Boron Cardiac Physio Review Flashcards
resistance in series
R + R + R
blood flow in given organ
- single artery supplies organ
- goes to ateries > arterioles > capillaries > veins
resistance in parallel
1/R + 1/R + 1/R
systemic circulation
-arteries that branch off aorta to organs
three kinds of pressure in circulation
1 driving pressure - axial
2 transmural pressure - radial - intravascular vs. tissue pressure
3 hydrostatic pressure - gravity on column of fluid
CO = ?
HR x SV
poiseuilles law
flow = deltaP x r^4 / 8nl
r = radius n = viscosity l = length of vessel
flow directly proportional to pressure difference and inversely to radius of vessel to the fourth and inversely to length and viscosity
reynolds number
determines when blood flow becomes turbulent
- laminar below 2000
- turbulent above 3000
increases in reynolds number
**more turbulent flow
decreased blood viscosity - decreased hematocrit, anemia
increased blood velocity - narrow vessel
also increased vessel diameter
pulse pressure
difference between SBP and DBP
four factors generating presure in circulation
1 - gravity
2 - compliance of vessels
3 - viscous resistance
4 - inertia
gravity
P difference when difference in height
-ex/ when patient standing
standing pressure
high in feet
reference at heart
low in head
driving pressure when standing?
remains the same in head and heart
- difference between SBP and DBP
- slightly higher at heart
gravity does not affect
driving pressure that governs flow
palpatory method of BP
radial artery at wrist
-systolic ONLY
auscultatory method of BP
systolic and diastolic
fick principle
allows you to measure CO
CO = O2 consumption / O2 arteries - O2 veins
highest cross sectional area
capillaries
slowest velocity of blood
capillaries
blood volume distribution
20% systemic arterial
65% systemic venous
10% pulmonary
5% heart chambers
arteries
resistance vessels
veins
volume reservoirs
-capacitance vessels
compliance
distensibility of blood vessels
-greater in veins (if low pressure)
-change in volume with change in pressure
veins at “arterial pressure”
not as compliant
-sudden increase in volume leads to large increase in transmural pressure
case with saphenous vein in CABG
transmural pressure
distending force - increases circumference of vessel
laplaces law
describe how tension in vessel wall increases with transmural pressure
-for given transmural pressure - wall tension gets larger as radius increases
convection
main mechanism for net transfer of fluid across capillary membrane
determined by hydrostatic pressure and colloid osmotic pressure
starling equation used
standing
increased capillary pressure - due to increased hydrostatic forces
-results in edema
pulmonary edema
pulmonary HTN - increased hyrostatic pressure
-with left-sided heart failure
nephrotic syndrome
loss of protein
-decreased plasma colloid oncotic pressure - edema
pregnancy
plasma protein synthesis too slow
-decreased plasma colloid oncotic pressure - edema
during ischemia
blood vessels deteriorate
-with reperfusion - local edema
lymph flow
dependent on interstitial pressure
slow APs
SA and AV nodes
fast APs
atrial myocytes
purkinje fibers
ventricular myocytes
phase 0
upstroke
- Ca slow
- Na and Ca fast
phase 1
rapid repolarization
- inactivation of Na and Ca
- activaiton of K
phase 2
plateau phase
-Ca and Na
Phase 3
repolarization
-K
Phase 4
electrical diastolic phase
- most negative - maxi diastolic potential
- SA, AV nodes - changes in K, Ca, and F currents
- produce pacemaker activity
If
non-selective cation channels
SA node phase 4
outward K
inward I-f
slight inward Ca
SA node phase 0
depolarization
-calcium
three ways to slow SA node
- decrease phase 4 steepness
- max diastolic potential more negative
- threshold more positive
acetylcholine on SA and AV nodes
PS activity
-slows pacemaker - all three mechanisms
1 - decreases If - reduces phase 4 steepness
2 - opens GIRK channels - increasing K conductance - making maximum diastolic potential more negative
3 - reduces I-Ca in SA node - reduces steepness of phase 4 and moves threshold more positive
ACh on AV node
not usually the pacemaker
-PS innervation slows conduction velocity
-inhibition of I-Ca that makes threshold more positive
sympathetics on heart
increase heart rate
- increase I-f in nodal cells - increase phase 4 steepness
- increase I-Ca - steepens phase 4 depolarization and makes threshold more negative
**no large change in maximum diastolic potential
sympathetics in heart muscle
atria and ventricles
- positive inotropic - contraction
- 4 ways
1 - increased I-Ca - more Ca in muscle cell - greater Ca induced Ca release
2 - increase sensitivity of SR Ca release channel to cytoplasmic Ca
3 - enhance Ca pumping into SR - stimulate SERCA Ca pump
4 - increased I-Ca presents more Ca to SERCA - so SR Ca stores increase over time
**all more Ca to troponin C - more forceful contraction
