Cardiovascular System Physiology Year 2 PDF
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University of Basrah
Areej H.S. Aldhaher
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These lecture notes cover the Cardiovascular System, focusing on different aspects of physiology, such as abnormal heart sounds, cardiac output, and regulation. Provides detailed explanations and diagrams.
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Physiology , Year 2 The Cardiovascular System 1 LEC 2 Department: Basic Sciences Colleg...
Physiology , Year 2 The Cardiovascular System 1 LEC 2 Department: Basic Sciences College of Dentistry University of Basrah By Assist. Prof. Dr. Areej H.S. Aldhaher ABNORMAL HEART SOUNDS * An abnormal sound is called a murmur and is usually due to faulty valve action. * For example, if a valve fails to close tightly and blood leaks back, a murmur is heard. * Another condition giving rise to an abnormal sound is the narrowing, or stenosis (sten-O-sis), of a valve opening. * The many conditions that can cause abnormal heart sounds include congenital (birth) defects, disease, and physiologic variations. * An abnormal sound caused by any structural change in the heart or the vessels connected with the heart is called an organic murmur. 2 Cardiac OUT The volume of blood pumped by each ventricle in 1 minute is termed the cardiac output (CO). CO = HR X SV SV It is the product of the stroke volume (SV)—the volume of blood ejected from the ventricle with each beat HR The heart rate (HR)—the number of times the heart beats per mi Normal CO = heart rate (HR) x stroke vol.(SV) = 72 B/ min Å~ 70 ml = 5040 ml/min= (about 5L/ min) 5L/ 3 4 Regulation of Cardiac OUT Regulation of C.O.: C.O. = H.R. X S.V. A. regulation of H.R.: 1. By the A.N.S. Sympathetic→ Tachycardia→ ↑C.O.(example exercise). Parasympathetic→ Bradycardia→ decrease C.O 2. Hormonal Circulating catecholamines→ Act on non innervated B1 receptors of the S.A. node→↑ H.R. →↑ C.O. ( people with transplanted heart suffer from tachycardia). 5 CONTROL OF THE HEART RATE Although the heart’s fundamental beat originates within the heart itself, the heart rate can be influenced by the nervous system, hormones, and other factors in the internal environment. * During a fight-or-flight response, the sympathetic nerves can boost the cardiac output on average four to five times the resting value. Sympathetic fibers increase the contraction rate by stimulating the SA and AV nodes. They also increase the contraction force by acting directly on the fibers of the myocardium. These actions translate into increased cardiac output. * Parasympathetic stimulation decreases the heart rate to restore homeostasis. The parasympathetic nerve that supplies the heart is the vagus nerve (cranial nerve X). It slows the heart rate by acting on the SA and AV nodes These ANS influences allow the heart to meet changing needs rapidly. * The heart rate is also affected by substances circulating in the blood, including hormones, such as epinephrine and thyroxine; ions, primarily K+, Na+, and Ca2+; and drugs. * Regular exercise strengthens the heart and increases the amount of blood ejected with each beat. Consequently, the body’s circulatory needs at rest can be met with a lower heart rate. Trained athletes usually have a low resting heart rate. 6 The following variations in heart rate occur commonly. Note that these variations do not necessarily indicate pathology: Bradycardia (brad-e-KAR-de-ah) is a relatively slow heart rate of less than 60 beats/min. During rest and sleep, the heart may beat less than 60 beats/min, but the rate usually does not fall below 50 beats/min. Tachycardia (tak-e-KAR-de-ah) refers to a heart rate of more than 100 beats/min. Tachycardia is normal during exercise or stress, or with excessive caffeine intake, but may also occur with certain disorders. Sinus arrhythmia (ah-RITH-me-ah) is a regular variation in heart rate caused by changes in the rate and depth of breathing. It is a normal phenomenon. Premature beat, also called extrasystole, is a beat that comes before the expected normal beat. In healthy people, premature beats may be initiated by caffeine, nicotine, or psychologic stresses. They are also common in people with heart disease. 7 Regulation of C.O.: C.O. = H.R. X S.V. B. regulation of SV 1. Preload 2. contractility 3. afterload 8 9 3- afterload Is the load that the heart must eject blood against Or the forces that oppose ejection of blood out of the chamber 10 11 1.The arteries : The walls of the aorta & other arteries of large diameter contain large amount of elastic tissue which stretched during systole to prevent increase in systolic pressure more than 120 mmHg & recoil on the blood during diastole to maintain a high arterial pressure between heart beats (80 mmHg diastolic Bp), so that blood can continue to flow to tissues without interruption 2. The arterioles: Their walls contain less elastic tissue but much more smooth muscles , so they are the major site of resistance & small changes in their caliber cause large changes in the Total peripheral resistance & blood flow to the tissue. 3. Capillaries: The wall thickness of the cap. is about 1μm which is made up of a single layer of endothelial cells, which join with themselves to permit passage of molecules as large as 10 nm. the function of cap. is to exchange fluid, nutrients , electrolytes & other substances between the blood & the interstitial spaces. Each arteriole supply 10-100 capillaries. The opening of the arterial side of the cap. is surrounded by minute smooth muscle (precapillary sphincters 12 4 & 5- The venules & veins: The venules collect blood from the capillaries, they gradually coalesce into large veins which act as conduits for transport of blood from the tissues to the heart & Since the pressure in the venous system is very low, the venous walls are thin , contain few amount of elastic tissue so they have lower elastane & higher compliance. 13 Arterial blood Pressure is the force exerted by the blood on the wall of the arterial tree Systolic B.P. Diastolic B.P. maximum pressure exerted by the blood on the wall of the arterial tree during the cardiac cycle normally = ( 100-140 mmHg.) minimum pressure exerted by the blood on the wall of the arterial tree during the cardiac cycle normally=(60-90mmHg) Pulse pressure = systolic B.P - diastolic B.P. mean arterial B.P = diastolic + 1/3 pulse pressure 14 15 Peripheral resistance, it is affected by conditions that affect either or both of these factors. BP=CO*PVR ( CO: cardiac output, PVR: peripheral vascular resistance) C.O. determines systolic BP. Total peripheral resistance determines diastolic BP ↑TPR → ↑ DBP (arteriolar contraction) ↓TPR → ↓ DBP (arteriolar dilatation) So in exercise, sympathetic stimulation lead to increase in systolic pressure &Decrease in diastolic pressure. Figure1 expansion and elastic recoil of arterial wall during systole and diastole 16 Blood Pressure Must Be Regulated Low Blood Pressure High Blood Pressure Blood will not reach all Heart is placed Tissues specifically under great stress those Where gravity is acting Excess plasma against flow. leakage Most importantly the At the extreme, brain. capillaries burst 17 Physiological variations in BP Age During exercise ↑C.O Sex ↓TPR Body mass index ↑ systolic B.P ↓ diastolic B.P Meals female has lower B.P. than male Exercise because : Posture vlower Anxiety lower HR S.V. ↓ Slightly during inspiration and ↑ vlower TPR. Slightly during expiration 18 19 20 21 22 Mechanism of transduction Stretching of the wall of the blood vessels (example by an increasing level of blood pressure) causes stretching of the baroreceptors which contain stretch activated Na channels. With opening of these channels sodium ion move from the extracellular to intracellular fluid of the baroreceptors causing depolarization. So the rate of discharging of the baroreceptors will increases. Therefore, excitation of the baroreceptors by high pressure in the arteries reflexly causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in cardiac output. Conversely, low pressure has opposite effects, reflexly causing the pressure to rise back toward normal. Medulla oblongata 23 24 25 Reflexes initiated by stretching of the baroreceptors The baroreceptors are stimulated by distention of the structures in which they are located, and so they discharge at an increased rate when the pressure in these structures rises. Their afferent fibers pass via the glossopharyngeal and vagus nerves to the nucleus of the tractus solitarius in the medulla oblongata. These 2 nerves will inhibit the cardioexcitatory center (C.E.C.) and vasomotor center (VMC) and stimulate the cardioinhibitory center (CIC). The net effects are (1)vasodilation of the veins and arterioles throughout the peripheral circulatory system (2) decreased heart rate and strength of heart contraction 26 27 28 Long-term regulation The rennin – angiotensin – aldosteron system Angiotensin II has many effects that can elevate arterial pressure. 1. It is one of the most potent vasoconstrictors known, being four to eight times as active as norepinephrine.Vasoconstriction occurs intensely in the arterioles and much less so in the veins. Constriction of the arterioles increases the total peripheral resistance>>>↑DBP. The mild constriction of the veins promotes increased venous return of blood to the heart>> ↑EDV>> ↑SV>> ↑CO>> ↑SBP 29 2. Angiotensin II causes the adrenal glands to secrete aldosterone, and an important subsequent function of aldosterone is to cause marked increase in sodium reabsorption by the kidney tubules, thus increasing the total body extracellular fluid sodium. This increased sodium then causes water retention promotes increased venous return of blood to the heart>> ↑EDV>> ↑SV>> ↑CO>> ↑BP. 3. Angiotensin II acts on the hypothalamas and stimulate the thirst center to increase water intake. it also increase the secretion of vasopressin hormone 4. Direct effect on the kidney Angiotensin II causes consitriction of the efferent arterioles to maintain the GFR 5 Angiotensin II also increases the release of norepinephrine from the postgang. nerve endings >> (vasoconstriction + ↑CO) >> ↑BP 30 31