The Cardiovascular system: Heart Lab and Lecture Notes

Lab Material

Location Thoracic cavity between two lungs surrounded by pericardium: ~2/3 to left of midline surrounded by pericardium: Fibrous pericardium- Inelastic and anchors heart in place Inside is serous pericardium- double layer around heart Parietal layer fused to fibrous pericardium Inner visceral layer adheres tightly to heart Filled with pericardial fluid- reduces friction during beat.

Figure 15.1

Heart Wall Epicardium- outer layer Myocardium- cardiac muscle Two separate networks via gap junctions in intercalated discs- atrial & ventricular Networks- contract as a unit Endocardium- Squamous epithelium lines inside of myocardium

Figure 15.2a

Figure 15.2b

Figure 15.2c

Chambers 4 chambers 2 upper chambers= Atria Between is interatrial septum Contains fossa ovalis- remnant of foramen ovalis 2 lower chambers = ventricles Between is interventricular septum Wall thickness depends on work load Atria thinnest Right ventricle pumps to lungs & thinner than left

Great Vessels Of Heart- Right Superior & inferior Vena Cavae Delivers deoxygenated blood to R. atrium from body Coronary sinus drains heart muscle veins R. Atrium Tricuspid Valve R. Ventricle pumps through Pulmonary Trunk R & L pulmonary arteries  lungs

Great Vessels Of Heart-Left Pulmonary Veins from lungs oxygenated blood L. atriumBicusid (Mitral) Valve Left ventricle ascending aorta body Between pulmonary trunk & aortic arch is ligamentum arteriosum fetal 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) valves Between atria and ventricles Right = tricuspid valve (3 cusps) Left = bicuspid or mitral valve Semilunar 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 Heart Blood flow through vessels in myocardium = coronary circulation L. & Right coronary arteries branch from aorta branch to carry blood throughout muscle Deoxygenated blood collected by Coronary Sinus (posterior) Empties into R. Atrium

Lecture Material

Conduction System 1% of cardiac muscle generate action potentials= Pacemaker & Conduction system Normally begins at sinoatrial (SA) node Atria & atria contract AV node -slows AV bundle (Bundle of His) bundle branches Purkinje fibers  apex and up- then ventricles contract

Pacemaker Depolarize spontaneously sinoatrial node ~100times /min also AV node ~40-60 times/min in ventricle ~20-35 /min Fastest 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 depolarization Contraction begins right after peak Repolarization is masked in QRS QRS complex= Ventricular depolarization Contraction of ventricle T-wave = ventricular repolarization Just after ventricles relax

Figure 15.7

Cardiac Cycle after T-wave ventricular diastole Ventricular pressure drops below atrial & AV valves open  ventricular filling occurs After P-wave atrial systole Finishes filling ventricle (`25%) After QRS ventricular systole Pressure pushes AV valves closed Pushes semilunar valves open and ejection occurs Ejection until ventricle relaxes enough for arterial pressure to close semilunar valves

Action Potential Review muscle Heart 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 nerves Cardiovascular center in Medulla parasympathetic- ACh slows Via vagus nerve Sympathetic - norepinephrine speeds Sensory 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 tachycardia Ions Increased 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