Resuscitation in Hypovolaemic Shock

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Hypovolaemic shock occurs when the volume of the circulatory system is too depleted to allow adequate circulation to the tissues of the body. The aim of resuscitation is to correct the hypovolaemia and hypoperfusion of vital organs such as the kidneys before irreversible damage occurs.

Remember there are also other causes of shock:

  • Cardiogenic - eg, massive myocardial infarction or other cause of primary cardiac (pump) failure.
  • Obstructive - eg, massive pulmonary embolism, tamponade, tension pneumothorax.
  • Distributive - vasodilatation +/- leakage from endothelium; with the following subtypes: septic, anaphylactic and neurogenic.

A healthy adult can withstand the loss of half a litre from a circulation of about five litres without ill effect; however, larger volumes and rapid loss cause progressively greater problems. Risk is very much related to the degree of hypovolaemia and the speed of correction. In children tachycardia is one of the earliest signs of hypovolaemia but in young adults the circulatory system is much better able to cope with the rigours of loss. The risk of morbidity and mortality is much greater as age increases. Pathology in the cardiovascular, respiratory and renal systems increases risk.

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  • The individual may feel cold, unwell, anxious, faint and short of breath.
  • There may be faintness on standing or even on sitting up, due to postural hypotension.
  • There may be symptoms related to the cause of the hypovolaemia, such as pain from a bleeding ulcer, dissecting aneurysm, ruptured ectopic pregnancy, trauma or burns.
  • Gut ischaemia can lead to nausea and vomiting but the significance is often overlooked.


  • The patient may look pale and sweaty.
  • There may be tachypnoea.
  • The periphery may be cold from poor perfusion, and capillary refill time may be prolonged. However, this can be a poor indicator of hypovolaemia.
  • There may be tachycardia and a fall in blood pressure (BP) or postural hypotension. However, tachycardia is a later feature than the cold periphery and a fall in BP occurs still later. This is particularly so in a young person (not child), compared with an elderly person.
  • Young people may show little rise in pulse rate and no fall in BP despite significant exsanguination. It is very easy to underestimate the severity of loss in a young person.
  • Late features include confusion or even coma.

The causes of hypovolaemic shock are:[1] 

  • Loss of blood, which may be revealed or occult.
  • Trauma, which may lead to visible bleeding or rupture of an internal organ like the spleen or liver. A fractured femur will bleed about half a litre and a fractured pelvis will lose about one litre of blood - note these volumes vary according to age/weight. The volume of haematemesis gives little indication of the degree of bleeding. Bleeding from ectopic pregnancy is also occult with little or no vaginal loss, and 30% of ectopic pregnancies rupture before a menstrual period has been missed. It is important to maintain a high level of clinical suspicion.
  • Leakage of plasma and often some blood as in burns.
  • Severe loss of water and salt. This may occur with vigorous exercise in a hot environment, poor intake, loss from diarrhoea and vomiting, and inappropriate diuresis.

The surface area of burns should be estimated using the rule of nines; alternatively, calculators are available.[2] The larger the area involved, the more severe the problem, especially in children and the elderly. In children, the rule of nines does not apply but, as a guide, the child's palm represents about 1% of surface area. Children need relatively more fluid than adults. Severe diarrhoea and vomiting will cause marked loss of salt and water. In cholera, diarrhoea can be up to 20 litres a day. Exercise in extreme heat can cause serious loss of water and salt. As the rate of sweating rises, the concentration of sodium in the sweat rises, so that the total loss of sodium rises exponentially. Ability to remove sodium from sweat improves with acclimatisation. Other causes of shock include:

  • Poor cardiac output as in massive myocardial infarction, ruptured aortic valve or massive pulmonary embolism.
  • Septic shock and acute pancreatitis leading to a fall in vascular resistance.
  • High transection of the spine or a high spinal anaesthetic.
  • Check Hb, U&E, LFT and, in haemorrhage and burns, group and cross-match.
  • Coagulation screen.
  • Blood gases (arterial or venous) may show a metabolic acidaemia from poor perfusion; lactate levels particularly reflect hypoperfusion.
  • Monitor urine output, which may require a catheter.
  • Ultrasound can be useful for differentiating hypovolaemic from cardiogenic shock; the vena cava can be assessed for adequate filling and echocardiogram can show any pump failure.
  • Central venous pressure (CVP) monitoring may be useful where there is evidence of shock.

For adults, the clinical staging relating to loss of blood volume can be classified as:[1] 

  • Class 1: 10-15% blood loss; physiological compensation and no clinical changes appear.
  • Class 2: 15-30% blood loss; postural hypotension, generalised vasoconstriction and reduction in urine output to 20-30 ml/hour.
  • Class 3: 30-40% blood loss; hypotension, tachycardia over 120, tachypnoea, urine output under 20 ml/hour and the patient is confused.
  • Class 4: 40% blood loss; marked hypotension, tachycardia and tachypnoea. No urine output and the patient is comatose.

Physiologically, three stages of hypovolaemic shock are recognised:[3] 

  • Compensated shock: baroreceptor reflexes result in increase in myocardial contractility, tachycardia and vasoconstriction. They maintain cardiac output and BP and lead to the release of vasopressin, aldosterone and renin.
  • Progressive or uncompensated shock: occurs with myocardial depression, failure of vasomotor reflexes and failure of the microcirculation, with increase in capillary permeability, sludging and thrombosis, resulting in cellular dysfunction and lactic acidosis.
  • Irreversible shock: failure of vital organs with inability to recover.

These stages are also applicable to children but their period of compensated shock may be relatively longer than in adults. However, their cardiac reserve is less, so that the shift to uncompensated shock can progress more rapidly to the irreversible stage.

General measures

  • Oxygen should be given.
  • Venous access must be secured early. It is more difficult to achieve once further circulatory collapse has occurred. There may be some concern that fluid replacement before arrest of haemorrhage may encourage further bleeding but maintaining adequate perfusion of vital organs is more important.[4]
  • Resuscitation is usually started with crystalloid, such as normal saline or Hartmann's solution, although some people prefer colloids from the outset.[3][5] Studies have shown that there is remarkably little to choose between the two.[6][7] Albumin has previously been avoided in the seriously ill patient, as it has been associated with a worse outcome but it may play a role in those requiring substantial amounts of crystalloid to maintain their mean arterial pressure in the setting of septic shock.[8] In haemorrhage, blood should be given as soon as possible. Rapid infusion devices and autologous blood transfusion may be employed if blood loss is massive and fast.[3][9]
  • There is some debate around fluid replacement where haemorrhage is ongoing. Modern ideas include avoiding excessive crystalloid fluid resuscitation by allowing permissive hypotension and early use of blood and massive transfusion protocols with damage control surgery to combat the lethal triad of hypothermia, coagulopathy and acidosis.[10] 
  • A CVP line may be required. CVP is far more sensitive to the balance between loss and replacement than pulse or BP and, in the elderly, it can prevent over-transfusion and pulmonary oedema. Particularly in young patients, there is a tendency towards over-replacement to prevent tissue ischaemia, although the evidence base is surprisingly scarce.[6] In burns, a high CVP may be required to maintain adequate output of urine.
  • As a first aid measure in burns, Clingfilm® or some such polyethylene film is very useful, both to prevent infection that can convert a superficial burn to full thickness and to reduce fluid and plasma loss.


  • Traditional teaching is that vasopressors have no part to play, as they will only increase tissue ischaemia. They may have a place if there is failure to respond to volume replacement; however, the evidence is inconclusive.[11]
  • Vasodilator therapy is for the intensive care specialist. It is used more for septic shock. If hypovolaemia is the problem, volume should be replaced.
  • If there is pain, analgesia must be given by the IV route, as any other route will be ineffective. Pain increases metabolic rate and so aggravates tissue ischaemia.


  • If bleeding continues, surgery may be needed to stem the flow. It is usual to resuscitate first to reduce the risk, especially as induction of anaesthesia can lead to collapse of a fragile circulation. In some cases like ruptured ectopic pregnancy and placenta praevia, the rate of bleeding cannot be matched by transfusion and the cause must be treated before resuscitation can be effective.
  • In trauma, first aid measures may help stem blood loss. In gunshot wounds look for not just the entrance but also the exit wound. The latter may be significantly larger than the former. If a high-powered weapon was used, primary closure of the wound should not be attempted.
  • Blood is directed away from the kidneys and gut. This can produce acute kidney injury and complications of gut ischaemia.
  • In obstetric shock, acute tubular necrosis can occur.
  • Inadequate perfusion leads to hypoxia and metabolic acidosis.
  • About 75% of the blood flow to the right ventricle and 100% to the left ventricle occurs in diastole. A fall in diastolic pressure will predispose to cardiac arrhythmias and even arrest. Upset of acid-base balance, hypoxia and disturbance of electrolytes will aggravate the problem.
  • In those who are susceptible, dehydration may lead to haemoconcentration and sludging of the circulation with such complications as venous sinus thrombosis.

Prognosis is worse in the elderly than in the young. Physical fitness improves outcome. Rapid and adequate replacement of the circulating volume may prevent the complications of hypoperfusion, including renal failure, ischaemic damage to the gut, brain damage and cardiac arrest.

  • Loss of circulating volume must be diagnosed and treated before the condition becomes critical. This is often difficult when bleeding is internal and hence occult. It is often poorly done.
  • Where the loss is simply salt and water, oral replacement will be adequate in the early stages.
  • In other cases, venous access and adequate replacement are required at an early stage.
  • Small children are very susceptible to dehydration, as are the elderly.
  • Nowadays sportsmen are very much more aware of the problems of dehydration. Even slight dehydration has a marked adverse effect on fitness.

Further reading & references

  1. Mulholland MW and Doherty GM; (2012) Complications in Surgery, 2nd Ed., Lippincott Williams and Wilkins: Philadelphia.
  2. Bonsall AM; Resuscitation Fluids in Burns
  3. Adult Trauma Clnical Practice Guidelines: Management of hypovolaemic shock in the trauma patient; NSW Institute of Trauma and Injury Management, 2007
  4. Nolan J; Fluid resuscitation for the trauma patient.; Resuscitation. 2001 Jan;48(1):57-69.
  5. Shafi S, Kauder DR; Fluid resuscitation and blood replacement in patients with polytrauma.; Clin Orthop Relat Res. 2004 May;(422):37-42.
  6. Moore FA, McKinley BA, Moore EE; The next generation in shock resuscitation; Lancet. 2004 Jun 12;363(9425):1988-96.
  7. Perel P, Roberts I, Ker K; Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2013 Feb 28;2:CD000567. doi: 10.1002/14651858.CD000567.pub6.
  8. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med. 2013 Feb;39(2):165-228. doi: 10.1007/s00134-012-2769-8. Epub 2013 Jan 30.
  9. Stammers AH, Murdock JD, Klayman MH, et al; Utilization of rapid-infuser devices for massive blood loss; Perfusion. 2005 Mar;20(2):65-9.
  10. Chak Wah K, Wai Man C, Janet Yuen Ha W, et al; Evolving frontiers in severe polytrauma management - refining the essential principles. Malays J Med Sci. 2013 Jan;20(1):1-12.
  11. Mullner M, Urbanek B, Havel C, et al; Vasopressors for shock.; Cochrane Database Syst Rev. 2004;(3):CD003709.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Gurvinder Rull
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1253 (v23)
Last Checked:
Next Review:

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