Physiology of Blood pressure - February 12 and Ch 9 Control of Blood pressure

Question 1

Formula for BP

Answer 1

CO x SVR

Question 2

Property of blood vessel that modifies BP

Answer 2

The radius of the blood vessel:

• determines rate of flow through blood vessel (increased flow due to decreased SVR= decreased BP, decreased flow due to increased SVR = increased BP)
• vessel resistance (SVR) = 1/radius^4

Question 3

Vasodilation effects (what can see + what is happening)

Answer 3

1. Bigger diameter
2. Lower resistance (SVR)
3. More blood flow
4. Blood is warm and red = patient extremities will be warm and pink

Question 4

Vasoconstriction effects (what can see + what is happening)

Answer 4

1. Smaller diameter
2. Higher resistance (SVR)
3. Less blood flow
4. Patient extremities will be cool and pale

Question 5

Methods to measure SVR

Answer 5

1) PA catheter (less common now)
2) On physical exam -estimate
a) Signs of increased SVR:
- cool
- pale
- weak pulse
b) Signs of decreased SVR:
- warm
- pink
- bounding pulses

Question 6

What are the baroreceptor-stimulated mechanisms called into play to restore blood pressure/blood volume (4 mechanisms with net effect to restore BP)

Answer 6

1. Increased SNS activity = increased norepinephrin (noradrenalin) release - targets B1 receptor in heart, activated B1 receptor:
   a)increased HR
   b)increased SV
   c)increased SVR
   all leading to increased BP
2. Decreased PNS activity = decreased acetylcholine release which normally activate muscuarinic receptor in heart, less activation of muscarini:
   - increased HR = increased BP
3. Increased activation of renin-angiotensin cascade = increased release angiotensin II = increased SVR (increased BP) and aldosterone (increased BV)
4. Increased release Vasopressin (AVP) = Increased H20 reabsorption to restore BV and increased SVR = increased BP

NET effect = BP restored to pre-hemorrhage level

Question 7

Effect of norepinephrine on vascular muscle cell (steps)

Answer 7

1. Increases Ca2+ concentration in vascular muscle cell
2. More Ca2+ = increased complexing with calmodulin
3. Ca2+ -calmodulin complex binds to MLCK activates it
4. MLCK phosphorylates myosin - activated myosin associated with actin to begin contraction

Question 8

Effect of vasopressin (ADH ) and angiotensin II on vascular muscle cell (steps)

Answer 8

1. Increase Ca2+ concentration
2. More Ca2+ - increased Ca2+calmodulin complex
3. Increased MLCK activation
4. Increased phosphorylation of myosin to bind wih actin and begin contraction (how both angII, ADH –> massive amounts V1 receptor - not physiologic)

Question 9

Short term compensation blood loss

Answer 9

BP and BV restored due to baroreceptors stimulating the autonomic system and hormones (4 methods increase SNS, decrease PNS, activation RAAS, release vasopressin)

Question 10

Long term compensation blood loss (3)

Answer 10

1. BV restored due to fluid shifts
2. RBC’s and Hct restored (% of RBC in blood)
3. Blood proteins restored

Question 11

Postural (or Orthostatic) hypotension - how this develops (i.e. why we faint)

Answer 11

1. Blood pools in legs upon standing (gravity)
2. Failure to increase SVR and restore BP (due to delay autonomic response)
3. Insufficient blood to brain (due to fall in CO & BP)
4. Fall to ground - blood equally distributed at same level as heart - ensures good blood flow to brain.

Question 12

2 local regulators of vasoconstriction/dilation

Answer 12

1) Endothelin

2) Nitric Oxide

Question 13

Endothelin-origin

Answer 13

Synthesized and released from endothelial cells

Question 14

Endothelin function

Answer 14

Vasoconstriction

Question 15

Stimulus for endothelin release

Answer 15

Hypoxia in lung vasculature –> stimulates vasoconstriction to direct blood away from poorly oxygenate regions (preventing V/Q mismatch)

Question 16

Origin/formation nitric oxide

Answer 16

• synthesized and released from endothelial cells

- L arginine is converted to NO by nitric xide synthase

Question 17

Nitric oxide function

Answer 17

-acts on vascular smooth muscle cells to cause vasodilation

Question 18

Endothelin MOA

Answer 18

• Increase intracellular calcium in vascular smooth muscle cells
• calcium binds to calmoduin
• calcium calmodulin complex binds to MLCK
• MLCK activates myosin - promoting myosin/actin interaction causing contraction

Question 19

Nitric oxide MOA

Answer 19

• increased cGMP concentration
• activate PKG
• phosphorylation of MLCK –> deactivation of MLCK
• inhibit myosin and actin interaction
• relax

Question 20

Sublingual nitroglycerin MOA

Answer 20

breaks down to NO -same MOA as NO

Question 21

2 mechanisms how Nitroglycerin is treatment for angina pectoris

Answer 21

• decreased preload (decreased O2 demand- increase contractility (which requires more E))
• coronary artery vasodilation (increased O2 supply)

Question 22

Case 1:
Bridget a 32 year old woman brought ED
Her BP is 60/38 mmHg (after 3 L of normal saline)
Extremities are warm and pink
She has a fever
a) what do her warm extremities suggest
b) normal response do decrease in BP (via baroreceptors)
c) what does this suggest about bridgits current BP and SVR

Answer 22

a) Vasodilation
so decreased SVR in the periphery and therefore decreased BP (as seen by vitals)
b)
-increased SNS activation and decreased PNS activation
-activation renin angiotensin cascade
-production of AVP
c) that the decrease in BP and SVR is pathological
d) Diagnosis:
Septic Shock

Question 23

Case 2:
Joseph is a 63 year old man that presents with sweating, chest pain and shortness of breath
His BP is 120/88 mmHg
Extremities are very cool
What is his diagnosis?

Answer 23

Sweating = increased activation of SNS, chest pain and shortness of breath= angina, extremities are cool = poor CO or increased SVR

Diagnosis = myocardial infarction

Question 24

Case 4
Alicia is a 49 year old woman with Type I diabetes
She tells teh doctor that she has recently been getting dizzy when she stands up from a lying down position
Diagnosis

Answer 24

Diabetic autonomic neuropathy (impaired autonomic functioning leading to postural /orthostatic hypotension)