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 barorecepto

rs•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 reflexBlood pressure

falls

Aortic archAortic arch Carotid sinusCarotid sinus

Constriction of veins &

arterioles

Constriction of veins &

arterioles

Increased stroke volume

Increased stroke volume

Increased heartrate

Increased heartrate

VasoconstrictionVasoconstriction Cardiac stimulationCardiac stimulation Cardiac inhibitionCardiac inhibition

Nucleus tractus solitariusNucleus tractus solitarius

Increased peripheral resistance

Increased cardiac output

Increased blood pressure

Neural integrationNeural integration

SensorsSensors

EffectorsEffectors

Baroreceptor reflex is afeedback loopfeedback loop

Read temperatur

e

Is temperaturetoo high?

No

Yes

Boiler on

Negative feedback

Example: central heating systemSet

temperature

Baroreceptor reflex is afeedback loopfeedback loop

“Read” pressure

Is pressuretoo high?

Two way negative feedback

Yes

Increase CO

Increase TPR

No

Reduce CO

Reduce TPR

Yes

No

Positive feedback loopPositive feedback loop

Read temperatur

e

Is temperaturetoo high?

Yes

No

Boiler on

Positive feedback

UnstableSet

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 afferentsunmyelinatedmyelinated

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

ArteriesArteries

VeinsVeins

Reduced renalblood flow

Reduced renalblood flow

Juxtaglomerularapparatus

Juxtaglomerularapparatus

ReninRenin

AngiotensinogenAngiotensinogen

Angiotensin IAngiotensin I

Angiotensin IIAngiotensin II

Increasedpre-loadIncreasedpre-load

Increasedafter-loadIncreasedafter-load

vasoconstrictionvasoconstriction

Increased aldosteronesecretion

Increased aldosteronesecretion

Sodium retentionSodium retention

Fluid re-absorptionFluid re-absorption

Increasedblood volumeIncreased

blood volume

Renin/angiotensin/ aldosterone system

LV filling pressure)

(LV pressurebeginning 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

ShockDefinition: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