Bio-Med 350 Normal Heart Function and Congestive Heart Failure

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

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???

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

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

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

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

Bio-Med 350 Volume change during LV filling

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

Bio-Med 350 The Cardiac Cycle

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

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

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

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

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

Bio-Med 350 Mediators of Cardiac Output

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)

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

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

Bio-Med 350 The Cardiac Cycle

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

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

Bio-Med 350 The Cardiac Cycle

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??

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)

Bio-Med 350 Frank-Starling Curves in CHF

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

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

Bio-Med 350 The Swan-Ganz Catheter

Bio-Med 350 Werner Forssman – 1929

Bio-Med 350 Right heart catheterization

Bio-Med 350 Right Heart Catheterization

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

Bio-Med 350 The Fick Principle Lungs Body O2

Bio-Med 350 Measuring O2 consumption The Waters Hood

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

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

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)

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

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

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

Bio-Med 350 Left Heart Failure

Bio-Med 350 Left Heart Failure

Bio-Med 350 Left Heart Failure

Bio-Med 350 Left Heart Failure

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

Bio-Med 350 Diastolic dysfunction due to LVH

Bio-Med 350 Diastolic dysfunction: Pressure – Volume Loop

Bio-Med 350 Left Heart Failure

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

Bio-Med 350 Frank –Starling mechanism

Bio-Med 350 Neuro-humoral mediators

Bio-Med 350 Neuro-humoral mediators

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

Bio-Med 350 End results of “compensatory mechanisms”

Bio-Med 350 Left Heart Failure

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

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

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