Cardio- Lecture (Steiner) Hypertension

Front 1

Flow (Q)= delta P/R

delta P =

Back 1

arterial pressure

Q * R

(flow * resistance)

Front 2

flow * resistance quickly falls:

Back 2

at level of arterioles and stays low

- points at highest resistance

Front 3

highest pressure is at the:

Back 3

narrowing points

Front 4

where is the place to change resistance:

Back 4

arterioles

Front 5

the pressure is highest in:

Back 5

the widest section just before the narrowing

Front 6

Is flow the same thoughout?

Back 6

Flow is the same
Amount of blood in the heart has to equal the amount leaving the heart

Front 7

Blood Pressure=

Back 7

Cardiac output (CO) X Peripheral resistance (PR)

Front 8

stroke volume =

Back 8

Amount of blood leaving the heart with each beat

Front 9

cardiac output

Back 9

stroke volume (SV) x heart rate (HR)

Front 10

increased blood pressure will do what do afterload?

Back 10

increase

Front 11

increase afterload leads to:

Back 11

Dysfunctional hypertrophy

Front 12

increase blood pressure leads to overstressing of vessels which leads to:

Back 12

blood vessel rupture

and
Inflammation-atherosclerosis

Front 13

increase afterload leads to:

Back 13

Dysfunctional hypertrophy

Front 14

increase blood pressure leads to over stressing of vessels which leads to:

Back 14

blood vessel rupture

and
Inflammation-atherosclerosis

Front 15

Types of hypertension:

essential hypertension

Back 15

95% of cases, unknown cause

Front 16

Types of hypertension:

secondary hypertension

Back 16

5% of cases, defined cause

Front 17

why is it called "essential" hypertension?

Back 17

originally thought that high bp was needed for perfusion in the tissues…

Front 18

baroreceptors are important for _____ but not _____

Back 18

short term but not long term BP regulation

Front 19

why are baroreceptors not good for the long term?

Back 19

pressure goes up, more firing, then adapts. baroreceptor resets

because of this there is minute to minute regulation.

Front 20

the kidney's and long term regulation of BP

water excretion:

Back 20

determines osmolarity (tightly controlled, ±1%)

Front 21

the kidney's and long term regulation of BP

sodium excretion

Back 21

determines extracelullar volume (due to tight osmolarity control)

Front 22

review of osmolarity:

Back 22

Kidney retains sodium, osmolarity increases, then water goes up, creates higher volume, bp goes down

Conc = m/v

Front 23

Increased blood:

Back 23

increased pressure

Front 24

more blood in veins, more pressure in veins, so:

Back 24

more pressure driving into the heart

Front 25

more blood entering the heart, more blood leaving the heart. so:

Back 25

so increase in HR and SV so increase CO

Front 26

heart ejecting more blood so tissues receive more blood. Tissues don't want more blood so they:

Back 26

autoregulate.
-increase resistance to maintain bloodflow, total peripheral resistance, -increase pressure

Front 27

diuretics decrease:

Back 27

blood volume

Front 28

diuretics autoregulate by:

Back 28

vasodilation

PR is reduced
BP is reduced

Front 29

no sustained increase in BP as long as kidneys are working properly

initial disturbance:

Back 29

increased BP= increased CO X PR

Front 30

no sustained increase in BP as long as kidneys are working properly

corrective action:

Back 30

there is increased BP
and increased sodium excretion
and decreased extracellular volume
which leads to :
decreased BP= decreased CO X PR

Front 31

common causes of secondary hypertension:

Back 31

Chronic renal disease
Primary aldosteronism
Renovascular malfunction
Cushing syndrome

Front 32

all of the secondary causes of hypertension effect:

Back 32

kidney excretion of sodium (directly or indirectly )

Front 33

abnormalities in essential hypertension

Blood Vessel: Functional

Back 33

decrease NO secretion
increase endothelin production
ca++ or Na+/K+ channel defects
hyperresponsiveness to catecholamines

Front 34

abnormalities in essential hypertension

Blood Vessel: structural

Back 34

exaggeraged medial hypertrophy

Front 35

abnormalities in essential hypertension

adrenal

Back 35

catecholamine leak or malregulation

Front 36

abnormalities in essential hypertension

CNS

Back 36

-increase basal sympathetic tone
-abnormal stress response
-abnormal response to signals from baroreceptors and volume receptors

Front 37

abnormalities in essential hypertension

pressure volume receptors

Back 37

desensitization

Front 38

abnormalities in essential hypertension

kidney complicity

Back 38

-RAA dysfuntion
-ion channel defects: (Na+/K+/2Cl- cotransporter, basolateral Na+/K+ ATPase, Ca++ ATPase

** RAA = renin-antiontensin-aldosterone system.