1. Chapter 18 --The Heart Use the video clip, CH 18 Heart Anatomy for a review of the gross anatomy of the heart J.F. Thompson, Ph.D. & J.R. Schiller, Ph.D. & G.R. Pitts, Ph.D.

2. Pericardium The sac containing the heart

3. 3 Layers Form the Heart’s Wall - Epicardium (outer) Myocardium (middle) Endocardium (inner)

4. Pericarditis inflammation of the pericardium painful may damage the lining tissues may damage myocardium fibrinous pericarditis

5. Cardiac Tamponade a buildup of pericardial fluid, or bleeding into the pericardial cavity may result in cardiac failure Elizabeth, Empress of Austria (d. 1898) by assassination with a hat pin

6. Internally - 4 compartments R/L atria with auricles R/L ventricles Interatrial septum separates atria Interventricular septum separates ventricles Left ventricular wall is much thicker because it must pump blood throughout the body and against gravity Chambers of the Heart RA LA LV RV

7. Blood Flow through the Heart Right atrium (RA) - receives deoxygenated blood from three sources superior vena cava (SVC) inferior vena cava (IVC) coronary sinus (CS) ( CS SVC IVC RA

8. Right ventricle (RV) receives blood from RA pumps to lungs via Pulmonary Trunk (PT) Pulmonary Trunk (PT) - from RV branches into the pulmonary arteries (PA) Pulmonary arteries deoxygenated blood from the heart to the lungs for gas exchange right and left branches for each lung blood gives up CO 2 and picks up O 2 in the lungs Pulmonary veins (PV) - oxygenated blood from the lungs to the heart Blood Flow through the Heart RA PT PA RV

9. Pulmonary Circulation

10. Left atria receives blood from PV pumps to left ventricle Left ventricle (LV) sends oxygenated blood to the body via the ascending aorta aortic arch curls over heart three branches off of it feed superior portion of body thoracic aorta abdominal aorta LA LV Aortic arch PV Blood Flow through the Heart

11. Schematic of Circulation Know the names of the valves indicated here.

12. Schematic of Circulation Review Routes

13. Myocardial Blood Supply Myocardium has its own blood supply coronary vessels simple diffusion of nutrients and O 2 into the myocardium is impossible due to its thickness Collateral circulation = duplication of supply routes and anastomoses (crosslinked connections) Heart can survive on 10- 15% of normal arterial blood flow

14. Arteries first branches off the aorta blood moves more easily into the myocardium when it is relaxed between beats  during diastole blood enters coronary capillary beds [note the collateral circulation] Myocardial Blood Supply

15. Coronary veins deoxygenated blood from cardiac muscle is collected in the coronary veins and then drains into the coronary sinus deoxygenated blood is returned to the right atrium Myocardial Blood Supply

16. Coronary Circulation Pathologies Compromised coronary circulation due to: emboli: blood clots, air, amniotic fluid, tumor fragments fatty atherosclerotic plaques smooth muscle spasms in coronary arteries Problems ischemia (decreased blood supply) hypoxia (low supply of O 2 ) infarct (cell death)

17. Pathologies (cont.) Angina pectoris - classic chest pain pain is due to myocardial ischemia – oxygen starvation of the tissues tight/squeezing sensation in chest labored breathing, weakness, dizziness, perspiration, foreboding often during exertion - climbing stairs, etc. pain may be referred to arms, back, abdomen, even neck or teeth silent myocardial ischemia can exist

18. Pathologies (cont.) Myocardial infarction (MI) - heart attack thrombus/embolus in coronary artery some or all tissue distal to the blockage dies if pt. survives, muscle is replaced by scar tissue Long term results size of infarct, position pumping efficiency? conduction efficiency, heart rhythm

19. Pathologies (cont.) Treatments clot-dissolving agents angioplasty (bypass surgery) Reperfusion damage re-establishing blood flow may damage tissue oxygen free radicals - electrically charged oxygen atoms with an unpaired electron radicals indiscriminately attack molecules: proteins (enzymes), neurotransmitters, nucleic acids, plasma membrane molecules further damage to previously undamaged tissue or to the already damaged tissue

20. Valve Structure Dense connective tissue covered by endocardium AV valves chordae tendineae - thin fibrous cords connect valves to papillary muscles

21. Valve Function Opening and closing a passive process when pressure low, valves open, flow occurs with contraction, pressure increases papillary muscles contract pull valves together

22. Valves of the Heart Function to prevent backflow of blood into/through heart Open and close in response to changes in pressure in heart Four key valves: tri- and bi-cuspid (mitral) valves between the atria and ventricles and semi-lunar valves between ventricles and main arteries Valves also close the entry points to the atria Tricuspid Bicuspid (Mitral) Semi-lunar

23. Separate the atria from the ventricles bicuspid (mitral) valve – left side tricuspid valve – right side note the feathery edges to the cusps Atrioventricular (AV) valves bicuspid tricuspid anterior

24. in the arteries that exit the heart to prevent back flow of blood to the ventricles pulmonary semilunar valves aortic semilunar valves Pathologies Incompetent – does not close correctly Stenosis – hardened, even calcified, and does not open correctly Semilunar valves

25. Normal Action Potential Review in Chapter 11

26. Cardiac Muscle Action Potential Contractile cells  near instantaneous depolarization is necessary for efficient pumping  much longer refractory period ensures no summation or tetany under normal circumstances

27. Cardiac Muscle Action Potential electrochemical events

28. Cardiac Muscle Action Potential sarcolemma’s ion permeabilities  opening fast Na + channels initiates depolarization near instantaneously  opening CA ++ channels while closing K + channels sustains depolarization and contributes to sustaining the refractory period  closing Na + and Ca ++ channels while opening K + channels restores the resting state repolarization

29. Cardiac Muscle Action Potential long absolute refractory period permits forceful contraction followed by adequate time for relaxation and refilling of the chambers inhibits summation and tetany

30. Pacemaker Potentials leaky membranes spontaneously depolarize creates autorhythmicity the fact that the membrane is more permeable to K + and Ca ++ ions helps explain why concentration changes in those ions affect cardiac rhythm

31. Conduction System and Pacemakers Autorhythmic cells cardiac cells repeatedly fire spontaneous action potentials Autorhythmic cells: the conduction system pacemakers SA node origin of cardiac excitation fires 60-100/min AV node conduction system AV bundle (Bundle of His) R and L bundle branches Purkinje fibers It’s as if the heart had only two motor units: the atria and the ventricles!

32. Conduction System and Pacemakers Arrhythmias irregular rhythms: slow (brady-) & fast (tachycardia) abnormal atrial and ventricular contractions Fibrillation rapid, fluttering, out of phase contractions – no pumping heart resembles a squirming bag of worms Ectopic pacemakers (ectopic focus) abnormal pacemaker controlling the heart SA node damage, caffeine, nicotine, electrolyte imbalances, hypoxia, toxic reactions to drugs, etc. Heart block AV node damage - severity determines outcome may slow conduction or block it

33. Conduction System and Pacemakers SA node damage (e.g., from an MI) AV node can run things (40-50 beats/min) if the AV node is out, the AV bundle, bundle branch and conduction fibers fire at 20-40 beats/min Artificial pacemakers - can be activity dependent

34. Atrial,Ventricular Excitation Timing

35. Sinoatrial node to Atrioventricular node about 0.05 sec from SA to AV, 0.1 sec to get through AV node – conduction slows allows atria time to finish contraction and to better fill the ventricles once action potentials reach the AV bundle, conduction is rapid to rest of ventricles

36. Extrinsic Control of Heart Rate basic rhythm of the heart is set by the internal pacemaker system central control from the medulla is routed via the ANS to the pacemakers and myocardium sympathetic input - norepinephrine parasympathetic input – acetylcholine

37. Electrocardiogram measures the sum of all electro- chemical activity in the myocardium at any moment P wave QRS complex T wave

38. Electrocardiogram

39. Cardiac Cycle Relationship between electrical and mechanical events Systole Diastole Isovolumetric contraction Ventricular ejection Isovolumetric relaxation

40. Cardiac Output Amount of blood pumped by each ventricle in 1 minute Cardiac Output (CO) = Heart Rate x Stroke Volume HR = 70 beats/min SV = 70 ml/beat CO = 4.9 L/min * *Average adult total body blood volume = 4-6 L

41. Cardiac Reserve Cardiac Output is variable Cardiac Reserve = maximal output (CO) – resting output (CO) average individuals have a cardiac reserve of 4X or 5X CO trained athletes may have a cardiac reserve of 7X CO heart rate does not increase to the same degree

42. Regulation of Stroke Volume SV = EDV – ESV EDV End Diastolic Volume Volume of blood in the heart after it fills 120 ml ESV End Systolic Volume Volume of blood in the heart after contraction 50 ml Each beat ejects about 60% of the blood in the ventricle

43. Regulation of Stroke Volume Most important factors in regulating SV: preload, contractility and afterload Preload – the degree of stretching of cardiac muscle cells before contraction Contractility – increase in contractile strength separate from stretch and EDV Afterload – pressure that must be overcome for ventricles to eject blood from heart

44. Preload Muscle mechanics Length-Tension relationship? fiber length determines number of cross bridges cross bridge number determines force increasing/decreasing fiber length increases/decreases force generation Cardiac muscle How is fiber length determined/regulated? Fiber length is determined by filling of heart – EDV Factors that effect EDV (anything that effects blood return to the heart) increases/decreases filling Increases/decreases SV

45. Preload Preload – Frank-Starling Law of the Heart Length tension relationship of heart Length = EDV Tension = SV As the ventricles become overfilled, the heart becomes inefficient and stroke volume declines. “cardiac reserve”

46. Contractility Increase in contractile strength separate from stretch and EDV Do not change fiber length but increase contraction force? What determines force? How can we change this if we don’t change length?

47. Sympathetic Stimulation Increases the number of cross bridges by increasing amount of Ca ++ inside the cell Sympathetic nervous stimulation (NE) opens channels to allow Ca ++ to enter the cell

48. Positive Inotropic Effect increase the force of contraction without changing the length of the cardiac muscle cells

49. Afterload if blood pressure is high, it is difficult for the heart to eject blood more blood remains in the chambers after each beat heart has to work harder to eject blood, because of the increase in the length/tension of the cardiac muscle cells

50. Regulation of Heart Rate Intrinsic Pacemakers Bainbridge effect Increase in EDV increases HR Filling the atria stretches the SA node increasing depolarization and HR

51. Regulation of Heart Rate Extrinsic Autonomic Nervous System Sympathetic - norepinephrine Parasympathetic – acetyl choline hormones – epinephrine, thyroxine ions (especially K + and Ca ++ ) body temperature age/gender body mass/blood volume exercise stress/illness

52. Regulation of Heart Rate Overview

53. End Chapter 18