Peripheral Circulation Flashcards
(43 cards)
1
Q
Compliance
A
- the higher the compliance of a vessel, the more
volume it can hold at a given pressure. - Compliance of the veins is high; the veins hold large volumes of blood at low pressure.
- Compliance of the arteries is much lower than that of the veins; the arteries hold much less blood than the veins, and they do so at high pressure.
- Aging decreases the compliance of arteries.
2
Q
Cross-Sectional area and Velocity relationship?
A
- increased cross sectional area causes decrease in velocity
- capillaries have the largest cross sectional area and lowest velocity
- aorta has greatest velocity (it is the smallest vessel in cross sectional area)
3
Q
Velocity of Blood Flow Equation:
A
V= Q/A
V= velocity
Q= Blood Flow
A= Cross sectional area
** velocity is inversely proportional to cross sectional area
4
Q
What factors impact vessel resistance?
A
- diameter (increased = decrease R)
- length (increased = increased R)
- blood viscosity (increased = increased R)
5
Q
Pressure Difference
A
- “pressure gradient” along the
vessel. It is the force that
pushes the blood through the
vessel
6
Q
What is Conductance?
A
- opposite of resistance
- ease with how blood can flow
- measure of the blood flow through a vessel for a given pressure difference
7
Q
How much does the conductance of a vessel increase in proportion of the diameter?
A
- FOURTH POWER diameter
- fourfold increase in vessel
diameter can increase the flow as much as 256-fold.
Thus, this fourth power law makes it
possible for the arterioles, responding with only small changes in diameter to nervous
signals or local tissue chemical signals, either to turn off almost completely the blood flow to the tissue or at the other extreme to cause a vast increase in flow.
8
Q
When does Laminar flow occur?
A
- The velocity of flow in the center of the vessel is far greater than that
toward the outer edges. - The layer of fluid adjacent to the vessel wall has hardly moved,
- The layer slightly away from the wall has moved a small distance,
- The layer in the center of the vessel has moved a long distance.
- This effect is called the “parabolic profile for velocity of blood flow.”
9
Q
When does Turbulent flow occur?
A
- Turbulent flow means that the blood flows crosswise in the
vessel as well as along the vessel, usually forming whorls in
the blood called eddy currents - Blood flow may become turbulent or disorderly when:
1. It passes by an obstruction in a vessel,
2. It makes a sharp turn, or
3. It passes over a rough surface
Laminar flow is silent, while turbulent flow is audible.
10
Q
When are Korotkoff sounds heard?
A
auscultatory measurement of blood pressure are caused
by turbulent flow.
Blood vessel stenosis (narrowing) and cardiac valve disease can cause turbulent flow and
often are accompanied by audible vibrations called bruits/murmurs.
11
Q
Factors that impact Turbulent Flow?
A
- The tendency for turbulent flow increases in direct proportion to the:
1. velocity of blood flow,
capillaries: small diameter = less chance
2. diameter of the blood vessel, - inversely proportional to the:
1. viscosity of the blood
(anemia decreases viscosity which decreases resistance, and increases velocity)
12
Q
Effect of Blood Hematocrit and Blood Viscosity on Vascular Resistance and Blood Flow
A
- The percentage of the blood that is cells is called the
hematocrit. - The viscosity of blood increases drastically as the
hematocrit increases - The viscosity of whole blood at normal hematocrit is
about 3; this means that three times as much
pressure is required to force whole blood as to force
water through the same blood vessel. - When the hematocrit rises to 60 or 70, which it
often does in polycythemia, the blood viscosity can
become as great as 10 times that of water, and its
flow through blood vessels is greatly retarded.
13
Q
Pressure Profile in the Vasculature
A
Mean pressure in the aorta is high, (averaging 100 mm Hg) because of:
-the large cardiac output
-the low compliance of the arterial wall.
The pressure remains high in the large arteries, because of the high elastic recoil of the arterial walls.
In the small arteries, particularly in the arterioles, mean pressure drops significantly (approximately
30 mm Hg) because:
-a high resistance to flow
-the constant flow across the cardiovascular system
In the capillaries, pressure decreases further because:
-frictional resistance to flow
-filtration of fluid out of the capillaries
In the venules and veins, pressure decreases even further (vena cava 4 mm Hg).
-high capacitance of the veins is high, the veins can hold large volumes of blood
Pressure in the right atrium is even lower at 0–2 mm Hg.
14
Q
Two Major Determinants of Pulse Pressure?
A
- Stroke volume
- Stroke volume is the amount of blood pumped by the ventricles during
each beat. - It is the major determinant of Systolic Blood Pressure.
- Stiffness of Aorta (Elasticity) – Compliance
- Stiffness can change with age and disease of aorta
- Keeping stroke volume constant, if the aorta becomes stiffer, SBP
increases. - As age increases Systolic blood pressure increases.
15
Q
Aortic Compliance (stiffness of Aorta)
A
- Aortic compliance decreases with age due to structural changes, thereby producing age-dependent increases in pulse pressure.
Because the aorta is compliant, as blood is ejected into the aorta, the walls of the aorta expand to
accommodate the increase in blood volume.
* This helps to dampen the pulsatile output of the left ventricle, thereby reducing the pulse pressure (systolic minus diastolic arterial pressure). If the aorta were a rigid tube, the pulse
pressure would be very high.
- As the aorta expands, the increase in pressure is determined
by the compliance of the aorta. The more compliant the
aorta, the smaller the pressure change during ventricular
ejection (i.e., smaller pulse pressure)
16
Q
Arteriosclerosis
A
-plaque deposits decrease the diameter of the arteries
-arteries are stiffer and less compliant
-increased pulse pressure
-Increased arterial pressure
17
Q
Aortic stenosis
A
-reduction in opening through which blood can be
ejected
-stroke volume is decreased
-decreased systolic pressure
-decreased pulse pressure
18
Q
Patent ductus arteriosus
A
-ejected blood flows back into pulmonary artery
-decreased diastolic pressure
-increased systolic pressure
-increased pulse pressure
19
Q
Aortic regurgitation
A
Valve does not close completely
-ejected blood flows back into left ventricle
-decreased diastolic pressure
-increased systolic pressure
-increased pulse pressure
20
Q
Explain Baroreceptor Properties
A
- discharge rate is at high and low BP
- sensitive range is 60-160mm Hg
- respond more rapidly to changing BP than to stationary high/low levels of BP
21
Q
What is CNS Ischemic Response?
A
If blood flow is decreased to the vasomotor centre in the lower brainstem and CO2 accumulates, the CNS ischemic response is initiated
- very stron sympathetic stimulator causing major vasoconstriction and cardiac acceleration
- called the last ditch stand
22
Q
When does the RAAS come into play?
A
When blood pressure falls
Decreased blood flow causes decreased flow to the kidneys, decreased flow to kidneys decreases GFR.
23
Q
Explain 3 mechanisms of RAAS
A
- Nervous: JG cells are specialized smooth muscle cells innervated by sympathetic nerves. More action potentials causes more renin secretion
- Baroreceptor: Blood pressure falling causes decreased afferent arteriole wall stretch and more renin secretion
- Chemical: DIstal tubule macula densa cells sense Na in tubular fluid and with decreased GF rate because of decreased blood pressure, there is less Na filtered into the tubular fluid, and more renin is secreted
24
Q
Explain how RAAS works
A
- Decreased renal blood flow causes release of renin, which converts angiotensinogen (from the liver) to angiotensin I
- Angiotensin I then gets converted to active angiontensin II by angiotensin converting enzyme that is found in the lungs
- angiotensin II acts on the adrenal cortex, brain, and blood vessels
1. Adrenal cortex: release of aldosterone which causes sodium and water retention in kidneys which bring the BP up
2. Brain: causes increased thirst and vasopressin (ADH release) which also causes sodium and water retention
3. Blood vessels: vasoconstriction and restoration of blood pressure
25
Explain the role of ADH (Vasopressin)
- ADH is synthesized by neurons in the hypothalamus and transported to posterior pituitary where it is stored
- V1: causes vasoconstriction which increases systemic vascular resistance and increases arterial pressure
- V2: in the kidneys it causes fluid reabsorption which increases blood volume and that increases arterial pressure
26
What factors cause the hypothalamus and posterior pituitary to release ADH (Vasoporesin)?
1. Hyperosmolarity
2. Angiotensin II
3. decreased atrial receptor firing
4. sympathetic stimulation
27
Where is Atrial Natriuretic Peptide (ANP) secreted from?
Atrial myocytes
28
Where is Brain Natriutetic Peptide (BNP) secreted from?
Ventricular myocytes
29
What is the role of ANP?
- it is secreted when blood volume is high (increased secretion with increased wall stretch or stress)
1. ANP dilates the afferent arteriole leading to increased blood flow and filtration = diuresis
2. ANP suppresses reabsorption of Na+ in the collecting duct and other segments of the nephron = naturesis
- increases excretion of water and sodium, loss of sodium
30
Explain the BrainBridge Reflex
When too much blood returns to the heart (increased blood volume), the atrium walls stretch from the extra blood. The stretch receptors in the atria sense this stretch and send a signal to the brain (via the Vagus Nerve). The brain responds by sending commands through both the Vagus and sympathetic nerves to increase the heart rate and pump harder. This reflex helps move blood out faster, preventing the backup into veins and lungs (RS HF).
The stretch receptors elicit the Reflex by:
- the afferent signals are through the vagus nerve to the medulla of the brain
- the efferent signal are transmitted back through vagal and sympathetic nerves to increase HR and strength of heart contraction
31
Where is Renin released from?
Renin is released from the JG cells in the afferent arteriole of the kidneys, specifically in the JG apparatus near the glomerulus
These cells release renin in response to:
- low blood pressure
- low sodium levels in the distal tubule (sensed by macula densa cells)
- sympathetic nervous system activation (via B1 receptors): THIS MEANS that the kidneys can stimulate the release of renin through the B1 adrenergic receptors because the JG cells in the kidneys have B1 receptors on their surface. When stressed, dehydrated or have low blood pressure, your sympathetic nerves release norepinephrine. NE binds to B1 receptors on the JG cells and this binding causes renin release which helps raise BP.
32
Explain Aldosterone
aldosterone is from the adrenal cortex and tells kidneys to reabsorb sodium and water, which increases blood volume
33
Differences between Aldosterone and ADH (Vasopressin)?
ADH: when you are dehydrated (blood is too concentrated or blood pressure is too low), brain releases ADH from the posterior pituitary and travels to the kidneys telling them to hold onto water ONLY. ADH makes the collecting ducts in kidneys more permeable to water, allowing rater to be reabsorbed back into the bloodstream and making the urine MORE concentrated and LOWER in volume. It does not touch salt or electrolytes -- just water
Aldosterone: it is released from the adrenal glands (cortex) when blood pressure is low, potassium levels are high, and the RAAS system is activated.
Aldosterone acts on the distal tubule and collecting duct, saying to reabsorb sodium and get rid of potassium. Since water follows sodium, this leads to an increase in blood volume and pressure. Aldosterone doesn't make urine more concentrated, but it reduces the total amount of sodium (and water) lost in urine. Remember that Renin activating angiotensin II causes aldosterone to be released when there is low blood pressure or low sodium.
34
Heart Failure and the role of ADH (vasopressin) and Aldosterone
When your heart isn't working well, your kidneys think there is low blood pressure, even if there is enough fluid in the body.
If the body thinks there isn't enough blood pressure or volume, the RAAS system kicks in causing renin to create angiotensin II which stimulates the adrenal cortex to release aldosterone. Now, more sodium and water are reabsorbed. ADH is released as well from the posterior pituitary causing more water to be backed up in body.
The body has now held onto too much fluid, causing an increase in blood volume but the weak heart cannot pump it well.
Now, fluid backs up causing edema, pulmonary congestion and worsened heart failure
35
Hypertension due to stenosis of the renal artery
When there is stenosis in one or both of the renal arteries (such as due to atherosclerosis), this means that less blood reaches the kidneys and it will think that blood pressure is too low.
The kidney reacts by releasing renin from the JG cells.
Renin stimulates the RAAS system -- making angiotensin II and aldosterone
This causes the body to retain salt and water which will increase the blood volume and blood pressure.
This is a secondary hyperaldosteronism because aldosterone is released due to trigger from high renin (found in low blood volume/dehydration, chronic heart failure, renal artery stenosis)
36
Secondary vs. Primary hyperaldosteronism
Secondary is when the adrenal gland is obeying renin signals = high renin, high aldosterone
Primary is when adrenal gland is misbehaving = high aldosterone, low renin because body can see there is enough fluid and pressure
** Conns syndrome is a aldosterone-producing adrenal tumor
37
Goal and role of Natruiretic Peptides (ANP/BNP)
These peptides want to increase urine output (get rid of salt and water) and lower blood volume and pressure.
To do that, the kidneys need to filter more blood into urine, and that happens at the glomerulus.
How to increase filtration?
You boost glomerular capillary pressure, which increases GFR. To do this effectively, we need to dilate the afferent arteriole (more blood enters glomerulus) and constrict the efferent arteriole. This increases the pressure inside the glomerulus (because we constrict efferent) so more pressure builds up causing even greater filtration.
ANP also decrease kidney Na+ absorption, decrease aldosterone synthesis and renin secretion, increase capillary/venule filtration and decrease plasma volume.
Na+ and H2O excreted in urine = natriuresis and diuresis
38
Explain the Stress Relaxation mechanism
When blood pressure goes up (exercise, stress, extra fluid), this causes the walls of blood vessels to stretch. In response, the smooth muscle in the vessel walls relaxes (stress relaxation).
When the muscles relax, the blood vessels widen and increase capacity. This makes space for more blood, which lowers the pressure inside.
Blood vessels stretch and relax to help buffer rising blood pressure
39
Explain difference between Stress relaxation, Autoregulatiion and Baroreceptor Reflex
1. Stress relaxation: slow response, happens in veins and arteries and is triggered by persistent stretch. It lowers BP after its been high for a while as a mechanical buffer system by relaxing vessels
2. Autoregulation: tissue- level local control to maintain constant blood flow, even if blood pressure changes. It is local and rapid, common in brain, kidneys and heart. If BP drops, vessels dilate and if BP rises vessels constrict to prevent over-perfusion. Keeps blood flow constant to organs.
3. Baroreceptor: neural (nervous system) reflex to adjust HR and vessel tone to regulate BP. It is the fastest response and involves the carotid sinus and aortic arch baroreceptors. If BP rises, baroreceptors fire MORE which decrease the sympathetic tone, and lower heart rate + dilate vessels.
40
Why does diastolic pressure decrease in both Patent Ductus Arteriosus and Aortic regurgitation?
First, know that diastolic pressure is the pressure in the arteries once the heart is relaxing and no blood is being pumped. It reflects how well the arteries hold onto pressure between beats.
When the heart pumps (systole), the blood rushes into the arteries and stretches them. During diastole (relaxation), the arteries recoil and keep pushing the blood forward, maintaining a certain baseline pressure (diastole).
In PDA and AR, blood that is supposed to stay in the aorta/arteries and keep pressure up or at baseline during diastole is leaking backwards into either the pulmonary arteries (in PDA) or left ventricle (in AR).
If blood is escaping the arteries during diastole, theres less blood in system to hold the pressure up and diastolic pressure drops
** systolic pressure increases for both because there is extra volume the heart has to pump out again
41
What is incisura (dicrotic notch)?
During systole, the left ventricle contracts and pumps blood into the aorta (pressure rises).
When the ventricle finishes pumping and relaxes, the aortic valve snaps shut to stop blood from leaking back in.
The sudden closure causes a brief back flow of blood, which bounces against the closes valve and makes a little dip (notch) in the pressure curve.
** There is absent incisura in aortic regurgitation because the valve does not close properly and there is no sudden snap shut, no bounce, no dip.
42
Aortic Compliance and Pulse Pressure
Compliance shows how stretchy the aorta is. A stretchy aorta can expand easily when blood is pumped into it.
When the aorta is stretchy, it can absorb some of the pressure from the heartbeat so systolic pressure stays lower and pulse pressure stays narrower.
When the aorta is stiff (low compliance), it cant expand well, so pressure rises more during systole and pulse pressure becomes wider.
Normal compliance: for a given change in volume, the pressure increase is small (the aorta absorbs the pulse gently).
Low compliance: same amount of blood, but pressure goes up a lot. This means the aorta is stiff, so it resists the incoming blood and causes a big spike in pressure.
The aorta becomes less elastic (stiffer) with age, so older adults have higher systolic pressure and wider pulse pressure.
43
Blood Hematocrit and Blood Viscosity
Hematocrit is the percentage of blood made up of cells, mostly RBC.
Normal is about 40-45%.
Viscosity is how thick or sticky the blood is.
As your hematocrit increases, your blood becomes thicker (more viscous). This makes it harder for your heart to pump and for blood to flow through the vessels. Blood is already 3x thicker than water.
In Polycythemia, there is very high hematocrit (60-70%) and blood becomes 10x thicker. This can increase risk of clots, strokes, and heart strain.
In polycythemia you have too many RBC.
Primary Polycythemia (P. Vera): it is a bone marrow disorder where RBC are made in excess for no good reason (JAK2+ mutation)
Secondary Polycythemia: RBC production increases in response to something else, usually low oxygen. This is where COPD and high altitude come into play. In COPD, your lungs cant get enough oxygen into your blood, the body compensates by making more RBC (to carry more oxygen) which leads to secondary polycythemia and thicker blood, leading to vascular resistance and strain on the heart.
Dehydration doesn't increase RBC, but it reduces the plasma (fluid) volume, so even though the RBC stay the same, the percentage of hematocrit appears higher and can make blood more viscous.
