1. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Human Anatomy & Physiology, Sixth Edition Elaine N. Marieb PowerPoint ® Lecture Slides prepared by Vince Austin, University of Kentucky 18 The Cardiovascular System: The Heart

2. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Pathway of Blood Through the Heart and Lungs  Right atrium  tricuspid valve  right ventricle  Right ventricle  pulmonary semilunar valve  pulmonary arteries  lungs  Lungs  pulmonary veins  left atrium  Left atrium  bicuspid valve  left ventricle  Left ventricle  aortic semilunar valve  aorta  Aorta  systemic circulation

3. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Pathway of Blood Through the Heart and Lungs Figure 18.5

4. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Muscle Contraction  Heart muscle:  Is stimulated by nerves and is self-excitable (automaticity)  Contracts as a unit  Cardiac muscle contraction is similar to skeletal muscle contraction  Autorhythmic cells:  Initiate action potentials  Have unstable resting potentials called pacemaker potentials  Use calcium influx (rather than sodium) for rising phase of the action potential

5. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Pacemaker and Action Potentials of the Heart Figure 18.13

6. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Muscle Contraction  Depolarization opens voltage-gated fast Na + channels in the sarcolemma  Reversal of membrane potential from –90 mV to +30 mV  Depolarization wave in T tubules causes the SR to release Ca 2+  Depolarization wave also opens slow Ca 2+ channels in the sarcolemma  Ca 2+ surge prolongs the depolarization phase (plateau)

7. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.12 Absolute refractory period Tension development (contraction) Plateau Action potential Time (ms) 1 2 3 Depolarization is due to Na + influx through fast voltage-gated Na + channels. A positive feedback cycle rapidly opens many Na + channels, reversing the membrane potential. Channel inactivation ends this phase. Plateau phase is due to Ca 2+ influx through slow Ca 2+ channels. This keeps the cell depolarized because few K + channels are open. Repolarization is due to Ca 2+ channels inactivating and K + channels opening. This allows K + efflux, which brings the membrane potential back to its resting voltage. 1 2 3 Tension (g) Membrane potential (mV)

8. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Muscle Contraction  Ca 2+ influx triggers opening of Ca 2+ -sensitive channels in the SR, which liberates bursts of Ca 2+  E-C coupling occurs as Ca 2+ binds to troponin and sliding of the filaments begins  Duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle  Repolarization results from inactivation of Ca 2+ channels and opening of voltage-gated K + channels

9. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Heart Physiology: Sequence of Excitation  Sinoatrial (SA) node generates impulses about 75 times/minute  Atrioventricular (AV) node delays the impulse approximately 0.1 second  Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)  AV bundle splits into two pathways in the interventricular septum (bundle branches)  Bundle branches carry the impulse toward the apex of the heart  Purkinje fibers carry the impulse to the heart apex and ventricular walls

10. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Heart Physiology: Sequence of Excitation Figure 18.14a

11. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.17 Atrial depolarization, initiated by the SA node, causes the P wave. P R T Q S SA node AV node With atrial depolarization complete, the impulse is delayed at the AV node. Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. P R T Q S P R T Q S Ventricular depolarization is complete. Ventricular repolarization begins at apex, causing the T wave. Ventricular repolarization is complete. P R T Q S P R T Q S P R T Q S DepolarizationRepolarization 1 2 3 4 5 6

12. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Extrinsic Innervation of the Heart  Heart is stimulated by the sympathetic cardioacceleratory center  Heart is inhibited by the parasympathetic cardioinhibitory center Figure 18.15

13. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Electrocardiography  Electrical activity is recorded by electrocardiogram (ECG)  P wave corresponds to depolarization of SA node  QRS complex corresponds to ventricular depolarization  T wave corresponds to ventricular repolarization  Atrial repolarization record is masked by the larger QRS complex

14. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Electrocardiography Figure 18.16

15. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.18 (a) Normal sinus rhythm. (c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1. (d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock. (b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min.

16. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Heart Sounds  Heart sounds (lub-dup) are associated with closing of heart valves  First sound occurs as AV valves close and signifies beginning of systole  Second sound occurs when SL valves close at the beginning of ventricular diastole

17. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.19 Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space Aortic valve sounds heard in 2nd intercostal space at right sternal margin Pulmonary valve sounds heard in 2nd intercostal space at left sternal margin Mitral valve sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle

18. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle  Cardiac cycle refers to all events associated with blood flow through the heart  Systole – contraction of heart muscle  Diastole – relaxation of heart muscle

19. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle  Ventricular filling – mid-to-late diastole  Heart blood pressure is low as blood enters atria and flows into ventricles  AV valves are open, then atrial systole occurs  Ventricular systole  Atria relax  Rising ventricular pressure results in closing of AV valves  Isovolumetric contraction phase  Ventricular ejection phase opens semilunar valves

20. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle  Isovolumetric relaxation – early diastole  Ventricles relax  Backflow of blood in aorta and pulmonary trunk closes semilunar valves  Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves

21. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle Figure 18.20

22. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Output (CO) and Reserve  CO is the amount of blood pumped by each ventricle in one minute  CO is the product of heart rate (HR) and stroke volume (SV)  HR is the number of heart beats per minute  SV is the amount of blood pumped out by a ventricle with each beat

23. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Output: Example  CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)  CO = 5250 ml/min (5.25 L/min)

24. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Stroke Volume  SV = end diastolic volume (EDV) minus end systolic volume (ESV)  EDV = amount of blood collected in a ventricle during diastole  ESV = amount of blood remaining in a ventricle after contraction  Example:  CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)  CO = 5250 ml/min (5.25 L/min)

25. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Factors Affecting Stroke Volume  Preload – amount ventricles are stretched by contained blood  Contractility – cardiac cell contractile force due to factors other than EDV  Afterload – back pressure exerted by blood in the large arteries leaving the heart

26. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Frank-Starling Law of the Heart  Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume  Slow heartbeat and exercise increase venous return to the heart, increasing SV  Blood loss and extremely rapid heartbeat decrease SV

27. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Preload and Afterload Figure 18.21

28. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Extrinsic Factors Influencing Stroke Volume  Contractility is the increase in contractile strength, independent of stretch and EDV  Increase in contractility comes from:  Increased sympathetic stimuli  Certain hormones  Ca 2+ and some drugs  Agents/factors that decrease contractility include:  Acidosis  Increased extracellular K +  Calcium channel blockers

29. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Contractility and Norepinephrine  Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second- messenger system Figure 18.22

30. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.21 Norepinephrine Adenylate cyclase Ca 2+ uptake pump Ca 2+ channel  1 -Adrenergic receptor G protein (G s ) Ca 2+ Sarcoplasmic reticulum (SR) Active protein kinase A Extracellular fluid Cytoplasm Phosphorylates SR Ca 2+ pumps, speeding Ca 2+ removal and relaxation Phosphorylates SR Ca 2+ channels, increasing intracellular Ca 2+ release Phosphorylates plasma membrane Ca 2+ channels, increasing extra- cellular Ca 2+ entry Inactive protein kinase A Ca 2+ Enhanced actin-myosin interaction Cardiac muscle force and velocity ATP is converted to cAMP binds to SR Ca 2+ channel GDP Troponin a b c

31. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Factors Involved in Regulation of Cardiac Output Figure 18.23

32. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Chemical Regulation of Heart Rate 1.Hormones  Epinephrine from adrenal medulla enhances heart rate and contractility  Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine 2.Intra- and extracellular ion concentrations (e.g., Ca 2+ and K + ) must be maintained for normal heart function

33. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Other Factors that Influence Heart Rate  Age  Gender  Exercise  Body temperature

34. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Homeostatic Imbalances  Tachycardia: abnormally fast heart rate (>100 bpm)  If persistent, may lead to fibrillation  Bradycardia: heart rate slower than 60 bpm  May result in grossly inadequate blood circulation  May be desirable result of endurance training

35. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Congestive Heart Failure (CHF)  Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs  Caused by  Coronary atherosclerosis  Persistent high blood pressure  Multiple myocardial infarcts  Dilated cardiomyopathy (DCM)