Heart Location

Cardiovascular System:The Heart1Heart Size, Shape, MassAbout the size of a closed fist:3.5 wide (at widest pt) X 5 long. 2.5 thick

Cone-shaped: Base & Apex

8 oz in adult females, 10 oz in adult males

28 oz = hamburger weightHeart LocationIn the mediastinum (tissue between sternum & vertebral column)2/3 of its mass is left of midlineA cone lying on its side:Base is toward your right shoulder, apex points to your left hipAnterior surface - deep to sternumInferior surface on diaphragmRight border against right lung.Left border (pulmonary border) against left lung

3Notice esophagus between heart & vertebral column - think heartburnBecause heart lies between two rigid structures, the vertebral column and the sternum, external compression on the chest can be used to force blood out of the heart and into the circulation. (CPR)2007 japanese study - chest compression alone is equally as effective if niot better than chest compression w mouth to mouth lung ventilation

pericardiumFibrous, Serous (Visceral & Parietal)Fibrous & Serous pericardium

Pericardium the sac that surrounds, protects, anchors heart to diaphragm. It is composed of 2 layers - the fibrous & serous (visceral & parietal layers) pericardium5What if the heart were just beating without this serous pericardium?Rubbing up against the fibrous pericardium - friction burn?What if the pericardium were inflamed? Pericarditis - take an aspirin, call me in the morningCardiac tamponade - too much fluid in the pericardial cavity - from chronic pericarditisThe FIBROUS PericardiumFIBROUS PERICARDIUMOutermost layerTough, inelastic, dense irregular CTPrevents overstretching of heartAnchors heart to diaphragm. Prevents rising of heart

6Can you figure out what part of the heart we are looking at in the picture on the right?The SEROUS PERICARDIUMSEROUS pericardium: thinner, delicate, inner layers that form a fluid-filled sac. It has 2 continuous layers:Parietal layer: is adhered to fibrous pericardiumVisceral layer aka Epicardium: is adhered to heart

The pericardial cavity is filled with Pericardial fluid. The pericardial cavity is the space between parietal & visceral layers.

The pericardial fluid PREVENTS FRICTION

7Double-bag it - like groceries. One layer will rip, 2 wont Base of pericardium fused with the central tendon of the diaphragmPericardium is attached to central tendon of diaphragmFluid is from leakage from myocardial capillaries & drained by the lymphSystemic & Pulmonary CirculationsTwo closed circulatory systems:Body Lungs

The output of one becomes the input of the other with each beat of the heart

8Circulation makes a cross -Horizontal (lungs) & vertical (body)

Blood Flow Within the 4 Heart ChambersFYI: is it just a pump?

10Anthroposophical medicine - enlivens the blood with spiraling hemodynamics. http://www.anthromed.org/Article.aspx?artpk=89What does the heart do? It pumps faster, slower, stronger, weaker.Cardiac Output (CO)

Heart pumps 5 L bloodPER MINUTETotal volume of blood in the body is approximately 5L. CO is typically about 5L/min

CO= Amount of blood pumped by left or right ventricle PER MINUTE

CO depends on Heart Rate & Stroke Volume

HEART RATE ie number of beats per minute. Normal is 75BPM

STROKE VOLUME ie. the amount of blood ejected from one Ventricle PER BEAT. Normal is 70ml/beat in a 70 kg healthy man

11Preload - think rubberband or water balloonThink of squeezing a water bottle - if sqeeze stronger, more will squirt out than if squeeze gentlyCardiac reserve - difference between CO at rest & max CO (4-5x more is possible)

Electrical activity of the heartAutorhythmic vs Contractile myocytesThe Heart has 2 kinds of cells:Autorhythmic myocytes (purple circle / yellow cell) spontaneously depolarize and generate action potentials

Contractile myocytes (pink cells) contract together to pump blood as the action potential spreads across them

13Assuming the coronary arteries are supplying oxygen, how does the coronary artery In skeletal muscle, each cell had a nerve supplying it - imagine if the heart had a nerve to each cell?The Sinoatrial (SA) Node or PacemakerThe SinoAtrial (SA) node is an area of modified cardiac myocytes within the R atrium.Cells here spontaneously depolarize (become more positive) 100 x/minPacemaker potential: the spontaneous depolarization from -60 to -35mV that precedes the action potentialAction potential: the depolarization that occurs after threshold of -35 mV

14Autorhythmic fibers have much higher resting membrane potential than working fibers or contractile fibers -60 vs -90-60 to -45 If channels open (funny current) Na/K channel that is more permeable to Na - net positive influx-45 T-type Ca channels open (Transient) -open & close for a very short time-35 voltage gated L-type Ca channels open & cause action potential spike to 0 mV

Action Potential at the SA NodeSA node cells do not restNa+ channels spontaneously open at -60mV. (If funny current) Na+ leaks into SA node cells which initiates the pacemaker potential2 Ca2+ channels open. One at low voltage, one at high voltage. Ca2+ enters the cell, causing part of pacemaker potential & then the action potentialAt 0mV, K+ channels openK+ exits cell which repolarizes the cell membrane to -60mV

15CaT = transient - open & close quicklyCaL = long - open & close slowlyHyperpolarization-activated cyclic nucleotide-gated (HCN) channel = HCN4 excpressed in heart generates funny currentHCN has dual activation by voltage and by cyclic nucleotidesFeatures of Cardiac Contractile CellsExhibit branchingIntercalated disks: at end of each myocyte, its sarcolemma thickensStair-step appearance2 disks are held together by Desmosomes Gap junctions connect cytoplasm of adjoining cellsStriated/Sarcomeres: same structure as skeletal muscle cells: bands & zones of actin &myosin, z-discs, m-linesSarcoplasmic reticulum: smaller w less Ca2+ reserveT-tubules: 1 per sarcomere. located at the z-diskMitochondria: Larger, more numerous (25% of cytosol)One central nucleus: cardiac myocytes are shorter in length

16Intercalate - insert betweenWHY BRANCHING? Have a conical strucutre. Goal is to spread the AP in a circular direction - so need BRANCHING or else would just have long cells that radiate out from the central SA NODE.GAP JUCTIONS only work to spread AP because cells are shorter in lengthPositive ions pass from SA to Contractile Cells through Gap Junctions Gap junction: a channel formed between two cells by 2 adjoined connexons. Connects cytoplasm of 2 cells, allowing ions & small molecules to pass through to adjoining cells quickly.

Positive ions (Ca2+ & Na+) pass from the autorhythmic cells, through gap junctions, to enter the adjacent contractile cells

17In a skeletal muscle, the depolarization = ion flow is triggered by a neurotransmitterIn cardiac muscle, ion flow is initated by pacemaker cellContractile Cell Depolarization Fast Na ChannelsGap Junction: Positive ions (Na+ & Ca2+ enter through gap junctions which triggers:

Rapid Depolarization: Fast voltage-gated Na+ channels on the sarcolemma open. The cell instantly becomes positive on the inside.

Plateau Phase: at +20mV Ca2+ & K+ channels open. Influx and efflux of positive ions is balanced so AP graph plateaus.

In myocardial cells, magnesium is a cofactor for the sodium-potassium adenosine triphosphatase enzyme[6] and antagonizes both the L-type and T-type calcium channels in the atria18Action Potential Plateau & Repolarization

Ca2+ channels and K+ channels are open at the same voltage (+20 mV).

Thus, Ca2+ enters the cell, while K+ leaves. Influx and efflux of positive ions is equal, the cell does not become more positive or negative, creating a plateau in the AP graph.

Ca2+ channels close, while K+ channels remain open and K+ keeps leaking out so the cell becomes more negative inside, or, repolarizes

Calcium-Triggered Calcium Release plateau and contractionNa+ & Ca2+ influx from an adjacent cell changes voltage

Voltage-gated Ca channels on cell surface open & Ca enters the cell from Extra Cellular Fluid

Calcium-triggered calcium release: Ca entering cell binds to ryanodine receptors, which are Ca channels on the sarcoplasmic reticulumSarcoplasmic Ca stores are released into cell. Ca binds to troponin, tropomyosin moves off myosin binding sites, myosin binds to actin & the sarcomeres shorten

20Xanthines like caffeine and pentifylline activate it by potentiating sensitivity to native ligand Ca.cardiac excitation-contraction coupling

21Action potential vs contraction

The action potential is generated first in the SA node. Then the action potential spreads to contractile myocytes.After the contractile myocytes depolarize, the sarcomeres shorten and a contraction is generated.

TetanusUnlike skeletal muscle, cardiac muscle cannot enter tetanus (sustained contraction).The cardiac cell has a refractory period that is almost as long as the entire muscle twitch

23You can fit another action potential into a skeletal muscle contraction. Cardiac muscle is still in plateau when muscle contraction is already endingHeart rate REGULATIONSympathetic & Parasympathetic

The Vagus nerve (Parasympathetic) innervates SA, AV nodes & atrial myocardium. It releases ACETYLCHOLINE which binds to muscarinic receptors on cardiac mm.Binding of Ach to muscarinic receptors causes K+ to leave the cells. Thus:

SLOWS rate of depolarization of SA & AV nodes, thus HEART RATE DECREASESThe Vagus N. slows SA node to make the normal HR. Normal HR = 70-100 BPM. (Contractile Fibers: little effect on contractility because does not innervate ventricles)

HR slows due to Vagus Nerve(Ach): Parasympathetic25Max heart rate about 200bpmHR & Contractility increase due to Sympathetic Nerves (NE)Sympathetic Cardiac Accelerator Nerves innervate SA & AV nodes, and most of the myocardium. They release NOREPINEPHRINE which binds to 1 receptors. Binding of NE to 1 enhances Ca2+ entry to cell, thus, at:SA & AV nodes, it speeds rate of depolarization so HEART RATE INCREASESContractile Fibers,more crossbridges form and CONTRACTILITY INCREASES100-150 (simple tachycard), 150-200 (paroxysmal), 250-350 (flutter), 350+ (fibrillation)

26Max heart rate about 200bpmInputs affecting Heart RateInput to the Cardiovascular Center in medulla oblongata comes from:Brain - cortex, limbic system (eg anxiety), hypothalamus Sensory Receptors - proprioceptors (limb position), chemoreceptors, baroreceptors (artery & vein stretch, blood pressure changes)

Chemical & Other Regulation of HRINCREASES HEART RATE & CONTRACTILITY Hormones:EpinephrineNorepinephrineThyroid hormonesCations:Ca2+ Other:Increased body temperature (fever, exercise)

TACHYCARDIA: increased resting heart rate (>100bpm for adult)DECREASES HEART RATE & CONTRACTILITYCations:K+ blocks generation of AP (Hyperkalemia)Na+ blocks Ca inflow during APOther:Decreased body temperature (hypothermia)

BRADYCARDIA: decreased resting heart rate (50%), calcification of congenital bicuspid aortic valve (30-40%), HTN, diabetes, hyperlioproteinemia, uremia all can speed up process. Acute Rheumatic fvr (10%) can scar MITRAL STENOSIS - almost all from Rheumatic ht dz dt rhem fvr. - uncommon - calcification dt congenital. When severe, get AfibTRICUSPID STENOSIS is rare & almost always together with mitral stenosis. Can also be dt carcinoid synd, endocarditis, lupus e, r atrial myxoma, congenital TRICUSPID INSUFFICIENCY - R ventricular dilation messes up anatomy of valve dt L ventricular dilation, R ventricular infarction, inferior MI, cor PAORTIC INSUFFICIENCY - 50 aortic root dialtion of which 80% is idiopathic. aging, syphillitic aortitis, aortic dissection, osteogenesis imperfecta, SSRIs, dopmine aginists, Systemic HTN, 15% bicuspidal aortic valve, 15% retraction of cusps from rheumatic endocarditis, collagen vascular dz, marfans, ehlers-danlos, ankylosing spond, lupus, ACUTE - infective endocarditisHeart Valve Disorders: Insufficiency w RegurgitationMost common valves affected:Mitral insufficiency backflow of blood from L ventricle to L atriumMitral valve prolapse (MVP) one or both valve cusps protrude into L atrium during ventricular contractionAortic insufficiency backflow of blood from aorta into L ventricle

63Congestive Heart FailureIn CHF, the heart is a failing pump:Stroke Volume decreases, blood remains in ventricle (end systolic volume increases)End diastolic volume increases gradually (ventricle enlarges)If Left ventricle fails first,blood backs up into lungs, get Pulmonary edemaIf Right ventricle fails first, blood backs up in body, get Peripheral edemaCHF may be due to: coronary artery disease, congenital defects, long-term high blood pressure (increases afterload), myocardial infarctions, valve disorders.

64Either ventricles are too dilated & cant contract or they cant relax and let blood in