1. THE CIRCULATORY SYSTEM By PROF. IBTISAM EL MILEEGY

2. The circulatory system is a closed system of vessels filled with blood which continuously circulates by the pumping action of the heart. The actual transport and regulatory functions of a given animal's circulatory system depends on factors such as the size of the animal the range of activities and the particular species. 3. Components of the circulatory system: 1-The heart: It is analogous to mechanical pump whose function is rhythmic pumping of blood which it receives from veins and pumps it into 4. 2- The blood vessels: They are elastic tubes filled with continuously circulating blood. a- Arteries and arterioles: They distribute the blood from the heart to the tissues of the body. So, they act as a distributing 5. b- Capillaries: The blood vessels continue to divide into smaller and smaller branches to reach the smallest units, the capillaries. They allow diffusion of gases, substances and fluids between the tissue cells and the blood. So, they act as interchange system. 6. c- Venules and veins: The capillaries fuse into collecting vessels, the venules, which in turn fuse into large vessels, the veins. The venous side of the circulation returns blood directly to the heart for re- circulation and re oxygenation. 7. 3- Valves: The heart and most of veins possess valves allowing the blood to circulate in one direction from the heart to arteries to capillaries to veins back to the heart and prevent regurgitation of blood in the opposite direction. 8. Valves are structured to close when the pressure is greater on one side than on the other, and to open when the pressure difference reverses. 9. Lymphatic vessels: The lymphatic vessels are channels that are not connected with the blood vessels of the body, but serve as an additional drainage and transport system for lymph. 10. The pulmonary and systemic circulations In birds and mammals, animals that depend almost on the lungs for obtaining oxygen, the circulatory system consists of two complete circuits 11. 1-The systemic (general) circulation: It is also called the greater or peripheral circulation. The left ventricle pumps its arterial blood into the aorta and its branches; arteries arterioles capillaries where the blood gives its O2 to the tissues and takes CO2 to become venous blood venules veins superior and inferior vena cava right atrium right ventricles where the pulmonary circulation begins. 12. 2- The pulmonary (lesser) circulation: The right ventricle pumps venous blood into the pulmonary artery and its branches ; pulmonary capillaries ( where the blood is oxygenated and CO2 removed to air and become arterial in nature ) pulmonary veins left atrium and then to left ventricle where systemic circulation begins. 13. General features of the heart Physiological anatomy of the heart: The heart lies slightly to the left of the centre of the thoracic cavity partly behind the sternum. It is shaped roughly like an inverted triangle with the pointed end, the apex, directed downward and to the left. 14. The broader portion of the heart is called the base and is directed upward and to the right. It weighs about 300 gm (vary with species). The heart is a four- chambered organ: *- Right and left atria (auricles) which are separated from each other by the inter-atrial septum. They act mainly as reservoirs for blood and play only a minor role in pumping blood. 15. *- Right and left ventricles which are separated from each other by the inter-ventricular septum. They act as pumps that must supply the power for moving blood through the circulatory system. Therefore, the muscular layer of the atria is very thin as compared with the thick muscular wall of the ventricles. 16. The musculature of both atria is continuous with each other but both atria are completely separated from both ventricles by a fibrous ring. 17. The heart is composed entirely of a muscle which is known as the myocardium. The exterior surface is referred to as the pericardium (a thin membranous sac envelops the heart, and the space between this sac and the heart contain a small amount of fluid which serves to lubricate the heart surface as it moves during contraction). The interior surface is called the endocardium. 18. Types of cardiac muscle fibers: There are two types of cardiac muscle fibers: a- The ordinary contractile cardiac muscle fibers of the auricles and ventricles b- Specialized fibers which are essential for the initiation and propagation of normal excitation of the heart (pace maker and conductive system of the heart). 19. Cardiac muscle as a syncytium: It was believed that the cardiac muscle form a histological syncyitium, i.e. one protoplasmic mass with many nuclei. The electron microscope, however, showed that the cardiac muscle fibers are made up of many cardiac muscle cells connected with each other. 20. The cell membrane at the site of contact is called the intercalated-discs. The intercalated discs allow complete free diffusion of ions. Thus, ions move with ease inside the cardiac muscle and the action potentials travel from one cardiac muscle cell to another very rapidly. 21. Therefore, the cardiac muscle is a syncytium in which cardiac muscle cells are so tightly bound that when one of these cells become excited, the action potential spread to all of them. So, the all or none rule is applied to the entire functional syncytium of the heart rather-than to a single muscle fibers as in case of skeletal muscle fibers. 22. The heart is composed of two separate syncytium: The atrial syncytium. The ventricular syncitium. These are separated from each other by fibrous tissue surrounding the valvular rings but an action potential can be conducted from the atrial syncytium into the ventricular syncytium by the way of the AV bundle. 23. The valves of the heart: Valves of the heart are four and required to maintain one way flow of blood. *-The mitral valve and the tricuspid valve, which lie between the atria and the ventricles, are called the atrio- ventricular valves. They prevent leakage of blood backward from the ventricles into the atria when the ventricles are contracting to eject blood into the great 24. *- The other valves lie between the ventricles and the great arteries and called semi lunar valves. The aortic valve prevents blood from leaking backwards from the aorta into the left ventricle, and the pulmonary valve performs a similar function between the pulmonary artery and the right 25. The coronary circulation. The coronary arteries are the first branches to arise from the aorta, and flow through these vessels supplies oxygen and nutrients to the heart itself. Since the heart is an active organ, the coronary circulation provides a rich blood supply to the myocardium. 26. The autonomic innerrvation of the heart: Sympathetic fibers. Parasympathetic fibers. 27. The electrical activity of the heart (Electrical impulse formation and conduction) Electrical impulses (action potentials) that derive the heart originate in a group of pacemaker cells lying in the sinoatrial (SA) node, and these action potentials spread rapidly to the cardiac cells by the conductive system, causing them to 28. If the membrane potential of the cardiac muscle fiber is measured during rest, it is known as the resting membrane potential. If it is measured during activity, it is known as the action potential or the impulse and the membrane is said to be a depolarized membrane. 29. The resting membrane potential of atrial or ventricular muscle is about - 85 to - 95 mv. The resting membrane potential of the pacemacker region (SA node) is - 55 to - 60 mv. Action potential: The rapid transient changes in membrane potential during activity is called action potential 30. The shape and duration of action potential will differ according to the type of cardiac muscle fiber: 31. 1-Action potentials of atrial and ventricular muscle: Phase 0: when the cardiac muscle fiber is excited, the potential difference between the inside and the outside surfaces of the muscle fiber is quickly lost (depolarization) followed by reversal of polarity i.e. the outer surface becomes negative in relation to the inner surface of the fiber (overshoot to +20 mv). Soon after the reversal of polarity, 32. When the resting membrane potential reaches a level of about -58 mv (threshold level), the action potential occurs very rapidly and is irreversible. 33. Phase 1 of the action potential starts the process of repolarization of the membrane. It is small but fast repolarization. Phase 0 and phase 1 are due to activation of fast Na+ channels which cause rapid increase in Na+ permeability from the outside to the inside of the cell membrane of the cardiac muscle fibers. Maximum entry occurs at the threshold level. 34. Phase 2: repolarization slows down and results in a plateau due to activation of slow Na+ -Ca++ channels causing slow inward flow of Ca++ and Na+ . 35. Phase 3: following the plateau there is once gain a fairly rapid repolarization until the resting potential is reached. It is due to: inactivation of the Na+ and Ca++ channels. Activation of K+ channels causes flow of K+ ions from the inside to the outside of the cell membrane. 36. Phase 4: represents the resting action potential. Na+ - K+ pump removes Na+ ions that enters the cell during the action potential to the outside, and K+ ions which left the cell during repolarization are also returned by this pump to the inside of the cell. 37. 2- Action potential of SA node and the conductive system. The action potentials of these cells are characterized by: - Low level of resting membrane potential (-55 to -60). - Slow depolarization. - Less amplitude of action potential, and - Slow repolarization 38. The cardiac impulse starts from SA node because the SA node is more leaky to Na ions than other cardiac muscle fibers. So, the threshold value of depolarization (- 40 mv) needed for starting cardiac impulse is reached in SA node before other cardiac muscle fibers. 39. Cells in the pacemaker and the conducting system do not exhibit constant resting membrane potential, but are capable of spontaneous depolarization (pacemaker potential). 40. Cardiac automatic rhythmicity means the ability of SA node and the conducting system to generate spontaneously a propagated impulse (self- excitation). It is the function of pacemaker (SA node) and the conducting system. 41. Physiological properties of cardiac muscle The different cardiac muscle fibers possess the properties of: I- Excitability. II- Rhythmicity. III- Conductivity. IV- Contractility. 42. Excitability Heart muscle has the ability to respond to a stimulus of adequate strength and duration. This response consists of generation of a propagated action potential followed by a mechanical contraction. 43. Excitability changes during cardiac activity: 1- Absolute refractory period (ARP): During which the excitability is completely abolished. No stimulus whatever strong can excite. During it the membrane is completely depolarized. 44. In the cardiac muscle the ARP is: Very long and occupies the whole period of systole and early part of diastole A second stimulus applied during the contracted state is ineffective to prevent tetanus of the heart. If tetanus occurs for few seconds it will stop the heart. In addition, ARP is long to give time for the heart to recover completely from contraction before a next one can occur. 45. Whereas in voluntary muscle the ARP is: Very short and equal to the latent period. A second stimulus applied during the contraction phase is effective to maintain the contracted state which fits with the function of these muscles. 46. 2- Relative refractory period (RRP): During which the excitability gradually recovers until it reaches the normal value. During it the membrane is not completely depolarized (during diastole). A stimulus applied during the RRP produces weak contraction (extrasystole). 47. 3- Supernormal phase: During which the excitability rises above the normal. A weaker stimulus is needed to excite, and stronger contraction is produced. Stimuli adjusted to occur during supernormal phase of their predecessors would produce systole of increasing strength. This is called the staircase phenomenon. 48. Extrasystole (premature beats or ectopic beats) Premature beats (extrasystole) have been found in clinical ECG studies in the horse and in the dog. In the dog they are regarded as pathological signs. A premature contraction is a contraction of the heart prior to the time that normal contraction would have been expected. 49. Causes: Most premature contractions result from ectopic foci in the heart, which transmit abnormal impulses at any time during the cardiac cycle. Among the possible causes of ectopic foci are: Local area of ischemia. Small calcified areas in the heart. Toxic irritation of the AV node, purkinje system, or myocardium caused by drugs. Anxiety and lack of sleep. 50. According to the site of ectopic foci, extrasystole may be: * Atrial extrasystole, in which the ectopic focus is present in the atria. * Nodal (junctional) extrasystole, in which the ectopic focus is present in the AV node or in the AV bundle. * Ventricular extrasystole, in which the ectopic focus is present in the ventricles. 51. Rhythmicity Rhythmicity is the power of the heart to beat regularly. It is an inherent property of the cardiac muscle and is not dependent on nerve supply of the heart. This means that it is myogenic and not the neurogenic. 52. Rhythmicity in different cardiac fibers: Rhythmicity is not possessed to the same extend by the different muscle fibers of the heart. In the mammalian heart: 1-SA node: 120 beat/minute. This is the hightest rythmicity in the normal heart. The SA node is therefore the normal cardiac pacemaker. 2- AV node: 100 beat/minute. 3- AV bundle: 45 beat/minute. 4- Purkinje fibers: 35- 40 beat/minute 5- Atrial muscle: 30-40 beat/minute. 6- Ventricular muscle: 25-40 beat/minute (idioventricular rhythm). 53. In the frog, s heart: It is greatest in the sinus venosus (pacemaker), then in the atria and last in the ventricle. 54. Factors affecting rhythmicity: Nervous factor: *-Mild stimulation of parasympathetic nerve to the heart (the vagi) inhibit rhythmicity and *- strong stimulation can completely stop rhythmic contraction of the SA node. The ventricle stops beating for 4 to 10 seconds, then develop its own rhythm 55. *-Stimulation of sympathetic nerves to the heart increases rhythmicity of the whole heart including the ventricles. 56. Conductivity Conductivity is the ability of the heart muscle to transmit the excitation wave from one part of the heart to another. i.e. passage of a wave of depolarization along the membrane. The cardiac impulse is initiated from the SA node and rapidly propagated to the atrial and ventricular musculature by the conductive system. 57. Cardiac pacemaker and the conductive system I-The nodal fibers:a- The sinoatrial (SA) node is located in the posterior wall of the right atrium immediately beneath and medial to the superior vena cava. The SA node is the mammalian cardiac pacemaker. It is the part of the heart which has the highest rhythmicity and 58. b- Atrioventricular (AV) node is located on the right side of the interatrial septum at the junction of the atria and the ventricles close to the opening of the coronary sinus. The node continues into the bundle of His or AV bundle. 59. II- Specialized conducting fibers. a-Internodal or interatrial tracts constitute the pathways from SA node to both atria and to the AV junction: *-The anterior internodal pathway sends fibers to the right and left atrium and to AV node, *- The middle internodal tract goes only to the AV node, and *- The posterior internodal tract goes to the left atrium. 60. b- The bundle of His (AV bundle) is continuous with the AV node and pass through the fibrous skeleton between the atria and the ventricles. 61. c- The right and left bundle branches: The AV bundle breaks into two branches, right and left, that run down the right and left side of the inter ventricular septum beneath the endocardium to the apex of the heart where they reflect upward along the lateral walls of the ventricles to the heart base. 62. d- Purkinje fibers: The bundle branches, along their length, give many branches which penetrate the ventricular muscle fibers and form the peripheral purkinje network. 63. Propagation of the cardiac impulse: 1- Transmission through the atria: From the SA node, the depolarization wave passes from right to left by the internodal pathway over both atria, resulting in atrial systole. Within 70 m sec, all portions of both atria have started to contract. The velocity of conduction in the atrial 64. 2- Transmission at the AV node: The tissue which lies between the atria and the ventricle is an insulator and will not conduct the depolarization wave. The internodal pathways conduct, also, the depolarization wave to the AV node at a velocity of 0.5 to 0.6 meter/sec. The AV node conducts the depolarization wave very slowly at a velocity of 0.2 meter/sec. In fact, it delay its progress for approximately 70 m 65. The slow conductivity of the AV node has very important functions: *- It delays the start of activity of the ventricles till the end of atrial activity. This give enough time for blood to pass from the atria to the ventricles. *- Protect the ventricles from pathological high rhythms of atrial flutter (200-400 beat/minute) and fibrillation 66. 3- Transmission in purkinje system From the AV node, the depolarization wave moves to the bundle of His and its bundle branches. These lie in the inter ventricular septum and conduct the depolarization wave to the apex of the heart at a rapid rate of velocity of 1.5 to 4.0 meter/ sec. 67. 4- Transmission in the ventricular muscle: From the bundle branches, the depolarization wave rapidly travels through the purkinje network of highly conductive fibers which cover the endocardial (inner) surface of both ventricles. *-The depolarization wave moves through the ventricular muscle from the endocardial surface to myocardium, then to to the epicardial surface at a velocity of 0.4 0.5 meter/ sec. 68. *-Myocardial contraction begins in the ventricular septum, then the apex of the heart and finally the base. *- Myocardial repolarization (relaxation), is opposite to that of depolarization proceeding from the epicardial to the endocardial surfaces of the ventricle. 69. Factors affecting conductivity: 1- Nervous factors: *- Mild stimulation of parasympathetic nerves decrease conductivity of the impulse and *- Strong stimulation of the vagi can completely block transmission of the cardiac impulse. *- Sympathetic stimulation increases conductivity. 70. 2- Drugs: Acetylcholine decreases conductivity. Adrenaline increases conductivity. 71. Contractility Contractility is the ability of the heart muscle to contract and push blood into the circulation. The contractile response of cardiac muscle fibers begins just after depolarization and lasts about 1.5 times as long as the action potential 72. Properties of cardiac contraction: 1- All or None rule:- Because of syncytial nature of cardiac muscle, stimulation of any single atrial muscle fiber causes the action potential to travel over the entire atrial muscle mass, and similarly, stimulation of any single ventricular fiber causes excitation of the entire ventricular muscle mass. This is called the all or none rule. 73. All or non rule stated that the cardiac muscle either contracts maximally or does not contract at all, provided the conditions under which cardiac contraction occurs remain constant. Maximal contraction occurs on using threshold (minimal) stimulus or strong. 74. No contraction at all occurs on using a subthreshold (subminimal) stimulus. It is to be noted that all stimuli stronger than threshold stimulus give the same maximal contraction. 75. When comparing the effect of applying single stimulation to a voluntary muscle and to the heart, it will be seen that in voluntary muscle the strength of contraction of each single fiber obeys the all or none rule. In the heart, this rule is applies to the whole cardiac muscle fibers. The whole heart acts as a single unit because it is a functional syncytium. 76. The whole heart means either both atria and both ventricles but not the 4 chambers together. That the whole cardiac fibers have to contract together is of fundamental importance to the pumping action. If each fiber were to contract separately, the fractionate conditions would be ineffective in rising the intracardiac pressure, the pumping of the blood would not occur. 77. 2- Frank-Starling law of the heart. Within physiological limits, the force of contraction of the cardiac muscle is directly proportional to its initial length. 78. Physiological significance: The initial length of the fiber is determined by the degree of diastolic filling of the heart. As diastolic filling increases, the force of contraction of the ventricles is increased, and the heart pumps all the blood that comes to it not allowing excessive damming of blood in the veins. 79. Therefore, the heart can pump either a small amount of blood or a large amount. For example, during muscular exercise when the venous return increases, the diastolic volume increases, ventricular systole becomes stronger and cardiac output increases to prevent damping of blood in the veins. 80. Mechanism: When the cardiac muscle becomes stretched, the stretched muscle contracts with a greatly increased force, thereby automatically pumping the extra blood into the arteries. The increased force of contraction is probably caused by the fact that the actin and myosin filaments are brought to a more nearly optimal degree of interdigitation for achieving contraction. 81. Limitation: When the total quantity of incoming blood rises above the physiological limit that the heart can pump, the muscle fibers of the heart become over stretched which causes marked decrease in contractility as in heart failure where the heart is very dilated but the contraction is week. 82. 3- Staircase phenomenon. This phenomenon means gradual increase in muscle contraction following rapidly repeated stimulation or HR. If the cardiac muscle is stimulated repeatedly at the end of each diastole (during supernormal phase of excitability), each systole becomes stronger than the 83. It will usually be found that the first four to five contractions represented graphically as a stepwise or staircase. After a number of contractions, the strength of contraction remains stable. 84. The possible cause of the staircase is that the first stimulus produces thermal, chemical and other changes which improve the physiological state of the cardiac muscle. So, the second stimulus finds the muscle in a better condition and produces a stronger contraction and so on. The staircase phenomenon does contradict the all or non rule because this rule is good only when the conditions of the heart remain constant. 85. 4- Mechanical activity of the heart. The heart performs two types of contraction: a- Isometric contraction: The tension of the muscle is increased without change in muscle length. b- Isotonic contraction: The tension of the muscle 86. Factors affecting contractility. I- Nervous factor a- Stimulation of the parasympathetic nerves to the heart (the vagi) causes release of Ach at the vagal endings. Ach decreases the permeability of the membrane to Ca++ which decreases contractility of the atria in man and mammals. Vagus does not 87. b- Stimulation of the sympathetic nerves to the heart causes release of norepinephrine at the sympathetic nerve endings. Norepinephrine increases the permeability of the membrane to Ca++ which is responsible for increased contractility. 88. 2- Effect of ions: a- Effect of Ca ++: Excess Ca++ ions favours systole at the expense of diastole until the heart stop in a contracted state (calcium rigor ). b- Effect of K+ ions: Excess K+ ions favours cardiac diastole at the expense of systole and finally lead to stoppage of the heart in diastole. 89. 3-Effect of temperature: *- Moderate increase in temperature increases contractility of the heart due to increased permeability of the membrane to ions resulting acceleration of self excitation process. *-Moderate decrease in temperature decreases contractility. *- Excess warming to 45 C or excess cooling to 15 C stop the heart. 90. 4- Reaction of the blood: Acids decrease contractility and alkalies increases contractility. 5-Effect of drugs: *-Adrenaline and noradrenaline increase contractility of the heart. *-Ach, ether, chloroform and bacterial toxin decreases contractility of the heart. 6- Oxygen lack: decreases 91. Electrocardiogram Electrocardiogram (ECG) is a record of the electrical potentials generated by the heart during the cardiac cycle. Electrocardiograph is the apparatus. Electrocardiography is the method. 92. The cardiac impulse spreads as a wave of depolarization. The active region becomes electronegative in relation to the resting region. Recovery occurs as a process of repolarization, the recovered region becomes electropositive in relation to the still active regions. 93. Therefore, the difference in electrical potential can be recorded during either the process of incomplete depolarization or repolarization, but there is no record when the heart is completely depolarized or repolarized and the record remains isoelectric. 94. Because the body fluids are good electrical conductors, changes in potential are distributed throughout the body and can be recorded from the surface by applying electrodes to the skin. 95. Normal ECG The normal ECG is composed of 3 positive waves above the isoelectric line: P, R and T waves and 2 negative waves, below the isoelectric line: Q and S waves. 96. *- The first P wave represents atrial depolarization. End of P wave marks complete depolarization (excitation) of the whole atrial muscle. *-The second QRS complex represents ventricular depolarization. End of S wave marks complete depolarization of the whole ventricular muscle. 97. *-The final T wave represents ventricular repolarization. No waves are recorded at complete depolarization or repolarization ( the end of P,S and T). *-No manifestation of atrial repolarization is evident. *-Sometimes, another wave called U wave follows the T wave. It is not always present and it has no pathological importance. It represents supernormal phase of excitability. 98. P wave: - It represents the spread of excitation wave over the surface of both atria and has a duration of 0.1 sec. - It starts about 0.02 sec before the mechanical response of the atria (systole). - The start of P wave coincides with and is caused by the start of cardiac impulse in the SA node. The AV node receives the impulse at the top of P Wave. 99. - When the P wave reaches the isoelectric line, all atrial muscle is equally depolarized. - When QRS complex is absent as in heart block, atrial repolarization appears as a slow shallow negative wave following P wave and is called auricular T or Ta. 100. QRS complex: Represents the spread of excitation wave over the surface of both ventricles. Its duration is 0.04 to 0.08 sec. It starts about 0.02 sec before the mechanical response of the ventricles. 101. Q wave: It is a small negative wave representing spread of excitation wave in the interventricular septum. It is 0.02 sec. R wave: It is the largest positive wave and represents the excitation of the apex and most of the ventricular wall and base of the ventricles. It is 0.04 sec. S wave: It is a small negative wave represents the excitation of the remaining part of the base of the ventricles. It is 0.02 sec. 102. T wave: It is a positive represents repolarization of the ventricles. It is 0.25 sec in duration. U wave: Is a small positive wave, usually absent and when presents represents supernormal phase of excitability. It has duration of 0.25 sec. 103. Electrocardiographic leads: The ECG is recorded using a set of bipolar and unipolar leads. In bipolar electrocardiography a lead is the connection of two parts of the body by electrodes and wires with the electrocardiograph. 104. In the standard bipolar limb lead, the electrodes are connected with the limbs of the animal in three different types of connection: Lead I: right arm (R) and left arm (L). Lead II: right arm (R) and left leg (F). Lead III: left arm (L) and left leg (F). The potential difference between these two electrodes is recorded. 105. The cardiac cycle The contraction and relaxation of various chambers of the heart result in the characteristic pressure changes and valve movements comprising the cardiac cycle. The cycle repeat with every heart beat and includes systole (isovolumetric contraction, ejection), diastole (isovolumetric relaxation and filling), and then back to systole. 106. The right and left ventricular cycle are basically identical except for the beak pressures. The right ventricle will usually only achieve peak systolic pressure of 20 to 40 mm Hg while the left ventricle will develop pressures of 100 to 160 mm Hg in the resting animal. 107. *- The cardiac cycle start by systole of both atria followed by systole of both ventricles then diastole of the whole heart. *- Atrial systole lasts 0.1 sec while atrial diastole lasts 0.7 sec. *- Ventricular systole lasts 0.3 sec while ventricular diastole lasts 0.5 sec. 108. The cardiac cycle can be divided into the following phases: 1- Atrial systole. 2- Isovolumetric contraction phase. 3- Maximum ejection phase. 4- Reduced ejection phase. 5- Protodiastolic phase. 6- Isovolumetric relaxation phase 7- Increased inflow phase. 109. 1- Atrial systole: During the late ventricular diastole, the auricles contract causing flow of the remaining 30 of blood into the ventricles. - Duration: 0.1 second. - Atrial pressure increases - Ventricular pressure increases. - Ventricular volume increases. - Phonocardiogram: atrial systole causes vibration of the ventricular walls that is responsible for the fourth heart sound. - ECG: The P wave starts 0.O2 sec before the beginning of atrial systole. 110. 2- Isovolumetric contraction phase: - Duration: 0.05 sec. - The isovolumetric contraction raises the ventricular pressure which is enough to close the AV valves. - Auricular pressure increases (+ ve wave) due to bulging of AV cusps into the atria. - Ventricular pressure: increases. - Ventricular volume: no change. - Phonocardiogram: sudden closure of AV valves is responsible for the first heart sound - ECG: Q wave starts about 0.02 sec before the beginning of ventricular contraction and the rest of QRS complex occur during this phase. --- 111. 3- Maximum ejection phase: Ventricular contraction rises the left ventricular pressure above 80 mm Hg ( that exceed the aortic pressure) and the right ventricular pressure above 8 mm Hg (that exceed the pulmonary pressure) leading to opening of the aortic and pulmonary valves at the onset of this phase. About 60 of the blood is pumped rapidly into the aorta. - Duration: 15 second. - Atrial pressure: at the beginning of this phase show negative wave followed by gradual rise: 112. *- Negative wave caused by contraction of the ventricular muscle pulling down the AV ring. The auricles become distended, their capacity increases and the pressure drops. *- The gradual increase is due to the accumulation of blood in the auricles. - Ventricular pressure: increases. - Ventricular volume: decreases rapidly due to ejection of most of ventricular blood into the aorta. 113. - Aortic pressure: as the blood pumped by the ventricles into the aorta is greater than that which leaves the aorta into the periphery, the aortic pressure rises to a maximum (systolic) of about 120 mm Hg. The corresponding systolic pressure in the right ventricles and pulmonary artery is about 26 mm Hg. - Phonocardiogram: the vibrations of the first heart sound continue during most of this period. - ECG: T wave starts during this period. 114. 4-Reduced ejection phase: The ejection of the blood continues but at a reduced rate than the previous period. Only the remaining 40 of the blood is pumped during this period. The systole ends by the end of this phase. - Duration: 0.1 second. - Atrial pressure: increases due to accumulation of venous blood. 115. - Ventricular pressure: decreases. - Ventricular volume: decreases. Aortic pressure: shows some decline because the blood pumped into the aorta is greater than that leaving the aorta into the periphery. ECG: T wave continues during this phase and its summit ends the electrical systole. 116. 5- Protodiastolic phase: At the end of ventricular systole, the ventricular muscle remains contracted till the closure of the aortic (and pulmonary) valves at the end of this phase. Duration: 0.04 sec. Atrial pressure: increases due to accumulation of venous blood. Ventricular pressure: decreases rapidly and become lower than aortic pressure. Ventricular volume: remain constant. 117. Aortic pressure shows: a negative wave (incisura or dicrotic notch) due decrease in aortic pressure by the sudden closure of the aortic valve behind the moving column of blood. Positive wave, the dicrotic wave. Then, the aortic pressure decreases gradually due to the flow of blood from the aorta into the periphery. The decrease in the aortic pressure continues during the subsequent phases until the minimum (or diastolic pressure of the next cycle (80 mm Hg) at the end of isometric contraction phase. - ECG: the T wave continues during this phase. 118. 6- Isovolumetric relaxation phase: The ventricles relax without change in the volume allowing the ventricular pressure to fall rapidly. The high pressure in the auricle caused by accumulation of the venous blood open the atrioventricular valve at the end of this phase. - Duration: 0.06 sec. 119. - Auricular pressure: increased: gradually due to accumulation of venous blood. - Ventricular pressure: decreases rapidly. - Ventricular volume remains constant. Phonocardiogram: Sudden closure of the aortic (or pulmonary) valves that occur at the end of the previous phase is responsible for the second heart sound that heard during this phase. - ECG: T wave ends during this phase. 120. 7- Increased inflow phase: During isotonic relaxation, approximately 70 of the accumulated blood in the atria flow passively from the atria into the ventricles. For a short period of time about 50 of the blood flows rapidly. - Duration: 0.1 sec. - Atrial pressure: decreases. - Ventricular pressure: increases. - Ventricular volume: increases. - Phonocardiopgram: the rapid flow of blood into the relaxed ventricles produces vibrations that cause the third heart sound. - ECG: when a U wave is present, it takes origin mainly during this period. 121. 8- Reduced inflow phase: Only a small amount of blood flows slowly into the ventricles. - Duration: 0.2 sec. - Atrial pressure: marked decrease. - Aortic pressure: still decreasing. - Vetricular pressure: marked increase. - Ventricular volume: shows a steady increase. 122. 8- Reduced inflow phase: During this phase, only a small amount of blood flows slowly into the ventricles. - Duration: 0.2 sec. - Atrial pressure: marked decrease. - Aortic pressure: still decreasing. - Vetricular pressure: marked increase. - Ventricular volume: shows a steady increase. 123. The heart sounds Vibrations associated with the pulsatile events during the cardiac cycle produce sounds. Contraction of the normal heart produces vibrations by direct and indirect mechanisms. Many of these vibrations are transmitted to certain location on the surface of the thorax, but only a portion possesses sufficient frequency or amplitude to be audible. 124. Groups of audible vibrations are perceived as heart sounds when the ear or a stethoscope is placed at appropriate location on the thoracic surface. The phonocardiogram (PCG) is a graphic recording of the heart sounds after they have been transduced to an electrical signal with a microphone. 125. First heart sound: The first heart sound (S1) is longer and lower pitched than the second heart sound (S2) and occurs at the onset of ventricular ejection. Causes: *- The major cause for S1 is the sudden closure of the AV valves. Causes of less importance include: *- Contraction of ventricular muscle, *- Vibration of chordae tendineae, *- The vibrations set in the aortic and pulmonary walls as blood is ejected into these arteries at the onset of systole. In the dog, S1 is more intense than S2. The opposite is true for many horses under basal condition. 126. Second heart sound: S2 is a shorter higher pitched sound than S1 and occurs during isometric relaxation phase. Causes: *- The most important cause is sudden closure of semilunar valves. The other causes are: *- Vibrations of the blood. *- Vibrations of the walls of the aorta, pulmonary artery and to less extent the ventricle. The intensity of S2 seems to be related to arterial pressure. 127. Splitting or doubling of S2 occurs in: Normal human and dog as a respiratory related phenomenon appearing during inspiration only. Certain cardiac abnormalities in the dog. Most normal horses and it tend to be fixed rather than related to respiration. 128. Third heart sound (S3) : S3 occurs early in diastole near the end of rapid ventricular filling. It is caused by sudden tension of the chordae tendineae and vibrations arising in the walls of the ventricles. S3 is detected in phonocardiogram. It is rarely audible in normal dog and audible in many dogs with congestive heart failure. It is readily audible in apparently normal horses and in CHF where as in dog is frequently very intense. It is occasionally audible in man. 129. Forth heart sound: The fourth heart sound is seldom heard in dogs. It is common in apparently normal horses. S4 is associated with atrial contraction, acceleration of blood into the ventricles and tension of the AV valves at the end of atrial systole. S4 is heard after P wave and immediately precedes S1. 130. The pulse pressure wave The PolyGram During ventricular systole, blood is powerfully pumped by the left ventricles into the aorta which causes sudden increase of pressure and expansion of the elastic aortic wall. This expansion rapidly propagated along the walls of the arteries in the form of a wave called pulse pressure wave or arterial pulsation. The pulse is a wave of expansion of the arterial walls produced by variations in arterial pressure during each beat of the heart 131. Palpation: The pulse may be palpated in many of the superficial arteries, the site most varying in different species. In the horse: the pulse is palpated in the external maxillary artery. In the cow: the pulse is palpated in the external maxillary, the saphenous or the middle coccygeal artery. In the sheep, goat, dog, and cat: the pulse is palpated in the femoral artery. Palpation of the radial pulse, near the wrist, where the radial artery lies superficial to the lower end of the radius is a very old clinical method. 132. Significance of the pulse. It gives information about: a- The heart rate, its regularity, the presence of missed beats or extrasystole. b- The force of ventricular systole. c- The state of the arterial wall, whether soft and elastic or cord-like rigid. d- The level of the arterial blood pressure. 133. The jugular venous pulse It is a record of pressure changes in the external jugular vein. The curve obtained is similar to intra-atrial pressure changes. It is visible in some animals over the jugular veins in the region of the neck as in ox. 134. Cardiac Innervation The cardiac nerves arise bilaterally from sympathetic and parasympathetic (vagal) trunks. The atria are extensively innervated by noradrenergic, cholinergic, and afferent fibers, and cholinergic ganglion cells present especially on their 135. Ventricular innervation, with the exception of the bundle of His, is much less profuse than atrial innervation (in mammals, not in birds), and most species have only moderate cholinergic innervation, primarily following the course of coronary arteries. 136. Diving mammals may be exceptions since they can slow their hearts well below the AV node rate as part of diving reflex. The ventricular myocardium receives its modest innervation from the coronary plexuses that follow these arteries. They are predominantly composed of noradrenergic fibers. 137. The activity of the heart is adjusted to meet the need of the body mainly by the neural control system which has afferent fibers (inputs) from the heart to the cardio inhibitory centre (CIC) in the CNS and efferent fibers (outputs) from CNS to the circulatory system. The CNS control circulation through the autonomic nervous system. 138. The afferent fibers: They arise from the vaso- sensory areas. These areas are regions in the circulatory system which contain receptors sending impulses along afferent nerves to CIC causing reflexes controlling circulation. The most important vasosensory areas are: *- The aortic arch and carotid sinus: containing baroreceptors present in the aortic wall in the region of the aortic arch and at the base of each internal carotid artery 139. *- Aortic and carotid bodies: lying near the aortic arch and carotid sinus and containing chemoreceptors. The afferent fibers pass toward the CNS from aortic arch and aortic bodies in the aortic nerve which is a branch of the vagus nerve, whereas afferent fibers from the carotid sinus and carotid bodies pass in the sinus nerve which is a branch of the glossopharyngeal nerve. 140. The cardio inhibitory centre: It receives afferent connection from the baroreceptors and chemopeceptors via the vagi and glossopharyngeal nerves. The efferent fibers: The autonomic nerve supply to the heart consists of many mixed fibers containing both sympathetic 141. Functions of sympathetic stimulation: - Excite all cardiac properties, excitability, rhythmicity, conductivity and contractility. - Cause dilatation of coronary blood vessels. - Increase rate of oxygen consumption of the heart. Section of the sympathetic produces little or no slowing of the heart. Contrary to the vagus there is no sympathetic tone at the resting level of the ABP. 142. Function of vagal stimulation: - Inhibition of all cardiac properties. - Constriction of coronary blood vessels. - Decrease the rate of oxygen consumption of the heart. 143. The vagal tone. Definition: Normally the vagi at rest are continuously transmitting inhibitory impulses to the heart to check the inherently high rhythm of the SAN. This is because the CIC is continuously active at rest. Evidence: Section of both vagi leads to increase in heart rate from 90-120 to about 140-160 beat/ min in dogs. 144. Mechanism: Vagal tone is a reflex mechanism in which the stimulus is the normal resting ABP which stimulates the baroreceptors situated in the walls of the aortic arch and carotid sinus. From these receptors afferent excitatory impulses are transmitted from the arch of the aorta by the aortic nerve ( branch of the vagus ) and from the carotid sinus by the sinus nerve ( branch of glossopharyngea nervel ) to stimulate the CIC. 145. The CIC send efferent inhibitory impulses to the heart through the vagus nerve which decrease HR from the sinus rhythm to the normal average of HR. The normal intensity of the inhibitory tone, and the subsequent increase in HR following section of the vagi, varies in different animals. 146. Vagal escape: Moderate stimulation of the vagi depress all properties of the heart leading to slowing of the HR. Strong vagal stimulation causes strong inhibition of the SA node and stop the heart completely. The ventricles stop beating for 410 sec then develop their own rhythm and contract at a rate of 25 40 beats/min (idioventricular rhythm). This phenomenon is known as ventricular escape (vagal escape). This is because the ventricles in human are not supplied by the vagus nerve i.e. the ventricles escape from the inhibitory effect of the vagus. 147. The heart rate Normal standard and variations: Under the standard basal conditions of energy expenditure, the average rate/min: Elephant 30 Cat 120 Horse 40 Chicken 300 Cow 60 Mouse 600 Sheep & goat 70 Rat 400 Pig 70 Guinea pig 300 Dog 100 Man 70 148. Causes of variations: 1-size: smaller animals have a faster HR than larger animals due to higher MR/unit BW. This occur both within the species and among the different species. A small dog may have resting HR of 120, and a larger dog only 80 beat/minute. The HR of mouse is 600, of the rat is 400, while that of the elephant is 30 beat/minute. Comparing HR of cow and horse, the horse was found to have lower HR. 149. 2- Age: Young animals have a faster rate than mature animals due to their smaller size and less developed vagal tone . 3- Sex: The heart HR is faster in female than in male animals. 4- Standing: HR 5-7 beats/minute over lying in dairy cows. 5- Rumination: Caused a slight HR. 6- Eating: Caused a definite HR. 150. 7- HR during the last three months of gestation and during lactation. 8- Sleep: HR. 9- Excitement and muscular exercise: HR. 151. Regulation of the heart rate I- Nervous regulation A) Impulses from the circulatory system 1- Impulses from baroreceptors: Mary's law: The heart rate is inversely proportional to the level of arterial blood pressure (ABP) provided the other factors affecting the heart rate remain constant. 152. Exceptions: Both BP and HR increase in muscular exercise and in hyperthyroidism and decrease during sleep and in myxoedema. Mechanism: It is a baroreceptor reflex. Pressure receptors (or baroreceptors) are present in the adventitia of the aortic arch and the carotid sinuses. These receptors are mechanically stimulated by the level of the ABP which stretches the walls of the blood vessels. 153. As the ABP rises above the normal level, more and more of the receptors will be stimulated. Lowering of the pressure decreases the number of discharging receptors. At pressure levels below 30 mm Hg all the receptors are inactive. The afferent impulses are transmitted from the arch of the aorta by the aortic nerve a branch of the vagus. From the carotid sinus the impulses pass in the sinus nerve, a branch of the glossopharyngeal. 154. On reaching the medullary centers these impulses produce: Stimulation of the CIC. Inhibition of vasoconstrictor C. Response: 1- HR and strength of heart contraction COP. 2- Vasodilatation throughout the peripheral circulatory system which lead to PR. 155. Therefore, excitation of the baroreceptors by high ABP causes ABP to decrease because of both PR andCOP. Conversely, low pressure has opposite effects, reflexly causing the pressure to rise back toward normal. 156. 2- Impulses from the right atrium The Bainbridge reflex: An increase of pressure at the venous side of the heart lead to reflex cardiac acceleration. Mechanism: Increased venous return (VR) increases venous pressure in the right auricle and in big veins opening into it. This stimulates mechanical receptors present in their walls, which send stimulatory impulses to the medullary centers through afferent vagal fibers. 157. On reaching the medullary centers, these impulses produce the following effects: 1- Inhibition of CIC. 2- Stimulation of vasoconstrictor centre. The net effects are: 1- HR which lead to COP. 2- Vasoconstriction throughout the peripheral circulatory system which lead to VR. Significance: It helps pumping the excess VR into the arterial side of the circulation and prevents blood stagnation in veins. 158. Anrep's reflex: Another important effect produced by a rise in VR or of the right auricular pressure is the reflex inhibition of the vasoconstrictor tone to the coronary blood vessels. The blood supply to the cardiac muscle itself is thus increased. 159. B- Impulses from other parts Alarm-Smirk reflex: It is a reflex cardiac acceleration caused by contraction of voluntary muscle even small muscles of one finger. Afferent impulses originate from the proprioceptors in the muscle ascend in the spinal cord to medulla oblongata to inhibit CIC. The efferent is sympathetic. 160. Significance: During muscular exercise it supplies the active muscle with more blood and, thus, more O2 and nutrients. Carotid sinus syndrome: Stimulation of pressure receptors in the carotid sinus by an intrasinusal rise in pressure caused reflex cardiac inhibition and low 161. C) Impulses from the respiratory center: With inspiration the heart accelerates and with expiration is slow (the respiratory sinus arrhythmia). 162. D) Impulses from higher center 1- The cerebral cortex: Experimental stimulation of the orbital surface of the frontal lobe and of the cingulated gyrus in animals and in man produces acceleration or slowing of the heart among other autonomic effect depending upon the nature of the stimulus. 163. 2-The hypothalamus: The hypothalamus as a higher center of autonomic nervous system, it can influence the medullary cardiac centre. *-The anterior and middle nuclei are parasympathetic in function and produce bradycardia. *- The posterior and lateral nuclei are sympathetic in function and produce tachycardia. 164. For example, in emotion (a generalized sympathetic stimulation) the heart accelerates and during sleep the heart slows due to impulses from the hypothalamus, increasing the vagal tone. 165. II- Changes in the chemical composition of the blood 1-Changes in the tensions of CO2 and O2: CO2 excess, O2 lack and increase in (H+) increase HR through several mechanism: a-Direct inhibition of the CIC in the medulla. b-Stimulation of the chemical receptors in the carotid and aortic bodies, leading to a reflex cardiac acceleration. c-Reflex secretion of adrenaline. 166. 2-Hormones: a- Adrenaline: *-It HR, due to the direct effect of adrenaline on the SA node. *-It the strength of contraction and COP and thus raises the systolic BP. b- Noradrenaline: Has a marked vasoconstrictor effect and raises the ABP. HR is reflexly slowed due to ABP (Mary's law). 167. C-Thyroxin: HR through: -Direct action on SA node increasing its rhythmicity. -The sensitivity of SA node to the action of circulating adrenaline. -The general metabolism leading to production of large amounts of metabolites which causes peripheral vasodilatation and VR. HR is reflexly accelerates by means of Bainbridge reflex. -body temperature which causes HR. 168. III-The effect of blood temperature A rise in the temperature of the blood accelerates, while a drop in temperature slows the heart. The action of temperature is partly on the hypothalamus and the cardiac centers and partly a direct effect on the rhythmicity of the SA node. A rise of 1C leads to an increase of about 15 beats/min. 169. The cardiac output Definitions: -The cardiac output (minute volume) is the volume of blood pumped by each ventricle/min. It equals the product of the stroke volume and the heart rate. COP = Stroke volume X Heart rate. 170. -The stroke volume is the volume of blood pumped by each ventricle/beat. Cardiac index is the COP per square meter of body surface area. Cardiac index = COP Body surface area 171. Regulation of cardiac output The COP will vary under changing the physiological conditions and in disease process. Changes in COP depend on changes in stroke volume and heart rate. A) Regulation of stroke volume through: 1-Venous return. 2-Strength of myocardial contraction. 172. I-The effect of venous return The cardiac output is determined by the volume of blood returned by the veins from the tissues. According to the Starling law of the heart, within physiological limit the strength of the cardiac contraction is directly proportional to 173. When the venous return increases, the ventricles will fill more during diastole. The subsequent systole becomes stronger and the cardiac output increases. If the venous return is reduced, the diastolic volume decreases, the contraction becomes weaker and the cardiac output decreases. Normally it may thus be stated that the venous return and cardiac output are proportionally related. 174. Factors that influence the venous return: 1-The pressure gradient: The blood pressure in small veins is higher than in big veins just outside the thorax which in turn is higher than the blood pressure in the intra thoracic veins. Therefore the effective pressure gradient moves the blood 175. 2-The respiratory movements: -Inspiration VR and expiration VR. 3-Voluntary muscle contraction: This squeezes the blood from the capillaries and small veins that lie between the fibers into the veins towards the heart. During relaxation, the valves prevent regurgitation of blood 176. 4-The diameter of the arterioles:- If the arterioles are dilated, the blood flow from the arterioles to the veins are accelerated VR and COP. -Constriction of the arterioles VR and 177. 5-The tone of the capillaries: It is essential for the maintenance of VR. If all the capillaries are dilated (histamine release in shock), they will accommodate great volume of blood and little blood will return to the heart COP. 178. Such condition occurs after sever burns, extensive surgical operation or sever allergy due to tissue damage and release of dilator substances as histamine. The cardiac output would be markedly diminished and the ABP would drop to a fetal level (shock). 179. 6-The tone of the veins: The tone in veins prevents their complete distension. When veins are fully distended they accommodate most of the blood volume VR & COP. 7-Contraction of the spleen: Contraction of the spleen, ejects its store of blood into the circulation and increases VR & COP. 180. 8-The arterial pulsation: Help venous return in places where veins run parallel to arteries. The arterial pulsation are mechanically conducted to the venous wall and help to drive the blood towards the heart. 181. 9-Gravity: In the erect position, gravity helps to increase the VR from parts above the level of the heart to it, but it decreases the VR from parts below the heart. 182. B-The effect of heart rate on the cardiac output When the venous return remains constant: Physiological or moderate changes in HR have no effect on the cardiac output because it is associated with changes in stroke volume. 183. Excessive changes in HR as in paroxysmal tachycardia (200/min) or complete heart block (25-40/min) produce a decrease in cardiac output. This is due to excessive reduction in stroke volume (say 20) in the first and excessive slowing of the HR in spite of increase stroke volume (say 120) in the second condition. COP = 200 X 20 = 4000 ml/min. ( in paroxysmal tachycardia) = 30 x 120 = 3600 ml/min. ( in complete heart block) 184. When the venous return is increased as in muscular exercise, COP is increased due to: - Increased rate of blood flow, the heart can fill to maximum in a short diastolic period, so the stroke volume increase to a maximum of 200 ml. - Simultanious increase in HR to 200/min. COP = 200 X 200 = 4000 ml/min 185. II The strength of the mocardium The contractility (strength) of the myocardium exerts a major influence on stroke volume. The greater the strength of myocardial contractility (in sympathetic stimulation and increase in the initial length of cardiac muscle fibers), the greater will be the the stroke volume and the COP. Damage to the myocardium as in coronary thrombosis 186. III- The effect of the arterial blood pressure Provided the VR is kept constant, the changes in the arterial blood pressure have no strong effect on the COP. After the first few beats following the increase or decrease in ABP, the strength of the ventricular systole becomes adequate to give normal stroke 187. The cardiac reserve Cardiac reserve is the maximum percentage that COP increase above normal. There are three mechanisms of cardiac reserve: 1- Acceleration. The HR may be accelerated from 70 beats/min to a maximum of 200, which increases the COP nearly 188. 2- Increased stroke volume. In severe muscular effort the stroke volume may be increased by 3 folds, from an average of 70 ml/beat during rest to a maximum of about 200 ml. In this manner the COP may increase 9 folds (in man). 189. 3- Hypertrophy ( of limited value). Cardiac hypertrophy occurs when the heart is subjected to constant stress. Hypertrophy of the left ventricle occurs in hypertension and in aortic regurgitation. Hypertrophy of the right ventricle occurs in mitral stenosis and in pulmonary hypertension. 190. The arterial blood pressure Definition: The arterial blood pressure (ABP) is the lateral pressure exerted by the blood on the arterial walls, resulting in their distention. It vibrates during each cardiac cycle between a maximum (systolic) and a minimum (diastolic) pressure. It is written as systolic pressure / diastolic pressure. 191. Pulse pressure is the difference between systolic and diastolic pressure. Mean ABP is the average pressure tending to push the blood through the systemic circulation. Therefore, it is important for tissue fluid formation. It equals diastolic pressure +1/3 of the pulse pressure. 192. Normal standards : Under basal condition of complete physical, mental and digestive rest, the following table shows the systemic blood pressure (mmHg) of different species 193. Species Systolic Diastolic Mean Equine 130 95 107 Bovine 140 95 110 Ovine 140 90 107 Porcine 140 80 100 Canine 120 70 87 Feline 140 90 106 Giraffe 260 160 193 194. Factors maintaining normal arterial blood pressure I-The cardiac output: Provided the other factors that determine the ABP remain constant, an increase in the COP produces a corresponding increase in the ABP and a decrease in the COP leads 195. II- Elasticity of the arterial wall: The elasticity of the aorta and its large branches buffers excessive changes in the ABP during the cardiac cycle. During systole, the aortic wall distends and accommodates the stroke volume without great rise in the systolic BP. During diastole, the elastic walls recoil, their capacity decreases to prevent excessive drop in the diastolic BP and maintain a sufficient high diastolic BP. If the arterial walls were completely rigid (arteriosclerosis) leads to an increase in the systolic and a decrease in the diastolic pressure. 196. III- The peripheral resistance It is the resistance which the blood meats during its passage through the peripheral arterioles and capillaries. The peripheral resistance is determined by : 1- The diameter of the arterioles 2- Viscosity of the blood. 197. 1- The diameter of the arterioles: * A decrease in the diameter of the arterioles increases the peripheral resistance and increases the diastolic pressure more than the systolic pressure. * Vasodilatation decreases the diastolic pressure but the systolic pressure remains constant. 198. 2- Viscosity of the blood. It is due to plasma proteins and RBCs. * The increase in viscosity as in polycythaemia and in dehydration increases the resistance to the flow of blood through the small vessels and increases the diastolic pressure. * In vasodilatations and decreased viscosity of blood, the blood leaves the arteries more rapidly and diastolic blood pressure decreases. At the same time the increase in the venous return leads to an increase in the stroke volume which keeps the systolic pressure unaffected. 199. IV- The total blood volume in relation to the capacity of the circulatory system: 1- Changes in the blood volume: a) Moderate changes in BV do not affect significantly the ABP due to reflex alteration in the capacity of the circulatory system (vasodilatation and vasoconstriction). b) Severe decrease in BV as in severe hemorrhage leads to drop in the ABP in spite of vasoconstriction. On the other hand, if a large amount of blood is injected into a normal animal or in case of salt and water retention, the COP increases and the ABP rises. 200. 2- Changes in the circulatory capacity: a) Increase in capacity (vasodilatation), e.g. in case of allergy where large amount of histamine is released, leads to drop in the ABP. b) Decrease in capacity (vasoconstriction) e.g. in high sympathetic activity or injection of nor adrenaline, leads to increase in the ABP. 201. Vet UniteD Kfs We Do The Best.... To Be The Best