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38 Cards in this Set
- Front
- Back
Flow (Q)= delta P/R
delta P = |
arterial pressure
Q * R (flow * resistance) |
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flow * resistance quickly falls:
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at level of arterioles and stays low
- points at highest resistance |
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highest pressure is at the:
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narrowing points
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where is the place to change resistance:
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arterioles
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the pressure is highest in:
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the widest section just before the narrowing
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Is flow the same thoughout?
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Flow is the same
Amount of blood in the heart has to equal the amount leaving the heart |
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Blood Pressure=
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Cardiac output (CO) X Peripheral resistance (PR)
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stroke volume =
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Amount of blood leaving the heart with each beat
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cardiac output
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stroke volume (SV) x heart rate (HR)
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increased blood pressure will do what do afterload?
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increase
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increase afterload leads to:
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Dysfunctional hypertrophy
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increase blood pressure leads to overstressing of vessels which leads to:
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blood vessel rupture
and Inflammation-atherosclerosis |
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increase afterload leads to:
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Dysfunctional hypertrophy
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increase blood pressure leads to over stressing of vessels which leads to:
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blood vessel rupture
and Inflammation-atherosclerosis |
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Types of hypertension:
essential hypertension |
95% of cases, unknown cause
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Types of hypertension:
secondary hypertension |
5% of cases, defined cause
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why is it called "essential" hypertension?
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originally thought that high bp was needed for perfusion in the tissues…
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baroreceptors are important for _____ but not _____
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short term but not long term BP regulation
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why are baroreceptors not good for the long term?
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pressure goes up, more firing, then adapts. baroreceptor resets
because of this there is minute to minute regulation. |
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the kidney's and long term regulation of BP
water excretion: |
determines osmolarity (tightly controlled, ±1%)
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the kidney's and long term regulation of BP
sodium excretion |
determines extracelullar volume (due to tight osmolarity control)
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review of osmolarity:
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Kidney retains sodium, osmolarity increases, then water goes up, creates higher volume, bp goes down
Conc = m/v |
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Increased blood:
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increased pressure
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more blood in veins, more pressure in veins, so:
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more pressure driving into the heart
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more blood entering the heart, more blood leaving the heart. so:
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so increase in HR and SV so increase CO
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heart ejecting more blood so tissues receive more blood. Tissues don't want more blood so they:
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autoregulate.
-increase resistance to maintain bloodflow, total peripheral resistance, -increase pressure |
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diuretics decrease:
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blood volume
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diuretics autoregulate by:
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vasodilation
PR is reduced BP is reduced |
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no sustained increase in BP as long as kidneys are working properly
initial disturbance: |
increased BP= increased CO X PR
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no sustained increase in BP as long as kidneys are working properly
corrective action: |
there is increased BP
and increased sodium excretion and decreased extracellular volume which leads to : decreased BP= decreased CO X PR |
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common causes of secondary hypertension:
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Chronic renal disease
Primary aldosteronism Renovascular malfunction Cushing syndrome |
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all of the secondary causes of hypertension effect:
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kidney excretion of sodium (directly or indirectly )
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abnormalities in essential hypertension
Blood Vessel: Functional |
decrease NO secretion
increase endothelin production ca++ or Na+/K+ channel defects hyperresponsiveness to catecholamines |
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abnormalities in essential hypertension
Blood Vessel: structural |
exaggeraged medial hypertrophy
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abnormalities in essential hypertension
adrenal |
catecholamine leak or malregulation
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abnormalities in essential hypertension
CNS |
-increase basal sympathetic tone
-abnormal stress response -abnormal response to signals from baroreceptors and volume receptors |
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abnormalities in essential hypertension
pressure volume receptors |
desensitization
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abnormalities in essential hypertension
kidney complicity |
-RAA dysfuntion
-ion channel defects: (Na+/K+/2Cl- cotransporter, basolateral Na+/K+ ATPase, Ca++ ATPase ** RAA = renin-antiontensin-aldosterone system. |