Mr. Michael Aprill Lakeshore Technical College Ch. 18: The Heart (pp. 662-680)

1. Advanced Anatomy & PhysiologyLearning Plan 5: Correlation of Cardiovascular Physiology to Human Health Mr. Michael Aprill Lakeshore Technical College Ch. 18: The Heart (pp. 662-680) Ch. 19: Blood Vessels (pp. 694-713) MARIEB 8th Edition Revised: 6/14/11

2. HEART ANATOMY—Size, Location, & Orientation (p. 663; Fig. 18.1) • The heart is the size of a fist and weighs 250–300 grams. • The heart is found in the mediastinum and two-thirds lies left of the midsternal line. • The base is directed toward the right shoulder and the apex points toward the left hip.

3. HEART ANATOMY—Coverings of the Heart (p. 663; Fig. 18.2) • The heart is enclosed in a doubled-walled sac called the pericardium. • Fibrous Pericardium: loosely fitting superficial sac • Serous Pericardium: deep to the fibrous pericardium • Parietal pericardium: superficial layer • Pericardial space: between the two layers of the serous pericardium. • Visceral pericardium: covers the surface of the heart. Also called the epicardium.

4. HEART ANATOMY—Layers of the Heart Wall (pp. 663-664; Fig. 18.3) • The myocardium is composed mainly of cardiac muscle and forms the bulk of the heart. • The endocardium lines the chambers of the heart.

5. HEART ANATOMY—Chambers & Associated Great Vessels (pp. 668-669; Fig. 18.5) • The right and left atria are the receiving chambers of the heart. • The right ventricle pumps blood into the pulmonary trunk; the left ventricle pumps blood into the aorta.

6. HEART ANATOMY—Pathway of Blood Through the Heart (pp. 668-669; Fig. 18.5) • The right side of the heart pumps blood into the pulmonary circuit • The left side of the heart pumps blood into the systemic circuit.

7. HEART ANATOMY—Coronary Circulation (pp. 669-670; Fig. 18.7) • The heart receives no nourishment from the blood as it passes through the chamber. • The coronary circulation provides the blood supply for the heart cells. • In a myocardial infarction, there is prolonged coronary blockage that leads to cell death.

8. HEART ANATOMY—Heart Valves (pp. 670-672; Figs. 18.8-18.10) • The tricuspid and mitral valves prevent backflow into the atria (AV Valves) when the ventricles contract. • When the heart is relaxed the AV valves are open, and when the heart contracts the AV valves close. • The aortic and pulmonary valves (SL Valves)are found in the major arteries leaving the heart. They prevent backflow of blood into the ventricles. • When the heart is relaxed the aortic and pulmonary valves are closed, and when the heart contracts they are open.

9. HEART ANATOMY—Heart Valves (pp. 670-672; Figs. 18.8-18.10)

10. HEART ANATOMY—Heart Valves (pp. 670-672; Figs. 18.8-18.10)

11. CARDIAC MUSCLE FIBERS—Microscopic Anatomy (pp. 672-673; Fig. 18.11) • Cardiac muscle is striated and contraction occurs via the sliding filament mechanism. • The cells are: • Short • Fat • Branched • interconnected by intercalated discs.

12. CARDIAC MUSCLE FIBERS—Microscopic Anatomy (pp. 672-673; Fig. 18.11)

13. CARDIAC MUSCLE FIBERS—Mechanisms & Events of Contraction (pp. 673-675; Fig. 18.12) • Some cardiac muscle cells are self-excitable. • The heart contracts as a unit or not at all. • The heart’s absolute refractory period is longer than a skeletal muscle’s, preventing tetanic contractions.

14. CARDIAC MUSCLE FIBERS—Energy Requirements (p. 675) • The heart relies exclusively on aerobic respiration for its energy demands. • Cardiac muscle is capable of switching nutrient pathways to use whatever nutrient supply is available.

15. HEART PHYSIOLOGY—Electrical Events (pp. 676-680; Figs. 18.13-18.18) • The intrinsic conduction system is made up of specialized cardiac cells that initiate and distribute impulses, ensuring that the heart depolarizes in an orderly fashion. • The autorhythmic cells have an unstable resting potential, called pacemaker potentials, that continuously depolarizes. • Impulses pass through the autorhythmic cardiac cells in the following order: • sinoatrial node • atrioventricular node • atrioventricular bundle • right and left bundle branches • Purkinje fibers.

16. HEART PHYSIOLOGY—Electrical Events (pp. 676-680; Figs. 18.13-18.18)

17. HEART PHYSIOLOGY—Electrical Events (pp. 676-680; Figs. 18.13-18.18) • The autonomic nervous system modifies the heartbeat • The sympathetic center increases rate and depth of the heartbeat • the parasympathetic center slows the heartbeat. • An electrocardiograph monitors and amplifies the electrical signals of the heart and records it as an electrocardiogram (ECG).

18. HEART PHYSIOLOGY—Electrical Events (pp. 676-680; Figs. 18.13-18.18)

19. HEART PHYSIOLOGY—Heart Sounds (p. 681; Fig. 18.19) • Normal • The first heart sound, lub, corresponds to closure of the AV valves, and occurs during ventricular systole. • The second heart sound, dup, corresponds to the closure of the aortic and pulmonary valves, and occurs during ventricular diastole. • Abnormal • Heart murmurs are extraneous heart sounds due to turbulent backflow of blood through a valve that does not close tightly.

20. HEART PHYSIOLOGY—Heart Sounds (p. 681; Fig. 18.19)

21. HEART PHYSIOLOGY—Mechanical Events: The Cardiac Cycle (p. 682; Fig. 18.20) • Systole is the contractile phase of the cardiac cycle and diastole is the relaxation phase of the cardiac cycle. • A cardiac cycle consists of a series of pressure and volume changes in the heart during one heartbeat. • Ventricular filling occurs during mid-to-late ventricular diastole, when the AV valves are open, semilunar valves are closed, and blood is flowing passively into the ventricles. • The atria contract during the end of ventricular diastole, propelling the final volume of blood into the ventricles.

22. HEART PHYSIOLOGY—Mechanical Events: The Cardiac Cycle (p. 682; Fig. 18.20) • Cardiac Cycle (Cont.) • The atria relax and the ventricles contract during ventricular systole, causing closure of the AV valves and opening of the semilunar valves, as blood is ejected from the ventricles to the great arteries. • Isovolumetric relaxation occurs during early diastole, resulting in a rapid drop in ventricular pressure, which then causes closure of the semilunar valves and opening of the AV valves.

23. HEART PHYSIOLOGY—Mechanical Events: The Cardiac Cycle (p. 682; Fig. 18.20)

24. HEART PHYSIOLOGY—Cardiac Output (pp. 682-687; Figs. 18.21-18.23) • Cardiac output is defined as the amount of blood pumped out of a ventricle per beat, and is calculated as the product of stroke volume and heart rate. • Regulation of Stroke Volume • Preload: the Frank-Starling law of the heart states that the critical factor controlling stroke volume is the degree of stretch of cardiac muscle cells immediately before they contract. • Contractility: contractile strength increases if there is an increase in cytoplasmic calcium ion concentration. • Afterload: ventricular pressure that must be overcome before blood can be ejected from the heart.

25. Figure 18.22 Factors involved in regulation of cardiac output. Exercise (by skeletal muscle and respiratory pumps; see Chapter 19) Bloodborne epinephrine, thyroxine, excess Ca2+ Exercise, fright, anxiety Heart rate (allows more time for ventricular filling) Venous return Sympathetic activity Parasympathetic activity Contractility EDV (preload) ESV Heart rate Stroke volume Cardiac output Initial stimulus Physiological response Result

26. HEART PHYSIOLOGY—Cardiac Output (pp. 682-687; Figs. 18.21-18.23) • Regulation of Heart Rate • Sympathetic stimulation of pacemaker cells increases heart rate and contractility • While parasympathetic inhibition of cardiac pacemaker cells decreases heart rate. • Epinephrine, thyroxine, and calcium influence heart rate. • Age, gender, exercise, and body temperature all influence heart rate.

27. HEART PHYSIOLOGY—Cardiac Output (pp. 682-687; Figs. 18.21-18.23) • Homeostatic Imbalance of Cardiac Output • Congestive heart failure occurs when the pumping efficiency of the heart is so low that blood circulation cannot meet tissue needs. • Pulmonary congestion occurs when one side of the heart fails, resulting in pulmonary edema.

28. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Structure of Blood Vessel Walls (p. 695; Figs. 19.1-19.2; Table 19.1) • The walls of all blood vessels except the smallest consist of three layers: • tunica intima • tunica media • tunica externa(p. 695; Fig. 19.1). • The tunica intimareduces friction between the vessel walls and blood • the tunica media controls vasoconstriction and vasodilation of the vessel • The tunica externaprotects, reinforces, and anchors the vessel to surrounding structures (p. 695; Fig. 19.2; Table 19.1).

29. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Structure of Blood Vessel Walls (p. 695; Figs. 19.1-19.2; Table 19.1)

30. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Arterial System (pp. 695-698; Fig. 19.2; Tables 19.1-19.2) • Elastic (conducting) arteries contain large amounts of elastin, which enables these vessels to withstand and smooth out pressure fluctuations due to heart action (p. 697; Fig. 19.2; Table 19.1). • Muscular (distributing) arteries deliver blood to specific body organs, and have the greatest proportion of tunica media of all vessels, making them more active in vasoconstriction (p. 698; Table 19.1). • Arterioles are the smallest arteries and regulate blood flow into capillary beds through vasoconstriction and vasodilation (p. 698).

31. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Arterial System (pp. 695-698; Fig. 19.2; Tables 19.1-19.2)

32. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Capillaries (pp. 698-700; Figs. 19.3-19.4; Table 19.1) • Capillaries are the smallest vessels and allow for exchange of substances between the blood and interstitial fluid (pp. 698–699; Fig. 19.3; Table 19.1). • Continuous capillaries are most common and allow passage of fluids and small solutes. • Fenestrated capillaries are more permeable to fluids and solutes than continuous capillaries. • Sinusoidal capillaries are leaky capillaries that allow large molecules to pass between the blood and surrounding tissues.

33. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Capillaries (pp. 698-700; Figs. 19.3-19.4; Table 19.1) • Capillary beds are microcirculatory networks consisting of a vascular shunt and true capillaries, which function as the exchange vessels (pp. 699–700; Fig. 19.4). • A cuff of smooth muscle, called a precapillary sphincter, surrounds each capillary at the metarteriole and acts as a valve to regulate blood flow into the capillary (p. 700; Fig. 19.4).

34. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Capillaries (pp. 698-700; Figs. 19.3-19.4; Table 19.1) • Capillary beds are microcirculatory networks consisting of a vascular shunt and true capillaries, which function as the exchange vessels (pp. 699–700; Fig. 19.4). • A cuff of smooth muscle, called a precapillary sphincter, surrounds each capillary at the metarteriole and acts as a valve to regulate blood flow into the capillary (p. 700; Fig. 19.4).

35. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Capillaries (pp. 698-700; Figs. 19.3-19.4; Table 19.1)

36. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Venous System (pp. 700-701; Fig. 19.5; Table 19.1) • Venules are formed where capillaries converge and allow fluid and white blood cells to move easily between the blood and tissues (p. 700; Table 19.1). • Venules join to form veins, which are relatively thin-walled vessels with large lumens containing about 65% of the total blood volume (pp. 700–701; Fig. 19.5; Table 19.1).

37. OVERVIEW OF BLOOD VESSEL STRUCTURE & FUNCTION—Vascular Anastomoses (pp. 701, 703) • Vascular anastomoses form where vascular channels unite, allowing blood to be supplied to and drained from an area even if one channel is blocked (p. 701).

38. PHYSIOLOGY OF CIRCULATION—Introduction to Blood Flow, Blood Pressure, and Resistance (pp. 703-704) • Blood flow is the volume of blood flowing through a vessel, organ, or the entire circulation in a given period, and may be expressed as ml/min (p. 703). • Blood pressure is the force per unit area exerted by the blood against a vessel wall, and is expressed in millimeters of mercury (mm Hg) (p. 703). • Resistance is a measure of the friction between blood and the vessel wall, and arises from three sources: blood viscosity, blood vessel length, and blood vessel diameter (p. 704).

39. PHYSIOLOGY OF CIRCULATION—Introduction to Blood Flow, Blood Pressure, and Resistance (pp. 703-704) • Relationship Between Flow, Pressure, and Resistance (p. 704) • If blood pressure increases, blood flow increases; if peripheral resistance increases, blood flow decreases. • Peripheral resistance is the most important factor influencing local blood flow, because vasoconstriction or vasodilation can dramatically alter local blood flow, while systemic blood pressure remains unchanged.

40. PHYSIOLOGY OF CIRCULATION—Systemic Blood Pressure (pp. 704-706; Figs. 19.6-19.7) • The pumping action of the heart generates blood flow; pressure results when blood flow is opposed by resistance (p. 704). • Systemic blood pressure is highest in the aorta, and declines throughout the pathway until it reaches 0 mm Hg in the right atrium (p. 705; Fig. 19.6).

41. PHYSIOLOGY OF CIRCULATION—Systemic Blood Pressure (pp. 704-706; Figs. 19.6-19.7) • Arterial blood pressure reflects how much the arteries close to the heart can be stretched (compliance, or distensibility), and the volume forced into them at a given time (p. 705; Fig. 19.6). • When the left ventricle contracts, blood is forced into the aorta, producing a peak in pressure called systolic pressure (120 mm Hg). • Diastolic pressure occurs when blood is prevented from flowing back into the ventricles by the closed semilunar valve, and the aorta recoils (70–80 mm Hg). • The difference between diastolic and systolic pressure is called the pulse pressure. (For example 120/80 mm Hg has a pulse pressure = 40 mm Hg) • The mean arterial pressure (MAP) represents the pressure that propels blood to the tissues.

42. PHYSIOLOGY OF CIRCULATION—Systemic Blood Pressure (pp. 704-706; Figs. 19.6-19.7)

43. PHYSIOLOGY OF CIRCULATION—Systemic Blood Pressure (pp. 704-706; Figs. 19.6-19.7) • Capillary blood pressure is low, ranging from 40–20 mm Hg, which protects the capillaries from rupture, but is still adequate to ensure exchange between blood and tissues (p. 705; Fig. 19.6). • Venous blood pressure changes very little during the cardiac cycle, and is low, reflecting cumulative effects of peripheral resistance (pp. 705–706; Fig. 19.7).

44. PHYSIOLOGY OF CIRCULATION—Systemic Blood Pressure (pp. 704-706; Figs. 19.6-19.7)

45. PHYSIOLOGY OF CIRCULATION—Maintaining Blood Pressure (pp. 706-713; Figs. 19.8-19.12; Table 19.2) • Blood pressure varies directly with changes in blood volume and cardiac output, which are determined primarily by venous return and neural and hormonal controls (p. 706; Fig. 19.8).

46. Example: • SV = 80 mL/beat • HR = 60 beats/min • Calculate CO • CO = SV x HR • CO = 80 mL/beat x 60 beats/min • =4800 mL/min • =4.8 L/min

47. Calculated: CO = 4.8 L/min • Is this a normal value?

48. PHYSIOLOGY OF CIRCULATION—Maintaining Blood Pressure (pp. 706-713; Figs. 19.8-19.12; Table 19.2) • Short-term neural controls of peripheral resistance alter blood distribution to meet specific tissue demands, and maintain adequate Mean Arterial Pressure (MAP) by altering blood vessel diameter (pp. 706–709; Fig. 19.9). • The vasomotor center is a cluster of sympathetic neurons in the medulla that controls changes in the diameter of blood vessels. • Baroreceptorsdetect stretch and send impulses to the vasomotor center, inhibiting its activity and promoting vasodilation of arterioles and veins. (Fig. 19.11) • Chemoreceptors detect a rise in carbon dioxide levels of the blood, and stimulate the cardioacceleratory and vasomotor centers, which increases cardiac output and vasoconstriction. (Fig. 19.11) • The cortex and hypothalamus can modify arterial pressure by signaling the medullary centers.

49. Figure 19.11 Factors causing an increase in MAP. Fluid loss from hemorrhage, excessive sweating Crisis stressors: exercise, trauma, body temperature Bloodborne chemicals: epinephrine, NE, ADH, angiotensin II; ANP release Activity of muscular pump and respiratory pump Release of ANP Dehydration, high hematocrit Body size Conservation of Na+ and water by kidney Blood volume Blood pressure Blood pH, O2, CO2 Blood volume Baroreceptors Chemoreceptors Venous return Activation of vasomotor and cardiac acceleration centers in brain stem Diameter of blood vessels Blood viscosity Blood vessel length Stroke volume Heart rate Cardiac output Peripheral resistance Initial stimulus Physiological response Result Mean systemic arterial blood pressure

50. Figure 19.9 Baroreceptor reflexes that help maintain blood pressure homeostasis (1 of 2). 3 Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center. 4a Sympathetic impulses to heart cause HR, contractility, and CO. 2 Baroreceptors in carotid sinuses and aortic arch are stimulated. 4b Rate of vasomotor impulses allows vasodilation, causing R 5 Stimulus: Blood pressure (arterial blood pressure rises above normal range). CO and Rreturn blood pressure to homeostatic range.