Download Physio Lecture 18 Vessels and Flow Dynamics

Lecture 18 Vessels and Flow Dynamics
REVIEW OF ANATOMY OF BLOOD VESSELS
END OF REVIEW OF ANATOMY OF BLOOD VESSELS
The driving force of BP is from high to low pressure. Too low BP means that the tissues in the body are
not well perfused with blood.
Arterial Pulsations and Pulse Pressure
• The height of the pressure pulse is the systolic pressure (120mmHg), while the lowest point is
the diastolic pressure (80mmHg).
• The difference between systolic and diastolic pressure is called the pulse pressure (40mmHg).
Factors Affecting Pulse Pressure
• Stroke volume —increases in stroke volume increase pulse pressure, conversely decreases
in stroke volume decrease pulse pressure.
•
Arterial compliance —decreases in compliance increases pulse pressure; increases in
compliance decrease pulse pressure.
HR x SV = CO = MAP/ TPR
MAP= (0.4 SP) + (0.6 DP)
PP= SP- DP
Damping of Pulse Pressures in the Peripheral Arteries
• The intensity of pulsations becomes progressively less in the smaller arteries.
•
The degree of damping is proportional to the resistance of small vessels and arterioles and the
compliance of the larger vessels.
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The intensity of pulsations becomes progressively less in the smaller arteries.
The degree of damping is proportional to the resistance of small vessels and arterioles and the
compliance of the larger vessels.
How Arteries help modify blood pressure before getting to the capillaries
• Elastic arteries: large radii, low resistance, some pressure reservoir
• Muscular arteries
– Smaller radii
– Little more resistance
– More pressure reservoir
• Arterioles
– Thick tunica media vs. radius
– major pressure reservoir
Central Venous Pressure
• Pressure in the right atrium is called central venous pressure.
• determined by the balance of the heart pumping blood out of the right atrium and flow of blood
from the large veins into the right atrium.
• normally 0 mmHg, but can be as high as 20-30 mmHg.
• More vigorous heart contraction (lower CVP).
•
Less heart contraction (higher CVP)
• Factors that increase CVP:
increased blood volume
increased venous tone (peripheral pressure)
dilation of arterioles
decreased right ventricular function
Skeletal and respiratory pumps
Resistance makes a difference for the two sides of the heart!
• Let’s say the CO (flow) is roughly 100ml/sec (easier math).
• To calculate systemic resistance vs. pulmonary resistance we need to know pressure
differences.
• Pulmonary resistance is 16-2/100
• Systemic resistance is 100/100
• So, CO is same on each side of heart (has to be!), but right side generates less pressure due to
lower resistance (1/7th than systemic).
What organ starts the pressure gradient? The heart.
Does the blood flow only when the heart is beating? No.
The pressure gradient is continued in the large arteries with their expansion and recoil.
Pressure is the driving force for blood flow.
What is the clinical importance of blood pressure? When we take someone’s BP, we evaluate the blood
flow and perfusion to tissues, accumulation of waste products. It tells us if they have adequate
perfusion.
Viscosity
• What are the major contributors to blood viscosity? Anemic people have reduced amount of
blood cells, reduced viscosity, get increased flow. Polycythemia are too many RBCs, increases
viscosity.
• As viscosity increases, resistance will…increase.
• An increase in plasma EPO will cause resistance to…
Radius
The larger the radius, the less resistance
This is the most important factor to resistance. It is to the power of four. If the radius doubles, blood
flow will increase 16x
Total Vessel Length
• Longer the vessel.....more opportunity for resistance.
Viscosity and BV length are numbers in the denominator of the equation. Length and viscosity have a
linear relationship. If length increases, flow decreases. If viscosity increases, flow decreases.
If radius increases, flow extremely increases. Radius is not linear, it is to the power of 4. Radius is
inversely to viscosity and length.
If you want to increase pressure to increase flow, what can you do?
1) Increase stroke volume (contractility of the heart)
2) Increase resistance (Remember, vasoconstriction does not mean there is no flow, they just
reduce their diameter). This creates more flow. Increase vasomotor activity. Reduce the
compliance.
A dehydrated person has decreased blood flow; BP drops, and needs compensation.
If you are bleeding out, sympathetic system causes vasoconstriction to non critical organs. Blood will be
shunted to other vessels, and BP to those vessels will increase. Vasomotor activity means that more
pressure is applied, more blood will flow. Vasoconstriction means that the blood vessel has closed so
much that there is reduced blood flow to that vessel.
Flow (amount of blood/time) MUST be the same through vessels in series!
If a pipe’s diameter changes over its length, a fluid will flow through narrower segments faster than it
flows through wider segments because the volume of flow per second must be constant throughout the
entire pipe.
Flow (volume/time) vs. velocity (distance/time) are NOT synonyms!
If resistance decreases, what will happen to flow? Increases
If pressure increases, what will happen to flow? Increases
If radius increases, what will happen to flow? Increases 16-81x
Whatever goes in a vessel has to leave the vessel, or it will pop.
If a hose diameter suddenly gets smaller, rate of flow has to increase.
If capillaries have such a small diameter, why is the velocity of blood flow so slow?
Let’s say 5ml of blood flows through an artery, then through an arteriole, then to a capillary.
What happens to the velocity as it goes there? You would predict that it would increase, but it actually
decreases, otherwise it would rupture the capillary. You have only one aorta, but you have 10 billion
capillary beds, so collectively they would have a much larger lumen than the aorta. So the pressure
goes down by the time it gets to the capillaries. The blood flow starts to slow as soon as it leaves the
aorta because it flows into several other muscular arteries, which flows to more arteries, into many
more arterioles, etc.
Control of blood flow through vessels- Why is this important? Tissues need perfusion
• Perfusion vs. ischemia vs. hypoxia vs. anoxia vs. infarction
– Ischemia is lack of blood flow
– Hypoxia is reduced oxygen content in the tissues
– Anoxic means there is no oxygen
– Infarction is death of tissue from lack of oxygen
• Tissue Perfusion Dependent on:
– Cardiac output
– Peripheral resistance; vasoconstriction will cause decreased flow downstream.
• Infections cause increase nitrous oxide in tissues, which causes vasoconstriction,
so BP drops
– Blood pressure: when you stand up too fast and feel dizzy, it is called orthostatic
hypotension. Brain needs time to compensate.
• Regulation of perfusion dependent on:
– Autoregulation (Acute, local, intrinsic)
– Neural mechanisms (acute)
– Endocrine mechanisms (long-term)
Metabolically active tissues and organs produce a lot of waste products, such as lactic acid, C02, etc.
Some of these products are vasodilators. They trigger the precapillary sphincters to relax, so blood flows
more through the capillary beds. This helps to remove the wastes. Therefore, the precapillary sphincters
will contract, shutting down the capillary bed again. We don’t want oxygen in areas where it is not
needed. When waste products build up again, capillary bed will open. This is Autoregulation. Capillary
beds control their own blood flow.
Autoregulation of Blood Flow to specific tissues (Know this list)
• Vasodilator agents
Histamine
Nitric oxide
Elevated temperatures
Potassium/hydrogen ions
Lactic acid
Carbon dioxide
Adenosine/ ADP
• Vasoconstrictors
Norepinephrine and epinephrine
Angiotensin
Vasopressin (ADH)
Thromboxane
Oxygen
Note: in the kidneys and the lungs, some of the above substances have the opposite effect than in the
rest of the capillary beds. We will talk about these exceptions to the rule later.
Brain Centers involved in Short Term BP Control
• Vasomotor
– Adjusts peripheral resistance by adjusting sympathetic output to the arterioles
• Cardioinhibitory- transmits signals via vagus nerve to heart to decrease heart rate.
(parasympathetic)
• Cardioacceleratory/ contractility-sympathetic output
Vasomotor control: Sympathetic Innervation of Blood Vessels
• Sympathetic nerve fibers
1) Innervate all vessels except capillaries and precapillary sphincters (precapillary
sphincters follow local control)
2) Innervation of small arteries and arterioles allow sympathetic nerves to increase
vascular resistance.
Large veins and the heart are also sympathetically innervated
Anatomy of the Baroreceptors
• Spray type nerve endings located in the walls of the carotid bifurcation called the carotid sinus
and in the walls of the aortic arch-pressoreceptors that respond to stretch.
• Signals from the carotid sinus are transmitted by the glossopharyngeal nerves.
• Signals from the arch of the aorta are transmitted through the vagus into the NTS.
• Important in short term regulation of arterial pressure.
They are unimportant in long term control of arterial pressure because the baroreceptors adapt.
Carotid and Aortic Chemoreceptors
• Chemoreceptors are chemosensitive cells sensitive to oxygen lack, CO2 excess, or H ion excess.
• Chemoreceptors are located in carotid bodies near the carotid bifurcation and on the arch of the
aorta.
• Activation of chemosensitive receptors results in excitation of the vasomotor center.
Nervous control also found in the heart- Bainbridge Reflex
• Prevents damming of blood in veins, atria and pulmonary circulation.
• Increase in atrial pressure increases heart rate.
• Stretch of atria sends signals to VMC via vagal afferents to increase heart rate and contractility.
The Microcirculation
• Important in the transport of nutrients to tissues.
• Site of waste product removal.
• Over 10 billion capillaries with surface area of 500-700 square meters perform function of solute
and fluid exchange.
Determinants of Net Fluid Movement across Capillaries-Starling forces
• Capillary hydrostatic pressure (Pc)-tends to force fluid outward through the capillary membrane.
(30 mmHg arterial; 10mmHg venous- average 17.3mmHg)
• Interstitial fluid hydrostatic pressure (Pif)- opposes filtration when value is positive (but it’s not!
Due to lymphatic drainage! – 3mmHg).
• Plasma colloid osmotic pressure (p c)- opposes filtration causing osmosis of water inward
through the membrane
• Colloid osmotic pressure of the blood plasma. (28mmHg)
• 75% from albumin; 25% from globulins
• Interstitial fluid colloid pressure (p if) promotes filtration by causing osmosis of fluid outward
through the membrane
• Colloid osmotic pressure of the interstitial fluid. (8mmHg)
• 3gm%
The four Starling pressures are: two hydrostatic pressures and two colloid osmotic pressures.
There is a hydrostatic pressure in the capillaries and a colloid osmotic pressure in the capillaries.
There is a hydrostatic pressure in the interstitial space and a colloid osmotic pressure in the interstitial
space.
The hydrostatic pressure in the capillaries is fluid exerting pressure outward on the vessel wall.
The colloid osmotic pressure is from proteins in the plasma that have osmotic draw from the interstitial
space into the capillary bed. There are also proteins in the interstitial space that have osmotic draw of
fluid from the capillary bed into the interstitial space. You might think that the interstitial hydrostatic
pressure would push against the vessel wall. However, there is another series of vessels (lymphatic)
around capillary beds that produce suction, and they actually drain the interstitial fluid. So the
hydrostatic pressure in the interstitial space is actually negative instead of positive. It favors outward
movement of fluid.
The Starling pressures are not the only factors affecting fluid movement. There is also a permeability
coefficient (Kf). There are times when Kf fluctuates, such as when there is a copious amount of
histamine production from mast cells. Histamine makes the capillaries more porous, so there are more
gaps for fluids to leak out into the interstitial space. When Kf increases, permeability is increased, and
the amount of fluid leaving the capillary increases, and the fluid moves into the interstitial space.
In the renal lecture, you will also need to understand these forces in the capillary bed of the glomerulus
of the kidney. If the capillary hydrostatic pressure is higher than the capillary osmotic pressure, you get
filtration. If it is lower, fluid moves back into the vessel. The glomerulus is not just a flat capillary bed. It
is all balled up into a cup shape, so we don’t see drastic changes in hydrostatic pressure there. The Kf of
the glomerulus is very high because the capillaries are fenestrated. A lot of fluid will leave the plasma in
the glomerulus.
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Lymphatic vessels collect lymph from loose connective tissue
– Fluid flows only toward the heart
– Collect excess tissue fluid and blood proteins and carry to great veins in the neck
– All three tunics
– NO pump! It relies on the skeletal muscles to push on the lymph vessels to move the
fluid upward toward the heart.
– Has valves!
contains plasma, water, ions, sugars, proteins, gases, amino acids- is colorless, but low in protein
compared to blood
Lymph can contain hormones and large things such as bacteria, viruses, cellular debris, traveling
cancer cells, macrophages. The large things get trapped in the lymph vessel, blocked in by the
valves, and are forced into the lymph nodes upstream. Within the lymph nodes are large
amounts of WBCs that are waiting to phagocytize these large particles.
Causes of Edema
• Excessive accumulation of tissue fluid.
• Edema may result from:
– High arterial blood pressure.
– Venous obstruction.
– Leakage of plasma proteins into interstitial fluid.
– Valve problems
– Cardiac failure
– Decreased plasma protein.
– Obstruction of lymphatic drainage. Elephantiasis- Wuchereria bancrofli
Be able to understand what force, what factor, is changed as a result of edema.
For example, what if the patient was hypovolemic? That means low blood volume. The force that was
impacted directed is capillary hydrostatic pressure, which drops. The fluid that leaves the capillary bed
to go into the interstitial compartment would decrease. The oxygen can still diffuse across since it is a
gas, but there will be a decrease in nutrients to the tissues. This can lead to shock. Less filtration of
fluids, metabolic wastes accumulate, leads to cell death.
If the patient was ischemic (lack of blood flow), tissue can die from lack of oxygen.
If tissues are deprived of nutrients, they can begin programmed cell death. The lysosomes release their
contents, ATP is reduced to ADP, phosphates come off, and tissues die. In excess, can lead to shock, they
can no longer recover.
More salt leads to greater blood volume, which leads to an increase in blood pressure.
Decreased plasma proteins means decreased capillary colloid osmotic pressure, fluid moves back into
the capillary. Proteins can leak out in a burn or crush injury. Burns increase Kf and decreased colloid
osmotic pressure. The proteins leave the capillary. Block of lymph return causes increased fluid in
interstitial fluid. Also understand if edema would be systemic or pulmonary.