1. Ch 12 Heart and Circulatory System The Body’s Transport System

2. 4 Chambered Heart – size of clenched fist 2 Atria 2 Ventricles Arteries (efferent vessels) Veins (afferent vessels) Layers of the Heart Epicardium – outmost layer; covers surface of heart Myocardium – muscle layer; contains cardiac muscle, blood vessels and nerves Endocardium – lines heart’s chambers and valves; composed of simple squamous tissue

3. Two Circuits for Blood Pulmonary Circuit: right side of heart; receives blood and transports de-oxygenated blood to lungs. Systemic Circuit: left side of heart; supplies body with oxygenated blood.

4. Pericardium is the shiny covering around the heart. Function: To reduce friction between surrounding surfaces as heart beats Protect the heart Anchor the surrounding structures

5. Characteristics of Heart Muscle Intercalated discs Involuntary Striated One nuclei per cell

6. Intercalated disks; allows heart to beat as one unit

7. Location of Heart

8. Structure of the Heart

9. Main Veins into heart –Coronary Sinus –Superior Vena Cava –Inferior Vena Cava –Pulmonary Vein Main Arteries –Coronary Artery –Pulmonary Artery –Aorta 1 2 5 6

10. Blood flow through the Heart De-oxygenated blood from the body enters the R atrium and is pumped to the R ventricle. From the R ventricle deO 2 blood is sent to the lungs where gas exchange occurs. Oxygenated blood enters the L atria and is sent to the L ventricle where it is sent to the body via the aorta.

11. Flow of blood through heart 1 1.Superior Vena Cava 2.Inferior Vena Cava 3.R. atrium 4.R. ventricle 5.Pulmonary trunk (artery) 6.Pulmonary vein 7.L. atrium 8.L. ventricle 9.Aorta A. Brachiocephalic B. L. Common Carotid C.L. Subclavian 2 3 4 5 6 7 8 9 A BC

12. Difference in myocardium thickness between R. ventricle and L. ventricle. Why?

13. Valves of the Heart Atrioventricular Valves - one way valves; prevent back flow of blood -chordae tendineae - papillary muscles Tricuspid – 3 flaps –Found between R atrium and R. ventricle Bicuspid (mitral) – 2 flaps –Found between L atrium and L. ventricle

14. Anatomy of AV valves One-way valves Atrioventricular valves Chordae tendineae Papillary muscles

15. Semilunar Valves Located in Pulmonary Artery and Aortic Artery 3 flaps Prevents blood from flowing back into ventricles

16. Valve position when ventricles relaxed

17. Valve position when ventricles contract

18. Heart Sounds Two sounds (lubb-dupp) 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 Heart murmurs: abnormal heart sounds most often indicative of valve problems

19. 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

21. Cardiac Muscle Contraction Rapid Depolarization: Threshold is reached along the membrane. Causes Na + channels in the sarcolemma to open Na + enters cell reversing membrane potential from –90 mV to +30 mV (Na + gates close) Plateau: Calcium channels open and Ca +2 enters sarcoplasm Ca +2 also is released from SR Ca +2 surge prolongs the depolarization phase and delays repolarization (excess + ions in cell) Repolarization: Ca +2 begin to close; K + channels open and K + leaves the cell.

22. In Cardiac muscle, depolarization lasts longer. Thus cardiac muscle can’t increase tension with another impulse; tetanus doesn’t occur. Why is this important?

23. Heart Physiology: Electrical Events Intrinsic cardiac conduction system –A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart –Nodes – cells that are responsible for starting the impulse –Conducting cells – distribute the impulse to the myocardium –1 % of the heart’s cardiac cells have this capability

24. Internal Conduction System 1. Sinoatrial node 2. AV node 3. AV bundle or Bundle of HIS 4. R and L bundle branches 5. Purkinge fibers Nodes – cluster of nervous tissue that begins an impulse. 5

25. 1.Sinoatrial (SA) node (pacemaker) Generates impulses about 70-80 times/minute (sinus rhythm) Depolarizes faster than any other part of the myocardium

26. 2.Atrioventricular (AV) node –Delays impulses approximately 0.1 second Allows for Atria to contract –Depolarizes 40-60 times per minute in absence of SA node input

27. Conducting Cells 3.Atrioventricular (AV) bundle (bundle of His) 4.Right and left bundle branches –Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

28. 5.Purkinje fibers –Complete the pathway into the apex and ventricular walls

29. Figure 18.14a (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Internodal pathway Superior vena cava Right atrium Left atrium Purkinje fibers Inter- ventricular septum 1 The sinoatrial (SA) node (pacemaker) generates impulses. 2 The impulses pause (0.1 s) at the atrioventricular (AV) node. The atrioventricular (AV) bundle connects the atria to the ventricles. 4 The bundle branches conduct the impulses through the interventricular septum. 3 The Purkinje fibers depolarize the contractile cells of both ventricles. 5

30. 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 (AV node) 3.T wave: ventricular repolarization

31. Normal EKG has 3 distinct waves. 1 st wave (P) - SA node fires - Natural Pacemaker - fires around 70-80 times/minute The atria depolarize Impulse is being generated across R and L atria via diffusion..1s after P wave, atria contract.

32. 2 nd wave (QRS) AV Node fires; depolarization of ventricles. Q-R interval represents beginning of atrial repolarization and AV node firing; ventricles depolarize R-S interval represents beginning of ventricle contractions S-T End of Ventricular depolarization AV node – back up pacemaker - Beats 40-60 times/minute - Impulse is delayed at bundle of HIS until Atria contract.

33. 3 rd Wave (T) T wave repolarization of ventricles Ventricles return to normal relaxed state. In a healthy heart, size, duration and timing of waves is consistent. Changes reveal a damage or diseased heart.

34. Figure 18.16 Sinoatrial node Atrioventricular node Atrial depolarization QRS complex Ventricular depolarization Ventricular repolarization P-Q Interval S-T Segment Q-T Interval

35. 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

37. 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

38. Problems with Sinus Rhythms Tachycardia: Heart rate in excess of 100 bpm when at rest –If persistent, may lead to fibrillation Bradycardia: Heart rate less than 60 bpm when at rest –May result in grossly inadequate blood circulation –May be desirable result of endurance training

39. Homeostatic Imbalances Defective SA node may result –Ectopic focus: abnormal pacemaker takes over –No P waves; If AV node takes over, there will be a slower rhythm (40–60 bpm) Defective AV node may result in –Partial or total heart block –Longer delay at AV node than normal –No all impulses from SA node reach the ventricles Ventricular fibrillation: –cardiac muscle cells are overly sensitive to stimulation; no normal rhythm is established –

40. Problems with Sinus Rhythms 2 nd degree heart block; Missed QRS complex SA node is sending impulses, but the AV node is not sending the impulses along the bundle branches 1 st degree is represented by a longer delay between P & QRS

41. 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.

44. Pacemaker Used to correct nodes that are no longer are in rhythm. Becomes the new heart’s pacemaker.

45. Myocardial Infarction A Heart Attack is caused by oxygen not getting to the heart muscle usually by blockages in the coronary arteries

46. Stopping a Heart Attack Breaking apart the blockage is done with: –Medication –Angioplasty –Stents –Coronary bypass surgery (CABG)

47. 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

48. Mechanical Events: The Cardiac Cycle Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat –Systole—contraction –Diastole—relaxation

49. 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

50. Phases of the Cardiac Cycle 2.Ventricular systole –Atria relax and ventricles begin to contract –Rising ventricular pressure results in closing of AV valves –In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the Semilunar valves open –End systolic volume (ESV): volume of blood remaining in each ventricle

51. One Cardiac Cycle Events during one complete heartbeat

52. Phases of the Cardiac Cycle 3.Ventricles relax –Decrease in pressure causes blood to flow backward –Backflow of blood in aorta and pulmonary trunk closes SL valves

53. Systole Diastole

54. EKG and One Cardiac Cycle

55. Cardiac Cycle & BP describes the contracting and relaxing stages of the heart. Includes all events that occur in the heart during one complete heart beat. Blood Pressure Systolic pressure: (top number) measurement of the force on the arterial walls when the L ventricle contracts. Diastolic pressure: (bottom number) measurement of the force on the arterial walls when the L ventricle is relaxed. Normal BP = 120/80 Hypertension Hypotension

56. Cardiac Output Volume of blood pumped by each ventricle in 1 minute. CO = Heart rate (HR) x Stroke volume (SV) –Heart Rate (beats/minute) –Stroke Volume – volume of blood pumped out of the L. ventricle with each beat. Why Left ventricle? SV = EDV(end diastolic volume) – ESV (end systolic volume) Stroke volume can be determined by subtracting systolic BP volume from diastolic BP volume Stroke volume/pulse pressure = SBP – DBP

57. Cardiac Output in a normal adult is 4.5 – 5 Liters of blood per minute –At rest: CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat) = 5.25 L/min Varies with body’s demands –Change in HR or force of contraction Cardiac Reserve – the heart’s ability to push cardiac output above normal limits –difference between resting and maximal CO –Healthier hearts can have a large increase in C.R. Athlete 7X C.O. = 35L/minute Nonathlete 4X C.O. = 20L/minute

58. Factors that Influence Heart Rate Age Gender Exercise Body temperature

59. Regulation of Stroke Volume Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV Factors which increase contractility –Increased Ca 2+ influx due to sympathetic stimulation –Hormones (thyroxine and epinephrine) Factors which decrease contractility –Increased extracellular K + –Calcium channel blockers

60. Factors that Control Cardiac Output Blood volume reflexes Autonomic Nervous System with assistance from neurotransmitters and hormones –Norepinephrine –Acethylcholine –Thyroxine Ions Temperature

61. Blood Volume Reflexes Frank Starling Law of the Heart –Stroke volume is controlled by Preload - the degree to which cardiac muscles are stretched just before they contract. “More blood in = More blood out” –Increase in stretch is caused by an Increase in the venous return to the right atrium which causes the walls of the right atrium to stretch. Increase in stretch causes SA node to depolarize faster; increasing HR Increase in stretch also increases force of contraction; Stroke volume At rest heart walls are not overstretched; ventricles don’t need forceful contractions

62. Autonomic Nervous System Controlled by Medulla oblongata Parasympathetic (Resting and Digesting) –Stimulates Vagus nerve (CN X) – decreases SV and HR; decreasing CO –Acetylcholine – decreases HR and SV; opposite action on cardiac muscle then on skeletal muscle (stimulates) Sympathetic (Fight or Flight) – prepares the body for stress –Secretes Norephinephrine and epinephrine – increases HR and SV; increasing CO –Increasing HR causes overstretch (Frank S. law) –Beta blockers-

63. Figure 18.15 Thoracic spinal cord The vagus nerve (parasympathetic) decreases heart rate. Cardioinhibitory center 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

64. Ions CalciumPotassiumSodium Hypercalcemia Excess Ca ions in muscle cell Extended state of contraction; fatal Hypocalcemia Low Ca levels; results in no/weak contractions Hyperkalemia High levels of K Interferes with depolarization of SA and AV nodes Results in heart block Increase in Na Blocks Ca No Ca; no T&T moving out of way No/weak contractions

65. Temperature HyperthermiaHypothermia Temp > 98.6°F Increases HR and SV Increase CO Temperature < 95° F Slows depolarization Slows contraction Decrease CO

66. Figure 18.22 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