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CARDIOVASCULA R SYSTEM  CIRCULATORY SYSTEM  Parts of circulatory system: 1. Heart 2. Blood vessels: a)Arteries b)Veins c)Lymphatic vessels HEART  Heart is approximately the size of your fist. (Wt. = 250- 300 grams)  Location a) In the mediastinum between...

CARDIOVASCULA R SYSTEM  CIRCULATORY SYSTEM  Parts of circulatory system: 1. Heart 2. Blood vessels: a)Arteries b)Veins c)Lymphatic vessels HEART  Heart is approximately the size of your fist. (Wt. = 250- 300 grams)  Location a) In the mediastinum between the lungs b) On the superior surface of diaphragm c) ⅔’s of it lies to the left of the midsternal line d) It is anterior to the vertebral column, posterior to the sternum.  PERICARDIUM  Covering of the Heart is called Pericardium.  It is a double-walled sac around the heart.  Composed of: 1. A superficial fibrous pericardium 2. A deep two-layer serous pericardium a) The parietal layer lines the internal surface of the fibrous pericardium b) The visceral layer or epicardium lines the surface of the heart (They are separated by the fluid-filled space called the pericardial cavity) Functions:  Protects and anchors the heart  Prevents overfilling of the heart with blood  Allows for the heart to work in a relatively friction-free environment  LAYERS OF HEART WALL  Layers of the Heart Wall: 1. Epicardium – visceral pericardium 2. Myocardium – cardiac muscle layer forming the bulk of the heart 3. Endocardium– endothelial layer of the inner myocardial surface  EXTERNAL MARKINGS OF HEART External markings:  Apex - pointed inferior region  Base - upper region  Coronary sulcus  Indentation that separates atria from ventricles  Anterior and posterior interventricular sulcus Separates right and left ventricles CHAMBERS OF THE HEART  The heart is divided into four chambers that are connected by valves.  The upper two chambers of the heart are called the left atrium and the right atrium.  The lower two chambers of the heart are called the left ventricle and the right ventricle.  ATRIA  Receiving chambers of the heart  Receive venous blood returning to heart 1. Right atrium: receives blood returning to the heart from the superior and inferior vena cava. 2. Left atrium: receives blood returning to the heart from the pulmonary veins.  Atria pump blood into ventricles.  Separated by an interatrial septum (wall).  Fossa ovalis - remnant of foramen ovale seen in right atrium.  VETRICALS  discharging chambers of the heart: 1. Right ventricle pumps blood into the pulmonary trunk. 2. Left ventricle pumps blood into the aorta, hence myocardium is thicker due to greater work load.  Papillary muscles and trabeculae carnae mark ventricular walls  Separated by an interventricular septum  Contains components of the conduction system  VALVES  Flap-like structures that allow blood to flow in one direction.  The heart has two kinds of valves, atrioventricular and semilunar valves.  The atrioventricular valves are thin structures that are located between the atria and the ventricles 1. The tricuspid valve is located between the right atrium and the right ventricle. 2. The mitral (bicuspid) valve between left atrium and left ventricle.  The semilunar valves are located between the aorta and the left ventricle and between the pulmonary artery and the right ventricle.  CONDUCTION SYSTEM OF HEART  Cardiac muscle cells have unique intrinsic property of spontaneous rhythmical contractions.  The conduction system consists of nodes and networks of specialized myocardial cells organized into four basic components: 1. Sinu-atrial node 2. Atrioventricular node 3. Atrioventricular bundle with its right and left bundle branches 4. Subendocardial plexus of conduction cells (Purkinje fibers). CORONARY CIRCULATION Functional blood supply to the heart muscle itself. Right and Left Coronary arteries are branches off the ascending aorta Coronary sinus (vein) empties into R. atrium  BLOOD VESSELS FUNCTIONAL CLASSIFICATION 1. Distributing vessels– Arteries (End Arteries do not anastomose with their neighbours Example  central artery of retina) 2. Resistance vessels-- arterioles and precapillary sphincters. 3. Exchange vessels-- 2. Capillaries (Microscopic endothelial tubes ) 3. Sinusoids (Large, irregular, vascular spaces) 4.Postcapillary venules cell 5. Reservoir vessels-- endothelium (one cell thick) large venules and veins. 6. Anastomosis– lumen (Communication between neighboring vessels )  Histology of Blood Vessels The blood vessels are made of three layers, called from the luminal side outward: Tunica intima (endothelium & subendothelium) Tunica media (smooth muscle & elastic fibres) Tunica adventitia or externa (connective tissue layer) Thickness of these three layers varies greatly depending upon the size and type of vessel (large, medium & small arteries and veins; capillaries).  Arteries Arteries carry blood away from the heart. They are classified into three types according to their size: 1. Large or elastic arteries 2. Medium arteries(or muscular or distributive) 3. Small arteries or arterioles which are less than 0.5 mm in diameter. elastic arteries large vein muscular medium-sized arteries vein arterioles venules capillaries Arteries – always carry blood away from heart Veins – always return blood to heart,  Large arteries (Elastic arteries or Conducting arteries) Large include the aorta and its largest main branches: a. Tunica intima - thin (relative to other layers in this type of vessel) (1) Endothelium (2) Subendothelial layer (3)Internal elastic lamina (a prominent sheet of elastin) separates tunica intima and media. c. Tunica media – thick - 40 - 60 distinct, concentrically arranged elastic fibers - smooth muscles cells are less abundant. d. Tunica adventita –Thin connective tissue layer.  Medium to small arteries ( muscular arteries) a.Tunica intima – thin - Internal elastic lamina c. Tunica media – Thick (1) Circular smooth muscle, 5 - 40 layers which are intermingled with a variable number of elastic lamellae (2) Thickness decreases as diameter of vessel decreases d. Tunica adventita – thick, loose connective tissue. The muscular wall resists damage due to relatively high blood pressure in these vessels.  Arterioles Peripheral resistance vessels. Structure: a. Tunica intima - very thin consisting only of endothelium - Internal elastic lamina - usually present except in smaller arterioles c. Tunica media - 1 to 5 layers of smooth muscle, some elastic fibers d. Tunica adventita – thin.  Capillaries Structure – consist only of endothelium. Three types of capillaries may be distinguished a. Continuous (type I) capillaries : The capillary wall is continuous ( in most organs.) b. Fenestrated (type II) capillaries : the capillary wall is perforated at intervals by pores or fenestrations (in kidney and in endocrine glands.) c. Sinusoidal capillaries: are larger in diameter and have wide spaces between adjacent endothelial cells ( in the spleen, liver, and bone marrow).  Venules Postcapillary venules similar structurally to capillaries and contain endothelium. These venules converge into larger collecting venules which have more contractile cells. With greater size the venules become surrounded by recognizable tunica media with two or three smooth muscle layers and are called muscular venules. A characteristic feature of all venules is the large diameter of the lumen compared to the overall thinness of the wall.  Veins Small to medium veins 1. Structure: a. Tunica intima - thin (1) Endothelium (2) Subendothelial layer (3) May be folded to form valves b. Tunica media - thin; contain smooth muscle, collagen fibers, some elastic fibers c. Tunica adventita - well developed.  Large veins vena cavae and larger branches 1. Structure: a. Tunica intima - thicker (1) Endothelium (2) Subendothelial layer (3)Internal elastic lamina - usually distinguishable. c. Tunica media - thin, few layers of smooth muscle and abundant connective tissue d. Tunica adventita - The adventitial layer is thick in large veins and frequently contains longitudinal bundles of smooth muscle with spirally arranged collagen fibers, elastic laminae.  TYPES OF CIRCULATION Systemic (greater) circulation: The blood flows from the left ventricle, through the arteries and veins which traverse the various parts of the body, to the right atrium. This circulation is responsible for keeping the body tissues alive by supplying a continuous stream of blood to them. Pulmonary (lesser) circulation:  The blood flows from the right ventricle, through the lungs, to the left atrium.  This circulation is responsible for oxygenation of blood. Portal circulation:  It is a part of systemic circulation, which has the following characteristics. 1. The blood passes through two sets of capillaries before draining into a systemic vein. 2. The vein draining the first capillary network is known as portal vein which branches like an artery to form the second set of capillaries or sinusoids.  Examples: hepatic portal circulation, hypothalamo hypophyseal portal circulation and renal portal circulation.  PHYSIOLOGY OF CARDIOVASCULAR SYSTEM OBJECTIVES By the end of this part students should be able to know:- 1- Properties of the cardiac muscle. 2- Pace maker of the heart. 3- Cardiac out put and factors affecting it. 4- Innervations of the heart and heart rate. 5- Arterial blood pressure and factors maintenance it. 6- Vascular system and capillary circulation.  PART I THE HEART CARDIAC MUSCLE HEART  What is heart? Is it only a pump?  It is not just a pump it is secret hormones (oxytocin, atrial natriuretic factor)  It is contain more than 40,000 ganglia.  It has a electromagnetic field extend few feet away from body.  There is a heart - brain connection.  Some's considered the heart as a little brain. FUNCTIONAL HISTOLOGY OF CARDIAC MUSCLE (MYOCARDIAC)  Cardiac muscle characteristic by a connection between fibers in both atria and another connection in both ventricles.  This connections is called syncytium, so heart has two syncytiums one in both atria and another in both ventricles.  Physiologically both atria act as a one muscle cell (all or nothing) and both ventricles act as a one muscle cell (all or nothing). Cardiac syncytium  PROPERTIES OF THE CARDIAC MUSCLE  There are 4 properties for the cardiac muscle:- 1- Rhythmicity (autorhythmicity). 2- Conductively. 3- Contractility. 4- Excitability.  1- RHYTHMICITY  Definition: It the ability of the cardiac muscle to beat regularly without nerve or hormone.  The impulse start from part in the right atrium called (Sino-Atrial node)=SAN.  The action potential AP(excitation) from SAN is 100-120/min.  Heart beat (heart rate) is 70-90 beat/ min. this is under the effect of vagus.  Then AP transport through atrium muscle to atrio- ventricular node (AVN).  Then transport from AVN to AV-bundle, then AVB branch (right and left).  Then transport to all ventricular muscle (right and left) through purkinje fibers.  FACTORS AFFECTING RHYTHMICITY 1- Effect of ANS: A- Sympathetic increase rhythmicity. B- Parasympathetic (vagus) decrease rhythmicity. 2- Effect of Temperature: increase temperature increase rhythmicity and cold will decrease it. 3- Effect of pH: (normal pH of blood= 7.36-7.40) a- acidic will decrease rhythmicity. b- alkaline increase rhythmicity.  WHAT IS THE PACE MAKER OF THE HEART?  Rhythm of SAN is 120/min.  Rhythm of AVN is 45/min.  The highest rhythmicity is the pace maker of the heart so, SAN is the pace maker of the heart.  If the SAN is destructed the pace maker is AVN and if AVN is destructed pace maker will be the prkinki fibres.  2- CONDUCTIVITY  Definition: It is the ability of the cardiac muscle to transmitted excitation waves of cardiac muscle from point to point.  Excitation start in SAN and conduct through atrium muscles to both atria then to AVN then to AVB and bundle branches to Purkinje to all ventricular muscle.  The transmit of excitation in AVN is slower to reach both ventricles when both atria are starting their relaxation.  Sympathetic increase conductivity and parasympathetic decrease it (in AVN).  Temperature: cold decrease conductivity and hot increase it. 3- EXCITABILITY  Definition: It is the ability of the cardiac muscle to response to stimulus.  Excitability of cardiac muscle during stimulation is three phases:- 1- Absolute refractory period (ARP), it is the excitability of muscle shortly after stimulation (excitability is zero), muscle can not response to stimuli. * ARP is prolong in cardiac muscle and short in skeletal muscle. 2- Relative refractory period (RRP), the excitability return but not completely, during relaxation of muscle it is need strong stimulus. 3- Supernormal phase of excitability, after complete relaxation to response to another stimulus. 4- CONTRACTILITY  Definition: It is the ability of the cardiac muscle to contract as a response to stimulus.  Contractility of cardiac muscle called inotropism.  +ve inotropic effect on heart means increase cardiac muscle contractility.  -ve inotropic effect on heart means decrease cardiac muscle contractility. Frank-Starling law:- * Within limit, the force of myocardium muscle contraction is directly proportional to the length of cardiac muscle fibers.  Increase venous return will lead to stretch myocardium and increase the force of its contraction to overcome the increase in venous return but this within limit.  Over increase in venous return will decrease the force of contraction according to Frank-Starling law.  This will accumulate blood in the heart and over increase in myocardium stretching and heart failure occur.  Myocardium hypertrophy  Hypertrophy in cardiac muscle in case of :  Hypertension (pathological) and in athletes (Physiological).  Factors affecting myocardial contractility: 1- Length of cardiac muscle (Frank Starling’s law). 2- ANS: sympathetic increase contractility will parasympathetic decrease it. 3- Thyroxin (hormone), has +ve inotropic effect. 4- Effect of ions:- A- Increase sodium (hypernatremia) has -ve inotropic. b- increase potassium (hyperkalemia) has -ve inotropic effect. C- increase calcium has +ve inotropic effect. 5- Coffee and tea have +ve inotropic effect. HEART SOUNDS  Lup-Dup * 1st heart sound is Lup.  It is due to closure of atrioventricular valve (between atria and ventricles). * 2nd heart sound is Dup.  It is due to closure of semilunar valve (between aorta and pulmonary artery and left and right ventricle respectively).  Murmurs: abnormality in heart sounds by splitting of the sound or absence of one sound or duplicate of one sound.  PART II HEART RATE ,CARDIAC OUTPUT AND ARTERIAL BLOOD PRESSURE INNERVATIONS OF THE HEART  Autonomic NS is innervate cardiac muscle  Autonomic NS is not initiate cardiac rhythmicity, it is autorhythmicity  Autonomic NS regulates cardiac muscle rhythmicity  Sympathetic increases heart rate and parasympathetic (vagus) decreases heart rate HEART RATE  Heart beat is autorhthmicity, but it is regulate by ANS.  Sympathetic increase HR and parasympathetic decrease HR.  Normal range of heart rate in rest= 60-90 beat/min.  Normal heart rate= 75 beat /min. Physiological variation of heart rate: 1- Age: decrease with age. 2- Sex: faster in female than male. 3- Physical training: heart rate is high in non-athlete than athlete persons at rest. 4- Exercise: during exercise heart rate increase. 5- Sleep: decrease heart rate during quite sleep. REGULATION OF HEART RATE (HR) I- Nervous regulation: 1- Blood pressure: (Mary’s law)  Increases blood pressure stimulate nerve receptors in aortic arch and carotid bodies (baroreceptors= pressorecptors) to decrease heart rate (through vagus).  Mary’s law: Heart rate is inversely proportional to blood pressure (increase blood pressure will reflexly decrease heart rate). 2- Venous return:  Increase venous return will increase heart rate (Bainbridge reflex): impulse start from right atrium (via sympathetic and decrease venous return decrease HR (via parasympathetic). 3- Chemoreceptor: in aorta and carotid artery A- Decrease O2 increase heart rate. B- Increase CO2 increase heart rate. 4- Higher centers (in brain): A- Respiratory center: inspiration increase HR and expiration decrease HR. B- Emotion and hypothalamus: * stimulation of posterior hypothalamic area (or emotion) will stimulate sympathetic and increase HR. * stimulation of anterior hypothalamic area will stimulate parasympathetic and decrease HR. II- Chemical regulation: 1- Adrenalin and nor adrenalin: increase HR. 2- Thyroxin hormone: increase HR. III- Effect of body temperature and other parts of body: a- Increase body temperature increase HR (increase body temperature one degree will increase HR 15 beat), and decrease body temperature decrease HR. b- Light and moderate pain increase HR by sympathetic. c- Sever pain decrease HR by parasympathetic. d- Skeletal muscle contraction increases HR, even contraction of the thumb. Important Notes: Contraction of the heart is called systole. Relaxation of the heart is called diastole.  CARDIAC OUTPUT (COP)  Itis the volume of blood pumped by each ventricle / min.  COP = Stroke volume X HR = 70 ml X 70 = 4900 ml= blood volume (blood volume =5000 ml).  Stroke volume, is the volume of blood pumped by each ventricle/ heart beat.  Venous return, is the volume of blood return to heart (atrium) by veins. Cardiac output is controlled to maintain the proper amount of flow to tissues and to prevent undue stress on the heart. Cardiac Index (CI)=Cardiac output/body surface area= 3L/min/m2 Body surface area= BSA = 0.007184 × W0.425 × H0.725 REGULATION OF COP THROUGH 1- Regulation of stroke volume. 2- Regulation of heart rate. 1-Regulation of stroke volume: A- Venous return:  increase venous return will increase stroke volume and increase COP.  Decrease venous return will decrease stroke volume and decrease COP.  Venous return affected by: a- exercise increase VR b- during inspiration increase VR and expiration decrease VR c- Pressure gradient of blood (pressure is high in arteries then decreases in capillaries then decreases in small veins and very low in large veins). B- Strength of myocardium muscle:  Increase strength of myocardium (+ve inotropic) increase stroke volume then increase COP and vice versa.  +ve inotropic like, sympathetic NS, digitalis, coffee, stress.  -ve inotropic like, parasympathetic Ns, damage of myocardium muscle (angina). 2- Heart Rate (HR):  Increase HR increase COP and decrease HR decrease COP.  N.B.: Sever increase in heart rate decrease COP, because will lead to decrease in stroke volume (if HR is 200 stroke volume will become 20 ml so, COP = 200 X 20 = 4000 ml ARTERIAL BLOOD PRESSURE (ABP)  Definition: It is the pressure of blood on the wall of the arteries.  Blood pressure is two; the first is systolic blood pressure and the second is diastolic blood pressure.  Systolic BP means the pressure of blood on wall of arteries during systole of the heart.  Diastolic BP means the pressure of blood on the wall of arteries during diastole of the heart.  Normal ABP is 120/80 mmHg.  Normal range of ABP from 90/60 to 140/90 mmHg.  Pulse pressure: it is the difference between systolic BP and diastolic BP normally equal= 40 mmHg.  Mean arterial pressure= diastolic BP + 1/3 (systolic BP-diastolic BP) PHYSIOLOGICAL VARIATION OF ABP 1- Age: ABP increase with age. 2- Sex: ABP is more in male than female but after postmenopause will increase. 3- Body weight: increase ABP in obese. 4- After meals: increase ABP after meals. 5- Emotion: increases ABP about 30 mmHg (sympathetic). 6- Exercise: increases during exercise and after exercise decrease ABP.  FACTORS MAINTAINED NORMAL ABP 1- COP: increase COP increase ABP and decrease COP decrease ABP. 2- Elasticity and elastic recoil of arterial wall:- * Elasticity: it decreases systolic BP. * Elastic recoil: it prevents decrease of diastolic BP and it is responsible for developments of BP. 3- Blood volume: * Increase blood volume will increase ABP. * Decrease blood volume will decrease ABP (as in hemorrhage). * Decrease blood volume (by diuretics drugs) will also decrease BP as in hypertensive patients. 4- Circulatory capacity: * Vasoconstriction (as in sympathetic) decrease capacity of blood vessels and increase ABP. * Vasodilatation (as in parasympathetic) increase capacity of blood vessels and decrease ABP. 5- Viscosity of blood: * Increase blood viscosity (increase blood cells, or increase plasma proteins or dehydration) increase ABP. * Decrease blood viscosity (decrease blood cell as in anemia) will decrease ABP. RELATION BETWEEN BLOOD PRESSURE AND CARDIAC OUTPUT  No effect of blood pressure on cardiac output if the blood pressure is increased or decreased but sever increase in blood pressure (over 200 mmHg) will decrease COP.  This is mean increase blood pressure load (up to limit) does not decrease COP.  Normotensive patient: patient with normal ABP.  Hypertensive patient: patient with high ABP (above normal range).  Hypotensive patient : patient with low ABP (below normal range). REGULATION OF ARTERIOLAR DIAMETER  Diameter of arterioles is very important to keep the blood flow through circulatory system.  Two major factors regulate it: I- Central mechanism: A- Neural mechanism: a- Vasoconstrictor nerves: Sympathetic causes constriction in all arterioles except in skeletal muscle and heart. b- Vasodilator nerves: Sympathetic supply skeletal muscle and heart, and parasympathetic c- antidromic impulses. B- Vasoactive substances: substances that causes vasoconstriction ( adrenalin or noradrenalin angiotensin II) or vasodilatation(bradykinin and atrial natriuretic peptide, (secreted from atrium of heart). II- Local regulatory mechanism: A- Autoregulation: It is the capacity of tissues to regulate their blood flow. Increase activities in certen tissues will increase the flow of blood in this tissues than others. B- Endothelium of blood vessles , it secreted some substances like thromboxane A2 (causes V.D) or endothelins which produce (V.C). EDEMA  Definition: Increase extracellular fluid.  Types: a- general or b- local  Causes: 1- Increase capillary blood pressure, mainly due to increase arterial blood pressure. 2- Decrease colloid osmotic pressure, due to decrease plasma protein as in liver diseases. 3- Lymphatic obstruction, lymph remove excess extracellular fluid. If it is obstructed as in elephantiasis it will lead to edema.