1. The Cardiovascular System: The Heart18
P A R T A
The Cardiovascular System: The Heart

2. Approximately the size of your fist Location
Heart Anatomy
Approximately the size of your fist
Location
Superior surface of diaphragm
Left of the midline
Anterior to the vertebral column, posterior to the sternum

3. Heart Anatomy
Figure 18.1

4. Coverings of the Heart: Physiology
The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively friction-free environment

5. Pericardial Layers of the Heart
Figure 18.2

6. Cardiac Muscle Bundles
Figure 18.3

7. External Heart: Vessels that Supply/Drain the Heart (Posterior View)
Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove)
Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein

8. Aorta Superior vena cava Left Right pulmonary artery pulmonary artery
Left atrium
Pulmonary trunk
Left
pulmonary veins
Right atrium
Right
pulmonary veins
Mitral
(bicuspid) valve
Fossa
ovalis
Aortic
valve
Pectinate
muscles
Pulmonary
valve
Tricuspid
valve
Left ventricle
Papillary
muscle
Right ventricle
Chordae
tendineae
Interventricular
septum
Myocardium
Trabeculae
carneae
Visceral
pericardium
Inferior
vena cava
Endocardium
(e)
Figure 18.4e

9. Right and Left Ventricles
Figure 18.6

10. Figure 18.5

11. Coronary Circulation
Coronary circulation is the functional blood supply to the heart muscle itself
Collateral routes ensure blood delivery to heart even if major vessels are occluded

12. Coronary Circulation: Arterial Supply
Figure 18.7a

13. Coronary Circulation: Venous Supply
Figure 18.7b

14. Heart Valves
Figure 18.8a, b

15. Heart Valves
Figure 18.8c, d

16. Atrioventricular Valve Function
Figure 18.9

17. Semilunar Valve Function
Figure 18.10

18. Microscopic Anatomy of Heart Muscle
Cardiac muscle is striated, short, fat, branched, and interconnected
The connective tissue endomysium acts as both tendon and insertion
Intercalated discs anchor cardiac cells together and allow free passage of ions
Heart muscle behaves as a functional syncytium
InterActive Physiology ®:
Anatomy Review: The Heart, pages 3–7

19. Microscopic Anatomy of Cardiac Muscle
Figure 18.11

20. The Cardiovascular System: The Heart18
P A R T B
The Cardiovascular System: The Heart

21. Cardiac Muscle Contraction
Heart muscle:
Is stimulated by nerves and is self-excitable (automaticity)
Contracts as a unit
Has a long (250 ms) absolute refractory period
Cardiac muscle contraction is similar to skeletal muscle contraction

22. Heart Physiology: Intrinsic Conduction System
Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker potentials
Use calcium influx (rather than sodium) for rising phase of the action potential

23. Pacemaker and Action Potentials of the Heart
Figure 18.13

24. Cardiac Membrane Potential
Figure 18.12

25. Cardiac Intrinsic Conduction
Figure 18.14a

26. Heart Physiology: Sequence of Excitation
Sinoatrial (SA) node generates impulses about 75 times/minute
Atrioventricular (AV) node delays the impulse approximately 0.1 second
Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

27. Heart Physiology: Sequence of Excitation
AV bundle splits into two pathways in the interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex of the heart
Purkinje fibers carry the impulse to the heart apex and ventricular walls

28. Cardiac Intrinsic Conduction
Figure 18.14a

29. Cardiac Membrane Potential
Figure 18.12

30. Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
Impulse delayed
at AV node
Impulse passes to
heart apex; ventricular
excitation begins
Ventricular excitation
complete
SA node
AV node
Bundle
branches
Purkinje
fibers
Figure 18.17

31. Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
Figure 18.17

32. Heart Excitation Related to ECG
Impulse delayed
at AV node
AV node
Figure 18.17

33. Heart Excitation Related to ECG
Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
Figure 18.17

34. Heart Excitation Related to ECG
Ventricular excitation
complete
Purkinje
fibers
Figure 18.17

35. Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
Impulse delayed
at AV node
Impulse passes to
heart apex; ventricular
excitation begins
Ventricular excitation
complete
SA node
AV node
Bundle
branches
Purkinje
fibers
Figure 18.17

36. Electrocardiography
Figure 18.16

37. Electrical activity is recorded by electrocardiogram (ECG)
Electrocardiography
Electrical activity is recorded by electrocardiogram (ECG)
P wave corresponds to depolarization of SA node
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex
PLAY
InterActive Physiology ®:
Intrinsic Conduction System, pages 3–6

38. Defective heart valves:
Heart Murmurs
Abnormal heart sounds produced by abnormal patterns of blood flow in the heart.
Defective heart valves:
Valves become damaged by antibodies made in response to an infection, or congenital defects.
Mitral stenosis:
Mitral valve becomes thickened and calcified.
Impairs blood flow from left atrium to left ventricle.
Accumulation of blood in left ventricle may cause pulmonary HTN.
Incompetent valves:
Damage to papillary muscles.
Valves do not close properly.
Murmurs produced as blood regurgitates through valve flaps.

39. Septal defects: Heart Murmurs Usually congenital.
Holes in septum between the left and right sides of the heart.
May occur either in interatrial or interventricular septum.
Blood passes from left to right.

40. Electrocardiogram (ECG/EKG)
The body is a good conductor of electricity.
Tissue fluids have a high [ions] that move in response to potential differences.
Electrocardiogram:
Measure of the electrical activity of the heart per unit time.
Potential differences generated by heart are conducted to body surface where they can be recorded on electrodes on the skin.
Does NOT measure the flow of blood through the heart.

41. Ischemic Heart Disease
Ischemia:
Oxygen supply to tissue is deficient.
Most common cause is atherosclerosis of coronary arteries.
Increased [lactic acid] produced by anaerobic respiration.
Angina pectoris:
Substernal pain.
Myocardial infarction (MI):
Changes in T segment of ECG.
Increased CPK and LDH.

42. Arrhythmias Detected on ECG
Abnormal heart rhythms.
Flutter:
Extremely rapid rates of excitation and contraction of atria or ventricles.
Atrial flutter degenerates into atrial fibrillation.
Fibrillation:
Contractions of different groups of myocardial cells at different times.
Coordination of pumping impossible.
Ventricular fibrillation is life-threatening.

43. Arrhythmias Detected on ECG (continued)
Bradycardia:
HR slower < 60 beats/min.
Tachycardia:
HR > 100 beats/min.
First–degree AV nodal block:
Rate of impulse conduction through AV node exceeds 0.2 sec.
P-R interval.
Second-degree AV nodal block:
AV node is damaged so that only 1 out of 2-4 atrial APs can pass to the ventricles.
P wave without QRS.

44. Arrhythmias Detected on ECG (continued)
Third-degree (complete) AV nodal block:
None of the atrial waves can pass through the AV node.
Ventricles paced by ectopic pacemaker.

45. ECG Tracings
Figure 18.18

46. Extrinsic Innervation of the Heart
Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
Figure 18.15

47. Heart Sounds
Figure 18.19

48. Heart sounds (lub-dup) are 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

49. Cardiac Cycle
Cardiac cycle refers to all events associated with blood flow through the heart
Systole – contraction of heart muscle
Diastole – relaxation of heart muscle

50. Phases of the Cardiac Cycle
Ventricular filling – mid-to-late diastole
Heart blood pressure is low as blood enters atria and flows into ventricles
AV valves are open, then atrial systole occurs

51. Phases of the Cardiac Cycle
Ventricular systole
Atria relax
Rising ventricular pressure results in closing of AV valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves

52. Phases of the Cardiac Cycle
Isovolumetric relaxation – early diastole
Ventricles relax
Backflow of blood in aorta and pulmonary trunk closes semilunar valves
Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves
PLAY
InterActive Physiology ®: Cardiac Cycle, pages 3–18

53. Phase of contraction. Phase of relaxation. Cardiac Cycle
Refers to the repeating pattern of contraction and relaxation of the heart.
Systole:
Phase of contraction.
Diastole:
Phase of relaxation.
End-diastolic volume (EDV):
Total volume of blood in the ventricles at the end of diastole.
Stroke volume (SV):
Amount of blood ejected from ventricles during systole.
End-systolic volume (ESV):
Amount of blood left in the ventricles at the end of systole.

54. Figure 18.20

55. Cardiac Cycle (continued)
Step 1: Isovolumetric contraction:
QRS just occurred.
Contraction of the ventricle causes ventricular pressure to rise above atrial pressure.
AV valves close.
Ventricular pressure is less than aortic pressure.
Semilunar valves are closed.
Volume of blood in ventricle is EDV.
Step 2: Ejection:
Contraction of the ventricle causes ventricular pressure to rise above aortic pressure.
Semilunar valves open.
Ventricular pressure is greater than atrial pressure.
AV valves are closed.
Volume of blood ejected: SV.

56. Cardiac Cycle (continued)
Step 3: T wave occurs:
Ventricular pressure drops below aortic pressure.
Step 4: Isovolumetric relaxation:
Back pressure causes semilunar valves to close.
AV valves are still closed.
Volume of blood in the ventricle: ESV.
Step 5: Rapid filling of ventricles:
Ventricular pressure decreases below atrial pressure.
AV valves open.
Rapid ventricular filling occurs.

57. Cardiac Cycle (continued)
Step 6: Atrial systole:
P wave occurs.
Atrial contraction.
Push 10-30% more blood into the ventricle.

58. Cardiac Cycle (continued)

59. Correlation of ECG with Heart Sounds
First heart sound:
Produced immediately after QRS wave.
Rise of intraventricular pressure causes AV valves to close.
Second heart sound:
Produced after T wave begins.
Fall in intraventricular pressure causes semilunar valves to close.

60. Figure 18.20

61. Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by each ventricle in one minute
CO is the product of heart rate (HR) and stroke volume (SV)
HR is the number of heart beats per minute
SV is the amount of blood pumped out by a ventricle with each beat
Cardiac reserve is the difference between resting and maximal CO

62. Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)

63. Regulation of Stroke Volume
SV = end diastolic volume (EDV) minus end systolic volume (ESV)
EDV = amount of blood collected in a ventricle during diastole
ESV = amount of blood remaining in a ventricle after contraction

64. Factors Affecting Stroke Volume
Preload – amount ventricles are stretched by contained blood
Contractility – cardiac cell contractile force due to factors other than EDV
Afterload – back pressure exerted by blood in the large arteries leaving the heart

65. Cardiac Output (CO) Volume of blood pumped/min. by each ventricle.
Pumping ability of the heart is a function of the beats/ min. and the volume of blood ejected per beat.
CO = SV x HR
Total blood volume averages about 5.5 liters.
Each ventricle pumps the equivalent of the total blood volume each min. (resting conditions).

66. Frank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV

67. Preload and Afterload
Figure 18.21

68. Extrinsic Factors Influencing Stroke Volume
Contractility is the increase in contractile strength, independent of stretch and EDV
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs

69. Extrinsic Factors Influencing Stroke Volume
Agents/factors that decrease contractility include:
Acidosis
Increased extracellular K+
Calcium channel blockers

70. Heart Contractility and Norepinephrine
Extracellular fluid
Norepinephrine
b1-Adrenergic
receptor
Adenylate cyclase
Ca2+
Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Ca2+
channel
Cytoplasm
GTP 1
GTP
GDP
ATP
cAMP
Active
protein
kinase A
Inactive
protein
kinase A
Ca2+ 3
Ca2+
uptake
pump 2
Enhanced
actin-myosin
interaction
binds
Troponin to
Ca2+
SR Ca2+
channel
Cardiac muscle
force and
velocity
Sarcoplasmic
reticulum (SR)
Figure 18.22

71. Regulation of Heart Rate
Positive chronotropic factors increase heart rate
Negative chronotropic factors decrease heart rate

72. Circulatory Changes During Exercise (continued)

73. Regulation of Heart Rate: Autonomic Nervous System
Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone

74. Atrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria
Causes stimulation of the SA node
Stimulates baroreceptors in the atria, causing increased SNS stimulation

75. Chemical Regulation of the Heart
The hormones epinephrine and thyroxine increase heart rate
Intra- and extracellular ion concentrations must be maintained for normal heart function
InterActive Physiology ®: Cardiac Output, pages 3–9

76. Figure 18.23

77. Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is caused by:
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)

78. Baroreceptor Reflex (continued)

79. Renin-Angiotension-Aldosterone System (continued)

80. Dehydration or excess salt intake:
Regulation by ADH
Released by posterior pituitary when osmoreceptors detect an increase in plasma osmolality.
Dehydration or excess salt intake:
Produces sensation of thirst.
Stimulates H20 reabsorption from urine.