1. CARDIAC OUTPUT

2. Cardiac Output Amount of blood pumped out by each ventricle per minute
In an average adult L\min.
In infants & children it is low
In elderly it is less than in the adult.

3. Stroke Volume
The amount of Blood ejected out of each ventricle per beat.
In an average adult at rest =
40-60ml

4. Stroke Volume X Heart Rate
Cardiac Output
Stroke Volume X Heart Rate

5. Cardiac Output from each ventricle should be equal
or otherwise
damming of blood will take place

6. Under which normal condition is CO from both ventricles not equal?

7. Cardiac Output decides the rate of flow to the tissues.
Rate of flow to tissues depends on tissue needs
Therefore, cardiac output is proportional to the energy requirements of the tissues.

8. CO---5L\min. CO—3L\min child Adult Obese Adult 3.8L\min.Sqm

9. Cardiac Index Cardiac Output per body surface area.
In an average adult it is —3.2L\min.\Sqm

10. Cardiac Index Reflects the efficiency of the system
Helps to compare between 2 individuals or
In the same individual in different situations

11. Cardiac Index
Cardiac Index (CI): Approximately 3 liters/min/m2 of body surface area.
CI varies with age, peaking at around 8 years.

12. Determining Factors

13. Factors determining Cardiac Output
Extra Cardiac
Venous Return
Preload
Resist. offered
Afterload ?
Cardiac
Heart Rate
Myocardial Contractility

15. Venous Return

16. Sympathetic Stimulation
Venomotor Tone
Sympathetic Stimulation N 10
Mean circulatory Pressure 5
Volume - L

17. Venomotor Tone Symp. Stimulation Symp. Inhibition Volume - L10
Mean circulatory filling Pressure 7 5
Symp. Inhibition
Volume - L

18. Rt.Atrial Pressure Venous Return (L\min.)
Effect of Intra thoracic Pressure
Venous Return (L\min.) 5
- 8
Rt.Atrial Pressure

19. Rt. Atrial Pressure-mm Hg10
Venous Return (L\min.)
Mean filling \ Systemic filling Pressure 5
--4
Rt. Atrial Pressure-mm Hg

20. Determinants of Venous Return
Mean systemic filling pressure
Right Atrial Pressure
Venomotor Tone
Pressure change is slight. Thus, small increase in RA Pressure or a reduction in mean systemic filling pressure causes dramatic reduction in venous return.

21. Cardiac Output Curve
5 L/min
(CO) 7 -4
Rt. Atrial Pressure (mm Hg)

22. Plateau: collapse of large veins
Working Cardiac Output
5 L/min
Cardiac Output Curve
VR (CO) 7 -4
Mean systemic filling pressure ~
Rt. Atrial Pressure (mm Hg)

23. Gravity

24. Simulates Muscle Pump
water
Legs immersed in water

25. The filling of the ventricle is dependent on the stiffness
&
therefore the Diastolic tension
Stiffness dependes on
Quality of muscle
Thickness of the walls
Dimension of the cavity
Shape
The angles of adj. muscle fibers

26. Compliance of the Ventricle
In the aged the compliance decreases
Replacement by fibrous tissue decreases the compliance.
Massive hypertrophy also decreases
Aneurism of Ventricles inc.

27. Inc. stiffness of chamber
Normal
LV End Diastolic Pressure
LV End Diastolic Diameter
Chamber stiffness increases as the chamber contracts because there is increase in thickness

28. The Rt.Ventricle is more compliant than the Lt. because it is thinner.

29. Atrial Systole increases the blood flow into the ventricles by 30% ,
Significant when the compliance of ventricles are low
Atrial Booster Pump .

30. LVEDP Length Pericardium Intact Constrictive Pericarditis
Pericardial Effusion
W\O Pericardium
LVEDP
Normal
Length

31. Ventricular Inter dependance
Alteration of filling in one chamber will alter the pressure –vol. relation in the other.
because of the resulting encroachment of Inter ventricular septum.

32. Venous Return Total Blood Volume Distribution of the Blood
Body Position
Intrathoracic Pressure
Venomotor Tone

33. Venous Return Rt.Atrial Pressure Atrial Booster Pump
Intrapericardial Pressure
Ventricular Compliance

34. Frank Starling’s Phenomenon
Based on length active tension relation
Force of contraction & extent of shortening depends on the initial length of the muscle

35. Tension (Percednt of maximum)
Skeletal Muscle
Tension (Percednt of maximum)
Cardiac Muscle
Card. Musc. Fetus
Sarcomere Length (microns)

36. Cardiac muscle is more stiff.
Length at Lmax averages 2.2 u.
At 20% beyond Lmax sarcomere elongate very little but the tension falls substantially
Diastolic sarcomere length is prevented from exceeding 2.3u
Contraction always happens in the steep portion of the curve

37. LV Pressure filling - mm Hg Tension --g 1 2 3 4 5 6
Actively Developed
Tension
LV Pressure filling - mm Hg
Tension --g
Sarcomere Length (microns)

38. The active Tension developed during isometric contraction is due to the extent of overlapping

39. Ca++ 5mM\l
Active Tension
Ca++ 2mM\l
Sarcomere Lentgh

40. The mechanical performance is more sensitive to changes in extracellular Ca++ at longer than at shorter muscle length----
increased contractility

41. The disengagement of myofilaments cannot explain the decrement in Active Tension
Cellular damage with stretching is responsible for reduction in tension development

42. The Vmax is little altered
Force Velocity relation
Increasing Muscle length
Velocity of shortening
Load

43. Stroke volume
Preload

44. In the intact heart the increase in preload augments the stroke volume & the velocity of wall shortening.
The maximum velocity of wall shortening at zero load Vmax does not change with length (preload)

45. Venous Return in Pregnancy Max.Inc. in Blood vol.—II Trimester

46. SUPINE POSITION
IVC
Gravid Uterus
LEFT LATERAL POSITION

47. Immediate Post Partum.
IVC
Gravid Uterus

48. What can increase the VR in the Fetus?

49. Myocardial Contractility
Inotropy is the contractile property independent of the EDV or Preload

50. The midwall fibers are circumferential-perpendicular to the long axis
The subendocardial fibers & subepicardial fibers run parallel to the long axis
Major axis
Minor axis
The midwall fibers are circumferential-perpendicular to the long axis
Isometric contraction- chamber becomes sperical

51. Isotonic contraction-The fibers shorten & thicken.
During ejection-
internal minor axis accounts for 85-90% of stroke volume.
Ratio of Major to Minor axis becomes
1.93 from 1.49
Change in shape & the arrangement of fibers will reduce the extent of shortening.

52. Inotropic agent At any given length, increases
Velocity & extent of wall shortening.
Peak force developed
Time to reach peak force developed decreases
Increases Stroke vol. & decreases duration of contraction.

53. Force Velocity relation with NE
Control
+NE
Velocity of shortening
Load

54. Adrenergic stimulation (Intrinsic)
Alpha receptors mediate inc.inotropy by inc. in Ca++ influx
Beta receptors through cyclic AMP
Sensitivity to Ca++ increases
Enhanced pumping of Ca++ into SR
Good Lusiotropic effect

55. Exogenous Inotropic agents
Loss of contractile mass
Physiological & Pharmacological depressants
Intrinsic Myocardial depression

56. Cardiac Output Curve
5 L/min
(CO) 7 -4
Rt. Atrial Pressure (mm Hg)

57. Cardiac Output Curve
5 L/min
(CO) 7 -4
Rt. Atrial Pressure (mm Hg)

58. Force Frequency Relation
A simple inc. in frequency in the Physiological range augments contractility
but
This effect is seen with depressed function rather than in the normal heart

59. Contractile state of Myocardium
Force Frequency Relation
Sympathetic & Catecholamines
Exogenous Inotropic agents
Contractile state of Myocardium
Intrinsic depression
Physio. & Pharmacologic depressants
Ioss of Myocardium

60. After Load
Force (Tension) or stress per unit of cross sectional area, acting on the fibers after the onset of shortening.

61. Peripheral Vascular Resistance
The physiological characteristics of the
Arterial tree (Aorta)
Blood column in the arterial system
Viscosity of blood

62. In diseased conditions what else can decide the After Load?
Valve size
Circumferential wall stress or Tension

63. After Load
Force (Tension) or stress per unit of cross sectional area, acting on the fibers after the onset of shortening.

64. Laplac’s Law
The Circumferential Wall Stress or Tension is directly related to the Intra ventricular pressure & the Radius & indirectly so to the wall thickness.
T = PR\h

65. What is the afterload during the different phases of cardiac cycle?
T = PR\h
During systole P increases, R decrease & h increases
therefore T tends not to increase too high.
Diastole-P decreases, R increases & h also dec.,
T –not much of a change

66. Force –Velocity Relation
The extent & maximum velocity of shortening for each contraction depends on the load at any given preload

67. Force Velocity relation
At a given muscle length
Velocity of shortening
Load

68. Force Velocity relation
Vmax
Normal
RVH
CHF
Velocity of shortening
Load

69. In mild Hypertrophy T = PR\h h increases, P increases
therefore T remains the same or dec.
However Myocardial contractility decreases.

70. Wall Tension decides the Myocardial O2 consumption.
Moderate or severe Hypertrophy
Hypertrophy
Muscles becomes more stiff because of Ischemia
-Wall Tension increases
Wall Tension decides the Myocardial O2 consumption.

71. Velocity of shortening
Normal
Velocity of shortening
Severe Hypertrophy
Circumferential wall tension

72. Circumferential wall tension
Normal
Ejection Fraction
Aortic Stenosis
Circumferential wall tension

73. Stroke volume
Active LV Pressure

74. In Pregnancy, what decides the After Load?
Why is Ejection into the Pulmonaary Artery more prolonged?
What decides the After Load to the LV in the fetus?

75. After Load to LV
AO with MI
PDA
Anemia
Ischemia

76. Homeometric Autoregulation Anrep Effect
A positive inotropic effect follows an abrupt inc. in systolic Aortic & LV Pressure
Reactive Hyperemia occurs
Related to recovery from transient subendocardial Ischemia

77. After load & Preload can also be influenced by the Heart under abnormal conditions

78. What is the minimum CO necessary to sustain life?