quick questions for pecchiari Flashcards
VISCOSITY determinants
HC
temp
shear rate
diameter of vessel
(axial migration and sigma effect)
why are rouleaux bad
happens when Shear rate decreases
causes shift of WBC from center to periphery hence inflammatory and thrombotic response
Msf graph axis
y = msf
x = volume
affected by sympathetic stim to the left
main points for shematic org of CVS
- in series
- average flow at steady state is CO = 5 (av flow bcos pulsatile, and steady bcos VR=CO)
- 5% CO is shunts and can ause hypoxia
how we model blood with equations
ideal (visc 0) bernoulli
newtonian (ok for physiological, visc constant) pouseille
in path the non newtonian characteristics come out
reasons why issues can occur for ECG in heart
re-entry
triggered activity
(bcos cardiac muscle has the property of refractory period, no summation is possible)
leads in ECG summary
12 leads overall.
6 pericordial (unipolar)
3 bipolar (einhover) LA,LL,RA
3 unipolar (goldberg augmented voltage LRF)
in ECG when the voltage is positive what direction is it going in
right to left
venous pulse the three waves correspond to what
JUGULAR, CVP INDEX
a - contraction
c - bulging of tricuspid into RA
v - atrial filling
(c is a bulge, a is atrial contraction stands for atrium, v is for ventricle so the opposite happens so FILL)
charges of the einhover leads
RA –
LA +-
LL ++
valve closure
MTAP (high low)
cardiac sounds
MTAP
1st av valves
2nd semilunar
3rd in apex in children during filling
4th if augmented due to atrial systole
AV in 5th intercostal space
Aorta in 2nd intercostal RIGHT
pulm in 2nd intercostal LEFT
receptors on the heart + autonomic stim
symp = adrenergic beta 1 Gq CAMP PKA phospholamban SERCA +Ve.
paras = vagal = muscarinic M2 Ach, Gi response -ve
digitalis effects
inhibits Na/K pump
NCX decrease
more Ca stuck in cell
contraction increases
propanolol type of drug and action
BETA BLOCKER
inhibits beta 1 adrenergic response hence -ve contractility
frank starling heart lung prep
cut aort awith manometer to measure aortioc P
sterling resistor to control arterial P hence afterload
lungs ventrillated mechanically
frank starling 2 experiments
1 change preload (RAP) and meaasure SV and CO
2 change afterload (AP) and measure SV and CO
clinical necessity for frank starling
pulm edema equilibrium
standing up
standing exercise
hypotension
contractility changes
name of 4 graphs for otto frank
diastolic PV (EDP)
isovolumic max (sys P)
isobaric max (P, no A)
afterloaded max (P&A)
what determines O2 use of heart
basal met = 2
added met due to EW, EW+PE = PVA, 8-10
CCP axis on graph and effect of NS
y = blood flow
X= arterial pressure
X intercept = CCP
ss to the right
(sos T=RP bcos tension is exerted against the Ptm)
situations that can cause a change in VR
increase in exercise due to action of the muscles
decreases from sitting to standinf bcos blood pools at he bottom
things that affect the Frank starling line
y axis = SV
x axis = EDV
so up if contractility increases or afterload decreases (and vice versa for down)
effect if contractility on ESPVR
increases the slope (Ees) so shifts to the left
