1. The Cardiovascular System: Cardiac Function

2. Anatomy of the Heart Four Chambers Valves Interventricular septum Base
Two atria
Two ventricles
Valves
Atrioventricular
Semilunar
Interventricular septum
Base
Apex
Figure 13.1
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3. Path of Blood Flow Cardiovascular system = closed system
Flow through systemic and pulmonary circuits is in series
Left ventricle  aorta  systemic circuit  vena cavae  right atrium  right ventricle  pulmonary artery  pulmonary circuit  pulmonary veins  left atrium  left ventricle
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4. Path of Blood Flow Figure 13.2
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5. Heart Location
Figure 13.5
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6. Ventricular Muscle Figure 13.6
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7. Properties of Cardiac Muscle
Cells are smaller than cells of skeletal muscle
Cells demonstrate branching
Striations are evident
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8. Properties of Cardiac Muscle
Intercalated disks
Gap junctions
Cause heart to contract as a unit
Desmosomes
Resist stress
Atria and ventricles
Separate units
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9. Properties of Cardiac Muscle
Aerobic muscle
No cell division after infancy—growth by hypertrophy
99% contractile cells (for pumping)
1% autorhythmic cells (set pace)
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10. Function of Cardiac Muscle
Rhythmic contraction and relaxation generates heart pumping action
Contraction pushes blood out of heart into vasculature
Relaxation allows heart to fill with blood
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11. Heartbeat Wave of contraction through cardiac muscle
Atria contract as a unit
Ventricles contract as a unit
Atrial contraction precedes ventricle contraction
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12. Valves and Unidirectional Blood Flow
Pressure within chambers of heart vary with heartbeat cycle
Pressure difference drives blood flow
High pressure to low pressure
Normal direction of flow
Atria to ventricles
Ventricles to arteries
Valves prevent backward flow of blood
All valves open passively based on pressure gradient
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13. Atrioventricular Valve Action
Figure 13.7
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14. Semilunar Valve Action
Figure 13.8
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15. Autorhythmic Cells Cardiac cells are linked by gap junctions
Location Firing Rate at Rest
SA Node APs/min*
AV Node APs/min
Bundle of His APs/min
Purkinje Fibers 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
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16. Cardiac Electrical Connections
Figure 13.9
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17. Conduction System of Heart
Figure 13.10
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18. Pathway of Depolarization
Figure 13.11
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19. Electrical Activity: Pacemaker Cell
Figure 13.12
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20. Electrical Activity: Pacemaker Cell
Table 13.1
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21. Electrical Activity: Contractile Cell
Figure 13.13
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22. Electrical Activity: Contractile Cell
Table 13.2
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23. Cardiac Cycle Figure 13.18 Ventricular filling Ventricular filling
Mid-to-late
diastole
Atrial contraction
Isovolumetric
contraction
ejection
relaxation
Left atrium
Right atrium
Right
ventricle
Left ventricle
Systole
Early diastole
Open
Atrioventricular valves
Aortic and pulmonary
(semilunar) valves
Phase
Closed 1 2 3 4
Figure 13.18
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24. Ventricular Systole Isovolumetric ventricular contraction
AV and aortic valves closed
Ventricular pressure increases until it exceeds atrial pressure
Ventricular ejection
Aortic valve opens
Blood moves from ventricle to aorta
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25. Ventricular Diastole Isovolumetric ventricular relaxation
Ventricle muscle relaxes so that pressure is less than aorta
Aortic valve closes
Pressure in ventricle continues dropping until it is less than atrial pressure
Ventricular filling
AV valve opens
Blood moves from atria to ventricle
Passive until atrium contracts
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26. Ventricular Pressure Figure 13.19
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27. Aortic Pressure Figure 13.20
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28. Ventricular Volume
EDV = end-diastolic volume, volume of blood in ventricle at the end of diastole
ESV = end systolic volume, volume of blood in ventricle at the end of systole
SV = stroke volume, volume of blood ejected from ventricle each cycle.
SV = EDV -ESV
Figure 13.21
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29. Stroke Volume Volume of blood ejected by the ventricle each beat
end diastolic volume – end systolic volume =
130 mL – 60 mL = 70 mL
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30. Ejection Fraction
Fraction of end-diastolic volume ejected during a heartbeat
Ejection fraction =
stroke volume / end diastolic volume
= 70 mL / 130 mL = 0.54
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31. Heart Sounds Due to turbulent flow when valves close First heart sound
Soft lubb
AV valves close simultaneously
Second heart sound
Louder dubb
Semilunar valves close simultaneously
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32. Heart Sounds
Figure 13.22
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33. Cardiac Output Volume of blood pumped by each ventricle per minute
Cardiac output = CO = SV x HR
Average CO = 5 liters/min at rest
Average blood volume = 5.5 liters
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34. Regulation of Cardiac Output
Regulate heart rate and stroke volume
Extrinsic and intrinsic regulation
Extrinsic—neural and hormonal
Intrinsic—autoregulation
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35. Autonomic Inputs to Heart
Figure 13.23
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36. Heart Rate - Determined by SA Node Firing Rate
SA node intrinsic firing rate = 100/min
No extrinsic control on heart, HR = 100
SA node under control of ANS and hormones
Rest: parasympathetic dominates, HR = 75
Excitement: sympathetic takes over, HR increases
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37. Effects of Sympathetic Activity on Heart Rate
Increased sympathetic activity (nerves or epinephrine)
Beta 1 receptors in SA node
Increase open state of If and calcium channels
Increase rate of spontaneous depolarization
Increase heart rate
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38. Effects of Parasympathetic Activity on Heart Rate
Increased parasympathetic activity (vagus nerve)
Muscarinic Cholinergic Receptors in SA Node
Increase open state of K channels and closed state of calcium channels
Decrease rate of spontaneous depolarization and hyperpolarize cell
Decrease heart rate
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39. Sympathetic Effects: SA Potentials
Figure 13.25
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40. Factors Affecting Cardiac Output: Stroke Volume
Primary factors affecting stroke volume
Ventricular contractility
End-diastolic volume
Afterload
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41. Stroke Volume Ventricles never completely empty of blood
More forceful contraction will expel more blood
Extrinsic controls of SV
Sympathetic drive to ventricular muscle fibers
Hormonal control
Intrinsic controls of SV
Changes in EDV
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42. Extrinsic Control of Stroke Volume
Sympathetic innervation of contractile cells
Cardiac nerves
NE binds to 1 adrenergic receptors
Increases cardiac contractility
Parasympathetic innervation of contractile cells
Not significant
Hormones
Thyroid hormones, insulin and glucagon increase force of contraction
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43. Sympathetic Effects on Contractility
Increased sympathetic activity
Increased epinephrine release
Increases strength of contraction
Increases rate of contraction
Increases rate of relaxation
Figure 13.27
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44. Principle of Frank-Starling’s Law
Increased EDV stretches muscle fibers
Fibers closer to optimum length
Optimum length = greater strength of contraction
Result = Increased SV
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45. Intrinsic Control - Frank-Starling’s Law
Increase venous return
Increase strength of contraction
Increase stroke volume
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46. Starling’s Law
Figure 13.28
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47. Starling’s Law
Figure 13.29
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48. Factors Affecting End-Diastolic Volume
End-diastolic pressure = preload
Filling time
Atrial pressure
Central venous pressure
Afterload = pressure in aorta during ejection
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49. Factors Influencing Stroke Volume
End-diastolic
volume
Venous return
Contractility
Arterial pressure
(afterload)
Sympathetic
activity or
Epinephrine
Ventricle
Figure 13.30
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50. Factors Influencing Stroke Volume
End-diastolic
volume
Venous return
Ventricle
Figure 13.30, step 1
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51. Factors Influencing Stroke Volume
End-diastolic
volume
Venous return
Contractility
Sympathetic
activity or
Epinephrine
Ventricle
Figure 13.30, step 2
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52. Factors Influencing Stroke Volume
End-diastolic
volume
Venous return
Contractility
Arterial pressure
(afterload)
Sympathetic
activity or
Epinephrine
Ventricle
Figure 13.30, step 3
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53. Regulation of Cardiac Output
Figure 13.31
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