1. Chapter 9
Cardiac Physiology

2. Credit: © L. Bassett/Visuals Unlimited
97935
Human heart.

3. Credit: © L. Bassett/Visuals Unlimited
97936
Human heart with coronary arteries exposed.

4. Outline Circulatory system overview Transplant surgery Anatomy
Electrical activity
Mechanical events
Cardiac output
Coronary circulation

5. Circulatory System Three basic components Heart Blood vessels Blood
Serves as pump that establishes the pressure gradient needed for blood to flow to tissues
Blood vessels
Passageways through which blood is distributed from heart to all parts of body and back to heart
Blood
Transport medium within which materials being transported are dissolved or suspended
Pulmonary circulation
Closed loop of vessels carrying blood between heart and lungs
Systemic circulation
Circuit of vessels carrying blood between heart and other body systems

6. Transplant

7. Circulatory System Anatomy Heart
Hollow, muscular organ about the size of a clenched fist
Positioned between two bony structures – sternum and vertebrate
Dual pump
Right and left sides of heart function as two separate pumps
Divided into right and left halves and has four chambers
Atria
Upper chambers
Receive blood returning to heart and transfer it to lower chambers
Ventricles
Lower chambers which pump blood from heart

8. Circulatory System Heart Arteries Veins Septum
Carry blood away from ventricles to tissues
Veins
Vessels that return blood from tissues to the atria
Septum
Continuous muscular partition that prevents mixture of blood from the two sides of heart

9. Outline Anatomy Thoracic cavity, base, apex AV and semilunar valves
endothelium, myocardium, epicardium
cardiac cells, intercalated disks
Comparison of cardiac cells to skeletal and smooth muscle cells
pericardium

10. Blood Flow Through and Pump Action of the Heart
What are the parts and what do they do?
Know the flow of blood in order.

11. Heart Valves Atrioventricular (AV) valves
Right and left AV valves are positioned between atrium and ventricle on right and left sides
Prevent backflow of blood from ventricles into atria during ventricular emptying
Right AV valve
Also called tricuspid valve
Left AV valve
Also called bicuspid valve or mitral valve
Chordae tendinae
Fibrous cords which prevent valves from being everted
Papillary muscles

12. Heart Valves Semilunar valves Aortic and pulmonary valves
Lie at juncture where major arteries leave ventricles
Prevented from everting by anatomic structure and positioning of cusps
No valves between atria and veins
Reasons
Atrial pressures usually are not much higher than venous pressures
Sites where venae cavae enter atria are partially compressed during atrial contraction

13. Heart Valves

14. Consists of three distinct layers Endothelium
Thin inner tissue
Epithelial tissue which lines entire circulatory system
Myocardium
Middle layer
Composed of cardiac muscle
Constitutes bulk of heart wall
Epicardium
Thin external layer which covers the heart
Pericardium
the fluid filled sac that surrounds the heart
Endocardium
Myocardium
fig. 18-9; pg: 563
Epicardium

15. Heart is enclosed by pericardial sac Pericardial sac has two layers
Tough, fibrous covering
Secretory lining
Secretes pericardial fluid
Provides lubrication to prevent friction between pericardial layers
Pericarditis
Inflammation of pericardial sac

16. The next series of slides compares cardiac, skeletal, smooth muscle cells.

17. Cardiac Muscle Fibers
Interconnected by intercalated discs and form functional syncytia
Within intercalated discs – two kinds of membrane junctions
Desmosomes
Gap junctions

18. Credit: © Dr. Donald Fawcett/Visuals Unlimited
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Cardiac muscle in longitudinal section showing intercalated discs. TEM.

19. Skeletal Muscle Fiber Basal lamina Sacrolemma Myofibrils Longitudinal
system
Mitochondria
Transverse
tubule
Nucleus
Intercalated
disc
Myofibril
Opening of
Transverse
tubule
fig 16-8b, pg 487

20. Credit: © Dr. Richard Kessel/Visuals Unlimited
310127
Credit: © Dr. Richard Kessel/Visuals Unlimited
Myofibrils within skeletal muscle fibers. All bands (A, I, Z, M) are evident as well as elements of the sarcoplasmic reticulum and small dots of glycogen. TEM X32,000.

21. Smooth Muscle Fiber Rough Endoplasmic reticulum Glycogen granules
Nucleus
Mitochondria
Thin filament
Thick filament
Dense
bodies
Plasma
membrane
fig 16-9a, pg 479

22. Dense bodies Smooth muscle Cells Fig. 8-27b, p. 288
Figure 8.27: Microscopic view of smooth muscle cells.
(b) Electron micrograph of smooth muscle cells at 14,000× magnification. Note the presence of dense bodies and lack of banding.
Fig. 8-27b, p. 288

23. Outline Electrical activity of the heart Autorhymicity
Pacemaker (function, ions)
Conductive system (SA, AV, bundle of His, Purkinje fibers)
Abnormal rhythms
Spread of cardiac excitation
Cardiac cell action potentials
Characteristics vary by location

24. Electrical Activity of Heart
Heart beats rhythmically as result of action potentials it generates by itself (autorhythmicity)
Two specialized types of cardiac muscle cells
Contractile cells
99% of cardiac muscle cells
Do mechanical work of pumping
Normally do not initiate own action potentials
Autorhythmic cells
Do not contract but send electrical signals to the contractile cells
Specialized for initiating and conducting action potentials responsible for contraction of working cells

25. Electrical Activity of Heart
Locations of noncontractile cells capable of autorhymicity
Sinoatrial node (SA node)
Specialized region in right atrial wall near opening of superior vena cava
Pacemaker of the heart
Atrioventricular node (AV node)
Small bundle of specialized cardiac cells located at base of right atrium near septum
Bundle of His (atrioventricular bundle)
Cells originate at AV node and enters interventricular septum
Divides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls
Purkinje fibers
Small, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium

26. Specialized Conduction System of Heart

27. Electrical Activity of Heart
Cardiac impulse originates at SA node
Action potential spreads throughout right and left atria
Impulse passes from atria into ventricles through AV node (only point of electrical contact between chambers)
Action potential briefly delayed at AV node (ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling)
Impulse travels rapidly down interventricular septum by means of bundle of His
Impulse rapidly disperses throughout myocardium by means of Purkinje fibers
Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions

28. Spread of Cardiac Excitation

29. Open K channels Closure of K channels Open Ca channels
Figure 9.7: Pacemaker activity of cardiac autorhythmic cells.
The first half of the pacemaker potential is due to closure of K+ channels, whereas the second half is due to opening of T-type Ca2+ channels. Once threshold is reached, the rising phase of the action potential is due to opening of L-type Ca2+ channels, whereas the falling phase is due to opening of K+ channels.
Open Ca channels
Closure of K channels
Fig. 9-7, p. 305

30. Relationship of an Action Potential and the Refractory Period to the Duration of the Contractile Response in Cardiac Muscle

31. Figure 9.11: Action potential in contractile cardiac muscle cells.
The action potential in cardiac contractile cells differs considerably from the action potential in cardiac autorhythmic cells (compare with Figure 9-7).
Fig. 9-11, p. 310

32. fig ; pg: 564

33. Atrial muscle Atrioventricular Bundle branch Purkinje fibers
SA node
pacemaker
Atrial muscle
Atrioventricular
Bundle branch
Purkinje fibers
Ventricular
muscle
Milliseconds
fig ; pg: 568

34. Electrical Activity of Heart
Atria contract as single unit followed after brief delay by a synchronized ventricular contraction
Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction
Ensures adequate ejection time
Plateau primarily due to activation of slow L-type Ca2+ channels

35. Electrical Activity of Heart
Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum
Ca2+ induced Ca2+ release leads to cross-bridge cycling and contraction

36. Excitation-Contraction Coupling in Cardiac Contractile Cells

37. Electrical Activity of Heart
Because long refractory period occurs in conjunction with prolonged plateau phase, summation and tetanus of cardiac muscle is impossible
Ensures alternate periods of contraction and relaxation which are essential for pumping blood

38. Relationship of an Action Potential and the Refractory Period to the Duration of the Contractile Response in Cardiac Muscle

39. Electrocardiogram (ECG)
Record of overall spread of electrical activity through heart
Represents
Recording part of electrical activity induced in body fluids by cardiac impulse that reaches body surface
Not direct recording of actual electrical activity of heart
Recording of overall spread of activity throughout heart during depolarization and repolarization
Not a recording of a single action potential in a single cell at a single point in time
Comparisons in voltage detected by electrodes at two different points on body surface, not the actual potential
Does not record potential at all when ventricular muscle is either completely depolarized or completely repolarized

40. Electrocardiogram (ECG)
Different parts of ECG record can be correlated to specific cardiac events

41. Credit: © Mediscan/Visuals Unlimited
3202
Normal ECG.

42. Abnormalities in Rate Tachycardia
Rapid heart rate of more than 100 beats per minute
Bradycardia
Slow heart rate of fewer than 60 beats per minute

43. Abnormalities in Rhythm
Regularity or spacing of ECG waves
Arrhythmia
Variation from normal rhythm and sequence of excitation of the heart
Examples
Atrial flutter ( BPM)
Atrial fibrillation
Ventricular fibrillation
Heart block

44. Cardiac Myopathies Damage of the heart muscle Myocardial ischemia
Inadequate delivery of oxygenated blood to heart tissue
Necrosis
Death of heart muscle cells
Acute myocardial infarction (heart attack)
Occurs when blood vessel supplying area of heart becomes blocked or ruptured

45. Representative Heart Conditions Detectable Through ECG

46. Outline Mechanical events Systole, diastole
animation (volumes, pressures, sounds and EKG)

47. Specialized Conduction System of Heart

48.
Figure 9.17: Cardiac cycle.
This graph depicts various events that occur concurrently during the cardiac cycle. Follow each horizontal strip across to see the changes that take place in the electro-cardiogram; aortic, ventricular, and atrial pressures; ventricular volume; and heart sounds throughout the cycle. The last half of diastole, one full systole and diastole (one full cardiac cycle), and another systole are shown for the left side of the heart. Follow each vertical strip downward to see what happens simultaneously with each of these factors during each phase of the cardiac cycle. See the text (pp. 317–318) for a detailed explanation of the circled numbers. The sketches of the heart illustrate the flow of O2-poor (dark blue) and O2-rich (bright red) blood in and out of the ventricles during the cardiac cycle.
Fig. 9-17, p. 316

49. Cardiac Output Volume of blood ejected by each ventricle each minute
Determined by
heart rate times
stroke volume

50. Cardiac Output
Heart rate is varied by altering balance of parasympathetic and sympathetic influence on SA node
Parasympathetic stimulation slows heart rate
Sympathetic stimulation speeds it up

51. = Inherent SA node pacemaker activity
Threshold
potential
= Inherent SA node pacemaker activity
= SA node pacemaker activity on parasympathetic stimulation
= SA node pacemaker activity on sympathetic stimulation
Fig. 9-20, p. 322

52. Heart rate Sympathetic activity (and epinephrine) Parasympathetic
Fig. 9-20b, p. 322

53. Cardiac Output Stroke volume
Determined by extent of venous return and by sympathetic activity
Influenced by two types of controls
Intrinsic control
Extrinsic control
Both factors increase stroke volume by increasing strength of heart contraction

54. Frank-Starling Law of the Heart
States that heart normally pumps out during systole the volume of blood returned to it during diastole

55. Figure 9.22: Intrinsic control of stroke volume (Frank–Starling curve).
The cardiac muscle fiber’s length, which is determined by the extent of venous filling, is normally less than the optimal length for developing maximal tension. Therefore, an increase in end-diastolic volume (that is, an increase in venous return), by moving the cardiac muscle fiber length closer to optimal length, increases the contractile tension of the fibers on the next systole. A stronger contraction squeezes out more blood. Thus, as more blood is returned to the heart and the end-diastolic volume increases, the heart automatically pumps out a correspondingly larger stroke volume.
Fig. 9-22, p. 323

56. Figure 9.23: Effect of sympathetic stimulation on stroke volume.
(a) Normal stroke volume. (b) Stroke volume during sympathetic stimulation. (c) Stroke volume with combination of sympathetic stimulation and increased end-diastolic volume.
Fig. 9-23, p. 324

57. Figure 9.24: Shift of the Frank–Starling curve to the left by sympathetic stimulation.
For the same end-diastolic volume (point A), there is a larger stroke volume (from point B to point C) on sympathetic stimulation as a result of increased contractility of the heart. The Frank–Starling curve is shifted to the left by variable degrees, depending on the extent of sympathetic stimulation.
Fig. 9-24, p. 324

58. Outline
Coronary circulation

59. Nourishing the Heart Muscle
Muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation, not from blood within heart chambers
Heart receives most of its own blood supply that occurs during diastole
During systole, coronary vessels are compressed by contracting heart muscle
Coronary blood flow normally varies to keep pace with cardiac oxygen needs

60. Coronary Artery Disease (CAD)
Pathological changes within coronary artery walls that diminish blood flow through the vessels
Leading cause of death in United States
Can cause myocardial ischemia and possibly lead to acute myocardial infarction
Three mechanisms
Profound vascular spasm of coronary arteries
Formation of atherosclerotic plaques
Thromboembolism

61. Collagen-rich smooth muscle cap of plaque Plaque Normal blood
vessel wall
Lipid-rich core
of plaque
Endothelium
Fig. 9-29, p. 328

62. Fig. 9-30, p. 330 Figure 9.30: Consequences of thromboembolism.
(a) A thrombus may enlarge gradually until it completely occludes the vessel at that site. (b) A thrombus may break loose from its attachment, forming an embolus that may completely occlude a smaller vessel downstream. (c) Scanning electron micrograph of a vessel completely occluded by a thromboembolic lesion.
Fig. 9-30, p. 330

63. Area of cardiac muscle deprived of blood supply if coronary vessel
is blocked at
point
Area of cardiac
muscle deprived
of blood supply
if coronary vessel
is blocked at
point
Left
coronary
artery
Right
coronary
artery
Left
ventricle
Right
ventricle
Fig. 9-31, p. 331

64. Possible Outcomes of Acute Myocardial Infarction (Heart Attack)