1. Control of blood pressure
Outline
Short term control (baroreceptors)
Location
Types of baroreceptor
Baroreceptor reflex
Other stretch receptors
Long-term control
Renin/ angiotensin/ aldosterone system
Vasopressin
Atrial natiuretic peptide
Response to blood loss (shock)

2. Control of blood pressure
Mean blood pressure is controlled by changing total peripheral resistance and or cardiac output. P = CO x TPR (compare Ohm’s law)
Cardiac output is controlled by sympathetic and para sympathetic nerves which effect:
heart rate
force of contraction
TPR controlled by nervous and chemical means to effect constriction/dilatation of
arterioles and venules

3. Regulation of blood pressure
How is pressure “measured”?
Short term
Baroreceptors
Long term
Kidney via renin angiotensin system

4. Location of baroreceptors
Baroreceptors sense stretch and rate of stretch by generating action potentials (voltage spikes)
Located in highly distensible regions of the circulation to maximise sensitivity
Pressure/bp012 baroreceptor anat.gif

5. Baroreceptor output (from single fibres)
Rapid increase in mean pressure
Rapid decrease in mean pressure
Response to pulse pressure
From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)

6. Two types of baroreceptor
From “An Introduction to Cardiovascular Physiology”
J.R. Levick
Type A
High sensitivity
High firing rate
Type C
Lower sensitivity
Lower firing rate
Higher threshold (before firing starts)
Therefore can deal with higher pressures than type A which become “saturated”

7. Response of single baroreceptor fibre to change in pressure
From “An Introduction to Cardiovascular Physiology” J.R. Levick

8. Baroreceptor reflex Sensors Neural integration Effectors
Blood pressure falls
Aortic arch
Carotid sinus
Sensors
Vasoconstriction
Cardiac stimulation
Cardiac inhibition
Nucleus tractus solitarius
Neural integration
Constriction of veins & arterioles
Increased stroke volume
Increased heart
rate
Effectors
Increased peripheral resistance
Increased cardiac output
Increased blood pressure

9. Baroreceptor reflex is a
feedback loop
Example: central heating system
Set temperature
Read temperature
Is temperature
too high?
Yes No
Boiler on
Negative feedback

10. Baroreceptor reflex is a
feedback loop
“Read” pressure No
Reduce CO
Reduce TPR
Is pressure
too high?
Yes
Increase CO
Increase TPR
Two way negative feedback

11. Positive feedback loop
Unstable
Set temperature
Read temperature
Is temperature
too high?
Yes No No
Yes
Boiler on
Positive feedback

12. Other stretch receptors
Coronary artery baroreceptors
Respond to arterial pressure but more sensitive than carotid and aortic ones
Veno-atrial mechanoreceptors
Respond to changes in central blood volume
Lie down, lift your legs and cause peripheral vasodilatation
Unmyelinated mechanoreceptors
Respond to distension of heart
Ventricular ones during systole; atrial ones during inspiration

13. Location of receptors in and near the heart
Nucleus tractus solitarius
Cardiac vagal afferents
Cardiac pain
myelinated
unmyelinated
Spinal cord
Baroreceptors in coronary arteries and aortic arch
Sympathetic afferents & unmyelinated nociceptors
From “An Introduction to Cardiovascular Physiology” J.R. Levick

14. Other receptors Heart chemosensors Arterial chemosensors
Cause pain in response to ischaemia
K+, lactic acid, bradykinin, prostaglandins
Arterial chemosensors
Stimulated in response to
Hypoxaemia, hypercapnia*, acidosis, hyperkalaemia**
Regulate breathing
Lung stretch receptors
Cause tachycardia during inspiration
*too much CO2
**too much K+

15. Overview of short-term control mechanisms
From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)

16. Long term control of blood pressure
Involves control of blood volume/sodium balance by the kidneys
Hormonal control
Renin-angiotensin-aldosterone system
Antidiuretic hormone (vasopressin)
Atrial natiuretic peptide
Pressure natriuresis

17. Renin/angiotensin/ aldosterone system
Reduced renal
blood flow
Increased
blood volume
Juxtaglomerular
apparatus
LV filling pressure)
Increased
pre-load
after-load
Fluid re-absorption
Renin
(LV pressure
beginning of systole)
Angiotensinogen
Sodium retention
Increased blood volume in the thorax
Angiotensin I
Increased aldosterone
secretion
Angiotensin II
Arteries
Veins
vasoconstriction

18. Vasopressin Enhances water retention Causes vasoconstriction
Secretion increased by unloading of aortic Baroreceptors and atrial sensors

19. Atrial natiuretic peptide
Increases salt excretion via kidneys
By reducing water reabsorption in the collecting ducts
relaxes renal arterioles
inhibits sodium reabsorption in the distal tubule
Released in response to stimulation of atrial receptors

20. Summary of long term BP control
Cardiac output and BP depend on renal control of extra-cellular fluid volume via:
Pressure natriuresis, (increased renal filtration)
Changes in:
Vasopressin
Aldosterone
Atrial natiuretic peptide
All under the control of altered cardiovascular receptor signaling

21. Shock Definition: Symptoms
A pathophysiological disorder characterised by acute failure of the cardiovascular system to perfuse the tissues of the body adequately.
Levick J.R. “An Introduction to Cardiovascular Physiology”
Symptoms
Cold, clammy skin
Muscular weakness
Rapid and shallow breathing
Rapid and weak pulse
Low pulse pressure (and sometimes mean pressure)
Reduced urine output
Confusion

22. Types of shock Hypovolaemia Septic Cardiogenic Anaphylactic
Caused by drop in blood (plasma) volume
e.g. haemorrhage, diarrhoea, vomiting, injury
Septic
Caused by bacterial endotoxins
e.g. salmonella
Cardiogenic
An acute interruption of of cardiac function
e.g. myocarditis (inflammation of the heart muscle) or myocardial infarction
Anaphylactic
Caused by allergic reaction

23. Effect of blood loss less than 10%, no serious symptoms
e.g. blood transfusion
% blood loss not usually life threatening
greater than 30%, severe drop in BP and, often, death due to impaired cerebral and coronary perfusion

24. Response to moderate blood loss (compensated haemorrhage)
Blood volume falls therefore pulse pressure and stroke volume fall. (Frank-Starling mechanism: reduced LV contractile force)
Cardiopulmonary stretch receptor and baroreceptor activity falls
Arterial chemoreceptor activity increases, due to hypoxia and acidosis
 rapid breathing
 release of vasoconstrictors
Vasopressin, angiotensin etc.

25. Response to moderate blood loss
More serious blood loss can be treated by transfusion to lessen the effects shown here

26. Uncompensated shock
If compensation is not sufficient, organ failure occurs due to inadequate perfusion
Heart
Kidney
Brain