Chapter 20

1. Chapter 20 the heart

2. Anatomy review Electrical activity of the whole heart (EKG) Electrical activity of the heart cells The Cardiac Cycle Cardiac Input and Output (dynamics)

3. Heart review 4 chambers 2 atria 2 ventricles 4 valves 2 AV valves 2 semilunar valves 2 circuits systemic pulmonary receive send

4. external heart anatomy fig. 20-9

5. internal heart anatomy fig. 20-6

6. 100 keys (pg. 678) “The heart has four chambers, two associated with the pulmonary circuit (right atrium and right ventricle) and two with the systemic circuit (left atria and left ventricle). The left ventricle has a greater workload and is much more massive than the right ventricle, but the two chambers pump equal amounts of blood. AV valves prevent backflow from the ventricles into the atria, and semilunar valves prevent backflow from the aortic and pulmonary trunks into the ventricles.”

7. cardiac conduction system modified cardiac muscle cells • SA node (sinoatrial node) • wall of RA • AV node (atrioventricular node) • between atrium and ventricle • conducting cells • AV bundle (of His) • conducting fibers • Purkinje fibers

8. conducting system of heart fig. 20-12a

9. prepotential cannot maintain steady resting potential gradually drift toward threshold SA node 80-100 bpm AV node 40-60 bpm

10. fig. 20-12b

11. because SA node is faster… …it controls the heart rate (pacemaker) but heart rate is normally slower than 80-100 bpm (parasympathetics) if SA node is damaged, heart can still continue to beat, but at a slower rate

12. if heartbeat is slower than normal… … bradycardia if heartbeat is faster than normal… … tachycardia

13. impulse conduction fig. 20-13

14. impulse conduction SA node atria get signal - contract signal to AV Node AV node sends signal to ventricles (time delay) ventricles contract after atria are done damage to any part of conducting system may result in abnormalities (EKG)

15. ECG’s EKG’s electrocardiagram recording of the electrical activity of the heart (from the surface of the body) fig 20-14

16. ECG’s different components: P wave QRS complex T wave depolarization of the atria depolarization of the ventricles bigger stronger signal repolarization of the ventricles

17. ECG’s fig 20-14 EKG

18. ECG’s to analyze: size of voltage changes duration of changes timing of changes intervals

19. ECG’s fig 20-14 EKG

20. ECG’s intervals: P-R interval from start of atrial depolarization to start of QRS complex time for signal to get from atrium to ventricles if longer than 200 msec can mean damage to conducting system

21. ECG’s intervals: Q-T interval time for ventricular depolarization and repolarization (ventricular systole) if lengthened, may indicate, [ion] disturbances, medications, conducting problems, ischemia, or myocardial damage.

22. ECG’s intervals: T-P interval from end of ventricular repolarization to start of next atrial depolarization the time the “heart” is in diastole the “isoelectric line”

23. fig 20-14 EKG T-P interval

24. ECG’s intervals: abnormalities cardiac electrical activity = cardiac arrhythmias some are not dangerous others indicate damage to heart

25. 100 keys (pg. 688) “The heart rate is normally established by cells of the SA node, but that rate can be modified by autonomic activity, hormones, and other factors. From the SA node the stimulus is conducted to the AV node, the AV bundle, the bundle branches, and Purkinjie fibers before reaching the ventricular muscle cells. The electrical events associated with the heartbeat can be monitored in an electrocardiagram (ECG).”

26. Electrical activity of the heart cells 99 % of heart is contractile cells similar to skeletal muscle AP leads to Ca2+ around myofibrils Ca2+ bind to troponin on thin filaments initiates contraction (cross-bridges) • but there are differences… • nature of AP • location of Ca2+ storage • duration of contraction

27. Electrical activity of the heart cells The action potential resting potential of heart cells ~ -90mV threshold is reached near intercalated discs signal is AP in an adjacent cell (gap junctions)

28. Electrical activity of the heart cells The action potential review skeletal muscle fig. 20-15

29. Electrical activity of the heart cells The action potential once threshold is reached the action potential proceeds in three steps.

30. Electrical activity of the heart cells The action potential - step 1 rapid depolarization (like skeletal muscle) Na+ into cell through voltage-gated channels (fast channels)

31. Electrical activity of the heart cells The action potential - step 2 the plateau Na+ channels close Ca2+ channels open for a “long” time (slow calcium channels) Ca2+ in balances Na+ pumped out

32. Electrical activity of the heart cells The action potential - step 3 repolarization Ca2+ channels begin closing slow K+ channels begin opening K+ rushes out restoring resting pot.

33. Electrical activity of the heart cells The action potential - step 3 repolarization Na+ channels are still inactive cell will not respond to stimulus = refractory period

34. fig. 20-15a

35. Electrical activity of the heart cells The role of calcium extracellular Ca2+ enters cells during the plateau phase (20%) Ca2+ entering triggers release of Ca2+ from sarcoplasmic reticulum ... heart is highly sensitive to changes in [Ca2+] of the ECF

36. Electrical activity of the heart cells The role of calcium in skeletal muscle, refractory period ended before peak tension developed… …summation was possible …tetanus. in cardiac muscle refractory period lasts until relaxation has begun… …no summation …no tetanus.

37. Clinical note: Heart attacks blockage of coronary vessels myocardium without blood supply… …cells die (infarction) myocardial infarction (MI) = heart attack

38. Clinical note: Heart attacks blockage of coronary vessels due to: CAD (coronary artery disease) (plaque in vessel wall) blocked by clot (thrombosis)

39. Clinical note:Heart attacks blockage of coronary vessels as O2 levels fall, cardiac cells will: accumulate anaerobic enzymes die and release enzymes LDH SGOT CPK CK-MB lactose dehydrogenase serum glutamic oxaloacetic transaminase creatine phosphokinase cardiac muscle creatine phosphokinase

40. to here 3/26 lec # 31

41. Clinical note:Heart attacks anticoagulants (aspirin) clot-dissolving enzymes quick treatment will help reduce damage due to blockage

42. Clinical note:Heart attacks risk factors: smoking high blood pressure high blood cholesterol high [LDL] diabetes male severe emotional stress obesity genetic predisposition sedentary lifestyle any 2 more than doubles your risk of MI

43. The cardiac cycle contraction (systole) relax (diastole) fluid (blood) moves always moves from higher pressure… …toward lower pressure

44. fig. 20-16

45. together The cardiac cycle atrial systole atrial diastole ventricular systole ventricular diastole generic heart rate 75 bpm

46. fig. 20-17

47. The cardiac cycle atrial systole (100 msec) blood in atria is pushed through AV valves into ventricles “tops off” the ventricles blood in ventricles is called EDV (end diastolic volume) 1+2 (follows path of least resistance) end of atrial systole ventricular diastole begins 3…

48. The cardiac cycle ventricular systole (270 msec) pressure start to rise in ventricle when it is greater than pressure in atria, the AV valves will close (chordae tendineae and papillary m.) …3 “lubb” pressure continues to build until it can force open the semilunar valves 4

49. The cardiac cycle ventricular systole (270 msec) up until now, ventricles have been contracting but no blood has flowed: isovolumetric contraction 4 ventricular volume has not changed but the pressure has increased

50. The cardiac cycle ventricular systole (270 msec) when pressure in ventricle is greater than pressure in the arteries, the semilunar valves will open 5 ventricular ejection stroke volume some blood left behind end systolic volume (ESV)