Physiology of Blood pressure - February 12 and Ch 9 Control of Blood pressure Flashcards
1. Relate CO, resistance, blood pressure 2 Neural and humoral factors that regulate blood pressure
Formula for BP
CO x SVR
Property of blood vessel that modifies BP
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
Vasodilation effects (what can see + what is happening)
- Bigger diameter
- Lower resistance (SVR)
- More blood flow
- Blood is warm and red = patient extremities will be warm and pink
Vasoconstriction effects (what can see + what is happening)
- Smaller diameter
- Higher resistance (SVR)
- Less blood flow
- Patient extremities will be cool and pale
Methods to measure SVR
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
What are the baroreceptor-stimulated mechanisms called into play to restore blood pressure/blood volume (4 mechanisms with net effect to restore BP)
- 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 - Decreased PNS activity = decreased acetylcholine release which normally activate muscuarinic receptor in heart, less activation of muscarini:
- increased HR = increased BP - Increased activation of renin-angiotensin cascade = increased release angiotensin II = increased SVR (increased BP) and aldosterone (increased BV)
- Increased release Vasopressin (AVP) = Increased H20 reabsorption to restore BV and increased SVR = increased BP
NET effect = BP restored to pre-hemorrhage level
Effect of norepinephrine on vascular muscle cell (steps)
- Increases Ca2+ concentration in vascular muscle cell
- More Ca2+ = increased complexing with calmodulin
- Ca2+ -calmodulin complex binds to MLCK activates it
- MLCK phosphorylates myosin - activated myosin associated with actin to begin contraction
Effect of vasopressin (ADH ) and angiotensin II on vascular muscle cell (steps)
- Increase Ca2+ concentration
- More Ca2+ - increased Ca2+calmodulin complex
- Increased MLCK activation
- Increased phosphorylation of myosin to bind wih actin and begin contraction (how both angII, ADH –> massive amounts V1 receptor - not physiologic)
Short term compensation blood loss
BP and BV restored due to baroreceptors stimulating the autonomic system and hormones (4 methods increase SNS, decrease PNS, activation RAAS, release vasopressin)
Long term compensation blood loss (3)
- BV restored due to fluid shifts
- RBC’s and Hct restored (% of RBC in blood)
- Blood proteins restored
Postural (or Orthostatic) hypotension - how this develops (i.e. why we faint)
- Blood pools in legs upon standing (gravity)
- Failure to increase SVR and restore BP (due to delay autonomic response)
- Insufficient blood to brain (due to fall in CO & BP)
- Fall to ground - blood equally distributed at same level as heart - ensures good blood flow to brain.
2 local regulators of vasoconstriction/dilation
1) Endothelin
2) Nitric Oxide
Endothelin-origin
Synthesized and released from endothelial cells
Endothelin function
Vasoconstriction
Stimulus for endothelin release
Hypoxia in lung vasculature –> stimulates vasoconstriction to direct blood away from poorly oxygenate regions (preventing V/Q mismatch)
Origin/formation nitric oxide
- synthesized and released from endothelial cells
- L arginine is converted to NO by nitric xide synthase
Nitric oxide function
-acts on vascular smooth muscle cells to cause vasodilation
Endothelin MOA
- 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
Nitric oxide MOA
- increased cGMP concentration
- activate PKG
- phosphorylation of MLCK –> deactivation of MLCK
- inhibit myosin and actin interaction
- relax
Sublingual nitroglycerin MOA
breaks down to NO -same MOA as NO
2 mechanisms how Nitroglycerin is treatment for angina pectoris
- decreased preload (decreased O2 demand- increase contractility (which requires more E))
- coronary artery vasodilation (increased O2 supply)
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
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
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?
Sweating = increased activation of SNS, chest pain and shortness of breath= angina, extremities are cool = poor CO or increased SVR
Diagnosis = myocardial infarction
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
Diabetic autonomic neuropathy (impaired autonomic functioning leading to postural /orthostatic hypotension)
