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Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Human Anatomy & Physiology SEVENTH EDITION Elaine N. Marieb Katja Hoehn PowerPoint.

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Presentation on theme: "Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Human Anatomy & Physiology SEVENTH EDITION Elaine N. Marieb Katja Hoehn PowerPoint."— Presentation transcript:

1 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Human Anatomy & Physiology SEVENTH EDITION Elaine N. Marieb Katja Hoehn PowerPoint ® Lecture Slides prepared by Vince Austin, Bluegrass Technical and Community College C H A P T E R 18 The Cardiovascular System: The Heart P A R T A

2 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Anatomy  Approximately the size of your fist  Location  Superior surface of diaphragm  Left of the midline  Anterior to the vertebral column, posterior to the sternum

3 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Anatomy Figure 18.1

4 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coverings of the Heart: Physiology  The pericardium:  Protects and anchors the heart  Prevents overfilling of the heart with blood  Allows for the heart to work in a relatively friction- free environment

5 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Pericardial Layers of the Heart Figure 18.2

6 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Muscle Bundles Figure 18.3

7 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings External Heart: Vessels that Supply/Drain the Heart (Posterior View)  Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove)  Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein

8 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.4e (e) Superior vena cava Right pulmonary artery Pulmonary trunk Right atrium Right pulmonary veins Fossa ovalis Pectinate muscles Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava Aorta Left pulmonary artery Left atrium Left pulmonary veins Pulmonary valve Aortic valve Mitral (bicuspid) valve Left ventricle Papillary muscle Interventricular septum Myocardium Visceral pericardium Endocardium

9 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Right and Left Ventricles Figure 18.6

10 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.5

11 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coronary Circulation  Coronary circulation is the functional blood supply to the heart muscle itself  Collateral routes ensure blood delivery to heart even if major vessels are occluded

12 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coronary Circulation: Arterial Supply Figure 18.7a

13 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coronary Circulation: Venous Supply Figure 18.7b

14 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Valves Figure 18.8a, b

15 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Valves Figure 18.8c, d

16 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Atrioventricular Valve Function Figure 18.9

17 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Semilunar Valve Function Figure 18.10

18 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Microscopic Anatomy of Heart Muscle  Cardiac muscle is striated, short, fat, branched, and interconnected  The connective tissue endomysium acts as both tendon and insertion  Intercalated discs anchor cardiac cells together and allow free passage of ions  Heart muscle behaves as a functional syncytium InterActive Physiology ®: Anatomy Review: The Heart, pages 3–7

19 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Microscopic Anatomy of Cardiac Muscle Figure 18.11

20 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Human Anatomy & Physiology SEVENTH EDITION Elaine N. Marieb Katja Hoehn PowerPoint ® Lecture Slides prepared by Vince Austin, Bluegrass Technical and Community College C H A P T E R 18 The Cardiovascular System: The Heart P A R T B

21 Copyright © 2006 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  Has a long (250 ms) absolute refractory period  Cardiac muscle contraction is similar to skeletal muscle contraction

22 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Physiology: Intrinsic Conduction System  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

23 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Pacemaker and Action Potentials of the Heart Figure 18.13

24 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Membrane Potential Figure 18.12

25 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Intrinsic Conduction Figure 18.14a

26 Copyright © 2006 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)

27 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Physiology: Sequence of Excitation  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

28 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Intrinsic Conduction Figure 18.14a

29 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Membrane Potential Figure 18.12

30 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA nodeAV nodePurkinje fibers Bundle branches Figure 18.17 Heart Excitation Related to ECG

31 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings SA node generates impulse; atrial excitation begins SA node Figure 18.17 Heart Excitation Related to ECG

32 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Impulse delayed at AV node AV node Figure 18.17 Heart Excitation Related to ECG

33 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Impulse passes to heart apex; ventricular excitation begins Bundle branches Figure 18.17 Heart Excitation Related to ECG

34 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Ventricular excitation complete Purkinje fibers Figure 18.17 Heart Excitation Related to ECG

35 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA nodeAV nodePurkinje fibers Bundle branches Figure 18.17 Heart Excitation Related to ECG

36 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Electrocardiography Figure 18.16

37 Copyright © 2006 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 PLAY InterActive Physiology ®: Intrinsic Conduction System, pages 3–6

38 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings  Abnormal heart sounds produced by abnormal patterns of blood flow in the heart.  Defective heart valves:  Valves become damaged by antibodies made in response to an infection, or congenital defects.  Mitral stenosis:  Mitral valve becomes thickened and calcified.  Impairs blood flow from left atrium to left ventricle.  Accumulation of blood in left ventricle may cause pulmonary HTN.  Incompetent valves:  Damage to papillary muscles.  Valves do not close properly.  Murmurs produced as blood regurgitates through valve flaps. Heart Murmurs

39 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Murmurs  Septal defects:  Usually congenital.  Holes in septum between the left and right sides of the heart.  May occur either in interatrial or interventricular septum.  Blood passes from left to right.

40 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Electrocardiogram (ECG/EKG)  The body is a good conductor of electricity.  Tissue fluids have a high [ions] that move in response to potential differences.  Electrocardiogram:  Measure of the electrical activity of the heart per unit time.  Potential differences generated by heart are conducted to body surface where they can be recorded on electrodes on the skin.  Does NOT measure the flow of blood through the heart.

41 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Ischemic Heart Disease  Ischemia:  Oxygen supply to tissue is deficient.  Most common cause is atherosclerosis of coronary arteries.  Increased [lactic acid] produced by anaerobic respiration.  Angina pectoris:  Substernal pain.  Myocardial infarction (MI):  Changes in T segment of ECG.  Increased CPK and LDH.

42 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Arrhythmias Detected on ECG  Arrhythmias:  Abnormal heart rhythms.  Flutter:  Extremely rapid rates of excitation and contraction of atria or ventricles.  Atrial flutter degenerates into atrial fibrillation.  Fibrillation:  Contractions of different groups of myocardial cells at different times.  Coordination of pumping impossible.  Ventricular fibrillation is life-threatening.

43 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Arrhythmias Detected on ECG (continued)  Bradycardia:  HR slower < 60 beats/min.  Tachycardia:  HR > 100 beats/min.  First–degree AV nodal block:  Rate of impulse conduction through AV node exceeds 0.2 sec.  P-R interval.  Second-degree AV nodal block:  AV node is damaged so that only 1 out of 2-4 atrial APs can pass to the ventricles.  P wave without QRS.

44 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Arrhythmias Detected on ECG (continued)  Third-degree (complete) AV nodal block:  None of the atrial waves can pass through the AV node.  Ventricles paced by ectopic pacemaker.

45 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings ECG Tracings Figure 18.18

46 Copyright © 2006 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

47 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Sounds Figure 18.19

48 Copyright © 2006 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

49 Copyright © 2006 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

50 Copyright © 2006 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

51 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle  Ventricular systole  Atria relax  Rising ventricular pressure results in closing of AV valves  Isovolumetric contraction phase  Ventricular ejection phase opens semilunar valves

52 Copyright © 2006 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 PLAY InterActive Physiology ®: Cardiac Cycle, pages 3–18

53 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle  Refers to the repeating pattern of contraction and relaxation of the heart.  Systole:  Phase of contraction.  Diastole:  Phase of relaxation.  End-diastolic volume (EDV):  Total volume of blood in the ventricles at the end of diastole.  Stroke volume (SV):  Amount of blood ejected from ventricles during systole.  End-systolic volume (ESV):  Amount of blood left in the ventricles at the end of systole.

54 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.20

55 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle (continued)  Step 1: Isovolumetric contraction:  QRS just occurred.  Contraction of the ventricle causes ventricular pressure to rise above atrial pressure.  AV valves close.  Ventricular pressure is less than aortic pressure.  Semilunar valves are closed.  Volume of blood in ventricle is EDV.  Step 2: Ejection:  Contraction of the ventricle causes ventricular pressure to rise above aortic pressure.  Semilunar valves open.  Ventricular pressure is greater than atrial pressure.  AV valves are closed.  Volume of blood ejected: SV.

56 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle (continued)  Step 3: T wave occurs:  Ventricular pressure drops below aortic pressure.  Step 4: Isovolumetric relaxation:  Back pressure causes semilunar valves to close.  AV valves are still closed.  Volume of blood in the ventricle: ESV.  Step 5: Rapid filling of ventricles:  Ventricular pressure decreases below atrial pressure.  AV valves open.  Rapid ventricular filling occurs.

57 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle (continued)  Step 6: Atrial systole:  P wave occurs.  Atrial contraction.  Push 10-30% more blood into the ventricle.

58 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Cycle (continued)

59 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Correlation of ECG with Heart Sounds  First heart sound:  Produced immediately after QRS wave.  Rise of intraventricular pressure causes AV valves to close.  Second heart sound:  Produced after T wave begins.  Fall in intraventricular pressure causes semilunar valves to close.

60 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.20

61 Copyright © 2006 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  Cardiac reserve is the difference between resting and maximal CO

62 Copyright © 2006 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)

63 Copyright © 2006 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

64 Copyright © 2006 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

65 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings  Volume of blood pumped/min. by each ventricle.  Pumping ability of the heart is a function of the beats/ min. and the volume of blood ejected per beat.  CO = SV x HR  Total blood volume averages about 5.5 liters.  Each ventricle pumps the equivalent of the total blood volume each min. (resting conditions). Cardiac Output (CO)

66 Copyright © 2006 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

67 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Preload and Afterload Figure 18.21

68 Copyright © 2006 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

69 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Extrinsic Factors Influencing Stroke Volume  Agents/factors that decrease contractility include:  Acidosis  Increased extracellular K +  Calcium channel blockers

70 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings GTP GDP Inactive protein kinase A Active protein kinase A ATP cAMP GTP SR Ca 2+ channel Ca 2+ binds to Troponin Enhanced actin-myosin interaction Extracellular fluid Cytoplasm Adenylate cyclase Ca 2+ channel Ca 2+  1 -Adrenergic receptor Norepinephrine Ca 2+ uptake pump Sarcoplasmic reticulum (SR) Cardiac muscle force and velocity 1 3 2 Heart Contractility and Norepinephrine  Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system Figure 18.22

71 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Heart Rate  Positive chronotropic factors increase heart rate  Negative chronotropic factors decrease heart rate

72 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Circulatory Changes During Exercise (continued)

73 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings  Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise  Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS  PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone Regulation of Heart Rate: Autonomic Nervous System

74 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Atrial (Bainbridge) Reflex  Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria  Causes stimulation of the SA node  Stimulates baroreceptors in the atria, causing increased SNS stimulation

75 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Chemical Regulation of the Heart  The hormones epinephrine and thyroxine increase heart rate  Intra- and extracellular ion concentrations must be maintained for normal heart function InterActive Physiology ®: Cardiac Output, pages 3–9

76 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.23

77 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Congestive Heart Failure (CHF)  Congestive heart failure (CHF) is caused by:  Coronary atherosclerosis  Persistent high blood pressure  Multiple myocardial infarcts  Dilated cardiomyopathy (DCM)

78 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Baroreceptor Reflex (continued)

79 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Renin-Angiotension-Aldosterone System (continued)

80 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Regulation by ADH  Released by posterior pituitary when osmoreceptors detect an increase in plasma osmolality.  Dehydration or excess salt intake:  Produces sensation of thirst.  Stimulates H 2 0 reabsorption from urine.


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