1. CARDIAC OUTPUT

2. Cardiac Output, Venous Return and their Regulation
Cardiac output is controlled to maintain the proper amount of flow to tissues and to prevent undue stress on the heart.

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

4. Frank-Starling Law What goes into the heart comes out.
Increased heart volume stretches muscles and causes stronger contraction.
Stretch increases heart rate as well.
Direct effect on sino-atrial node
Bainbridge reflex (through the brain)

5. Cardiac Output
Depends on venous return, which, in turn, depends on the rate of flow to the tissues.
Rate of flow to tissues depends on tissue needs (i.e. it depends on Total Peripheral Resistance). Therefore, cardiac output is proportional to the energy requirements of the tissues.

6. Limit of Cardiac Output
Normal CO – 5 L/min
Plateau – 13 L/min
Hypereffective heart plateau – 20 L/min
Hypoeffective heart plateau – 5 L/min

7. Hypereffective Heart Effected by: Nervous excitation.
Cardiac Hypertrophy
Exercise – Marathon runners may get 30 to 40 L/min
Aortic Valve Stenosis

8. Hypoeffective Heart Valvular disease Increased output pressure
Congential heart disease
Myocarditis
Cardiac anoxia
Toxicity

9. Autonomic Nervous System
Causes increased cardiac output when vessels become dilated (dinitrophenol).
Causes venous constriction during exercise.

10. Disease States Lowering Total Peripheral Resistance
Beriberi: insufficient thiamine – tissues starve because they cannot use nutrients.
AV fistula: e.g. for dialysis.
Hyperthyroidism: Reduced resistance caused by increased metabolism
Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues.

11. Disease States Lowering Cardiac Output
Heart attack, valvular disease, myocarditis, cardiac tamponade, shock.
Shock: Nutritional deficiency of tissues.
Decreased venous return caused by:
Reduced blood volume
Venous dilitation (increased circulatory volume)
Venous obstruction

12. Changes in Intrapleural Pressure
Pericardial Sac
Generally shift the cardiac output curve in proportion to pressure change (breathing, Valsalva maneuver).
Cardiac Tamponade (filling of pericardial sac with fluid) lowers rate of change of CO with right atrial pressure
Heart
Rt. Atrial Pressure CO
tamponade
15 L/min

13. Determinants of Venous Return
Mean systemic filling pressure
Right Atrial Pressure
Resistance to Flow
Pressure change is slight. Thus, small increase in RA Pressure causes dramatic reduction in venous return. (mean systemic filling pressure).

14. Normal Venous Return Curve
Plateau: collapse of large veins ( => increased resistance)
Working Cardiac Output
5 L/min
Venous return with heart and lung removed.
Cardiac Output Curve
VR (CO) -4
Mean systemic filling pressure ~ 7 mm Hg
Rt. Atrial Pressure (mm Hg)

15. Filling Pressure
Mean Circulatory: The pressure within the circulatory system when all flow is stopped (e.g. by stopping the heart).
Mean Systemic: Pressure when flow is stopped by clamping large veins.
The two are close numerically.

16. Venous Return & Cardiac Output
Cardiac output increases with atrial pressure.
Normal atrial pressure is about 0 mm Hg.
Venous return (with heart and lungs removed) decreases with atrial pressure.
Working cardiac output is where venous return curve meets cardiac output curve.

17. Compensation for Increased Blood Volume
Increased CO increases capillary pressure, sending more fluid to tissues.
Vein volume increases
Pooling of blood in the liver and spleen
Increased peripheral resistance reduces cardiac output.

18. Effects of Sympathetic Stimulation
Increases contractility of the heart.
Decreases volume by contracting the veins.
Increases filling pressure
Increases resistance

19. Effects of Sympathetic Inhibition
Shifts CO to the right
Shifts venous return down and to the left
- Reduced CO
Venous return with heart and lung removed.
5 L/min
VR (CO) -4
Rt. Atrial Pressure (mm Hg)

20. Effects of AV Fistula Decreased VR resistance.
Slight increased CO because of reduced peripheral resistance.
After restoration of pressure (sympathetic)
Further CO increase.
Increased filling pressure.
Decreased kidney output (leads to higher fluid volume and more increase in CO).
Cardiac hypertrophy (caused by increased workload).

21. Measurement of CO
Electromagnetic/ultrasonic (transit time) flow meter.
Oxygen Fick method:
CO = (Rate of O2 absorbed by lungs)
[O2]la - [O2]rv
Indicator dilution method:
Inject cold saline (or dye) into RA, measure temperature (or concentration) in aorta.