Lecture 7 Neural Control

From Iusmphysiology

Revision as of 15:37, 31 January 2011 (edit) 24.15.60.132 (Talk) ← Older edit		Revision as of 06:50, 9 March 2012 (edit) (undo) 192.162.19.21 (Talk) (uZCg7F Fantastic blog post.Thanks Again. Great.) Newer edit →
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-	==Neural Control==	+	uZCg7F Fantastic blog post.Thanks Again. Great.
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-	===Objectives===	+
-	*How do the sympathetic and parasympathetic nervous systems change each of the following:  Heart rate, Cardiac Contractility, Arterial Resistance, and venous constriction	+
-	*As the mean arterial pressure is increased, how does the arterial baroreceptor activity (firing rate) change?  If the artery containing the baroreceptor sensors could not expand as the pressure is increased, how would baroreceptor activity change?	+
-	*What are atrial and ventricular baroreceptors? During which phases of the heart cycle are they active?  When excessively active, what general types of modifications of neural and hormonal control occur?	+
-	*At a conceptual level, there are four centers in the brain stem which interact to regulate the sympathetic and parasympathetic nervous systems. What are the four centers and what major functions does each have?	+
-	*Compare the effects of pleasurable emotions versus fear versus anger on neural control of the cardiovascular system.	+
-	*Complete loss of neural cardiovascular control would result in a very low arterial blood pressure, a heart rate of about 100-110 beats/min (no vagal control), and low cardiac output.  Why do these problems occur?	+
-	*How does an increase in the intracranial pressure progressively cause decreased brain blood flow even if the arterial blood pressure is elevated?	+
-		+
-	===Overview of Neural Vascular Regulation===	+
-	*Looking at the flow chart.	+
-	*Work through it backward from arterial pressure.	+
-		+
-	====Without regulatory system====	+
-	*If we stopped neural control to the cardiovasc system, we would faint.	+
-	**Standing and walking would be very difficult.	+
-	**Mean pressure ~50 mmHg	+
-		+
-	====Range of Activity====	+
-	*When sleeping, we use only use 80% of our normal awake function of the neural control.	+
-	*When exercising, CV flow icnreases 5-10 fold, at least.	+
-	*BP and cardiac output goes up because of the symp nervous system	+
-		+
-	====Must adapt to life span of >80  years====	+
-	*Most of us will see 2100	+
-	*Our bp will change very little over time if we stay lean and active	+
-	*Even from little babies to full grown, our BP doesn't change much:	+
-	**Increase in about 20-30 mmHg.	+
-	**This occurs as the child starts to stand.	+
-		+
-	====Set Point Pressure====	+
-	*Setpoint pressure:	+
-	**The moment at which the body will try to maintain the bp.	+
-	**When sleeping, the pressure is about 80.	+
-	**awake = 90	+
-	**walking and talking = 95	+
-	**Walk fast = 105	+
-	**Run in the hall 140-150.	+
-	**These are each new setpoints	+
-	*Resistance and volume and what not get fixed to maintain these set points.	+
-		+
-	====E.  Regulated variables====	+
-	*Let's look at at 24 hour cycle: noon to noon with a healthy, normal male	+
-	*Variables that are regulated:	+
-	**Mean arterail pressure, pretty constant:	+
-	***BP drops off with sleep	+
-	***BP goes up with alarm clock	+
-	****BP usually highest in the mornings	+
-	**Heart rate:	+
-	***Low while sleeping	+
-	***High in the morning	+
-	**Stroke volume	+
-	***Boringly constant	+
-	***Except when exercising	+
-	***Can increase 40%	+
-	**Cardiac output	+
-	***Low while sleeping	+
-	***Up during exercise, though not much	+
-	***50% in increase is a nice walk, not a run or anything	+
-	**Total peripheral resistance	+
-	***Went up during sleep	+
-	***Went down when "busy" in the evening	+
-		+
-		+
-	*24 hours with an athlete:	+
-	**Mean arterail pressure, pretty constant:	+
-	***Decreases where it needs to, goes up where the blood isn't needed.	+
-	**Heart rate:	+
-	***Heart rate is lower because cardiac output is higher	+
-	***can go really low, too.	+
-	***Max heart rate isn't really that different as sedentary people; may even be that athletes can't quite as high.	+
-	**Stroke volume	+
-	***Larger in this athlete	+
-	**Cardiac output	+
-	***Higher	+
-	**Total peripheral resistance	+
-	***Low	+
-	**Venous constriction follows directional changes in heart rate	+
-	***Constrict to make sure the blood is in the right places (organs, arteries).	+
-	**Blood Volume:	+
-	***Exercise training increases blood volume, first by increased plasma.	+
-	***Then RBCs are added later.	+
-	***Volume stays up 5-10% for as long as you exercise.	+
-	***Temperature during the seasons change the blood volume:	+
-	****In the summer the plasma is warmer and the volume increases appropriately	+
-	****The blood volume even changes by the night day cycles (higher in the day, lower in the night when it is cooler).	+
-		+
-		+
-	*stopped here on 01/27/11 at 9AM.	+
-	*started here on 01/27/11 at 11AM.	+
-		+
-		+
-	===Short  Term Sensor Systems for Neural Regulation===	+
-	*This is moment to moment regulation.	+
-	*CV system can respond very quickly.	+
-	*How does it know?	+
-		+
-	====Peripheral Arterial Baroreceptors====	+
-	*The first two lines of defense are baroreceptors:	+
-	*Baroreceptors are found in the arch of aorta and the bifurcation area of common carotid arteries in the neck	+
-	*Mixed into wall of vessel	+
-	*Associated with smooth muscle cells	+
-	*As diameter gets larger, the baroreceptors fire	+
-	*They sense tension of themselves too and will fire	+
-	*As BP goes up they fire faster and faster	+
-	*Carotid baroreceptor is	+
-	**innervated by glossopharyngeal  nerve	+
-	**It is the main receptor becasue it works over a wider range	+
-	*Aortic arch receptor	+
-	**Vagus	+
-	**Only over pressures over MAP; stops working over 100 mmHg	+
-	**Can signal when the pressure drops under 100 to tell the brain pressure is low	+
-		+
-	=====Baroreceptor function=====	+
-	*How do they work?	+
-	*Mechanosensitive Na and Ca channels	+
-	*Ions rush in	+
-	*More depolarization, the faster the signal to the brain trhough glosso and vagus nerves	+
-		+
-	=====Influences on baroreceptor function=====	+
-	*This firing is influenced by things in our bodies like abnormal lipid levels, normal or abnomral production of prostacyclins and NO, etc.	+
-	*Prostacylins and NO (vasodilators):	+
-	**When smooth muscles relaxed, there is more tenstion on the barorecptors because there is more tension	+
-	**So baroreceptors fire	+
-	**This is good because sympathetics should calm when pressure is going up.	+
-	*When lipids are high:	+
-	**Too much LDLs	+
-	**endothelial cells aren't healthy, don't make NO or prostacyclins	+
-	**So we don't get relaxation of smooth muscle	+
-	**We don't get baroreceptor stretch	+
-	**We don't get sympathetic inhibition	+
-	**Blood pressure rises as sympathetics keep signaling smooth muscle to flex and narrow arteries	+
-	*Platelet activation:	+
-	**Usually act as vasoconstrictyors	+
-	**BAroreceptors are inhibited	+
-	**Parasympathetics are signaled to fire	+
-	**Body thinks blood pressure is going up but it isn't	+
-		+
-	====Low pressure baroreceptors====	+
-	*There are baroreceptors in the heart.	+
-	**They can cause increase or decrease of neural stimulation at the heart.	+
-	*Atrial Type A baroreceptors:	+
-	**These monitor atrial contract; tell the brain if it is going well or not.	+
-	*Atrial type B	+
-	**Sense how venous pressure is stretching the atrium.	+
-	**Brain stops getting signal if not stretching correctly.	+
-	*Ventricular receptors	+
-	**These sense how well the ventricle is being passively stretched.	+
-	*Different ventricular receptors	+
-	**Detect tension generated during systole	+
-	*If Atrial type a or b are over active, brain is told that atria are doing too much (too much stretch in diastole, or something)	+
-	**Antidiuretic hormone is suppressed to reduce blood volume.	+
-	**Sympathetic activity will also be suppressed.	+
-	*If too much ventricular activit / stretch is detected:	+
-	**Symnpathetic activity is decreased.	+
-	**These are more important than the atrial baroreceptors.	+
-	**Renal lectures will tell us about how atria can release hormones to talk to the kidneys, too.	+
-		+
-	===Integration of Input and Output Neural Signals in the Medulla Excitatory Centers===	+
-	*Higher the bp pressure, more firing of baroreceptors.	+
-	*This is a '''reciprocal innervation system''': the more the baroreceptors fire, the more they inhibit cardiac excitatory systems (in the brain stem).	+
-	**Brain stem is generally where sympathetics originate.	+
-		+
-	====Pressor Center - sympathetic  nervous system to blood vessels====	+
-	*The pressor center is part of the sympahetics.	+
-	*It talks to the blood vessels	+
-	*When inhibited, less activity to the arteries so they are less constricted.	+
-	*Tries to bring bp up through: venus constriction, arterial constriction, increased heart contractility	+
-		+
-	====Cardiac inhibitory center====	+
-	*This is the beginning of the parasympathetics.	+
-	*When these fire, the vagus nerve gets stimulated	+
-	*Vagus goes to SA node, AV node and slows the heart rate	+
-	**Most effective at SA node but also at AV node.	+
-	*Notice that vagus does not (nor does any of the parasymp) affect blood vessels.	+
-		+
-	====Cardiac Excitatory Center - sympathetic nervous system to heart====	+
-	*The sympthetic system is tonically active.	+
-	**it must be inhibited or it will fire very fast.	+
-	**Baroreceptors are all calming the parasymp down.	+
-		+
-		+
-	====Overall outcome of the baroreceptor and central nervous system interaction====	+
-	*As baroreceptor activity is increased, the medulla will reflexively decrease the sympathetic nervous system activity; vagal activity usually changes in the opposite direction of sympathetic activity.	+
-	*The cardiovascular system without sympathetic or parasympathetic activity:	+
-	**Heart rate about 100-110 beats/min,	+
-	***SA node has an inherent rate of about 100, so as we rest, parasympathetics dominate HR control (ach > ne)	+
-	**Arterial pressure 65/40 mmHg,	+
-	***pretty low	+
-	**Cardiac output about 70% of normal,	+
-	***Need sympath NE to generate proper heart contraction	+
-	**Vasculatures very dilated,	+
-	***need sympath NE to keep vessels a little constricted	+
-	**Skin warm,	+
-	**mucus membranes flushed,	+
-	**very little tolerance to sitting or standing	+
-	***Because of low cardiac output	+
-	*The Full Neural Control System:	+
-	**Heart rate should be 70-80 beats / min,	+
-	**arterial pressure 120/70 mmHg,	+
-	**cardiac output 70 ml/min per kg,	+
-	**skin cool and	+
-	**mucus membranes pink,	+
-	***not too much blood flow to the skin	+
-	**able to perform to the maximum ability of the skeletal muscle system.	+
-		+
-	===Modifications of Neural Control By Higher Brain Centers===	+
-	*This is the conscious brain working on our unconscious systems.	+
-		+
-	====Emotion====	+
-	*Pleasurable sensations	+
-	**BP goes down	+
-	**People who pet dogs or have pets brings down bp.	+
-	**Pleasure lowers sympathetic and increases parasympathetic activity	+
-	*Anger	+
-	**Excites the sympathetics	+
-	**Acts in the brain, increase firing rate of sympathetic neurons	+
-	**Can be so potent as to cause an heart attack	+
-	**Anger also decreases sensitivity of the baroreceptors	+
-	*Fear and depression	+
-	**Inhibits sympathetic activity	+
-	**Works from conscious centers in brain	+
-	**There is a depression of the sympathetics in the medulla	+
-	**There is a stimulation of the parasympathetic system; this can cause fainting because of the slowed heart rate and low vascular resistance.	+
-		+
-	====Pain====	+
-	*Sharp pain - activate sympathetic system	+
-	**jazzes up the sympathetics	+
-	*Visceral pain - suppress sympathetic system	+
-	**Childbirth, kidney stone, hit in the chest in car accident	+
-		+
-	====Exercise====	+
-	*Just knowing you're going to exercise causes increase in sympathetic activity	+
-	*The more emotional you are about it, the more the sympathetic effect to raise cardiac function!	+
-		+
-	====Loss of baroreceptor Input====	+
-	*Neck injuries can sever glossopharyngeal nerve, atherosclerosis of the larger arteries can prevent baroreceptors from deforming.	+
-	*MAP will remain pretty normal, actually, but will have a wider range of variation.	+
-	*Even though our average pressure is ok, we have trouble with body position changes.	+
-	**This is orthostatic hypotension; in ability to generate contractility increase and arterial constriction.	+
-	*We also have trouble responding to temperature appropriately.	+
-	*So we must have some long-term system other than baroreceptors to keep our bp over time.	+
-		+
-	====Loss of all neural control====	+
-	*Nerve block in the spine	+
-	**Useful for having surgery without depressing the brain.	+
-	**This will cause a decrease in bp mostly because peripheral vascular resistance drops	+
-	**Done routinely	+
-	**	+
-	*Pts with spinal cord injuries that inhibit the sympathetics will become supersensitive to NE where they are no longer getting neural stimulation	+
-		+
-	===The Brain as a Baroreceptor===	+
-	*The brain is a baroreceptor!	+
-	*All the areas we've talkeda bout in the brian stem will change their firing appropriately if they aren't getting enough oxygen	+
-		+
-	====Inadequate perfusion of the brain====	+
-	*Let's look at the different scenarios of brain perfusion issues.	+
-	**The theme is inadequate perfusion, oxygen availability decreases, carbon dioxide accumulates, tissue becomes acidotic, sympathetic activity increased dramatically to raise pressure.	+
-		+
-		+
-	*Arterial pressure too low for autoregulation	+
-	*Compromise of the carotid arteries	+
-	**Blood flow goes down in brain	+
-	**Sympathetic activity will go up to increase blood pressure so it is high enough to get to the deep part of the brain.	+
-	**If this is caused by arterial disease, it must be very advanced arterial disease such that the patient will have many problems other than getting blood to the brain.	+
-	*Increased intracranial pressure	+
-	**Bump on the head and bleeding into the brain	+
-	**Increased pressure squishes the microvessels and venules, then the arterioles	+
-	**This raises vascular resistance	+
-	**Decreased blood flow	+
-	**Too low oxygen to sympathetics	+
-	**Faster firing of sympathetics	+
-	**Tries to bring blood flow up	+
-	**Cushing reflex:	+
-	***Many pts in early 1900s would die after surgery	+
-	***This happened because of brain swelling after surgery.	+
-	***BP would go really high because of sympathetic response to swelling in the brain	+
-		+
-	===Long Term Regulation of Arterial Blood Pressure===	+
-	*From birth to death, bp on average only changes about 20-30 mmHg!	+
-	*How does the body know to keep bp constant over this long term?	+
-		+
-	====Intake of NaCl equals Renal loss of NaCl over a matter of a few days====	+
-	*There isn't much Na in the natrual environment of humans.	+
-	*NaCl was money in the past	+
-	**Not worth his salt	+
-	*As you consume high levels of salt:	+
-	**Increased NaCl does increase MAP	+
-	**Then body compensates by greater excretion of NaCl to lower blood volume	+
-	*It is generally assumed that the major mean arterial pressure effect of salt is on the central venous pressure and CO.	+
-	What?	+
-	*However, a second effect is the damage done to endothelial cells and vascular smooth muscle cells because of oxygen radical formation.	+
-	*Hypertensive state:	+
-	**Those who have generated a new bp setpoint at a higher level still excrete na and water just fine, it just takes a higher bp for the kidney to be signaled to react.	+
-		+
-	====If arterial pressure increases and baroreceptors work, less sympathetic nerve activity to kidney allows increased loss of NaCl====	+
-		+
-	====If intake of NaCl can not be properly excreted, arterial pressure will increase====	+
-	*Kidney function goes down with age.	+
-	*BP diseases go up with age, too.	+
-	*So, as one age, because the kidney's can't respond correclty, even if a pt has functional baroreceptors, they may not be able to control BP that is elevated because of NaCl.	+
-	**Eat salt, bp goes up, baroreceptors fire to brain, brain tells kidney to remove Na and water, kidneys try but fail, bp remains high.	+
-	**So we give them a diuretic to increase urination.	+
-	*Na intake is one of the most important long term control mechanisms for blood pressure control.	+
-	*Only one in four pts react to increase or decrease in dietary Na addition or reduction.	+
-	*Black americans are more salt sensitive than most caucasians.	+
-	**Africans have similar sensitivity to cuacasians.	+
-	**What happened?	+
-	***Some people think obesity is over represented in blacks than in africans.	+
-		+
-	====Obesity====	+
-	*Obesity has changed our understanding of hypertension.	+
-	*Obesity affects salt sensitivty, atherosclerotic lipids that affect baroreceptors, leptin production (ncreases sympath and icnreases salt sensitivity).	+
-	*More on this in a couple days.	+
-		+
-	===Clinical Example===	+
-	*24 yo	+
-	*Vigorous activity, heavy sweating	+
-	*Collapsed in tent, couldn't drink	+
-	*High heart rate; sympathetics are working	+
-	*BP = 80/50	+
-	*Neck veins and arm veins are flat when lying down; his blood volume is really low	+
-	*Facial and body skin : Sweating profusely	+
-	*Vascular refill in fingers: 6 seconds	+
-	**That is super slow!	+
-	*Unresponsive to name, but both pupils react rapidly to light, reacts sluggishly to sternal pain stimulus	+
-	**Brain is working, but not enough to make him conscious	+
-	*A. Intravascular clotting	+
-	**Not yet, though it will be a problem	+
-	*B. Failure of sympathetic nervous system	+
-	**Nope, high heart rate tells us sympt is working	+
-	*C. Elevated peripheral vascular resistance	+
-	**That's trying to save him to perfuse heart and brain so, no.	+
-	*D. Inadequate cardiac output	+
-	**That is true, but that's not what caused him to go bad	+
-	*E. Decreased blood volume	+
-	**Yes	+
-	*Give saline and some 5% glucose solution	+
-	**Glucose burned off will generate water	+
-		+
-		+
-	*continued on to [[Lecture 8 Shock]] on 01/27/11 at 11:40AM.	+

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Revision as of 06:50, 9 March 2012

• continued here from Lecture 6 Transcapillary Exchange on 01/27/11 at around 8:37 ish.

uZCg7F Fantastic blog post.Thanks Again. Great.