6 - Venous Return Flashcards
Conduit of blood that transport to periphery BACK to the <3
Veins
Difference of veins from arteries
Distribution of components!
Arteries - thicker
Veins - more compliant
Aka volume reservoir
Veins
T or F. Veins are major reservoir which is not controllable.
False! They are controllable. How? Because of pressure and sphincters which regulate blood flow from the arterial to the microcirculation to the venous system
Veins also have their own smooth muscles which maintains own tone. (Responsible for tone: ANS)
Compare the compliance and thickness of the veins in the Lower Ex from that of the Upper Ex
Lower Ex veins are less compliant and thicker
Venous compliance increases/decreases with age?
Decreases
-Elastin decreases while collagen increases
Unique feature of veins
Have valves!
Valves prevent backflow in your low pressure system.
T or F. Venous return is independent of your cardiac output.
FALSE!!! Venous return normally limits CO! Under steady state, CO should be equal to venous return.
Venous Pressure vs. Central Venous Pressure
Venous Pressure - average BP within the venous compartment
Central Venous Pressure - BP in the thoracic vena cava; filling pressure of RV -> reflects SV
Relationship of venous pressure to venous volume and venous compliance
Venous pressure is directly proportional to venous volume.
VP is inversely proportional to venous compliance.
Relationship of venous pressure and compliance
More compliant = lower P needed
Effect of gravity on venous pressure
Dependent areas = higher VP
Why do some people have varicose veins?
Incompetent valves = accumulation in dependent areas aka legs
Effect of skeletal muscle pump on venous return
Woman standing on tippy toes
-> Calf contracts -> distal valves close and proximal valves open -> venous blood pushed upward -> increased venous return
Woman no longer standing on tippy toes
-> Calf ms relaxes -> Proximal valve closes due to gravity pushing valve shut -> distal valves open -> decrease venous return
Effect of ankle pump to a bedridden patient with no possibility of DVD
> Help venous return and to maintain range of motion (inc venous return)
Effect of respiratory activity on venous return
Inspire:
Inc P in abdomen -> Inc vol of thoracic cavity -> dec P in thoracic cavity (Boyle’s Law) -> venous return increases bringing blood back to the <3
During inspiration
Diaphragm contracts -> Diaphragm goes down -> TC vol increases -> TC P dec (dec in P reflected in the structures inside the TC e.g. <3, VC (pulmo circ) -> VR inc in RA
In left side of <3, Venous return decreases
Why? Pulmonary vessels are more compliant (than systemic). If there’s (-) pressure inside thoracic cavity -> pressure in pulmo circ decreases so blood accumulates in more compliant pulmo vessels (not in LA) -> So VR during decreases
During expiration
Diaphragm goes back (relaxes) -> Vol dec -> P increases -> VR decreases
In the left side, VR increases because P would compress highly compliant pulmonary vessels in the thoracic cavity which would squeeze blood towards L side -> VR in L slide/LA increases
Thus, SV/CO/BP inc
During hyperventilation, CO increases/decreases?
Increases
Effect of blood volume on CVP
Inc BV -> Inc CVP -> Inc EDV -> Inc SV
- > Inc CO -> Inc MAP
- > Dec ESV
If you increase fiber length, why would you have an increase in tension?
If you increase ms fiber length -> increase sensitivity of troponin C to Ca2+ -> more tension produced in cross bridge cycling; If you stretch a ms -> bringing closer the distance between actin and myosin (shorter distance) -> more optimal interaction between actin and myosin
Effect of venomotor tone in CVP? VR? Venous capacity?
Venomotor tone
-tension created in a blood vessel
Veins can undergo constriction when the sympathetic NS dominates causing the smooth ms lining the veins to contract -> vasoconstriction -> inc tension -> inc venomotor tone
Remember: Role of vein - takes blood back to the heart
Vasoconstriction will inc CVP -> venous return will push the blood in front of constriction to the heart (like kinking a hose)
Inc venomotor tone -> Inc VR -> Decreases venous capacity
Effect of valsalva maneuver on venous return
When u poop (forceful expiration with a closed glottis) -> initially VR would increase bc of contraction of diaphragm and abdomen which increases abdominal P
Remember: Vessels in your abdomen are splanchnic = highly compliant so compress initially -> inc venous return but if prolonged expiration -> followed by prolonged decrease venous return
So effect: initially increase but eventually prolonged decreased venous return
Effect of venous filling pressure/VR on CO?
Effect of CO on VP?
Increase VR -> Inc CO because preload higher
Inc CO -> decreases VP
Why?
You increase amt of blood going out but right side connected to the venous side so you’re slowly drying up the well
(More blood being translocated to the arterial side)
*but eventually body will adjust to achieve homeostasis
Relationship of CVP and CO
Increase VR -> Increase CVP, Preload, SV -> Inc CO
But inc CO -> dec VP and Volume in the venous circ
Decreased VP -> Decreases CO
Venous Return formula
VR = (MAP - RAP)/SVR
*If high MAP (Pressure inside veins as compared to pressure inside atria) -> Flow proceeds from veins to RA
Venous return = CO (under steady conditions)
Under steady conditions, relate CO and VR. What happens if you have a congestive <3 failure?
Under steady conditions, VR = CO.
If you have a congestive <3 failure
If incompetent L side/failing L side of <3 that CO is so low -> there’s pooling of blood in the pulmonary area = PULMONARY CONGESTION
If incompetent R heart (RV) -> blood remains in periphery so patient will be edematous (liver congestion)
If patient is undergoing MRM bc of breast cancer (70 y.o.) -> tachycardia to 140 bpm 2’ to inadequate anesthesia and by ECG nagka ST elevations, T wave inversion, patient presented with pulmo congestion (may crackles)
What could have happened
Patient is undergoing MI (usually in MI, LV is affected) -> Won’t maintain CO (can’t pump blood back to <3 as efficiently as before so blood remains at the pulmo circ) -> *Give TropI!!!
Effect of CO on MAP and RAP
Increased CO = INC MAP AND DEC RAP
What is MCP? Depends on what factors?
Mean Circulatory Pressure
-Pressure throughout the vascular system when CO is 0/not pumping
-Pressure which keeps vessels open
~ 7 mmHg
-Depends on vascular compliance and blood volume
MCP curve:
Shift to the right implies? Left?
MCP curve: CO vs. P
Shift to the right
= increased MCP and blood vol -> Decreased venous compliance
Shift to the left: opposite
Increase vol and dec compliance -> inc RAP (& CVP) -> Inc CO -> shifts curve to the right
Systemic Vascular function curves
SVR vs. RAP
CO vs VP
Increased CO -> VP decreases
VP increases -> CO increases -> blood in R side of <3 decreases
Dec SVR -> inc RAP
Inc SVR -> dec RAP
Why?
Inc resistance in arterial system -> CVP & RAP decreases because…
You have highly constricted vessel -> harder to translocate blood from L to R side -> less blood translocating to arterial side which could have been translocated to the venous side which could have returned to RA
When CO = 0, VP = ?
MCP
Effect of RAP on CO?
Inc RAP -> Inc CO
Inc <3 performance -> Inc CO -> RAP decreases (shifts the curve up and to the left)
Dec CO -> shifts curve down to the right
Magnitude by which CO changes when cardiac performance is altered is determined by the state of systemic vascular fxn
Effect of hypervolemia and hypovolemia
Hypervolemia (increased venous tone) fill the CV system -> raises MCP (by squeezing blood contained in the veins and, in turn, raising their internal pressure)
Hypovolemia
Dec venous tone -> dec VP
Septic shock
- Albumin no effect
- Diuretics: SV affect which is not good; BP falls
- Give constrictors (but if too constricted, give inotropes tom improve SV and CO)
