Cardiovascular Physiology PDF

srOOr Objectives of CVS: 1- Introduction. 2- Know the properties of the cardiac muscle (Excitability, rhythmicity, conductivity and contractility) and factors affecting them. 3- Know the innervations of the heart and regulation of the heart rate. 4- Describe the cardiac out put and its...

srOOr Objectives of CVS: 1- Introduction. 2- Know the properties of the cardiac muscle (Excitability, rhythmicity, conductivity and contractility) and factors affecting them. 3- Know the innervations of the heart and regulation of the heart rate. 4- Describe the cardiac out put and its regulation. 5- Know arterial blood pressure, factors maintain ABP and regulation of ABP. 6- Describe hemorrhage and its compensatory mechanisms. 7- Know types and stages of shock. srOOr  Introduction The cardiovascular system is formed of the heart and a closed system of blood vessels f illed with blood. The pumping function of t he he a r t a l l ows cont i nuous ci r cul a t i on of t he bl ood a nd continuous exchange between the blood and interstitial fluid. srOOr The four major functions of the cardiovascular system are: 1 -To transport nutrients ,gases and waste products around the body 2 -To protect the body from blood loss 3 -To help the body maintain a constant body temperature‘( thermoregulation)’ 4 -To help maintain fluid balance within the body srOOr Properties of cardiac muscle 1- Rhythmicity. 2- Contractility 3- Excitability 4- conductivity 1- Rhythmicity: Definition: It’s the ability of cardiac muscle to beat regularly and spontaneously. It’ inherent, myogenic in nature, not nervous srOOr Factors affecting rhythmicity: 1- Nervous factor: Sympathetic system secrets adrenaline that increases rhythmicity Parasympathetic secrets acetyl choline that decreases rhythmicity 2- Ions and pH: Excess Na ions decrease rhythmicity Excess K favors diastoles and stops heart in diastole Excess Ca favors systoles and stops heart in systole Acid like K favors diastole Alkaline like Ca favors systole srOOr 3- Oxygen supply: absence of O2 stops heart after few beats 4- Drugs: adrenaline increase rhythmicity Acetyl choline decrease rhythmicity 5- Temperature: Moderate increase temperature lead to increaserhythmicity Moderated decrease temperature leads to decrease rhythmicity. Excess warming or cooling stop rhythmicity. srOOr 2- Contractility: Definition: It’ the ability of cardiac muscle to contract and push blood into the circulation. Whole heart either contracts max or does not contract at all (All or non rule) srOOr Factors affecting contractility:  Same factors as rhythmicity plus  Starling law: The force of cardiac contraction is direct proportional to the initial length of cardiac muscle provide other factors are constant. The signif icance of the law allow the heart to pump a small or large amount of blood enter the heart without damping of blood. srOOr 3- Excitability: Excitability change during cardiac cycle: 1- Absolute refractory period (ARP):  Definition: It’s the period during which the excitability is completely lost and the heart doesn't respond to any strong stimuli (depolarized membrane). srOOr 2- Relative refractory period (RRP):  Period during which gradual recovery of excitability until it reaches to normal.  Strong stimuli applied can produce weak contraction (extrasystole) 3- Supernormal phase:  The excitability is more than normal  Weak adequate stimuli produce strong contraction. srOOr 4- Conductivity: Def inition: It’s ability of cardiac muscle to transmit impulse from one part to another.  Conductive parts include the following:  SAN  Internodal  AVN  AVB  LT,  RT bundles srOOr Cardiac Innervations The activity of the heart is adjusted to meet the requirement of the body at different situations by several regulating mechanisms. The most important is the autonomic inervation of the heart. Sympathetic system secrets adrenaline that increases rhythmicity. Parasympathetic secrets acetyl choline that decreases rhythmicity. srOOr The Heart Rate  Normal heart rate ranges from 60-100 beat/minute with an averages 70 beat/minute in male adult during rest. A) Variation with age: The resting rate is faster in infancy B) Variation with sex: The resting rate is faster in female. C) Physical training: The heart rate in athletes is slower srOOr Factors Regulate Heart rate  The adjustment of the heart according to the requirements of the body is mainly carried out through the following issues: (I) Nervous Regulation (II) Humoral Regulation (III) Physical regulation. srOOr I- Nervous Regulation A - Impulses from the circulatory system: The most important are : Impulses from baroreceptors (Pressoreceptors) Mary's law  (Definition) The heart rate is inversely proportional to the arterial blood pressure, provided the other factors affecting the heart rate remain constant. srOOr Mechanism: It's a baroreceptor reflex.  Stimulus: Change in ABP  Receptors: Increase ABP stimulates the baroreceptors  Afferent: the aortic branch of vagus & sinus branch of glossopharyngeal nerves.  Center: CIC in the medulla.  Response: Increase ABP leading to decrease the hear t rate also associated with reflex vasodilatation of arteries.  Both ref le xes cause lowering ABP toward normal value so keep ABP within physiological level. srOOr B- Impulses from Respiratory center:  Effect: The heart accelerates during inspiration and slows during e x pi ra t i on; t hi s phe nom e non i s ca l l e d "Re spi ra t or y si nus arrhythmia". srOOr C) Impulses from higher centers: 1- Cerebral cortex: - Conditioned reflexes - Emotion 2- Hypothalamus: - Autonomic nervous system - Emotions srOOr II) Humoral Regulation 1- Adrenaline: increases H.R. by direct stimulation of S.A. Node. 2- Noradrenaline: decreases H.R., because it produces generalized vasoconstriction and elevation of ABP in intact animals 3-Thyroxine: accelerates the heart (sleeping pulse 90/min) through:  Direct action on S.A.N increasing its rhythmicity.  Increasing the sensitivity of S.A.N. to the action of circulating adrenaline and sympathetic stimulation.  Increasing the general body metabolism. srOOr  II) Physical regulation  A rise in the body temperature leads to increases the heart rate, while a drop in temperature slows the heart.  A rise of l°C leads to an increase about 15 beats/mm.  However, increase in the body temperature beyond 40°C, the heart rate may actually decrease. srOOr The Cardiac Output 1- Stroke volume: It is the amount of blood pumped out by each ventricle per beat (70 ml/ beat). 2- The cardiac output: The volume of blood ejected by ventricle per minute. The output of both ventricles is equal (70 x 70 = 4900 ml/ min). srOOr Factors controlling Cardiac out put: A-Stroke volume B- Heart rat A) Stroke Volume (SV) Stroke Volume is determined by three factors: 1- venous return 2- arterial blood pressure 3- contractility srOOr  (I)- Venous return: Factors affecting venous return (VR) 1-The pressure gradient:  The blood pressure in the venular end of the capillaries is about 15 mmHg and in the big veins just outside the thorax is zero.  This pressure difference is responsible for moving the blood towards the heart.  The VR is proportional to the pressure gradient. srOOr 2- The respiratory muscle:  During resting inspiration, VR increases because intrapleural pressure becomes more negative. So blood is sucked from extrathoracic to intrathoracic veins 3- Skeletal muscle pump:  During contraction of skeletal muscles, the increased muscle tension around the soft walled veins squeezes their blood content. 4- Diameter of arterioles:  Dilatation of the arterioles accelerates the blood f low from the arteries to the veins. The venous return and the COP are increased. srOOr 5- Capillary tone:-  If capillaries are widely dilated, they would accommodate a great volume of blood, the VR and COP are reduced 6- Venous tone:  Excess vasodilatation of veins may lead to pooling of blood in the venous system and decreases VR. 7- Arterial pulsation:  Helps VR in place where vein runs parallel to and near to artery.  When pulsations are mechanically transmitted to the venous wall, they propel blood towards the heart. 8- Contraction of spleen and blood reservoir  Increase venous return. srOOr  (II)-Contractility :  An increase in force of ventricle contraction (e.g., produced by sympathetic activation of the heart and positive inotropic agents, such as digoxin) increases COP.  While decrease in force of ventricular contraction as in coronary thrombosis lead to decrease COP (III) Arterial blood pressure:  An increase or decrease ABP (afterload) have no effect on COP in case of healthy normal heart. srOOr B- Heart rate In general physiological (moderate) changes in HR leads to non signif icant effect on COP because stroke volume can compensate for this change. However, excessive (pathological) changes in heart rate reduces cardiac output, because stroke volume can not compensate for these changes. srOOr  Arterial Blood Pressure (ABP) Definition and Physiological standers: ABP is the pressure exerted byb lood stream on the lateral walls of the arteries ,leading to their distension. The systolic blood pressure: is defined as the maximum pressure in the arteries ,which occurs at systole. The diastolic blood pressure: is the lowest pressure at diastole. Normal blood pressure in case of complete physical ,mental and digestive resting in healthy adult human are approximately 120 mmHg srOOr systolic and 80 mmHg diastolic( written as 120/80 mmHg) Physiological variations influence the ABP: l) Age: The ABP is very low at birth 50/30 mmHg. It rapidly rises during the f irst few weeks to 90/60 then gradually increases with age up to adult age to be about 120/80 mmHg. Then a progressive but slight increase is continued with advancing age. 2) Sex: A) In children: the ABP is more or less identical in both sexes before puberty. B) In adult age: the ABP is slightly lower in females than males. C) At menopause the ABP is higher in females than males srOOr 3) Body built: In obe se pe ople t he ABP is usually highe r t han t hat of norm al individuals. 4) Effect of Gravity: The pressure in any vessel below heart level is increased and that in any vessel above heart level is decrease by the effect of gravity. 5) Meals: During digestion the ABP increases 5-10 mmHg due to contraction of spleen 6) Circadian rhythm: (ABP shows lowest level at early morning (about 4 o'clock a.m.) and highest level at the afternoon (about 4 o'clock p.m srOOr 7) Emotions and muscular exercise: Emotions increase ABP by more than 30 mmHg due to increase in adrenaline secret ion. In m uscular exercise, t he ABP increases temporarily to high level (up to 180 mmHg.) and after exercise the ABP drops to the normal level. 8) Sleep: De e p qui e t sl e e p l owe r s t he ABP by 15- - 30 m m Hg, but whe n accompanied by dreams of emotional activity the ABP may rise to high level. 9) Pregnancy: ABP drops during normal pregnancy due to both hormonal factors and fetal circulation. srOOr 10) Physical factors:  Exposure to cold causes cutaneous vasoconstriction with increasing mean ABP by 10 mmHg.  Exposure to heat causes vasodilatation and decreased ABP. In severe hot weather, diastolic pressure may decrease markedly leading to hypotension and syncope. 11) Respiratory phases: ABP raises 4-6 mmHg during inspiration and falls towards normal level with expiration. srOOr Factors maintaining arterial blood pressure 1) Peripheral Resistance (PR): Definition of PR: It is the resistance, which the blood meets during its passage in the peripheral arteries and capillaries. The increase in PR lead to increase diastolic BP while systolic pressure remain constant The peripheral resistance depends on: A) The Diameter of Arteries: Decrease diameters (VC) leads to increase DBP B) Viscosity of Blood: Increase viscosity (increase plasma proteins or RBC ), leads to increase DBP srOOr 2-Cardiac output:  The ABP is directly proportional to the COP.  Increase SV lead to increase SBP ,while increase HR lead to increase DBP 3- Elasticity of arteries:  Normal physiological elasticity buffers the excessive change in ABP.  During systole the arteries distended to prevent excessive increase in SBP.  While in diastole the recoil of the wall prevents excessive decrease in DBP.  Arteriosclerosis: A pathological condition caused by precipitation of cholesterol in ar terial wall leading to lose the normal ar terial elasticity and converting the arteries into rigid tubes so, ABP is higher than normal. srOOr 4- Blood volume and capacity of circulation:  Moderate changes: are adjusted by corresponding changes in capacity and HR without change in ABP  Severe changes: as severe hemorrhage, ABP decrease in spite of change of HR and capacity srOOr  Haemorrhage Definition: It is the loss of blood from the heart and blood vessels Special effects of hemorrhage depends on : a) The amount of blood loss:  If it's less than 30% of blood volume, body can compensate for it. But if it's more than 30% (sudden loss), the body can’t compensate for it and death occurs, unless blood transfusion and other therapies are made. b) The speed of blood loss:  Small repeated haemorrage is not dangerous because the body can compensate for it. But rapid severe is dangerous srOOr The following characters occur after severe haemorrage: 1- The primary event is reduction in blood volume, cardiac output and arterial pressure. 2- The pulse is rapid and weak 3- Breathing is shallow and rapid 4- Skin is pale and cold 5- The mouth is dry and thirst is a common 6- Reduction in the urine output 7- Loss of conscious and death srOOr Compensatory reactions of haemorrage I-Rapid (immediate) compensatory mechanisms: Aim to: maintain adequate ABP. Onset: It starts within seconds to few minutes. I- Blood coagulation: It aims to closing the wound and preventing further blood loss. 2 -Cardiovascular changes: a- Increase heart rate: To increase DBP and maintain the blood f low through the cerebral and coronary blood vessels. srOOr Causes: 1- When ABP is decreased, arterial baroreceptors become stimulated with increase heart rate (Mary's law). 2- Hypoxia stimulates chemoreceptors that increase heart rate. 3- Increased adrenaline secretion directly stimulates SAN. b-Increased vasoconstrictor discharges: Effects: 1-Vasoconstriction affect mainly the blood vessels of less important areas (the skin and splanchnic area and muscle vascular beds) to redistribution of the blood f low and ensure an adequate circulation through coronary and cerebral vessels. Causes: 1- stimulation of VCC by impulses from barorecptor, chemoreceptor and Rt. atrium receptor. 2- Release of angiotensin II as a result of renal ischemia. 3- Adrenaline and noradrenalin release. srOOr 3 -Respiratory changes: Effects: The respiration is accelerated to increase venous return and ensure complete oxygenation of blood. Causes: The respiratory rate is increased due to:-. 1- Hypoxia stimulates chemoreceptors that activate respiratory center. 2- Local accumulation of metabolites in cells of respiratory center due to its ischemia. srOOr 4- Endocrine changes through increase secreation of: 1-Epinephrine and norepinephrine: They are responsible for: a) Enhance vasoconstriction of skin and splanchnic area. b) Dilate coronary arteries and helps coronary blood flow. c) Increases the heart rate and improves the contractility. D) Contraction of spleen 2-Aldosterone: Responsible for: sodium and water reabsorption by the kidney that leads to increase blood volume and return ABP towards the normal. srOOr 3-Antidiuretic hormone: Responsible for: water reabsorption by the kidney and restoration of blood volume and ABP. 4- Angiotensin II: Responsible for: 1-Generalized vasoconstricting effect. 5- Glucocorticoids: Responsible for: increase the resistance to stress condition 6-Erythropoietin. Responsible for: stimulation RBCs formation by the bone marrow. srOOr 5- Splenic contraction: Effe ct s: It sque e ze 200- 500 CC of blood r ich in RBCs int o circulation leads to restoration of blood volume, ABP and RBCs number. 6- Renal changes: Urine formation is decreased due to decrease ABP and renal blood flow, and increase secretion of ADH. srOOr II-Long term (Delayed) compensatory reactions Aim to: restore the blood volume. They include the following reactions: 1) Restoration of water and electrolytes: within 12-72 hours. This occurs through: a) Decrease ABP and f iltration force with normal reabsorption force. These lead to withdrawal water from interstitial space. b) A greater reabsorption of water by the kidney c) An increase in the amount of water intake srOOr 2-Restoration of plasma proteins: This occurs through:  Rapid addition: within one hour from labile protein of the liver and tissues.  Delayed addition: by synthesis of new protein in the 3-Restoration of red blood cells: This occurs through:  Rapid mechanism: This occurs through squeeze of spleen.  Slow mechanism: due to stimulation of BM by erythropoietin hormone produced by the kidney under effect of hypoxia. srOOr