Cardio 9

Question 1

Peripheral chemoreceptors in general and for cardio

Answer 1

In general: sense O2 and CO2 pp and pH, located near the carotid and aortic bodies
Main effect is to increase respiratory frequency to increase tidal volume in response to low O2 pp, but it also consequently increases HR, leading to more efficiency in pumping, exchange, etc

Question 2

What’s the kidneys role in long term BP control

Answer 2

Maintains plasma fluid and ion levels as well as remove waste
Controls BV long term, hours to days scale, negative feedback system that responds to MAP, thats what it sense/gauges
Brief: can do so via pressure diuresis or through RAAS

Question 3

Pressure diuresis

Answer 3

Main idea: when there’s increased MAP, more urine will be produced to lower total volume
Stimulus: increased MAP, kidney will trigger loss of sodium and (consequently) a loss of water, this resulting in lower plasma volume and therefore less blood aka lower MAP
On a bigger scale, leads to lower BV, lower venous return, lower end diastolic volume, lower stroke volume, lower CO, and then lower MAP

Question 4

RAAS (brief)

Answer 4

Renin Angiotensin Aldosterone System, hormonal system that regulates MAP over the long term, involved multiple organs systems

Question 5

Pressure sensors in the kidney

Answer 5

Sense filtration rates, specifically in terms of excreted sodium and water, lower rates mean less filtration is occurring and its a sign to increase it

Question 6

RAAS pathway, the angiotensinogen part

Answer 6

Pressure sensors in the kidney detect lower filtration rate, renin is produced in response, enters blood, it converts angiotensinogen (proenzyme made by the liver) to angiotensin 1, this is then converted to angiotensin 2 by ACE (angiotensin converting enzyme made by pulmonary epithelial), angiotensin 2 then goes around vasoconstricting, increasing TPR and consequently increasing BP and filtration, the initial issue
Negative feedback

Question 7

Pressure sensors in the brain

Answer 7

Osmoreceptors, can detect the osmolarity of your blood (ion concentration)

Question 8

Baroreceptors

Answer 8

Also sense pressure and can trigger the release of ADH from neurons in the hypothalamus
Note: more involved in large fluid losses, not so much the small maintenance stuff

Question 9

RAAS pathway, the baroreceptors part

Answer 9

Baroreceptors sense changes in pressure and trigger the release of ADH from the pituitary storage, anti-diuretic hormone or vasopressin, specifically there will be low pressure so well have low Baroreceptors activity, the presence of angiotensin 2 also triggers vasopressin release (an independent response to low BP within the RAAS),
Vasopressin causes systemic vasoconstriction, causing an increase in TPR, it also acts on the kidney, increasing water retention to raise volume
Also a negative feedback loop

Question 10

Where does ADH come from

Answer 10

ADH is synthesized by the hypothalamus but stored in the pituitary gland

Question 11

RAAS pathway, the adrenal gland part

Answer 11

Angiotensin 2 binds receptors in the adrenal gland, this causing the release of the hormone aldosterone
Aldosterone then binds to receptors in the kidneys, causes an increase in sodium and water retention, leading to increased BV…….. higher CO and consequently TPR
Another negative feedback system

Question 12

Drugs that help control hypertension (long term)

Answer 12

Aldosterone receptor antagonist: something to block aldosterone receptors in the kidneys to prevent the increase of sodium and water for raising BP
Angiotensin 2 receptor blockers: blocks the binding of angiotensin 2 in the brain, artérioles and adrenal gland, preventing the release of ADH, vasoconstriction, and release of aldosterone
ACE inhibitors: inhibit ACE such that it cant convert angiotensin 1 to 2, preventing it from doing its thing
Renin inhibitors: blocks the conversion of angiotensinogen to angiotensin, stopping the pathway early

Question 13

Orthostasis vs orthostatic hypotension

Answer 13

The maintenance of an upright standing posture
Orthostatic hypotension: BP dropping upon standing

Question 14

What happens to regulate your BP when you go from lying to standing

Answer 14

You stand up after lying down, you get a drop in systolic pressure and a raise in diastolic pressure, evening out to a pretty constant MAP, Baroreceptors reflex has to get it back up to normal
Your central BV falls (to you legs mostly), causing a drop in venous pressure and a decrease in venous return, this causes a decrease in SV (starlings law of the heart explains), these factors together drop CO (CO=SV xHR)
Based on teh equation, the only way to maintain cardiac output (which is liek required for life) you need to increase HR, that’s the baroreflex,
MAP= CO x TPR, based on this equation, to maintain the MAP then TPR must be increased

Question 15

What causes the big drop in BP upon standing

Answer 15

Leg veins are highly compliant so when you stand they can’t resist the gravitational weight of the blood that pooled in your torso/trunk
An additional 80mmHg can be felt on feet when you stand

Question 16

What can happen after standing for long periods of time

Answer 16

That can lead to fainting, the central BV will blood in the legs (in your not moving), this resulting in a significantly lower venous return and you may just pass out (happens when your brain specifically doesnt get enough, likely since its the farther from your feet)
You can also lose plasma, lose meaning it can shift from capillaires to interstitial space (not a useful place for it to be for use), happens due to hydrostatic pressure

Question 17

Muscle pump

Answer 17

Prevents the whole “fainting from standing thing” by contracting calf muscle, idea is that these periodic contractions force venous blood up the one way leg street and stop the pooling from being as intense as it is, keeping up venous return and consequently BP higher