Chapter 20



Chapter 20 The HeartAn Introduction to the Cardiovascular SystemLearning Outcomes20-1Describe the anatomy of the heart, including vascular supply and pericardium structure, and trace the flow of blood through the heart, identifying the major blood vessels, chambers, and heart valves.20-2Explain the events of an action potential in cardiac muscle, indicate the importance of calcium ions to the contractile process, describe the conducting system of the heart, and identify the electrical events associated with a normal electrocardiogram.An Introduction to the Cardiovascular SystemLearning Outcomes20-3Explain the events of the cardiac cycle, including atrial and ventricular systole and diastole, and relate the heart sounds to specific events in the cycle.20-4Define cardiac output, describe the factors that influence heart rate and stroke volume, and explain how adjustments in stroke volume and cardiac output are coordinated at different levels of physical activity.An Introduction to the Cardiovascular SystemThe Pulmonary CircuitCarries blood to and from gas exchange surfaces of lungsThe Systemic CircuitCarries blood to and from the bodyBlood alternates between pulmonary circuit and systemic circuitAn Introduction to the Cardiovascular SystemThree Types of Blood VesselsArteriesCarry blood away from heartVeinsCarry blood to heart CapillariesNetworks between arteries and veinsAn Introduction to the Cardiovascular SystemCapillariesAlso called exchange vessels Exchange materials between blood and tissuesMaterials include dissolved gases, nutrients, waste products An Introduction to the Cardiovascular SystemFour Chambers of the Heart Right atriumCollects blood from systemic circuit Right ventriclePumps blood to pulmonary circuit Left atriumCollects blood from pulmonary circuit Left ventriclePumps blood to systemic circuit 20-1 Anatomy of the HeartThe HeartGreat veins and arteries at the basePointed tip is apexSurrounded by pericardial sacSits between two pleural cavities in the mediastinum20-1 Anatomy of the HeartThe PericardiumDouble lining of the pericardial cavity Visceral pericardiumInner layer of pericardiumParietal pericardiumOuter layerForms inner layer of pericardial sac 20-1 Anatomy of the HeartThe PericardiumPericardial cavityIs between parietal and visceral layers Contains pericardial fluidPericardial sac Fibrous tissueSurrounds and stabilizes heart20-1 Anatomy of the HeartSuperficial Anatomy of the HeartAtriaThin-walledExpandable outer auricle (atrial appendage) 20-1 Anatomy of the HeartSuperficial Anatomy of the HeartSulciCoronary sulcus divides atria and ventriclesAnterior interventricular sulcus and posterior interventricular sulcusSeparate left and right ventriclesContain blood vessels of cardiac muscle20-1 Anatomy of the HeartThe Heart Wall Epicardium Myocardium Endocardium20-1 Anatomy of the HeartEpicardium (Outer Layer) Visceral pericardium Covers the heart20-1 Anatomy of the HeartMyocardium (Middle Layer)Muscular wall of the heartConcentric layers of cardiac muscle tissueAtrial myocardium wraps around great vesselsTwo divisions of ventricular myocardiumEndocardium (Inner Layer)Simple squamous epithelium20-1 Anatomy of the HeartCardiac Muscle TissueIntercalated discsInterconnect cardiac muscle cellsSecured by desmosomes Linked by gap junctionsConvey force of contraction Propagate action potentials20-1 Anatomy of the HeartCharacteristics of Cardiac Muscle CellsSmall sizeSingle, central nucleusBranching interconnections between cellsIntercalated discs20-1 Anatomy of the HeartInternal Anatomy and OrganizationInteratrial septum separates atria Interventricular septum separates ventricles20-1 Anatomy of the HeartInternal Anatomy and OrganizationAtrioventricular (AV) valvesConnect right atrium to right ventricle and left atrium to left ventricle Are folds of fibrous tissue that extend into openings between atria and ventricles Permit blood flow in one directionFrom atria to ventricles20-1 Anatomy of the HeartThe Right AtriumSuperior vena cavaReceives blood from head, neck, upper limbs, and chestInferior vena cava Receives blood from trunk, viscera, and lower limbsCoronary sinusCardiac veins return blood to coronary sinus Coronary sinus opens into right atrium 20-1 Anatomy of the HeartThe Right AtriumForamen ovaleBefore birth, is an opening through interatrial septum Connects the two atriaSeals off at birth, forming fossa ovalis20-1 Anatomy of the HeartThe Right AtriumPectinate musclesContain prominent muscular ridges On anterior atrial wall and inner surfaces of right auricle 20-1 Anatomy of the HeartThe Right VentricleFree edges attach to chordae tendineae from papillary muscles of ventriclePrevent valve from opening backwardRight atrioventricular (AV) valve Also called tricuspid valveOpening from right atrium to right ventricle Has three cuspsPrevents backflow20-1 Anatomy of the HeartThe Right VentricleTrabeculae carneaeMuscular ridges on internal surface of right (and left) ventricle Includes moderator bandRidge contains part of conducting systemCoordinates contractions of cardiac muscle cells20-1 Anatomy of the HeartThe Pulmonary CircuitConus arteriosus (superior end of right ventricle) leads to pulmonary trunkPulmonary trunk divides into left and right pulmonary arteries Blood flows from right ventricle to pulmonary trunk through pulmonary valvePulmonary valve has three semilunar cusps 20-1 Anatomy of the HeartThe Left AtriumBlood gathers into left and right pulmonary veins Pulmonary veins deliver to left atriumBlood from left atrium passes to left ventricle through left atrioventricular (AV) valveA two-cusped bicuspid valve or mitral valve20-1 Anatomy of the HeartThe Left VentricleHolds same volume as right ventricleIs larger; muscle is thicker and more powerfulSimilar internally to right ventricle but does not have moderator band20-1 Anatomy of the HeartThe Left VentricleSystemic circulationBlood leaves left ventricle through aortic valve into ascending aortaAscending aorta turns (aortic arch) and becomes descending aorta20-1 Anatomy of the HeartStructural Differences between the Left and Right VentriclesRight ventricle wall is thinner, develops less pressure than left ventricle Right ventricle is pouch-shaped, left ventricle is round20-1 Anatomy of the HeartThe Heart ValvesTwo pairs of one-way valves prevent backflow during contractionAtrioventricular (AV) valves Between atria and ventriclesBlood pressure closes valve cusps during ventricular contractionPapillary muscles tense chordae tendineae to prevent valves from swinging into atria20-1 Anatomy of the HeartThe Heart ValvesSemilunar valves Pulmonary and aortic tricuspid valvesPrevent backflow from pulmonary trunk and aorta into ventriclesHave no muscular supportThree cusps support like tripod 20-1 Anatomy of the HeartAortic Sinuses At base of ascending aorta Sacs that prevent valve cusps from sticking to aortaOrigin of right and left coronary arteries 20-1 Anatomy of the HeartConnective Tissues and the Cardiac Skeleton Connective tissue fibersPhysically support cardiac muscle fibersDistribute forces of contractionAdd strength and prevent overexpansion of heartProvide elasticity that helps return heart to original size and shape after contraction20-1 Anatomy of the HeartThe Cardiac Skeleton Four bands around heart valves and bases of pulmonary trunk and aortaStabilize valves Electrically insulate ventricular cells from atrial cells20-1 Anatomy of the HeartThe Blood Supply to the Heart = Coronary circulationSupplies blood to muscle tissue of heartCoronary arteries and cardiac veins20-1 Anatomy of the HeartThe Coronary Arteries Left and rightOriginate at aortic sinusesHigh blood pressure, elastic rebound forces blood through coronary arteries between contractions20-1 Anatomy of the HeartRight Coronary Artery Supplies blood to:Right atriumPortions of both ventriclesCells of sinoatrial (SA) and atrioventricular nodes Marginal arteries (surface of right ventricle)Posterior interventricular artery20-1 Anatomy of the HeartLeft Coronary Artery Supplies blood to:Left ventricleLeft atriumInterventricular septum20-1 Anatomy of the HeartTwo Main Branches of Left Coronary Artery Circumflex artery Anterior interventricular artery Arterial AnastomosesInterconnect anterior and posterior interventricular arteries Stabilize blood supply to cardiac muscle20-1 Anatomy of the HeartThe Cardiac VeinsGreat cardiac veinDrains blood from area of anterior interventricular artery into coronary sinusAnterior cardiac veinsEmpty into right atrium Posterior cardiac vein, middle cardiac vein, and small cardiac veinEmpty into great cardiac vein or coronary sinus20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseCoronary artery disease (CAD) Areas of partial or complete blockage of coronary circulationCardiac muscle cells need a constant supply of oxygen and nutrients Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance Reduced circulatory supply, coronary ischemia, results from partial or complete blockage of coronary arteries20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseUsual cause is formation of a fatty deposit, or atherosclerotic plaque, in the wall of a coronary vessel The plaque, or an associated thrombus (clot), then narrows the passageway and reduces blood flowSpasms in smooth muscles of vessel wall can further decrease or stop blood flow One of the first symptoms of CAD is commonly angina pectoris20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseAngina pectorisIn its most common form, a temporary ischemia develops when the workload of the heart increasesAlthough the individual may feel comfortable at rest, exertion or emotional stress can produce a sensation of pressure, chest constriction, and pain that may radiate from the sternal area to the arms, back, and neck20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseMyocardial infarction (MI), or heart attackPart of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygenThe death of affected tissue creates a nonfunctional area known as an infarctHeart attacks most commonly result from severe coronary artery disease (CAD) 20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseMyocardial infarction (MI), or heart attackConsequences depend on the site and nature of the circulatory blockageIf it occurs near the start of one of the coronary arteries: The damage will be widespread and the heart may stop beatingIf the blockage involves one of the smaller arterial branches:The individual may survive the immediate crisis but may have many complications such as reduced contractility and cardiac arrhythmias20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseMyocardial infarction (MI), or heart attackA crisis often develops as a result of thrombus formation at a plaque (the most common cause of an MI), a condition called coronary thrombosisA vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wallIndividuals having an MI experience intense pain, similar to that felt in angina, but persisting even at rest 20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseMyocardial infarction (MI), or heart attackPain does not always accompany a heart attack; therefore, the condition may go undiagnosed and may not be treated before a fatal MI occursA myocardial infarction can usually be diagnosed with an ECG and blood studiesDamaged myocardial cells release enzymes into the circulation, and these elevated enzymes can be measured in diagnostic blood tests The enzymes include:Cardiac troponin T, Cardiac troponin I, A special form of creatinine phosphokinase, CK-MB20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseTreatment of CAD and myocardial infarctionAbout 25 percent of MI patients die before obtaining medical assistance 65 percent of MI deaths among those under age 50 occur within an hour after the initial infarction20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseTreatment of CAD and myocardial infarctionRisk factor modificationStop smokingHigh blood pressure treatment Dietary modification to lower cholesterol and promote weight loss Stress reductionIncreased physical activity (where appropriate)20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseTreatment of CAD and myocardial infarctionDrug treatmentDrugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadinDrugs that block sympathetic stimulation (propranolol or metoprolol)Drugs that cause vasodilation, such as nitroglycerinDrugs that block calcium movement into the cardiac and vascular smooth muscle cells (calcium channel blockers)In a myocardial infarction, drugs to relieve pain, fibrinolytic agents to help dissolve clots, and oxygen20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseTreatment of CAD and myocardial infarctionNoninvasive surgeryAtherectomyBlockage by a single, soft plaque may be reduced with the aid of a long, slender catheter inserted into a coronary artery to the plaque20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseTreatment of CAD and myocardial infarctionNoninvasive surgeryBalloon angioplastyThe tip of the catheter contains an inflatable balloon Once in position, the balloon is inflated, pressing the plaque against the vessel wallsBecause plaques commonly redevelop after angioplasty, a fine tubular wire mesh called a stent may be inserted into the vessel, holding it open20-1 Anatomy of the HeartHeart Disease – Coronary Artery DiseaseTreatment of CAD and myocardial infarctionCoronary artery bypass graft (CABG)In a coronary artery bypass graft, a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary arteryAs many as four coronary arteries can be rerouted this way during a single operation The procedures are named according to the number of vessels repaired, so we speak of single, double, triple, or quadruple coronary bypasses20-2 The Conducting SystemHeartbeatA single contraction of the heartThe entire heart contracts in seriesFirst the atriaThen the ventricles 20-2 The Conducting SystemCardiac PhysiologyTwo types of cardiac muscle cells Conducting system Controls and coordinates heartbeat Contractile cellsProduce contractions that propel blood20-2 The Conducting SystemThe Cardiac Cycle Begins with action potential at SA nodeTransmitted through conducting systemProduces action potentials in cardiac muscle cells (contractile cells)Electrocardiogram (ECG or EKG)Electrical events in the cardiac cycle can be recorded on an electrocardiogram20-2 The Conducting SystemThe Conducting SystemA system of specialized cardiac muscle cellsInitiates and distributes electrical impulses that stimulate contraction AutomaticityCardiac muscle tissue contracts automatically20-2 The Conducting SystemStructures of the Conducting System Sinoatrial (SA) node – wall of right atriumAtrioventricular (AV) node – junction between atria and ventriclesConducting cells – throughout myocardium20-2 The Conducting SystemConducting CellsInterconnect SA and AV nodesDistribute stimulus through myocardiumIn the atriaInternodal pathwaysIn the ventriclesAV bundle and the bundle branches20-2 The Conducting SystemPrepotentialAlso called pacemaker potentialResting potential of conducting cellsGradually depolarizes toward thresholdSA node depolarizes first, establishing heart rate20-2 The Conducting SystemHeart RateSA node generates 80–100 action potentials per minuteParasympathetic stimulation slows heart rateAV node generates 40–60 action potentials per minute20-2 The Conducting SystemThe Sinoatrial (SA) NodeIn posterior wall of right atriumContains pacemaker cellsConnected to AV node by internodal pathwaysBegins atrial activation (Step 1)20-2 The Conducting SystemThe Atrioventricular (AV) NodeIn floor of right atriumReceives impulse from SA node (Step 2)Delays impulse (Step 3)Atrial contraction begins20-2 The Conducting SystemThe AV Bundle In the septumCarries impulse to left and right bundle branchesWhich conduct to Purkinje fibers (Step 4)And to the moderator bandWhich conducts to papillary muscles20-2 The Conducting SystemPurkinje FibersDistribute impulse through ventricles (Step 5)Atrial contraction is completedVentricular contraction begins20-2 The Conducting SystemAbnormal Pacemaker FunctionBradycardia – abnormally slow heart rateTachycardia – abnormally fast heart rateEctopic pacemakerAbnormal cells Generate high rate of action potentialsBypass conducting systemDisrupt ventricular contractions20-2 The Conducting SystemThe Electrocardiogram (ECG or EKG)A recording of electrical events in the heartObtained by electrodes at specific body locationsAbnormal patterns diagnose damage20-2 The Conducting SystemFeatures of an ECG P waveAtria depolarizeQRS complexVentricles depolarizeT waveVentricles repolarize20-2 The Conducting SystemTime Intervals between ECG WavesP–R intervalFrom start of atrial depolarizationTo start of QRS complexQ–T intervalFrom ventricular depolarizationTo ventricular repolarization20-2 The Conducting SystemContractile CellsPurkinje fibers distribute the stimulus to the contractile cells, which make up most of the muscle cells in the heartResting potentialOf a ventricular cell about –90 mVOf an atrial cell about –80 mV 20-2 The Conducting SystemRefractory PeriodAbsolute refractory periodLong Cardiac muscle cells cannot respondRelative refractory periodShortResponse depends on degree of stimulus20-2 The Conducting SystemTiming of Refractory PeriodsLength of cardiac action potential in ventricular cell250–300 msec30 times longer than skeletal muscle fiberLong refractory period prevents summation and tetany20-2 The Conducting SystemThe Role of Calcium Ions in Cardiac ContractionsContraction of a cardiac muscle cell Is produced by an increase in calcium ion concentration around myofibrils 20-2 The Conducting SystemThe Role of Calcium Ions in Cardiac Contractions20 percent of calcium ions required for a contractionCalcium ions enter plasma membrane during plateau phaseArrival of extracellular Ca2+Triggers release of calcium ion reserves from sarcoplasmic reticulum (SR)20-2 The Conducting SystemThe Role of Calcium Ions in Cardiac ContractionsAs slow calcium channels closeIntracellular Ca2+ is absorbed by the SROr pumped out of cellCardiac muscle tissueVery sensitive to extracellular Ca2+ concentrations20-2 The Conducting SystemThe Energy for Cardiac ContractionsAerobic energy of heartFrom mitochondrial breakdown of fatty acids and glucoseOxygen from circulating hemoglobinCardiac muscles store oxygen in myoglobin 20-3 The Cardiac CycleThe Cardiac Cycle Is the period between the start of one heartbeat and the beginning of the next Includes both contraction and relaxation20-3 The Cardiac CycleTwo Phases of the Cardiac CycleWithin any one chamberSystole (contraction)Diastole (relaxation)20-3 The Cardiac CycleBlood PressureIn any chamberRises during systoleFalls during diastoleBlood flows from high to low pressureControlled by timing of contractionsDirected by one-way valves20-3 The Cardiac CycleCardiac Cycle and Heart RateAt 75 beats per minute (bpm)Cardiac cycle lasts about 800 msecWhen heart rate increasesAll phases of cardiac cycle shorten, particularly diastole20-3 The Cardiac CyclePhases of the Cardiac CycleAtrial systoleAtrial diastoleVentricular systoleVentricular diastole20-3 The Cardiac CycleAtrial SystoleAtrial systole Atrial contraction beginsRight and left AV valves are openAtria eject blood into ventriclesFilling ventriclesAtrial systole ends AV valves closeVentricles contain maximum blood volumeKnown as end-diastolic volume (EDV)20-3 The Cardiac CycleVentricular Systole Ventricles contract and build pressureAV valves close causing isovolumetric contraction Ventricular ejectionVentricular pressure exceeds vessel pressure opening the semilunar valves and allowing blood to leave the ventricleAmount of blood ejected is called the stroke volume (SV)20-3 The Cardiac CycleVentricular SystoleVentricular pressure fallsSemilunar valves closeVentricles contain end-systolic volume (ESV), about 40 percent of end-diastolic volume20-3 The Cardiac CycleVentricular DiastoleVentricular diastole Ventricular pressure is higher than atrial pressureAll heart valves are closedVentricles relax (isovolumetric relaxation)Atrial pressure is higher than ventricular pressureAV valves openPassive atrial filling Passive ventricular filling20-3 The Cardiac CycleHeart SoundsS1Loud soundsProduced by AV valvesS2Loud soundsProduced by semilunar valves 20-3 The Cardiac CycleS3, S4 Soft soundsBlood flow into ventricles and atrial contractionHeart MurmurSounds produced by regurgitation through valves20-4 CardiodynamicsCardiodynamicsThe movement and force generated by cardiac contractionsEnd-diastolic volume (EDV)End-systolic volume (ESV)Stroke volume (SV) SV = EDV – ESVEjection fractionThe percentage of EDV represented by SV20-4 CardiodynamicsCardiac Output (CO)The volume pumped by left ventricle in one minuteCO = HR SVCO = cardiac output (mL/min)HR = heart rate (beats/min)SV = stroke volume (mL/beat)20-4 CardiodynamicsFactors Affecting Cardiac OutputCardiac outputAdjusted by changes in heart rate or stroke volumeHeart rateAdjusted by autonomic nervous system or hormonesStroke volumeAdjusted by changing EDV or ESV20-4 CardiodynamicsAutonomic Innervation Cardiac plexuses innervate heartVagus nerves (N X) carry parasympathetic preganglionic fibers to small ganglia in cardiac plexusCardiac centers of medulla oblongataCardioacceleratory center controls sympathetic neurons (increases heart rate)Cardioinhibitory center controls parasympathetic neurons (slows heart rate)20-4 CardiodynamicsAutonomic Innervation Cardiac reflexes Cardiac centers monitor:Blood pressure (baroreceptors)Arterial oxygen and carbon dioxide levels (chemoreceptors)Cardiac centers adjust cardiac activityAutonomic tone Dual innervation maintains resting tone by releasing ACh and NEFine adjustments meet needs of other systems20-4 CardiodynamicsEffects on the SA NodeMembrane potential of pacemaker cellsLower than other cardiac cellsRate of spontaneous depolarization depends on:Resting membrane potentialRate of depolarization20-4 CardiodynamicsEffects on the SA NodeSympathetic and parasympathetic stimulationGreatest at SA node (heart rate)ACh (parasympathetic stimulation)Slows the heartNE (sympathetic stimulation)Speeds the heart20-4 CardiodynamicsAtrial ReflexAlso called Bainbridge reflexAdjusts heart rate in response to venous returnStretch receptors in right atriumTrigger increase in heart rateThrough increased sympathetic activity20-4 CardiodynamicsHormonal Effects on Heart RateIncrease heart rate (by sympathetic stimulation of SA node)Epinephrine (E)Norepinephrine (NE)Thyroid hormone 20-4 CardiodynamicsFactors Affecting the Stroke VolumeThe EDV – amount of blood a ventricle contains at the end of diastoleFilling timeDuration of ventricular diastoleVenous returnRate of blood flow during ventricular diastole20-4 CardiodynamicsPreloadThe degree of ventricular stretching during ventricular diastoleDirectly proportional to EDVAffects ability of muscle cells to produce tension20-4 CardiodynamicsThe EDV and Stroke VolumeAt restEDV is lowMyocardium stretches lessStroke volume is lowWith exerciseEDV increasesMyocardium stretches moreStroke volume increases20-4 CardiodynamicsThe Frank–Starling PrincipleAs EDV increases, stroke volume increasesPhysical LimitsVentricular expansion is limited by:Myocardial connective tissueThe cardiac (fibrous) skeletonThe pericardial sac20-4 CardiodynamicsEnd-Systolic Volume (ESV)Is the amount of blood that remains in the ventricle at the end of ventricular systole 20-4 CardiodynamicsThree Factors That Affect ESV PreloadVentricular stretching during diastole ContractilityForce produced during contraction, at a given preload AfterloadTension the ventricle produces to open the semilunar valve and eject blood20-4 CardiodynamicsContractility Is affected by:Autonomic activity Hormones20-4 CardiodynamicsEffects of Autonomic Activity on ContractilitySympathetic stimulationNE released by postganglionic fibers of cardiac nervesEpinephrine and NE released by adrenal medullaeCauses ventricles to contract with more forceIncreases ejection fraction and decreases ESV20-4 CardiodynamicsEffects of Autonomic Activity on ContractilityParasympathetic activityAcetylcholine released by vagus nervesReduces force of cardiac contractions20-4 CardiodynamicsHormones Many hormones affect heart contractionPharmaceutical drugs mimic hormone actions Stimulate or block beta receptorsAffect calcium ions (e.g., calcium channel blockers)20-4 CardiodynamicsAfterload Is increased by any factor that restricts arterial blood flow As afterload increases, stroke volume decreases20-4 CardiodynamicsSummary: The Control of Cardiac OutputHeart rate control factorsAutonomic nervous systemSympathetic and parasympathetic Circulating hormones Venous return and stretch receptors20-4 CardiodynamicsSummary: The Control of Cardiac OutputStroke volume control factors EDVFilling time and rate of venous returnESVPreload, contractility, afterload20-4 CardiodynamicsCardiac ReserveThe difference between resting and maximal cardiac outputs20-4 CardiodynamicsThe Heart and Cardiovascular SystemCardiovascular regulationEnsures adequate circulation to body tissues Cardiovascular centersControl heart and peripheral blood vesselsCardiovascular system responds to:Changing activity patternsCirculatory emergencies ................
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