Exam questions Flashcards

(44 cards)

1
Q

What is the role of residual strain in the vessel wall?

A

Related to the remodelling of the blood vessel wall. Our blood vessels remodel themselves when stress changes. The stress-growth law provides a biomechanical foundation for tissue engineering.

The zero stress state of a blood vessel consists of open-sector segments whose opening angles vary along the longitudinal axis of the vessel. When the homeostatic state of the blood vessel is changed the opening angle will change. Thus, residual stresses are related to the remodeling of the blood vessel wall. Our blood vessel remodels itself when stress changes.

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2
Q

What are smooth muscle cells?

A

SMCs are present in most contractile organs. They serve as a contractile cell of arteries, arterioles and veins. They appear as spindle-shaped configurations. In blood vessels they are responsible for maintaining blood pressure. In the vessel wall SMCs are mainly aligned in circumferential vessel direction and they communicate with each other through tightor gap-junctions.

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3
Q

Explain the basic structure and physiological function of the adventitial layer of the large arteries?

A

Consists of:
Extracellular matrix components(Dense network of collagen fibres, and other connective tissue), fibroblasts(about 10%), vasa vasorum and nerves.

Physiological function:

  • anchoring blood vessel to surrounding tissues or binds structures together/holds the vessel in relative position.
  • nervous connection to SMCs in the medial layer
  • synthesis of collagen by fibroblasts
  • protect the media from overextension
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4
Q

Draw the hydraulic and electric representations of a three-element Windkessel model. Denote also the introduced parameters.

A

(((Flow q(t), pressure p(t) describe the system sate)))

ELECTRIC: impedance Za, capacitance C, resistance R

HYDRAULIC: aortic impedance, arterial capacity and vascular bed resistance

TRUE: veins, heart, elastic arteries(aorta), peripheral resistance

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5
Q

How is the rate of deformation tensor defined?

A

see fig deformation_tensor

can also be written:

d = 0.5( l + l^T)
(where l is the spatial velocity gradient)

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6
Q

How is the blood pressure distributed in the cardiovasular system?

A

It is higher in the systolic circuits than in the pulmonary circuits. Blood pressure drops beyond large arteries.

In general: higher in the largest vessels, lowest in capillaries …Highest in the aorta.

See fig P_distrib

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7
Q

Detail a generalised Maxwell model. Draw its mechanical representation as well as creep and relaxation responses.

A

See fig Maxwell

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8
Q

What determines the viscosity of blood and why?

A

Hematocrit accounts for about 50% of the difference between normal and high blood viscosity. Basically a higher percentage of RBCs to total blood volume, results in thicker blood

Hematocrit = volume RBCs/Total blood volume

Stationary the red blood cells are clumped together and at low shear they start to drift apart and the viscosity decreases. At high shear they elongate in the flow direction which decreases the viscosity even more. Because of that, blood behaves as a non-Newtonian fluid. As such, the viscosity of blood varies with shear rate. Blood becomes less viscous at high shear rates like those experienced with increased flow such as during exercise or in peak-systole. Therefore, blood is a shear-thinning fluid. Contrarily, blood viscosity increases when shear rate goes down with increased vessel diameters or with low flow, such as downstream from an obstruction or in diastole.

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9
Q

How is the first Piola-Kirchoff stress defined?

A

see fig PK

Transpose of the nominal stress: P = N^T = JsigF^-T

Where sigma is the Cauchy stress tensor, F^-T the transposed inverse of the deformation gradient and J = det F (volume change).

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10
Q

Sketch and explain the basic structures of a sarcomere.

A

See fig sarcomere

Contractile units in muscles. Composed of long, fibrous proteins as filaments that slide past each other when a muscle contracts or relaxes. Two of the important proteins are myosin, which forms the thick filament, and actin, which forms the thin filament

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11
Q

Explain methods to estimate arterial compliance.

A

1) C = ΔV/ΔP
2) During the diastolic phase, the flow is 0. The arterial compliance is then determined using the model’s governing equations and either the decay time method or area method.

IN VIVO:
Arterial compliance is an index of the elasticity of large arteries (such as the thoracic aorta) and is an important cardiovascular risk factor!

1) Ultrasound
2) Magnetic Resonance Imaging (MRI)

IN VITRO:
uniaxial and biaxial tensile testing

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12
Q

Why do the Maxwell and Kelvin-Voigt fail to represent a solid?

A

Maxwell model does not exhibit strain recovery, even at small strains, so it is usually thought of as a fluid model. Kelvin-Voigt does exhibit strain recovery, so qualitatively, it behaves like a solid. However, neither of these models describes the behavior of fluids or solids quantitatively.

KELVIN VOIGT: The deformation of a dashpot connected in parallel to a spring, as in the Kelvin–Voight model, is restricted by the response of the spring to the applied loads. The dashpot in the Kelvin–Voight model cannot undergo continuous deformations. Therefore, the Kelvin–Voight model represents a viscoelastic solid behavior.

MAXWELL: The Maxwell model does not exhibit strain recovery, not even at small strains. The spring is used to represent the elastic solid behavior and there is a limit to how much a spring can deform. The dashpot represent the fluid behavior and is assumed to deform continuously as long as there is a force there to deform them. A force applied will cause both the spring and the dashpot to deform. The deformation of the spring
will be finite but the dashpot will keep deforming as long as the force is maintained. Therefore, the overall behavior of the Maxwell model is more like a fluid than a solid.

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13
Q

What is model verification and validation?

A

Model validation: The assurance that the model meets its PURPOSE and represents the real system. (Are the correct equations solved – Does the model reflect the
particular feature of the real object?)

Model verification: The evaluation of whether or not the model matches SPECIFICATIONS and assumptions deemed acceptable for the given purpose of application. (Are the equations solved correctly?)

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14
Q

Compute the matrix representation of the deformation gradient, the right and the left Cauchy-Green strains for simple shear.

A

See fig GL_simple_shear

Deformation gradient: F(X) = dx/dX =
(1 gamma 0 ;
0 1 0;
0 0 1)

right Green-Lagrange strain: C = F^T F =
(1 gamma 0 ;
gamma 1 + gamma^2 0;
0 0 1)

left Green-Lagrange strain: b = F F^T
(1 + gamma^2 gamma 0 ;
gamma 1 0;
0 0 1)

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15
Q

Describe the basic mechanism that causes the typical non-linear properties of vascular tissue. Draw a sketch that indicates the role of collagen and elastin.

A

see fig collagen_vs_elastin

Elastin is activated first while collagen provides stiffness att higher stress levels. These two properties combined create the following curve.

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16
Q

Provide the Navier-Stokes equation.

A

see fig Navier_stokes

div sig + f = rho (Dv/Dt)

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17
Q

Frank Starling effect

A

The Frank Starling effect stipulates that if blood volume of the heart increases then the heart muscle will contract(at the end of the diastolic phase)

..increased filling pressure of the right heart results in increased cardiac output.

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18
Q

Explain the basic structure and physiological function of the medial layer of large arteries.

A

The medial layer consists of smooth muscle cells (30 - 60%), an extracellular
matrix which is made of elastin fibrins (from elastin sheets 5 - 25%), collagen fibres/bundles (15 - 40%) and other connective tissue like proteoglycan (15 - 25%).

Physiological functions:
• Regulate flows by vasocontriction/vasodilation (Muscular acitivity regulated by autonomous nervous system. Related to physical activity or thermal regulation.)
• Key for the physiological mechanical properties (Cardiovascular system function)
• Synthesis of connective tissue (Collagen, elastin)
• Regulates wall stress by thickness adaption (Tension of a medial lamellar units (MLU) keeps constant at about 2.0 +-0.4 N/m.)

19
Q

Provide a matrix representation of the engineering strain tensor and detail the
meaning of the different components.

A

See picture eng_strain.

u = (u1, u2, u3) is the displacement vector and x1, x2 and x3 are the directions in the coordinate system.

Example: epsilon_11 is the change in length in the x1-direction divided by the original length in the same direction.

20
Q

Give the elasticity tensor for a linear transversely isotropic material.

A

See fig Elas_LinTranIso

21
Q

Compute the matrix representation of the deformation gradient, the right and left
Green-Lagrange strains for simple tension.

A

see fig GL_simple_tension

F = [lam 0 0
0 1/sqrt(lam) 0
0 0 1/sqrt(lam)]

22
Q

Detail a Kelvin-Voigt model. Draw its mechanical representation as well as creep and relaxation responses.

A

See fig Kelvin_Voigt

23
Q

Sketch the dependence of blood viscosity from the shear rate.

A

see fig blood_shear

24
Q

How can the Cauchy stress for a general isotropic fluid be written?

A

see fig Iso_fluid

25
How is the hydraulic resistance of blood vessel distributed over the cardiovascular system?
The resistance against flow in the vascular system is defined by the smallest vessels. The resistance can be determined by R = delta p/q = 8*eta*l/pi*r^4 see Resistance_formulas where r is the radius of the vessel. Since the resistance is dependent on the radius to the power of four, only small vessel can change the resistance.
26
What are principal stresses?
The principal stresses are mathematically defined as the eigenvalues of the stress matrix. In the principal directions the shear stress vanishes, only stress acts on them. There are three independent principal stresses usually ordered as sigma 1 > sigma 2 > sigma 3. The maximum normal stress that acts on any plane in a point is defined by the largest principal stress s1. Correspondingly, the minimum stress is given by the smallest principal stress s3.
27
What is polar decomposition?
Polar decomposition of a square matrix separates the matrix into a component that stretches the space along a set of orthogonal axes and one part that rotates. Example: F = RU where F is the deformation gradient, U the unitary matrix that stretches and R the rotation matrix.
28
How is the Cauchy stress defined?
...defined as sigma = P/A where P is the force acting in the same direction as the stress considered and A is the area which the force acts on (after deformation). ...the measure of loading, how much force acts on a particle. ...used for stress analysis of material bodies experiencing small deformations: It is a central concept in the linear theory of elasticity. see fig Cauchy_stress
29
Show that the time derivative of the Cauchy stress is not objective.
See fig Cauchy_not_objective
30
Sketch and explain the steps of a cross-bridge cycle known from skeleton muscle?
see fig Crossbridge 1) Myosin heads hydrolyse ATP and become reoriented and energised 2) Myosin heads bind to actin, forming crossbridges 3) Myosin cross bridges rotate toward center of the sarcomere (power stroke) 4) As myosin heads bind ATP, the cross bridges detach from actin 1) ...
31
Give the governing equations for resistance, capacity and inertance (inductivity) used in Windkessel models.
2-ELEMENT: q(t) = q_r(t) + q_c(t) .......= p(t)/R + C(dp(t)/dt) 3-ELEMENT: q(t) = q_r(t) + q_c(t) .......= p*(t)/R + C(dp*(t)/dt) p(t) = p*(t) + Zq(t) 4-ELEMENT: q(t) = q_r(t) + q_c(t) .......= p*(t)/R + C(dp*(t)/dt) p(t) = p*(t) + Zq(t) L(dq_l(t)/dt) = Zq_z(t) q(t) = q_l(t) + q_z(t)
32
How does the length of a muscle fibre (sarcomere) influence the contractile force? Draw a schematic diagram.
see fig Sarcomere_length Muscles exist in this state to optimize the force produced during contraction, which is modulated by the interlaced myofilaments of the sarcomere. When a sarcomere contracts, myosin heads attach to actin to form cross-bridges. Then, the thin filaments slide over the thick filaments as the heads pull the actin. This results in sarcomere shortening, creating the tension of the muscle contraction. If a sarcomere is stretched too far, there will be insufficient overlap of the myofilaments and the less force will be produced. If the muscle is over-contracted, the potential for further contraction is reduced, which in turn reduces the amount of force produced.
33
Compute the matrix representation of the deformation gradient, the right and left Green-Lagrange strains for equi-biaxial tension.
see fig GL_equi_biaxial
34
What is the hemolysis index and what does it characterize?
The hemolysis index reflects RBC damage. Hemolysis index = Free hemoglobin in plasma / Total hemoglobin in blood Hemolysis is the rupturing (lysis) of red blood cells (erythrocytes) and the release of their contents (cytoplasm) into surrounding fluid. One cause of hemolysis is the action of hemolysins, toxins that are produced by certain pathogenic bacteria or fungi. Hemolysins damage the red blood cell’s cytoplasmic membrane, causing lysis and eventually cell death.
35
What are the objectives of blood and how is blood composed?
OBJECTIVES: • Delivers nutrients and oxygen to the cells. • Transports metabolic waste produvts away from cells. • Has key immunological functions. • Coagulates, which is the firts step of healing a wound. • Transports information in the form of hormones. • Regulates temperature and PH. CONSISTS OF: • Erythocytes (red blood cells) - transport oxygen and they are highly deformable • Leukocytes (white blood cells - immune response • Thrombocytes (platelets) - coagulates • Plasma
36
Explain the basic mechanism of the Windkessel principle.
The walls of large arteries contain elastic fibres formed of elastin. These arteries distend when the blood pressure rises during the systolic phase and recoil when the blood pressure falls during the diastolic phase. Since the rate of blood entering these arteries exceeds the rate which leaves them, there is a net storage of blood in the aorta and the large arteries during the systolic phase, this blood then discharges during the diastolic phase. Thus the blood never stops running. The compliance of the aorta and the large arteries can because of this be considered analogous to a capacitator.
37
Explain the different steps of the cardiac cycle.
The cardiac cycle comprises all of the physiological events associated with a single heartbeat. The cardiac cycle is essentially split into two phases, systole (the contraction phase) and diastole (the relaxation phase). Each of these is then further divided into an atrial and ventricular component. The cardiac cycle therefore proceeds in four stages: 1. Atrial systole: lasts about 0.1 seconds - both atria contract and force the blood from the atria into the ventricles. 2. Ventricular systole: lasts about 0.3 seconds - both ventricles contract, blood is forced to the lungs via the pulmonary trunk, and the rest of the body via the aorta. 3. Atrial diastole: lasting about 0.7 seconds - relaxation of the atria, during which the atria fill with blood from the large veins. 4. Ventricular diastole: lasts about 0.5 seconds - begins before atrial systole, allowing the ventricles to fill passively with blood from the atria.
38
What are the hydrostatic and deviatoric stresses?
The stress tensor sigma can be split into two parts, one hydrostatic and one deviatoric. sigma = sigma_hyd + sigma_dev = tr(sigma)/3 + sigma_dev The deviatoric part is zero for a fluid at rest, thus only the hydrostatic part is relevant. Whereas at plastic deformation only the deviatoric part is relevant. For an incompressible material the pressure is independent of material deformation. The BCs depend on the hydrostatic part but the deformation and stress in the material depend on the deviatoric part. The hydrostatic stress is simply the average of the three normal stress components of any stress tensor. Hydrostatic stress is the same in all directions, think a particle in water under pressure from the water. Deviatoric stress uneven, and applied, not necessarily constant
39
Compute the matrix representation of the deformation gradient, the right and left Green-Lagrange strains for pure shear.
see fig GL_pure_shear
40
Explain the basic structure and physiological function of the intima layer of large arteries.
Structure: -A thin layer of tightly connected endothelial cells, elongated in the direction of blood flow Physiological function: -Senses wall shear stress (WSS) due to blood flow -Smooth and anti-thrombogenic surface -Selective barrier for nutrients, leukocytes… The intima layer is a thin layer of tightly connected endothelial cells, elongated in the direction of blood flow. The intima layer can sense wall shear stress due to blood flow. The surface of the intima layer is smooth and anti-thrombogenic and its barrier can select to let nutrients in. The layer also controls SMCs, tonus and clotting. It remodels and synthesises the extra cellular matrix (ECM).
41
What are typical macroscopic homeostasis mechanisms of the vessel wall?
Homeostasis is the tendency to resist change in order to maintain a stable, relatively constant internal environment. For us, the interesting parameters to maintain constant are mainly WSS and circ./axial stress. The vessel regulates these by altering the geometry (for example increasing the radius of the vessel) or by changing the structure.
42
What determines the transport across the wall of micro-vessels?
The transport of water and solutes(electrolytes and small molecules) between blood and tissue fluid is determined by: * Wall permeability to water * Hydrostatic pressure difference * Osmotic pressure difference * Diffusion, Advection * Transcytosis
43
What is the material time derivative for Eulerian and Lagrangian approaches?
see fig MTD_eul_lagr
44
What forces do act on particles? What forces do act on blood particles? (what..)
Forces from or related to.... - Drag - Gravity and inertia - Fluid pressure - Velocity gradient(shear) - Collisions - Chemical and electrical