Cardiac Flow And O2 Delivery

Front 1

how does body incr CO in response to exercise?

Back 1

local tissues need more oxygen -> incr local mediators like adenosine -> vasodilation -> SVR decr -> baroreceptors sense decr MAP and thus incr HR/inotopy -> CO incr to keep MAP constant

Front 2

indicator dilution technique of measuring CO: what does indicator concentration change relate to? (2), types of indicator dilution

Back 2

magnitude of concentration change is related directly to indicator addition rate and inversely to stream flow rate; types: Fick (oxygen), thermal dilution

Front 3

Fick principle equation for CO

Back 3

CO = VO2 (consumed O2)/AVO2D (arterial venous O2 difference)

Front 4

normal mixed venous O2 sat at rest

Back 4

75 (one third of max O2 transport -> 3 fold change in metabolic reqs can be met w/o change in CO) --- if mixed venous O2 sat is low, then patient is in trouble (can't change CO to meet metabolic reqs)

Front 5

maximum incr in CO

Back 5

HR can be improved by 3x, SV by 3x, so max is 9x

Front 6

stroke volume depends on (3)

Back 6

preload, afterload, inotropic state

Front 7

preload det by (4)

Back 7

det by venous vasodilation, by intravascular volume, by diastolic ventricular compliance, and by HR -> incr HR means diastole is decr and preload is decr, altho normal HR range doesn't usually affect preload since most filling occurs during first 1/3 of diastole

Front 8

response of CO to temp

Back 8

heat stress causes skin vasodilation -> decr SVR -> baroreceptors signal heart to incr HR and incr inotropy (incr CO); opposite happens in cold stress -> decr CO to keep MAP normal despite skin vasoconstriction

Front 9

intrinsic control of vascular smooth muscle (3)

Back 9

myogenic autoregulation -> increases SVR in response to increased inflow P (mech unknown) ; endothelium-mediated autoregulation -> decr SVR (via NO) in response to incr shear stress (flow rate); metabolic-mediated autoregulation -> decr SVR vai adenosine

Front 10

O2 carrying capacity

Back 10

total amount of O2 which blood can carry if all its hemoglobin binding sites are occupied; = Hb x 1.34

Front 11

O2 sat and PO2

Back 11

O2 sat det by lung health and % O2 in room air; % sat remains very high (>90%) for a wide range of pO2 (from 60 to 100), therefore a drop in O2 sat below 90% in lungs is very troublesome (= hypoxia) - it means that pO2 is around 60 mmHg (very low for lungs), and that with any further loss in oxygen, O2 sat will plummet

Front 12

O2 content equation

Back 12

bound + dissolved oxygen = (Hb x 1.34 x O2 sat) + (pO2 x .003)

Front 13

O2 sat and PO2 at room air, alveolar gas, venous blood, and what is pO2 for 50% O2 sat?

Back 13

room air 100% sat, 150 mmHg pO2; alveolar gas 97% sat, 100 pO2; venous blood 75% sat, 40 pO2; 50% sat = 28 mmHg pO2

Front 14

Fick principle general equation

Back 14

flow rate = rate of addition/change in concentration ---- for CO, means that CO = VO2 (consumed O2)/AVO2D

Front 15

fetal circulation modification (5)

Back 15

ductus venosus (umbilical vein -> IVC), foramen ovale (RA -> LA), ductus arteriosus (pulm artery -> aorta); pulmonary vascular resistance > systemic vascular resistance; R ventricular diastolic compliance < L ventricular diastolic compliance b/c R ventricle hypertrophied to deal w/ elevated pulmonary resistance

Front 16

circulatory changes at birth and cause/effect/time (3)

Back 16

decrease in pulmonary vascular resistance (begins w/ lung inflation and progresses over first week, allows for incr. pulm flow and decr. DA flow); increased venous return from lungs (incr LA pressure and opposes flow across FO); closure of ductus arteriosus (stim by incr O2 and decr PGE2, us. complete by day 4)

Front 17

cardiac output definition and unit

Back 17

volume of blood per unit time (liters/min)

Front 18

cardiac index definition and normal range

Back 18

cardiac output normalized to body size by dividing by body SA; 2.5-3.5 L/min/m^2

Front 19

stroke volume definition and normal value

Back 19

volume of blood ejected per beat; 100 mL for an adult

Front 20

LVEF definition and normal range

Back 20

left ventricular ejection fraction: % of blood volume in left ventricle at end-diastole that is ejected during systole = (LVEDV - LVESV)/LVEDV = SV/EDV; normally .55-.65

Front 21

driving pressure definition

Back 21

axial P difference (difference between upstream and downstream Ps - measures F moving blood from one location to another)

Front 22

transmural pressure definition

Back 22

radial P difference (difference between pressure inside vessel vs. outside vessel - measures F on chamber wall)

Front 23

compliance definition

Back 23

pressure or force required to distend or stretch a structure; = dV/dP or dr/dP (strain/stress)

Front 24

flow rate vs flow velocity

Back 24

flow rate = volume per time (L/min or mL/sec) vs flow velocity = distance per time (cm/sec)

Front 25

flow resistance determined by

Back 25

vessel radius and blood viscosity

Front 26

Bernoulli's law; when to use it

Back 26

P + .5pv^2 = constant; relation btwn P and v is quadratic (if flow velocity doubles, then P decr by x4); use to determine pressure drops across obstructions (how severe?) from velocity measurements

Front 27

LaPlace's law, when to use it (2)

Back 27

tension = pressure x radius / 2 x thickness; used to determine force on vessel walls (risk for aneurysm) from BP and vessel radius; determine force that heart has to generate in order to generate pressure (can determine contractile performance of enlarged/diseased hearts)

Front 28

Poiseulle's law, when to use it (2)

Back 28

flow = dP x pi x r^4 / (8 x viscosity x length); relates the diameter of a vessel and the resistance to flow through it; note that radius is raised to the fourth (decr radius causes flow to decr by 4 - small radial changes can cause large changes in flow volume); defines the mechanism by which pressure and flow are regulated (decr radius by muscle contraction and thus incr P x 4 or decr flow x 4); implications for disorders affected blood viscosity (incr viscosity causes decr P or decr flow)

Front 29

Reynold's law and when to use it

Back 29

maximum laminar flow velocity = K x viscosity / (pr) ; determines when flow will be turbulent and thus generate murmurs or bruits

Front 30

use of Ohm's in blood flow

Back 30

V = IR becomes P = q(flow) x R, therefore q(flow) = Pressure/Resistance; not perfect though (blood flow is pulsatile and therefore more similar to AC than DC)

Front 31

SVR equation

Back 31

SVR = MAP - RAP (venous P) / CO

Front 32

pulmonary venous resistance eq

Back 32

PVR = PAP - LAP / CO

Front 33

total pulmonary resistance eq

Back 33

TPR = PAP/CO

Front 34

diff between PVR and TPR

Back 34

PVR takes into account LAP, TPR doesn't (makes TPR > PVR)

Front 35

how do we measure afterload?

Back 35

PVR is afterload on RV; SVR is afterload on LV

Front 36

normal values for SVR, TPR, PVR

Back 36

SVR = 12-18 Wood units; TPR = 1.5 - 3; PVR <1.5

Front 37

transport vs delivery; equations

Back 37

transport is quantity transported per unit time (= O2 content x CO = Hb x 1.34 x CO); delivery is quantity transferred from blood to tissue per unit time (= CO x AVO2D)

Front 38

what factors det max VO2, and which matters most in healthy people?

Back 38

resp sys max rate of O2 exchange; circ sys max ability of O2 transport; max metabolic rate of skeletal muscle; circ sys matters most

Front 39

normal rest VO2 for adult

Back 39

3.5 mL/kg/min, or rather 125 mL/m2/min (divide by 125/BSA to get VO2)

Front 40

MET

Back 40

metabolic equivalent = resting oxygen consumption

Front 41

untrained vs trained athletes max MET

Back 41

untrained healthy person can get 8-12 METs, athletes can get 20-25+ METs

Front 42

limitations to AV O2 extraction

Back 42

pO2 in mitochondrion us 1 mm Hg and a 20 mm Hg gradient is needed to drive diffusion, so therefore min achievable capillary pO2 is 20-21 mmHg, which corresponds to 15% O2 sat, meaning max AVO2D is 85% (assuming 100% sat in lungs)

Front 43

CV response to exercise in untrained healthy pt: VO2, VCO2, O2 sat/AVO2D, CO/HR/SV, MAP, SVR

Back 43

VO2 rises rapidly and plateaus when max CO is reached; VCO2 rises quickly and continues to rise even more rapidly after VO2 plateaus because of switch to nonaerobic respiration; mixed venous sat quickly drops from max at 75% to min at 15% (AVO2D rises while O2 sat drops); CO rises rapidly as a result of initial increase in both SV and HR followed by later incr in HR when SV reaches max, CO plateaus when HR reaches max (220-age); MAP rises as CO rises; SVR declines as CO rises (SVR drop is what causes CO rise to compensate MAP)

Front 44

resting CV parameters in marathon runner

Back 44

resting SVR, venous sat, AVO2D, VO2, CO relatively normal; resting SV very high though, and as a result HR is very low and MAP on the lower side

Front 45

CV response to exercise in marathon runner: VO2, O2 sat/AVO2D, CO/HR/SV, MAP, SVR vs regular pt

Back 45

VO2 reaches much higher level than in average pt b/c CO so much higher; mixed venous sat drops from max at 75% to min at 13% (AVO2D rises while O2 sat drops) - this is a larger drop than in an average pt; CO rises rapidly as a result of initial large increase in SV w/ small incr in HR, when SV peaks (much later and higher than average pt), HR begins to climb more steeply (starts much lower than in average pt so can climb higher), CO peaks when HR reaches max (220-age); MAP rises as CO rises (final MAP much > average pt); SVR declines as CO rises (final SVR much < average pt)

Front 46

major diff btwn average pt and marathon runner

Back 46

marathon runner has much larger SV at rest, allowing for lower HR at rest (and thus larger increase to final HR, which is similar to average person); marathon runner can incr their SV to a much higher level than an average person, yielding a much larger CO for the same HR; marathon runner has lower SVR at peak, lower venous O2 sat at peak, and much higher O2 consumption, CO, SV, and MAP at peak