Volume Resuscitation

Updated: Oct 17, 2019
Author: Griffin L Davis, MD, MPH; Chief Editor: Erik D Schraga, MD 



Volume depletion takes place when fluid is lost from the extracellular space at a rate exceeding net intake. Acute hemorrhage is the leading cause of acute life-threatening intravascular volume loss requiring aggressive fluid resuscitation to maintain tissue perfusion until the underlying cause can be corrected. Intravascular volume depletions may also result from gastrointestinal disorders (eg, vomiting, diarrhea, or ascites), burns, environmental exposure, or renal salt wasting. Volume depletion may result from acute sequestration in the body in a “third space” that is not in equilibrium with the intracellular fluid, as seen in septic shock.

When volume loss occurs, the body reacts by triggering a wide range of physiologic regulatory responses to maintain perfusion in the vascular beds of the most important organs, namely the heart, brain, and kidneys. Decreases in circulating blood volume lead to a drop in arterial blood pressure, and diminished venous return reduces preload, stroke volume, and, therefore, cardiac output. This stimulates aortic baroreceptors, cardiac stretch receptors, and the sympathetic nervous system to increase ventricular contractility, venous and arterial vasoconstriction, and fluid shifts into the intravascular system.

The kidneys react through the rennin-angiotensin-aldosterone system by retaining sodium and water and releasing antidiuretic hormone to increase intravascular volume. The coagulation system responds through the release of local mediators such as thromboxane and platelet-aggregating factor and controls sites of bleeding through vasoconstriction, platelet plug formation, and fibrin deposition.

Without adequate fluid resuscitation, tissue hypoperfusion leads to lactate production and metabolic acidosis. Once the physiologic response to hypovolemia is overwhelmed by prolonged tissue hypoxia, myocardial contractility is depressed and hypoxia and acidosis result in the loss of peripheral vasoconstriction, release of inflammatory mediators and activation of cellular apoptotic pathways, eventually leading to death.


The normal circulating volume of an averaged-size adult is approximately 5 L for a 70 kg person, or 7% of body weight. This volume is further divided into 3 L plasma and 2 L RBC volume (see the image below).

Table 1: Body Fluid Spaces Table 1: Body Fluid Spaces

Disturbances between the intravascular and extravascular volumes or acute blood loss are all indications for fluid resuscitation. The image below lists the various types of intravascular volume loss.

Table 2: Causes of Intravascular Volume Loss Table 2: Causes of Intravascular Volume Loss

Assessment of the need for fluid resuscitation begins with the clinical history. If significant volume loss is reported, volume resuscitation is likely required regardless of laboratory findings or relatively normal vital signs. Signs of orthostatic or persistent hypotension should prompt the provider to begin resuscitation as well.

An even earlier sign that is sometimes missed is a narrow pulse pressure. The pulse pressure is calculated as the systolic pressure minus the diastolic pressure. This should be at least 25% of the systolic pressure. Although a pressure of 110/90 is normal, the pulse pressure of 20, which is only 18% of the systolic pressure, can be an indication of volume loss. Changes in mental status such as confusion, restlessness, or obtundation may be the chief symptoms for a patient that has loss of at least 30% of their circulating volume.[1]

Several physical examination findings may suggest the need for fluid resuscitation. These include the following:

  • Skin: The skin is cool and clammy, except in the cases of septic shock or a “warm shock” in which patients may be febrile. Skin tenting (loss of skin turgor) and dry mucous membranes may be present.

  • Cardiac: Tachycardia becomes more pronounced with increasing volume loss.

  • Renal: Acute renal failure with decreased urine output.

  • Extremities: Weak and faint pulses, slow capillary refill, and muscle weakness may be present.

  • Neurological: Early findings include altered mental status exhibited by restlessness, agitation, or general CNS depression. Later findings include more severe CNS depression, seizure, obtundation, or coma.

  • Ultrasound: Two possible sonographic markers that may be measured at the bedside as surrogates for hypovolemia are the diameters of the inferior vena cava and the right ventricle. Complete collapse of the inferior vena cava on inspiration is usually an indication of hypovolemia requiring immediate fluid resuscitation.[2]


Few contraindications exist to volume resuscitation. The benefit and need for fluid resuscitation to maintain adequate profusion of tissues far outweighs the risks associated with transfusing fluid and/or blood products. The question of “permissive” hypotension in the setting of hemorrhage has not been conclusively answered by the literature. Concerns exist that fluid resuscitation to a normal blood pressure before controlling sites of bleeding may exacerbate ongoing hemorrhage by inhibiting or damaging the formation of clots in areas of vascular injury.[3] Additionally, some fears exist regarding replacing volume with fluids that lower the oxygen-carrying capacity of circulating blood.[4] The adverse affects of “permissive” hypotension are sustained tissue hypoxia regional hypoperfusion, which can be particularly devastating to splanchnici circulation.[5]

Technical Considerations

Best practices

Vascular access and monitoring are essential for proper volume resuscitation. Establish IV access early with awareness that the rate at which crystalloid can be infused is dependent on the catheter diameter and the driving pressure. Large bore peripheral IVs may be as adequate for volume resuscitation as central lines. Maintaining vascular access above the diaphragm is important if concern exists regarding vascular injury in the abdomen or pelvis. For adults and especially children, an intraosseous (IO) line may be placed in the distal femur or proximal tibia within 90 seconds for a truly unstable patient with inadequate peripheral access.

Initial fluid resuscitation is generally accepted to begin with the infusion of crystalloids.[6] If no acceptable hemodynamic improvement occurs after 2-3 L infusion of crystalloids in patients with shock, a blood transfusion may be needed. In the setting of massive hemorrhage, beginning blood transfusion immediately is appropriate. For children, an initial fluid bolus of 20 mL/kg of crystalloids over 0-20 minutes may be repeated twice, followed by a transfusion of 10 mL/kg warm pack red blood cells (PRBCs) if the patient remains unstable.

Procedure Planning

Complication prevention

Post-transfusion reactions with dyspnea are major causes of morbidity and death after blood transfusion. Transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO) are most dangerous, while transfusion-associated dyspnea (TAD) is a milder respiratory distress.[7] TRALI is defined as the onset of acute hypoxia within 6 hours of a blood transfusion in the absence of hydrostatic pulmonary edema. Factors causing TRALI are divided into antibody-mediated and non–antibody-mediated TRALI. Antibody-mediated TRALI is caused by passive transfusion of cognate antibodies and non–antibody-mediated TRALI is caused by transfusion of aged cellular blood products.[8]

TACO can occur in any patient, but elderly persons, small children, and/or patients with cardiac dysfunction are at greatest risk. A transfusion rate of approximately 2-2.5 mL/kg/h is acceptable, meaning that one unit of packed red blood cells should be transfused over a 1.5- to 2-hour period. Patients deemed to be at risk of TACO should have their transfusion rate reduced to 1 mL/kg/h.[9]

A review published in 2007 summarized the data from studies that evaluated the use of premedication to decrease the incidence of febrile nonhemolytic transfusion reactions.[10] The authors concluded that no evidence supports the use of premedication with antihistamines and/or acetaminophen for the prevention of these reactions.

A blood warmer should be used when transfusion of more than 3 units of blood at one time to avoid the complications of hypothermia.

Although blood collections are now routinely separated into various components, allowing for the storage of RBC up to 42 days,[11] avoiding transfusion-related hyperkalemia may be minimized by using blood that was collected less than 5 days prior to transfusion. An alternative is to wash stored red with saline to remove extracellular potassium. These options may not be available in the acute setting.

Leukocyte-reduced red cell preparations are expensive but can be made available to patients with a history of transfusion reactions, patients undergoing cardiovascular surgery, or chronically transfused patients.[12]


Each unit of packed red blood cells PRBC has a volume of 300 mL and contains about 200 mL of red blood cells, which should raise the hemoglobin by about 1 g/dL or the hematocrit by 3-4% in the setting of controlled or slow bleeding.

The ultimate outcome measure is mortality. Adequate volume resuscitation should lead to stabilization of vital signs and the ability of the body to recover from whatever insult is the etiology of the need for volume. Please see the Monitoring and Follow-Up section for what should be monitored during resuscitation. These are interim outcome measures to follow.


Periprocedural Care

Patient Education & Consent

Elements of informed consent

Informed consent for a blood product transfusion requires an appreciation of both benefits and risks. Often, the patient refusing blood transfusion may be more concerned about the risks than the benefits. The clinician should present as balanced a discussion as possible. Benefits may be life-saving, patient stabilization, and/or symptomatic relief. Risks generally include infection, varying types of allergic transfusion reactions, graft versus host disease, volume overload, and electrolyte and clotting factor disturbances.

Therapeutic alternatives for patient unwilling to undergo transfusions include the following:

  • Using “blood substitutes” if available and permissible by patient

  • Reducing blood loss through minimizing the volume of blood used for laboratory testing

  • Reducing the oxygen requirement (eg, 100% oxygen, sedation, mechanical ventilation, control of body temperature, hyperbaric chamber)

  • Increasing the patient’s red cell production with autologous transfusion and/or erythropoietin (if acceptable) and supplemental iron and vitamins as needed

The idea that competent adults have the right to refuse medical treatment, including fluid resuscitation, is well established. Children are minors and therefore not capable of informed consent. The clinician’s duty is to seek legal intervention when a child is placed at "clear and substantial" risk by parental decisions.[13] In the event of a life-threatening clinical scenario that requires blood transfusion, a court order is not needed in order to transfuse a minor.

Monitoring & Follow-up

General parameters

Several diagnostic studies can aid in evaluation of a hypovolemic patient. Basic vital signs of hypotension and tachycardia are used to initially identify patient who are in need of volume resuscitation and can be followed to monitor their progress.

Arterial blood pressure

The first changes in arterial blood pressure that may indicate hypovolemia is a narrow pulse pressure, as previously mentioned. Orthostatic hypotension followed by hypotension regardless of position rapidly follow. Consider that while the normal blood pressure is considered 120/80 mmHg, hypovolemia may be indicated by a pressure above the normal range in a patient who is normally hypertensive. Additionally, arterial blood pressure does not adequately reflect cardiac output or regional hypoperfusion.

Central venous pressure

The venous circulation contains 70% of blood volume; therefore CVP response to fluid administration is useful for monitoring volume status. In general, if the CVP does not rise after infusion of a bolus of fluids, then the vascular system must still be very compliant, meaning that the “tank “ is not full. If a patient does not have intravenous monitoring, volume status may also be evaluated at the bedside by assessing jugular venous distension (JVD) or using ultrasound to visualize the IVC collapse in response to patient inspiration.


Central venous oximetry is a useful parameter for monitoring the global oxygen supply-demand balance. SvO2 less than 70% indicates global hypoperfusion leading to increased tissue oxygen extraction in response to poor oxygen delivery. SvO2 is not sensitive to regional hypoperfusion such as splanchnic hypoperfusion.

Urine output

Oliguria or low urine output may be a sign of volume depletion since the kidney's response to hypovolemia is to resorb sodium and water. As urine output increases, it can be a useful proxy for adequate volume resuscitation. Note that urine output may differ for patients with impaired renal function but is usually 30 mL/hr as a minimum.

Physical examination

During fluid resuscitation, looking for signs of extravascular leak, such as pulmonary and interstitial edema, is important. Frequent physical examinations of the heart, lungs, JVD, and bowel sounds should be documented during the resuscitation process.


Ultrasonography has been suggested as a useful noninvasive tool for the detection and monitoring of hypovolemia. Two possible sonographic markers for hypovolemia are the diameters of the inferior vena cava (and the right ventricle. In general, inferior vena cava size of less than 1.5 cm with total collapse on inspiration equates to a central venous pressure of 0-5, whereas a size greater than 2.5 cm with no collapse on inspiration equates to central venous pressure over 20.[14]


Children have a tendency to decompensate quickly. Thus, close attention to vitals and signs of shock are extremely important. Capillary refill is largely affected by ambient temperature and is not a reliable sign of hypotension. A child with pallor has likely suffered profound blood loss. The best signs to monitor are tachycardia, which is the earliest sign of volume loss in children; blood pressure; and the quality of central and peripheral pluses. Remember that blood pressure in children is dependent on size and age. A general rule to follow is 70 + (2 times age in years) = systolic for children over 1 year old. Diastolic blood pressure is usually 2/3 systolic.



Approach Considerations

Several types of fluids are available for resuscitation. They are generally divided into isotonic crystalloid solutions (most commonly used), colloids, hypertonic solutions, oxygen therapeutic agents and blood products (see the image below). Clinicians should adopt an individualized fluid approach based on the clinical scenario and best available evidence.[15]

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Blood Transfusion

The American Society of Anesthesiologist set the lower threshold for blood transfusion at hemoglobin less than 6 g/dL or hematocrit less than 18% in a healthy individual. Transfusing a patient with a hemoglobin greater than 10 g/dL or a hematocrit over 30 is not recommended.[16, 17] This leaves a relatively wide range for practitioners to choose when blood transfusion is necessary based on the etiology of hypovolemia, comorbidities, and disease processes, in addition to the stability of the patient and their laboratory abnormalities.

The Transfusion Requirements in Critical Care (TRICC) trial showed that patients on a restrictive transfusion strategy where red cells were transfused for Hgb less than 7 g/dL and maintained at 7-9 g/dL showed a lower in-hospital mortality rate than a liberal strategy, although 30-day mortality was similar.[18] Also, literature exists that supports maintaining a hematocrit above 30 for patients with a history of coronary artery disease.

When time is available, typed and cross-matched blood is preferred. Unstable patients may be transfused with low-titer O-negative blood (see the image below). In the setting of hemorrhage, 4 classes exist for which specific clinical responses are demonstrated requiring different levels of fluid resuscitation.

Table 4: Classes of Hemorrhage Table 4: Classes of Hemorrhage

Massive Transfusion

Massive transfusion is defined as a transfusion of more than 10 units PBRC at one given time. In the setting of massive hemorrhage, when large volumes of crystalloid and blood have been given, FFP and platelet transfusion may be required to address the effects of dilutional coagulopathy. Some debate exists in the literature, but it is generally suggested that when initiating a massive transfusion protocol, patients should be transfused PRBC, FFP, and platelets in a ratio close to 1:1:1 if multiple units of blood will be necessary.[19]

Whole blood should be considered only when dealing with a patient with an acute hemorrhage[20] and then only after the patient has received approximately 5-7 units of red cells plus crystalloids.[21] Reinfusion of autologous red cells is a good approach for patients for who have large quantities of blood collected from chest tubes or aspirated from peritoneal cavities reducing the need for an allogenic transfusion. Proper collecting devices are necessary for this type of transfusion but should be considered in patients who present with massive hemorrhage or patients such as Jehovah’s Witnesses who do not accept any donor products.

Crystalloids versus Colloids

Colloids have larger molecular-weight particles that give them oncotic plasma pressures similar to natural plasma proteins. This theoretically allows for better volume resuscitation by remaining in the intravascular space and supporting circulating volume as compared to crystalloids, which may have extravascular shift causing pulmonary and interstitial edema. However, in patients with increased vascular permeability as seen in sepsis and late hemorrhagic shock, leakage of these larger colloid molecules also exists. Physiologically balanced crystalloids may be the default fluid for critically ill patients, whereas the role for colloids remains unclear.

Several studies have compared the use of crystalloid and several different types of colloids as resuscitation fluids and have found no difference in mortality.[22, 23] Furthermore, most evidence shows there is no clear evidence that one colloid solution is more effective or safer than any other.[24] Newer studies have shown that differences in chloride load and strong ion difference appear to be clinically important. Quantitative toxicity can be mitigated when dosing is based on dynamic parameters that measure volume responsiveness. Qualitative toxicity for colloids and isotonic saline remain a legitimate concern.[25] Given the cost associated with colloids, no clear benefit exists to using these agents over the more affordable and generally available crystalloids.

Hypertonic Fluids

Hypertonic saline has been proposed as a crystalloid alternative that may have some benefit in head injury and trauma patients by limiting tissue edema effects associated with volume resuscitation. Recent studies have shown that hypertonic saline plus dextran does not reduce mortality or the risk of acute respiratory distress syndrome (ARDS) compared to resuscitation with lactated Ringer solution in trauma patients.[26] Evidence from the SAFE trial demonstrated that albumin and saline have similar outcomes for fluid resuscitation in patients receiving volume resuscitation in intensive care units.[27]

Oxygen-Carrying Fluids

Two classes of agents are under development in hopes of replicating the oxygen-carrying capacity of native RBC that may be lost during hemorrhage.[28, 29, 30] Hemoglobin-based oxygen carriers are not currently approved for human use in the United States and fluorocarbon-based oxygen carriers have yet to show any effectiveness in large-volume resuscitation.

Tranexamic Acid

Tranexamic acid (TXA) has been demonstrated to reduce bleeding in patients undergoing elective surgery. The CRASH-2 trial aimed to determine the effect of early administration of TXA on death and transfusion requirement in bleeding trauma patients. Early administration of TXA safely reduced the risk of death in bleeding trauma patients and may be cost-effective. However, treatment beyond 3 hours of injury is unlikely to be effective.[31]


Laboratory Medicine

Laboratory Medicine Summary

Several laboratory values will be useful both in the diagnostic evaluation of acute hemorrhage as well as in monitoring patients during volume resuscitation. Hemoglobin/hematocrit baseline should be established and frequently checked to assess for appropriate accommodation when transfusing blood or in the setting of acute hemorrhage. Each unit of packed red blood cells (PRBC) has a volume of 300 mL and contains about 200 mL of red blood cells, which should raise the hemoglobin by about 1 g/dL or the hematocrit by 3-4% in the setting of controlled or slow bleeding.

Arterial or venous blood gases will provide information about the pH and degree of metabolic acidosis from tissue hypoxia. Lactate, electrolytes, BUN, Cr, glucose, and calcium are all important markers of tissue and organ hypoxia and ensuing organ failure. All patients receiving a blood transfusion should have coagulation studies, platelet counts and be typed and cross-matched.