STRUCTURE OF THE VENTRICLE AND PHYSIOLOGICAL DETERMINANTS OF SYSTOLIC AND DIASTOLIC FUNCTION

1. STRUCTURE OF THE VENTRICLE AND PHYSIOLOGICAL DETERMINANTS OF SYSTOLIC AND DIASTOLIC FUNCTION Dr. MansiArora University College of Medical Sciences & GTB Hospital, Delhi

2. 1)Structure of the Heart and the ventricle 2)Diastolic function of the ventricle • Factors • Clinical implications 3)Systolic function of the ventricle • Factors • Clinical implications

3. STRUCTURE OF THE HEART CHAMBERS • Atria • Right and left • Superior • Separated by interatrial septum • Ventricles • Right and left • Inferior • Separated by interventricular septum

4. STRUCTURE OF THE HEART… PERICARDIUM • Double-walled sac • Encloses heart • Contains pericardial fluid (5-30 ml) • Greatly reduces friction

5. STRUCTURE OF THE HEART… HEART WALL • Epicardium (outer) • Also known as visceral pericardium • Myocardium • Thickest layer • Cardiac muscle • Endocardium • Smooth inner lining • Continuous with blood vessels

6. Left Ventricle • Largest chamber of the heart • Majority of the anterior and left lateral surfaces of the heart and also the apex • Wall is 8-15 mm thick • Tip of the apex 2mm thick-ellipsoidal shape

7. Left Ventricle • Laminar layering of spiral bundles • Subepicardial myocardium-longitudinal orientation • Middle segment-circumferential • Subendocardial myocardium-longitudinal • Eject blood in a cork-screw type motion (Base to apex)

8. Right ventricle • Wall thickness for an adult is 4-5 mm • Separated from left ventricle by interventricular septum • Crescent shaped

9. DIASTOLIC FUNCTION • Diastology- important focus of cardiac physiology • Heart failure may result from primary diastolic dysfunction in absence of, or before the appearance of systolic dysfunction eg:- • Ischemic heart disease • Hypertrophic obstructive cardiomyopathy • Pressure or volume overload hypertrophy

10. Determinants Of Left Ventricular Diastolic Function • EXTRINSIC FACTORS • Pericardium • Right ventricle • Intrapleural and mediastinal pressures • PHYSICAL PROPERTIES OF THE LEFT VENTRICLE • Volume • Wall thickness • Composition(scar, amyloid)

11. Determinants Of Left Ventricular Diastolic Function • MYOCARDIAL RELAXATION • Load • Inactivation • Spatial and temporal nonuniformity

12. Phases Of Diastole

13. PRESSURE VOLUME LOOP • a : Ventricular Filling • b : Isov. Contraction • c : Ejection • d : Isov. Relaxation • 1 : MV closes • 2 : Aortic valve opens • 3 : Aortic valve closes • 4 : MV opens

14. Factors Influencing LV Relaxation

15. RAPID FILLING AND DIASTASIS PHASE • Occurs after the mitral valve opens • Composes one-third of diastole • 60-80% of total LV volume enters the left ventricle • Initial portion of the phase - DIASTOLIC SUCTION • DIASTASIS PHASE - Follows rapid filling phase • No flow/slow filling - 5% of the total LV volume • LV and LA pressure almost equalizes

16. Determinants Of Transmitral Flow • MAJOR • LV compliance (stiffness) • Rate of rise of transmitral gradient • OTHERS • Pericardial constraints • MV recoil • Ventricular diastolic suction

17. Determinants Of Transmitral Flow… LV compliance Flow Diastolic dysfunction • Aging • Angina • Coronary artery disease • HOCM Various drugs to reduce myocardial stiffness-ACE inhibitors

18. Ventricular End Diastolic P- V Relation • Nonlinear relation • A : normal • B : increased compliance • C : decreased compliance

19. Determinants Of Transmitral Flow… • Rate of rise of transmitral gradient  if increased  accelerate the flow rate • High atrial pressure

20. ATRIAL SYSTOLE At the end of diastole just before closing of MV Only 15-20% of LV volume Essential in presence of diastolic dysfunction • Atrial systole continues to compensate for decreased LV compliance and LV filling initially maintained in diastolic dysfunction

21. Measurement Of Diastolic Function Small area of diastasis between E and A wave Measured by - Transmitral pulsed wave doppler pattern E wave - early passive flow A wave - represents atrial systole

22. Factors Leading To Diastolic Dysfunction FIBROSIS CELLULAR DISARRAY PASSIVE CHAMBER STIFFNESS HYPERTROPHY ASYNCHRONY ABNORMAL LOADING ISCHEMIA ABNORMAL Ca++ FLUX RELAXATION INCREASED DIASTOLIC PRESSURE

23. SYSTOLIC FUNCTION SYSTOLE • Period between closure of mitral valve& start of contraction  ejection of blood from the heart • Ventricular systolic function most often equated with CARDIAC OUTPUT • Volume of blood pumped by heart per minute • Both ventricles function in series, so their output are normally equal

24. SYSTOLIC FUNCTION… • C.O.= S.V. × H.R. • STROKE VOLUME -Ejected blood volume in each cardiac cycle Determined by- • Preload • Afterload • Myocardial contractility • Heart rate

25. PRELOAD • Volume of blood contained in LV cavity at end-diastole - LVEDV • Equal to ventricular wall stress at end-diastole • The relationship between the cardiac output and EDV is known as Frank Starling’s law of heart

26. FRANK STARLING LAW • The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank- Starling mechanism of the heart • When an extra amount of blood flows into the ventricles, the cardiac muscle itself is stretched to greater length • The muscle contract with increased force because the actin and myosin filaments are brought to a more nearly optimal degree of overlap force generation

27. Frank Starling Law Of The Heart = Increased blood volume = increased stretch of myocardium Increased force to pump blood out.

28. Effect Of Changes In Myocardial Contractility On Frank Starling Curve

29. FactorsAffecting Ventricular Preload • Venous return • Most imp. Determinant of RV preload & also LV preload (in absence of pulm./RV dysfunction) • Skeletal muscle pump • Blood volume • ↑ in total blood volume  ↑ in venous return.

30. Factors Affecting Ventricular Preload • Distribution of blood volume • Venous tone : major determinant of venous return • ↑ venous tone : • Sympathomimetics • Exercise • Anxiety • Marked hypotension • ↓ venous tone : • Sympatholytics • Nitrates • Spinal /epidural anaesthesia

31. Factors Affecting Ventricular Preload • Posture : positioning during surgery, ↓ in standing position. • Intrathoracic pressure : IPPV , thoracotomy. • Pericardial pressure : pericardial diseases. • Heart rate and rhythm • Increases in HR assoc. with greater reduction in diastole as compared to systole. • Vent. Filling impaired at high HR (>120 beats/min). • Absent/ ineffective atrial contractions  ↓ vent. Filling by 20 – 30%

32. FactorsAffecting Ventricular Preload • Ventricular compliance • Early diastolic compliance (rate of relaxation) reduced in : • Hypertrophy • Ischemia • Asynchrony • Late diastolic compliance (passive stiffness of ventricles) reduced in : • Hypertrophy • Fibrosis • Extrinsic factors : • Pericardial disease • Tumors • surgical compression

33. Perioperative Ventricular Hypovolemia/Decreased Preload CAUSES DIMINISHED INTRAVASCULAR VOLUME • Surgical bleeding • Extravasation • Excessive diuresis • Reduced fluid intake REDUCED VENOUS RETURN • Increased capacitance—anaesthetic, vasodilator, sympatholytic • Increased resistance to venous flow—atrial mass, tamponade, PEEP, pulmonary embolism

34. Perioperative Ventricular Hypervolemia/Increased Preload CAUSES • Regurgitantvalvular heart disease • Ischemic heart disease • Viral and idiopathic cardiomyopathy • Chronic pulmonary and systemic hypertension CONSEQUENCES • Increase wall tension • Increase myocardial oxygen consumption • Reduced contractility

35. AFTERLOAD • Equated with—

36. LAPLACE’S LAW If ventricle assumed to be spherical— Wall tension/stress=P × R/2H • P=Intraventricular pressure • R=Ventricular radius • H=Wall thickness LV– Ellipsoidal shape, then also this formula is applied

37. Intraventricular Pressure Depends on— 1) Force of ventricular contraction 2) Viscoelastic properties of the Aorta & its proximal branches 3) Viscosity & density of blood 4) Systemic vascular resistance(SVR)—Most imp. • Arteriolar tone is the primary determinant of SVR

38. Systemic/ Pulmonary Vascular Resistance Afterload mainly depends on SVR SVR= 80 x (MAP – CVP)/CO Right ventricular afterload mainly depends onPVR PVR=80 × PAP-LAP/CO RV wall is thinner than LV – More sensitive to increase in afterload

39. Effect of changes in afterload on cardiac muscle shortening during afterloaded contractions and on ventricular stroke volume

40. ANAESTHETIC IMPLICATION Cardiac output in patients with RV or LV impairment- • Very sensitive to acute increase in afterload as in presence of myocardial depression—as often occurs during anaesthesia

41. MYOCARDIAL CONTRACTILITY • It is intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload. • Depends on the rate of myocardial muscle shortening. • Depends on intracellular calcium concentration. • Increased contractility = Increased CO (SV) (positive ionotropism)

42. Factors Increasing Contractility 1) Sympathetic stimulation- e.g. catecholamines,exercise Increase force of Increase heart rate contraction (rate treppe effect or Bowditch phenomenon) 2) Parasympathetic inhibition 3) Positive ionotropic agents- e.g. digitalis

43. Factors Decreasing Contractility • Parasympathetic stimulation - decrease heart rate • Sympathetic inhibition - e.g. withdrawal of catecholamines, blockade of adrenergic receptors • Drugs - beta-blockers, calcium channel blockers • Myocardial depressants e.g. most anesthetic agents • Myocardial ischemia & infarction • Hypoxia • Acidosis

44. Determinants Of Systolic Function • ISOVOLUMIC CONTRACTION PHASE INDICES • dp/dt – change in ventricular pressure over time during systole • Derived from volume/pressure curves • As a measure of contractility • EJECTION PHASE INDICES • Most common use-measurement of systolic function • EF = EDV - ESV/EDV • Normal value=0.67±0.08

45. SYSTOLIC DYSFUNCTION Systolic dysfunction shifts the isovolumic pressure–volume curve to the right, decreasing the stroke volume from b–c to b'–c'.

46. DIASTOLIC DYSFUNCTION Diastolic dysfunction decreasesend-diastolic volume and shifts the diastolic pressure-volume relationship upward and to the left. This reduces the stroke volume from b–c to b'–c'

47. SUMMARY

48. Factors Leading To Diastolic Dysfunction FIBROSIS CELLULAR DISARRAY PASSIVE CHAMBER STIFFNESS HYPERTROPHY ASYNCHRONY ABNORMAL LOADING ISCHEMIA ABNORMAL Ca++ FLUX RELAXATION INCREASED DIASTOLIC PRESSURE

50. REFERENCES • Kaplan JA. Kaplan’s cardiac anesthesia. 5th ed. Cardiac physiology. p. 71-90. • Mohrman DE, Heller LJ. Lange cardiovascular physiology. 2006. The heart pump. • Guyton and Hall. Textbook of Medical Physiology. 11th edition. Heart muscle; the Heart as a pump and function of the Heart valves. • Ganong WF. 22nd edition. The heart as a pump. • Miller RD. Miller’s Anesthesia. 7th edition. Cardiac physiology.