Blood Pressure



Arterial blood pressure is the pressure exerted by the circulating blood upon the walls of the blood vessels.
Normal blood pressure for a healthy resting individual on average is approximately 120/80 mmHg. In the UK blood pressures are categorised into three groups; low (90/60 or lower), normal (90/60 – 130/80) or high (140/90 or higher).
​Mean arterial pressure is the average over a cardiac cycle:

Pressure changes through circulation

Regulation of BP

Baroreceptors detect changes in arterial pressure. These baroreceptors send signals to the medulla of the brain stem. The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart’s contractions, as well as the total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.

Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II.

Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.

Baroreceptors in low pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the atria) result in feedback by regulating the secretion of antidiuretic hormone (ADH/Vasopressin), renin and aldosterone. The resultant increase in blood volume results in an increased cardiac output by the Frank–Starling law of the heart, in turn increasing arterial blood pressure.

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in order to return the blood pressure to a more appropriate level.

The blood pressure fall is detected by a decrease in blood flow and thus a decrease in GFR.
Decrease in GFR is sensed as a decrease in Na+ levels by the macula densa.
The Macula Densa cause an increase in Na+ reabsorption, which causes water to follow in via osmosis and leads to an ultimate increase in plasma volume.
Further, the macula densa releases adenosine which causes constriction of the afferent arterioles.
At the same time, the juxtaglomerular cells sense the decrease in blood pressure and release renin.
Renin converts angiotensinogen (inactive form) to angiotensin I (active form).
Angiotensin I flows in the bloodstream until it reaches the capillaries of the lungs where angiotensin converting enzyme (ACE) acts on it to convert it into angiotensin II.
Angiotensin II is a vasoconstrictor which will increase blood flow to the heart and subsequently the preload, ultimately increasing the cardiac output.
Angiotensin II also causes an increase in the release of aldosterone from the adrenal glands.
Aldosterone further increases the Na+ and H2O reabsorption in the distal convoluted tubule of the nephron.


When arterial pressure and blood flow decrease beyond a certain point, the perfusion of the brain becomes critically decreased (i.e., the blood supply is not sufficient).
Causes of hypotension eg., hypovolaemic shock i.e. the loss of circulating blood volume for a variety of reasons, septic shock with an associated vasodilation and low resistance or drug related reactions.
Shock is a complex condition which leads to critically decreased perfusion. The usual mechanisms are loss of blood volume, pooling of blood within the veins reducing adequate return to the heart and/or low effective heart pumping. Low arterial pressure, especially low pulse pressure, is a sign of shock and contributes to and reflects decreased perfusion.


BP is the result of CO increased by peripheral resistance: blood pressure = cardiac output X peripheral resistance. As a result, an abnormal change in blood pressure is often an indication of a problem affecting the heart’s output, the blood vessels’ resistance, or both. Hypertension can be acute or chronic.

​NOTE: Blood pressure can be ‘normal’ yet flow can be abnormal
If an intervention is considered on blood pressure alone, there may be many clinical scenarios that are missed because there are other layers below pressure that need to be considered. Consider the following example (although BP is obviously low here, treatment may vary when there is more information available:

slide 1 – under pressure?
Slide 2 – What is happening?
slide 3 – now add central
slide 4 – scenario 1
slide 5 – scenario 2
slide 6 – line chart
slide 7 – text for chart
Slide 8 – general text

Further Reading re Under Pressure

​​Bayliss et al. Bedside haemodynamic monitoring: experience in a general hospital. Br Med J (Clin Res Ed). 1983 Jul 16;287(6386):187-90. PubMed link –
Connors et al. Assessing hemodynamic status in critically ill patients: Do physicians use clinical information optimally? Journal Crit Care. PubMed link –
Deltex Medical Ltd and
Hamilton-Davis et al. Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Medicine 1997 23:276-281. PubMed link –
Iregui et al. Physicians’ estimates of cardiac index and intravascular volume based on clinical assessment versus transesophageal Doppler measurements obtained by critical care nurses. Am J Crit Care 2004 12(4):336-42. PubMed link –
NHS England
Patient safety
Price et al. Haemodynamic and metabolic effects of haemorrhage in man with particular reference to the splanchnic circulation. Circulation Research 1966 18:469-474. PubMed link –
Reisner. Academic assessment of arterial pulse contour analysis: missing the forest for the trees? Br J Anaesth. 2016 Jun;116(6):733-6. PubMed link –
Singer et al. Effects of alterations in left ventricular filling, contractility and systemic vascular resistance on the ascending aortic blood velocity waveform of normal subjects. Critical Care Medicine 1991 19:1132-1145 PubMed link –
Singer and Glynne. Treating critical illness: the importance of first doing no harm. PLosMed 2005 Jun;2(6):e167. PubMed link –
Singer. Oesophageal Doppler. Current Opinion in Critical Care 2009, 15:244 – 248. PubMed link –
Urrunaga et al. Hemodynamic evaluation of the critically III in the emergency department: A comparison of clinical impression versus transesophageal doppler measurement Annals of Emergency Medicine 1999 34(4):S46. Link –​
US AHRQ your paragraph here.

Other Suggested Reading

NHS choices: What is blood pressure?
NHS choices: High blood pressure (hypertension).
Kladbunde R.E., Cardiovascular Physiology Concepts. 2005. Lippincott Williams & Wilkins.