Physiology Flashcards
What is the equation for velocity of blood flow?
V=Q/A
- *V**= velocity in cm/s
- *Q **= cardiac output/flow in mL/min
- *A **= cross sectional area of vessel
What is the equation for CO/ blood flow?
Q = ΔP/R
“Ohm’s law” I = ΔV/R
- *Q **= flow/CO in mL/min
- *ΔP **= pressure in mmHg
- *R **= total peripheral resistance in mmHg/mL/min
What is the Law of Laplace?
τ = Pr/2H
- *τ** = tension in vessel wall (or wall stress in ventricles)
- *P** = transmural pressure
- *r** = radius of vessel (or cavity for ventricle)
- *H** = wall thickness (negligble for capillaries)
When can you apply the Law of Laplace? What is its clinical relevance?
Can be applied to vessels or ventricles
This law explains why LV thickens in response to high BP to decrease wall stress
What is Poiseuille’s equation?
R = 8ηℓ/πr4
R = resistance
η = viscosity of blood
ℓ = length of blood vessel
r = radius of blood vessel
What is the total resistance for a series arrangement?
RT = R1 + R2 + R3 …
What is the total resistance for a parallel arrangement?
1/RT = 1/R1 + 1/R2 + 1/R3 …
What is the difference between laminar flow and turbulent flow?
Laminar flow = streamlined, parallel to vessel
Turbulent flow = in axial/radial directions; it’s audible
What is Reynbold’s number?
NR = ρdv/η
- *NR** = Reynold’s number
- *ρ** = density of blood
- *d** = diameter of blood vessel
- *v** = velocity of blood flow
- *η** = viscosity of blood
If <2000, blood flow usually laminar
If >3000, blood flow usually turbulent
Why does decreasing the diameter of a blood vessel cause an increase in Reynold’s number?
It’s puzzling bc diameter is on top in Reynold’s number equation
But rememer that v = Q/A = Q/πr^2. This shows that velocity increases as radius decreases, which takes over because r is to the second power here. Therefore this effect is greater nd since v is also on top in the Reynold’s equation, as radius decreases, Reynold’s number increases.
What is capitance?
C = V/P
C=capitance/compliance mL/mmHg
V=volume mL
P=pressure mmHg
What is the meaning of capitance/compliance?
What is the result of changes in compliance?
Capitance describes the volume of blood that a vessel can hold at a given pressure… veins are more compliant bc they are less stressed: can hold more volume at lower pressure
Changes in compliance (i.e. due to vasoconstriction) cause redistribution of blood
Also loss of elasticity in arteries due to aging means that compliance decreases: at a given pressure, arteries hold less blood. So to hold the same volume of blood, bp must increase…this is how you get hypertension
What is the relationship between CO, MAP, RAP, and TPR?
CO = (MAP - RAP)/TPR
- *CO** = cardiac output
- *MAP** = mean arterial pressure
- *RAP** = right atrial pressure
- *TPR** = total peripheral resistance
*Multiply by 80 to convert from mmHg min/L to dyne sec/cm5
What is the Fick equation?
CO = O2 consumption/([O2]PV - [O2]PA)
- *O2 consumption** = O2 use by body in mL O2/min
- *[O2]PV** = O2 content in pulmonary vein (mL O2/mL blood)
- *[O2]PA** = O2 content in pulmonary artery (mL O2/mL blood)
How do you calculate MAP? 3 equations
MAP = (SBP+2DPB)/3
MAP = DBP + (1/3)PP
MAP = DBP + (1/3)(SBP - DBP)
What is the equation for pulmonary vascular resistance?
PVR= (MPAP-PCWP)/CO in L/min
What is the Frank-Starling law?
SV increases in response to an increase in preload volume
Up to a point– bc when you overwhelm the system, pulmonary venous pressure increases & fluid leaks out of the capillaries –> impaired gas exchange
Preload
Load on ventricle at end of diastole
Measures include: end diastolic volume, end diastolic pressure, end diastolic wall stress, venous return
Afterload
Load on ventricle during ejection– determined by arterial system: force that LV must generate to eject blood
Measures: aortic pressure, total peripheral resistance, ejection wall stress
Stroke volume
SV=EDV-ESV
EDV=end diastolic volume
ESV=end systolic volume
Ejection Fraction=
EF= SV/EDV
Pressure Volume Loop: ID the following:
SV, EDV, ESV, aortic valve open/close, mitral valve open/close, EDPVR, ESPVR, end systole, end diastole
A= ventricle fills until end diastolic volume (when P in LV>LA –> mitral valve closure) = S1
A–>B=isovolumic contraction
B= aortic valve opens when P LV>P aorta
B –> C = ejection phase
C= end of systole, when P in LV
C –> D = isovolumic reduction
D = diastole, ventricle starts to fill. When P LV < LA, mitral valve opens & ventricle starts to fill
What happens to the PV-loop when you increase preload? Afterload? Contractility?
What’s an inotrope?
What is the effect of inotropes on the ESPVR?
Inotropes alter the force of contraction by altering Ca release, affinity of myofilaments for Ca, or number of myofilaments available
Positive inotropes make the relationship steeper
Negative inotropes make the relationship less steep
This is an index of contractility– if you change contractility, the ESPVR changes
