HypovolaemiaSigns of hypovolaemiaMeasuring blood volumeCentral venous pressureThe response to hypovolaemiaTreating hypovolaemia


Hypovolaemia is a loss of blood volume. This can occur because the body loses fluids (absolute hypovolaemia) or because fluids become redistributed from the blood into tissue compartments or cavities (relative hypovolaemia). Hypovolaemia leads to a reduction in blood pressure and inadequate perfusion of organs, potentially causing multiple organ failure. There are physiological responses to hypovolaemia which can compensate - in part - for the reduction in blood volume and potentially restore blood pressure. A fluid challenge can aid in diagnosis and subsequent treatment of hypovolaemia.


Hypovolaemia is a loss of blood volume. This can occur because the body loses fluids (absolute hypovolaemia) or because fluids become redistributed from the blood into tissue compartments or cavities (relative hypovolaemia):

Absolute hypovolaemia – blood or fluid loss from the body

  • Haemorrhage
  • Vomiting
  • Diarrhoea
  • Burns
  • Dehydration (e.g. polyuria in diabetes)
  • Evaporation (e.g. exposure)

Relative hypovolaemia – redistribution of blood or fluid elsewhere in the body

  • Capillary leak (e.g. during severe inflammation such as anaphylaxis or sepsis)
  • Effusion (into a body cavity such as the peritoneum or pleura)
  • Vasodilatation (e.g. during severe inflammation such as anaphylaxis or sepsis)

Signs of hypovolaemia

The obvious signs of hypovolaemia may only become apparent when clinical intervention is urgently required. These include:

Reduced skin turgor
If the skin is pinched and tented up it remains so rather than springing back. The skin on the back of the hand is often pinched as a simple test of this.

Due to lack of blood volume (absolute hypovolaemia), widespread vasodilatation and blood pooling and/or leakage of fluid from the blood into tissues or cavities (relative hypovolaemia).

Reduced cardiac output
Cardiac output depends on venous return to the right side of the heart. If blood volume is reduced, venous return will be low, stroke volume will be decreased and cardiac output will be reduced.

Baroreflex control of blood pressure responds to low pressure/volume by increasing the rate and force of the contractility of the heart. This, and other compensatory mechanisms (see below), may make hypovolaemia difficult to spot. On the other hand, in severe hypovolaemia where venous return is very low, increasing the rate of the heart pumping at necessarily low stroke volume will not compensate enough to restore blood pressure and organ perfusion.

Lack of perfusion of the kidneys will result in decreased urine production and potentially acute kidney injury.

Measuring blood volume

There isn’t a simple way to measure blood volume that can be used in a treatment setting. The best way to measure blood volume would be to intravenously inject something traceable (e.g. radioactive) and determine the extent to which it has been diluted in the blood volume soon after. Radio-labelled red blood cells can be used for this purpose, but the equipment required to perform such a test isn’t widely available. Generally, a surrogate measure of blood volume, such as central venous pressure (CVP) is used instead.

Central venous pressure

Recording central venous pressure (CVP) using a cannula inserted into a large vein and advanced near the heart provides a useful indication of blood volume and the effects of interventions such as a fluid challenge. Low CVP indicates that inadequate blood is returning to the heart. The effect of this will be reduced cardiac contractility due to the a href="tag/frank-starling-relationship">Frank-Starling relationship and low cardiac output. In haemorrhagic hypovolaemia, a fluid challenge should increase CVP and provide an indication of the extent to which further fluids are required to normalise blood pressure. In more complex situations a fluid challenge may have little effect. For example, in septic shock widespread plasma leak and vasodilatation cannot be overcome with a simple fluid challenge and a vasopressor such as noradrenaline may be required to increase blood pressure.

The physiological response to hypovolaemia

How does the body’s homeostatic processes respond to hypovolaemia? Firstly, the kidneys will be receiving a poorer blood supply than usual and this will initiate the release of renin, activating the renin-angiotensin system to increase blood pressure. This is achieved by the threefold functions of angiotensin II:

  • Direct contraction of vascular smooth muscle
  • Aldosterone secretion and hence water retention by the kidney
  • Potentiation of sympathetic contraction of vascular smooth muscle

Reduced blood pressure due to hypovolaemia will also activate baroreceptors in the carotid sinus and aortic arch which will initiate a reflex activation of the sympathetic nervous system. Release of noradrenaline from sympathetic nerve fibres innervating the heart and blood vessels will increase the rate and force of cardiac contraction (thereby increasing cardiac output [link]) and cause vasoconstriction, respectively. Both of these actions should increase blood pressure to improve the perfusion of vital organs, but compensation may be inadequate. Thus, it is possible to have tachycardia with reduced cardiac output and hypotension when this reflex cannot compensate for inadequate venous return to the heart due to a serious loss of blood volume.

Treatment of hypovolaemia

Hypovolaemia can be managed by fluid resuscitation. A fluid challenge is often performed to determine how successful this approach is likely to be. In sepsis, for example, administration of fluids may not substantially improve blood pressure because systemic vasodilation allows blood volume to pool. In such a circumstance, administration of vasopressors may be indicated. By contrast, when hypovolaemia occurs from blood loss due to trauma or after surgery, fluid resuscitation can be very effective in restoring blood pressure and organ perfusion.

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