Exam 1 - Control Of Cardiac Output Flashcards
3 basic principles of blood flow
1 - Control of flow to local tissues depends on metabolic need
2 - VR is sum of flow from local tissues and CO is driven by VR
3 - BP is independent of control of flow through local tissue and CO
Baroreceptors
- respond to moment to moment changes
- respond to increase or decrease in BP fro normal MAP
~ all others respond to drop in MAP
Responds to changes in pressure over all ranges
- Baroreceptors
- Cap fluid shift
- Stress relaxation/constriction
- Renal BP control (long term)
Responds to changes when MAP drops
- Chemoreceptors
- Renin-angiotensin / aldosterone
- CNS ischemic response
CO
CO = HR x SV
HR: autonomic innervation (para) / drugs
SV: autonomic innervation (symp) / preload / afterload
CO vs VR
- Over time…they must be equal
- May be different for a few beats
- CO affected by: metabolic activity / body mass / age
- VR determines CO
Frank-Starling law
- SV changes based on VR
- Increased VR produces more stretch which increases SV/HR
Q (sum of all VR) =
Q = P/SVR
- SVR changes based on metabolism…inversely proportional
~ only works if body maintains constant MAP
ANS and maintaining MAP
- ANS keeps MAP constant (baroreceptors)
- Allows CO to change based on metabolic need / SVR changes
- Without ANS…MAP drops as SVR drops with minimal CO change
Peak CI
- Age 8-10
- 4 to 4.5 L/min/m2
Affect of age on CI
- metabolic activity determines CO
- CI drops as you age due to drop in muscle mass / activity
~2.4 @ 80 yo
Average CO
- 5.0 L/min
- Male: 5.6
- Female: 4.9
- CI: 3.0
Hypereffective
- Increased CO from changes in contractility and HR
- Curve shifts UP and LEFT
- Causes: sympathetic / hypertrophy
Hypoeffective
- decreased CO
- curve shifts DOWN and RIGHT
- caused by: anything that makes the heart pump less effectively
RAP
Resting Atrial Pressure aka CVP
Normal ANS tone
Resting: RAP - 0 / CO - 5.0
Max: RAP > 4 / CO - 13.0
Hypereffective heart values (nervous only)
Max: RAP > 4 / CO - 25
Hypereffective heart values (hypertrophy and symp)
- Mass is 50 - 75% greater
- Max: RAP > 4 / CO - 30 to 40
CO vs External Pressure
- Intrapleural pressure usually -4 mmHg
- Increase intrapleural pressure increases RAP
~ 1:1 ratio - Hypereffective shifts cardiac function curve up (hypo is oppo)
- Increased intrapleural pressure shifts right (visa versa)
Cardiac tamponade
- fluid build up around heart
- heart cannot fill properly
- hypoeffective
- drop in pre-load
Factors that alter external pressure
- respiration cycle
- negative shifts left…positive shifts right
- open thoracic cage….move to 0 mmHg…. shift curve right 4
- cardiac tamponade
To get VR….
Need pressure drop from caps to RA
Central vs Peripheral venous compartment
Central: affected by intrathoracic pressure
Peripheral: not affected
VR = (peripheral venous p - CVP) / venous resistance
~ same equation as before
Ventricle values
Volume: 30
Compliance: 24
Resistance: 0
Artery values
Volume: 600
Compliance: 2
Resistance: 1
Arterioles values
Volume: 100
Compliance: 0
Resistance: 13
Capillary values
Volume: 250
Compliance: 0
Resistance: 5
PVC values
Volume: 2500
Compliance: 110
Resistance: 1
CVC values
Volume: 80
Compliance: 4
Resistance: 0
Entire body values
Volume: 3560
Compliance: 140
Resistance: 20
R in Wood units
Normal systemic volume
- 4500 mls
- 4500-3560 = 1000
- 1000/140 = 7 mmHg pressure when full but no flow
Mean systemic filling pressure
- Psf
- similar to Pmf (Mean circulatory filling pressure)
- Pmf includes pulmonary but it has minimal effect
Arteries vs Venous compliance
- change in volume has bigger pressure change in arteries
~ arteries have lower compliance (2 vs 110)
CVC
- RA and central veins in thorax
- volume depends on VR (in) vs CO (out)
Factors affecting VR
- Pressure in PVC (usually = Psf = 7 mmHg)
- Venous resistance: 2/3 veins and 1/3 arterioles (1.4)
- Pressure in CVC (usually 0 mmHg)
- VR = Psf - RA / Resistance -> 7/1.4 = 5 L/min
Venous function curve
- independent = RAP aka CVP
- dependent = VR
- RAP/CVP affect VR…not the other way around
Changing Psf and venous curve
- Can change Psf by adding CBV
- increase CBV….curve shifts right
- increase resistance….curve SLOPE drops down
~ up resistance….down VR
Intersection of Cardiac and Venous curves
- Shows CO / VR / CVP
Increase in CVP on cardiac and venous curves
- increase CO
- decrease VR
- more volume leaving CVP than coming in -> CVP drops until back to equilibrium (CO and VR are equal)
What has to happen to get a change in CO
- one or both curves have to shift
- Cardiac shifts: Change in cardiac effectiveness (hyper/hypo)
Change in external pressure - Venous shifts: Change in Psf aka CBV
Change in venous resistance (slope)
Effect of increasing CBV
- Increases Psf
- Distends vessels so resistance drops
- Venous curve shifts right and slope increases
- Kidneys will take off extra volume over time (big player)
~ fluid also moves to 3rd space (edema)
~ autoregulation constricts
~ fluid stored in liver and spleen
- all these try to bring Venous curve back to normal spot
Response to hemorrhage
- Loss of volume shifts venous curve left
- symp stimulation kicks in (cardiac curve up and left)
~baroreceptors / CNS ischemic / chemoreceptors / etc. - symp stimulation constricts veins (shifts venous curve back right a little)
Inotropic drugs
- increase cardiac curve (increases contractility)
Vasoactive drugs
Changes venous curve resistance (slope)
Diuretic drugs
- shifts venous curve based on loss or gain of volume
