THE CARDIOVASCULAR SYSTEM: HEART

CHAPTER 15

LOCATION

Thoracic cavity between two lungs~2/3 to left of midlinesurrounded by pericardium:Fibrous pericardium- Inelastic and anchors heart in placeInside is serous pericardium-

double layer around heartParietal layer fused to fibrous pericardiumInner visceral layer adheres tightly to heartFilled with pericardial fluid- reduces friction during beat.

FIGURE 15.1

HEART WALL

Epicardium- outer layerMyocardium- cardiac muscle Two separate networks via gap junctions in intercalated discs- atrial & ventricular

Networks- contract as a unitEndocardium- Squamous epitheliumlines inside of myocardium

FIGURE 15.2A

FIGURE 15.2B

FIGURE 15.2C

CHAMBERS

4 chambers2 upper chambers= AtriaBetween is interatrial septumContains fossa ovalis- remnant of foramen ovalis

2 lower chambers = ventriclesBetween is interventricular septum

Wall thickness depends on work load

Atria thinnestRight ventricle pumps to lungs & thinner than left

GREAT VESSELS OF HEART- RIGHT

Superior & inferior Vena CavaeDelivers deoxygenated blood to R. atrium from body

Coronary sinus drains heart muscle veinsR. Atrium R. Ventriclepumps through Pulmonary TrunkR & L pulmonary arteries lungs

GREAT VESSELS OF HEART-LEFT

Pulmonary Veins from lungsoxygenated bloodL. atrium Left ventricleascending aorta bodyBetween pulmonary trunk & aortic

arch is ligamentum arteriosumfetal ductus arteriosum remnant

FIGURE 15.3A

FIGURE 15.3B

FIGURE 15.3C

VALVES

Designed to prevent back flow in response to pressure changes

Atrioventricular (AV) valvesBetween atria and ventriclesRight = tricuspid valve (3 cusps)Left = bicuspid or mitral valveSemilunar valves near origin of

aorta & pulmonary trunk Aortic & pulmonary valves

respectively

FIGURE 15.4AB

FIGURE 15.4C

FIGURE 15.4D

FIGURE 15.5A

FIGURE 15.5B

BLOOD SUPPLY OF HEARTBlood flow through vessels in

myocardium = coronary circulationL. & Right coronary arteries branch from aortabranch to carry blood throughout muscleDeoxygenated blood collected by

Coronary Sinus (posterior)Empties into R. Atrium

CONDUCTION SYSTEM

1% of cardiac muscle generate action potentials= Pacemaker & Conduction system

Normally begins at sinoatrial (SA) node Atria & atria contractAV node -slowsAV bundle (Bundle of His) bundle branches Purkinje fibers apex and up- then ventricles

contract

PACEMAKER

Depolarize spontaneouslysinoatrial node ~100times /minalso AV node ~40-60 times/minin ventricle ~20-35 /minFastest one run runs the heart =

pacemaker Normally the sinoatrial node

FIGURE 15.6

ELECTROCARDIOGRAM

Recording of currents from cardiac conduction on skin = electrocardiogram (EKG or ECG)

P wave= atrial depolarizationContraction begins right after peakRepolarization is masked in QRSQRS complex= Ventricular

depolarizationContraction of ventricleT-wave = ventricular repolarizationJust after ventricles relax

FIGURE 15.7

CARDIAC CYCLE

after T-wave ventricular diastoleVentricular pressure drops below atrial & AV valves open ventricular filling occurs

After P-wave atrial systoleFinishes filling ventricle (`25%)

After QRS ventricular systolePressure pushes AV valves closedPushes semilunar valves open and ejection occurs

Ejection until ventricle relaxes enough for arterial pressure to close semilunar valves

ACTION POTENTIAL

Review muscleHeart has addition of External

Ca2+

creates a plateau prolonged depolarized period.Can not go into tetanus.

FIGURE 15.8

FLOW TERMS

Cardiac Output (CO) = liters/min pumped

Heart Rate (HR) = beats/minute (bpm)

Stroke volume (SV) = volume/beat CO = HR x SV

CONTROLS- STROKE VOLUME (S.V.)

Degree of stretch = Frank-Starling law

Increase diastolic Volume increases strength of contraction increased S.V.

Increased venous return increased S.V.increased sympathetic activity High back pressure in artery

decreased S.V.Slows semilunar valve opening

CONTROLS- HEART RATE

Pacemaker adjusted by nervesCardiovascular center in Medulla

parasympathetic- ACh slowsVia vagus nerve

Sympathetic - norepinephrine speedsSensory input for control:baroreceptors (aortic arch & carotid sinus)- B.P.Chemoreceptors- O2, CO2, pH

OTHER CONTROLS

Hormones: Epinephrine & norepinephrine increase H.R.

Thyroid hormones stimulate H.R.Called tachycardiaIonsIncreased Na+ or K+ decrease H.R. & contraction force

Increased Ca2+ increases H.R. & contraction force

FIGURE 15.9

EXERCISE

Aerobic exercise (longer than 20 min) strengthens cardiovascular system

Well trained athlete doubles maximum C.O.

Resting C.O. about the same but resting H.R. decreased

FIGURE 15.10