1. Cardiovascular Physiology
Chapter 14
Cardiovascular Physiology

21. Overview of the Cardiosvascular System
Heart and Blood vessels
Products transported to sustain all cells
Table 14-1: Transport in the Cardiovascular System

22. Circulation Reviewed Heart – "four chambered" Right atrium & ventricle
Pulmonary circuit
Left atrium & ventricle
Systemic circuit
Blood Vessels – "closed circulation"
Arteries –from heart
Capillaries– cell exchange
Veins – to heart

24. Figure 14-1: Overview of circulatory system anatomy
Circulation Reviewed
Figure 14-1: Overview of circulatory system anatomy

25. Blood Flow: Pressure Changes
Flows down a pressure gradient
Highest at the heart (driving P), decreases over distance
Hydrostatic (really hydraulic) pressure in vessels
Decreases 90% from aorta to vena cava

26. Blood Flow: Pressure Changes
Figure 14-2 : Pressure gradient in the blood vessels

27. Some Physic of Fluid Movement: Blood Flow
Flow rate: (L/min)
Flow velocity = rate/C-S area of vessel
Resistance slows flow
Vessel diameter
Blood viscosity
Tube length
Figure 14-4 c: Pressure differences of static and flowing fluid

28. Some Physic of Fluid Movement: Blood Flow
Figure 14-6: Flow rate versus velocity of flow

29. Figure 14-7 g: ANATOMY SUMMARY: The Heart
Heart Structure
Pericardium
Chambers
Coronary vessels
Valves- (one-way-flow)
Myocardium
Figure 14-7 g: ANATOMY SUMMARY: The Heart

30. Figure 14-10: Cardiac muscle
Cardiac Muscle Cells:
Autorhythmic
Myocardial
Intercalated discs
Desmosomes
Gap Junctions
Fast signals
Cell to cell
Many mitochondria
Large T tubes
Figure 14-10: Cardiac muscle

31. Mechanism of Cardiac Muscle Excitation, Contraction & Relaxation
Figure 14-11: Excitation-contraction coupling and relaxation in cardiac muscle

32. Modulation of Contraction
Graded Contraction: proportional to crossbridges formed
More [Ca++]: crossbridges, more force & speed
Autonomic n & epinephrine modulation

33. Modulation of Contraction
Figure 14-12: Modulation of cardiac contraction by catecholamines

34. More Characteristics of Cardiac Muscle Contraction
Stretch-length relationship
 stretch,  Ca++ entering
 contraction force
Long action potential
Long refractory period
No summation
No tetanus

35. More Characteristics of Cardiac Muscle Contraction
Figure 14-13: Length-tension relationships in skeletal and cardiac muscle

36. More Characteristics of Cardiac Muscle Contraction
Figure 14-15c: Refractory periods and summation in skeletal and cardiac muscle

37. Autorhythmic Cells: Initiation of Signals
Pacemaker membrane potential
I-f channels Na+ influx
Ca++ channels – influx, to AP
Slow K+ open – repolarization

38. Autorhythmic Cells: Initiation of Signals
Figure 14-16: Action potentials in cardiac autorhythmic cells

39. Sympathetic and Parasympathetic
Sympathetic – speeds heart rate by  Ca++ & I-f channel flow
Parasympathetic – slows rate by  K+ efflux &  Ca++ influx
Figure 14-17: Modulation of heart rate by the nervous system

40. Coordinating the Pump: Electrical Signal Flow
AP from autorhythmic cells in sinoatrial node (SA)
Spreads via gap junctions down internodal pathways and across atrial myocardial cells (atrial contraction starts)
Pause – atrioventricular (AV) node delay
AV node to bundles of His, branches & Purkinje fibers
Right and left ventricular contraction from apex upward

41. Coordinating the Pump: Electrical Signal Flow
Figure 14-18: Electrical conduction in myocardial cells

42. Coordinating the Pump: Electrical Signal Flow
Figure 14-19a: Electrical conduction in the heart

43. Electrocardiogram (ECG): Electrical Activity of the Heart
Einthoven's triangle
P-Wave – atria
QRS- wave – ventricles
T-wave – repolarization
Figure 14-20: Einthoven’s triangle

44. Electrocardiogram (ECG): Electrical Activity of the Heart
Figure 14-21: The electrocardiogram

45. Electrocardiography (ECG)
Measures galvanically the electric activity of the heart
Well known and traditional, first measurements by Augustus Waller using capillary electrometer (year 1887)
Very widely used method in clinical environment
Very high diagnostic value
1. Atrial depolarization
2. Ventricular depolarization
3. Ventricular repolarization

46. 12-Lead ECG measurement
Most widely used ECG measurement setup in clinical environment
Signal is measured non-invasively with 9 electrodes
Lots of measurement data and international reference databases
Well-known measurement and diagnosis practices
This particular method was adopted due to historical reasons, now it is already rather obsolete
Einthoven leads: I, II & III
Goldberger augmented leads: VR, VL & VF
Precordial leads: V1-V6

47. ECG Information Gained
(Non-invasive)
Heart Rate
Signal conduction
Heart tissue
Conditions
Figure 14-24: Normal and abnormal electrocardiograms

50. Vectorcardiogram (VCG or EVCG)
Instead of displaying the scalar amplitude (ECG curve) the electric activation front is measured and displayed as a vector (dipole model)
 It has amplitude and direction
Diagnosis is based on the curve that the point of this vector draws in 2 or 3 dimensions
The information content of the VCG signal is roughly the same as 12-lead ECG system. The advantage comes from the way how this information is displayed
A normal, scalar ECG curve can be formed from this vector representation, although (for practical reasons) transformation can be quite complicated
Plenty of different types of VCG systems are in use

51. Heart Cycle
Figure 14-25: Mechanical events of the cardiac cycle

52. Heart Cycle: Heart Chambers and the Beat Sequence
1. Late diastole: all chambers relax, filling with blood
2. Atrial systole: atria contract, add 20% more blood to ventricles
3. Isovolumic ventricular contraction: closes AV valves ("lub"), builds pressure

53. Heart Cycle: Finish and Around To the Start
4. Ventricular ejection: pushes open semi lunar valves, blood forced out
5. Ventricular relaxation: aortic back flow slams semi lunar valves shut ("dub") AV valves open refilling starts – back to start of cycle

54. Summary of Heart Beat: Electrical, Pressure and Chamber Volumes
Figure 14-27: The Wiggers diagram

55. Regulators of the Heart: Reflex Controls of Rate
Range: about 50 – near 200
Typical resting: near 70
AP conduction
Muscle Contraction
Parasympathetic slows
Sympathetic speeds

56. Regulators of the Heart: Reflex Controls of Rate
Figure 14-28: Reflex control of heart rate

57. Definition of Afterload
The "afterload" for any contracting muscle is the total force that opposes shortening, minus the stretching force that existed prior to contraction. For cardiac muscle, the afterload is the force against which the myocardial fibers must contact during the ejection phase of systole. Force equals pressure times area, by definition. The total force opposing LV contraction (i.e., the afterload) is the product of the LV pressure and the internal surface area of the LV cavity. In hypertensive subjects, of course, the arterial and LV pressures are abnormally high during systole and, therefore, the LV afterload tends to be high. The internal surface area of the LV varies directly with the volume of blood in the ventricle. If the hypertensive subject also has a dilated LV, the internal area of the LV will be greater than that for a normal subject. Hence, for any given pressure, the afterload tends to increase as the ventricular volume becomes greater. The internal surface area of the ventricular cavity is extremely difficult to measure precisely. Furthermore, both pressure and area change continually throughout ejection. Therefore, it is difficult to assess afterload accurately.

58. Cardiac Output: Heart Rate X Stroke Volume
Around 5L : (72 beats/m  70 ml/beat = 5040 ml)
Rate: beats per minute
Volume: ml per beat
EDV - ESV
Residual (about 50%)

59. Deep Vein Thrombosis

60. Clot

61. Leg Swelling from Deep Vein Thrombosis

62. Pulmonary Embolus

63. Vena Caval Filter

64. Cardiac Output: Heart Rate X Stroke Volume
Figure 14-26: The Wiggers diagram

65. Left Ventricular Pressure-Volume Loops
Pressure-volume loop plots LV pressure against LV volume through one complete cardiac cycle
Factors affecting:
Preload
Afterload
Contractility
IHSS
Valvular problems

67. Left Ventricular Pressure-Volume Loops
KNOW:
When the mitral and aortic valves are open and closed during each phase
When systole begins (B) and ends (D)
When diastole begins (D) and ends (B)
Diastolic filling occurs between points A and B
Ejection occurs between points C and D

68. Left Ventricular Pressure-Volume Loops
Acute changes in preload
Increased preload:
Filling increases
SV increases
Decreased preload:
Filling decreases
SV decreases
*NOTE: the ventricle empties to the same end-systolic volume after either an increase or decrease in preload

69. Left Ventricular Pressure-Volume Loops
Acute changes in Afterload
Increased afterload:
Ventricle empties less completely
SV decreases
Increase in BP
(shifts up and right)
Decreased afterload:
Ventricle empties more completely
SV increases
Decrease in BP
(shifts down and left)

70. Left Ventricular Pressure-Volume Loops
Altered contractility
Increased contractility:
Ventricle empties more completely
SV increases
BP increases
(shifts up and left)
Decreased contractility:
Ventricle empties less completely
SV decreases
BP decreases
(shifts down and right)

71. Left Ventricular Pressure-Volume Loops
Summary of concepts:
Alterations in preload: end-diastolic volume increases or decreases, but the amount of blood in the chamber at end-systole does not change
Stroke volume falls: result of either an increase in afterload or a decrease in contractility, the volume of blood in the LV chamber increases (chamber dilates)
Stroke volume increases: result of a decrease in afterload or an increase in contractility, the volume of blood in the LV chamber decreases (chamber shrinks)

72. Left Ventricular Pressure-Volume Loops
A = Normal
B = Mitral stenosis
C = Aortic stenosis
D = mitral regurgitation (chronic)
E = aortic regurgitation (chronic)

73. Regulators of the Heart: Factors Influencing Stroke Volume
Starlings Law – stretch
Force of contraction
Venous return:
Skeletal pumping
Respiratory pumping

74. Regulators of the Heart: Factors Influencing Stroke Volume
Figure 14-29: Length-force relationships in the intact heart

75. Regulators of the Heart: Factors Influencing Stroke Volume
Figure 14-31: Factors that affect cardiac output