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Bio-Med 350 Normal Heart Function and Congestive Heart Failure.

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Presentation on theme: "Bio-Med 350 Normal Heart Function and Congestive Heart Failure."— Presentation transcript:

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2 Bio-Med 350 Normal Heart Function and Congestive Heart Failure

3 Bio-Med 350 Basic Concepts: n The Cardiac Cycle n Myocardial Filling -- “Diastole” Compliance Left ventricular filling curves n Myocardial Emptying -- “Systole” Cardiac Output Frank-Starling Performance Curves n The relationship of filling and emptying: Pressure - Volume Loops

4 Bio-Med 350 Basic Definitions n Cardiac Output is defined as: Stroke Volume X Heart Rate n Blood Pressure is defined as: Cardiac Output X Systemic Vascular Resistance What happens to each of these during: Exercise? When LV filling is impaired?? When systolic function is impaired???

5 Bio-Med 350 What happens to the runner during exercise? OR “Why the jogger didn’t blow his top!”

6 Bio-Med 350 Basic Definitions n Cardiac Output is defined as: Stroke Volume X Heart Rate n Blood Pressure is defined as: Cardiac Output X Systemic Vascular Resistance

7 Bio-Med 350 Basic Concepts: #1 n The Cardiac Cycle

8 Bio-Med 350 The Normal Cardiac Cycle n Components of Diastole: Isovolumic relaxation Rapid Ventricular filling Atrial contraction (“kick”) n Components of Systole Isovolumic contraction L.V. Ejection

9 Bio-Med 350 Volume change during LV filling

10 Bio-Med 350 The Normal Cardiac Cycle n Let’s take a look at the cycle in some depth............

11 Bio-Med 350 The Cardiac Cycle

12 Bio-Med 350 Basic Concepts: #2 n The Cardiac Cycle n Myocardial Filling -- “Diastole” Compliance Left ventricular filling curves n Myocardial Contractility -- Systole Frank-Starling Performance Curves n The relationship of filling and emptying: Pressure - Volume Loops

13 Bio-Med 350 Left ventricular filling curves n Relationship of pressure to volume defines L.V. “stiffness” or “non-compliance” n At low pressures, almost linear

14 Bio-Med 350 Relationships to Remember n “Compliance” is proportional to change in volume over change in pressure n “Stiffness” is the inverse. n Stiffness is proportional to change in pressure over change in volume

15 Bio-Med 350 Normal vs “non-compliant” LV

16 Bio-Med 350 Basic Concepts: #3 n The Cardiac Cycle n Myocardial Filling -- “Diastole” Compliance Left ventricular filling curves n Myocardial Emptying -- “Systole” Cardiac Output Frank-Starling Performance Curves n The relationship of filling and emptying: Pressure - Volume Loops

17 Bio-Med 350 Mediators of Cardiac Output

18 Bio-Med 350 Relationships to Remember n “Preload” and “afterload” are defined as the wall tension during diastole and systole, respectively n Wall tension is defined as: P x r 2h (where h = wall thickness)

19 Bio-Med 350 Preload n Is the wall tension during ventricular filling n Is defined as P x r 2h during diastole!!!

20 Bio-Med 350 Why is volume the most important determinant of ventricular preload?? (Hint: look at the cardiac cycle)

21 Bio-Med 350 The Cardiac Cycle

22 Bio-Med 350 Afterload n Is the wall tension during ventricular ejection n Is defined as: P x r 2h during systole!!!

23 Bio-Med 350 Why is systolic pressure the most important determinant of ventricular afterload??? (Hint: look again at the cardiac cycle)

24 Bio-Med 350 The Cardiac Cycle

25 Bio-Med 350 How do we relate myocardial performance to: n Loading conditions: i.e. preload and afterload And how does “myocardial contractility” relate to all of the above??

26 Bio-Med 350 Frank - Starling Curves n L.V. “performance” curves relating: 1. L.V.E.D.P. (i.e." preload”) 2. L.V. “performance” (i.e. cardiac output)

27 Bio-Med 350 Frank-Starling Curves in CHF

28 Bio-Med 350 What happens to: n Heart rate n Blood pressure n Cardiac output n Vascular resistance n When: n LV filling falls n LV systolic function is impaired n The LV is non- compliant n Afterload increases

29 Bio-Med 350 How do we measure..... n Blood pressure n Cardiac output n Stroke volume n LVEDP n Systemic vascular resistance ?

30 Bio-Med 350 The Swan-Ganz Catheter

31 Bio-Med 350 Werner Forssman – 1929

32 Bio-Med 350 Right heart catheterization

33 Bio-Med 350 Right Heart Catheterization

34 Bio-Med 350 Measuring Cardiac Output n Fick Method -- O2 consumption A-V O2 difference n Thermodilution method -- “The Black Box”

35 Bio-Med 350 The Fick Principle Lungs Body O2

36 Bio-Med 350 Measuring O2 consumption The Waters Hood

37 Bio-Med 350 The Thermodilution Method n Similar in principle to the Fick method n Uses change in temperature per unit time, rather than change in O2 saturation n Requires a thermal probe in the right side of the heart

38 Bio-Med 350 Construction of Starling Curve for an individual patient

39 Bio-Med 350 Pressure - Volume Loops n Relate L.V. pressure to L.V. volume in a single cardiac cycle n Can be used to explore the effects of various therapies on stroke volume and L.V.E.D.P. Pressure (mm Hg)

40 Bio-Med 350 Pressure - Volume Loops n Holding afterload and contractility constant n Varying “preload”, measured as end- diastolic volume

41 Bio-Med 350 Heart Failure Forward Failure: Inability to pump blood forward to meet the body’s demands Backward Failure: Ability to meet the body’s demands, at the cost of abnormally high filling pressures

42 Bio-Med 350 Systolic vs. Diastolic Dysfunction n Systolic dysfunction Decreased stroke volume Decreased forward cardiac output Almost always associated with diastolic dysfunction as well n Diastolic Dysfunction One third of patients with clinical heart failure have normal systolic function – i.e. “pure” diastolic dysfunction

43 Bio-Med 350 Left Heart Failure

44 Bio-Med 350 Left Heart Failure

45 Bio-Med 350 Left Heart Failure

46 Bio-Med 350 Left Heart Failure

47 Bio-Med 350 Diastolic Dysfunction n Impaired early diastolic relaxation (this is an active, energy dependent process) n Increased stiffness of the left ventricle (this is a passive phenomenon) LVH LV fibrosis Restrictive or infiltrative cardiomyopathy

48 Bio-Med 350 Diastolic dysfunction due to LVH

49 Bio-Med 350 Diastolic dysfunction: Pressure – Volume Loop

50 Bio-Med 350 Left Heart Failure

51 Bio-Med 350 Compensatory Mechanisms for Heart Failure n Frank – Starling Mechanism n Neuro-humoral alterations n Left ventricular enlargement LV Hypertrophy  ↑ contractility LV “remodeling”  ↑ stroke volume

52 Bio-Med 350 Frank –Starling mechanism

53 Bio-Med 350 Neuro-humoral mediators

54 Bio-Med 350 Neuro-humoral mediators

55 Bio-Med 350 Left Ventricular enlargement n Concentric LVH Increased LVEDP Increased incidence of backward failure Decreased wall stress at expense of increased oxygen demand and increased LVEDP n Eccentric hypertrophy (cavity dilation and hypertrophy) Seen in volume-overload states Seen after acute MI (post-infarction “remodeling”) Increased stroke volume at the expense of increased wall stress, oxygen demand and LVEDP

56 Bio-Med 350 End results of “compensatory mechanisms”

57 Bio-Med 350 Left Heart Failure

58 Bio-Med 350 “Pseudo” Left Heart Failure Abnormally high filling pressure (PCW pressure) despite normal LV function and LVEDP

59 Bio-Med 350 Right Heart Failure n Very commonly a sequela of Left Heart Failure LVEDP PCW PA pressure Right heart pressure overload n Cardiac causes Pulmonic valve stenosis RV infarction n Parenchymal pulmonary causes COPD ILD n Pulmonary vascular disease Pulmonary embolism Primary Pulmonary hypertension

60 Bio-Med 350 Right heart vs. Left heart failure Left Heart failure Pulmonary congestion Reduced forward cardiac output: Fatigue Renal insufficiency Cool extremities Decreased mentation Right Heart failure Neck vein distension Hepatic congestion Peripheral edema Also may result in reduced forward cardiac output, but with clear lung fields


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