1. Physiology of Ventricular Function Dr. Chris Glover Interventional Cardiology Director of Education University of Ottawa Heart Institute January 12, 2015

2. Objectives  Define preload, afterload, and contractility  Define cardiac output, stroke volume  How does load and contractility interplay with pump function  Fick equation (not)  Everyday examples

3. Terms to Define  PRELOAD  AFTERLOAD  CONTRACTILITY  COMPLIANCE  STROKE VOLUME  CARDIAC OUTPUT

4. CARDIAC OUTPUT  Volume of blood ejected per minute

5. Factors Affecting Stroke Volume  Stroke Volume is amount of blood ejected during each cardiac cycle  Determinants are –Preload : +ve –Afterload : -ve –Contractility : +ve

6. PRELOAD  The load on the ventricle wall set just prior to systole (the end of diastolic volume) Greater distension = Greater contraction  End-diastolic volume (EDV) and/or End- diastolic pressure (EDP) correlate with myocardial stretch

7. Starling’s Law of the Heart  the extent to which cardiac muscle contracts is determined by the initial fiber length prior to initiation of contraction". The preload (end diastolic volume) determines the initial fiber length and hence the degree of overlap of the actin-myosin filaments in each sarcomere. The force generated is thus proportional to the end diastolic volume.

8. STARLING LAW OF THE HEART  The more blood that enters the heart, the more blood that is pumped out of the heart

9. Preload - Muscle Fiber  Relation between muscle length and tension is curvilinear  Isometric contraction – tension generated proportional to length of muscle at time of contraction  Stretching optimizes myosin-actin interaction and increases myofilament sensitivity to calcium

11. Preload – Muscle fiber  Relationship between fiber length and tension in intact heart is fundamental to understanding function  Larger diastolic ventricular volume = More stretch on muscle fibers = greater contraction  Frank-Starling mechanism

12. PRELOAD

13. Preload  ↑ Venous Pressure - ↑ Preload  ↑ Atrial Contractility - ↑ Preload  ↑ length of diastole - ↑ Preload  ↓ ventricular compliance - ↓ Preload

14. CARDIAC OUTPUT  Volume of blood ejected per minute

15. Factors Affecting Stroke Volume  Stroke Volume is amount of blood ejected during each cardiac cycle  Determinants are –Preload : +ve –Afterload : -ve –Contractility : +ve

16. Pressure-Volume loops

17. Afterload and contractility are constantPreload

18. PRELOAD

19. Preload  ↑ Venous Pressure - ↑ Preload  ↑ Atrial Contractility - ↑ Preload  ↑ length of diastole - ↑ Preload  ↓ ventricular compliance - ↓ Preload

20. Afterload  Pressure generated by ventricle and size of chamber at end of contraction depends upon load against which the ventricle contracts

21. Afterload  Muscle fibers contract against fixed load (isotonic contraction)  Length of muscle at end of contraction directly related to magnitude of load - ↑ load → ↓ shortening ( ↓ stroke volume)  Final length → independent of length prior to stimulation

22. AFTERLOAD  the "load" to be lifted by contraction i.e. the aortic pressure  Equals arterial systolic pressure in absence of aortic obstruction

23. Afterload Constant preload/contractility

25. Contractility  Changes in the force of contraction independent of the initial fiber length and afterload  Relation b/w initial fiber length and force developed during contraction shifted upward  Achieve shorter final length for fixed afterload  Changes due to chemical hormonal interaction

26. CONTRACTILITY  When contractility is increased, a greater force is generated by the contraction, starting from a given preload. When contractility is decreased, a smaller force is generated by the contraction, starting from a given preload.

27. Contractility Constant preload/afterload

28. Left ventricular performance

30. Compliance  Pressure-volume relationship of chamber during filling  Reflects ease or difficulty with which chamber can be filled  ΔP/ΔV  Decreased with ischemia, hypertrophy, infiltration  ?increased in athletes

31. Compliance

32. Clinical - ↓ Preload  Low Preload – hypovolemia, bleeding  ↓ stroke volume  ↓ cardiac output  Treatment – replace losses (fluid, blood)

33. Clinical - ↑ preload  High Preload – CHF, Mitral/Aortic insufficiency  ↑ preload → ↑ EDP → Pulmonary congestion  Treatment – optimize contractility (Digoxin); reduce preload (diet, diuretics); fix valve (MR/AR)

34. Clinical - ↑ afterload  High afterload – Hypertension, aortic obstruction (aortic stenosis, hypertrophic cardiomyopathy)  Cardiac muscle hypertrophy reduces tension  ↑ hypertrophy → ↓ compliance → ↑ EDP → may lead to Heart Failure  Treatment – antihypertensives for hypertension; relieve obstruction for aortic obstruction

35. Clinical - Contractility  ↓ Contractility → Myocardial Infarction/ Cardiomyopathy → ↓ SV → ↓ CO  Treatment - ↑ contractility (digoxin, catecholamines); optimize preload/afterloead  Treat cause

36. Clinical - Compliance  ↓ compliance ; hypertrophy, ischemia, scar, infiltration  ↓ compliance → ↑ EDP for given EDV  Pulmonary congestion occurs at lower preload

37. Thank you Questions?