Chapter 19: The HeartCirculatory system heart, blood vessels and bloodCardiovascular system heart, arteries, veins and capillaries; 2 major divisionsPulmonary circuit - right side of heartcarries blood to lungs for gas exchangeSystemic circuit - left side of heartsupplies blood to all organs of the body

Cardiovascular System Circuit

Size, Shape and PositionLocated in mediastinum, between lungsBase - broad superior portion of heartApex - inferior end, tilts to the left, tapers to point3.5 in. wide at base, 5 in. from base to apex and 2.5 in. anterior to posterior; weighs 10 oz

Heart Position

Pericardium (analogous to pleura)Allows heart to beat will less friction, gives room to expand and resists excessive expansionParietal pericardium consists of two layersfibrous layer outer, tough layer of connective tissueserous layerinner, thin, smooth, moist layer, produces lubricative serous fluid Pericardial cavity filled with pericardial fluidVisceral pericardium (a.k.a. epicardium of heart wall)thin, smooth, moist serous layer covers heart surface

Review: serous membranesEach serous membrane is composed of a secretory epithelial layer and a connective tissue layer underneath.The epithelial layer, known as mesothelium, consists of a single layer of avascular flat nucleated cells (simple squamous epithelium) which produce the lubricating serous fluid. This fluid has a consistency similar to thin mucus. These cells are bound tightly to the underlying connective tissue.The connective tissue layer provides the blood vessels and nerves for the overlying secretory cells, and also serves as the binding layer which allows the whole serous membrane to adhere to organs and other structures.For the heart, the surrounding serous membranes include:Outer: Parietal pericardiumInner : Visceral pericardium (epicardium) Other parts of the body may also have specific names for these structures. serosa of the uterus is called perimetrium.The three serous cavities in the body have lubricative roles:pericardial cavity (surrounding the heart), pleural cavity (surrounding the lungs) peritoneal cavity (surrounding most organs of the abdomen)The serous cavities are formed from the intraembryonic coelom and are basically an empty space within the body surrounded by serous membrane. Early in embryonic life visceral organs develop adjacent to a cavity and invaginate into the bag-like coelom. Therefore each organ becomes surrounded by serous membrane - they do not lie within the serous cavity. The layer in contact with the organ is known as the visceral layer, while the parietal layer is in contact with the body wall.

Heart WallEpicardium (a.k.a. visceral pericardium)serous membrane covers heartMyocardiumthick muscular layerfibrous skeleton - network of collagenous and elastic fibersprovides structural supportattachment for cardiac musclenonconductor important in coordinating contractile activityEndocardiumsmooth inner lining

Pericardium & Heart WallPericardial cavity contains 5-30 ml of pericardial fluid

Heart chambers and sulci4 chambersRight and left atria 2 superior, posterior chambersreceive blood returning to heartRight and left ventricles 2 inferior chamberspump blood into arteriesAtrioventricular sulcus - separates atria, ventriclesAnterior and posterior sulci = grooves that separate ventricles (next slide)

External Anatomy - AnteriorAtrioventricular sulcus

External Anatomy - Posterior

Heart Chambers - InternalInteratrial septumwall that separates atriaPectinate musclesinternal ridges of myocardium in right atrium and both auriclesInterventricular septumwall that separates ventriclesTrabeculae carneaeinternal ridges in both ventricles

Internal Anatomy Anterior Aspect

Internal Anatomy, Anterior Aspect

Heart Internal AnatomyHeart bisected in frontal plane, opened like a book

Heart ValvesEnsure one-way blood flowAtrioventricular (AV) valvesright AV valve has 3 cusps (tricuspid valve)left AV valve has 2 cusps (mitral, bicuspid valve) lambchordae tendineae = cords that connect AV valves to papillary muscles (on floor of ventricles)Semilunar valves - control flow into great arteriespulmonary: from right ventricle into pulmonary trunkaortic: from left ventricle into aorta

Heart Valves

Heart Valves

AV Valve MechanicsVentricles relax, pressure drops, semilunar valves close, AV valves open, blood flows from atria to ventriclesVentricles contract, pressure rises, AV valves close, (papillary m. contracts and pulls on chordae tendineae to prevent prolapse) pressure rises and semilunar valves open, blood flows into arteries

Operation of Atrioventricular Valves

Operation of Semilunar Valves

Blood Flow Through Heart

Coronary CirculationBlood vessels of heart wall nourish cardiac muscleLeft coronary artery - under left auricle, 2 branchesanterior interventricular arterysupplies interventricular septum + anterior walls of ventriclescircumflex artery passes around left side of heart in coronary sulcus, supplies left atrium and posterior wall of left ventricle Right coronary artery - supplies right atriumpasses under right auricle in coronary sulcus, divides:marginal artery - supplies lateral rt. atrium + ventricleposterior interventricular arterysupplies posterior walls of ventricles

Myocardial InfarctionSudden death of heart tissue caused by interruption of blood flow from vessel narrowing or occlusionAnastomoses defend against interruption by providing alternate blood pathwayscircumflex artery and right coronary artery combine to form posterior interventricular arteryanterior and posterior interventricular arteries join at apex of heart

Venous Drainage20% drains directly into right ventricle80% returns to right atriumgreat cardiac vein (anterior interventricular sulcus)middle cardiac vein (posterior sulcus)coronary sinus (posterior coronary sulcus) collects blood from these and smaller veins and empties into right atrium

Coronary Vessels - Anterior

Coronary Vessels - Posterior

BaroreceptorsChemoreceptors &

Coronary Flow and the Cardiac CycleReduced during ventricular contractionarteries compressedIncreased during ventricular relaxationopenings to coronary arteries, just above aortic semilunar valve, fill as blood surges back to valve

Structure of Cardiac MuscleShort, thick, branched cells, 50 to 100 m long and 10 to 20 m wide with one central nucleusSarcoplasmic reticulum T tubules much larger than in skeletal muscle, admit more Ca2+ from ECF during excitationIntercalated discs, join myocytes end to endinterdigitating folds - surface areamechanical junctions tightly join myocytesfascia adherens: actin anchored to plasma membranedesmosomes = mechanical junctionsgap junctions = electrical junctions that form channels allowing ions to flow directly into next cell

Structure of Cardiac Muscle Cell

Cardiac MuscleIn comparison to skeletal muscle, the cells are shorter, thicker, branched and linked to each other at intercalated discselectrical gap junctions allow cells to stimulate their neighbors & mechanical junctions keep the cells from pulling apartsarcoplasmic reticulum is less developed but T tubules are larger to admit Ca+2 from extracellular fluidStriatedmononucleated autorhythmic due to pacemaker cellsUses aerobic respiration almost exclusivelylarge mitochondria make it resistant to fatiguemakes sense

The fibers consist of separate cells with interdigitating processes where they are held together. These regions of contact are called the intercalated discs, which cross an entire fiber between two cells. The transverse regions of the steplike intercalated disc have abundant desmosomes (mechanical junctions) and other adherent junctions which hold the cells firmly together. Longitudinal regions of these discs contain abundant gap junctions, which form "electrical synapses" allowing contraction signals to pass from cell to cell as a single wave. Cardiac muscle cells have central nuclei and myofibrils that are less dense and organized than those of skeletal muscle. Also the cells are often branched, allowing the muscle fibers to interweave in a more complicated arrangement within fascicles that produces an efficient contraction mechanism for emptying the heart.

Metabolism of Cardiac MuscleAerobic respirationRich in myoglobin and glycogenLarge mitochondria Organic fuels: fatty acids, glucose, ketonesFatigue resistant

Cardiac Conduction SystemMyogenic - heartbeat originates within heartAutorhythmic - depolarize spontaneously regularlyConduction systemSA node: pacemaker, initiates heartbeat, sets heart ratefibrous skeleton insulates atria from ventriclesAV node: electrical gateway to ventriclesAV bundle (of His): pathway for signals from AV nodeRight and left bundle branches: divisions of AV bundle that enter interventricular septum and descend to apexPurkinje fibers: upward from apex spread throughout ventricular myocardium

Cardiac Conduction System

Cardiac RhythmSystole = contraction; diastole = relaxationSinus rhythmset by SA node, adult at rest is 70 to 80 bpmEctopic foci - region of spontaneous firing (not SA)nodal rhythm - set by AV node, 40 to 50 bpm intrinsic ventricular rhythm - 20 to 40 bpm Arrhythmia - abnormal cardiac rhythmheart block: failure of conduction systembundle branch blocktotal heart block (damage to AV node)

Depolarization of SA NodeSA node - no stable resting membrane potentialPacemaker potential gradual depolarization from -60 mV, slow influx of Na+Action potentialat threshold -40 mV, fast Ca+2 channels open, (Ca+2 in) depolarizing phase to 0 mV, K+ channels open, (K+ out)repolarizing phase back to -60 mV, K+ channels closeEach depolarization creates one heartbeatSA node at rest fires at 0.8 sec, about 75 bpm

SA Node Potentials

Impulse Conduction to MyocardiumSA node signal travels at 1 m/sec through atriaAV nodes thin myocytes slow signal to 0.05 m/secdelays signal 100 msec, allows ventricles to fill AV bundle and purkinje fibersspeeds signal along at 4 m/sec to ventriclesPapillary muscles - get signal first, contraction stabilizes AV valves Ventricular systole begins at apex, progresses upspiral arrangement of myocytes twists ventricles slightly

Contraction of MyocardiumMyocytes have stable resting potential of -90 mVDepolarization (very brief) stimulus opens Na+ gates, (Na+ in) depolarizes to threshold, rapidly opens more Na+ gates in a positive feedback cycleaction potential peaks at +30 mV, gates close quicklyPlateau - 200 to 250 msec, sustains contractionslow Ca+2 channels open, Ca+2 binds to fast Ca+2 channels on SR, releases Ca+2 into cytosol: contractionRepolarization - Ca+2 channels close, K+ channels open, rapid K+ out returns to resting potential

Myocardial Contraction & Action Potential1) Na+ gates open2) Positive feedback cycle3) Na+ gates close4) Plateau5) Ca+2 channels close K+ channels open

Electrocardiogram (ECG)Composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest

ECGP waveSA node fires, atrial depolarizationatrial systoleQRS complexatrial repolarization and diastole (signal obscured)AV node fires, ventricular depolarizationventricular systoleT waveventricular repolarization

Normal Electrocardiogram (ECG)

1)atria begin to depolarize2) atria depolarize3)ventricles begin to depolarize at apex; atria repolarize4)ventricles depolarize5) ventricles begin to repolarize at apex6) ventricles repolarize Electrical Activity of Myocardium

Diagnostic Value of ECGInvaluable for diagnosing abnormalities in conduction pathways, MI, heart enlargement and electrolyte and hormone imbalances

ECGs, Normal & AbnormalNo P waves or inverted P waves or retrograde P waves suggest junctional (nodal ) rhythm determined by AV node

ECGs, AbnormalArrhythmia: conduction failure at AV nodeNo pumping action occurs

Cardiac CycleOne complete contraction and relaxation of heartAtrial systoleAtrial diastoleVentricle systoleVentricle diastoleQuiescent period

Opposing pressuresalways positive blood pressure in aorta, holds aortic valve closedventricular pressure must rise above aortic pressure forcing open the valveChange in volume creates a pressure gradientPrinciples of Pressure and FlowMeasurement: compared to force generated by column of mercury (mmHg) - sphygmomanometer

Heart SoundsAuscultation - listening to sounds made by bodyFirst heart sound (S1), louder and longer lubb, occurs with closure of AV valvesduring isovolumetric contraction of ventriclesSecond heart sound (S2), softer and sharper dupp occurs with closure of semilunar valvesduring isovolumetric relaxation of ventricles S3 - rarely heard in people > 30

Phases of Cardiac CycleQuiescent periodall chambers relaxedAV valves openblood flowing into ventriclesAtrial systoleSA node fires, atria depolarizeP wave appears on ECGatria contract, force additional blood into ventriclesventricles now contain end-diastolic volume (EDV) of about 130 ml of blood

Isovolumetric Contraction of VentriclesAtria repolarize and relaxVentricles depolarizeQRS complex appears in ECGVentricles contractRising pressure closes AV valvesHeart sound S1 occursNo ejection of blood yet (no change in volume)compare to isometric muscle contractionmuscle length doesnt change, yet muscle exerts force

Ventricular EjectionRising pressure opens semilunar valvesRapid ejection of bloodReduced ejection of blood (less pressure)Stroke volume (SV): amount ejected, about 70 mlSV/EDV= ejection fraction, at rest ~ 54%, during vigorous exercise as high as 90%, diseased heart < 50%End-systolic volume: amount left in heart

Isovolumetric Relaxation of VentriclesT wave appears in ECGVentricles repolarize and relax (begin to expand)Semilunar valves close (dicrotic notch of aortic press. curve)AV valves remain closed Ventricles expand but do not fill yetHeart sound S2 occurs

Ventricular FillingAV valves openVentricles fill with blood - 3 phasesrapid ventricular filling - high pressurediastasis - sustained lower pressurefilling completed by atrial systoleHeart sound S3 may occur

Major Events of Cardiac CycleQuiescent periodAtrial systoleIsovolumetric contractionVentricular ejectionIsovolumetric relaxationVentricular filling

Rate of Cardiac CycleAtrial systole, 0.1 secVentricular systole, 0.3 secQuiescent period, 0.4 secTotal 0.8 sec, heart rate 75 bpm

Overview of Volume ChangesEnd-systolic volume (ESV)60 mlPassively added to ventricle during atrial diastole30 mlAdded by atrial systole40 mlTotal: end-diastolic volume (EDV) 130 mlStoke volume (SV) ejected by ventricular systole -70 mlEnd-systolic volume (ESV) 60 mlBoth ventricles must eject same amount of bloodSV refers to either ventricle

Unbalanced Ventricular Output

Unbalanced Ventricular Output

Cardiac Output (CO)Amount ejected by each ventricle in 1 minuteCO = HR x SVResting values, CO = 75 beats/min x70 ml/beat = 5,250 ml/min, usually about 4 to 6L/minVigorous exercise CO to 21 L/min for fit person and up to 35 L/min for world class athleteCardiac reserve: difference between maximum and resting CO

Heart RateMeasured from pulseInfants have HR of 120 beats per minute or moreYoung adult females avg. 72 - 80 bpmYoung adult males avg. 64 to 72 bpmHR rises again in the elderlyTachycardia: persistent, resting adult HR > 100stress, anxiety, drugs, heart disease or body temp.Bradycardia: persistent, resting adult HR < 60common in sleep and endurance trained athletes ( SV)

Chronotropic EffectsPositive chronotropic agents raise HR and negative chronotropic agents lower HRCardiac center of medulla oblongataan autonomic control center with 2 neuronal pools: cardioacceleratory center (sympathetic) cardioinhibitory center (parasympathetic)

Sympathetic Nervous SystemCardioacceleratory centerstimulates sympathetic cardiac accelerator nerves to SA node, AV node and myocardiumthese nerves secrete norepinephrine, which binds to -adrenergic receptors in the heart (+ chronotropic effect)CO peaks at HR of 160 to 180 bpmSympathetic n.s. can drive HR up to 230 bpm, (limited by refractory period of SA node), but SV and CO are less than at rest

Parasympathetic Nervous SystemCardioinhibitory centerstimulates vagus nervesright vagus nerve - SA nodeleft vagus nerve - AV nodesecrete ACh (acetylcholine), binds to muscarinic receptorsopens K+ channels in nodal cells, hyperpolarized, fire less frequently, HR slows downvagal tone: background firing rate holds HR to sinus rhythm of 70 to 80 bpmsevered vagus nerves - SA node fires at intrinsic rate-100bpmmaximum vagal stimulation HR as low as 20 bpm!

Inputs to Cardiac CenterHigher brain centers affect HRsensory and emotional stimuli - rollercoaster, IRS auditcerebral cortex, limbic system, hypothalamusProprioceptors inform cardiac center about changes in activity, HR before metabolic demands ariseBaroreceptors pressure sensors in aorta and internal carotid arteries send continual stream of signals to cardiac center in medulla oblongataif pressure drops, signal rate drops, cardiac center HRif pressure rises, signal rate rises, cardiac center HR

Inputs to Cardiac Center Chemoreceptorssensitive to blood pH, CO2 and oxygenaortic arch, carotid arteries and medulla oblongata primarily respiratory control, may influence HR CO2 (hypercapnia) causes H+ levels, may create acidosis (pH < 7.35)Hypercapnia and acidosis stimulates cardiac center to HR

Chronotropic ChemicalsNeurotransmitters - with cAMP as 2nd messengernorepinephrine and epinephrine (catecholamines) are potent cardiac stimulantsDrugs caffeine inhibits cAMP breakdownnicotine stimulates catecholamine secretionHormonesTH adrenergic receptors in heart, sensitivity to sympathetic stimulation, leads to HRElectrolytes - K has greatest chronotropic effects K+ makes myocardium less excitable, HR slow and irregularif extracellular K+ is greater, then repolarization (K+ flowing out of the cell) following an action potential will be incomplete; cell will be depolarized, refractive period will become longer K: cells more hyperpolarized (more intracellular K+ flows out after an AP), requires stimulation

Stroke VolumeGoverned by three factors:preload, contractility and afterload preload or contractility: SV afterload SV

PreloadAmount of tension in ventricular myocardium before it contracts preload causes contraction strengthexercise venous return, stretches myocardium ( preload) , myocytes generate more tension during contraction, CO matches venous returnFrank-Starling law of heart - SV EDVventricles eject as much blood as they receive, the more they are stretched ( preload) the harder they contract

ContractilityContraction force for a given preloadTension caused by factors that adjust myocytes responsiveness to stimulationfactors that contractility are positive inotropic agentshypercalcemia, catecholamines, glucagon, digitalisfactors that contractility are negative inotropic agentshyperkalemia (K+), hypocalcemia, hypoxia, hypercapnia

AfterloadPressure in arteries above semilunar valves opposes opening of valves before next contraction afterload SVany impedance in arterial circulation afterload Continuous in afterload (lung disease, atherosclerosis, etc.) causes hypertrophy of myocardium, may lead it to weaken and fail

Exercise and Cardiac OutputEffect of proprioceptorsHR at beginning of exercise due to signals from joints, musclesEffect of venous returnmuscular activity venous return causes SV HR and SV cause COEffect of ventricular hypertrophycaused by sustained program of exercise SV allows heart to beat more slowly at rest, 40-60bpm cardiac reserve, can tolerate more exertion