Exam 9 - Short Term Control Of BP Flashcards
Local flow to tissues
- Depends on constant pressure drop across tissues
- MAP - CVP = constant
Arterial compliance
2 mls/mmHg
Venous compliance
100 mls/mmHg
Hormonal mechanisms for controlling BP
- Aldosterone
- Renin-angiotensin-vasoconstriction
Nervous mechanisms for BP control
- Baroreceptors (moment to moment / normal changes)
- Chemoreceptors
- CNS ischemic response
Physiologic mechanisms for BP control
- Capillary fluid shift (normal to abnormal changes)
- Stress relaxation of vasculature (normal to abnormal changes)
Renal mechanism for BP control
- Renal-blood volume pressure control
- long term control….everything else short term
Filtration/absorption rate
- If MAP increase….filtration increase
- If MAP decrease….absorption increase
4 quickest activated mechanisms
- Within seconds
- Baroreceptors
- Chemoreceptors
- CNS ischemic response
- Stress relaxation
2 average reaction time mechanisms
- Within minutes
- Renin-angiotensin-vasoconstriction
- Capillary fluid shift
2 slowest reacting mechanisms
- Within hours
- Aldosterone
- Renal-blood volume pressure control
5 average strength mechanisms
- Max feedback of 4% increase relative
- Bring BP back CLOSE to normal
- Chemoreceptors
- Stress relaxation
- Renin-angiotensin-vasoconstriction
- Capillary fluid shift
- Aldosterone
2 strong mechanisms
- Max feedback of 7 & 11
- Bring BP back CLOSE to normal
- Baroreceptors
- CNS ischemic response
1 infinite strength response
- Renal-blood volume pressure control
- Can bring BP back to NORMAL
Which mechanisms play role on bypass
- All except Aldosterone and Renal-blood volume pressure
- CPB not on long enough to activate those two
- Average case only 90 minutes
- These two take 4 hours to activate
Which change in BP to these mechanisms respond to
- Mostly drops in BP
- Except Baroreceptors…they do both
Innervation of the heart
- Sympathetic and Parasympathetic
Innervation of arterioles
- Sympathetic
Parasympathetic control
- Regulates HR
- Small/No affect on contractility
- only atrial filling - Minimal regulation of circulation
Sympathetic control
- Regulate contractility
- Regulates circulation
Vasomotor center pathways
- Efferent pathways
- Parasympathetic impulses via vagus nerve
- Sympathetic impulses via spinal cord and peripheral sympathetic nerves to arteries, arterioles, and veins
Sympathetic nerve fibers
- Exit spinal cord via thoracic spinal nerves and first 2 lumbar
- Enter sympathetic chains either side of spinal cord
- To circulation 2 ways:
- specific nerves directly to heart and internal viscera
- peripheral portions of spinal nerves to peripheral vasculature
Which vessels innervated by sympathetic
- Arteries / Arterioles - change resistance and flow to tissue
- Veins / Venuoles - change volume held…changing return
- SOME metarterioles and pre-cap sphincters of mesenteric
- most are not - Most are vasoconstrictors: kidney/ intestines/ spleen/ skin
- weak vasoconstriction in skeletal muscle / brain - When impulses sent to vessels…also sent to adrenal medulla
- releases Epi and NE
Vasomotor center location
- Bilateral
- all efferent neurons come out of here
- In medulla and lower third of pons
- regulates amount of vascular constriction AND cardiac activity
- like HR and contractility
3 parts of vasomotor center
- Vasoconstrictor
- Vasodilator
- Sensory
Vasoconstrictor area
- Bilateral
- Anterolateral part of upper medulla
- sends out efferent neurons to all areas of spinal cord
- excite vasoconstrictor neurons of sympathetic
- increase cardiac activity (sympathetic)
Vasodilator area
- Bilateral
- Anterolateral part of lower medulla
- Sends efferent neurons to vasoconstrictor area
- fibers inhibit vasoconstrictor area
- decrease cardiac activity (parasympathetic)
Sensory area
- Bilateral
- In medulla and lower pons (tractus solitarius)
- Receives signal via vagus and glossopharyngeal nerves
- Sends output to vasoconstrictor and vasodilator areas
- based on input from circulatory system
Vasomotor center cardiac control
- Lateral portions: excitatory impulses to heart
- Sympathetic - Medial portion: impulses to vagus nerve which sends parasympathetic impulses to heart -> inhibitory
- Parasympathetic
Sympathetic vasoconstrictor tone
- more impulses -> constrict
- less impulses -> dilate
- vasoconstrictor center sends 1.5-2.0 impulses/sec
- normal vasomotor tone - If efferent paths blocked….MAP will drop by at least half
Vasomotor center control by CNS
- Pons / mesencephalon / diencephalon
- lateral/superior portions: excite
- medial/inferior portions: inhibit - hypothalamus
- posterolateral: excite
- anterior: mild excite or inhibit…..depends which part - cerebral cortex
- motor cortex: excites
- other areas: excite or inhibit depending
Effect of CNS control
- Can produce rapid increase in BP
- double within 5-10 seconds - stimulate vasoconstrictor area
- stimulate increase in cardiac activity
- inhibit parasympathetic Vargas signals to heart
If MAP drops…what is CNS response
- constriction of most arterioles
- increase SVR -> increase MAP - strong constriction of veins and larger arteries
- move volume -> more preload -> more SV -> increase MAP - increase cardiac performance
- increase HR (major effect) -> more CO -> increase MAP
- increase contractility -> up SV -> up MAP (curve up and left)
Barroreceptors
- Stretch receptors in large arteries of thorax and neck
- aortic and carotid bodies are big areas - Carotid: Hering nerve to glossopharyngeal nerve to sensory area
- Aortic: vagus nerve to sensory area of vasomotor center
- help maintain more constant MAP
- If removed….MAP is all over the place - CAN normalize to if pressure changes and remains at new level
- takes 1-2 days / no matter which way pressure changes
- may mediate changes of tone to kidneys
Carotid barroreceptors
- In play more often
- responds to lowest of 50 - 60 mmHg
- then stretch happens
Aortic barroreceptors
- In play when MAP is a bit higher
- 80 - 90 mmHg
- receptors produce greater response when pressure is changing
- not standing still….same with carotid receptors
Chemoreceptors
- sensitive to lack of O2 and excess CO2/H ions
- In carotid bodies (2)
- In aortic bodies (3)
- excite nerve fibers through Herring’s nerve and vagus nerve
- If flow to receptor drops -> impulse increase -> excites vasomotor
- kick in when pressure drops below 80 mmHg
CNS ischemic response
- Very powerful
- direct response of vasomotor center to ischemia
- increased levels of CO2 - can increase BP to 250 mmHg
- will cut off flow to less important tissues
- kicks in when BP below 60 mmHg
- greatest level of stimulation at 15-20 mmHg
Atrial / Pulmonary stretch receptors
- low pressure receptors
- minimize changes in atrial pressure due to sudden changes in blood volume (baroreceptors respond to stretch….these to flow)
- bigger help in maintaining BP due to increase in volume
Atrial reflex and Kidney - A
- increase atrial stretch
- reflex dilation of afferent arterioles in kidney
- increase glomerular cap pressure
- increase glomerular filtration
- increase urine output
- decrease CBV
- decrease venous return
- decrease CO
- brings pressure down / happens slowly
Atrial reflex and Kidneys - B
- Increase atrial stretch
- hypothalamus makes less ADH
- decrease reabsorption of H2O in renal tubes
- increased urine output
- decrease CBV
- decrease venous return
- decrease CO
- brings pressure down / happens slow…but little quicker than A
Bainbridge reflex
- increase atrial stretch -> increase in HR
- via vagus nerve
- 40-60% boost
Respiratory waves
- Change in arterial pressure 4-6 mmHg during each breath
- Inspiration: pressure negative…vessels expand…decrease CO
- Expiration: positive pressure…vessels constrict…increase CO
- These can trigger vascular and atrial stretch receptors
Vasomotor waves
- slow oscillation of MAP of 10-40 mmHg
- dynamic equilibrium
- cycle is 7-10 seconds
- oscillation due to baroreceptors / chemoreceptors