Flashcards in Nordgren Cardiac Phys week 2 Deck (40):
Passive transcapillary solute diffusion depends on (4 things):
1. concentration gradient
2. surface area
3. diffusion difference
4. permeability of capillary wall to the substrate
Net fluid OUT of capillary = ?
Net fluid INTO capillary = ?
Pressure of blood forcing fluid OUT of capillary?
Attraction of water IN to regions of higher protein concentration?
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?
total peripheral resistance
Adding and organ in parallel to the system will _______ the TPR.
compliancy (C) = ?
C = change in V / change in P
** veins have much greater C than 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)
MAP = 2/3Pdias + 1/3Psys
relate pulse pressure, stroke volume and compliance.
PP = SV/C arterial
Vascular smooth muscle contraction depends on?
Basic pathway for Ca2+ mediated VSM contraction:
1. Ca2+ + calmodulin
2. activation of myosin light chain kinase
3. MLC kinase + ATP --> phosphorylation of MLC protein --> MLC-PO4
4. 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:
1. 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:
2. chemical vasodilators --> Beta2 receptors --> increased cAMP/cGMP --> active protein kinase A --> lots of phoshorylation --> Ca2+ efflux, hyperpol, decreased contractile machinery sensitivity to Ca2+
Most important means of local arterial flow?
Dilation: low O2, high CO2/H+/K+, release of adenosine
Endothelial cells effect on arterial tone?
NO --> increased cGMP
NO production stimulated by?
Ach, bradykinin, vasoactive intestinal peptide
Other chemicals involved in control of arterial tone?
Active phase of VSM reacting to change in transmural pressure:
Most important means of reflex control in vasculature?
SNS vasoconstrictive nerves
NT and receptor for SNS vasoconstriction
Hormonal influence for vasoconstriction and its receptor?
Vasopressin (ADH) -- a1
Hormonal influence for vasodilation and its receptor?
Angiotensin II -- Beta2 (more sensitive to epi than a1)
Is venous tone subject to local metabolic needs?
What is the pressure of the circulatory system if there were no flow?
"Mean circulatory filling pressure"
Two major variables that affect mean circulatory filling pressure:
1. circulating blood volume
2. state of peripheral venous tone
Central integration of the baroreceptor reflex occurs where?
medullary cardiovascular centers
where are baroreceptors located?
1. aortic arch
2. carotid sinuses
When do PNS and SNS work in concert instead of reciprocally?