Cardiovascular System components

1. Cardiovascular System components • The heart • Blood vessels • Blood

2. Capillary beds of lungs where gas exchange occurs Pulmonary Circuit Pulmonary veins Pulmonary arteries Aorta and branches Venae cavae Left atrium Left ventricle Right atrium Heart Right ventricle Systemic Circuit Oxygen-rich, CO2-poor blood Capillary beds of all body tissues where gas exchange occurs Oxygen-poor, CO2-rich blood Figure 18.5

4. 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

5. Coverings of the Heart: Anatomy • The heart is enclosed in a double-walled sac called the pericardium. • Superficial fibrous pericardium • Protects, anchors, and prevents overfilling • The outer parietal pericardium consists of a tough fibrous layer of dense connective tissue. • The inner thin, smooth, moist serous layer turns in at the base of the heart, forming the visceral pericardium/epicardium covering the heart surface. • Between the parietal and visceral pericardia is a space called the pericardial cavity. • It contains pericardial fluid that lubricates the membranes and allows the heart to beat almost without friction.

6. Layers of the Heart Wall myocardium • Spiral bundles of cardiac muscle cells to allow “twisting” when contracting • Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue • Supply structural support for the heart • Anchors cardiocytes and give them something to pull against • Limits spread of action potentials to specific paths

7. Heart Chambers Atrium – single Atria - pleural Ventricle/s http://mtsu32.mtsu.edu:11259/heart3.jpg

8. Atria of the Heart • Atria are the receiving chambers of the heart – entering veins • Blood enters right atria from superior and inferior venae cavae and coronary sinus • Blood enters left atria from pulmonary veins • Each atrium has a auricle that increase atrial volume • Separated internally by the interatrial septum • Coronary sulcus (atrioventricular groove) encircles the junction of the atria and ventricles • Pectinate muscles mark the anterior atrial wall

9. Ventricles of the Heart • Ventricles are the discharging chambers of the heart • Right ventricle pumps blood into the pulmonary trunk • Left ventricle pumps blood into the aorta • Papillary muscles that attached to the valves

10. Figure 18.4e

11. Heart Valves • Heart valves ensure unidirectional blood flow through the heart (prevent backflow) • Atrioventricular (AV) valves lie between the atria and the ventricles • AV valves prevent backflow into the atria when ventricles contract • Chordae tendineae anchor AV valves to papillary muscles • Semilunar valves prevent backflow of blood into the ventricles • Aorticsemilunar valve lies between the left ventricle and the aorta • Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk

12. Heart Sounds • Two sounds (lub-dup) 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

13. Heart valves problems Valvular heart disease (VHD) When valve function has deteriorated to where heart cannot maintain adequate blood flow Can be due to: Congenital (present at birth) malformations Heart swelling (carditis) In severe cases, replacement with a prosthetic valve may be necessary Bioprosthetic valves come from pigs or cows

14. Vessels that Supply/Drain the Heart - coronary circulation Figure 18.7

15. Risk factors that can lead to heart diseases • Coronary artery disease • High blood pressure • Diabetes • Smoking • High cholesterol • Obesity • Excessive alcohol use • Drug abuse • Stress • Family history of heart disease • Advancing age

16. Arteriosclerosis and coronary artery disease Arteriosclerosis (arterio-, artery + sclerosis, hardness) Thickening or toughening of artery walls Related complications account for about half of all U.S. deaths

17. Arteriosclerosis and coronary artery disease Atherosclerosis (athero-, fatty degeneration) Formation of lipid deposits Most common form of arteriosclerosis Often associated with elevated cholesterol May form fatty tissue mass (plaque) in vessel that restricts blood flow Most common in older men Treatment can be removing damaged vessel or compressing plaque with balloon angioplasty

18. Heart Disease - Coronary Artery Disease (CAD) Areas of partial or complete blockage of coronary circulation Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance Reduced circulatory supply causes coronary ischemia One of the first symptoms of CAD is commonly angina pectoris– pain in the middle of the chest, left neck, left shoulder, or left arm

19. Myocardial infarction (MI), or heart attack Part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygen The death of affected tissue creates a nonfunctional area known as an infarct Heart attacks most commonly result from severe coronary artery disease (CAD)

20. Myocardial infarction (MI), or heart attack Consequences depend on the site and nature of the circulatory blockage If it occurs near the start of one of the coronary arteries: The damage will be widespread and the heart may stop beating If the blockage involves one of the smaller arterial branches: The individual may survive the immediate crisis but may have many complications such as reduced contractility and cardiac arrhythmias

21. Myocardial infarction (MI), or heart attack Pain does not always accompany a heart attack therefore, the condition may go undiagnosed and may not be treated before a fatal MI occurs A myocardial infarction can usually be diagnosed with an ECG and blood studies Damaged myocardial cells release enzymes into the circulation, and these elevated enzymes can be measured in diagnostic blood tests The enzymes include: Cardiac troponin T, Cardiac troponin I, A special form of creatinine phosphokinase, CK-MB

22. CAD and Myocardial Infarction prognosis About 25% of MI patients die before obtaining medical assistance 65% of MI deaths among those under age 50 occur within an hour after the initial infarction

23. Treatment of CAD and Myocardial Infarction Risk Factor Modification Stop smoking High blood pressure treatment Dietary modification to lower cholesterol and promote weight loss Stress reduction Increased physical activity (where appropriate)

24. Treatment of CAD and Myocardial Infarction Drug Treatment Drugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadin Drugs that block sympathetic stimulation (propranolol or metoprolol) – for hypertension Drugs that cause vasodilation, such as nitroglycerin Drugs that block calcium movement into the cardiac and vascular smooth muscle cells (calcium channel blockers)

25. Coronary Artery Bypass Surgery (CABG) In a coronary artery bypass graft, a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary artery

26. Pathway of Blood Through the Heart • The heart is two side-by-side pumps • Equal volumes of blood are pumped to the pulmonary and systemic circuits • Right side is the pump for the pulmonary circuit • Vessels that carry blood to and from the lungs • Pulmonary circuit is a short, low-pressure circulation • Left side is the pump for the systemic circuit • Vessels that carry the blood to and from all body tissues • Systemic circuit blood encounters much resistance in the long pathways

27. Cardiovascular system – the heart

28. The cells of the heart • Two types of cardiac muscle cells that are involved in a normal heartbeat: • Specialized muscle cells of the conducting system • Contractile cells • The heart is an autonomic system that can work without neural stimuli – an intrinsic conduction system. • The autonomic function of the heart results from: • The pacemaker function – Autorhythmic cells • The conductive system that transfer those impulses throughout the heart

29. Properties of Cardiac Muscle • Aerobic muscle • No cell division after infancy - growth by hypertrophy • 99% contractile cells (for pumping) • 1% autorhythmiccells (set pace)

30. Intrinsic cardiac conduction system – autorhythmic cells • Have unstable resting potentials/ pacemaker potentials • constantly depolarized slowly towards AP • At threshold, Ca2+ channels open • Ca2+ influx produces the rising phase of the action potential • Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels

31. Threshold Action potential 2 2 3 1 1 Pacemaker potential 3 2 1 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage. Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels. 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. Figure 18.13

32. Autorhythmic Cells Location Firing Rate at Rest SA node 70–80 APs/min* AV node 40–60 APs/min Bundle of His 20–40 APs/min Purkinje fibers 20–40 APs/min • Cardiac cells are linked by gap junctions • Fastest depolarizing cells control other cells • Fastest cells = pacemaker = set rate for rest of heart * action potentials per minute

33. Autorythmic cells - ectopic pacemakers • Autorythmic cells of the SA node (pacemaker) may be replaced by ectopic pacemakers • Ectopic pacemakers – other parts in the heart that can induce beating • The ectopic pacemakers may become dominant: • If their rythmicity increased • The pacemaker is inhibited/blocked • The conduction system pathways are blocked • First to take over will be the AV node

35. Cardiac contractile cells • Depolarization opens voltage-gated fast Na+ channels in the sarcolemma • Depolarization wave causes release Ca2+that causes the cell contraction • Depolarization wave also opens slow Ca2+ channels in the sarcolemma • Ca2+ surge prolongs the depolarization phase (plateau)

36. Myocardial Contractile Cells • Refractory period in skeletal muscle Figure 14-14a

37. Myocardial Contractile Cells • Refractory period in cardiac muscle Figure 14-14c

38. Action Potentials Table 14-3

39. Heart Physiology: Sequence of Excitation

40. Electrical Conduction in the Heart 1 SA node depolarizes. 1 SA node AV node Electrical activity goesrapidly to AV node viainternodal pathways. 2 2 Depolarization spreadsmore slowly acrossatria. Conduction slowsthrough AV node. 3 THE CONDUCTING SYSTEMOF THE HEART Depolarization movesrapidly through ventricularconducting system to theapex of the heart. 4 SA node 3 Internodalpathways Depolarization wavespreads upward fromthe apex. 5 AV node AV bundle 4 Bundlebranches Purkinjefibers 5 Figure 14-18, steps 1–5

41. Electrocardiography (ECG or EKG) • Body fluids are good conductors which allows the record of the myocardial action potential extracellularly • EKG pairs of electrodes (leads) one serve as positive side of the lead and one as the negative • Potentials (voltage) are being measured between the 2 electrodes • EKG is the summed electrical potentials generated by all cells of the heart and gives electrical “view” of 3D object (different from one action potential) • EKG shows depolarization and repolarization

42. Electrical Activity of Heart • P wave: atrial depolarization • QRS complex: ventricular depolarization and atrial repolarization • T wave: ventricular repolarization • PQ segment: AV nodal delay • QT segment: ventricular systole • QT interval: ventricular diastole

43. Correlation between an ECG and electrical events in the heart

44. Electrical Activity P wave: atrialdepolarization START P The end R PQ or PR segment:conduction throughAV node and AVbundle P T P Q S Atria contract T wave:ventricularrepolarization Repolarization ELECTRICAL EVENTSOF THECARDIAC CYCLE R T P Q S Q wave P ST segment Q R P R wave R Q S R Ventricles contract P Q P S wave Q S Figure 14-21 (9 of 9)

45. Homeostatic Imbalances • Defects in the intrinsic conduction system may result in • Arrhythmias: irregular heart rhythms • Uncoordinated atrial and ventricular contractions (heart block) • Fibrillation: rapid, irregular contractions; useless for pumping blood

46. ECG Arrhythmias: Abnormal Rates • Sinus rhythm = pace generated by SA node • Abnormal rates shown • Tachycardia = fast rhythm • Bradycardia = slow rhythm Figure 13.17 (1 of 4)

47. 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

48. First and second degree Heart Block • Slowed/diminished conduction through AV node occurs in varying degrees • First degree block • Increases duration PQ segment • Increases delay between atrial and ventricular contraction • Second degree block • Lose 1-to-1 relationship between P wave and QRS complex • Lose 1-to-1 relationship between atrial and ventricular contraction

49. Third Degree Heart Block Third degree block • Loss of conduction through the AV node • P wave becomes independent of QRS • Atrial and ventricular contractions are independent

50. ECG Arrhythmias: Fibrillation Ventricular Fibrillation • Loss of coordination of electrical activity of heart • Death can ensue within minutes unless corrected Figure 13.17 (4 of 4)