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Hypovolemia, also known as volume depletion or volume contraction, is a state of decreased intravascular volume.[1] This may be due to either a loss of both salt and water or a decrease in blood volume.[2][3] Hypovolemia refers to the loss of extracellular fluid and should not be confused with dehydration.[4] Dehydration refers to excessive total body water loss that results in cellular hypertonicity (a relatively substantial loss of fluid within individual cells).

Hypovolemia
Other namesOligemia, hypovolaemia, oligaemia, hypovolæmia, volume depletion
SpecialtyEmergency medicine
Symptomsheadache, fatigue, nausea, profuse sweating, dizziness

Hypovolemia is caused by a variety of different events, but these can be simplified into two categories: those associated with kidney function and those that are not.[5] The signs and symptoms of hypovolemia worsen as the amount of fluid lost increases.[6] Immediately or shortly after mild fluid loss, one may experience headache, fatigue, weakness, dizziness or thirst (as in blood transfusion, diarrhea, vomiting). Untreated hypovolemia or excessive and rapid losses of volume may lead hypovolemic shock[7]. Signs and symptoms of hypovolemic shock include increased heart rate, low blood pressure, pale or cold skin, and altered mental status. When these signs are seen, immediate action should be taken to restore the lost volume.

Signs and symptomsEdit

Signs and symptoms of hypovolemia progress with increased loss of fluid volume.[5]

Early symptoms of hypovolemia include headache, fatigue, weakness, thirst, and dizziness.

The more severe signs and symptoms are often associated with hypovolemic shock. These include oliguria, cyanosis, abdominal and chest pain, hypotension, tachycardia, cold hands and feet, and progressively altering mental status.

CausesEdit

The causes of hypovolemia can be characterized into two categories:[5]

KidneyEdit

  • Loss of body sodium and consequent intravascular water (due to impaired reabsorption of salt and water in the tubules of the kidneys)
    • Osmotic diuresis: the increase in urine production due to an excess of osmotic (namely glucose and urea) load in the tubules of the kidneys
    • Overuse of pharmacologic diuretics
    • Impaired response to hormones controlling salt and water balance (see mineralocorticoids)
    • Impaired kidney function due to tubular injury or other diseases

OtherEdit

  • Loss of bodily fluids due to:
    • Gastrointestinal losses; e.g. vomiting and diarrhea
    • Skin losses; e.g. excessive sweating and burns
    • Respiratory losses; e.g. hyperventilation (breathing fast)
  • Build up of fluid in empty spaces (third spaces) of the body due to:

PathophysiologyEdit

 
Pathophysiology of hypovolemia

The signs and symptoms of hypovolemia are primarily due to the consequences of decreased circulating volume and a subsequent reduction in the amount of blood reaching the tissues of the body.[9] In order to properly perform their functions, tissues require the oxygen transported in the blood.[10] A decrease in circulating volume can lead to a decrease in blood perfusion to the brain, resulting in headache and dizziness. Altered mental status progresses as hypovolemia continues.

Baroreceptors in the body (primarily those located in the carotid sinuses and aortic arch) sense the reduction of circulating fluid and send signals to the brain to increase sympathetic response (see also: baroreflex).[11] This sympathetic response is to release epinephrine and norepinephrine, which results in peripheral vasoconstriction (reducing size of blood vessels) in order to conserve the circulating fluids for organs vital to survival (i.e. brain and heart). Peripheral vasoconstriction accounts for the cold extremities (hands and feet), increased heart rate, increased cardiac output (and associated chest pain). Eventually, there will be less perfusion to the kidneys, resulting in decreased urine output.

DiagnosisEdit

Hypovolemia can be recognized by a fast heart rate, low blood pressure,[12] and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.[13]

In children, compensation can result in an artificially high blood pressure despite hypovolemia (a decrease in blood volume). Children typically are able to compensate (maintain blood pressure despite hypovolemia) for a longer period than adults, but deteriorate rapidly and severely once they are unable to compensate (decompensate).[14] Consequently, any possibility of internal bleeding in children should be treated aggressively.[15][16]

Signs of external bleeding should be assessed, noting that individuals can bleed internally without external blood loss or otherwise apparent signs.[16]

There should be considered possible mechanisms of injury that may have caused internal bleeding, such as ruptured or bruised internal organs. If trained to do so and if the situation permits, there should be conducted a secondary survey and checked the chest and abdomen for pain, deformity, guarding, discoloration or swelling. Bleeding into the abdominal cavity can cause the classical bruising patterns of Grey Turner's sign (bruising along the sides) or Cullen's sign (around the navel).[17]

InvestigationEdit

In a hospital, physicians respond to a case of hypovolemic shock by conducting these investigations:

StagesEdit

Untreated hypovolemia can lead to shock (see also: hypovolemic shock). Most sources state that there are 4 stages of hypovolemia and subsequent shock;[18] however, a number of other systems exist with as many as 6 stages.[19]

The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the stages of blood loss (under 15% of volume, 15–30% of volume, 30–40% of volume and above 40% of volume) mimic the scores in a game of tennis: 15, 15–30, 30–40 and 40.[20] It is basically the same as used in classifying bleeding by blood loss.

The signs and symptoms of the major stages of hypovolemic shock include:[21][22]

Stage 1 Stage 2 Stage 3 Stage 4
Blood loss Up to 15% (750 mL) 15–30% (750–1500 mL) 30–40% (1500–2000 mL) Over 40% (over 2000 mL)
Blood pressure Normal (Maintained
by vasoconstriction)
Increased diastolic BP Systolic BP < 100 Systolic BP < 70
Heart rate Normal Slight tachycardia (> 100 bpm) Tachycardia (> 120 bpm) Extreme tachycardia (> 140 bpm) with weak pulse
Respiratory rate Normal Increased (> 20) Tachypneic (> 30) Extreme tachypnea
Mental status Normal Slight anxiety, restless Altered, confused Decreased LOC, lethargy, coma
Skin Pale Pale, cool, clammy Increased diaphoresis Extreme diaphoresis; mottling possible
Capillary refill Normal Delayed Delayed Absent
Urine output Normal 20–30 mL/h 20 mL/h Negligible

TreatmentEdit

Field careEdit

The most important step in treatment of hypovolemic shock is to identify and control the source of bleeding.[23]

Medical personnel should immediately supply emergency oxygen to increase efficiency of the patient's remaining blood supply. This intervention can be life-saving.[24]

The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen the way blood does—however, researchers are developing blood substitutes that can. Infusing colloid or crystalloid IV fluids also dilutes clotting factors in the blood, increasing the risk of bleeding. Current best practice allow permissive hypotension in patients suffering from hypovolemic shock,[25] both avoid overly diluting clotting factors and avoid artificially raising blood pressure to a point where it "blows off" clots that have formed.[26][27]

Hospital treatmentEdit

Fluid replacement is beneficial in hypovolemia of stage 2, and is necessary in stage 3 and 4.[21] See also the discussion of shock and the importance of treating reversible shock while it can still be countered.

The following interventions are carried out:

  • IV access
  • Oxygen as required
  • Fresh frozen plasma or blood transfusion
  • Surgical repair at sites of bleeding

Vasopressors (such as dopamine and noradrenaline) should generally be avoided, as they may result in further tissue ischemia and don't correct the primary problem. Fluids are the preferred choice of therapy.[28]

HistoryEdit

In cases where loss of blood volume is clearly attributable to bleeding (as opposed to, e.g., dehydration), most medical practitioners prefer the term exsanguination for its greater specificity and descriptiveness, with the effect that the latter term is now more common in the relevant context.[29]

See alsoEdit

ReferencesEdit

  1. ^ McGee S (2018). Evidence-based physical diagnosis. Philadelphia, PA: Elsevier. ISBN 978-0-323-39276-1. OCLC 959371826. The term hypovolemia refers collectively to two distinct disorders: (1) volume depletion, which describes the loss of sodium from the extracellular space (i.e., intravascular and interstitial fluid) that occurs during gastrointestinal hemorrhage, vomiting, diarrhea, and diuresis; and (2) dehydration, which refers to the loss of intracellular water (and total body water) that ultimately causes cellular desiccation and elevates the plasma sodium concentration and osmolality.
  2. ^ "Hypovolemia definition - MedicineNet - Health and Medical Information Produced by Doctors". Medterms.com. 2012-03-19. Retrieved 2015-11-01.
  3. ^ "Hypovolemia | definition of hypovolemia by Medical dictionary". Medical-dictionary.thefreedictionary.com. Retrieved 2015-11-01.
  4. ^ Bhave G, Neilson EG (August 2011). "Volume depletion versus dehydration: how understanding the difference can guide therapy". American Journal of Kidney Diseases. 58 (2): 302–9. doi:10.1053/j.ajkd.2011.02.395. PMC 4096820. PMID 21705120.
  5. ^ a b c Jameson, J. Larry; Kasper, Dennis L.; Longo, Dan L.; Fauci, Anthony S.; Hauser, Stephen L.; Loscalzo, Joseph, eds. (2018-08-13). Harrison's principles of internal medicine (20th ed.). New York: McGraw-Hill Education. ISBN 9781259644030. OCLC 1029074059.
  6. ^ "Hypovolemic shock: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 2019-09-02.
  7. ^ Kolecki P (October 13, 2016). "Hypovolemic Shock". Medscape.
  8. ^ Danic B, Gouézec H, Bigant E, Thomas T (June 2005). "[Incidents of blood donation]". Transfusion Clinique et Biologique (in French). 12 (2): 153–9. doi:10.1016/j.tracli.2005.04.003. PMID 15894504.
  9. ^ Taghavi S, Askari R (2019), "Hypovolemic Shock", StatPearls, StatPearls Publishing, PMID 30020669, retrieved 2019-09-02
  10. ^ Carreau A, El Hafny-Rahbi B, Matejuk A, Grillon C, Kieda C (June 2011). "Why is the partial oxygen pressure of human tissues a crucial parameter? Small molecules and hypoxia". Journal of Cellular and Molecular Medicine. 15 (6): 1239–53. doi:10.1111/j.1582-4934.2011.01258.x. PMC 4373326. PMID 21251211.
  11. ^ Armstrong M, Moore RA (2019). "Physiology, Baroreceptors". StatPearls. StatPearls Publishing. PMID 30844199. Retrieved 2019-09-02.
  12. ^ "Stage 3: Compensated Shock". Archived from the original on 2010-06-11.
  13. ^ Alpert JS, Ewy GA (2002). Manual of Cardiovascular Diagnosis and Therapy. Lippincott Williams & Wilkins. p. 101. ISBN 978-0-7817-2803-4.
  14. ^ Henry MC, Stapleton ER, Edgerly D (26 July 2011). EMT Prehospital Care. Jones & Bartlett Publishers. pp. 471–. ISBN 978-0-323-08533-5.
  15. ^ Assuma Beevi (31 August 2012). Pediatric Nursing Care Plans. JP Medical Ltd. pp. 47–. ISBN 978-93-5025-868-2.
  16. ^ a b Clement I (20 May 2013). Textbook on First Aid and Emergency Nursing. Jaypee Brothers Publishers. pp. 113–. ISBN 978-93-5025-987-0.
  17. ^ Blaber A, Harris G (1 October 2011). Assessment Skills For Paramedics. McGraw-Hill Education. pp. 83–. ISBN 978-0-335-24199-6.
  18. ^ Hudson, Kristi. "Hypovolemic Shock - 1 Nursing CE". Archived from the original on 2009-06-06.
  19. ^ "Stage 1: Anticipation stage (a new paradigm)". Archived from the original on 2010-01-16.
  20. ^ Greaves I, Porter K, Hodgetts T, et al., eds. (2006). Emergency Care: A Textbook for Paramedics. Elsevier Health Sciences. p. 229. ISBN 9780702025860.
  21. ^ a b Agabegi ED, Steven S A (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 978-0-7817-7153-5.
  22. ^ Kumar, Vinay; Abbas, Abul K.; Aster, Jon C., eds. (2015). Robbins and Cotran pathologic basis of disease. Illustrated by Perkins, James A. (9th ed.). Philadelphia, PA: Saunders. ISBN 9781455726134. OCLC 879416939.
  23. ^ Bulger, E. M.; et al. (2014). "An evidence-based prehospital guideline for external hemorrhage control: American College of Surgeons Committee on Trauma". Prehospital Emergency Care. 18 (2): 163–173. doi:10.3109/10903127.2014.896962. PMID 24641269.
  24. ^ Takasu, A.; Prueckner, S.; Tisherman, S. A.; Stezoski, S. W.; Stezoski, J.; Safar, P. (2000). "Effects of increased oxygen breathing in a volume controlled hemorrhagic shock outcome model in rats". Resuscitation. 45 (3): 209–220. doi:10.1016/s0300-9572(00)00183-0. PMID 10959021.
  25. ^ "Permissive Hypotension". Trauma.Org. 1997-08-31. Retrieved 2015-11-01.
  26. ^ Kennamer M, American Academy of Orthopaedic Surgeons (AAOS) (30 September 2013). Intravenous Therapy for Prehospital Providers. Jones & Bartlett Publishers. pp. 63–. ISBN 978-1-4496-4204-4.
  27. ^ de Franchis R, Dell'Era A (25 January 2014). Variceal Hemorrhage. Springer Science & Business Media. pp. 113–. ISBN 978-1-4939-0002-2.
  28. ^ Nordin, A. J.; Mäkisalo, H.; Höckerstedt, K. A. (1996-08-31). "Failure of dobutamine to improve liver oxygenation during resuscitation with a crystalloid solution after experimental haemorrhagic shock". The European Journal of Surgery = Acta Chirurgica. Pubmed-NCBI. 162 (12): 973–979. Retrieved 2017-11-21.
  29. ^ Geeraedts LM, Kaasjager HA, van Vugt AB, Frölke JP (January 2009). "Exsanguination in trauma: A review of diagnostics and treatment options". Injury. 40 (1): 11–20. doi:10.1016/j.injury.2008.10.007. PMID 19135193.

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