CARDIOVASCULAR SYSTEM

INTERIOR OF THE HEART

Right atria separated from the left by interatrial septum. Right ventricle separated from left by interventricular septum. Right atria receives blood from superior venacava (svc) which drains the venous blood from head & neck as well as from upper limb- From here blood flows into right ventricles . The opening between right atria and right ventricle is guarded by the tricuspid valve (atrioventicular valve). Blood in the right ventricle is pumped into pulmonary trunk through an opening guarded pulmonary valve; this pulmonary trunk divides into pulmonary arteries that carry blood into lungs. In the lungs the venous blood (deoxygenated) is converted into arterial blood (oxygenated blood) and from here the blood, through pulmonary veins reaches the left atria. Pulmonary veins are the only veins that carry oxygenated blood. Blood from left atria moves into left ventricle through the (bicuspid) mitral valve. These mitral and tricuspid valves are called as atrioventicular valves. Blood in the left ventricle is pumped into aorta through an opening which is guarded by aortic valve. These aortic and pulmonary valves are called as semilunar valves. From the aorta the oxygenated blood is supplied to all over the body through different branches.

PULMONARY CIRCULATION OR LESSER CIRCULATION

The circulation of venous blood from the right ventricle (deoxygenated) of the heart to the lungs and oxygenated blood from lungs back to the left atrium of the heart.

SYSTEMIC CIRCULATION OR GREATER CIRCULATION

The circulation of oxygenated blood from the left ventricle of the heart to the various tissues of the body and of venous blood back to the right atrium of the heart.

VASCULAR SYSTEM
Aorta larger arteries medium sized arteries small arteries arterioles capillaries venules smaller veins medium sized veins large veins venacava RIGHT VENTRICLE Exchange of nutrients and metabolic waste products between the blood and tissues chiefly takes place at capillaries (exchange vessels).

2. Structure and Functions of Blood Vessels 3. Comparison between Arteries and Veins

Arteries
Transport blood away from the heart; Carry Oxygenated Blood (except in the case of the Pulmonary Artery); Have relatively narrow lumens Have relatively more muscle/elastic tissue; Transports blood under higher pressure (than veins); Do not have valves (except for the semi-lunar valves of the pulmonary artery and the aorta).

Veins
Transport blood towards the heart; Carry De-oxygenated Blood (except in the case of the Pulmonary Vein); Have relatively wide lumens Have relatively less muscle/elastic tissue; Transports blood under lower pressure (than arteries); Have valves throughout the main veins of the body. These are to prevent blood flowing in the wrong direction, as this could (in theory) return waste materials to the tissues.

The walls (outer structure) of arteries contain smooth muscle fibre that contract and relax under the instructions of the sympathetic nervous system. Arterioles Arterioles are tiny branches of arteries that lead to capillaries. These are predominantly under the control of the sympathetic nervous system and local control, and constrict and dilate, to regulate blood flow. Capillaries Capillaries are tiny (extremely narrow) blood vessels. There are networks of capillaries in most of the organs and tissues of the body. These capillaries are supplied with blood by arterioles

Arteries

Structure

Functions
Transport blood away from the heart; Transport oxygenated blood only (except in the case of the pulmonary artery). Transport blood from arteries to capillaries; Arterioles are the main regulators of blood flow and pressure.

Function is to supply tissues with components of, and carried by, the blood, and also to remove waste from the surrounding cells ... as opposed to simply moving the blood around the body

Venules

Veins

and drained by venules. Capillary Exchange of oxygen, carbon dioxide, walls are only one cell thick , water, salts, etc., between the blood and which permits exchanges of the surrounding body tissues. material between the contents of the capillary and the surrounding tissue. Venules are minute vessels that Drains blood from capillaries drain blood from capillaries and into veins, for return to the into veins. Many venules unite to heart form a vein. The walls (outer structure) of veins Transport blood towards the consist of three layers of tissues heart; that are thinner and less elastic Transport deoxygenated blood than the corresponding layers of only (except in the case of the arteries. pulmonary vein). Veins include valves that aid the return of blood to the heart by preventing blood from flowing in the reverse direction.

Histology of the Blood Vessels The blood vessels are made of three layers, called from the luminal side outward, the tunica intima, the tunica media and the tunica adventitia. These three layers are analogous to the endo-, myo- and epicardium, of heart respectively. The thickness of these three layers varies greatly depending upon the size and type of vessel (large, medium & small arteries and veins; capillaries). The tunica intima consists of an endothelium (present in all vessels) and any subendothelial connective tissue that may be present (highly variable depending on vessel). The tunica media is the layer of concentrically-arranged smooth muscle, the autonomic control of which can alter the diameter of the vessel and affect the blood pressure. Smooth muscle cells (in contrast to cardiac and skeletal) have Secretory capabilities. The tunica media of arteries is larger than that of veins of similar size. The tunica adventitia is made chiefly of longitudinally arranged collagen fibers. It tends to be much larger in veins than arteries. INNERVATION OF CARDIOVASCULAR SYSTEM: The neurons of the brain which controls the CVS is located in the medulla oblongata & Pons, here there is an area called vasomotor center. In this center certain neurons gives rise to sympathetic nerve fibres and certain group of neurons gives rise to parasympathetic fibres (vagus nerve). The sympathetic nerve fibres arising here descend downwards to enter the spinal cord; from here it emerges out of the spinal cord through the spinal nerves to Sympathetic ganglion, from here post ganglionic sympathetic fibers arise to supply the heart as well as the blood vessels. Parasympathetic fibres through vagus nerve emerge out of the base of the skull through jugular foramen then it descends along the neck to supply the thoracic structures (heart, lungs, etc) as well as major part of gastro intestinal system &etc.

Innervation of the heart Sympathetic innervation ; Sympathetic nerves supplies SA node, AV node, other parts of conducting system, atria, & ventricles. Sympathetic system amplifies the all actions (properties) of heart

Excitability of cardiac

Inotropy

Dromotropy

Lusitropy

Heart rate Chronotropy

Bathmotropy

Sympathetic system supplies almost all the blood vessels except the capillaries, precapillary sphincters, and metarterioles. The innervation of small arterioles and arterioles allows sympathetic stimulation to increase resistance to blood flow (helps in regulation of blood pressure) and there by decrease in rate of blood flow through the tissues. Innervation of large veins makes it possible for sympathetic stimulation to decrease the volume of these vessels. This can push blood into the heart and thereby play a major role in regulation of heart pumping and the cardiac output. IMPORTANT NOTE: Sympathetic system is always active(sympathetic tone) to stimulate the heart and blood vessels, so that smooth muscles in blood vessels are in constant contraction ( vasomotor tone) called as vasoconstriction . This results in reduction in internal diameter of blood vessels which causes increased resistance for blood to flow (maximum blood pressure drop in arteriolar region). This resistance to the blood flow is more in the arterioles as it receives more sympathetic innervations and it has more amount of smooth muscle Inhibition of sympathetic system causes relaxation of smooth muscles in the blood vessels results in vasodilatation of blood vessels. This causes increase in internal diameter and the resistance to blood flow decreases. These are the way through which nervous regulation of blood flow to tissue are regulated as well as the nervous regulation of blood pressure (see later) is maintained. Parasympathetic innervations (vagus nerve) Supplies the SA node, AV node and other parts of conducting system, apart from this it supplies atria but not the ventricles. Blood vessels lack the parasympathetic innervations (few exceptions)

Parasympathetic fibers are found associated with blood vessels in certain organs such as salivary glands, gastrointestinal glands, and in genital erectile tissue here it causes relaxation of smooth muscles in blood vessels (vasodilatation). Parasympathetic system slows down all most all the actions of heart*********** PHERIPHERAL RESISTANCE (PR) The resistance to the passage of blood through the small blood vessels (because it is in periphery), especially the arterioles. It is maximum at the arterioles so arterioles are the seat of maximum peripheral resistance. Vascular resistance is a term used to define the resistance to flow that must be overcome to push blood through the circulatory system. The resistance offered by the peripheral circulation is known as the systemic vascular resistance (SVR), while the resistance offered by the vasculature of the lungs is known as the pulmonary vascular resistance (PVR). The systemic vascular resistance may also be referred to as the total peripheral resistance. Vasoconstriction(i.e., decrease in blood vessel diameter) increases SVR, whereas vasodilation (increase in diameter) decreases SVR. Flow (F) of blood through a blood vessel is depend on Pressure gradient P (at the two ends of the blood vessel) R Resistance (peripheral) offered to flow of blood by the blood vessels F = P R PR = 8L r4 Viscosity of blood L- Length of the blood vessel r4 radius of blood vessel PROPERTIES OF CARDIAC MUSCLE A) ELECTRICAL PROPERTIES 1. Excitability 2. Auto rhythmicity 3. Conductivity B) MECHANICAL PROPERTIES 1. Contractility 2. Distensibility 1. Excitability RMP OF cardiac muscle is 90mv When appropriate strength of stimulus is applied the cardiac muscle responds by generating an action potential

CODUCTING SYSTESM OF THE HEART Parts of the conducting system 1. SA node 2. AV node 3. Internodal pathway which connects both AV node and SA node

4. Bundle of His 5. Right and left bundle branches 6. The bundle branches divides on each side into purkinje fibers to supply the ventricular muscle GENERATION AND TRANSMISSON OF IMPULSE (ACTION POTENTIAL) The action potentials generated by the SA node spread throughout the atria primarily by cell-to-cell conduction. There is some functional evidence for the existence of specialized conducting pathways within the atria (termed Internodal tracts), although this is controversial. As the wave of action potentials depolarizes the atrial muscle, the cardiomyocytes contract by a process termed excitationcontraction coupling. Normally, the only pathway available for action potentials to enter the ventricles is through a specialized region of cells (atrioventricular node, or AV node) located in the inferior-posterior region of the interatrial septum. The AV node is a highly specialized conducting tissue (cardiac, not neural in origin) that slows (AV nodal delay) the impulse conduction considerably (to about 0.05 m/sec) thereby allowing sufficient time for complete atrial depolarization and contraction (systole) prior to ventricular depolarization and contraction. The impulses then enter the base of the ventricle at the Bundle of His and then follow the left and right bundle branches along the interventricular septum. These specialized fibers conduct the impulses at a very rapid velocity (about 2 m/sec). The bundle branches then divide into an extensive system of Purkinje fibers that conduct the impulses at high velocity (about 4 m/sec) throughout the ventricles. This results in rapid depolarization of ventricular myocytes throughout both ventricles. ECG ELECTROCARDIOGRAM Graphical recording of summated electrical activity (action potential of cardiac muscle fibers) from the heart during a cardiac cycle. Electrocardiograph A device used for recording the electrical activity of the myocardium to detect transmission of the cardiac impulse through the conductive tissues of the muscle. Principle of ECG: Volume conductor principle Atrial repolarisation wave is masked by ventricular depolarisation so it is not recorded. Significance of ECG With this we can able to detect Arrhythmias irregular heart beats Decreased heart rate below 60 bts/minute is called bradycardia Increased heart rate above 100bts/minute is called Tachycardia Conduction blocks Myocardial infarction Relative size of chambers Arrhythmias An abnormal heart rhythm. In an arrhythmia the heartbeats may be too slow, too rapid, too irregular, or too early. Rapid arrhythmias (greater than 100 beats per minute) are called

tachycardias. Slow arrhythmias (slower than 60 beats per minute) are called bradycardias. Irregular heart rhythms are called fibrillations (as in atrial fibrillation and ventricular fibrillation). When a single heartbeat occurs earlier than normal, it is called a premature contraction. The term arrhythmia comes from the Greek a-, loss + rhythmos, rhythm = loss of rhythm.

CONTRACTILITY It refers to the mechanical change (shortening of muscle) brought about in the cardiac muscle when stimulated. The atrial and ventricular contractile phase is called Systole and where as relaxation phase is Diastole. At each beat ventricle contract to pump certain volume of blood which is about 70ml. Amount of blood pumped out by each ventricle per beat is called stroke volume which is about 70 ml. Heart rate is approximately 72 bts/min How much is the amount of blood pumped from each ventricle per minute = SV X HR =70ml X 72 bts/min = 5L approximately This 5L is the cardiac output. Sarcomere at CONTRACTED AND RELAXED STATE ANALYSE THE DIFFERENCES IN TWO STATES IN CONTRACTED STATE Z lines move closer that is sarcomere shortens I band decreases H zones decreases A band width remains same Types of muscle contraction Isometric and isotonic contraction In ISOTONIC CONTRACTION, The tension (force) in the muscle remains constant despite a change in muscle length. In this origin & and insertion move together (that is muscle shortens). This can occur only when a muscle's maximal force of contraction exceeds the total load on the muscle. ISOMETRIC CONTRACTION, An increase in muscular tension (force) without a change in muscle length, as in clenching the teeth. An example would be holding an object up without moving it; the muscular force precisely matches the load, and no movement results. isometric maintaining, or pertaining to, the same length; of equal dimensions.

Relation Of Sarcomere Length With Development Of Force

F O R C E

SARCOMERE LENGTH
Right hand side Above graph shows that when the sarcomere length increases the force of contraction decreases --- this is because as length of sarcomere increases the actin filaments are pulled away from the myosin head . So number of cross bridges binding with that of actin decreases resulting in decrease in force of contraction. Left hand side At shorter sarcomere length the actin filaments over ride with each other, in this case also the number of myosin head (cross bridges) attaching to actin decreases resulting in decreased force of contraction. At the point Io on the graph( that is center part ),the sarcomere length is such that the muscle can develop maximum force of contraction because the actin filament is exactly positioned on the myosin filaments so that maximum number of cross bridges (myosin head ) can bind to the actin. The sarcomere length where it can develop maximum tension (force) is called optimal length

PRE-LOAD & AFTER-LOAD Preload It is the load (tension) acting on the muscle before it starts to contract.

In cardiac muscle the preload is the pressure exerted by volume of blood present in the ventricles at the end of diastole (END DIASTOLIC PRESSURE) .This is the load acting on the ventricular muscle before its starts to contract called as preload. Afterload This is the load which acts on the muscle after its commencement of contraction In cardiac muscle afterload is the pressure in the arteries leading from the ventricles, this pressure in the arteries will act on the ventricle once its start to contract. IMPORTANT NOTE At normal physiological LEVELS OF increase in preload (end diastolic pressure) stretches the sarcomere of ventricles to optimal length, so that it increases the force of contraction of ventricles to pump out the extra volume of blood it received. DISTENSIBILITY It refers to extent to which heart can distend at the same venous pressure Heart is covered by pericardium, when the fluid or blood collect in the pericardial cavity (pericardial effusion) that limits the distensibility. STROKE VOLUME This is the amount of blood ejected out from each ventricle per beat. It is about 70 ml. CARDIAC OUTPUT ( CO) The amount of blood ejected out from the each ventricle in one minute is called CO. CO = SV X HR Heart rate is 75 bts/min CO = 70ml X 75bts/min = 5L approximately

Factors influencing the cardiac out put The factors which influences the SV &HR will influence the CO SV It is dependent on force of contraction (FOC) of ventricles If FOC is increased the amount of blood ejected out of ventricles increases (VICE VERSA) SV INCREASES CO INCREASES The FOC is increased by increasing the sympathetic impulses that is due to sympathetic stimulation CO increases. The other factor influencing the force of contraction is preload, if preload increases (within physiological limits) the sarcomere of cardiac muscle reaches the optimal length which results in increased in FOC. Preload effect was stated as franks starlings law The Frank-Starling law of the heart (also known as Starling's law or the FrankStarling mechanism) states that the greater the volume of blood entering the heart during diastole (end-diastolic volume or end-diastolic fiber length of ventricle), the greater the volume of blood ejected during systolic contraction (stroke volume) and vice-versa

The other factor which influences the stroke volume is VENOUS RETURN Venous return is venous blood entering into the heart. If venous return increases the amount blood in the ventricles at the end of diastole increases that is preload increases. The result of increase in preload is increased force of contraction followed by rise in stroke volume. Venous blood has to pump against the gravity to reach the heart; this pumping of venous blood from periphery is done the skeletal muscle. Calf muscle, soleus is called as peripheral heart. In the veins valves are present to prevent the back flow of blood. Veins Blood flows from capillaries into venules and then into veins. Some exchange of materials occurs between the interstitial fluid and the venules, just as in capillaries. The veins are the last set of tubes through which blood flows on its way back to the heart. In the systemic circulation, the force driving this venous returns is the pressure difference between the peripheral veins and the right atrium. The pressure in the first portion of the peripheral veins is generally quite lowonly 5 to 10 mmHgbecause most of the pressure imparted to the blood by the heart is dissipated by resistance as blood flows through the arterioles, capillaries, and venules. The right atrial pressure is normally approximately 0 mmHg. Therefore, the total driving pressure for flow from the peripheral veins to the right atrium is only 5 to 10 mmHg. This pressure difference is adequate because of the low resistance to flow offered by the veins, which have large diameters. Thus, a major function of the veins is to act as low-resistance conduits for blood flow from the tissue to the heart. The veins outside the chest, the peripheral veins, contain valves that permit flow only toward the heart. Why are these valves necessary if the pressure gradient created by cardiac contraction pushes blood only toward the heart anyway? The answer will be given below in the section on determinants of venous pressure. In addition to their function as low-resistance conduits, the veins perform a second important function: Their diameters are reflexly altered in response to changes in blood volume (hemorrhage), thereby maintaining peripheral venous pressure and venous return to the heart hence EDV SV CO BP. Thus, we now see that peripheral venous pressure is an important determinant of stroke Volume. Determinants of Venous Pressure The factors determining pressure in any elastic tube are, as we know, the volume of fluid within it and the compliance of its walls. Accordingly, total blood volume is one important determinant of venous pressure since, as we shall see, at any given moment most blood is in the veins. Also, the walls of veins are thinner and much more compliant than those of arteries. Thus, veins can accommodate large volumes of blood with a relatively small increase in internal pressure. Approximately 60 percent of the total blood volume is present in the systemic veins at any given moment, but the venous pressure averages less than 10 mmHg. (In contrast, the systemic arteries contain less than 15 percent of the blood, at a pressure of approximately 100 mmHg.) The walls of the veins contain smooth muscle innervated by sympathetic neurons. Stimulation of these neurons releases norepinephrine, which causes contraction of the venous smooth muscle, decreasing the diameter and compliance of the vessels and raising the pressure within them hence more volume of blood will be emptied in to ventricles rise in EDV SV CO BP.

Although the sympathetic nerves are the most important input, venous smooth muscle, like arteriolar smooth muscle, is also influenced by hormonal and paracrine vasodilators and vasoconstrictors. Two other mechanisms, in addition to contraction of venous smooth muscle, can increase venous Pressure and facilitate venous return. These mechanisms are the skeletal-muscle pump and the respiratory pump. During skeletal-muscle contraction, the veins running through the muscle are partially compressed, which reduces their diameter and forces more blood back to the heart. Now we can describe a major function of the peripheral-vein valves: The skeletal-muscle pump raises venous pressure locally, the valves permit blood flow only toward the heart and prevent flow back toward the tissues The respiratory pump work as follows during inspiration of air, the diaphragm descends, pushes on the abdominal contents, and increases abdominal pressure. This pressure increase is transmitted passively to the intra abdominal veins. Simultaneously, the pressure in the thorax decreases, thereby decreasing the pressure in the intrathoracic veins and right atrium. The net effect of the pressure changes in the abdomen and thorax is to increase the pressure difference between the peripheral veins and the heart. Accordingly, Venous return is enhanced during inspiration (expiration would reverse this effect if it were not for the venous valves). Larger the inspiration, the greater the effect. Thus, breathing deeply and frequently, as in exercise, helps blood flow from the peripheral veins to the heart. One might get the (incorrect) impression from these descriptions that venous return and cardiac output are independent entities. However, any change in venous return, due say to the skeletal-muscle pump, almost immediately causes equivalent changes in cardiac output, largely through the operation of the FrankStarling mechanism. Venous return and cardiac output therefore must be identical except for very brief periods of time. In summary the effects of venous smooth-muscle contraction, the skeletal-muscle pump, and the respiratory pump are to facilitate venous return and thereby to enhance cardiac output by the same amount. HEART RATE Sympathetic stimulation increases the frequency of generation of impulses from SA node so heart rises, as well as it increases the conductivity of impulses along the conducting system. Increase in HEART RATE Increase in STROKE VOLUME Increases the CO BLOOD PRESSURE Is the lateral pressure exerted by the flowing blood on the of the walls of Blood vessels . Types Systolic pressure is maximum pressure recorded in the arteries during ventricular systole Normal range is 100 to 140 mmHg. Mean is 120 mmHg in adult Diastolic pressure is the minimum pressure recorded in the arteries during ventricular diastole.

Normal range is 60 to 90 mmHg. MEAN is 80 mmHg PULSE PRESSURE ; It is the difference between systolic and diastolic pressure = 40 mmHg BP = CO X PERIPHERAL RESISTANCE (PR) CO = SV X HR 8L r4 From the above two equations , the factors maintaining the blood pressure are PR =
1. Cardiac output

2. Peripheral resistance Peripheral resistance Other two factors which influence BP is the BLOOD VOLUME & Elasticity of blood vessels. Systolic pressure denotes the cardiac out put Diastolic pressure denotes the peripheral resistance

REGULATION OF BLOOD PRESSURE Fall in blood pressure below the normal is called HYPOTENSION ,which results in failure of required amount of blood supply to the tissues . Rise in blood pressure above the normal is called HYPERTENSION . Blood vessels cannot with stand hypertension, so the blood vessels may undergo rupture. So it is important to maintain the BP precisely in day to day life. Before going to regulation BP we see some physiologic anatomy of nervous system that maintains the BP. Change in the blood pressure is sensed by the receptor called Baroreceptor. Location of baroreceptor: CAROTID SINUS & AORTIC ARCH. We will take a example of increase in BP. Stimulation of baroreceptor and generation of impulses, these impulses from baroreceptor present in the carotid sinus is carried by glossopharyngeal nerve (ix) and from aortic arch is by vagus nerve (x), these nerves are called afferent nerves. VASOMOTOR CENTRE This centre consists of group neurons that control BP; this centre is present in medulla oblongata and Pons. in this centre certain group of neurons gives rise to sympathetic fibers and the area where it is present is called vasoconstrictor area .

certain group of neurons in this center gives rise to parasympathetic fibers and the area where it is present is called vasodilator area. There are certain other group of neurons (sensory neurons )which receive all incoming impulses from baroreceptors as well as from other receptors ..That is ix & x nerve synapse with these sensory neurons to relay impulses about the BP. The area where these sensory neurons are present is called as NUCLEUS TRACTUS SOLITORIUS ( NTS) . These three areas 1. Vasoconstrictor area 2. Vasodilator area VASOMOTOR CENTER 3. NTS (SENSORY AREA) MEDULLA &PONS The above three areas constitute the vasomotor centre ,this centre located in the medulla oblongata and pons . RESULT OF STIMULATION OF VASOCONSTRICTOR AREA Increased impulses flow along the sympathetic fibers, this will result in 1. 2. Heart rate Force of contraction

3. Constriction of smooth muscles surrounding the arterioles especially because the arterioles have dense sympathetic innervations. This will raise the peripheral resistance CONCLUSION: STIMULATION OF SYMPATHETIC SYSTEM Causes rise in cardiac out and peripheral resistance. So end result is raise in BP Result of stimulation of parasympathetic area Increases the flow of impulses along the parasympathetic fibers (vagus nerve). This impuslse decreases the 1. Heart rate 2 Conduction of impulses along the conducting system

3. The force of contraction The net result of stimulation of parasympathetic system is decrease in CO

ROLE OF BARORECEPTOR REFLEX IN MAINTAINCE OF BP Consider the situation of Rise In Blood Pressure Stimulation of BARORECPTOR in Carotid sinus & Aortic arch

Ix nerve Impulses to NTS (SENSORY AREA)

x nerve

INHIBHITION OF VASOCONSTICTOR AREA SYMPATHETIC IMPULSES

STIMULATION OF VAODIATOR AREA PARASYMPATHETIC IMPULSES

VM C

Heart rate & FOC Cardiac output

Dilatation of blood vessels peripheral resistance

heart rate& FOC CARDIAC OUTPUT

ARTERIAL BLOOD PRESSURE

MICROCIRCULATION