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37 Cards in this Set

  • Front
  • Back
SV =
EDV - ESV
how much blood pumps out
EDV determines
preload
increase PL effect
inc EDV
inc SV
afterload determines
ESV
inc AL effect
inc ESV
dec SV
Ejection fraction
ejection fraction: what part of EDV is getting pumped out
EF =
EDV - ESV
_________

EDV
dec EF effect
dec LV function/ filling or ejection
inc EF effect
ejects more blood
inc EF inc SV
bowditch effect
preload plateaus: not enough time to refill

SERCA is maxed out (Ca+) can't take up anymore
increase myofiber length effect
inc cadiac sensitivity to Ca+/troponin (more cross bridges!)
determinants of in preload
venous tone
total BV
skeletal muscle activity
gravity/posture
isotonic
? vs ?
velocity vs. force
isotonic:
F=0 =
F=infinity =
Vmax
0
increase afterload effect
dec SV
afterload is dependent on
arterial pressure
system vascular resistance
resistance of valve
ventricular wall tension
inc Ca+ effect
inc contractility
swan ganz cath
into RA -> RV -> PV into PA
proximal: RA PRELOAD
distal: wedge in PA as a balloon: PCWP: into lungs and out estimate of LA to detect LV preload
swan ganz direct measurements
VO2 concentration (arterial/venous difference)
ability to oxygenate blood, pump out, tissues to take O2

system vascular resistance (afterload)
VO2 =
CO x A-V
driving pressure =
=MAP - RAP

=CO x SVR
MAP =
S + 2D
_____

3
hypovolemic shock effects
dec PL
dec CO
inc SVR
septic shock effects
dec PL
inc CO
dec SVR
cardiogenic effects
inc PL
dec CO
ince SVR
Tx of hypovolemic shock
fluids
tx of septic shock
treat SVR with DA, epi, NE, ABs
tx of cardiogenic shock
B1 stim and B2 to dec SVR
vasodilating dec AL
tx for elevated PCWP
inc filling pressure with diuretics
tx of low PCWP
dec filling pressure with fluids
Low CO tx
B agonist - milrinone or dobutamine
high SVR tx
vasodilator
low SVR tx
CA - NE, DA, a1 effect
myocardial relaxation
-SERCA removes inc Ca+
-1 ATP for 2 Ca+ reuptake
-Ca+ stored on calsequestrin
-dec Ca+ dec I-E
-tropomyosin returns to groove on A inhibiting A-M
Ca+ rises effect
Ca+ binds to TC which interacts with IT leading toa very strong bond
-strength increases position on actin; weaking top T and tropomyosin bond
-tropomyosin moves into the groove exposing A to M
EC coupling
diastole
-Ca+ inflow into myoctyre during AP plateau through voltage sensitive channels (occurs in T-tubules)
calcium-induced calcium released
systole
-Ca+ released from SR
-rise in intraCa+ during contraction phase