Microcirculation and Venous Return Flashcards
Why don’t capillaries burst?
Due to the law of Laplace, which equates wall stress and (pressure*radius)/thickness. Because radius is so small, wall stress is reasonable even with high pressure.
Wall stress in aorta vs capillaries
Aorta is 6x higher.
Law of Laplace
Wall stress = (pressure*radius)/thickness
How do gas/nutrients move across capillaries?
Via diffusion and filtration, thanks to slow velocity.
Where does most oxygen exchange occur?
At the beginning of the capillary.
Pc vs πc at beginning and end of capillary.
At beginning Pc (35mmHg) is higher than πc. At end, πc (25mmHg) is higher than Pc.
Starling equation
Q=k[(Pc-Pi) - (πc-πi)]. Filtration occurs on arterial end, absorption occurs on venous end.
Effect of Albumin in interstitial space?
Increased πi causing edema.
Effect of increased capillary hydrostatic pressure
Increased Pc leading to edema.
Will an increase in arteriolar pressure (MAP) lead to an increased Pc?
No, but increased pressure in veins will propagate back to capillaries increasing Pc.
What is autoregulation? Where does it occur?
In kidneys, heart, brain, muscle. If an increase in BP is sensed (which causes increased local flow), vasoconstriction occurs.
Active hyperemia
Metabolic activity, especially in skeletal muscle, causes the release of vasodilating agents
What is the effect of increased sheer stress (turbulent flow) on the vasculature?
Causes endothelial cells to produce activate eNOS, which converts arginine into NO, which diffuses to smooth muscle cells leading to vasodilation (cGMP mediated inhibition of MLCK).
eNOS
Turns arginine into NO. Activated in endothelial cells by increased sheer stress and CaM.
Three ways laminar flow becomes turbulent.
High velocity (v=Q/A), low viscosity, narrow BVs
Explain:
Starling curve. Cardiac output increases with increased preload. Indicative of the heart in isolation
Draw the venous return curve.
Couples function of heart to entire circulation.
When atrial pressure is lower, it is easier fror blood to flow into the atrium.
Draw cardiac output vs venous return graph
What happens to cardiac output if contractility is increased/decreased. Draw cardiac vs venous function graph.
Increased output leads to an increased pressure drop in arterioles, which leads to decreased venous pressures (because everything slows down), which leads to decreased venous return.
What happens to graph if there is a change in blood volume? Draw it.
Increased blood volume leads to increased cardiac output and increased right atrial pressure.
What happens to cardiac function x venous return graph with arteriolar constriction? Draw it.
Total peripheral resistance increases, causes a rotation of venous return curve and changes in the starling curve. No change in X intercept!
How will venoconstriction/change in venous compliance change the cardiac output x venous return graph.?
Change venous return curve. No change in y-intercept
What changes will increased blood volume cause on venous return graph?
Shift curve to the right. Will increase no flow pressure and increase maximal flow.
What changes will decreased TPR cause on venous return graph?
Will shift curve around same X intercept. No change in no-flow atrial pressure because most of the blood is in veins. Maximal flow increases because resistence decreases.
Four changes that occur in heart failure
1) Decrease in contractility due to damaged myocardium. This causes a decrease in cardiac output and an increase in venous pressure
2) Fluids are retained to increase preload further. This will increase CO, but will also further increase venous pressure.
3) Chronic sympathetic stimulation to improve myocardial performance. This increases contractility and HR, but can damage myocardium further.
