Laws and relationships Flashcards
What is Frank Starling law
Relationship btwn the EDV and cardiac performance
* Length-tension relationship
* incr volume of blood before contraction => more vigorous contraction force
o Beat to beat adjustment of SV to preload
Explain physiologic mechanism of Frank Starling law
↑ venous return → ↑ ventricular filling → ↑ preload → myocyte stretch prior to contraction → ↑ sarcomere length → ↑ inotropy → ↑ SV
* ↑ active tension of muscle fibers → more cross bridge are cycling
o Titin = length sensor
When stretched radial forces pull myosin toward actin
o ↑ velocity of fiber shortening (Vcf) for given afterload/inotropic state
* ↑ sarcomere length
o incr Troponin C sensitivity to Ca2+ => incr rate of cross bridge cycling
o availability of Ca2+ to intiate cycling
* More stretched myofibrils => more powerful contract => incr ES pressure
Explain graphic display of Frank Starling
- Y axis: parameter of systolic function
o CO, SV
o LV Pressure - X axis: preload
- Ascending limb: as EDV incr, generated pressure incr
- Descending limb: beyond certain point => generated pressure decr with further incr in EDV
o Diastolic ventricular interactions: dilated RV compress LV and impair its fct
o Titin play a role => progressively detach from myosin filament if stretched too much
Effect of changes in venous return on frank Starling curve
incr venous return => incr preload => incr initial stretching
o Move up and down a single curve
o Slope defined by afterload and inotropic state
Effect of changes in contractility and afterload on frank Starling curve
change the slope of the curve
o incr afterload or decr contractility: shift down and R
For given EDP = decr SV
o decr afterload or incr contractility: shift upward and L
For given EDP = incr SV
Equation of blood flow
Blood flow (Q) = change in pressure/Resistance
What is the primary determinant of blood pressure in vascular system
Resistance to blood flow
What determines resistance to blood flow
Physical properties of system
o Radius, Blood viscosity, Length
Concentrated in microcirculation (arterioles) R is inversely ∝ to body size All animals have same # of large vessels Small vessels w // connections incr in larger animals to accommodate > blood flow
Equation of SVR
BP/CO
Equation of resistance to blood flow
flow must be laminar, steady, cylindrical conduit, Newtonian viscosity
o Major variable: radius
Regulated by balance of vasodilatory and vasoconstrictive effects
o Length is stable
o Blood viscosity not important variable
R = 8nL/pi *r4
Units of vascular resistance
1 dyne sec/m5 = 80 mmHg/L/min
o dyne sec/m5
o mmHg/L/min (Wood’s unit)
Coronary vascular resistance
- Ao pressure/coronary flow
- 2 major types of arterial vessels
o Small resistance arterioles => major resistance to flow
o Large conductance arteries => govern qty of blood arriving to resistance vessels
Peripheral resistance units
- Peripheral resistance units (PRU)
o Normal arteriovenous pressure difference = 100mmHg
o Normal CO in Hu = 100ml/sec
o TPR = 100/100 = 1PRU
Vasodilation → ↓ pressure difference → ↓ TPR = 0.2PRU
Vasoconstriction → ↑ pressure difference → ↑ TPR = 4 PRU - Pulmonary vascular resistance = PAP-LAP/CO
o Normal arteriovenous pressure difference = 14mmHg
o Normal CO in Hu = 100ml/sec
o PVR = 14/100 = 0.14 PRU
Def conductance
- Measure of blood through a vessel for given pressure difference
o mL/sec/mmHg
o Reciprocal of resistance
Determinants of conductance
o Vessel diameter: ↑ diameter → markedly ↑ conductance
Larger vessels allow more rapid flow (laminar flow in center → ↑ velocity)
2/3 of total systemic resistance from small arterioles
Arrangement of systemic circulation vs resistance
- Series: arteries → arterioles → capillaries
o Total resistance = R1 + R2 + R3… - Parallel: blood supply to organs
o Total resistance = 1/R1 + 1/R2 + 1/R3…
o Each tissue regulates its own blood flow independently
o ↓ total resistance: higher amount of blood will flow vs single vessel
Each vessel provides pathway = ↑ conductance
Control of peripheral vascular resistance
- Integrated control
o Sympathetic outflow
If ↓ → decr renin release => decr Ang II mediated vasoconstriction
o Baroreflex activation
Vasoconstrictive A1 adrenergic R
o Low renal artery pressures + A1 adrenergic effect => stimulation of renin release by kidneys
o Excessive incr in BP:
Baroreflex inhibition of adrenergic system
Endothelial regulation - Normal endothelium: vascular shear force stimulates NO release
- Damaged endothelium: stimulate endothelin release vasoconstriction
- Diameter of arterioles control SVR
Major mechanism of control of peripheral vascular resistance
o Vasoconstrictor R: 3 major vascular R
incr intra¢ Ca2+ => arteriolar vasoconstriction
Respond to neurogenic, neurohumoral or endothelial agonists
* A1 adrenergic vasoconstrictor system: NE from terminal neuron w adrenergic stimulation
* RAAS: Ang II is end product of renin release
* Endothelin: released from damaged endothelium
o Cyclic nucleotide vasodilatory system
Inhibition of contraction w cGMP and cAMP: inhibit myosin light chain kinase that activate vascular contraction
B adrenergic vasodilation: cAMP
NO: synthetized by endothelium cGMP
o Endothelial control
Endothelin
ETB: vasodilation by NO release
ETA: vasoconstriction
Poiseuille’s law
Ratio of driving pressure to blood flow
* Motion of blood in tube depends on:
o Force applied (pression) at either side of the vessel
o Radius → MAJOR EFFECT
o Length
o Blood viscosity
* Applies for special conditions: steady laminar flow in cylindrical tube
Q = pir4PG/8nL
Law of Laplace
Calculate force producing a stretch
* Amount of sarcomere stretch: also determined by
o Compliance of chamber
o Orientation of sarcomere p/r to the force
o # sarcomeres in series
Which component has greatest effect on flow and resistance
Internal diameter of arterioles (radius)
Wall stress equation/units
develops when tension is applied to a CSA
Units: force/unit area
End diastolic wall stress (σ)
Pressure (P)
Radius (r)
Wall thickness (WT)
Sigma = P end diastolic * r end diastolic/2* wall thick end diastolic
Particularities of pulsatile flow
- Resistance is the primary but not the only factor determining flow
- Impedance contributes to 15% of interference to flow
o Factors: blood density, viscosity, Ao diameter, compliance, reflectance - SVR contribute to 85%
Def impedance
Sum of external factors opposing LV ejection (closely related to afterload)
Frequency dependent resistance
* Closely related to afterload
o Ao impedance is an index of afterload
= Ao pressure/Ao flow
Varies continuously during ejection
- Ao impedance: index of afterload
Factor determining impedance
- Determined by physical properties of arterial wall and blood:
o Blood density/viscosity
o Ao diameter
o Ao wall viscoelasticity
o Reflected flow
o Pressures in distal aterial system
Def compliance and equation
- Elastic behavior of vessel/chamber
- Changes in volume in response to transmural pressure
C = change volume/change pressure - Reciprocal to stiffness
Determinants of compliance
elasticity of constituents
Elastic: elastic fibers + smooth muscle ¢
Non elastic: collagen
Mechanical behavior: influenced by interconnections of constituents Simple elastical substance: force ∝ to distension Blood vessels: become stiffer as they distend => 2nd to stiffness of collagen
Def inertance
- Force required to initiate mvt of blood => inertia
Def reflectance
- Backward reflection of pressure and flow waveforms
o From branching sites of vasculature => abrupt change in vessels diameter
From decr diameter of Ao
o > force against which ventricle eject - Wave observed at any point: sum of forward + retrograde wave
What is Bernoulli equation
Used to calculate transvalvular pressure gradient
* Constant volume of blood moved through orifice/vessel => pressure incr proximal to obstruction => proportional incr in blood flow velocity
o incr in kinetic energy, decr potential energy
* Pressure gradient = convective acceleration + flow acceleration + viscous friction
o Forces of viscous friction and flow acceleration are negligible
o Value of 1/2(p) = mass density of blood = 4
* Greatest application to measure severity of valvular stenosis
modified Bernoulli equation
overestimate to a small degree when compared to cardiac KT gradients
Calculates instantaneous PG
* Peak to peak PG determined by calculating the difference btwn:
o Max LV pressure vs max Ao pressure
o Not at the same time
o Anesthesia: decr PG by 40-50%
* Doppler PG: calculate instantaneous pressure difference btwn Ao and LV pressure
o 30-40% higher vs invasive measurement
* More severe the stenosis: closer peak to peak and instantaneous pressure
o Highest LV pressures occur later in systole.
Limitations of Bernoulli
- Blood volume: will affect flow velocity
o PG calculation inaccurate if high flow state => creates a high proximal velocity (V1)
o Regurgitation through valve or stenotic region
AI, AS, shunt, anemia, sepsis - HR, blood pressure and contractility can also affect
o Sympathetic stimulation can incr PG - Tunnel lesions: overestimate PG => friction no longer insignificant
- Blood viscosity: decr blood viscosity overestimate, incr blood viscosity underestimate PG
o Not accurate when:
Large intercept angle
V1 is not negligible: high flow state or small PG - Simplified may be more accurate
Reynold’s # equation
= 2rvp/n
describe relationship of cardiac murmurs to vessel size, flow velocity, blood viscosity.
= radius x velocity x density/viscosity
Critical number: 2300
Define laminar flow
all fluid layers move in longitudinal direction
* Central velocity: most rapid motion
* Progressively decr toward tube’s walls
* Velocity profile => parabolic
Def turbulent flow
disturbed laminar flow
* Can occur at sharp bends or obstructions
Factors incr blood flow turbulence
o incr blood flow velocity
o decr viscosity
o Abrupt incr radius
Turbulent flow causes
HM
