology
Cardiovascular system
ASSIST. PROF. DR.
MAJIDA A. J. AL-QAYIM
Cardiovascular system
The cardiovascular system
consists of the heart and
two vascular systems.
The heart consists of two pumps,
pumps blood through two
vascular systems:
the low pressure pulmonary
circulation in which gas
exchange occurs
the systemic circulation, which
delivers blood to organs,.
The heart as a pump
The heart is a cone shape muscular organ
located in the thoracic cavity. The heart
wall consist of three distinct layers ;
Endocardium
Myocardium
Pricardium
The myocardium, or heart muscle, receives
nutrients via the coronary circulatation.
 Heart valves
Special structures of the
heart
1-Valves are outgrowths from the endocardium which prevent backflow of blood.
Heart valves ensure unidirectional blood flow through the heart
 Atrioventricular (AV) valves lie between the atria and the ventricles
 AV valves prevent backflow into the atria when ventricles contractSemilunar
 Aortic semilunar valve lies between the left ventricle and the aorta
 Pulmonary semilunar valve lies between the right ventricle and pulmonary
trunk
Valves contain three components.
a. Endothelium covers the valve.
b. chordae tendineae attach the flaps of the AV valves to the heart wall at the
apex of the heart..
C. papillary muscles
Heart Valves
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Chapter 18, Cardiovascular System
Figure 18.8a, b
2- The conducting system
The heart contains specialized cardiac musclefibers
that can self-generate an action potential, and are
therefore called autorhythmic fibers. These cells
do not require extrinsic neural input, and they can
continue to generate an action potential even
when the heart is removed from the body
1- SA nodeThe heart normally has a selffiring unit, located in the right atrium,
called the sinoatrial node or sinus node
(pacemaker cells),
2-The electric signal from the sinus node
activates the atrial walls to contraction,
and then reaches the main conduction
system at the level of the atrioventricular
node (AV node).
3-From the bundle of His, the signal is
transmitted down a rapid conduction
pathway
4- These bundle branches divide into a
network of conducting Purkinje fibres just
below the endocardial surface. Purkinje
fibres are large diameter cells without Ttubulesbundle of his
Molecular structure of the cardiac muscle

Cardiac muscle cells orcardiomyocytes(also known asmyocardiocytes[1]or cardiac
myocytes[2]) are the muscle cells (myocytes) that make up thecardiac muscle • cardiac muscle has
myofibrils that contain actin & myosin filaments almost identical to those found in skeletal muscle
these filaments lie side by side & slide along one another during contraction in the same manner a
occurs in skeletal muscle The cells are Y shaped and are shorter and wider than skeletal muscle cel
They are predominatly mononucleated.

The cardiac muscles, unlike skeletal ones, cannot rest, even for a moment. They must work
continuously.
cardiac muscle fibers arranged in a latticework, with the fibers dividing, recombining, & then
spreading again • cardiac muscle is striated in same manner as in skeletal muscle
Each myocardiocyte contains one nucleus.
The density of mitochondria (the energy generators of the body) in these cells is high, which lets th
produce an abundance of ATP molecules through aerobic respiration, to drive the muscle's
functioning. This is the reason why a heart's muscle tissue can work without fatigue and ensures a
lifetime of service.
The flexibility of the cell, along with the integrity of the cytosol is maintained by two proteins, calle
vimentin and desmin
These muscles have a very marginal store of glycogen, which is the raw material for energy
production in anaerobic conditions. So, in case of a heart attack, when the heart muscles fall short
oxygen, they simply die. Recent studies have shown that regeneration in heart cells is possible
The coronary arteries useful for the heart to be , rely on an available blood and electrical supply to
deliver oxygen and nutrients and remove waste products such as carbon dioxide
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The myocardium work as a Syncytium
The syncytium of cardiac muscle is important because it allows rapid coordinated contraction of
muscles along their entire length. Action potentials propagate along the surface of the muscle
fiber from the point of synaptic contact, through intercalated discs. Although a syncytium,
cardiac muscle differs because the cells are not long and multinucleated. Cardiac tissue is
therefore described as a functional syncytium, as opposed to the true syncytium of skeletal
muscle.
 There is an atrial syncytium and a ventricular syncytium that are connected by cardiac
connection fibres.[4]Electrical resistance through intercalated discs is very low, thus allowing
free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that
action potentials are able to travel from one cardiac muscle cell to the next, facing only slight
resistance. Each syncyntium obeys the all or none law.[5]
 Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an
electrochemical syncytium Under light microscopy, intercalated discs appear as thin, typically
dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run
perpendicular to the direction of muscle fibers
 Intercalated discs are described to consist of three different types of cell-cell junctions: the actin
filament anchoring adherens junctions, the intermediate filament anchoring desmosomes ,
and gap junctions. They allow action potentials to spread between cardiac cells by permitting
the passage of ions between cells, producing depolarization of the heart muscle intercalated
discs consist for the most part of mixed-type adhering junctions named area
composita (pl. areae compositae) representing an amalgamation of typical desmosomal
and fascia adhaerensproteins

 Cardiac muscle cells orcardiomyocytes are the muscle cells that make up
thecardiac muscle • cardiac muscle has myofibrils that contain actin & myosin
filaments almost identical to those found in skeletal muscle – these filaments lie
side by side & slide along one another during contraction in the same manner as
occurs in skeletal muscle The cells are Y shaped and are shorter and wider than
skeletal muscle cells.
 They are predominatly mononucleated.
 The cardiac muscles, unlike skeletal ones, cannot rest, even for a moment. The
density of mitochondria (the energy generators of the body) in these cells is high,
which lets them produce an abundance of ATP molecules through aerobic
respiration, to drive the muscle's functioning. This is the reason why a heart's
muscle tissue can work without fatigue and ensures a lifetime of service.
 These muscles have a very marginal store of glycogen, which is the raw material for
energy production in anaerobic conditions. So, in case of a heart attack, when the
heart muscles fall short of oxygen, they simply die.
 Recent studies have shown that regeneration in heart cells is possible
 The syncytium of cardiac muscle is important because it allows rapid coordinated
contraction of muscles along their entire length. Action potentials propagate along
the surface of the muscle fiber from the point of synaptic contact,
through intercalated discs. Although a syncytium, cardiac muscle differs because
the cells are not long and multinucleated. Cardiac tissue is therefore described as a
functional syncytium, as opposed to the true syncytium of skeletal muscle.
Cardiac muscle
Molecular structure of the myocardium
Myocardiocyte contraction
Main contractile elements
:
•Myosin: thick filaments with globular heads evenly spaced along their
length; contains myosin ATPase.
•Actin: smaller molecule (thin filaments) consisting of two strands
arranged as an alpha-helix, woven between myosin filaments.
Regulatory elements:
•Tropomyosin: double helix that lies in the groove between actin
filaments. It prevents contraction in the resting state by inhibiting the
interaction between myosin heads and actin.
•Troponin: complex with three subunits that sits at regular intervals along
the actin strands.
•Troponin T (TnT) – ties troponin complex to actin and tropomyosin
molecules.
•Troponin I (TnI) – inhibits activity of ATPase in actin-myosin
interaction.
•Troponin C (TnC) – binds calcium ions that regulate contractile
process.
Ionic basis of cardiac muscle contraction
 The mechanism of contraction of cardiac muscle
fibers is similar to that in skeletal muscle fibers. As
intracellular Ca 2+ concentrations increase, Ca 2+
binds to troponin, causing the tropomyosin to move
and thus uncovering the myosin binding sites on the
actin fi laments. Myosin then binds to actin, and the
actin is pulled across the myosin fi lament. Drugs
that alter the movement of calcium into the cardiac
muscle fibers can affect the strength of heart
contraction.
Molecular basis of cardiomyocyte contraction
Excitation-contraction coupling in a
cardiac fibre
The electrocardiogram (ECG)
 · The electrocardiogram (ECG) is a surface
recording of the electrical field generated in the
entire body by the heart. The sinus node is a
minimal muscle mass, and there is no potential
difference (wave in the ECG) before the atria
depolarise with a P-wave. When the
propagating wave is directed towards the
electrode (as in lead II) the atrial depolarization
will produce a positive P-wave. · The P-waves
correspond to the impulse distribution in the
atria, and the QRS-complex origin from
depolarisation of the strong ventricular
myocardium. · The QRS deflections in two of the
three standard leads can be drawn graphically
in a triangle and their resultant is the mean
QRS-axis of the heart. · The T-wave is caused by
the spread of repolarization over the ventricles.
· The small propagating wave moving away
from the electrode at the apex and to the right to
reach the right ventricle, is responsible for the
small, negative S-wave.
Cardiac cycle
The total of events associated with the movement of blood
during one heartbeat is called the cardiac cycle
Diastole represents the period of time when the ventricles are
relaxed ,blood is passively flowing from LA and RA into the
LV and RV, respectively . The blood flows through
atrioventricular valves (mitral and tricuspid) that separate the
atria from the ventricles.
Systole represents the time during which the left and right
ventricles contract and eject blood into the aorta and
pulmonary artery
Heart sounds
Four sounds are created during each heart beat, and two of these sounds are
clearly audible. These sounds are typically described as "lub-dup.
The first sound, lub, is louder and longer is the AV valves closing. This occurs at
the beginning of systole as the ventricular pressure increases above the atria
pressure, causing the AV valves to close as blood begins returning to the
atria.
The dup sound is caused by the semilunar valves closing at the beginning of
ventricular diastole.
The two other sounds, which are less audible, are due to the blood turbulence
during ventricular filling and atrial systole. Heart murmurs include clicking,
rushing, or gurgling sounds. Although not always due to a problem,
heart murmurs generally indicate a valve disorder. If the valve is stenotic,
meaning it has a narrowed opening, a click may be audible when the valve
should be fully opened. In contrast, if a swishing sound is heard when the
valve should be closed, it may indicate that blood is able to backfl ow through
the valve.
Cardiac output

Heart rate
Autonomic nervous
system
Circulating catecholamine
Chemoreceptors
Mechanoreceptor(priopro
receptor)
Baroreceptor
Temperature
Cations: Ca, Na, K
Stroke volume
Preload
End diastolic volume
Venousreturn
Body position
Muscular pumping
Venous pressure
Contractility
Force of contraction
Catecholamines
[Ca]
Hypertrophy
Afteload
Arterial pressure
Valve stenosis
 Cardiac output(CO) The amount of blood pumped by the heart per
minute, is a measure of how much work heart is doing. CO is equal to stroke
volume (SV), the amount of blood pumped by the ventricle per single heart
beat multiplied by the heart rate:
 CO (mL/min) = SV (mL/beat) × HR (beats/min). SV is equal to end diastolic
volume (EDV) minus end systolic volume (ESV). The heart pumps
approximately 60% of the blood in its chambers with each beat.
Circulating system
A- Arteries:There are types of arteries:
1. Elastic or conducting arteries, Largest in diameter , Have high pressure
fluctuations ,Provide pressure reservoir
2. Muscular or medium arteries distribution vessels. Smooth muscle allows vessels
to regulate blood supply by constricting or dilating
3. Arterioles Transport blood from small arteries to capillaries resistance vessels;,
Control the amount of resistance. Greatest drop in pressure occurs in arterioles
which regulate blood flow through tissues
B- Capillary Beds Capillaries form networks called capillary beds, the capillaries are
exchange vessels
C- venules and veins are capacitance vessels. The venous system can be expanded to
contain more than 75% of the total blood volume. The veins function as capacitance
vessels, and become very distended.
Severe exercise and loss of blood cause an increase in venous tone, which for a period
actually can increase the circulating blood volume. During hard work the muscular
venous pump provides up to 1/3 of the energy required for blood circulation (the
peripheral venous heart).
The venous system also plays an important role by its graded venous return to the heart.
Blood
flow
The total blood volume (5 l) is distributed with 60-75% in veins
and venules, 20% in arteries and arterioles, and only 5% in
capillaries at rest. Of the total blood volume only 12% are
found in the pulmonary low-pressure system.
The differences in BP within the vascular system provide the
driving force that keeps blood moving from higher to lower
pressure areas
Blood flow (F) is directly proportional to the difference in
blood pressure (ΔP) between two points in the circulation,
flows down a pressure gradient
Flow = ΔP /R
F = flow rate of blood through a vessel
ΔP = pressure gradient
R = resistance of blood vessels
R is more important than ΔP in influencing local blood
pressure
Blood vessels show resistance against blood flow, the affective
resistance from peripheral blood vessels resistances which is
regulated by: 1- Radios of blood vessel(SM activity)
 2- Viscosity of blood(RBCs )
 3-Length of blood vessel , which is fixed
Regulation of Blood pressure

Blood pressure (BP) is the pressure exerted by circulating blood upon the walls of blood vessels. Pressure of arterial blood is
regulated by blood volume, TPR, and cardiac rate.
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MAP=CO ´ TPR
Arteriole resistance is greatest because they have the smallest diameter.
Capillary BP is reduced because of the total cross-sectional area.
3 most important variables are HR, SV, and TPR.
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Increase in each of these will result in an increase in BP.
Long-Term Regulation of Blood Pressure
There are 5 mechanisms by which blood pressure is regulated over the long term:
1. Renin-Angiotensin-Aldosterone Mechanism
This mechanism detects a fall in blood pressure and initiates a series of events that help to bring blood pressure back to normal. For details
on the RAA mechanism.
2. Antidiuretic Hormone (ADH or Vasopressin) Mechanism
ADH is released by the posterior pituitary when osmoreceptors in hypothalamus detect an increase in plasma osmolality
Dehydration or excess salt intake:
Produces sensation of thirst
Stimulates water reabsorption from urine in kidneys, elevating blood volume
. Atrial Natriuretic Peptide Mechanism
Produced by the atria of the heart in response to increased blood pressure
Stretch of atria stimulates production of ANP.
Antagonistic to aldosterone and angiotensin II.
Promotes sodium and water excretion in the urine by the kidney.
Promotes vasodilation
4. Fluid Shift Mechanism: Administration of hypertonic fluids e.g. mannitolor hypertonic saline solution
Administration of plasma proteinssuch as albumin
5. Epinephrine/Norepinephrine Mechanism
Are produced by cells in the adrenal medulla in response to emergency or stressful situations
These hormones increase heart rate and blood vessel constriction, result in an increase in blood pressure
Regulation of Blood Pressure
 Short-Term Regulation of Blood Pressure
 Baroreceptor Reflexes
 Baroreceptors are sensory receptors that detect changes in blood pressure
 Baroreceptors are located in the carotid sinus, aortic arch, and other arteries
 Changes in peripheral resistance, heart rate, and stroke volume occur in response to changes in
blood pressure
 Chemoreceptor Reflexes
 Chemoreceptors are sensory receptors sensitive to oxygen, carbon dioxide, and pH
levels of blood
 Pressure of arterial blood is regulated by blood volume, TPR, and cardiac rate.
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Arteriole resistance is greatest because they have the smallest diameter.
Capillary BP is reduced because of the total cross-sectional area.
3 most important variables are HR, SV, and TPR.
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MAP=CO ´ TPR
Increase in each of these will result in an increase in BP.
BP can be regulated by:
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Kidney and sympatho-adrenal system
Intrinsic Regulation of Blood Flow (Autoregulation)
Most tissues (Kidneys, skeletal muscle, brain, liver , and myocardium) have an intrinsic
capacity to compensate for moderate changes in perfusion pressure by changes in vascular
resistance so blood flow remains constant. Blood flow can increase 7-8 times as a result of
vasodilation of metarterioles and precapillary sphincters .
Metabolic controle mechanism:
Response to increased rate of metabolism
 Intrinsic receptors sense chemical changes in environment
 Vasodilator substances produced as metabolism increases
Accumulation of metabolites [ increased CO2, H, adenosine/ k from tissue cells, lactic
acid, or decrease O2,pH, and ATP ], leads to vasodilation
↓BF→ accumulation of metabolites (adenosine, K+, lactate, ATP)
→ VD →↑BF
Myogenic control mechanism::-Occurs because of the stretch of the vascular smooth
muscle - maintains adequate flow.:Depends on the length- tension reletionship
↑ABP→ ↑ BF → stretch of vascular smooth muscle → stretch-induced ms contraction → ↓
BF back to normal)
↓ ABP → ↓BF→ inhibition of smooth ms→ vasodilatation→ ↑BF back to normal
A decrease in systemic arterial pressure causes vessels to dilate.
A increase in systemic arterial pressure causes vessels to contract
Endothelium secretions:
 Nitric Oxide (NO) causes vasodilation
 NO diffuses into smooth muscle:
 Activates cGMP (2nd messenger).
 Endothelin-1 causes vasoconstriction
Extrinsic Regulation of Blood Flow
 Extrinsic Regulation of Blood Flow
1- Neural regulation
 Sympathoadrenal
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Increase cardiac output
Increase TPR: Alpha-adrenergic stimulation - vasoconstriction of arteries in skin and viscera
 Parasympathetic
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Parasympathetic innervation limited, less important than sympathetic nervous system in
control of TPR.
Parasympathetic endings in arterioles promote vasodilation to the digestive
tract, external genitalia, and salivary glands
2- Hormonal:
Vasodilator Vasoconstrictor
Kinin
Adr & Nor-Adr
ANP
Angiotensine II
VIP
ADH ,Natriuretic
Blood flow during excersize
Heart failure
In a normal healthy heart, during each heartbeat a set amount of blood enters the
heart and is pumped out again, in heart failure, the heart cannot cope with
pumping the full amount of blood in each heartbeat. . Symptoms include fluid
retention, breathlessness and tiredness . Heart failure is usually classified on
which heart function or which side of the heart is most affected .
Systolic heart failure. This means that the ventricles of the heart do not contract
properly during each heartbeat so blood is not adequately pumped out of the
heart. In some cases there is only a slight reduction in the power of the ventricle,
which causes mild symptoms. If the power of the pumping action is more reduced
then symptoms become more severe.
Diastolic heart failure. This occurs when the ventricle does not fill up with blood
enough when the heart rests in between each heartbeat. This can sometimes be
due to the wall of the ventricle being stiffer than usual. This makes it more
difficult to stretch. 
.Ischaemic heart disease (IHD)
IHD (also called coronary heart disease) is the most common cause of heart failure.
In this condition, the blood flow to the heart muscle is reduced by narrowing of
the coronary arteries that supply the heart muscle with blood and oxygen. The
heart muscle may then not function as well as normal. Other symptoms of IHD
may occur such as angina (heart pains
Other causes
Diseases of the heart muscle (cardiomyopathy).
High blood pressure. Diseases of the heart valves. Diseases of the pericardium - Some types
of abnormal heart rhythms (arrhythmias). Drugs or chemicals that may damage the heart
muscle - for example, alcohol excess, cocaine and some types of chemotherapy.
 Various non-heart conditions that can affect the function of the heart - for example, severe
anaemia.
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Shock is a clinical condition
characterized by a gradual fall in
arterial pressure
 rapid heart rate and Respiration
 pale, moist and grey skin.
cardiac
insufficiency
Vascular
insufficiency
circulatory
insufficiency
the blood
flow to vital
tissues to be
inadequate
delivery of oxygen
and other nutrients as
well as elimination of
waste products is
insufficient
Cardiogenic shock can be caused by
restricted ventricular filling (bi- or tricuspidal stenosis,
pericardial fibrosis
myocardial disorders (infarctions, myocarditis etc)
Restricted ventricular ejection in cases with semilunar stenosis/insufficiency or
shunts.
Vascular shock caused by
Absolute hypovolaemia is caused by blood loss, plasma loss (burns , ascites,
hydrothorax etc) or dehydration (water deprivation, severe diarhoea or vomiting,
excessive sweating, intestinal obstruction with luminal fluid accumulation,
urinary loss of proteins/salt/water, excessive use of diuretics).
Relative hypovolaemia, vasodilatation , sometimes with universal vasodilatation,
is released by endotoxins (septic shock from viral or bacterial infections),
anaphylactic shock or by a neurogenic vasodilatation (neurogenic shock by severe
pains or stress, anaesthetics or brain stem lesions close to the vasoconstrictor
centre).
Oedema
 Oedema is an abnormal clinical state characterised by accumulation of
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interstitial or tissue fluid. Cutaneous oedemas can be diagnosed by the
simple test: pitting on pressure
Theoretically, oedemas are caused by three different mechanisms:
1. A hydrostatic pressure gradient, which is too great (so-called high
pressure oedema or cardiac oedema at heart failure with increased venous
and central venous pressure),
2. A colloid-osmotic pressure gradient, which is too low and caused by too
low concentrations of plasma proteins (so-called hunger oedema and renal
oedema),
3. Leakage in the capillary endothelium (so-called permeability oedema with
too much protein in the oedema fluid). Burns cause increased capillary
permeability for proteins, by infections or by allergy.
Chronic or congestive cardiac failure Congestive heart failure (CHF) is a
condition in which the heart's function as a pump is inadequate to meet the
body's needs. The symptoms of congestive heart failure vary, but can include
fatigue, diminished exercise capacity, shortness of breath, and swelling.
In chronic cardiac failure The weakened heart muscles may not be able to
supply enough blood to the kidneys, which then begin to lose their normal
ability to excrete salt (sodium) and water. This diminished kidney function
can cause the body to retain more fluid. This causes loss of fluid into the
interstitial fluid volume. Accumulation of abnormal volumes of interstitial
fluid is the definition of oedema.