Nordgren Cardiac Phys week 2 Flashcards
(40 cards)
Passive transcapillary solute diffusion depends on (4 things):
- concentration gradient
- surface area
- diffusion difference
- permeability of capillary wall to the substrate
Net fluid OUT of capillary = ?
filtration
Net fluid INTO capillary = ?
rebsorption
Pressure of blood forcing fluid OUT of capillary?
Hydrostatic
Attraction of water IN to regions of higher protein concentration?
Oncotic pressure
Starling’s Hypothesis:
Net filtration rate = ?
Positive net pressure gradient = ?
Negative net pressure gradient = ?
(P intracapillary - P interstitial) - (oncotic pressure of intracapillary fluid - oncotic pressure of interstitial fluid)
Positive net pressure gradient = filtration
Negative net pressure gradient = Reabsorption
***hydrostatic and oncotic pressure of IF are usually zero
***oncotic pressure usually does not change
Location of Filtration?
arteriole end of capillary
Location of Reabsorption?
venule end of capillary
What can cause the oncotic pressure to drop?
Histamine release–increases capillary permeability to protein.
Total resistance for vessels in a series = ?
the sum of each individual resistance
Q = total change in P / total R
Primary blood volume reservoir?
peripheral venous system
secondary blood volume reservoir?
central venous system
-great veins of the thorax and right atrium
Overall resistance to flow through the ENTIRE systemic circulation?
TPR
total peripheral resistance
Adding and organ in parallel to the system will _______ the TPR.
decrease
compliancy (C) = ?
C = change in V / change in P
** veins have much greater C than arteries
Pressure reservoir?
Arteries
**small change in V builds up a lot of P –> recoils to drive blood through the periphery
Relate MAP, CO, and TPR:
MAP = CO x TPR
**MAP also = Pdias + 1/3(Psys -Pdias…PP)
or
MAP = 2/3Pdias + 1/3Psys
relate pulse pressure, stroke volume and compliance.
PP = SV/C arterial
Vascular smooth muscle contraction depends on?
Ca2+
Basic pathway for Ca2+ mediated VSM contraction:
- Ca2+ + calmodulin
- activation of myosin light chain kinase
- MLC kinase + ATP –> phosphorylation of MLC protein –> MLC-PO4
- cross bridge formation and cycling, energy from ATP –> tension development/shortening
**5. removal of phosphate from MLC returns cell to relaxation
Resting membrane potential of VSM?
-40 to -65 mV
**determined by K+ permiability
two causes of VSM action potentials:
- slow inward Ca2+ current (like pacemaker cells)
2. stretch sensitive cation channels
In addition to membrane depol, how else can Ca2+ get into VSM cell?
Pharmacomechanical coupling (vasoconstrictor agonist)
G coupled protein receptor, IP3 (opens Ca2+ channels in SR)
2 methods for VSM relaxation:
- hyperpolarization
- chemical vasodilators –> Beta2 receptors –> increased cAMP/cGMP –> active protein kinase A –> lots of phoshorylation –> Ca2+ efflux, hyperpol, decreased contractile machinery sensitivity to Ca2+
