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

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 http://www.cvphysiology.com/Blood Pressure/bp012 baroreceptor anat.gif

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)

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”

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

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

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

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

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

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 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

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+

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

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

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: 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

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

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