Term
| What is the body's response to needing local blood flow? |
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Definition
| Local control by the capillaries, Cardiac output and tissue activity increases. An increase in local blood flow increases venous return --> Incr CO. |
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Term
| How is arterial pressure regulated? |
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Definition
Independent of local blood flow.
ANS responds by constriction
RAAS and regulation of BV. |
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Term
| How is blood flow/cardiac output determined? |
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Definition
| The pressure difference between 2 ends of a vessel and the vascular resistance. The greater the gradient of pressure, and the less the resistance --> more blood flow. |
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Term
| What is the difference between laminar flow and turbulent flow? |
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Definition
Opposites. Laminar flow is parabolic and streamlined, because flow closer to a membrane has more resistance
Turbulent flow - faster rate of ejection (aorta), obstruction, occlusion, sharp turn. |
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Term
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Definition
| A measure of the tendency of turbulence to occur. Turbulence is more likely to occur in a larger BV, with faster flow, and higher density of blood. Turbulence is less likely to occur with a higher blood viscocity |
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Term
| How does hematocrit affect blood flow? |
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Definition
| Hematocrit is the concentration of RBCs in the blood. A higher hematocrit = higher viscosity = greater resistance and less flow. |
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Term
| What is blood pressure, and how is it affected by autoregulation? |
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Definition
BP is what happens when flow is opposed by resistance. As flow increases, Pressure would increase as expected. However, there is a reflexive increase in resistance to bring pressure down
Autoregulation: SNS outflow, Local factors such as AngII, ADH, Endothelin reduce local blood flow. Local factors can also dilate to increase pressure. |
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Term
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Definition
How tissues adjust resistance to maintain normal blood flow during changes to arterial pressure. Via rapid changes to Arterioles, metarterioles, and capillary sphincters.
Ex: An oxygen deficit would increase metabolic rate (dilation), increasing blood flow |
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Term
| How does acute autoregulation occur? |
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Definition
2 theories:
- Vasodilators such as ADENOSINE dilate blood vessels, increasing blood flow. Has a different affect on the kidneys
- Oxygen lack - In a lack of oxygen, sphincters in capillaries relax --> increase in local blood flow. Vasomotion - opening and closing of sphincters. |
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Term
How is blood flow returned to normal acutely?
In the long term? |
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Definition
Acute:
- Metabolic theory - in increased pressure, increased blood flow eventually washes out vasodilators, returning blood flow to a plateau.
- Myogenic theory - Increased BF causes a stretch in SM and reactive contraction, counter-reducing BF
Long term - the need for increased BF promotes angiogenesis.
Therefore with and increase/decrease in pressure, blood flow remains relatively constant. |
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Term
| What happens if there is an increase in blood flow? |
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Definition
Want to reduce it to normal..
SNS outflow to constrict vessels, or vasoconstrictors such as endothelin
Metabolic theory - vasodilators washed out
Myogenic theory - vessel recoil. |
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Term
| What determines resistance to flow? |
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Definition
- diameter - smaller = greater resistance. Most important and easiest to change. An increase in diameter gives a d^4 increase in blood flow. Small change gives large results -- arteriole size and resistance.
- length - longer = greater resistance -- constant
- viscosity - greater = greater resistance -- constant |
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Term
| What is Poiseuille's law of conductance? |
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Definition
In a vessel with laminar flow, the flow rate is proportional to the fourth power of the pipe's radius (r^4)
Conductance and flow increases the greater the radius and the pressure gradient
Conductance = 1/resistance. |
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Term
| How is resistance different between in-series circuits and in-parallel circuits? |
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Definition
In series - Total resistance = sum of all resistances. Remember arterioles have greatest resistance, so to change aggregate resistance --> dilate arterioles
In parallel - The greater the # of vessels, the smaller the resistance, and total resistance is less than the vessel with the lowest resistance --
Rx = 1/(1/R1 + 1/R2)... |
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Term
| What is the difference between vascular distensibility and vascular compliance? |
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Definition
Distensibility - % increased volume per pressure, ability to stretch. Veins have 8x greater increase in volume than arteries
Compliance/capacitance - Tendency to resist recoil, inverse of elasticity. = Distensibility * volume.
-- Veins can receive more blood under less pressure |
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Term
| How do arteries and veins differ when compliance is changed? |
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Definition
- Arteries - SM contraction reduces compliance, decreases BV, and increases BP. A small change in volume in arteries has major pressure changes
- Veins - contraction of SM reduces compliance, pushes blood volume further downstream --> increased venous return and preload --> increased CO. A small change in pressure in veins has major volume changes.
-- The compliance of veins is greater at low pressures, nearly identical at high pressures. |
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Term
| How does stress-relaxation of smooth muscle explain delayed compliance? |
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Definition
When there is a major increase in volume/pressure in the vessel, SM relaxes to bring pressure back down.
When there is a drop in pressure, SM contracts to bring pressure back up.
Bladder has major stress-relaxation mechanisms. |
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Term
| What is the pressure pulse? |
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Definition
Starting in the aorta, arteries oscillate by distending and then relaxing to move blood along. PP = Systolic - Diastolic.
less resistance, increased SV = increased PP.
Sharp upstroke as blood enters aorta, max as ventricles finish contracting, then dicrotic notch as blood hits aortic valve. |
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Term
| What would cause the pressure pulse to be abnormal? |
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Definition
- Arteriosclerosis - causes HTN. Systolic increases, so increased PP
- Aortic stenosis - less blood flows through valve. Shallow dicrotic notch, diminished systolic
- PDA - Heart contracts at a greater force, reducing diastolic and increasing systolic
Aortic regurgitation - more blood in the ventricle -- more force of contraction, reducing diastolic and increasing systolic. NO dicrotic notch, |
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Term
| What is the formula for blood pressure? |
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Definition
BP = CO * PR
or (HR * SV) * PR |
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Term
| What factors influence systolic pressure? |
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Definition
Cardiac output and peripheral resistance mostly
Then blood volume and elasticity |
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Term
| What factors influence diastolic pressure? |
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Definition
| Blood volume and peripheral resistance |
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Term
| What are the Korotkoff sounds? |
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Definition
Sounds created by turbulence in the brachial artery from a blood pressure cuff, how we measure BP.
1st sound - some blood flow resumes, systolic pressure is measured
2nd/3rd/4th - between systolic and diastolic
5th sound - Pressure of cuff drops below pressure in the artery, no sound is heard as turbulent flow ceases. Diastolic pressure. |
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Term
| How is mean pressure calculated, and how does it change with age? |
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Definition
Mean pressure = Diastolic - 1/3(pulse pressure) and pulse pressure = systolic - diastolic)
So MP = diastole - 1/3(Systole - diastole)
Normal - mean closer to diastole. Increase in systole (HTN) leads to a line in the middle. |
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Term
| What is central venous pressure and the central venous trace? |
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Definition
CVP - pressure in the right atrium due to venous return, normally ~0
Central venous trace measures changes in CVP-
- A wave - atrial contraction. Absent in Afib, enlarged in tricuspid and pulmonary stenosis and pulmonary HT
- c wave - tricuspid valve bulges during ventricular contraction
- X descent - atrial relaxation, atria refills as ventricles are emptying
- v wave - Atrial pressure rises before tricuspid re-opens. Enlarged in tri-cuspid regurgitation
- y descent - atrial emptying into ventricle |
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Term
| What factors will increase venous return? |
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Definition
- Anatomy - respirator and muscle pump, venous valves
- Other:
- Right atrial pressure - increased preload and force of contraction, increased CO
- BV - increased BV = increased venous return. Salty foods, retention of sodium and water
- Muscle tone of SM
- dilation of arterioles decreases PR and increases venous return |
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Term
| How does increased venous return affect a P-V loop? |
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Definition
| Increases preload/fiber length, increases SV and force of contraction. Brings phase II line to the right. |
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Term
| What can affect peripheral venous flow? |
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Definition
- compression points in the ribs
- intraabdominal pressure affects leg venous pressure. Decreased venous return when standing for long periods.
- Gravitational pressure
- High right atrial pressure (CVP), which increases in heart failure. See Jugular distension, peripheral pressure, ascites, liver enlargement
- venous valvular insufficiency causes varicose veins |
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Term
| What is the function of microcirculation and vasomotion? |
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Definition
| Transport nutrients and oxygen by capillary into tissue. Vasomotion is the autoregulation by contraction of sphincters |
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Term
| How is pressure calculated in a capillary? |
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Definition
Calculate for arterial and venous end. Positive - fluid out. Negative - moving in.
(HPcap - HPif) - (OPcap - OPif) |
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Term
| How does local blood flow change during exercise? |
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Definition
| Skeletal muscles, skin, and heart need more oxygen. Kidneys and liver need less. Brain never changes |
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Term
| What is reactive hyperemia? |
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Definition
Increase in local blood flow where a period of ischemia or constriction was seen.
Reduction of O2 and adenosine in an area, replenishes with increase blood flow. Afrin. |
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Term
| What is a match/mismatch in the lungs? |
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Definition
-Match - Vasodilation to send blood to area with more oxygen in the lungs, want a 1:1 V/Q ratio. Opposite of in periphery.
- Mismatch - blood is sent to alveoli with the least amount of oxygen due to poor blood flow or poor oxygen. |
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Term
| Which factors affecting vascular smooth muscle produce dilation? |
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Definition
- decrease in pH and oxygen availability
- Increase in CO2 and potassium
- PgI and prostacyclin : prostaglandins
- Adenosine, NO, and bradykinin |
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Term
| Which factors affecting vascular smooth muscle produce constriction? |
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Definition
- Stretch in smooth muscle causes reflexing contraction
- Adrenergic NE/epi
- AngII, ADH (increase BV), Endothelin, Thromboxane |
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Term
| How does ANS control affect blood vessels? |
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Definition
No innervation of the capillaries.
Only SNS innervation of the blood vessels causing vasoconstriction. |
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Term
| Where are the baroreceptors located and how do they work? |
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Definition
On the common carotid and aortic arch. Detect BP changes, autoregulation to raise or lower BP. Reduces minute changes in BP
- Decreased BP - less inhibitory impulses sent. Stimulation of constriction and the SNS to raise BP and venous return.
- Raised BP - inhibitory signals dilate BV and increase vagal tone. |
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Term
| What are the mechanisms of short term blood pressure control? |
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Definition
- Baroreceptors - fastest mechanism
- Chemoreceptors - weak, same areas as baroreceptors, respond to CO2 changes. Fast acting.
- Stretch receptors - When volume is low, ADH released to retain Na/water --> constriction, increased BV and BP
- Volume reflex - in response to increased volume, kidney dilates afferent arteriole, increases GFR, and decreases ADH --> excretion of NA/water
- Bainbridge - response to volume, increases rate and force to prevent backup of blood
- CNS ischemic response - powerful vasoconstriction when BP very low. Quick changes. |
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Term
| What are the mechanisms of short term hormonal control? |
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Definition
- Adrenal medulla - releases NE/Epi to increase pressure
- AngII - increases pressure
- ADH - promotes retention of Na/water
- ANF - in high volume, excretion of Na/water |
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Term
| What are the direct renal mechanisms for blood pressure control? |
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Definition
Those that happen independent of hormones.
- Pressure diuresis - when pressure OR resistance increases as a result of increased volume, the kidneys excrete water to reduce blood volume.
- Pressure natriuresis - When the kidneys excrete water, sodium is also excreted. |
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Term
| What are indirect renal mechanisms for blood pressure control? |
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Definition
Alters BV through RAAS system
- Renin from J-G cells converts to Ang1, ACE converts to angII. Less ACE --> less angII (constrictor) and more bradykinin (dilator)
- AngII increases BP. Increases afterload, preload, constriction. Releases NE/epi and ADH for constriction and increased BV. Aldosterone also reabsorbes Na/water.
Constricts both arterioles for less filtration and promotes more reabsorption.
- RAAS responds in 8-10 min to bring up BP. |
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