4. Cardiac muscle mechanics
Page 1: Cardiac Muscle Mechanics
Introduction by Dr. Paul Leavis
Page 2: Lecture Objectives
Define preload, afterload, and contractility
Discuss factors affecting preload
Explain the Frank-Starling law of the heart
Identify events affecting afterload
Describe factors altering the inotropy of the heart
Page 3: Cardiac Output
Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)
Resting CO ≈ 72 beats/min x 70 ml/beat ≈ 5000 ml/min
HR max ≈ 220 - age
Stroke volume may increase up to 50% during exercise
Example exercise CO: 150 beats/min x 100 ml/beat = 15 l/min
Page 4: Heart Rate and Stroke Volume
Increased heart rate decreases diastole duration, possibly reducing stroke volume
Stroke volume paradoxically increases during exercise due to compensatory mechanisms
Page 5: Stroke Volume (SV) Regulation
SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
Three factors regulating SV:i) Preloadii) Afterloadiii) Contractility (Inotropy)
Page 6: Preload
Definition: Initial stretching of cardiac myocytes prior to contraction
Related to average ventricular sarcomere length at end diastole
Maximum wall stretch corresponds to EDV or EDP
Increases in EDV or EDP enhance contraction force
Page 7: Length-Tension Relationship
Isolated papillary muscle experiments demonstrate preload effects on force
Increased sarcomere length correlates with increased contractile force
Page 8: Early Experiments on Diastolic Stretch (Otto Frank, 1895)
Studied diastolic stretch by ligating the aorta and measuring peak isometric force
Found increases in EDV yield higher contractile forces
Page 9: Experiments with Ejecting Hearts (Ernest Starling, 1914)
Controlled filling pressure; increased filling pressure led to greater SV at constant aortic pressure
Page 10: Frank-Starling Law
More blood entering the heart during diastole results in greater stroke volume during contraction
Stretching cardiac fibers increases immediate contractile force
Page 11: Frank-Starling Law Details
X-axis: preload, EDV, EDP, sarcomere length, venous return
Y-axis: contractile force, SV
Page 12: Mechanisms Underlying Frank-Starling
Myofilament Overlap: Proper overlap facilitates optimal cross-bridge formation
Length-Dependent Activation: Stretch increases affinity of troponin C for Ca++
Page 13: Compliance Changes Affecting Preload
Compliance: volume change/pressure change ratio
Increased stiffness of ventricles decreases compliance
Ventricular hypertrophy lowers compliance
Dilation allows higher EDV at lower EDP
Page 14: Flow Volume Loops and Frank-Starling
Illustrations of SV regulation based on changes in EDV
Page 15: Summary of Preload Effects
Heart adjusts contraction force based on previous diastole filling volume
Increased/decreased venous return alters the ejected volume while maintaining ESV
Page 16: Afterload
Definition: Load against which the heart must contract to eject blood
Key components for left and right ventricle: aortic pressure and pulmonary arterial pressure
Wall stress equation: s = Pr/h
Page 17: Force-Velocity Relationship with Afterload
Increasing afterload reduces shortening velocity
Maximum shortening velocity reached at 0 afterload
Page 18: Effects of Increasing Aortic Pressure
Higher pressure yields reduced stroke volume due to increased force requirements and decreased velocity
Page 19: Flow-Volume Loop Implications
Increased afterload results in decreased SV and increased ESV in subsequent heartbeats
Page 20: Preload/Afterload Interrelationships
Increased afterload shifts Frank-Starling curve downward
Decreased afterload shifts curve upward
Page 21: Interrelationships Visualization
Changes in preload affect shortening velocity and isometric force generation
Changes in preload do not alter Vmax
Page 22: Contractility (Inotropy)
Inotropy: intrinsic cardiac function measure, independent of preload and afterload
Related to rate of force development during ejection
Increased by sympathetic stimulation, decreased by parasympathetic stimulation
Page 23: Impact of Inotropy on Frank-Starling Curve
Increased inotropy or decreased afterload enhances stroke volume at any preload
Page 24: Force-Velocity Curve and Inotropy
Increased inotropy raises velocity of shortening at any afterload
Page 25: Positive Inotropic Effects
Derived from increased Ca++ availability, binding to troponin C, and cross-bridge cycling
Chronic conditions can lead to loss of inotropy; drugs available for treatment
Page 26: LV Pressure and Preload Effects
Demonstrates relationship between preload and cardiac function
Page 27: LV Pressure and Inotropy Relationships
Illustrates how changing inotropy affects volume and pressure dynamics in the heart