Cardiovascular: Regulation Of Arterial Blood Pressure

Front 1

Relationship bw flow, pressure, & resistance

MAP

Back 1

Q = P/R

CO = MAP / TPR

CO x TPR = MAP

MAP: governed by how much blood pumped from LV

Front 2

MAP
1. Short Term Regulation
2. Long Term Regulation

Back 2

1. occurs w/in sec-min
-occurs prim via neural pathways
-targets the heart & BV

2. occurs w/in hrs-days
-occurs primarily via endocrine pathways
-targets the kidneys & BV

Front 3

Baroreceptors

Back 3

-short term regulation
-neural receptors located in the Carotid sinus & aortic arch
-participate in baroreceptor reflexes (also found in kidneys & brain)
-CN IX glossoph & X vagus carry signals from BR to medullary cardiovascuar (cardioregulatory) center of the brainstem

Front 4

Medullary Cardiovascular Center

Back 4

-highly complex
-consists of individual "mini-centers" such as vasomotor area & cardioinhibitory area
-makes decisions about what to do about hypertension
-employs SNS & paraNS to send orders to target tissues

Front 5

Baroreceptor Reflex
BP increases

Back 5

1. carotid & aortic arch BR detect
2. cardioregulatory center informed
3. decreases SNS cardiac nerve activity
-decrease SNS vasoconstrictor nerve activity
-increase paraNS cardiac nerve
4. decrease HR & decrease SV; vasodilation
5. decrease CO & TPR
6. BP decreases to normal

Front 6

Baroreceptor Reflex
BP decreases

Back 6

1. carotid & aortic arch BR detect
2. cardioregulatory center informed
3. increase SNS cardiac nerve activity
-increase SNS vasoconstrictor nerve
-decrease paraNS cardiac nerve activity
4. increase HR & SV; vasoconstriction
5. increase CO & TPR
6. BP increases to norm

Front 7

Baroreceptor Reflex in Response
to a Hemorrhage

Back 7

-losing blood = decrease BP
1. decrease MAP
2. decrease stretch on carotid sinus BR
3. decrease firing rate of carotid sinus nerve (Hering's nerve)
4a. decrease paraNS outflow to heart -> increase HR
4b. increase SNS outflow to heart & BV
-increase HR, contractility, constriction of arterioles (TPR)
-increase constrict of veins
-increase venous return
-increase mean systemic pressure

Front 8

How BR reflex works everyday?

Common ex of BR reflex slowing down?

Back 8

-adjust to change in gravity
-every morning when wake up
-stand up = decrease BP in neck & aorta (gravity pulls to feet but brain needs blood)
-BR adjust blood to increase HR & SV

Age (feel dizzy if get up too quickly)
orthostatic hypertension

Front 9

Sensitivity of BR altered by disease

Back 9

-chronic hypertension: BR do not see elevated BP as abnorm
0hypertension will be maintained rather than corrected
-mxn either decreased sensitivity of BR to increase in arterial pressure or an increase in the BP set point of the brainstem centers

Front 10

Kidney Anatomy

Back 10

nephron
-structural/fxnal unit of kidney
-filter blood & create urine
-glomerus (capillaries) in bowman's capsule: where filter blood
**population of cells that reside in nephron = juxtaglomerular cells
-JG cells: help regulate BP**

Front 11

Long-Term Regulation
RAA Pathway
Renin-angiotensin-aldosterone

Back 11

-decrease in renal perfusion pressure (BP) cause JG cells of afferent arterioles to secrete enzyme RENIN
-RENIN catalyzes the conversion of angiotensinogen to angiotensin I in the plasma

Front 12

ACE

Back 12

Angiotensin Converting Enzyme
-catalyzes conversion of angiotensin I into angiotensin II
-primarily occurs in the lungs
-angiotensin II has 3 prim effects:
1. hypothalamus: drink/thirst
2. vasoconstriction (increase BP)
3. Adrenal Cortex to make Aldosterone --> Kidney: salt & water retension

Front 13

RAA response to hemorrhage

Back 13

1. decrease arterial pressure
2. decrease renal perfusion pressure
3. increase renin
4. increase angiotensinogen to angiotesin I
5. ACE converts to angiotensin II
6. increase aldosterone
-increase Na-H exchange
-increase thirst
-vasoconstriction (increase TPR)

Front 14

ADH or Vasopressin

Back 14

anti-diuretic hormone
-stimulated by increased plasma osmolarity (solutes in blood)
-another stimulus is hypovolemia (volume contraction; hemorrhage)
-decrease in extracell fluid (ECF) of 10% or more cause decrease in arterial BP sensed by baroreceptor in L atria, carotid artery, & aortic arch

Front 15

2 Effects of ADH

Back 15

increasing BP:
1. potent vasoconstrictor that increases TPR by activating V1 receptors on the arterioles
2. increases water reabsorption by renal distal convoluted tubules & collecting ducts by activating V2 receptors

Front 16

ANP

Back 16

atrial naturetic peptide
-increase in BV result in increase in arterial pressure detected by te volume receptors
-input of volume receptors coordinated to return BV to norm
-prim by increasing excretion of NA & water
-response to an increase in BV include: increased secretion of ANP & decreased secretion of ADH
-opposing effects of ADH
-secreted by the atria in response to increased atrial pressure
-cause relax of vascular smooth muscle, vasodilation & decreased TPR
-kidney: vasodilation = increased Na & water excretion, decrease total ECP volume & BV

Front 17

Autoregulation

Parameters that affect the autoregulation of BP:

Back 17

-ability of tissues to regulate their own blood supply

1. metabolic factors: CO2, H; if tissue is inadequately perfused it becomes hypoxic & metabolites or waste is accum (stim vasodilation, increase perfusion)
2. chemical factors: blood platelet & endothelial cells secrete variety of vasoactive chem that stim vasodilation
-platelets secrete histamine which stim vasodilation under such conditions as trauma, inflamm & exercise
-endothelial cells secrete endothelin (vasoconstrictor) & nitric oxide (vasodilator)
3. Physical factors: temp, occlusion; reactive hyeremia increase above norm flow; when skin flushes after person comes in from cold or in forearm BP cuff is inflated for too long and then loosened

Front 18

Skeletal Muscle Pump

Back 18

-affect venous return
-when contract they force blood back to the heart while venous valves prevent the backflow of blood away from heart
1. before muscle contraction blood enters vein
2. muscle contract, upper valve opens further, lower valve closes, so blood moves up
3. muscle relax, upper valve close prevent back flow

Front 19

Hypertension

Back 19

-need series of elevation readings
-deadly
-not easily detected; silent asymptomatic
-diagnose often change screeing or person seeks medical care for other problem
-stim arterial vessels to thicken & strengthen
-less elastic & ability to change diameter lessens
-creates higher afterload, increasing heart's workload

Front 20

Primary (Essential) Hypertension

Back 20

-95%, most common
-chronic elevation in BP that occurs w/o any evidence of other disease
-has no identifiable causes
-related to:
>advanced age
>race
>gender
>family history
>obesity
>smoking
>heavy alcohol consumption

Front 21

Secondary Hypertension

Back 21

-only 5-10% of cases
-cause by a disorder of situation that increases TPR or CO (secondary to another disease)
>renal failure
>hyperthyroidism
>renin-producing tumors (aldosterone)
>cushing's syndrome (too much cortisol)
>hyperaldosteronism (tumor in adrenal, release lost of epi)
>pheochromocytoma

Front 22

Hypertension Treatments

Back 22

-diuretics
-ACE inhibitors
-Angiotensin II receptor blockers (antagonists)
-Ca Channel Blockers (antagonist)
-Beta blockers

Front 23

Diuretic Mxn

Back 23

-urinate; decrease blood volume
-venous return decreases
-cardiac output decreases (SV decreases)

Front 24

ACE Inhibitor

Back 24

-angiotensin converting enzyme inhibited
-not making angiotensin II
-vessls not going to constrict, BP decreases becuase more dilated
-not feel thirsty
-not release aldosterone: not retain Na in kidney thus water retention decreases in urine

Front 25

ARBs

Back 25

Angiotensin Receptor Blockers
-still making angiotensin II but like a hormone will bind to receptors on tissues
-so block receptors therefore AII doesn't work and don't get it's active effects

Front 26

Ca-Channel Blockers

Back 26

-block Ca channels in the ventricular myocytes (L-type)
-lower Ca level decreases force of contraction, not as much Ca into, less Ca released from SR = limited contraction
-can also block Ca channels in smooth muscles; depend on extracell Ca (not much SR) = don't contract = relax (vasodilate)

Front 27

Beta-Blockers

Back 27

-works in heart on B1 receptors
-NE can't bind
-heart rate and stroke volume decrease

Front 28

Arteriosclerosis/Athersclerosis

Back 28

-ath: thick due to plaques
-art: thick due to high BP
-abnormal thickening & hardening of the arterial walls (esp the tunica intima & media)
-not silent: blood flow = turbulent (Bruits: heart murmur in blood vessel)
-common complaint is pain in legs
-decrease ability of artery to change its radius
-lead to narrow of the arterial lumen (produce ischemia)
-no specific treatment

Front 29

Aneurysms

Back 29

-abnormal localized dilation or outpouching of the wall of an artery
-if untreated there is great risk of rupture