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)

• 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

How is pressure “measured”?
• Short term
– Baroreceptors
• Long term
– Kidney via renin angiotensin system

• Baroreceptors sense stretch and rate of stretch by generating action potentials (voltage spikes)
• Located in highly distensible regions of the circulation to maximise sensitivity http://www.cvphysiology.com/Blood Pressure/bp012 baroreceptor anat.gif

(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)

• 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

From “An Introduction to Cardiovascular Physiology” J.R. Levick

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

Example: central heating system
Set temperature
Read temperature
Yes
Is temperature too high?
No
Boiler on
Negative feedback

“Read” pressure
No
Is pressure too high?
Yes
Reduce CO Increase CO
Reduce TPR Increase TPR
Two way negative feedback

Unstable
Set temperature
Read temperature
Is temperature too high?
Ye
Yes s
Boiler on
Positive feedback

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

• 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 CO
2
** too much K +

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

• Involves control of blood volume/sodium balance by the kidneys
– Hormonal control
• Renin-angiotensin-aldosterone system
• Antidiuretic hormone (vasopressin)
• Atrial natiuretic peptide
– Pressure natriuresis

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

• Enhances water retention
• Causes vasoconstriction
• Secretion increased by unloading of aortic Baroreceptors and atrial sensors http://www.cvphysiology.com/Blood%20Pressure/BP016.htm

• 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

• 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

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

– 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

• 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

(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.

More serious blood loss can be treated by transfusion to lessen the effects shown here

If compensation is not sufficient, organ failure occurs due to inadequate perfusion
• Heart
• Kidney
• Brain