Cvs Physio

Front 1

Pressure

Back 1

F/A, cardiac muscle cx increases P, E

Front 2

Flow (Q)(Ohm's law)

Back 2

Pressure change/Resistance...
based on this, Paorta>Pveins or blood doesn't flow

Front 3

Resistance (R)

Back 3

opposition to fluid movement, Pressure gradient/Q

Front 4

Systolic P

Back 4

During contraction, usually 120mmHG

Front 5

Diastolic P

Back 5

During relaxation, usually 80 mmHg

Front 6

R Atrial P

Back 6

0-2mmHg

Front 7

Poiseulle's law (describes variables that alter resistance)

Back 7

8*viscosity*length/pi*r4
Radius greatly affects resistance
-high radius, low R
-low radius, hi R
only variable that our bodies can easily change is r

Front 8

Poiseulle's law with flow definition:
Q=Pdifference*pi*r4/8viscosity*length

Back 8

Flow decreased by increasing viscosity, increased by increasing radius/pressure

Front 9

Q=CO
Pdifference physiologically

Back 9

P=MAP because P2=Patrium~0

Front 10

CO =

Back 10

MAP/TPR

Front 11

Resistance in series

Back 11

Rseries=R1+R2+R3+R4..

Front 12

Resistance in parallel

Back 12

1/Rparallel=1/R1+1/R2+1/R3..
addition of parallel networks decreases R

Front 13

Velocity

Back 13

distance/time
Q/A, as cross sectional area of vessel decreases, velocity increases

Front 14

Bernoulli principle - V/P relationship

Back 14

increased velocity decreases transmural P, but increases kinetic P
Flow velocity increases through narrowed value, Pt decreases, reduction on driving pressure of flow

Front 15

Reynold's # - predicts laminar vs. turbulent flow

Back 15

= density*inner vessel diameter*velocity/viscosity

Front 16

Turbulence is favored by... (Re>2300)

Back 16

large vessel diameter, high velocity, low viscosity

Front 17

Turbulence in heart

Back 17

murmur

Front 18

Turbulence in arteries

Back 18

bruit

Front 19

Sheer stress

Back 19

sensed by endothelial cells, release NO in response, atherosclerotic plaques more common in areas of low sheer stress

Front 20

Compliance

Back 20

change in volume over change in pressure, veins highly compliant
measure of distensibility or flexibility,

decreased by atherosclerosis, endothelial smooth m. contraction

Front 21

Capacitance

Back 21

volume of blood contained in a vessel at a given Pt

Front 22

Path of wave of depolarization

Back 22

SA node -> internodal/interatrial fibers -> AV node -> bundle of His -> Purkinje fibers -> ventricular myocytes

Front 23

Fast response AP - Phase 0

Back 23

Rapid depolarization caused by opening of VG Na channels and resultant Na influx. Around -50mV, VG Ca channels open as well

Front 24

Fast response AP - Phase 1

Back 24

Partial repolarization caused by opening of transient outward K channels (and rapid subsequent closure)

Front 25

Fast response AP - Phase 2
Plateau

Back 25

Slow repolarization caused by continued influx of Ca and counterbalanced by VG delayed rectifier K channels (Iks, Ikr, Ikur)

Front 26

Fast response AP - Phase 3
repolarization

Back 26

Closure of VG Ca channels, continued K efflux through delayed rectifiers

Front 27

Fast response AP - Phase 4
RMP

Back 27

Inward rectifying K channel allows K to leak in.
diastolic/pacemaker potential phase in automatic tissues (SA/AV node)

Front 28

Fast response AP - Pre-Phase 0

Back 28

Suprathreshold stimulus from pacemaker, changing RMP to threshold (-65mV)

Front 29

Excitation contraction coupling in the heart

Back 29

Depolarization -> Ca influx -> CICRintracellular -> binding of Ca to TnC, exposing myosin active sites -> enables cross bridging

Front 30

Calcium channel characteristics

Back 30

VG, time sensitive, L-type Ca channels, activate more slowly than fast Na channels

Front 31

Effective refractory period

Back 31

similar to absolute, cell will not respond to any stimuli b/c VG Na channels are inactivated
- until end of phase 2

Front 32

Relative refractory period

Back 32

Some VG Na channels can open, but will result in a smaller AP

Front 33

Refractoriness and safety

Back 33

refractoriness prevents extraneous pacemakers from hijacking the heart.

Front 34

Slow response AP - Phase 4

Back 34

Diastolic/pacemaker potential. Slow depolarization due to opening of hyperpolarization activated cyclic nucleotide gated cation channels and consequent Na influx (funny current)
*decrease in K efflux b/c of inactivation of outward rectifiers

Front 35

Slow response AP - Phase 0

Back 35

During P4, as membrane potential passes -50mV, VG L-type Ca channels opening, leading to P0 upstroke (No fast response VG Na channels in SA/AV nodes)

Front 36

Slow response AP - Phase 3

Back 36

Outwardly rectifying K channels open, early repolarization and AP of ~3sec duration

Front 37

EKG - P wave

Back 37

sequential activation/depolarization of R and L atria

Front 38

EKG - PR interval

Back 38

time req'd for AP to travel from SA to AV node, blockage of conduction -> lengthened PR interval

Front 39

EKG - QRS complex

Back 39

simultaneous ventricular depolarization, 0.1 s or less

Front 40

EKG - ST segment

Back 40

isoelectric, coincides with plateau period and rapid ejection phase of cardiac cycle (end of QRS to beginning to T wave)
damage leads to ST elevation

Front 41

EKG - T wave

Back 41

ventricular repolarization - occurs in reverse to depolarization (ie - apex repolarized first)

Front 42

EKG - QT interval

Back 42

duration of depolarization + repolarization, inversely porportional to HR, if repolarization delayed QT prolonged

Front 43

Fick's law - gold std for calculating CO

Back 43

O2 uptake (gas) = Q (concentration O2 arteries - concentration O2 veins)

Front 44

CO=

Back 44

Vo2/(conc O2 art-conc O2 vein) or HRxSV