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Copyright © 2010 Pearson Education, Inc. Chapter 18: THE HEART.

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1 Copyright © 2010 Pearson Education, Inc. Chapter 18: THE HEART

2 Copyright © 2010 Pearson Education, Inc. Heart Anatomy Approximately the size of a fist Location In the mediastinum between second rib and fifth intercostal space On the superior surface of diaphragm Two-thirds to the left of the midsternal line Anterior to the vertebral column, posterior to the sternum Enclosed in pericardium, a double-walled sac

3 Copyright © 2010 Pearson Education, Inc. Figure 18.1a Point of maximal intensity (PMI) Diaphragm (a) Sternum 2nd rib Midsternal line

4 Copyright © 2010 Pearson Education, Inc. Figure 18.1c (c) Superior vena cava Left lung Aorta Parietal pleura (cut) Pericardium (cut) Pulmonary trunk Diaphragm Apex of heart

5 Copyright © 2010 Pearson Education, Inc. Pericardium 3 layers 1.Fibrous pericardium (superficial) 2.Serous pericardium (2 layers) Parietal layer Visceral layer lines the internal surface of the fibrous pericardium 3.Visceral layer (epicardium) on external surface of the heart

6 Copyright © 2010 Pearson Education, Inc. Pericardium: Layer Functions Fibrous layer Protects, anchors, and prevents overfilling Serous parietal layer lines the internal surface of the fibrous pericardium Parietal means relating to or forming the wall of a body part, organ, or cavity Serous visceral layer on external surface of the heart, known as the epicardium Visceral means organs

7 Copyright © 2010 Pearson Education, Inc. Percardium: Layer Functions The parietal and visceral serous pericardium form a sac or cushion of space around the heart This sac is called the pericardial cavity Filled with fluid Purpose = decrease friction

8 Copyright © 2010 Pearson Education, Inc. Figure 18.2 Fibrous pericardium Parietal layer of serous pericardium Pericardial cavity Epicardium (visceral layer of serous pericardium) Myocardium Endocardium Pulmonary trunk Heart chamber Heart wall Pericardium Myocardium

9 Copyright © 2010 Pearson Education, Inc. Layers of the Heart Wall 1.Epicardium—visceral layer of the serous pericardium

10 Copyright © 2010 Pearson Education, Inc. Layers of the Heart Wall 2.Myocardium Myo = muscle Spiral bundles of cardiac muscle cells Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue Anchors cardiac muscle fibers Supports great vessels and valves Limits spread of action potentials to specific paths

11 Copyright © 2010 Pearson Education, Inc. Layers of the Heart Wall 3.Endocardium is continuous with endothelial lining of blood vessels

12 Copyright © 2010 Pearson Education, Inc. Figure 18.2 Fibrous pericardium Parietal layer of serous pericardium Pericardial cavity Epicardium (visceral layer of serous pericardium) Myocardium Endocardium Pulmonary trunk Heart chamber Heart wall Pericardium Myocardium

13 Copyright © 2010 Pearson Education, Inc. Figure 18.3 Cardiac muscle bundles

14 Copyright © 2010 Pearson Education, Inc. Chambers Four chambers Two atria (receiving chambers) and two ventricles (discharging chambers) Left and right atrium, left and right ventricle Coronary sulcus (atrioventricular groove, AV groove) encircles the junction of the atria and ventricles Sulcus = deep, narrow groove Auricles (ears) increase atrial volume

15 Copyright © 2010 Pearson Education, Inc. Chambers Two ventricles (discharging chambers) Separated by the interventricular septum Pumping chambers R ventricle pumps blood into the lungs L ventricle pumps blood into the body Inter = between Intra = within

16 Copyright © 2010 Pearson Education, Inc. A note on vessels Direction of blood flow Artery = Away from the heart Vein = to the heart This is important to remember when looking at the heart; arteries do not always carry oxygenated blood and veins do not always carry deoxygenated blood i.e., pulmonary artery carries deoxygenated blood Pulmonary veins carry oxygenated blood

17 Copyright © 2010 Pearson Education, Inc. Figure 18.4b (b) Anterior view Brachiocephalic trunk Superior vena cava Right pulmonary artery Ascending aorta Pulmonary trunk Right pulmonary veins Right atrium Right coronary artery (in coronary sulcus) Right ventricle Inferior vena cava Left common carotid artery Left subclavian artery Left pulmonary artery Left pulmonary veins Left coronary artery (in coronary sulcus) Left ventricle Great cardiac vein Apex Aortic arch Auricle of left atrium

18 Copyright © 2010 Pearson Education, Inc. Figure 18.4d (d) Posterior surface view Aorta Left pulmonary artery Left pulmonary veins Auricle of left atrium Left atrium Great cardiac vein Posterior vein of left ventricle Left ventricle Apex Superior vena cava Right pulmonary artery Right pulmonary veins Right atrium Inferior vena cava Right coronary artery (in coronary sulcus) Coronary sinus Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein Right ventricle

19 Copyright © 2010 Pearson Education, Inc. Atria: The Receiving Chambers Walls are ridged by pectinate muscles Vessels entering right atrium Superior vena cava Inferior vena cava Coronary sinus Vessels entering left atrium Right and left pulmonary veins

20 Copyright © 2010 Pearson Education, Inc. Ventricles: The Discharging Chambers Walls are ridged by trabeculae carneae Papillary muscles project into the ventricular cavities (anchor valves) Vessel leaving the right ventricle Pulmonary trunk Vessel leaving the left ventricle Aorta

21 Copyright © 2010 Pearson Education, Inc. Figure 18.4e Aorta Left pulmonary artery Left atrium Left pulmonary veins Mitral (bicuspid) valve Aortic valve Pulmonary valve Left ventricle Papillary muscle Interventricular septum Epicardium Myocardium Endocardium (e) Frontal section Superior vena cava Right pulmonary artery Pulmonary trunk Right atrium Right pulmonary veins Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava

22 Copyright © 2010 Pearson Education, Inc. Pathway of Blood Through the Heart The heart is two side-by-side pumps Right side is the pump for the pulmonary circuit Vessels that carry blood to and from the lungs Left side is the pump for the systemic circuit Vessels that carry the blood to and from all body tissues

23 Copyright © 2010 Pearson Education, Inc. Figure 18.5 Oxygen-rich, CO 2 -poor blood Oxygen-poor, CO 2 -rich blood Capillary beds of lungs where gas exchange occurs Capillary beds of all body tissues where gas exchange occurs Pulmonary veins Pulmonary arteries Pulmonary Circuit Systemic Circuit Aorta and branches Left atrium Heart Left ventricle Right atrium Right ventricle Venae cavae

24 Copyright © 2010 Pearson Education, Inc. Pathway of Blood Through the Heart Right atrium Right ventricle Pulmonary trunk Pulmonary arteries Lungs Pulmonary veins Left atrium Left ventricle Aorta Systemic circulation

25 Copyright © 2010 Pearson Education, Inc. Pathway of Blood Through the Heart Pulmonary circuit is a short, low-pressure circulation Systemic circuit blood encounters much resistance in the long pathways As a result, the left ventricle has a much thicker wall (stronger muscle)

26 Copyright © 2010 Pearson Education, Inc. Figure 18.6 Right ventricle Left ventricle Interventricular septum

27 Copyright © 2010 Pearson Education, Inc. Heart Valves

28 Copyright © 2010 Pearson Education, Inc. Heart Valves Ensure unidirectional blood flow through the heart Atrioventricular (AV) valves (balloons) Prevent backflow into the atria when ventricles contract Tricuspid valve (right) Between R atrium and R ventricle Mitral valve (left) Between L atrium and L ventricle Chordae tendineae anchor AV valve cusps to papillary muscles

29 Copyright © 2010 Pearson Education, Inc. Heart Valves Semilunar (SL) valves (cups) Prevent backflow into the ventricles when ventricles relax Pulmonary valve between R ventricle and pulmonary trunk Aortic valve Between L ventricle and aorta

30 Copyright © 2010 Pearson Education, Inc. Figure 18.4e Aorta Left pulmonary artery Left atrium Left pulmonary veins Mitral (bicuspid) valve Aortic valve Pulmonary valve Left ventricle Papillary muscle Interventricular septum Epicardium Myocardium Endocardium (e) Frontal section Superior vena cava Right pulmonary artery Pulmonary trunk Right atrium Right pulmonary veins Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava

31 Copyright © 2010 Pearson Education, Inc. Blood flow through the heart with valves Right atrium  tricuspid valve  right ventricle  pulmonary semilunar valve  pulmonary trunk  pulmonary arteries  Lungs  pulmonary veins  left atrium  (mitral) bicuspid valve  left ventricle  aortic semilunar valve  aorta  systemic circulation

32 Copyright © 2010 Pearson Education, Inc. Figure 18.8a Pulmonary valve Aortic valve Area of cutaway Mitral valve Tricuspid valve Myocardium Tricuspid (right atrioventricular) valve Mitral (left atrioventricular) valve Aortic valve Pulmonary valve (b) Pulmonary valve Aortic valve Area of cutaway Mitral valve Tricuspid valve Myocardium Tricuspid (right atrioventricular) valve (a) Mitral (left atrioventricular) valve Aortic valve Pulmonary valve Fibrous skeleton Anterior

33 Copyright © 2010 Pearson Education, Inc. Figure 18.8b Pulmonary valve Aortic valve Area of cutaway Mitral valve Tricuspid valve Myocardium Tricuspid (right atrioventricular) valve Mitral (left atrioventricular) valve Aortic valve Pulmonary valve (b)

34 Copyright © 2010 Pearson Education, Inc. Figure 18.8c Pulmonary valve Aortic valve Area of cutaway Mitral valve Tricuspid valve Chordae tendineae attached to tricuspid valve flap Papillary muscle (c)

35 Copyright © 2010 Pearson Education, Inc. Figure 18.8d Pulmonary valve Aortic valve Area of cutaway Mitral valve Tricuspid valve Mitral valve Chordae tendineae Interventricular septum Myocardium of left ventricle Opening of inferior vena cava Tricuspid valve Papillary muscles Myocardium of right ventricle (d)

36 Copyright © 2010 Pearson Education, Inc. Physiology of Blood Flow through the Heart

37 Copyright © 2010 Pearson Education, Inc. Figure Blood returning to the heart fills atria, putting pressure against atrioventricular valves; atrioventricular valves are forced open. 1 Ventricles contract, forcing blood against atrioventricular valve cusps. 2 As ventricles fill, atrioventricular valve flaps hang limply into ventricles. 2 Atrioventricular valves close. 3 Atria contract, forcing additional blood into ventricles. 3 Papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria. (a) AV valves open; atrial pressure greater than ventricular pressure (b) AV valves closed; atrial pressure less than ventricular pressure Direction of blood flow Atrium Ventricle Cusp of atrioventricular valve (open) Chordae tendineae Papillary muscle Atrium Blood in ventricle Cusps of atrioventricular valve (closed)

38 Copyright © 2010 Pearson Education, Inc. Figure As ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar valves, forcing them open. As ventricles relax and intraventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar valves and forcing them to close. (a) Semilunar valves open (b) Semilunar valves closed Aorta Pulmonary trunk

39 Copyright © 2010 Pearson Education, Inc. Heart Sounds AV valves closing (tricuspid and mitral) = lub Semilunar valves closing (pulmonic, aortic) = dub

40 Copyright © 2010 Pearson Education, Inc. Coronary Circulation

41 Copyright © 2010 Pearson Education, Inc. Coronary Circulation The functional blood supply to the heart muscle itself Arterial supply varies considerably and contains many anastomoses (junctions) among branches

42 Copyright © 2010 Pearson Education, Inc. Coronary Circulation Arteries Right and left coronary (in atrioventricular groove) Veins Small cardiac, anterior cardiac, and great cardiac veins, coronary sinus Coronary sinus is where dexoygenated blood from coronary circulation pools and is returned to venous circulation via the inferior vena cava

43 Copyright © 2010 Pearson Education, Inc. Figure 18.7a Right ventricle Right coronary artery Right atrium Posterior interventricular artery Anterior interventricular artery Circumflex artery Left coronary artery Aorta Anastomosis (junction of vessels) Left ventricle Superior vena cava (a) The major coronary arteries Left atrium Pulmonary trunk

44 Copyright © 2010 Pearson Education, Inc. Figure 18.7b Superior vena cava Anterior cardiac veins Great cardiac vein Coronary sinus (b) The major cardiac veins

45 Copyright © 2010 Pearson Education, Inc. Figure 18.4d (d) Posterior surface view Aorta Left pulmonary artery Left pulmonary veins Auricle of left atrium Left atrium Great cardiac vein Posterior vein of left ventricle Left ventricle Apex Superior vena cava Right pulmonary artery Right pulmonary veins Right atrium Inferior vena cava Right coronary artery (in coronary sulcus) Coronary sinus Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein Right ventricle

46 Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Angina pectoris Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium Cells are weakened Myocardial infarction (heart attack) Prolonged coronary blockage Areas of cell death are repaired with noncontractile scar tissue

47 Copyright © 2010 Pearson Education, Inc. Histology of Cardiac Muscle

48 Copyright © 2010 Pearson Education, Inc. Microscopic Anatomy of Cardiac Muscle Cardiac muscle cells are striated, short, fat, branched, and interconnected Connective tissue matrix (endomysium) connects to the fibrous skeleton T tubules are wide but less numerous SR (sarcoplasmic reticulum) is simpler than in skeletal muscle SR stores Ca++, which plays an important part in cardiac cell APs and contraction Numerous large mitochondria Multiple nuclei per cell

49 Copyright © 2010 Pearson Education, Inc. Microscopic Anatomy of Cardiac Muscle Intercalated discs: junctions between cells anchor cardiac cells, cause heart to beat as a functional syncytium (as a group) Desmosomes prevent cells from separating during contraction Gap junctions allow ions to pass; electrically couple adjacent cells

50 Copyright © 2010 Pearson Education, Inc. Figure 18.11a Nucleus DesmosomesGap junctions Intercalated discsCardiac muscle cell (a)

51 Copyright © 2010 Pearson Education, Inc. Figure 18.11b Nucleus I band A band Cardiac muscle cell Sarcolemma Z disc Mitochondrion T tubule Sarcoplasmic reticulum I band Intercalated disc (b)

52 Copyright © 2010 Pearson Education, Inc. Physiology of Cardiac Muscle Contraction

53 Copyright © 2010 Pearson Education, Inc. Cardiac Muscle Cells

54 Copyright © 2010 Pearson Education, Inc. Cardiac Muscle Contraction 1.Depolarization opens voltage-gated fast Na + channels in the sarcolemma 1.Reversal of membrane potential from –90 mV to +30 mV 2.Slow Ca 2+ channels open (delayed), about 20% of Ca 2+ enters cell this way 1.Depolarization wave in T tubules causes the SR to release Ca 2+; 80% of Ca 2+ released thru SR 2.Ca 2+ surge prolongs the depolarization phase (plateau) 3.K + channels open and Ca 2+ channels close, repolarizing the membrane 1.Ca 2+ is pumped back into the SR and ECF

55 Copyright © 2010 Pearson Education, Inc. Cardiac Muscle Contraction Because of influx of Ca 2+ from slow Ca 2+ channels and the SR, the duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle Skeletal muscle AP is 1-2ms Contraction is ms Cardiac muscle AP is 200ms Contraction is 200ms

56 Copyright © 2010 Pearson Education, Inc. Cardiac AP and Ca++ Channel Ca++ Channel Open

57 Copyright © 2010 Pearson Education, Inc. Figure Absolute refractory period Tension development (contraction) Plateau Action potential Time (ms) 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 Tension (g) Membrane potential (mV)

58 Copyright © 2010 Pearson Education, Inc. Cardiac Muscle Physiology EPI B-1 Adrenergic receptor Beta blockers Ca ++ CA ++ Channels CA ++ Influx Adenylate cyclase Cyclase-a ATP cAMP Prot. Kinase Prot.Kinase-a “Phosphorylation” Tension Generation Cross Bridge Formation CA ++ Channel Blockers

59 Copyright © 2010 Pearson Education, Inc. Heart Conduction System

60 Copyright © 2010 Pearson Education, Inc. Heart Physiology: Electrical Events Intrinsic cardiac conduction system A network of noncontractile cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart The independent but coordinated activity of the heart is a function of Gap junctions Intrinsic conducting system

61 Copyright © 2010 Pearson Education, Inc. Cardiac Pacemaker Cells

62 Copyright © 2010 Pearson Education, Inc. Cardiac Pacemaker Cells Found in SA node, AV node, AV bundle, R and L bundle branches, Purkinje fibers; part of conduction system of the heart Autorhythmic cells (1% of cardiac muscle cells) Have unstable RMP (resting membrane potential) Cells continously depolarize because they drift toward threshold Depolarization of the heart is rhythmic and spontaneous Gap junctions ensure the heart contracts as a unit

63 Copyright © 2010 Pearson Education, Inc. Cardiac Pacemaker Cells Unstable resting potentials = pacemaker potential Pacemaker potential is due to slow Na + channels and closing of K + channels 1.Slow Na + channels leak positive ions into the cell, causing the RMP to creep up 2.At threshold, Ca 2+ channels open 1.Explosive Ca 2+ influx produces the rising phase of the action potential (not Na + ) 3.Repolarization results from inactivation of Ca 2+ channels and opening of voltage-gated K + channels

64 Copyright © 2010 Pearson Education, Inc. Figure Pacemaker potential This slow depolarization is due to both opening of Na + channels and closing of K + channels. Notice that the membrane potential is never a flat line. Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca 2+ influx through Ca 2+ channels. Repolarization is due to Ca 2+ channels inactivating and K + channels opening. This allows K + efflux, which brings the membrane potential back to its most negative voltage. Action potential Threshold Pacemaker potential

65 Copyright © 2010 Pearson Education, Inc. Heart Physiology: Sequence of Excitation 1.Sinoatrial (SA) node (pacemaker) Generates impulses about 75 times/minute (sinus rhythm) Depolarizes faster than any other part of the myocardium Atrial contraction

66 Copyright © 2010 Pearson Education, Inc. Heart Physiology: Sequence of Excitation 2.Atrioventricular (AV) node Smaller diameter fibers; fewer gap junctions Delays impulses approximately 0.1 second Want a delay between contract of atria and ventricles Depolarizes 50 times per minute in absence of SA node input

67 Copyright © 2010 Pearson Education, Inc. Heart Physiology: Sequence of Excitation 3.Atrioventricular (AV) bundle (bundle of His) Only electrical connection between the atria and ventricles

68 Copyright © 2010 Pearson Education, Inc. Heart Physiology: Sequence of Excitation 4.Right and left bundle branches Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

69 Copyright © 2010 Pearson Education, Inc. Heart Physiology: Sequence of Excitation 5.Purkinje fibers Complete the pathway into the apex and ventricular walls AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

70 Copyright © 2010 Pearson Education, Inc. Figure 18.14a (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Superior vena cava Right atrium Left atrium Purkinje fibers Inter- ventricular septum 1 The sinoatrial (SA) node (pacemaker) generates impulses. 2 The atrioventricular (AV) node. The atrioventricular (AV) bundle 4 The bundle branches 3 The Purkinje fibers 5

71 Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Defects in the intrinsic conduction system may result in 1.Arrhythmias: irregular heart rhythms 2.Uncoordinated atrial and ventricular contractions 3.Fibrillation: rapid, irregular contractions; useless for pumping blood because atria, and more importantly ventricles, are not getting filled with blood

72 Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Defective SA node may result in Ectopic focus: abnormal pacemaker takes over If AV node takes over, there will be a junctional rhythm (40–60 bpm) Defective AV node may result in Partial or total heart block Few or no impulses from SA node reach the ventricles

73 Copyright © 2010 Pearson Education, Inc. Electrocardiography

74 Copyright © 2010 Pearson Education, Inc. Electrocardiography Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given time Three waves 1.P wave: depolarization of SA node 2.QRS complex: ventricular depolarization 3.T wave: ventricular repolarization

75 Copyright © 2010 Pearson Education, Inc. Figure Sinoatrial node Atrioventricular node Atrial depolarization QRS complex Ventricular depolarization Ventricular repolarization P-Q Interval S-T Segment Q-T Interval

76 Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 1 Atrial depolarization, initiated by the SA node, causes the P wave. P R T Q S SA node Depolarization Repolarization 1

77 Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 2 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. P R T Q S Depolarization Repolarization 1 2

78 Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 3 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 Depolarization Repolarization 1 2 3

79 Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 4 Ventricular depolarization is complete. P R T Q S Depolarization Repolarization 4

80 Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 5 Ventricular depolarization is complete. Ventricular repolarization begins at apex, causing the T wave. P R T Q S P R T Q S Depolarization Repolarization 4 5

81 Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 6 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 Depolarization Repolarization 4 5 6

82 Copyright © 2010 Pearson Education, Inc. Figure 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

83 Copyright © 2010 Pearson Education, Inc. (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 beats/min.

84 Copyright © 2010 Pearson Education, Inc. Mechanical Events of the Cardiac Cycle

85 Copyright © 2010 Pearson Education, Inc. Mechanical Events: The Cardiac Cycle Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat Systole—contraction Diastole—relaxation Normal heart rate (HR) = bpm

86 Copyright © 2010 Pearson Education, Inc. Heart Sounds Two sounds (lub-dub) associated with closing of heart valves First sound occurs as AV valves close and signifies beginning of systole Second sound occurs when semilunar valves close at the beginning of ventricular diastole Heart murmurs: abnormal heart sounds most often indicative of valve problems

87 Copyright © 2010 Pearson Education, Inc. Figure 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

88 Copyright © 2010 Pearson Education, Inc. Cardiac Cycle: A Note on Pressure REMEMBER: Blood will always flow from high pressure to low pressure

89 Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle 1.Ventricular filling—takes place in mid-to-late diastole AV valves are open 80% of blood passively flows into ventricles Atrial systole occurs, delivering the remaining 20% End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

90 Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle 2.Ventricular systole Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase (all valves are closed) In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open End systolic volume (ESV): volume of blood remaining in each ventricle

91 Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle 3.Isovolumetric relaxation occurs in early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk closes semilunar valves and causes brief rise in aortic pressure

92 Copyright © 2010 Pearson Education, Inc. Figure a2b3 Atrioventricular valves Aortic and pulmonary valves Open Closed Open Phase ESV Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction Ventricular filling (mid-to-late diastole) Ventricular systole (atria in diastole) Isovolumetric contraction phase Ventricular ejection phase Early diastole Isovolumetric relaxation Ventricular filling 112a2b3 Electrocardiogram Left heart P 1st2nd QRS P Heart sounds Atrial systole Dicrotic notch Left ventricle Left atrium EDV SV Aorta T Ventricular volume (ml) Pressure (mm Hg)

93 Copyright © 2010 Pearson Education, Inc. Cardiac Output (CO) Volume of blood pumped by each ventricle in one minute CO = heart rate (HR) x stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by a ventricle with each beat

94 Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume SV = EDV – ESV Three main factors affect SV Preload Contractility Afterload

95 Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart) Cardiac muscle exhibits a length-tension relationship At rest, cardiac muscle cells are shorter than optimal length (as opposed to skeletal muscle fibers which are kept near optimal length) This degree of stretch produces more contractile force Increased venous return distends (stretches) the ventricles and increases contraction force Higher preload = higher SV

96 Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV Contractility rises when more Ca 2+ is released into the ICF via the SR Positive inotropic agents increase contractility Ino = muscle, fiber Ca 2+, hormones (thyroxine, glucagon, and epinephrine) Negative inotropic agents decrease contractility Acidosis (increased H + ) Increased extracellular K + Calcium channel blockers

97 Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume Afterload: pressure that must be overcome for ventricles to eject blood The back pressure that arterial blood exerts on the aortic (80mg) and pulmonary (10mg) valves Hypertension increases afterload, resulting in increased ESV and reduced SV

98 Copyright © 2010 Pearson Education, Inc. Regulation of Heart Rate Positive chronotropic factors increase heart rate Chrono = time Negative chronotropic factors decrease heart rate Can be neural, chemical, or physical factors

99 Copyright © 2010 Pearson Education, Inc. Autonomic Nervous System Regulation

100 Copyright © 2010 Pearson Education, Inc. Autonomic Nervous System Regulation Exerts the most important extrinsic controls affecting HR Sympathetic nervous system is activated by emotional or physical stressors Sympathetic nerves release norepinephrine which binds to β 1 adrenergic receptors on the heart, causing the pacemaker to fire more rapidly It also increases contractility

101 Copyright © 2010 Pearson Education, Inc. Autonomic Nervous System Regulation Parasympathetic nervous system opposes the sympathetic effects and reduces HR when a stressful situation has passe Parasympathetic-initiated cardiac responses are mediated by Acetylcholine (ACh) ACh hyperpolarizes the membranes by opening K + channels

102 Copyright © 2010 Pearson Education, Inc. Autonomic Nervous System Regulation At rest, the heart exhibits vagal tone At rest, both SNS and PNS send impulses to SA node, but the dominant influence is inhibitory (PNS) The heart rate is slower than if the vagus nerve was not innervating it

103 Copyright © 2010 Pearson Education, Inc. Figure Thoracic spinal cord The vagus nerve (parasympathetic) decreases heart rate. Cardio- acceleratory center Sympathetic cardiac nerves increase heart rate and force of contraction. Medulla oblongata Sympathetic trunk ganglion Dorsal motor nucleus of vagus Sympathetic trunk AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons

104 Copyright © 2010 Pearson Education, Inc. Figure Venous return Contractility Sympathetic activity Parasympathetic activity EDV (preload) Stroke volume Heart rate Cardiac output ESV Exercise (by skeletal muscle and respiratory pumps; see Chapter 19) Heart rate (allows more time for ventricular filling) Bloodborne epinephrine, thyroxine, excess Ca 2+ Exercise, fright, anxiety Initial stimulus Result Physiological response

105 Copyright © 2010 Pearson Education, Inc. Chemical Regulation of Heart Rate 1.Hormones Epinephrine from adrenal medulla increases HR and contractility Thyroxine increases HR 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 Electrolyte imbalances pose serious danger to the heart

106 Copyright © 2010 Pearson Education, Inc. Other Factors that Influence Heart Rate Age Gender Exercise Body temperature

107 Copyright © 2010 Pearson Education, Inc. 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

108 Copyright © 2010 Pearson Education, Inc. 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)

109 Copyright © 2010 Pearson Education, Inc. Figure Occurs in about 1 in every 500 births Occurs in about 1 in every 1500 births Narrowed aorta Occurs in about 1 in every 2000 births Ventricular septal defect. The superior part of the inter- ventricular septum fails to form; thus, blood mixes between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger. (a)Coarctation of the aorta. A part of the aorta is narrowed, increasing the workload of the left ventricle. (b) Tetralogy of Fallot. Multiple defects (tetra = four): (1) Pulmonary trunk too narrow and pulmonary valve stenosed, resulting in (2) hypertrophied right ventricle; (3) ventricular septal defect; (4) aorta opens from both ventricles. (c)

110 Copyright © 2010 Pearson Education, Inc. QUESTIONS TO TEST WHAT YOU NOW KNOW!!!

111 Copyright © 2010 Pearson Education, Inc. The principle of complementary structure and function is evident when examining the coverings of the heart. In what way is this relationship evident? A.The pericardium surrounds the heart. B.The epicardium and visceral layer of the pericardium are synonymous. C.The pericardial cavity surrounds the heart. D.The visceral and parietal membranes of the pericardium are smooth and slide past each other, providing a low-friction environment for heart movement.

112 Copyright © 2010 Pearson Education, Inc. Of the following layers of the heart wall, which consumes the most energy? A.Epicardium B.Myocardium C.Endocardium D.Visceral pericardium

113 Copyright © 2010 Pearson Education, Inc. Which of the following structures is an exception to the general principle surrounding blood vessel oxygenation levels? A.Pulmonary artery B.Aorta C.Pulmonary veins D.Both a and c

114 Copyright © 2010 Pearson Education, Inc. What purpose does the coronary circuit serve? A.None; it is a vestigial set of vessels. B.It delivers 1/20 of the body’s blood supply to the heart muscle itself. C.It delivers blood to the anterior lung surface for gas exchange. D.It feeds the anterior thoracic wall.

115 Copyright © 2010 Pearson Education, Inc. A heart murmur would be detected when blood is heard flowing from the ________ to the __________ through the ___________. A.right atrium; right ventricle; tricuspid valve B.right atrium; left atrium; tricuspid valve C.left ventricle; left atrium; mitral valve D.left atrium; left ventricle; mitral valve

116 Copyright © 2010 Pearson Education, Inc. The presence of intercalated discs between adjacent cardiac muscle cells causes the heart to behave as a _____________. A.single chamber B.contractile myofibril C.desmosome D.functional syncytium

117 Copyright © 2010 Pearson Education, Inc. Cardiac muscle cells have several similarities with skeletal muscle cells. Which of the following is not a similarity? A.The cells are each innervated by a nerve ending. B.The cells store calcium ions in the sarcoplasmic reticulum. C.The cells contain sarcomeres. D.The cells become depolarized when sodium ions enter the cytoplasm.

118 Copyright © 2010 Pearson Education, Inc. The plateau portion of the action potential in contractile cardiac muscle cells is due to: A.an increased potassium permeability. B.an influx of calcium ions. C.an influx of sodium ions. D.exit of calcium ions from the sarcoplasmic reticulum.

119 Copyright © 2010 Pearson Education, Inc. The stimulus for the heart’s rhythmic contractions comes from _________. A.intercalated discs B.acetylcholine C.a neuromuscular junction D.a pacemaker potential

120 Copyright © 2010 Pearson Education, Inc. The major ionic change that initiates the rising phase of the autorhythmic cell action potential is __________. A.potassium ion exit B.sodium ion entry C.calcium ion entry D.calcium ion exit

121 Copyright © 2010 Pearson Education, Inc. For which type of heart condition might a doctor prescribe calcium channel blockers? A.Depressed heart rate B.Heart irritability C.Heart murmur D.Weak heart rate

122 Copyright © 2010 Pearson Education, Inc. In a normal heart, which of the following structures is responsible for setting the heart’s pace? A.Sinoatrial node B.Atrioventricular node C.Atrioventricular bundle D.Purkinje fibers

123 Copyright © 2010 Pearson Education, Inc. Predict the nature of an ECG recording when the atrioventricular node becomes the pacemaker. A.There would continue to be a normal sinus rhythm. B.The P wave would be much larger than normal. C.The rhythm would be slower. D.The T wave would be much smaller than normal.

124 Copyright © 2010 Pearson Education, Inc. The primary input to the heart by the cardioinhibitory center is primarily found in the ___________. A.sinoatrial node and atrioventricular node B.Purkinje fibers C.the cardiac contractile fibers D.bundle of His

125 Copyright © 2010 Pearson Education, Inc. The “lub-dup” heart sounds are produced by: A.the walls of the atria and ventricles slapping together during a contraction. B.the blood hitting the walls of the ventricles and arteries, respectively. C.the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”). D.the closing of the semilunar valves (“lub”) and the closing of the atrioventricular valves (“dup”).

126 Copyright © 2010 Pearson Education, Inc. Atrial systole occurs _______ the firing of the sinoatrial node. A.before B.after C.simultaneously with D.alternately with

127 Copyright © 2010 Pearson Education, Inc. The majority (80%) of ventricular filling occurs ___________. A.during late ventricular systole B.passively through blood flow alone C.with atrial systole D.both a and b

128 Copyright © 2010 Pearson Education, Inc. In terms of blood flow, why is it important that atrial diastole occurs just as ventricular systole begins? A.Blood is continually propelled in a forward motion down its pressure gradient. B.The atria need that time to prepare for the next contraction. C.Ventricular systole pulls the remaining 20% of blood volume from the atria. D.Blood would flow too fast otherwise.

129 Copyright © 2010 Pearson Education, Inc. Cardiac output is determined by________. A.heart rate B.stroke volume C.cardiac reserve D.both a and b

130 Copyright © 2010 Pearson Education, Inc. Predict what would happen to the end systolic volume (ESV) if contraction force were to increase. A.It would decrease. B.It would increase. C.It would remain constant. D.ESV is not affected by contraction force.

131 Copyright © 2010 Pearson Education, Inc. The Frank-Starling law of the heart can be demonstrated when an individual takes a deep breath. This is because: A.the heart expands during inhalation. B.the negative intrathoracic pressure induces a larger than normal venous return to the right atrium, thereby stretching the wall of the right ventricle. C.sympathetic impulses are sent to the heart during inspiration. D.both a and c occur.

132 Copyright © 2010 Pearson Education, Inc. Your heart seems to “pound” after you hear a sudden, loud noise. This increased contractility is: A.because you were startled. B.because when a gasp of surprise is emitted, the Frank-Starling law of the heart is evident. C.due to norepinephrine causing threshold to be reached more quickly. D.because acetylcholine release is inhibited.

133 Copyright © 2010 Pearson Education, Inc. Predict what happens to end diastolic volume when an increase in heart rate is not accompanied by an increase in contractility. A.End diastolic volume is increased. B.End diastolic volume is decreased. C.End diastolic volume is unchanged. D.End diastolic volume is not affected by heart rate.

134 Copyright © 2010 Pearson Education, Inc. What is the nature of acetylcholine’s inhibitory effect on heart rate? A.Acetylcholine induces depolarization in the sinoatrial node. B.Acetylcholine causes closing of sodium channels in the sinoatrial node. C.Acetylcholine causes opening of fast calcium channels in contractile cells. D.Acetylcholine causes opening of potassium channels in the sinoatrial node, thereby hyperpolarizing it.

135 Copyright © 2010 Pearson Education, Inc. Why is high blood pressure damaging to the heart? A.With high blood pressure, the blood is more viscous and harder to pump. B.The heart rate slows down to dangerously low levels if blood pressure is too high. C.Due to increased afterload, the left ventricle must contract more forcefully to expel the same amount of blood. D.Sodium concentration increases during high blood pressure and is toxic to the myocardium.


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