AdAP Chapter 25 Notes on the Heart PDF

CHAPTER 25: THE HEART REVIEW OF THE HEART : 1. the blood flows into 2 closed circuits; the systemic and pulmonary circulation’s 2. systemic circulation: a) the left side of the heart is the pump b) it receives fresh, oxygenated blood from the lungs...

CHAPTER 25: THE HEART REVIEW OF THE HEART : 1. the blood flows into 2 closed circuits; the systemic and pulmonary circulation’s 2. systemic circulation: a) the left side of the heart is the pump b) it receives fresh, oxygenated blood from the lungs c) it propels the blood from the lungs  the aorta systemic arteries organs (except lungs) capillary arterioles capillary beds 3. pulmonary circulation: a) the right side of the heart is the pump b) it receives deoxygenated blood returning form the venules  blood from the right side of the heartflows into the pulmonary trunk-branches into pulmonary arteries & carries blood to right & left lungspulmonary capillaries (picks up O2 , unloads C02)oxygenated blood returns to left side of the heart. Ligamentum arteriosum is a fetal connection between the pulmonary trunk and the aorta. It redirects a small amount of blood to the developing, nonfunctional lungs. After birth it closes and is a ligament ANATOMY OF THE HEART 1. Located in the area in the middle of the thorax containing the heart and other tissues (mediastinum) 2. the heart sits on the diaphragm and is more on the left side of the body 3. the pointed end of the heart is the apex, which is directed anteriorly, inferiorly and to the left; the broad base part of the heart opposite the apex is the base, which is directed posteriorly, superiorly and to the right 4. pericardium:  is the 3-layered sac that surrounds the heart; layers include a) superficial fibrous pericardium (made of dense, irregular CT); it attaches inferiorly to the diaphragm and superiorly to the CT around the major vessels coming from the heart. It serves to anchor the heart in the mediastinum b) deeper, serous pericardium is divided into 2 layers. There is an outer parietal layer (fused to the outer fibrous pericardium). There is an inner visceral layer called the epicardium which is attached to the heart. c) between the visceral and parietal layers is a fluid filled space called the pericardial cavity filled with pericardial fluid. This serves to reduce friction. Pericarditis is an inflammation of the pericardium resulting from the rubbing together of the parietal and visceral layers. Fluid collected in the cavity compresses the heart and is dangerous, b/c it can compress the heart , a condition known as cardiac tamponade (it can stop the beating of the heart) Cardiopulmonary Resuscitation (CRP) involves periodic compressions on the chest that can be used to force blood out of the heart into the circulation when the heart stops. This can be done because the heart lies between 2 rigid structures – the vertebral column & the sternum. 5. layers of the heart wall  epicardium: is the visceral layer of the serous pericardium; it is composed of mesothelium ( s.sq. epithelium that lines serous membranes)  myocardium: muscle layer is the bulk of the heart weight ;consists of cardiac muscle fibers (striated, involuntary, branching) ;fibers form 2 independent networks (atrial & ventricle); contain intercalated disc - with gap junctions (for transfer of action potentials) & desmosomes for adherence to each other during contraction  endocardium: innermost is a thin layer if endothelium continuous with the endothelium in the vessels leaving the heart 6. heart chambers:  4 chambers; 2 ventricles and 2 atria  each atrium (atria) has an auricle appendage to increase the size of the chamber, to hold greater volumes of blood  on the surface of the heart are a series of grooves called sulci that contain coronary vessels and fat; each sulcus marks the  external boundary between 2 chambers of the heart. These include the deep coronary sulcus, encircling most of the heart and marks the boundary between the superior atria and the inferior ventricles; the anterior interventricular sulcus, a shallow groove on the anterior surface of the heart that marks the boundary between the right and left ventricles; the posterior interventricular sulcus, which marks the boundary between the ventricles on the posterior aspect of the heart  right atrium receives blood from superior, inferior vena cava & coronary sinus; left atrium receives blood from 4 pulmonary veins; the posterior wall is smooth, the anterior wall is rough due to the presence of muscular ridges called pectinate muscles ; a interatrial septum divides the right & left atria; in the interatrial septa is an indentation (the fossa ovalis) which is open in fetal heart and closed at birth.; Blood passes from the right atria into the right ventricle thru the tricuspid valve (has 3 cusps)  right ventricle forms most of the anterior surface of the heart and contains a series of ridges formed by raised bundles of cardiac muscle fibers called trabeculae carneae. Some of these convey part of the conduction system of the heart; the cusps of the tricuspid valve are connected to tendon like cords, the chordae tendineae which, in turn are connected to cone-shaped trabeculae carneae called papillary muscles.; an interventricular septum separates the atria and the ventricles  left atrium forms most of the base of the heart, and receives blood from 4 pulmonary veins; in this artia, the anterior and posterior walls are smooth; blood passes from the left atria into the left ventricle thru a bicuspid valve (mitral)  left ventricle forms the apex of the heart and also contains trabeculae carneae and chordae tendinae; blood passes from the left ventricle thru the aortic valve into the aorta; some of the blood in the aorta, flows into the coronary arteries which branch from the ascending aorta and carry blood to the heart wall. The remainder of the blood passes into the arch of the aorta and the descending aorta and branches carry blood throughout the body.  During fetal life, a temporary vessel called the ductus arteriosus shunts blood from the pulmonary trunk into the aorta so that only a small amount of blood enters the nonfunctioning fetal lungs. This closes shortly after birth, leaving a remnant known as the ligamentum arteriosum 7. Myocaridal thickness and Function 1) varies with chambers 2) atrial walls are thin, sufficient to deliver the blood to ventricles 3) ventricle walls are thick, pump same amount blood simultaneously 4) right ventricle pumps blood at low pressure to lungs; have smaller workload 5) myocardium of left ventricle is 4 x thicker than right ventricle b/c it has to pump much harder to get blood at higher pressure to rest of body 8. Fibrous skeleton of heart : consist of dense connective tissue rings that surround the valves of the heart, fuse with one another, and merge with the interventricular septum. Four fibrous rings support the 4 valves of the heart and are fused to each other. The fibrous skeleton prevents over-stretching of the valves as blood passes thru them and acts as an electrical insulator that prevents the direct spread of action potentials from the atria to the ventricles 9. Heart valves and Circulation of blood valves prevent backflow or ensure a one-way flow; they are composed of dense CT covered by endocardium as each chamber of the heart contracts, it pushes a volume of blood into a ventricle or out of the heart into an artery. Valves open & close in response to pressure changes as the heart contracts and relaxes. Each of the 4 valves ensure the one way flow of blood by opening to let blood thru and then closing to prevent the backflow of blood.  AV (atrioventricular valve) (1) found between the atria & ventricles, & consist of cusps or fibrous flaps covered with epithelium. The right AV valve is the tricuspid (3 flaps)/ left AV valve is bicuspid (2 flaps) (2) the flaps are pointed at one end, which projects into the ventricle, the chordae tendineae (3) connect these pointed ends to papillary muscles located in the inner surface of the ventricles (4) the opening & closing o f the heart valves is the result of pressure gradients from one side of the valve cusps to the other. (5) When AV valves are open and relaxed, blood moves from the atria into the ventricles thru the open AV valves when atrial pressure is higher than ventricular pressure. At this time the papillary muscles are RELAXED, and the chordae tendinae are SLACK. (6) When the ventricles contract, the pressure of the blood drives the cusps upward until their edges meet and close the opening. At the same time the papillary muscles are also contracting, which pulls on & tightens the chordae tendinae, preventing the valve cusps from everting (prolapse like a windblown umbrella being forced to open in the opposite direction into the atria due to the high ventricular pressure). If the AV valves or chordae tendinae are damaged, blood may regurgitate (flow back) into the artia when the ventricles contract.  SL (semilunar valves):  (1) pulmonary semilunar valves lie between the pulmonary trunk vessel and the right ventricle; aortic semilunar valve guards the opening between the left ventricle and the aorta (2) each consist of 3 flaps (cusps) that attaches to the vessel wall. (3) The semilunar’s are forced OPEN when the ventricle contracts & pushes blood thru them into the aorta (b/c the pressure builds up within the chambers and the valves open when the pressure in the ventricles exceeds the pressure in the arteries, permitting ejection of blood from the ventricles into the pulmonary trunk & aorta). They CLOSE again as the ventricles relax, and the blood seeps backwards towards the ventricles and the blood fills the pocket-like cusps Heart Valve Disorders occur when the heart valve fails to open fully (stenosis) or they fail to properly close (insufficiency / incompetence). In mitral stenosis, scar formation or a congenital defect causes narrowing of the mitral valve. Mitral insufficiency allows backflow of blood from the left ventricle into the left atrium. One cause is mitral valve prolapse (MVP)m in which one or both cusps of the mitral valve protrude into the left atrium during ventricular contraction. Although a small volume of blood may flow back into the left atrium during ventricular contraction, mitral valve prolapse doesn’t always pose a serious threat. Rheumatic fever is an infection caused by Strep. Pyogenes which usually starts as a sore throat and result in antibody production as the body wards off the infection. These antibodies may attack (and weaken) similar molecules in the heart valves and walls. Coronary Circulation: the arteries of the heart encircle it like a crown & while contracting, the heart receives little oxygenated blood via the coronary arteries. When the heart relaxes, the high pressure of blood in the aorta propels blood thru the coronary arteries into capillaries and then into coronary veins a) coronary arteries: the myocardium contains many anastomoses that connect branches of a given coronary artery or extend between branches of different coronary arteries. They provide detours for arterial blood if a main route becomes obstructed – the heart muscle may receive sufficient oxygen even if one of its coronary arteries is partially blocked; in the CA’s flow is GREATER when the ventricles are relaxed, b/c contraction of the ventricles compresses the coronary vessels and impedes flow, and b/c when the ventricle relaxes, blood backflows into the aortic cusps, and the opening of the CA’ s is near there. b) coronary veins: the coronary veins drain into the coronary sinus which empties into the right atrium ANGINA PECTORIS is severe pain that accompanies myocardial ishemia. Ishemia is a reduction of blood flow and is caused by clots, plaques of spasms of smooth muscle, it is faulty coronary circulation. Hypoxia (loss of 02) usually results after ishemia. Angina occurs usually after exercise or exertion and is often referred to the neck, chest, chin arm. It disappears with rest. REPERFUSION is the reintroduction of 02 to a oxygen deprived area. When this happens, this reintroduction may end up being more harmful than the initial damage b/c of the introduction of oxygen “free radicals” at the site that causes reperfusion damage. Free radicals are unstable, electrically charged (have an unpaired electron), and highly reactive. They take electrons from other molecules (enzymes, proteins, neurotransmitters) and start a chain reaction leading to cellular damage and death. They are implicated in aging, Alzheimer’s, cancer, Parkinson’s cataracts, rheumatoid disease. To counter the effects of oxygen free radicals, the body cells produce enzymes that convert free radicals to less reactive substances, these are superoxide dismutase and catalase. Some nutrients like vitamins E & C and beta- carotene & selenium are also antioxidants. Drugs that lessen reperfusion damage after a heart attack or stroke are being developed. Structure of Cardiac Muscle:  Cardio-myocytes are short, thick, branching cells with central nucleus; 25% of cell volume is filled with mitochondria (as opposed to 2% like in skeletal muscle); they have a typical sarcomere arrangement; they have scant SR & limited stored Ca+  myocytes are joined end to end by thick connections called intercalated discs which have 3 distinct features: a) the 2 plasma membranes from opposing cells are interdigitated and folded together like corrugated cardboard b)the cells are tightly joined by desmosomes which keep them from pulling apart c) there are gap junctions (electrical synapses) between cells –ion channels from the cytosol so that the cells can electrically stimulate each other. The entire myocardium of the atria and the ventricles each acts as if it were a single cell (functional syncytium) Regeneration of cardiomyocytes: in heart attack patients there are regions of infarcted cardiac muscle tissue that is typically replaced by fibrous , scar tissue, so that we can not regenerate cardiac muscle cells. Recent evidence shows that in male heart transplant patients (XY) who receive a female’s heart (XX), 7-16% of the transplanted heart now has myocytes and endothelial cells that are from the recipient (XY), showing some evidence of the migration of stem cells into the heart and differentiation into myocytes, Autorhythmic cells : The Conduction System These are specialized muscle fibers that are self-excitable b/c they repeatedly generate spontaneous action potentials that trigger heart contractions ; during development, about 1% of the cardiac muscle fibers become autorhythmic ; these cells act as: (1) they are the pacemakers of the heart setting the rhythm for the entire heart (2) and they form the conduction system –the route for propagating the AP thru the heart. The conduction system ensures that the chambers become stimulated to contract in a coordinated manner CARDIAC CYCLE  in a normal cardiac cycle, 2 atria contract while 2 ventricles relax and vice versa; it is 1 heartbeat. The human adult heartbeat is 75 beats/min, and a cardiac cycle last 0.8 sec.  a cardiac cycle refers to a systole and diastole in both atria plus systole/diastole of ventricles VENTRICULAR SYSTOLE & DIASTOLE  systole is divided into 2 periods – ISOVOLUMETRIC CONTRACTION & EJECTION PERIODS ISOVOLUMETRIC CONTRACTION PERIOD (SYSTOLE) 1- Begins with closure of AV valves and the occurrence of 1st heart sounds (S1). After AV closure for 0.02-03sec – (during which SL valves are ALSO closed) there is a building of ventricular pressure which rises rapidly b/c BOTH sets of valves are CLOSED and no blood is leaving ventricles while the muscles is contracting. This is the period of isovolumetric contraction (systole). Thus the muscle contraction at this point is isometric (same length) and b/c all 4 valves are shut, ventricle volume remains the same (isovolumetric) 2- Continued contraction of the ventricles causes ventricular pressure to increases so that when ventricular pressure surpasses aortic & pulmonary trunk pressure the SL valves open & blood is ejected; this is the period of ventricular ejection EJECTION PERIOD - the ejection of blood begins when the ventricle pressure is higher than the pressure in the large vessels ; ventricle pressure peaks @ 125 mmHg (left) and 30 mmHg (right) 1- about 60% of the stroke volume is ejected in first quarter of systole and the 40% in last 2 quarters. 2- The left ventricle ejects about 70 mls blood into the aorta , and the right ventricle ejects the same volume. The ejected volume is the stroke volume (SV)= 70 mls,. The stroke volume, the volume ejected per beat from each ventricle is the end-diastolic volume minus end-systolic volume : SV = EDV -- ESV = SV SV = EDV -ESV (with exercise the SV can rise to 90%) = 120/130 – 60 ml = 70 mls end-systolic volume (ESV) =~ 60 mls ; 3- The ejection fraction is the SV/EDV = or the percentage of the EDV that is ejected from the heart. Left ejection fraction should be 55-75% as determi9ned via angiocardiography or ecocardio.. DIASTOLE or RELAXATION PERIOD (last 0.4sec.) 1- isovolumetric relaxation (quiescent period)- occurs at end of cycle (for ~0.03-06 sec) when none of the heart chambers are contracting and ALL of the valves are closed WHILE the ventricular volume doesn’t change, and the ventricular pressure drops; relaxing of ventricle muscles causes a drop in pressure in the ventricles this causes the ejected blood to fall back towards ventricles which causes the semilunar valves to close in the major vessels to prevent back flowing of the blood; THIS IS MARKED by the second heart sound S2 2- As the ventricles continue to relax, the pressure falls. When the ventricular pressure drops BELOW atrial pressure, the AV valves open and ventricular filling begins. The major part of filling occurs after the AV valves open, and blood that has been building up in the atria during ventricular systole, rushes into the ventricles. At the end of relaxation period, the ventricles are ¾ full. Most of the filling occurs in first 1/3 (rapid filling period) of diastole. The last 1/3 of diastole is marked by atrial contraction – which gives an additional thrust to ventricular filling and acc’ts for 20% of blood in ventricles (when heart this rapid filling acc’ts for a 3rd heart sound) 3- Aortic Pressure – reflects the changes in the ejection of blood from left ventricle. There is a RISE in pressure & stretching of elastic fibers in aorta as blood is ejected into the aorta onset of systole. The aortic pressure continues to rise and then falls at the last ¼ of systoles as blood flows past aortic arch. The INCISURA or notch in the aortic pressure tracing represents the closure of the AV (caused by the back flow of blood as ventricular pressure falls during relaxation). During diastole, the recoil of the highly elastic aorta serves to MAINTAIN aortic pressure. ATRIAL SYSTOLE & DIASTOLE  There are 3 main atrial pressure waves that occur in a cycle.  1- The a wave occurring at end of diastole (caused by atrial contraction) 2-The c wave –occurs as ventricles begin to contract and increased interventricular pressure causes AV valves to bulge into the atria. 3-The v wave – occurs at end of systole when the AV values are closed and there is a buildup of blood in the atria 4-The right atrial pressures are transmitted to the jugular vein and observed visually (abnormal pulsing of JV can be the result of impaired emptying from rgt atria into rgt ventricle due to blockage etc.) +  Right Atrial pressure is regulated by the: (1) the balance between the ability to move into the right ventricle and the tendency of blood to flow from periphery INTO the atria. When the heart pumps strongly, right atrial pressure is decreased and atrial filling is ENHANCED! (2) interthoracic pressure – right atrial pressure is DECREASED during INSPIRATION (b/c the diaphragm contracts downward into abdomen) - when interthoracic pressure becomes more negative (pulling up on syringe) and it is INCREASED during coughing or forced expiration when interthoracic pressure becomes more positive (pushing in on syringe)  Venous return is a reflection of the amt of blood filled in the right atria and pumped by ventricle thru circulation returning to right atria. Venous return is increased when blood volume is expanded or when right atrial pressure falls (as in increased CO capacity); venous return is decreased in hypovolemic shock or when right atrial pressure rises…  Atrial filling becomes imp’t during times of increased HR b/c the ventricle filling time is decreased. Good venous return is needed then (atrial contraction can contribute 20% of cardiac reserve during periods of increased HR – but has little effect on CO during rest). Heart disease impairs this and decreases CO. REGULATION OF CARDIAC PERFORMANCE Efficiency of the heart is measured via CO which varies with boyd size and metabolic needs of tissues CARDIAC OUTPUT  is the amount of blood (CO) ejected by the ventricles into the vessels per minute  output is equal to the SV X ( heart rate) HR CO = SV X HR for a typical male 70ml/beat an d75 beats/min CO = 70 X 75 = 5.25 L/min  the entire blood volume ( 4-6.0 liters) flow thru the pulmonary and systemic system about I x min. ---faster if demand is accelerated.  During normal exercise, the SV +/or HR may increase to fulfill the bodies needs providing a CO = 19 L/min.  Cardiac reserve is the ratio between a person’s maximum CO and CO at rest. A cardiac reserve of 3-4 X the resting value is average with top athletes having a reserve of 19X their resting CO. People with heart disease have little to no cardiac reserve. Normal CR us 300-400%  3-4 factors affect CO - and ensure that right & left ventricles pump equal volumes of blood; preload, afterload, cardiac contractibility & heart rate Preload (stretching) = it represents the volume work of the heart; it is work imposed on heart before contraction begins  the preload is the amount of blood that fills the ventricles by the end of diastole (EDV) ; the preload is proportional to the EDV. Normally the greater the greater the EDV, the more forceful the next contraction..  within limits, the more the ventricles fill during diastole (due to greater ventricular muscle stretching ), the greater the force of contraction – a relationship known as Frank- Starling law of the heart  the preload is largely determined by : (1) the venous return, the volume of blood returning to the right ventricle (2) stretching of cardio- muscle cells. The size of the sarcomere in the muscle cells is such that the tension or force of contraction depends on the degree to which the muscle fibers are stretched (by filling) just before the ventricles begin to contract. The maximum force of contraction (max CO) is achieved when the venous return increases preload such that the muscle fibers are stretched to ~2/3 of normal resting length.   The F-S mechanism allows the heart to ADJUST its pumping ability to accommodate various levels of venous return. When there is a greater am’t of blood flow into ventricles, the muscle is stretched, eventually providing more force of contraction and more CO.  The F-S law equalizes the output of both sides of the heart so the same volume of blood is pumped into both circulations and compensates for changes in EDV. If the left side of the heart pumps a little more blood than the right side, the volume of blood returning to the right side (venous return) increases. The increased EDV causes the right ventricles to contract more forcefully on the next beat, bringing the 2 sides back into balance  In hypertension,the HR increases- so the duration of ventricle diastole is short, it means a smaller EDV b/c the ventricles may contract before completely filled, and the preload is lower. When venous pressure increases, a greater volume of blood is forced into the ventricles and EDV increases. Afterload = is the pressure that must be exceeded by the ventricles to force open the SL valves for ejection.  If the afterload increase, the SV will decrease and more blood will remain in the ventricles at the end of systole.  Increases in afterload can be caused by hypertension and narrowing of the arteries (stenosis) Cardiac Contractility = is the strength of contraction at a given preload.  Substances that increase contractility are called positive inotropic agents. These include Ca+ enhancers like digitalis which increase Ca+ in ECF and NOR & EPI which stimulate the ANS.  Negative inotropic agents decrease contractility via Ca+ blocking agents (reduce Ca+ inflow) , thereby decreasing the strength of the heartbeat. Hypoxia exerts a negative ionotropic effect. Heart Rate = at normal rate of 75 bpm one cardiac cycle is 0.8 sec (0.3 sec is systole , 0.5 sec is diastole).  As HR increases , time in systole is same, but time in diastole DECREASES, leading to decreased SV, at high HR, and decreased CO.  One of dangers of tachy is reduced CO ANS CONTROL of BLOOD FLOW Autonomic Centers in the medulla receives input from sensory receptors and form the limbic system & cortex. Sensory receptors include chemoreceptors (monitor chemical changes) and baroreceptors (monitor BP in the major vessels) Short Term Autoregulation - BF to vital organs must remain constant and predictable (Kidney, brain etc) – even if the BP vary over range 60-180mmHg -this is du to autoregulation of BF via changes in bv tone (hypotension of the arterial system due to hypovolemic shock leads to (vasoconstriction) of vessels in kidney etc.. to maintain GFR and O2 in brain.  An increase in LOCAL BF to organ system is called reactive hyperemia.. Functional hyperemia during exercise is one example. Transient redness seen on an arm after leaning on hard surface is another example of reactive hyperemia. This reaction can not occur if the major feeding arteries are blocked or occluded  Endothelial control of vascular function can result in vasodilation and control of BF.  L arginine + O2 (iNOS) = NO gas (aka endothelium-derived relaxing factor) Agonist of NO release= AcH, bradykinin, histamine, thrombin & sheer stress (resulting from high BP or increased BF) NO – also inhibits platelet aggregation (which causes vasoconstriction) NO - is released into lumen (inhibit thrombosis) and away from the lumen to relax smooth muscle (promote vasodilation ) Nitroglycerin = treatment for angina causes release of NO = vasodilation and increase BF to counteract potential Hypoxia causing angina. Bradykinin – kinin present in fluids/tissues that cause INTENSE vasodilation of arterioles and increased capillary permeability – play role in inflammation & help to regulate BF to skin and GI Histamine- powerful vasodilator (like bradykinin) – released from mast cells in injured tissue and leads to emigration in injured areas Serotonin- released from platelets- causes vasoconstriction – plays role in bleeding ; m found in brain and lung – may play a role in vascular spasm assoc. with migraines and pulmonary rxnx Long Term Autoregulation Angiogenesis – making new bv. Innervate an area to increase tissue O2 delivery and also increased metabolism  VEGF (vascular endothelial growth factor and FGF, and angiotensin – are found in tissue to promote new vessel growth in tissues ; collateral circulation ensures adequate blood flow ot area  Angiostatin and endostatin – can promote the disappearance of bv in a tissue CHAPTER 25: Vessels AND Principles of Blood Flow  Artery ; is a vessel that carries blood from the heart to the tissues  Veins are vessels that carry blood from tissue to the heart  arteries arterioles capillaries - venules - veins ARTERIES:  several kinds which indicate the size of the vessel : elastic (large) ; muscular ( medium size)  an increase in the lumen diameter is vasodilatation; a decrease in the lumen diameter is vasocontriction Histology : consist of a lumen and 3 coats (layers) 1. tunica interna (intima) - composed of an endothelial layer resting on a BM, between this layer and the tunica media is an internal elastic membrane (Swiss cheese) 2. tunica media - middle coat; thickest part of the wall, composed of an interlacing membrane of elastic fibers and smooth muscle cells arranged circularly around the lumen; there is an external elastic lamina layer in the largest of the elastic arteries 3. tunica adventicia - the outermost layer, consist of elastic and collagen fibers Types of ARTERIES 1. Elastic arteries: are conducting arteries; eg. aorta, brachiocephalic, common carotid, subclavian, iliac, pulmonary ; also called conducting arteries - they conduct blood from the heart to the medium sized, muscular arteries 2. walls are heavily ladened with elastic fibers in order to be stretched by the sudden surge of blood from the contraction of the heart; they help propel blood onward while the ventricles are relaxing ; by stretching, the elastic fibers store mechanical energy. 3. functioning as a pressure reservoir. Then the elastic fibers recoil and convert stored (potential) energy in the vessels into kinetic energy of the blood  Muscular arteries: are distributing arteries which shunt the blood from the elastic arteries to the tissue’s; These are the femoral, splenic, popliteal, brachial, radial mesenteric 1. in comparison with the elastics, they contain more smooth muscle and fewer elastic fibers in the tunica media 2. they are capable of greater vasodilatation/constriction to adjust the rate of blood flow 2. most tissue’s receive blood from more than one artery/veins etc.. This is called anastomosis (coming together). Anastomosis can occur between veins and arterioles and venules. Anastomosis, allows for an alternative route for blood to reach a tissue. This kind of an alternate is called collateral circulation. ANASTOMOSES: 1) Most tissue receives blood from more than one artery and the union of branches of 2 or more is anastomosis; it may occur between veins or arterioles or venules 2) The alternate route of blood flow is called collateral circulation. ARTERIOLES 1) is a very small artery that provides the route of circulation between the arteries and capillary bed 2) the tunica media made up of smooth muscle have few elastic fibers compared to muscle cells. As they branch and lessen in diameter, the layers become little more than an endothelium with a few smooth muscle cells around it. 3) Arterioles play a role in regulating blood flow from arteries into capillaries by regulating resistance, the opposition to flow. In vessels, resistance is due to the friction between blood and the inner walls of blood vessels. When blood vessels diameter is smaller, the friction is greater. 4) Arterioles are known as resistance vessels and contraction of the arteriolar smooth muscle causes vasoconstriction, which increases resistance and decreases blood flow into capillaries supplied by that arteriole, and the reverse is also true. A change in diameter of arterioles can affect BP. CAPILLARIES  are microscopic vessels conducting blood between the arterioles and the venules; they are known as the microcircualtion b/c they are found near almost every cell in the body ( except for in cartilage, few in tendon and ligament, covering and lining epithelium, cornea and lens of eye); tissues with high metabolic rates have more extensive capillary networks (liver, kidney and nervous system)  primary function is to permit the exchange of waste and nutrients between tissue interstitial fluid and the blood  this is achieved easily b/c the capillary wall contains an endothelial layer and a BM. There is NO tunic media or adventicia  a metarteriole is a vessel that emerges from an arteriole and supplies a group of 10-100 capillaries that constitute a capillary bed. The proximal end of the metarteriole is surrounded by scattered smooth muscle fibers whose contraction and relaxation help regulate  there are several types of capillaries: a) continuous - found in muscle, (smooth, skeletal), CT, lungs; the plasma membrane forms a continuous tube interrupted by intercellular clefts (gaps between neighboring cells); they have a continuous, intact plasma membrane b) fenestrated - differ b/c they have fenestration’s (pores) in their plasma membrane (70-100nm) ; they are found in the kidneys, villi of GI, choriod plexus of brain, ciliary processes of eye, endocrine glands; usually a thin membrane stretched over these fenestration’s c) sinusoid - found in the liver, spleen bone marrow ; the P.M. is punctuated with wide gaps that allow proteins to pass from tissue into bloodstream , and the B.M. is also inconsistent; phagocytic cells remove bacteria in the sinusoids of the spleen and liver VENULES  when several capillaries unite they form a venule which collects blood from the capillaries and drains it into the veins  when the venule is closest to the capillary it looks like the capillary (tunica intima of single layer of endothelium with a tunic media of a few smooth muscle cells)  as the venules become larger and converge to form veins, they contain the tunica externa characteristic of veins VEINS  composed of a tunica intima and a media which is thinner than the corresponding artery, but consist of a tunica adventicia that is much thicker (collagen and elastic fibers) ** with some smooth muscle cells in this layer; tunic media is thinner  there is no internal or external elastic lamina --- and the lumen is much larger than artery  b/c of the thin, non-muscular walls and no elastic component, the walls of the veins always looked collapsed  the blood pressure in the vein is MUCH lower than in the artery. Blood leaving a cut artery is spurted out vs. from a vein; veins aren’t designed to withstand high pressure; they appear flattened or collapsed  some veins, especially in the limbs, have valves – which are thin folds of tunica interna that form flap-like cusps pointing to the heart. They are needed b/c the blood pressure in the veins is SO LOW. When you stand, the blood pressure pushing  blood up the veins in the legs is barely enough to overcome gravity. When the leg muscles contract, the valves of the veins (lying in between them) contracts preventing the blood from flowing back down into the leg away from the heart – moving the blood toward the heart Varicose veins = result when leaky valves cause the veins to become dilated and twisted ; occur throughout the body by is common in esophagus and superficial veins of lower limbs. The valve defect may be congenital or result from mechanical stress (prolonged standing or pregnancy) or aging. The leaky valve allows the backflow of blood, causing pooling of blood, this in turn creates pressure that distends the vein and allows fluid to leak into tissue - this may lead to pain and inflammation. BLOOD DISTRIBUTION  About 60% of the blood at rest is in the systemic veins and venules. They are called the blood reservoirs, and serve as storage depots for blood when needed quickly as in the case of exercise or after a large blood loss. The principle reservoirs are the veins of the abdominal organs (spleen & liver) and of the skin  Systemic capillaries contain 5% of blood volume, arteries about 15% HEMODYNAMICS OF BLOOD FLOW Hemodynamics describe the effects of BP , vessel radius , vessel length, vessel cross-sectional area and blood viscosity on each other. Relationship between blood flow , BP and resistance:  Blood flow (BF) thru a vessel is determined by pressure differences (P1-P2) between the 2 ends of vessel and the resistance (R) that blood overcomes as it moves thru the vessel F = ∆P/R VASCULAR RESISTANCE:  Resistance (R) is the opposition to flow that blood must overcome as it moves; caused by friction. in peripheral system , collective R is called peripheral resistance (PVR) or SVR (systemic). R to flow is determined by (1) vessel radius (2) blood viscosity (3) parallel or series flow (total cross sectional area). Systemic vascular resistance (SVR) aka. Total peripheral resistance (TPR) refers to all of the vascular resistance offered by all of the systemic vessels. The arterioles, venules and capillaries offer most of the resistance. The major function of the arterioles is to control SVR, by vasoconstriction/ vasodilatation.(change in diameter) in response to the vasomotor centers of the brain. VESSEL RADIUS: Poiseuille (PWAA-ZUH-EE) Law - Resistance is inversely proportional to the forth power of the radius (R ~ 1/D4). The smaller the radius the greater the resistance it offers to blood flow (for example: if the diameter of a vessel decreases by ½, its resistance to blood flow increases 16 times). As arterioles dilate, resistance decreases, and BP falls; as arterioles constrict, resistance increases, and BP rises. BLOOD VISCOSITY: meaning thickness which increases if more particles are present in solution. RBC’s determine the viscosity (Hmcrit 38 = 38% RBC’s in blood) the viscosity increases by 2% with each DECREASE of 1 °C body temp (hypothermia leads to sluggish blood flow). ; If the blood is more viscous, the resistance is greater eg. Polycthymia or dehydration. A depletion of plasma proteins or RBC’s due to anemia or hemorrhage, decreases viscosity and thus decreases BP TOTAL X-SECTIONAL AREA: blood velocity (forward flow) is affected by X-sectional area of vessel b/c as the X-sec increases the blood must flow laterally as well as forward to fill the vessel and then the velocity DECREASES. In contrast when the x-sec area deceases, the lateral flow is decreased and the mean Linear velocity INCREASES. In addition , Total blood vessel length has effect on resistance in blood. The longer a blood vessel, the greater the resistance. Obese people often have hypertension, due to an increase in total blood vessel length caused by additional blood vessels in their adipose tissue. An estimated 650 km (400 miles) of additional blood vessels is needed for each extra 2.2 lbs of fat tissue Lateral flow Linear flow LAMINAR vs TURBULENT FLOW: laminar flow is the layered flow of blood in which a thin layer of plasma adheres to the vessel wall while the inner layers of RBCs and platelets shear against this layer in the middle of the vessel- giving the central area the greatest velocity. Turbulent blood flow occurs when vortices develop (vessel narrowing or low blood viscosity) – more energy is required to push blood radially( cross sec) and axially (lengthwise); the blood is not in layers (lamina) and develop vortices and turbulence. Murmurs or bruits (BROOD) are audible vibrations of blood turbulence in the CV system. Heart murmur in diseased valve that may be too narrow, stiff or floppy causes turbulence and can be heard with stethoscope Venous Return  Is the volume of blood flowing back to the heart thru the systemic veins, occurs due to the pressure generated by the contractions of the heart’s left ventricle.  the pressure difference from venules (16 mmHg) to the right ventricle (0 mmHg) normally is sufficient to cause venous return to the heart. If pressure increases in the right atrium or ventricle, venous return will decrease. One cause of increased pressure in the right atrium is an incompetent (leaky) tricuspid vale, which lets blood regurgitate (flow backward) as the ventricles contract. The result is decreased venous return and buildup of blood on the venous side of the systemic circulation.  When you stand, the pressure pushing blood up the veins in lower limbs is barely enough to overcome the force of gravity. So there are 2 mechanisms that “pump” the blood from the lower back to the heart: (1) the skeletal muscle pump (2) the respiratory pump skeletal muscle pumps: when the in the lower limbs skeletal muscle contracts it tightens around the veins passing thru it. This serves to squeeze the vein, increasing the blood pressure in the vein. This drives the blood with greater pressure towards the heart. At this time valves in the vein (pointing towards the heart) are open. When the muscle relaxes, the valves close so that the blood can’t flow backward b/c of gravity. Respiratory pump: is based on alternating compression and decompression of veins. During inhalation, the diaphragm moves downward decreasing the pressure in thorax and increasing pressure in abdomen. As a result, abdominal veins are compressed and greater volume of blood moves form the compressed abdominal veins into the decompressed thoracic veins and into the right atrium. When the pressure reverses during exhalation, the vein valves present backflow of blood