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Cardiovascular Biomechanics Instructor n n n n n n Robin Shandas, Ph.D. Associate Professor of Pediatric Cardiology and Mechanical Engineering [email protected] (303) 837-2586 (MWF) / (303) 492-0553 (T,Th) Office: ECME 265 Office Hours: T, Th 10-11 a.m. or by appointment (Please give me ~1-2 days notice for appointments). Cardiovascular Biomechanics, Spring 2004 1 Scope of the Course Mechanics and fluid mechanics of the cardiovascular system. Why take this course ? n n n n Bioengineering as applied to the cardiovascular area. Focused examination on the systems level. Understand challenges of some of the most severe health problems. Apply modeling and design principles. Cardiovascular Biomechanics, Spring 2004 2 Tentative outline Anatomy and Physiology of the Cardiovascular System Basic concepts n n Solid mechanics. Fluid mechanics. Blood rheology. Blood flow through arteries. Cardiac dynamics. Microcirculation (if time permits). Cardiovascular Biomechanics, Spring 2004 3 Textbook and Grading Required book: n Cardiovascular Physiology by Berne and Levy, Mosby. Homework Assignments (~ 10): 40% n n Most homework assignments will require independent research. Several HW assignments will involve class presentations. Midterm (1): 25% Final project and presentation: 35% Cardiovascular Biomechanics, Spring 2004 4 Plumber or Cardiologist ? Fixes leaky pipes (arterial dissections & aneurysms). Repairs valves in the main pump (valvular regurgitation). Expands blocked pipes (percutaneous transluminal coronary angioplasty – PTCA, stents) Replaces main pumping system (cardiac transplantation). Filters and purifies the water (dialysis). Cardiovascular Biomechanics, Spring 2004 5 Where does the engineer fit ? Understand physics of cardiovascular processes. n Models w mathematical; experimental; animal. n n Provide insight into how healthy systems work and how unhealthy systems adapt. New information on effect of treatment. Design diagnostics and prosthetics. n n Imaging and measurement. Artificial hearts; pacemakers; prosthetic valves… Cardiovascular Biomechanics, Spring 2004 6 History of Cardiovascular Study Galen (130-200 A.D.) n Palpated the pulse and classified according to strength, rate n Wrote On the Uses of the Parts of the Body of Man n First to disprove that arteries carried air William Harvey (1628) n First to postulate importance of blood circulation. Cardiovascular Biomechanics, Spring 2004 7 History - contd Stephen Hales (1733) n First to measure arterial pressure in an animal. n Correlated loss of pressure to loss of blood volume. n Likened arterial elasticity to “Windkessel” model. J.P. Poiseuille (1840) n Established relationship between flow, pressure gradient and diameter in tube flow. Moens (1878) n Pressure pulse transmission in elastic arteries. Osborne Reynolds (1883) n Description of transition from laminar (ordered) to turbulent (chaotic) flow in a tube. Fick (1864) n First use of a manometer to measure pressure. Otto Frank (1903) n Stipulated the relationship between ventricular filling and contraction. John Womersley (1954) n Mathematical relationship between pressure and flow. Cardiovascular Biomechanics, Spring 2004 8 Scope of the problem Mechanics: n Heart w 3 layered fiber-reinforced structure with multiple fiber orientations. w Highly dynamic. n Arteries w Multilayered thick walled structures with a combination of linear and non- linear viscoelastic elements. w Combination of passive and active elements. n Capillaries w Thin walled dynamic structures with predominantly active elements. n Veins w Mainly passive multilayered structures, easily collapsible. Cardiovascular Biomechanics, Spring 2004 9 Scope of the problem Fluid Mechanics n n Unsteady flow. Large range of flow conditions. w Reynolds number: <1 in capillaries ‡ >10,000 in turbulent jets within the heart. w Tube flow, suddenly started jets, fully and transitionally turbulent pulsating jets, sheet flow, entrance flow, curved pipe flow, boundary layer separation, etc. n n Non-newtonian fluid (shear-thinning). Complex fluid-structure interactions. Cardiovascular Biomechanics, Spring 2004 10 How to tackle this problem ? Simplify, simplify, simplify… Couple clinical/physiological need with modeling approach. Newtonian fluid n Ok assumption for larger vessels w High shear conditions. From steady to oscillating to pulsatile flow. n Steady flow assumption ok for veins, capillaries. Linear to quasi-linear mechanics. n Ok for certain arteries (pulmonary artery). Simplify fluid-structure interactions. n No viscoelasticity, limited or no pressure pulse reflection interactions, harmonic analysis. Cardiovascular Biomechanics, Spring 2004 11 The Cardiovascular system One of 3 major systems. n Endocrine – Chemical w Regulation of various body functions (long term). n Nervous – Electrical w Communication & short-term regulation and control. n Cardiovascular – Mechanical w Delivery of nutrients, removal of waste w Thermal & pressure regulation. w Efficient regulation of gas/nutrients. Cardiovascular Biomechanics, Spring 2004 12 The Cardiovascular system Essentially a plumbing system to deliver nutrients to tissue. Components: n n n n n Pump (heart) Major tubing (arteries) Minor connections and branches (arterioles). Nutrient transfer (capillaries) Return tubing (venules and veins). Capillary network is the focus of the plumbing since this is where nutrient/waste transfer takes place. Cardiovascular Biomechanics, Spring 2004 13 Cardiovascular System Heart: 2 Chambers in Series Pulmonary circulation in between right heart and left heart. Systemic circulation refers to remaining circulatory systems. Left heart provides major component of work to drive blood through the systemic circulation. Heart pulsation: Systole (Contraction) and Diastole (Relaxation/Filling) Cardiovascular Biomechanics, Spring 2004 14 Flow through the heart Superior Vena Cava RV RA O2 In + CO2 Out via Diffusion Right & Left Lungs LA LV Valves Inferior Vena Cava RA -- Right Atrium RV -- Right Ventricle Cardiovascular Biomechanics, Spring 2004 LA -- Left Atrium LV -- Left Ventricle 15 Anterior Surface of the Heart Cardiovascular Biomechanics, Spring 2004 16 Interior of the Left Ventricle Cardiovascular Biomechanics, Spring 2004 17 Mechanical Events in the Left (Right) Ventricle Relaxation or Diastole • Blood fills ventricle from atrium -- mitral (tricuspid) valve opens. Atrial Systole or Contraction • Atrium contracts to expel remaining blood and “prime” ventricular pump. Contraction or Systole • Ventricle contracts, aortic (pulmonic) valve opens, blood is ejected into the aorta. Cardiovascular Biomechanics, Spring 2004 18 Major Arteries and Veins Arteries and Veins usually adjacent to each other. Large arteries and veins: 25 - 30 mm in diameter. Many interventional procedures (cardiac angiography, catheterization) use the femoral artery (left side) or femoral vein (right heart) as the origin for access to the heart. Cardiovascular Biomechanics, Spring 2004 19 Major Arteries and Veins Original contraction is pulsatile. However, flow in capillaries and veins is almost steady state, due to the elasticity of the large arteries. Pulse Pressure = Systolic Pressure - Diastolic pressure Cardiovascular Biomechanics, Spring 2004 20 Pressure Drop in Cardiovascular System Small arteries produce the largest pressure drop Cardiovascular Biomechanics, Spring 2004 21 Functional Flow Area Capillaries contain maximum crosssectional area Cardiovascular Biomechanics, Spring 2004 22 Organization of Skeletal/Cardiac Muscle Cardiovascular Biomechanics, Spring 2004 23 Heart Muscle - Cardiomyocyte Sarcomere = Fundamental contractile apparatus; Actin, Myosin - Proteins Cardiovascular Biomechanics, Spring 2004 24 Sliding Filaments - Key to Contraction Cardiovascular Biomechanics, Spring 2004 25 Properties of Skeletal & Cardiac Muscle Active -vs- Resting Tension Cardiovascular Biomechanics, Spring 2004 26 Differences Between Skeletal & Cardiac Muscle 1 Many more structures present in cardiac muscle (more interconnections among cells. Cardiovascular Biomechanics, Spring 2004 27 Differences Between Skeletal & Cardiac Muscle 2. Many more mitochondria within cardiac muscle cells. Foodstuff + O2 · CO2 + H2O + Energy (ATP) Glucose is a common food • Energy for cellular processes provided by Adenosine TriPhospate (ATP) • Chemical (potential) energy stored in the covalent bonds between atoms of a molecule. • ATP has much higher (≈ 2X) potential energy stored in its terminal bonds. • Release of one of the terminal phosphates releases ≈ 7300 calories / mole (Compare to ≈ 3000 cal/mole for typical chemical bonds) • Mitochondria are part of the cellular apparatus responsible for providing energy to the cell. Cardiovascular Biomechanics, Spring 2004 28 Differences Between Skeletal & Cardiac Muscle 2. Many more mitochondria within cardiac muscle cells. • Skeletal muscle can build an “oxygen debt” by transforming glucose into lactate - “Glycolysis.” -- Anaerobic (absence of O2) activity. • However, cardiac muscle cannot withstand oxygen debt Constant aerobic activity. • Mitochondria in cardiac muscle cells function to constant energy supply for cellular processes and muscular contraction. Cardiovascular Biomechanics, Spring 2004 29 Differences Between Skeletal & Cardiac Muscle 3. Many more capillaries feeding cardiac muscle cells. • Skeletal muscle: 1 capillary feeds ≈ 5 - 10 muscle fibers. • Cardiac muscle: 1 capillary per fiber (cardiomyocyte). • Constant aerobic activity requires constant input of O2 and removal of CO2. • However, cardiac muscle cannot withstand oxygen debt Constant aerobic activity. • Mitochondria in cardiac muscle cells function to constant energy supply for cellular processes and muscular contraction. Cardiovascular Biomechanics, Spring 2004 30 The Heart Wall Interior of ventricular chamber (Endocardium) Middle of ventricular wall (Myocardium) Exterior of wall (Epicardium) Cardiovascular Biomechanics, Spring 2004 31 Ventricular Contraction A Normal Contraction B Hyperdynamic, via the use of a positive inotropic agent C Heart Failure Inotrope - Affects cardiac contraction Chronotrope - Affects heart rate Cardiovascular Biomechanics, Spring 2004 32 The Frank-Starling Mechanism Heart contraction is largely dependent on loading. Heart muscle expands to maximum during filling. Maximal length produces maximum tension on the muscle, resulting in forceful contraction. Therefore, greater filling (more volume entering the heart) produces greater ejection (more volume leaving). Cardiovascular Biomechanics, Spring 2004 33 Starling’s Original Experiment Venous pressure increased Venous pressure back to baseline Control Period Cardiovascular Biomechanics, Spring 2004 34 The Frank-Starling Mechanism Experimental Validation Cardiovascular Biomechanics, Spring 2004 35 The Frank-Starling Mechanism Increase in preload (more blood entering ventricle during diastole) Extra amount entering ventricle is ejected (Balance is maintained) End Diastolic Volume (EDV) increases Move further on the length/tension curve of cardiac muscle T/Ao Increased cardiac contraction L’/Lo Cardiovascular Biomechanics, Spring 2004 36 The Frank-Starling Mechanism • Compensation for increased preload or afterload via increase in cardiac contraction so that cardiac output matches venous return. Preload • Left ventricular filling pressure (End Diastolic pressure and/or volume in the ventricle). Afterload • Peripheral resistance (Resistance in the arterial system downstream of the left ventricle). Why would preload and/or afterload increase ? Cardiovascular Biomechanics, Spring 2004 37 The Frank-Starling Mechanism Cardiovascular Biomechanics, Spring 2004 38 Pressure-Volume Loops Cardiovascular Biomechanics, Spring 2004 39 Effect of a Positive Inotrope on PV Loop Cardiovascular Biomechanics, Spring 2004 40 Atrioventricular Valves: Tricsupid & Mitral Semilunar Valves: Pulmonary & Aortic Cardiovascular Biomechanics, Spring 2004 41 Aortic Valve -- Longitudinal View Cardiovascular Biomechanics, Spring 2004 42 Mechanism of mitral valve closure Henderson Y, Johnson FE: Two modes of closure of the heart valves, Heart, 4:69-82, 1912 Cardiovascular Biomechanics, Spring 2004 . 43 Mechanism of mitral valve closure Development of an adverse pressure gradient Assume: No-viscous or gravity effects, uniform flow, no flow in C initially: Momentum equation: ∂U + U ∂U = - 1 ∂P r ∂x ∂t ∂x No acceleration with x, So, according to continuity: ∂U/∂x = 0 During deceleration, ∂U/∂t < 0 ---> ∂P/∂x > 0 --> PB > PA Cardiovascular Biomechanics, Spring 2004 44 Flow downstream of the aortic valve Cardiovascular Biomechanics, Spring 2004 45 “Windkessel” Model for Aortic Flow • Aorta represented by an elastic chamber. • Peripheral blood vessels represented as a rigid tube with constant resistance. • Ventricle pulses --> energy used to distend the aortic walls and to drive flow downstream. • Energy used to extend the walls is subsequently used to maintain forward flow during diastole. • In the elastic chamber, rate of change of volume is assumed to be proportional to pressure. • Flow rate out is assumed to be proportional to pressure gradient and resistance (electrical analog). Cardiovascular Biomechanics, Spring 2004 46 “Windkessel” Model for Aortic Flow dp p Q = K dt + R Q = Flow rate; p = pressure; R = Resistance Cardiovascular Biomechanics, Spring 2004 47 Electrical Activity of the Heart Action Potential: Cycle of changes in transmembrane electrical potential that characterizes excitable tissue. Cell Voltage = 0 + - + - Cell Voltage = -90 mV Cardiovascular Biomechanics, Spring 2004 48 Fast -vs- slow response cardiac fibers Cardiovascular Biomechanics, Spring 2004 49 Muscle twitch occurs after peak action potential is reached Cardiovascular Biomechanics, Spring 2004 50 Chemical and electrical gradients around a resting cardiac cell Cardiovascular Biomechanics, Spring 2004 51 Conduction system of the heart Cardiovascular Biomechanics, Spring 2004 52 The Electrocardiogram (EKG) Cardiovascular Biomechanics, Spring 2004 53 Action Potential SA Node Atrial Muscle AV Node HIS Bundle Bundle Branches Purkinje Fibers Ventricular Muscle Cardiovascular Biomechanics, Spring 2004 54 Cardiovascular Biomechanics, Spring 2004 55