Transcript Slide 1
CARDIOVASCULAR SYSTEM THE HEART Cardiovascular System • • • • • • • • series of tubes-blood vessels filled with a fluid-blood connected to a pump-heart Arteries – carry blood away from heart Veins – carry blood to heart pressure generated in heart pumps blood continuously through system Blood flow – movement of blood through heart & around body to peripheral tissues Circulation Circulation • right side of bodyPulmonary Circuit – carries blood to & from lungs for gas exchange • Systemic Circuit – carries newly oxygenated blood from lungs to body & back to heart • each circuit begins & ends at heart • • • • • • • • • • • Heart Anatomy hollow, small organ about size of clenched fist weighs from 250-350 grams located in middle of chest in mediastinum surrounded by pericardial cavity lining of pericardial cavity is pericardium – visceral & parietal part visceral pericardium -epicardium – superficial layer that covers surface of heart parietal pericardium – lines inner surface of pericardial sac which surrounds heart between these two-pericardial cavity filled with pericardial fluid to lubricate & reduce friction Heart Wall • 3 layers • Epicardium-visceral pericardium – covers outer surface • Myocardium – muscular wall • Endocardium – simple squamous epithelium Microscopic Anatomy • different from skeletal muscle in several ways • cells are smaller • uninucleated • have branching interconnections between have intercalated discs – location of gap junctions & desmosomes – convey action potentials from cell to cell – ensure cells contract simultaneously Heart Anatomy • top of heart-base • pointed, lower part-apex • 4 chambers – 2 atria & 2 ventricles • coronary sulcus (atrioventricular sulcus) • anterior & posterior interventricular sulci – mark external boundary of right & left ventricle Coronary Sulcus Heart Anatomy • each atrium has expandable extensions- auricles – hold extra blood • right atrium receives blood from systemic circuit via superior & inferior vena cavae & coronary sinus • superior vena cava – returns blood from body areas superior to diaphragm • inferior vena cava – drains areas below diaphragm • coronary sinus – delivers blood from myocardium of heart Internal Heart Anatomy • blood passes into right ventricle via right AV (atrioventricular) valve or tricuspid valve – keeps blood flowing in one direction from atrium to ventricle – prevents backflow into atrium • tiny, white collagen cordschordae tendineae attach to each flap • originate at papillary muscles – help to close valves • chordae tendineae & papillary muscles anchor flaps in closed position Internal Heart Anatomy • pectinate muscles-right atrium • fossa ovalis also found here • muscular ridges- ventriclestrabeculae carnae • moderator band extends horizontally from right ventricle wall – coordinates contraction of muscle cells – insures chordae tendinae tense before ventricles contract Internal Anatomy • • • • • • • • • from right ventricle blood is pumped to pulmonary circuit valves between ventricles & vesselssemilunar valves – prevent back flow into ventricles each made of 3 pocket-like flaps shaped like crescent moons blood travels via pulmonary semilunar valve into pulmonary trunk – start of pulmonary circuit from pulmonary trunk, blood goes to left & right pulmonary arteries and to lungs for gas exchange after being oxygenated, blood reenters heart via 2 left & 2 right pulmonary veins-open into left atrium blood goes from left atrium to left ventricle via left AV valve bicuspid or mitral valve from here blood is ejected through aortic semi lunar valveinto aortic arch Heart Anatomy • • • • • • • left ventricle – discharging chamber contractsblood propelled into circulation equal volumes are pumped to both circuits right pumps blood to pulmonary circuit through pulmonary trunk – short path with low pressure left pumps blood through systemic circuit – long path-runs through entire body – 5X more resistance to flow – functional difference between left & right ventricle is reflected in anatomy left ventricle walls are 3X as thick as right ventricle wall – allows left ventricle to generate more pressure pulmonary trunk is attached to aortic arch by ligamentum arteriosum Ligamentum arteriosum Label Me Valve Function • atrioventricular & semilunar valves • open & close in response to blood pressure differences AV VALVES • relaxed heart • AV valve flaps hang limply in ventricle – blood flows from atria into ventricle • when ventricles contract intraventricular pressure increases – forces blood superiorly against flaps causing flap edges to meet & close valve Semi-Lunar Valves • ventricles contractintraventricu lar pressure rises • blood pushes against valvesopen • ventricles relax intraventricular pressure fallsblood flows back from arteriesfills cuspsvalve closes Coronary Circulation • heart muscle must have its own source of oxygenated blood • supplied by coronary arteries – originate at base of ascending aorta – blood pressure • right coronary artery follows coronary sulcus & supplies right atrium, parts of both ventricles & parts of conducting system • left coronary artery supplies: left ventricle, left atrium & interventricular septum • great cardiac vein – begins anterior surface of ventricles along interventriuclar sulcus • curves around left side of heart in coronary sulcus • empties into coronary sinus Heart Beat • myocytes-autorhythmic – depolarize spontaneously at regular time intervals – initiate contraction without signals from brain • each beat begins with action potential generated at SA node (sino-atrial)pacemaker – generates impulses at regular intervals • to ensure four chambers of heart are coordinated electrical signals travel through cardiac conduction system • sympathetic & parasympathetic connections to heart can modify heart beat – not involved in normal contractions Conducting System • autorhythmic cells in SA node (sinoatrial node) – right atrium • AV-atrioventricular node – junction of atria & ventricles • atrioventricular bundle or bundle of his • right & left bundle branches • purkinje fibers Initiation of Contraction • action potentials are spontaneously initiated by autorhythmic cells in SA node • possess leaky membranes – – – – – have unstable resting potentials exchange Na, K & Ca ions causes changes in polarization cells are continuously depolarized drift slowly toward threshold • spontaneously changing membrane potentials are pacemaker potentials • initiate action potentials which spread throughout heart Impulse Conduction • • • • • • • • SA node contract 75X/minute sets pace for heart beat – no other area has faster depolarization rate – pacemaker action potential- conducted to AV nodebottom of right atrium – conduction delayed about 0.1 sec – AV delay allows atria to respond & have complete contraction before ventricles contract impulse travels to Bundle of Hisatrioventricular bundle splits into right & left bundle branches bundle branches go along interventricular septum toward apex divide into purkinje fibersmoderator band papillary muscle of right ventricle contracts before rest of ventricleapplies tension on chordae tendineaebraces AV valvesprevents back flow into atria when ventricles contract contraction proceeds from bottom of ventricles blood is pushed toward base of heart Label Parts of Conducting System ECG-EKG-Electrocardiography • electrical currents can be detected by placing electrodes (leads) on skin’s surface • electrocardiograph amplifies signals • produces record-EKG, ECG or electrocardiogram • measures rate & regularity of beats • measures size & position of heart chambers • sum of all electrical potentials generated by all cells of heart at any moment • each component of EKG reflects depolarization and/or repolarization of a part of heart • because depolarization is signal for contractionelectrical events shown as waves on EKG can be associated with contraction or relaxation of atria & ventricles EKG Trace-Deflection Waves • P Wave – represents depolarization of atria • QRS complex – represents ventricular depolarization – atrial repolarization occurs during this time but is obscured by QRS complex • T Wave – represents ventricular repolarization EKG Trace • size, duration & timing of waves tend to be consistent • any change may reflect damage to or problems with conduction system Abnormal EKG Traces • lowered P – AV block • enlarged R – may indicate enlarged ventricle • flattened T – cardiac ischemia • prolonged Q – repolarization problem Contraction • purkinje fibers distribute action potential to contractile cells of heart • action potentialsCa appears among myofibrils binds to troponin cross bridges form contraction • differences from skeletal muscle contraction • action potentials-30X longer, from 250300msec • source of Ca is different • duration of contraction longer Action Potential • resting potential of ventricular contractile cell is -90mV • action potential begins when membrane of ventricular cell is brought to threshold • depolarization travels from cell to cell by ions passing through gap junctions • action potential proceeds in 3 steps • rapid depolarization • plateau • repolarization Action Potential • rapid depolarization • fast Na channels openNa rushes indepolarization • plateau phase – action potential flattens as membrane potential nears +30mV – Na channels close & slow Ca channels open • slow Ca channels remain open 175msec – as long as Ca enters cellcell contracts • repolarization – takes place as plateau phase ends – slow Ca channels close & slow K channels open – K rushes out of the cell – restores resting potential Muscle Tension • develops during plateau phase • peaks just after plateau ends • long plateau helps prevent sustained contraction or tetanus • refractory period – time when muscle is inexcitable – in cardiac muscle lasts as long as contraction • important since cardiac muscle must relax between contractions so ventricles can fill with blood – would stop pumping action Cardiac Cycle • time between start of one heartbeat & start of next • includes one contraction & one relaxation • for each chamber-cycle is divided into 2 phases: • contraction or systole – chamber contracts & pushes blood into adjacent chamber or arterial trunk • relaxation or diastole – chamber fills with blood • fluids flow from areas of higher to areas of lower pressures • blood flows only if one chamber’s pressure is higher than another Phases of Cardiac Cycle • beginning all chambers relaxed • atria & ventricle diastole • AV valves between atria & ventricles are opened • semilunar valves areclosed • blood flows from veins into atria & into ventricles-Passive Filling • • • • -ventricles 70% filled with blood atria contractatrial systole complete ventricular filling end of atrial systole-end of ventricular diastole • ventricular volume is greatest at this time – end-diastolic volume or EDV – maximum amount of blood ventricles can hold Phases of Cardiac Cycle • • • • • • • • • • • • atria relax atrial diastole continues until start of next cardiac cycle begins at same time as ventricular systole ventricles contractpressure in ventricles rises above pressure in atriaAV valves close – first heart sound-lubb both AV & semilunar valves are closed – blood has nowhere to goventricles continue to contract isometric contractionpressure increasestension no change in ventricular volume – isovolumetric contraction once pressure in ventricles is greater than pressure in arterial trunks, semilunar valve open blood flows into pulmonary & aortic trucks beginning of ventricular ejection each ventricle ejects 70 ml of blood = stroke volume-SV as ventricle systole endsventricular pressure falls rapidly blood in aorta & pulmonary trunks flows towards ventricles & fills cusps of semilunar valves causing them to close – second heart sound-dupp ventricular Phases of Cardiac Cycle • • amount of blood remaining in ventriclesESV or end systolic volume Ventricular Diastole – ventricles relax – all valves are closed • • • • • • • • • • ventricular pressure-still high no change in ventricular volume since all valves are closed this is isovolumetric relaxation ventricular pressure falls rapidly now when ventricular pressure falls below pressures in aortaatrial pressure forces AV valves openblood flows from atria to ventricles both atria & ventricles are in diastole ventricular pressure continues to fall as chambers fill passively cycle repeats when heart rate increasesall phases shorten greatest reduction in diastole ventricular Blood Pressure • Systolic blood pressure – pressure in aorta – 120 mmHg • Diastolic blood pressure – 80mmHg • when semilunar valves close, aortic pressure rises as elastic arterial walls recoil • small, temporary rise in pressure-dicrotic notch Heart Sounds • Ausculation – listening to heart using stethoscope • several areas on chest where these are best heard • Aortic Area • Pulmonic Area • Tricuspid Area • Mitral Area Heart Sounds • S1 – AV valves close-lubb • S2 – semilunars closedupp • S3 – ventriclular filling • S4 – atrial contraction • third & forth are faint • seldom detected in normal people Cardiodynamics • need to review some terms • EDV – amount of blood in ventricles at end of ventricular diastole • ESV – amount of blood in each ventricle at end of ventricular systole • Stroke Volume – amount of blood pumped out of each ventricle during one beat • SV = EDV – ESV Cardiodynamics • Stroke volume – most important factor when examining single cardiac cycle – largest when EDV is as large as can be & ESV is as small as can be • Cardiac Output – most important when looking at cardiac function over time – amount of blood pumped by each ventricle/minute • • • • – represents blood flow through peripheral tissues or total blood flow through body CO (ml/min) = heart rate (beats/min) X SV (ml/beat) CO = 75bpm X 70mL/beat = 5.250L/minute-average total blood volume not constant – varies with body’s state of activity • exercise increases CO CO precisely adjusted so peripheral tissues receive adequate supply of blood under variety of conditions Control of Cardiac Output • adjusted by changing SV or HR • changes generally reflect change in both SV & HR • HR can be adjusted with autonomic nervous system & hormones • SV can be adjusted by changing EDV, ESV or both Factors Affecting Stroke Volume • Preload –degree of stretch on heart before contraction • Contractility –forcefulness of contraction • Afterload –pressure that must be exceeded before ejection of blood can occur • • • • • • Preload indicates degree of stretch prior to contraction – directly proportional to EDV greater EDVgreater preload the more the heart fills with blood during diastolethe greater force of contraction during systole relationship-Frank-Starling Law of the Heart greater EDVgreater SV due to stretch on muscle fibers SV is directly proportional to EDV Factors Affecting EDV • Two key factors determine EDV: • duration of ventricular diastole • venous return • volume of blood returning to right atrium Contractility • amount of force produced during contraction at a given preload • factors that increase contractility are positive inotropic agents • those that reduce it-negative inotrophic agents • positive ionotropic factors typically stimulate Ca entry into cells • negative ionotropic factors function to block Ca Afterload • blood pressure outside semilunar valves • opposes opening of these valves – amount of tension ventricles must produce to force semilunar valves open & eject blood • increased afterload reduces stroke volume • greater afterload longer isovolumetric contraction • shorter time of ventricular ejection, and larger ESV • as afterload increasesSV decreases • afterload can be increased by any factor that restricts blood flow through arterial system – constriction of peripheral blood vesselsdecreases BP & increases afterload Regulation of Heart Rate • nervous system does not initiate heart beat • modulates rhythm & force • sympathetic & parasympathetic fibers innervate heart via cardiac plexus • sympathetic & parasympathetic fibers SA & AV nodes & atrial muscle cells • ventricles also innervated by sympathetic fibers Tonic Control of Heart • both centers are involved • both fire at steady level • vagus nerve maintains constant background firing rate – inhibits nodes • if vagus is cutHR increases because SA node fires on its own at about 100X per minute • vagus intact • keeps heart rate 75bpm Cardiac Center • located in medulla oblongata • has cardioacceleratory & cardioinhibitory part • cardioacceleratory center sends signals by sympathetic fibers to SA node, AV node & myocardium • secrete norepinephrine – binds to beta-1 receptors in heart – increases heart rate – Increases the entrance of calcium – Increases contractility Cardiac Center • cardioinhibitory centers • send signals via parasympathetic fibers in vagus nerve to SA & AV nodes • secretes acetylcholine • opens potassium channels in nodal cells • as potassium leaves cellsbecome hyperpolarizedfire less frequentlyheart rate slows Receptors to Cardiac Centers • receive & integrate information from many sources • sensory & emotional stimuli can act by cerebral cortex, limbic system & hypothalamus to change heart rate • Proprioceptors in muscles & joints report changes in physical activity • Baroreceptors or pressure receptors in aorta & internal carotid arteries send continuous information to cardiac centers • Chemoreceptors send information about Na, K, hydrogen ions and oxygen Chemoreceptors • responses to fluctuations in blood chemistry are called chemoreflexes • in aortic arch, carotid arteries & medulla oblongata • monitor ph, carbon dioxide & oxygen levels in blood • more important in respiratory rate-can function to change HR • carbon dioxide accumulates in blood & cerebral spinal fluidpH lowers acidosis • stimulates cardiac center to increase heart rate • oxygen deficiencyslows heart rate Hormones • Catecholamines –epinephrine & norepinephrine –adrenal medulla –increase heart rate & contractility