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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)
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
Regulation of blood pressure
How is pressure “measured”?
• Short term
– Baroreceptors
• Long term
– Kidney via renin angiotensin system
http://www.cvphysiology.com/Blood Pressure/bp012 baroreceptor anat.gif
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
Baroreceptor output
(from single fibres)
Rapid decrease in mean pressure
From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
Rapid increase in mean pressure
Response to pulse pressure
Two types of baroreceptor
• 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”
From “An Introduction to Cardiovascular Physiology”
J.R. Levick
Response of single baroreceptor
fibre to change in pressure
From “An Introduction to Cardiovascular Physiology” J.R. Levick
Baroreceptor reflex
Blood pressure falls
Aortic arch Carotid sinus
Constriction of veins
& arterioles
Increased stroke
volume
Increased heart
rate
Vasoconstriction Cardiac stimulation Cardiac inhibition
Nucleus tractus solitarius
Increased peripheral
resistance
Increased cardiac
output
Increased blood
pressure
Neural integration
Sensors
Effectors
Baroreceptor reflex is a
feedback loop
Read
temperature
Is temperature
too high?
No
Yes
Boiler on
Negative feedback
Example: central heating system
Set temperature
Baroreceptor reflex is a
feedback loop
“Read”
pressure
Is pressure
too high?
Two way negative feedback
Yes
Increase CO
Increase TPR
No
Reduce CO
Reduce TPR
Yes
No
Positive feedback loop
Read
temperature
Is temperature
too high?
Ye
s
No
Boiler on
Positive feedback
Unstable
Set temperature
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
Location of receptors in and near the heart
From “An Introduction to Cardiovascular Physiology” J.R. Levick
Spinal cord
Baroreceptors in
coronary arteries and
aortic arch
Sympathetic afferents &
unmyelinated nociceptors
Cardiac pain
Nucleus tractus solitarius
Cardiac vagal afferents
unmyelinated
myelinated
Other receptors
• Heart 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+
Overview of short-term control mechanisms
From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003)
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
Arteries
Veins
Reduced renal
blood flow
Juxtaglomerular
apparatus
Renin
Angiotensinogen
Angiotensin I
Angiotensin II
Increased
pre-load
Increased
after-load
vasoconstriction
Increased aldosterone
secretion
Sodium retention
Fluid re-absorption
Increased
blood volume
Renin/angiotensin/
aldosterone system
LV filling pressure)
(LV pressure
beginning of systole)
Vasopressin
• Enhances water retention
• Causes vasoconstriction
• Secretion increased by unloading of
aortic Baroreceptors and atrial sensors
http://www.cvphysiology.com/Blood%20Pressure/BP016.htm
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
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
Shock
Definition:
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
Types of shock
– Hypovolaemia
• 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
Effect of blood loss
• less than 10%, no serious symptoms
– e.g. blood transfusion
• 20 - 30% blood loss not usually life
threatening
• greater than 30%, severe drop in BP
and, often, death due to impaired
cerebral and coronary perfusion
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.
Response to moderate blood loss
More serious blood loss
can be treated by
transfusion to lessen the
effects shown here
Uncompensated shock
If compensation is not sufficient, organ
failure occurs due to inadequate perfusion
• Heart
• Kidney
• Brain

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BP_Control.ppt physology1.ppt

  • 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. http://www.cvphysiology.com/Blood Pressure/bp012 baroreceptor anat.gif 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
  • 5. Baroreceptor output (from single fibres) Rapid decrease in mean pressure From: Introduction to Cardiovascular physiology. J.R. Levick. Arnold 4th edition (2003) Rapid increase in mean pressure Response to pulse pressure
  • 6. Two types of baroreceptor • 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” From “An Introduction to Cardiovascular Physiology” J.R. Levick
  • 7. Response of single baroreceptor fibre to change in pressure From “An Introduction to Cardiovascular Physiology” J.R. Levick
  • 8. Baroreceptor reflex Blood pressure falls Aortic arch Carotid sinus Constriction of veins & arterioles Increased stroke volume Increased heart rate Vasoconstriction Cardiac stimulation Cardiac inhibition Nucleus tractus solitarius Increased peripheral resistance Increased cardiac output Increased blood pressure Neural integration Sensors Effectors
  • 9. Baroreceptor reflex is a feedback loop Read temperature Is temperature too high? No Yes Boiler on Negative feedback Example: central heating system Set temperature
  • 10. Baroreceptor reflex is a feedback loop “Read” pressure Is pressure too high? Two way negative feedback Yes Increase CO Increase TPR No Reduce CO Reduce TPR
  • 11. Yes No Positive feedback loop Read temperature Is temperature too high? Ye s No Boiler on Positive feedback Unstable Set temperature
  • 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 From “An Introduction to Cardiovascular Physiology” J.R. Levick Spinal cord Baroreceptors in coronary arteries and aortic arch Sympathetic afferents & unmyelinated nociceptors Cardiac pain Nucleus tractus solitarius Cardiac vagal afferents unmyelinated myelinated
  • 14. Other receptors • Heart 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. Arteries Veins Reduced renal blood flow Juxtaglomerular apparatus Renin Angiotensinogen Angiotensin I Angiotensin II Increased pre-load Increased after-load vasoconstriction Increased aldosterone secretion Sodium retention Fluid re-absorption Increased blood volume Renin/angiotensin/ aldosterone system LV filling pressure) (LV pressure beginning of systole)
  • 18. Vasopressin • Enhances water retention • Causes vasoconstriction • Secretion increased by unloading of aortic Baroreceptors and atrial sensors http://www.cvphysiology.com/Blood%20Pressure/BP016.htm
  • 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: 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 • 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 • 20 - 30% 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