March 14 Physiology II Lecture Notes
How baroreceptors helps deals with acute blood loss?
There is baroreceptor reflex-mediated response,When the baroreceptor reflex is
activated it always prompts PNS and always inhibits SNS.
The response we see during severe blood loss, is shutting off baroreceptor reflex-
mediated response, from occurring, that allows the body to response the way it does.
Slide 1 Composite response to haemorrhage
There are two phases:
What is the initial and direct effect of having a loss of blood?
What the reflex compensation is?
Haemorrhage situation: There is an acute blood loss.
--Tracking cardiovascular changes in diagram
--DIRECT effect: Venous return has been reduced, due to loss of vol of blood. Stroke
vol is going to be reduced. Cardiac output is reduced due to drop in the stroke vol. **
Heart rate is not directly affected by blood loss**
MAP is determined by CO which is dependant on stroke vol and TPR, therefore if
CO is reduced, MAP will be reduced but TPR is set by vasoconstriction of the arterioles,
Arterioles don’t care about blood loss, they are not directly sensing it NOT AFFECTED
by blood loss, they are just smooth muscles, (constricting it) that is setting the TPR. MAP reduction will reduce the stretch on baroreceptors and reduce signals on the brain.
Reduce PNS and increase SNS activation, will be the reflex compensation that
occurs. As a result, of that a slight increase STROKE vol.
Reduction in PNS will lead to increase in heart rate. Doubling effect both STROKE
VOL AND HEART VOL are being used. Together they are contributing to CO(cardiac
output) come closer to what it was before. There is a GAP between the CO used to be
and now, this response on its own, will not be able to store MAP.
Vasoconstriction of the arterioles which will increase TOTAL PERIPHRAL
RESISTANCE. That will happen in the peripheral side of things, which will increase the
MAP. The cardiac output needs TPR increase to get the MAP closer to its original
The actual extent of these changes will depend on how severe the haemorrhage is ,
and how severely the SNS is activated ,
The ability to increase the stroke will depend on how much blood you lost and have to
**STROKE VOL, CARDIAC, OUTPUT, MAP = Accute (direct effect)
**Heart rate & Total Peripheral Resistance = Compensations ( are not direct but are
used to compensation to allow to manage the blood pressure**
Times when your blood pressure is not regulated properly
The major consequence Its more severe in situation where you have drop in blood pressure. If you don’t
maintain enough pressure in the arterial system that means you cannot get enough
blood flow to your brain. The neurons get oxygen starved and start to dysfunction.
When neurons dysfunction you lose consciousness= Syncope (fainting, short term loss
There are different variations, that are largely attributed to where the problems may lie.
Orthostatic hypertension when go from lying/sitting to standing position, the blood in
the veins tends to go down, that can cause short term reduction in venous return
(REDUCES STROKE VOL)
As a result the blood pressure drops, the brain suddenly is not receiving an adequate
amount of oxygen, and syncope occurs.
(NORMAL PERSON ; the baroreceptor will reduce PNS and increase SNS activity in
order to maintain MAP)
Heart rate is simple indicator for nerve activity and get a good idea, whether you are
activating SNS system or not.
People that helping change the PNS and SNS activity, then we would not be able to
Situations where Vasomotor Syncope could happen:- (baroreceptors lose their
sensitivity over time, they are not responding to the changes in the stretch of aorta)
Prolonged bed rest or low gravity; The astronauts subject to low gravity when come
back to earth they can pass out.
Viral infection; Dehydration; Parkinson’s;
To compensate for MAP, we need Total Peripheral Resistance needs to be increased;
Bacterial or viral infection can cause massive release of nitric oxide ( vasodilator). If all
arterioles are getting vasodilatory signal , and activtiting SNS , to relea