1. Cardiac cycle Phase1. Atrial systole: AV valves open; aortic and pulmonic valves closed Phase1. Atrial systole: AV valves open; aortic and pulmonic valves closed

2. Cardiac cycle Phase2. Isvolumetric contraction: all valves closed Phase2. Isvolumetric contraction: all valves closed

3. Cardiac cycle Phase3. Rapid ejection: Pulmonic valves open AV valves closed Phase3. Rapid ejection: Pulmonic valves open AV valves closed

4. Cardiac cycle Phase4. Reduced ejection: Pulmonic valves open AV valves closed Phase4. Reduced ejection: Pulmonic valves open AV valves closed

5. Cardiac cycle Phase5. Isvolumetric relaxation All valves closed Phase5. Isvolumetric relaxation All valves closed

6. Cardiac cycle Phase 6: Rapid filling: AV valves open Semilunar valves closed Phase 6: Rapid filling: AV valves open Semilunar valves closed

7. Cardiac cycle Phase7. Reduced filling: AV valves open; aortic And pulmonic valves closed Phase7. Reduced filling: AV valves open; aortic And pulmonic valves closed

9. Summary of intracardiac pressures

10. At heart rates up to about 180, filling is adequate as long as there is ample venous return

11.  Preload is the initial stretching of the cardiac myocytes prior to contraction. Preload

12. 12 Tricuspid valve stenosis Pulmonic valve stenosis Pulmonary Hypertension Factors Determining Ventricular Preload

13. 13 Plays an important role in balancing the output of the two ventricles. ventricular function curve Frank-Starling Mechanism

14. 14 Frank-Starling Mechanism

15. 15  length-dependent activation. The intact heart under physiologic conditions operates at sarcomere lengths in the range of 1.8–2.2  Experimental evidence supports three possible explanations: 1.Increased sensitization of troponin C to calcium 2.Change in calcium homeostasis within the cell 3.Closer of myosin molecules to each other  length-dependent activation. The intact heart under physiologic conditions operates at sarcomere lengths in the range of 1.8–2.2  Experimental evidence supports three possible explanations: 1.Increased sensitization of troponin C to calcium 2.Change in calcium homeostasis within the cell 3.Closer of myosin molecules to each other What mechanisms are responsible for the increase in force generation with increased preload in the heart?

16.  Afterload

17.  Inotropy

19.  ↑ Heart Rate  ↑ Inotropy  ↑ Afterload  ↑ Preload* Changes in preload affect oxygen consumption much less than do changes in the other factors Factors Increasing Myocardial Oxygen Consumption Increasing the end-diastolic volume by 50% (by a factor of 1.5) represents only a 14% (cube root of 1.5) increase in wall stress at a given ventricular pressure, whereas a 50% increase in pressure increases wall stress by 50%.