Volume Resuscitation
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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).
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.
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]
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. 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.
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. [6] 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. [7]
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. [8]
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. [9] 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, [10] 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. [11]
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.
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Jeromy T Boucher, DO Resident Physician, Department of Emergency Medicine, George Washington University Hospital
Jeromy T Boucher, DO is a member of the following medical societies: American Osteopathic Association, Association of Military Osteopathic Physicians and Surgeons, Florida Osteopathic Medical Association, Student Osteopathic Medical Association, Texas Osteopathic Medical Association
Disclosure: Nothing to disclose.
Griffin L Davis, MD, MPH Chair, Department of Emergency Medicine, Prince George’s Hospital Center; Assistant Professor, Department of Emergency Medicine, George Washington University School of Medicine
Griffin L Davis, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, National Medical Association, Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Elizabeth M Phillips, MD, MA Resident Physician, Department of Emergency Medicine, George Washington University Medical Center
Disclosure: Nothing to disclose.
Volume Resuscitation
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