Cardiovascular lecture 4: regulation of arterial pressure and cardiovascular reflexes week 4

Question 1

What are the 2 purposes of regulating MAP?

Answer 1

Maintaining MAP serves 2 purposes:

If delta P across the system is maintained, TPR can be changed to change flow and therefore control CO to the various tissue beds

Regulating MAP prevents pressure from becoming high enough to cause damage to blood vessels or too low to provide adequate tissue perfusion

Question 2

CO and TPR regulate MAP (long/short) term. BV (blood volume) regulates MAP (long/short) term.

Answer 2

CO and TPR vary short term

BV varies long term

Question 3

Where in the body are the cardiovascular control centers? Where does it receive inputs from? Of these inputs, what ar the primary sensory inputs that determine cardiovascular function? What do the outputs of the cardiovascular control centers determine?

Answer 3

The cardiovascular control centers are in the medulla oblongata. There are a large number of inputs to it from the cortex and sensory receptors. Its outputs drive the sympathetic and parasympathetic pathways that control the cardiovascular effectors. So it:
1. receives inputs from “higher” centers such as the cortex and the hypothalamus
2. receives sensory inputs from a variety of receptors located throughout the body and all can influence cardiovascular function. These include temperature receptors, pain receptors and chemoreceptors
However, the primary sensory inputs that determine cardiovascular function are:
1. the baroreceptors
2. the atrial volume receptors

Question 4

Outputs from the medulla reach the cardiovascular effectors (____, ____, _____) via both sympathetic fibers that innervate the ___, ____, and ____ (same as previous blanks). Outputs from the medula also reach the cardiovascular effectors via parasympathetic fibers to the ______.

Answer 4

Outputs from the medulla reach the cardiovascular effectors (SA node, myocardium, blood vessels) via both sympathetic fibers (to SA node, myocardium and vessels) and parasympathetic fibers (to SA node).

Question 5

There are tonic outputs from the CV center. Tonic outputs are more or less always there at rest. Tonic outputs to the cardiac pacemaker establishes a resting HR of approximately 70 bmp. What does this mean for the output of the medulla to the SA node?

Answer 5

This rate is slower than the spontaneous rate of SA node firing in the absence of input. This means that the medulla is always sending out some parasympathetic signals, releasing acetylcholine and keeping the heart rate down at rest.

Question 6

The ventricular myocardium receieves tonic output as well which determines what?

Answer 6

inotropic state of the heart

Question 7

____ _____ also are always receiving output from the medulla, causing vasoconstriction and venoconstriction (determines total peripheral resistance). Indeed, if this tonic output wasn’t maintained and all of the arterioles were allowed to dilate, the MAP would drop substantially.

Answer 7

Blood vessels

Question 8

True or false: Naturally enough, it is the modulation of tonic outflow which results in control (increase or decrease) of the function of the effectors (SA node, myocardium, blood vessels). Hence we talk of increasing and decreasing sympathetic and parasympathetic tone which means nothing more than dialing a signal which is already there up or down. The sympathetic tone is high when the sympathetic output from the medulla is high, tending to cause more of a sympathetic response at the effector organs.

Answer 8

True.

Question 9

The baroreceptor reflex is important for adequate (long/short) term regulation of MAP.

What kind of receptors is it driven by? Where are these receptors located?

Answer 9

Short term!

baroreceptors in the carotid sinus

Question 10

List and describe the steps of the baroreceptor reflex when MAP is decreased.

Answer 10

1. impulses from the baroreceptors to the CNS integrating centers (the medulla) decrease
2. sympathetic output increases from the medulla and parasympathetic output decreases from
   the medulla
3. increased heart rate (SA node – sympathetic and parasympathetic) dc parasympathetic tone, increase sympathetic tone
4. increased inotropic state (sympathetic)
5. increased TPR (resistance vessels in the splanchnic, skin and muscle beds).
6. increased circulating blood volume (capacitance vessels - i.e. veins - in the splanchnic beds contract – sympathetic). Veins (capacitance vessels constrict. This somewhat increases resistancebut more importantly, compliance of veins decreases. At same pressure have less volume in veins. This increases the circulating blood volume. Get less blood in veins and more in arteries

Question 11

The baroreceptors are (tonically/periodically) active.

Answer 11

tonically

Question 12

What are the 2 locations of the barorecptors? Which is more important in man and for this class?

How do the signals from the baroreceptors travel to the medulla oblongata?

Answer 12

1. carotid sinus and aortic arch. carotid sinus are more important in man and ones we will focus on
2. Through afferent nerves from the aortic baroreceptor carried in the X cranial nerve (vagus) and afferents from the carotid sinus baroreceptor are carried in the IXth cranial nerve (carotid sinus nerve)

Question 13

The baroreceptor reflex is a (positive/negative) feedback system that functions to minimize changes in MAP (the regulated variable).

Answer 13

negative. increased firing with increases in MAP that causes a decrease in MAP. When MAP declines, decreasd frequency of firing.

Question 14

How does the final MAP compare to the original value after changes are made to MAP through the baroreceptor reflex?

Answer 14

The compensation is never quite complete and the final MAP will always end up slightly in the direction of the original change.

Question 15

What 3 phases make up a baroreceptor reflex response?Discuss in terms of a pt hemorrhaging.

Answer 15

1. Some disturbance causes a change in MAP (a fall in the attached figure). This is known as the direct response (DR). It takes place before any reflexes occur-reflex independent reaction to whater the inital perturbation is. (in reality, reflexes automatically kick in). If a pt hemorrhages, you lose blood volume. When BV goes down, MAP goes down.
2. The eventual Reflex Response (RR) returns MAP towards its nrmal level. In our hemorrhage case, the drop in MAP causes the HR, SV, and TPR to rise. THis causes MAP to return toward the original level
3. Evetually, after 2-3 minutes at most, a new Steady State (SS) level of MAP is achieved. Remember that the reflex response never completely compensates for the intial change in the DR. The new SS level in our hemorrhage victim is close to teh orginal level but the baroreflex never quite gets it all the way back up.

Any change in the CV system (as illustrated in attached figure) or any disturbance introduced into the system that porudces a change in MAP (DR) will give rise to a RR and eventually a new SS

Question 16

In representation of the baroreceptor reflex, MAP represents the regulated variable. The pathways from BR-CNS to Ra (arterial pressure), HR, and IS are neural pathways (ANS).

Question 17

When MAP is altered, what are the 4 effectors whose functions are reflexively altered?

Answer 17

The effectors whose functions are reflexively altered include:

1. SA node (pacemaker) - determines HR
2. Ventricular myocardium - determines inotropic state, or contractility (an important, but not the sole, determinant of stroke volume)
3. Resistance vessels in splachnic, skin, and muscle beds (determine TPR)
4. Capacitance vessels in the splanchnic circulation

Question 18

The maintenance of blood volume contributes to (long/short) term regulation of MAP.

Answer 18

long

Question 19

Where are blood volume receptors located? What kind of receptors are they?

Answer 19

There are atrial and central venous volume receptors (mechano/stretch receptors). These receptors are located in atria, large veins, and pulmonary circulation.

Question 20

The activity of blood volume receptors is

a. tonic
b. phasic

Answer 20

The activity of these receptors is tonic. They fire every cardiac cycle. An increae or decrease in BV is signaled by changes in firing frequency.

Question 21

What are the 2 types of atrial volume receptors? What do these 2 receptors fire in response to?

Answer 21

Atrial volume receptor type A fires on contraction, resumably in response to pressure. Note
Figure 4.7 (attached). The pressure in the atrium goes up just after the P wave, which signals electrical excitation and the beginning of atrial contraction. As the pressure rises, the type A receptor fires.
On the other hand, atrial volume receptor type B fires on stretch. Note again the figure. Atrial pressure declines with the appearance of the T wave, indicating ventricular relaxation and opening of the AV valve. As filling takes place, the atrial walls stretch causeing the type B receptor to fire.

Question 22

The afferent inputs to the CV controller from atrial volume receptors are

a. stimulatory
b. inhibitory

explain answer.

Answer 22

These afferent inputs are inhibitory to the CV controller (i.e. more firing indicates that blood volume must decrease).

Question 23

Note again that the frequency of firing from teh atrial volume receptors i decreased in response to decreased atrial pressure and stretch of the walls when there is a decrease in blood volume. What is released from the hypothalamus in response and what is the effect?

Answer 23

The signals lead to the release of anti-diuretic hormone (ADH) from the hypothalamus. ADH acts at the kidneys to increase water reabsorption and increase blood volume. The increased blood volume leads to increased CVP (i.e. atrial pressure), thus increasing the firing from the atrial volume receptors, eventually bring the firing frequency back to normal.

Note that the above response is long-term. The kidneys don’t retain enough water over a period of seconds or minutes to make a significant difference. The short term response is, of course, dominated by the baroreflex. Decreased blood volume leads to decreased CVP and decreased ventricular filling. The decreased filling decreases SV and CO. This decreases MAP. Baroreceptors sense the fall in MAP that accompanies decreased blood volume and their firing frequency declines. This, of course, leads to the now familiar response described on the previous pages of this section.

Question 24

Increased sympathetic outflow to the kidneys activates what system? What effect does this have on MAP?

Answer 24

Incraed sympathetic outflow to the kidneys activates Renin-Angiotensin-Aldosterone system and helps to sustain MAP. Renin is released from the kidneys and converts angiotensinogen to antiotensin I which is eventually converted to angiotensin II, a vasoconstrictor which increases TPR and therefore increases MAP. Angiotensin II also leads to the release of aldosterone from the adrenal cortex. Aldosterone increases Na absorption which leads to increased water retention. Increased water retention means increased blood volume.

Question 25

What is the chemoreceptor reflex? In answer, include stimuli, receptors, primary response, and secondary response.

Answer 25

Chemoreceptor reflex

1. Stimuli: decreased arterial PO2, decreased pH, increased PCO2
2. Receptors: carotid and aortic bodies (peripheral chemoreceptors)
3. Primary response is respiratory (increased rate and depth of breathing)
4. Secondary response is cardiovascular (reflex vasoconstriction in muscle and increased heart rate). Increases cardiac output and mean arterial pressure (body assumes these stimulia are result of low tissue perfusion so it increases MAP)
5. When severe hypoxia is present the resulting cardiovascular response assists in delivery of oxygen to the tissues, particularly the brain and heart (where vasoconstriction DOES NOT occur)

Question 26

What is the CNS ischemic response (Cushing reflex)? Include the stimulus and repsonse in answer.

Answer 26

CNS ischemic response - Cushing reflex

1. Stimuli: MAP below 50 mm Hg or increased intracranial pressure (stimulates neurons in CV control centers via as yet unknown agents, possibly decreased O2, decreased pH, increased PCO2, increased [K+])
2. Response: massive sympathetic outflow which leads to increased TPR (vasoconstriction) which gives rise to increased MAP (partially overcomes effects of increased intracranial pressure); this in turn leads to reflex bradycardia (vagal)

increased intracranial pressure: increase MAP to increase perfusion to brain (increased pressure would compress vessels so want to increase perfusion). bradycardia works against this reflex a little bit but still get increase in MAP