Hypovolemic Shock


Article Author:
Sharven Taghavi


Article Editor:
Reza Askari


Editors In Chief:
Jason Nagle


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
6/18/2019 2:39:40 AM

Introduction

Patients with hypovolemic shock have severe hypovolemia with decreased peripheral perfusion. If left untreated, these patients can develop ischemic injury of vital organs, leading to multi-system organ failure. The first factor to be considered is whether the hypovolemic shock has resulted from hemorrhage or fluid losses, as this will dictate treatment. When etiology of hypovolemic shock has been determined, replacement of blood or fluid loss should be carried out as soon as possible to minimize tissue ischemia. Factors to consider when replacing fluid loss include the rate of fluid replacement and type of fluid to be used. [1]

Etiology

The annual incidence of shock of any etiology is 0.3 to 0.7 per 1000, with hemorrhagic shock being most common in the intensive care unit. Hypovolemic shock is the most common type of shock in children, most commonly due to diarrheal illness in the developing world. Hypovolemic shock occurs as a result of either blood loss or extracellular fluid loss. Hemorrhagic shock is hypovolemic shock from blood loss. Traumatic injury is by far the most common cause of hemorrhagic shock. Other causes of hemorrhagic shock include gastrointestinal (GI) bleed, bleed from an ectopic pregnancy, bleeding from surgical intervention, or vaginal bleeding. 

Hypovolemic shock as a result of extracellular fluid loss can be of the following etiologies: 

Gastrointestinal Losses

GI losses can occur via many different etiologies. The gastrointestinal tract usually secretes between 3 to 6 liters of fluid per day. However, most of this fluid is reabsorbed as only 100 to 200 mL are lost in the stool. Volume depletion occurs when the fluid ordinarily secreted by the GI tract cannot be reabsorbed. This occurs when there is retractable vomiting, diarrhea, or external drainage via stoma or fistulas.

Renal Losses

Renal losses of salt and fluid can lead to hypovolemic shock. The kidneys usually excrete sodium and water in a manner that matches intake. Diuretic therapy and osmotic diuresis from hyperglycemia can lead to excessive renal sodium and volume loss. In addition, there are several tubular and interstitial diseases beyond the scope of this article that cause severe salt-wasting nephropathy.

Skin Losses

Fluid loss also can occur from the skin. In a hot and dry climate, skin fluid losses can be as high as 1 to 2 liters/hour. Patients with a skin barrier interrupted by burns or other skin lesions also can experience large fluid losses that lead to hypovolemic shock.

Third-Space Sequestration

Sequestration of fluid into a third-space also can lead to volume loss and hypovolemic shock. Third-spacing of fluid can occur in intestinal obstruction, pancreatitis, obstruction of a major venous system, or any other pathological condition that results in a massive inflammatory response. [1]

Epidemiology

While the incidence of hypovolemic shock from extracellular fluid loss is difficult to quantify, it is known that hemorrhagic shock is most commonly due to trauma. In one study, 62.2% of massive transfusions at a level 1 trauma center were due to traumatic injury. In this study, 75% of blood products used were related to traumatic injury. Elderly patients are more likely to experience hypovolemic shock due to fluid losses as they have a less physiologic reserve.[1]

Pathophysiology

Hypovolemic shock results from depletion of intravascular volume, whether by extracellular fluid loss or blood loss. The body compensates with increased sympathetic tone resulting in increased heart rate, increased cardiac contractility, and peripheral vasoconstriction. The first changes in vital signs seen in hypovolemic shock include an increase in diastolic blood pressure with narrowed pulse pressure. As volume status continues to decrease, systolic blood pressure drops. As a result, oxygen delivery to vital organs is unable to meet oxygen demand. Cells switch from aerobic metabolism to anaerobic metabolism, resulting in lactic acidosis. As sympathetic drive increases, blood flow is diverted from other organs to preserve blood flow to the heart and brain. This propagates tissue ischemia and worsens lactic acidosis. If not corrected, there will be worsening hemodynamic compromise and, eventually, death. [2]

History and Physical

History and physical can often make the diagnosis of hypovolemic shock. For patients with hemorrhagic shock, a history of trauma or recent surgery is present. For hypovolemic shock due to fluid losses, history and physical should attempt to identify possible GI, renal, skin, or third-spacing as a cause of extracellular fluid loss. Symptoms of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid-base disorders that accompany hypovolemic shock.

Patients with volume depletion may complain of thirst, muscle cramps, and/or orthostatic hypotension. Severe hypovolemic shock can result in mesenteric and coronary ischemia that can cause abdominal or chest pain. Agitation, lethargy, or confusion may result from brain malperfusion. 

Although relatively nonsensitive and nonspecific, physical exam can be helpful in determining the presence of hypovolemic shock. Physical findings suggestive of volume depletion include dry mucous membranes, decreased skin turgor, and low jugular venous distention. Tachycardia and hypotension can be seen along with decreased urinary output. Patients in shock can appear cold, clammy, and cyanotic.[3]

Evaluation

Various laboratory values can be abnormal in hypovolemic shock. Patients can have increased BUN and serum creatinine as a result of prerenal kidney failure. Hypernatremia or hyponatremia can result, as can hyperkalemia or hypokalemia. Lactic acidosis can result from increased anaerobic metabolism. However, the effect of acid-base balance can be variable as patients with large GI losses can become alkalotic. In cases of hemorrhagic shock, hematocrit and hemoglobin can be severely decreased. However, with a reduction in plasma volume, hematocrit and hemoglobin can be increased due to hemoconcentration.

Low urinary sodium is commonly found in hypovolemic patients as the kidneys attempt to conserve sodium and water to expand the extracellular volume. However, sodium urine can be low in a euvolemic patient with heart failure, cirrhosis, or nephrotic syndrome. A fractional excretion of sodium under 1% is also suggestive of volume depletion. Elevated urine osmolality can also suggest hypovolemia. However, this number also can be elevated in the setting of impaired concentrating ability by the kidneys.

Central venous pressure (CVP) is often used to assess volume status. However, its usefulness in determining volume responsiveness has recently come into question. Ventilator settings, chest wall compliance, and right-sided heart failure can compromise CVPs accuracy as a measure of volume status. Measurements of pulse pressure variation via various commercial devices has also been postulated as a measure of volume responsiveness. However, pulse pressure variation as a measure of fluid responsiveness is only valid in patients without spontaneous breaths or arrhythmias. The accuracy of pulse pressure variation also can be compromised in right heart failure, decreased lung or chest wall compliance, and high respiratory rates.

Similar to examining pulse pressure variation, measuring respiratory variation in inferior vena cava diameter as a measure of volume responsiveness has only been validated in patients without spontaneous breaths or arrhythmias. Measuring the effect of passive leg raises on cardiac contractility by echo appears to be the most accurate measurement of volume responsiveness, although it is also subject to limitations. [3][[4]

Treatment / Management

For patients in hemorrhagic shock, early use of blood products over crystalloid resuscitation results in better outcomes. Balanced transfusion using 1:1:1 or 1:1:2 of plasma to platelets to packed red blood cells results in better hemostasis. Anti-fibrinolytic administration to patients with severe bleed within 3 hours of traumatic injury appears to decrease death from major bleed as shown in the CRASH-2 trial. Research on oxygen-carrying substitutes as an alternative to packed red blood cells is ongoing, although no blood substitutes have been approved for use in the United States.

For patients in hypovolemic shock due to fluid losses, the exact fluid deficit cannot be determined. Therefore, it is prudent to start with 2 liters of isotonic crystalloid solution infused rapidly as an attempt to quickly restore tissue perfusion. Fluid repletion can be monitored by measuring blood pressure, urine output, mental status, and peripheral edema. Multiple modalities exist for measuring fluid responsiveness such as ultrasound, central venous pressure monitoring, and pulse pressure fluctuation as described above. In general, for hypovolemic shock, vasopressors should not be used because they can worsen tissue perfusion.

Crystalloid fluid resuscitation is preferred over colloid solutions for severe volume depletion not due to bleeding. The type of crystalloid used to resuscitate the patient can be individualized based on the patients’ chemistries, estimated volume of resuscitation, acid/base status, and physician or institutional preferences. Isotonic saline is hyperchloremic relative to blood plasma, and resuscitation with large amounts can lead to a hyperchloremic metabolic acidosis. Several other isotonic fluids with lower chloride concentrations exist, such as lactated Ringer's solution or PlasmaLyte. These solutions are often referred to as buffered or balanced crystalloids. Some evidence suggests that patients who need large volume resuscitation may have a less renal injury with restrictive chloride strategies and use of balanced crystalloids. Crystalloid solutions are equally as effective and much less expensive than colloid. Commonly used colloid solutions include those containing albumin or hyperoncotic starch. Studies examining albumin solutions for resuscitation have not shown improved outcomes, while other studies have shown resuscitation with hyperoncotic starch leads to increased mortality and renal failure. 234234[5][6][7][8][9][5]

Pearls and Other Issues

  • In patients with hypovolemic shock due to extracellular fluid loss, the etiology of fluid loss must be identified and treated.
  • Monitoring electrolytes and acid/base status in patients in hypovolemic shock is of utmost importance.
  • Trauma is the leading cause of hemorrhagic shock.
  • The hemorrhagic shock should be treated with balanced transfusion of packed red blood cells, plasma, and platelets.
  • Determining whether patients will be responsive to volume resuscitation should not rely on a single modality such as ultrasound, pulse pressure wave variation, passive leg raises, or central venous pressure. The decision for fluid administration should be based on the entire clinical presentation, laboratory values, and the aforementioned modalities.
  • For patients with hypovolemic shock due to fluid loss, the crystalloid solution is preferred over colloid.

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Hypovolemic Shock - Questions

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Which is false about hypovolemic shock?



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A patient is involved in a motor vehicle collision and suffers multiorgan trauma. He is brought to the emergency department by emergency medical services and found to be hypotensive, tachycardic and his abdomen is distended. He is disoriented and confused. He has a Glasgow coma scale of 9 and his legs are cool and the pulses thready. What is the most likely cause of his shock state?



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Which of the following is the first compensatory response to hypovolemic shock?



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A trauma patient is taken to the OR for a pelvic fracture. In the OR he becomes hypotensive with a low CVP, is oliguric, and febrile. What is the most likely diagnosis?



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A patient was stabbed in the abdomen. He is seen in the emergency room and appears to be in shock. His abdomen is distended and his blood pressure is 70/40 mm Hg. What is the first parameter to change in the early phase of hypovolemic shock?



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Once an airway has been controlled in a patient with hypovolemic shock, what is the next step?



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A 7-month-old infant has had profuse watery diarrhea for 6 days and is brought to the emergency department very lethargic. The blood pressure is 60/35 mm Hg, heart rate 180 bpm, and respiratory rate 50. The skin is mottled and cold. The peripheral pulses are weak. An intravenous line is started. What fluids should be given?



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Select the incorrect statement about hypovolemic shock.



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A 22-year-old Jehovah's Witness was involved in a motor vehicle accident and required surgery for a ruptured spleen. His estimated blood loss was 1800 mL. Which of the following is most accurate regarding his resuscitation?



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Which is the most common cause of hypovolemic shock?



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Which is not associated with hypovolemic shock?



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Which is not seen in severe hypovolemic shock?



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Which is not an acute compensatory mechanism in hypovolemic shock?



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Which is true regarding the treatment of hypovolemic shock in trauma?



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What is not true regarding resuscitation in hypovolemic shock in trauma?



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Which finding is not seen in patients with hypovolemic shock?



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A patient is brought to the emergency room after being shot in the leg. There is profuse bleeding. Vital signs show blood pressure 85/55 mm Hg, heart rate 115 bpm, and respirations 26. Which of the following is most probable?



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What kind of shock occurs secondary to acute blood loss?



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A parent brings a 16-month-old into the emergency department for severe vomiting and diarrhea. Hypovolemic shock is suspected, and pediatric intensivist is at the bedside. No cardiac abnormalities are suspected. What is the appropriate initial bolus dose of an isotonic crystalloid solution?



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An infant is brought to the emergency department by their caregiver for a 2-day history of vomiting and diarrhea. On exam, the infant's heart rate is 180 beats/min, the skin is mottled, capillary refill is more than 2 seconds, and the infant has a weak cry and is lethargic. What interventions would the nurse anticipate carrying out as part of the immediate treatment plan and admission stay? Select all that apply.



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A client presents in hypovolemic shock. What nursing interventions are needed to manage the care of this client emergently? Select all that apply.



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What decrease of blood volume to causer stage 2 hypovolemic shock in an adult?



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Why does pulse increase in hypovolemic shock?



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Hypovolemic Shock - References

References

Hooper N,Armstrong TJ, Shock, Hemorrhagic 2018 Jan;     [PubMed]
Gayet-Ageron A,Prieto-Merino D,Ker K,Shakur H,Ageron FX,Roberts I, Effect of treatment delay on the effectiveness and safety of antifibrinolytics in acute severe haemorrhage: a meta-analysis of individual patient-level data from 40 138 bleeding patients. Lancet (London, England). 2018 Jan 13;     [PubMed]
Annane D,Siami S,Jaber S,Martin C,Elatrous S,Declère AD,Preiser JC,Outin H,Troché G,Charpentier C,Trouillet JL,Kimmoun A,Forceville X,Darmon M,Lesur O,Reignier J,Abroug F,Berger P,Clec'h C,Cousson J,Thibault L,Chevret S, Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: the CRISTAL randomized trial. JAMA. 2013 Nov 6;     [PubMed]
Bentzer P,Griesdale DE,Boyd J,MacLean K,Sirounis D,Ayas NT, Will This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? JAMA. 2016 Sep 27;     [PubMed]
Zarychanski R,Abou-Setta AM,Turgeon AF,Houston BL,McIntyre L,Marshall JC,Fergusson DA, Association of hydroxyethyl starch administration with mortality and acute kidney injury in critically ill patients requiring volume resuscitation: a systematic review and meta-analysis. JAMA. 2013 Feb 20;     [PubMed]
Yunos NM,Bellomo R,Glassford N,Sutcliffe H,Lam Q,Bailey M, Chloride-liberal vs. chloride-restrictive intravenous fluid administration and acute kidney injury: an extended analysis. Intensive care medicine. 2015 Feb;     [PubMed]
Self WH,Semler MW,Wanderer JP,Wang L,Byrne DW,Collins SP,Slovis CM,Lindsell CJ,Ehrenfeld JM,Siew ED,Shaw AD,Bernard GR,Rice TW, Balanced Crystalloids versus Saline in Noncritically Ill Adults. The New England journal of medicine. 2018 Mar 1;     [PubMed]
Better OS, Impaired fluid and electrolyte balance in hot climates. Kidney international. Supplement. 1987 Aug;     [PubMed]
Miller TR,Anderson RJ,Linas SL,Henrich WL,Berns AS,Gabow PA,Schrier RW, Urinary diagnostic indices in acute renal failure: a prospective study. Annals of internal medicine. 1978 Jul;     [PubMed]

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