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2.00 Review of literature : 2.1 Introduction The muscle fibers of the human heart are excitable cells like other muscles, but they have a unique property that each cell in the heart will spontaneously contract at a regular rate because the electrical properties of the cell membrane spontaneously alter with time and regularly depolarize (kestin 1993). The normal human heart acts as a strong muscular pump; a little larger than a fist of the hand. It pumps blood continuously through the circulatory system. Each day the average heart expansions and contractions is about 100,000 times, and pumps about 2,000 gallons of blood. In a 70 years lifetime, an average human heart beats more than 2.500.000.000 beats/min (Levick 1998). 2.1.1 Conductive system of the heart For the heart to function properly, the four chambers must beat in an organized manner. A chamber contracts when an electrical impulse or signal moves across it through specific anatomical structure fibers called conductive system. A signal starts in a small bundle of highly specialized cells located in the right atrium at its junction with the superior vena cava, called the sinoatrial node (SA node) or pacemaker of the heart. The SA node generates and discharges electrical impulses at a given rate, but under steady state of emotional reaction and hormonal factors. Depolarization of the SA node triggers a wave front of depolarization, which travels through the both atria causing them to contracts and sending blood into ventricles. Direct conduction to the ventricles is prevented by fibrous ring, which separates the atria from the ventricles. The atrioventricular node is situated beneath the right atrial endocardium at the lower end of the interatrial septum. It conducts slowly and regulates the frequency of conduction to the ventricles. From the atrioventricular (AV) node, the bundle of His passes through the fibrous ring, and it is divided into right and left bundle branches which pass down to the respective sides of the ventricular septum. The bundle branches are subdivided into anterior and posterior hemibundles, and all fibers of the bundle of His radiate out the Purkinje network (Berne and Levy 1992). 2 2.1.2 Pacemaker of the heart Pacemaker tissue is found in the SA node, the AV node and the purkinje tissue, but because the rate of depolarization of the SA node is faster than the other pacemaker tissues and depolarization impulses spread via the conducting pathway to other pacemaker tissues before they become spontaneously depolarized, so the SA node is the pacemaker of human heart (Guyton and Hall 1996). Pacemaker of the heart has unstable resting membrane potential, which equals -55 to -60 mV. This negativity in the SA node is due to an inherent leakage in Na+ channels. The high concentrated level of Na+ ion in extracellular fluid and the negative electrical charge inside the SA fiber lead to leakage of Na+ ions from outside to inside the membrane of the SA node. Influx of Na+ ions helps for rising membrane potential until reaching the threshold voltage (-40mV), and at that time (Ca – Na) channels become activated. This activation leads to rapid entry of both Ca++ and Na+ ions, so that the action potential will occur in SA node (Ganong 1997). The Ca – Na channel will stay open for about 100 to 150 ms, and at the same time potassium (K+) channels will start to open. These two causes help to prevent depolarization of the SA node all the time, K+ channels remain open for another few tenths of a second carrying a great excess of positive K+ charges out of the cells, which temporarily causes excess negativity inside the cells, this is called hyperpolarization. K+ channels start to be closed, and now the inward leaking Na+ ions once again become over balance the outward flux of K+ ions, which cause the resting membrane potential to start again. Then, reexcitation will occur in the SA node to elicit another cycle (Levick 1998). The frequency of pacemaker firing is controlled by the activity of both divisions of autonomic nervous system (sympathetic and parasympathetic). Changes in autonomic neural activity often induce a pacemaker shift. Where the site on initiation of impulse may shift to a different locus within the SA node or to a different component of the atrial pacemaker complex (Hainsworth 1995). 2.1.3 Cardiac innervations centers The autonomic nerve supply to the heart has the important function of rapid adjustment of the heart rate and vasomotor tone according to different conditions in the body. There are higher centers in the medulla oblongata which control the sympathetic and parasympathetic discharge to cardiovascular system. These centers are called the cardiovascular centers. The cardiovascular centers have no sharp boundaries. They are 3 found as diffuse areas in the medullary reticular formation with a great deal of anatomical and functional overlap (Abusitta et al 1995). 2.1.3.1 The pressor or vasoconstrictor area This area is also called the vasomotor area or vasomotor center (VMC). It is located bilaterally in the anterolateral portions of the upper medulla oblongata and it is connected with preganglionic sympathetic nerves in the spinal cord. However, this area contains two centers; cardiac acceleratory center (CAC), which is also known as cardiac stimulatory center (CSC) and the vasoconstrictor center (VCC). Stimulation of the pressor area leads to circulatory sympathetic effects; which result in generalized vasoconstriction of the arterioles, acceleration of the heart rate and increasing in myocardial contractility force. On the other hand, under normal resting conditions, the VCC discharges impulses continuously at a certain rate. This is called vasomotor tone which leads to partial vasoconstriction of the arterioles and venules (Guyton and Hall 2000). 2.1.3.2The depressor or vasodilator area It is found bilaterally in the anterolateral portions of the lower of the medulla oblongata and it contains a cardio inhibitory center (CIC) which is an inhibitory area. It is present in the dorsal motor nucleus of the vagus nerve or nucleus ambiguus. Stimulation of this area produces parasympathetic (vagal) effects on the heart which will lead to a decrease in the heart rate and atrial contractility force. This area is equally discharges a continuous inhibitory impulses along the vagus nerve to the heart. This is called vagal tone which checks the high inherent rhythm of the S.A node (Guyton and Hall 2000). 2.1.3.3 The medullary sensory area This area located bilaterally in the tractus solitarius in the posterolateral portions of the medulla and lower pons. The neurons of this area receive sensory nerve signals mainly through the vagus and glossopharyngeal nerves, and the output signals from this sensory area then help to control the activities of both the vasoconstrictor and vasodilator areas of the vasomotor center, thus providing "reflex" control of many circulatory functions. (Guyton and Hall 2000). 4 2.1.4 Innervation of the Heart The major controlling influence on reflex cardiac activity is the autonomic nervous system. In terms of it's regulation, the autonomic nervous system exerts it's functions via two counter balancing influences provided by the sympathetic and parasympathetic systems. 2.1.4.1 The sympathetic innervation of the heart The preganglionic sympathetic fibers originated from the lateral horne of the upper four thoracic segments of the spinal cord (T1-T4). These preganglionic fibers relay in the cervical ganglia (superior, middle & inferior) and the upper four thoracic ganglia of the sympathetic chain. However, these fibers arise from these ganglia to supply the atria and the ventricles of the heart including the specialized tissues of the cardiac conducting pathway as well the coronary vessels. The main results of stimulation of these fibers are activation of all properties of the cardiac muscle, vasodilatation of the coronary arteries and increasing of the oxygen consumption of the cardiac muscles (Guyton and Hall 2000 and Sukker et al. 2000). Under resting normal conditions, the sympathetic nervous system discharges impulses continuously to the heart. The effect of this impulses has an positive inotrophic tone which increase the pumping capacity of the heart by 20-25% as well, it also increase the heart rate up to 120 beats/min. However, this positive inotrophic tone is abolished by more dominant negative chronotrophic vagal tone (Guyton and Hall 2000). 2.1.4.2 The parasympathetic innervations of the heart The parasympathetic supply to the heart is take place via two vagi: the preganglionic vagal fibers arise from the dorsal vagal nucleus (CIC) in the medulla oblongata and the preganglionic fibers relay in terminal ganglia located in the atria. However, the postganglionic fibers are short, they arise from the terminal ganglia to supply the atrial muscle, S A node, AV node, main stem of the AV bundle. Stimulation of these fibers will lead to inhibition of all cardiac muscle properties, vasoconstriction of coronary arteries and decrease the oxygen consumption of the heart (Guyton and Hall 2000 and Sukker et al. 2000). Vagal tone is the continuous inhibitory impulses carried by the vagus nerve from the CIC to the heart to inhibit the high inherent rhythm of the S.A. node. This is equally occurs under resting condition and produces a 5 basal heart rate (about 70 beats/min). At rest, the vagal tone to the heart is dominant over the weak sympathetic tone. However, during muscular exercise heart rate is increased due to a decrease in vagal tone and an increase in sympathetic activity (Guyton and Hall 2000). 2.1.5 Regulation of Heart Rate Heart rate is normally determined by the rate of depolarization cardiac pacemaker (Hainsworth 1995). Rhythmical beating of the heart at a rate of approximately 100 beats/min. will occur in complete absence of any nervous and hormonal influences, but under normal resting the heart rate is about 72 beats/min. The resting heart rate can vary widely in different individuals during different physiological and physical conditions (Vander et al. 1994). The heart rate indirectly affects the force of the contraction. As the heart rate is increased, the duration of diastole becomes shorter and the end diastolic volume (EDV) becomes smaller, the stroke volume according to Starling's low is decreased. The diastolic filling will be affected when heart rate exceeds 120 beats/min. But during exercise there is compensation for any increase in sympathetic stimulation with increase in strength of cardiac contraction (Guyton and Hall 1996). 2.1.5.1 Autoregulation of the heart rate (intrinsic control) Cardiac muscle has myogenic rhythm, that has ability to contract Rhythmically without nervous input (Ganong 1997). The heart will continue to beat even when it is completely removed from the body. At least some cells in the walls of all four cardiac chambers are capable for initiating beats, such as nodal tissues or specialized conducting fibers of the heart. When the SA node and other components of atrial pacemaker complex are excised or destroyed, pacemaker cells in the A V node usually are the next most rhythmic and they become the pacemaker for the entire heart. When the AV Junction is unable to conduct the cardiac impulses from the atria to ventricles, idioventricular pacemakers in the Purkinje fiber network initiate the ventricular contractions at frequency 30 to 40 beats per minute. Other regions of the heart that initiate beats under special circumstances are called ectopic foci or ectopic pacemaker. Ectopic foci may become pacemaker when their own rhythmicity become enhanced, or the rhythmicity of the higher order pacemakers becomes depressed, or all 6 conduction pathways between the ectopic focus and these regions with greater rhythmicity become blocked (Berne and Levy 1992). 2.1.5.2 Nervous regulation of the heart rate(extrinsic control) The S.A node is usually under the tonic influence of both divisions of the autonomic nervous system. The sympathetic system enhances automaticity where as the parasympathetic system inhibits it. Changes in the heart rate usually involves a reciprocal action of the two divisions of autonomic nervous system (Berne and Levy 1992). 2.1.5.2.1 Action of cardiac sympathetic fibers Increased activity in the sympathetic nerves results in increases both heart rate and the force of contraction. In addition, the rate conduction through the heart of cardiac impulse is increased due shorting in the AV nodal delay and the duration of the contraction shortened (Hainsworth 1995). in of to is Most of the norepinephrine released during sympathetic stimulation is taken up again by the nerve terminals and much of remainder is carried away by the blood stream, these processes are relatively slow. Therefore, at the beginning of sympathetic stimulation, the facilitatory effects on the heart attain steady state values much more slowly due to the inhibitory effects of vagal stimulation (Berne and Levy 1992). Increase in the heart rate leads to decrease of the time available for diastolic filling, but the quicker contraction and relaxation induced simultaneously by sympathetic nerve partially compensate for this problem by permitting a large traction of cardiac cycle to be available for filling. In other words, increasing in heart rate above critical level, the heart strength itself will decrease due to overuse of metabolic substance in cardiac muscles, at the same time decrease the duration of systolic contraction and allows more time for filling during diastole (Vander et al. 1994). There is a greater effect on heart rate from stimulation of right sympathetic nerve than left at low frequency of stimulation. The left sympathetic nerve is more concerned with regulation of cardiac inotropic state (Hainsworth 1995). 2.1.5.2.2 Action of cardiac parasympathetic fibers The parasympathetic (vagal) nerves innervate the A.V conducting pathways, and the atrial muscle. The question of whether the vagi provide an efferent control of ventricular muscle remains controversial (Hainsworth 1995). 7 The stimulation of vagus nerve slows the heart rate, reduces force of contraction of atrial muscle, increases delay of A.V node, and prolongs action potential. Minimum duration of atrial action potential has about 120 ms (Bary 1999). The right vagus nerve has a greater effect than the left due to different innervations in both sides and frequency of stimulation (Berne and Levy 1992). Strong vagal stimulation can decrease the heart rate to zero or almost zero, and then the heart after being stopped for few seconds, then start to beat again at rate 20-40 beats/min due to Autoregulation in AV node and the purkinje fibers. Also strong stimulation of vagus nerve to the heart leads to decrease of the strength of the heart contraction by 20-30 percent. This decrease is not great because vagal fibers are distributed mainly to the atria but not much to ventricles where the power of cardiac contraction occurred. Greater decrease in the heart rate combined with slight decrease in heart contraction can decrease ventricle pumping to 50% or more (Guyton and Hall 1996). 2.1.5.3 Reflexes influencing the heart rate Heart rate, at any instant of time, represents the resultant of many influences on the vagal and sympathetic centers. Some reflexes may increase heart rate through a decease in vagal tone, an increase in sympathetic activity, or both. Others exert the opposite effects. 2.1.5.3.1 Baroreceptors reflex Baroreceptors or stretch receptors are found in the wall of each internal carotid artery slightly above the carotid bifurcation in an area known as carotid sinus, also in the wall of the aortic arch (Vander et al. 1994). The Baroreceptors system opposes either increases or decreases in arterial pressure, it is often called pressure buffer system and the nerves from these receptors which send their afferent impulses called buffer nerves Normally. the carotid sinus Baroreceptors are not stimulated at all by pressure between 0 and 60 mmHg, but above 60 mmHg, they respond progressively more rapidly and reach a maximum at about 180 mmHg. The responses of the aortic Baroreceptors are similar to those of carotid receptors except that they operate, in general, at pressure levels about 30 mmHg higher. Stimulation of Baroreceptors results in increase in efferent 8 cardiac vagal activity and decrease in sympathetic activity. After the Baroreceptors signals have entered the tractus solitarius of the medulla, secondary signals eventually inhibit the vasoconstrictor center of medulla and excite of the vagal center. The net effects are vasodilatation of the veins and arterioles throughout the peripheral circulatory system, decreased heart rate and strengthen heart contraction. Therefore, excitation of the Baroreceptors by increased pressure in the arteries reflexly causes the arterial pressure to decrease because of both decrease in peripheral resistance and in cardiac output. Conversely, low pressure has opposite effects, reflexly causing the pressure to rise back towards normal (Guyton and Hall 2000). 2.1.5.3.2 Atrial and pulmonary artery reflexes Both the atria and the pulmonary arteries have stretch receptors, called low pressure receptors, in their walls similar to the baroreceptor stretch receptors of the large systemic arteries. These low pressure receptors play an important role in minimizing arterial pressure changes in response to changes in blood volume. With the arterial baroreceptors denervated, the ptessure will rise 40 mm Hg. If the low pressure receptors are also denervated, the pressure may rise 100 mm Hg(Guyton and Hall 1997). Thus, one can see that even though the low pressure receptors in the pulmonary artery and in the atria connot detect the systemic arterial pressure, these receptors nevertheless do detect simultaneous increases in pressure in the low pressure areas of the circulation caused by an increase in volume, and they elicit reflexes parallel to the baroreceptor reflexes to make the total reflex system much more potent for control of arterial pressure (Guyton and Hall 1997). Mechanoreceptors have reflex effects on respiration and heart rate. These receptors are found in upper respiratory airway, bronchi, alveoli and pulmonary artery (Haslettetal1999). In pulmonary blood vessels there are end unmyelinated ( C ) fibers innervated an area called Juxtacapillary receptors. These receptors are stimulated by hyperinflation of the lung and the response of the stimulation is apnea followed by rapid breathing, bradycardia and hypotension (Vander et al. 1994). 9 Stretch receptors exist in the wall of the pulmonary artery and they are excited by increase in pulmonary arterial pressure, the reflex response is an increase in pulmonary vascular resistance but it seems to have no direct effect on the heart rate (Guyton and Hall 1997). 2.1.5.4 Chemical regulation of the heart 2.1.5.4.1 Arterial chemoreceptor The chemoreceptor is the chemosensitive cells that respond to hypoxia, hypercapnia and acidosis of arterial blood. Chemoreceptors include two main types: peripheral and central chemoreceptors. The peripheral chemoreceptors are situated mainly in carotid and aortic bodies. The most obvious effects of peripheral chemoreceptor stimulation are increases in rate and depth of respiration (Hainsworth 1995). However, then- influence on the circulation is slight at normal gas tensions. Peripheral chemoreceptor afferent fibers accompany the baroreceptor afferent in Xth and IXth cranial nerves(Levick 1998). Each carotid or aortic body is supplied with an abundant blood flow through a small nutrient artery, so that chemoreceptors are always in close contact with arterial blood. However, the chemoreceptor reflex is not a powerful arterial pressure controller in the normal arterial pressure range because the chemoreceptors themselves are not stimulated strongly by pressure changes until arterial pressure falls below 80 mmHg. When excitation of these chemoreceptors is increased by hypoxia and hypercapnia, they elicit a sympathetically mediated constriction of resistance vessels (except in the skin), constriction of splanchnic capacitance vessels, bronchoconstriction, increase secretion of antidiuretic hormone and release of adrenaline. The results of all of these changes will help in increasing the arterial blood pressure, increase heart rate, and by the short time return P02, PC02 and PH to normal level (Guyton and Hall 2000). Central chemoreceptors on the other hand, are located at near the ventrolateral surface of medulla oblongata, this area is highly sensitive to change in either blood PC02 or hydrogen ions concentrations which are the only important direct stimulus of central chemoreceptors, that affect mainly the respiratory center in the medulla and also have slight effect on the adjacent vasomotor center (Guyton and Hall 2000). 10 2.1.5.5 Hormonal and acetylcholine regulation of the heart 2.1.5.5.1 The action of thyroid hormone of the heart rate Cardiac activity is sluggish patients with inadequate thyroid function (Hypothyroidism); that is the heart rate is slow and cardiac output is diminished. The converse in true in-patient with over activity of thyroid gland (Hyperthyroidism) (Berne and Levy 1992). 2.1.5.5.2 The action of adrenomedullary hormones on the heart The adrenal medulla is essentially a component of the autonomic nervous system. The principal hormone secreted by the adrenal medulla is epinephrine, although some norepinephrine is also released (Berne and Levy 1992). Adrenaline and noradrenalin show both similarities and differences in their effect on the circulation, but both adrenaline and noradrenalin have stimulatory effects on the cardiac beta-adrenoceptors, so their action is to increase heart rate and contractility (Hainsworth 1995). 2.1.5.5.3 The action of acetylcholine on the heart Acetylcholine (Ach) is released by vagal stimulation and it reduces the heart rate by increasing K+ ion conductance of pacemaker cells in the SA node and also it interacts with muscarinic receptors in cardiac cell membrane which lead to a decrease in myocardial contractility (Noma et al. 1990). 11