Hypovolemic Shock

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Continuing Education Activity

Hypovolemic shock is due to a critical loss in the effective circulating blood volume with systemic hypoperfusion. If left untreated, hypovolemic shock can lead to ischemic injury of vital organs, leading to multi-system organ failure and death. The first step in management is to rule out other forms of shock, which will dictate treatment. Hypovolemic shock may be due to loss in total body fluids versus bleeding. When the etiology of hypovolemic shock has been determined, blood or fluid loss replacement should be carried out as soon as possible to minimize tissue ischemia. Factors to consider when replacing fluid or blood volume loss include the type and rate of fluid replacement. This activity reviews the causes, pathophysiology, and presentation of shock and highlights the role of the interprofessional team in its management.

Objectives:

  • Identify the etiology of hypovolemic shock.
  • Outline the presentation of hypovolemic shock.
  • List the treatment and management options available for hypovolemic shock.
  • Discuss interprofessional team strategies for improving care coordination and communication to advance the treatment of hypovolemic shock and improve outcomes.

Introduction

Hypovolemic shock is a potentially life-threatening condition. Early recognition and appropriate management are essential.[1] Hypovolemic shock is circulatory failure due to effective intravascular volume loss (fluids or blood). This effective circulatory volume loss leads to tissue hypoperfusion and tissue hypoxia. If left untreated, hypovolemic shock can lead to ischemic injury of vital organs, leading to multiorgan failure (MOF).[1] 

Early recognition and treatment with volume resuscitation to restore euvolemia are life-saving. When the etiology of hypovolemic shock is determined, prompt replacement of volume together with source control should be performed to minimize tissue ischemia.[2] Factors to consider when replacing fluid or blood loss include the rate and type of replacement.[3]

Etiology

Shock is defined as a global tissue hypoperfusion state, leading to cellular hypoxia and dysfunction. Shock is generally classified into four types according to etiology; Distributive shock (DS), hypovolemic shock (HS), cardiogenic shock (CS), and obstructive shock (OS).[4] Distributive septic shock is the most common type of shock in adults admitted to the emergency department and intensive care unit.[4] However, hypovolemic shock is the most common type of shock in children due to diarrheal illness in the developing world. Hypovolemic shock can be divided into hemorrhagic and non-hemorrhagic. Hemorrhagic shock is due to an acute reduction in the effective intravascular volume from bleeding.

In contrast, non-hemorrhagic is due to reduced effective intravascular volume from body fluid loss. Traumatic injury is by far the most common cause of hemorrhagic shock. Other causes of hemorrhagic shock include gastrointestinal (GI), genitourinary, and bleeding from surgical intervention. 

Non-hemorrhagic hypovolemic shock can be due to one of the following etiologies: 

Gastrointestinal Losses

A GI source of hypovolemic shock is the leading source. The gastrointestinal tract usually secretes between 3 to 6 liters of fluid daily. However, most of this fluid gets reabsorbed, and only 100 to 200 mL is lost in the stool. Volume depletion occurs when the GI secretion exceeds the reabsorbed. This fluid loss occurs in the presence of intractable vomiting, diarrhea, bowel obstruction, 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, several tubular and interstitial diseases beyond the scope of this article cause severe salt-wasting nephropathy.

Skin Losses

Excessive fluid loss can also 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 significant fluid losses that lead to hypovolemic shock.[5]

Third-Space Sequestration

Sequestration of fluid occurs when intravascular fluid leaves the interstitial compartment leading to effective intravascular volume depletion and hypovolemic shock. Third-spacing of fluid can occur in intestinal obstruction, pancreatitis, burn, post-operatively, obstruction of a major venous system, or any other pathological condition that results in a massive inflammatory response.[3]

Epidemiology

While the incidence of hypovolemic shock from a non-hemorrhagic source with extracellular fluid loss is more common, 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 injuries. Elderly patients are more likely to experience hypovolemic shock due to fluid losses as they have reduced physiologic reserves.[3]

Pathophysiology

Hypovolemic shock results from depletion of intravascular volume, whether by extracellular fluid loss or blood loss. The pre-shock stage is characterized by compensatory mechanisms with increased sympathetic tone resulting in increased heart rate, increased cardiac contractility, and peripheral vasoconstriction.[2] Due to the increased sympathetic activity, the early changes in vital signs seen in hypovolemic shock with the loss of 10% body volume include an increased diastolic blood pressure with narrowed pulse pressure. The net result is normal or mildly elevated blood pressure.

As volume status continues to decrease, specifically when it is 25 to 30% of the effective blood volume patient gets into a shock state with a drop in systolic blood pressure, tachycardia, and oliguria.[6] As a result, oxygen delivery to vital organs cannot meet oxygen demand. Here cells switch from aerobic 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 blood flow diversion propagates tissue ischemia and worsens lactic acidosis. If untreated, this will lead to hemodynamic compromise, refractory acidosis, and a further reduction in cardiac output, leading to a multiorgan failure (MOF) and, eventually, death.[7]

History and Physical

History and physical can often make the diagnosis of hypovolemic shock. A history of trauma, overt bleeding, or recent surgery is present for patients with hemorrhagic shock. For the non-hemorrhagic hypovolemic shock due to fluid losses, history and physical should attempt to identify possible GI, renal, open wounds, 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.[2]

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. In addition, agitation, lethargy, or confusion may result from brain malperfusion. 

Although relatively nonsensitive and nonspecific, a physical exam can help determine 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.[8]

As stated above, early signs of shock can be associated with normal or elevated blood pressure. As effective circulating blood volume is further reduced, hypotension and tachycardia ensue. This is associated with reduced central venous pressure (CVP), increased peripheral vascular resistance, and decreased cardiac output. 

Evaluation

Various laboratory values can be abnormal in hypovolemic shock. Patients can have increased BUN and serum creatinine due to prerenal kidney failure. Also, hypernatremia or hyponatremia can result, as can hyperkalemia or hypokalemia. Lactic acidosis can be found as a result of anaerobic metabolism. However, the effect of acid-base balance can be variable, as patients with significant GI losses can become alkalotic. In cases of hemorrhagic shock, hematocrit and hemoglobin can be critically low. However, with a reduction in relative 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, urine sodium can be low in a euvolemic patient with heart failure, cirrhosis, or nephrotic syndrome. Fractional excretion of sodium under 1% suggests 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. Central venous catheter position, Ventilator settings, chest wall compliance, and right-sided heart failure can compromise CVPs accuracy as a measure of volume status. The measurements of pulse pressure variation via various commercial devices are sometimes used to measure volume responsiveness with variable effectiveness. 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.[9]

Treatment / Management

It is important to identify the type of shock before starting specific management, knowing that it is sometimes difficult to identify the specific shock type. This is sometimes referred to as undifferentiated shock. Please see the differential diagnosis section below. For patients presenting with hypovolemic shock, it is important to differentiate between hemorrhagic versus non-hemorrhagic hypovolemic shock, as this would dictate management. Early resuscitation with prompt bleeding source control is crucial for hemorrhagic hypovolemic shock to improve survival and reduce blood products transfusion. Bleeding source control is performed by endoscopic, surgical, or, more frequently, interventional radiology. In terms of hemorrhagic shock resuscitation, using blood products over crystalloid resuscitation resulted in improved outcomes.[10] Balanced transfusion using 1:1:1 or 1:1:2 of plasma to platelets to packed red blood cells results in better hemostasis.[11] 

Anti-fibrinolytic administration to patients with severe bleeding within 3 hours of traumatic injury appears to decrease death from major bleeding, as shown in the CRASH-2 trial.[12] Research on oxygen-carrying substitutes as an alternative to packed red blood cells is ongoing. However, no blood substitutes have been used in the United States.[11]

For patients in non-hemorrhagic hypovolemic shock, volume resuscitation must be started as soon as possible to restore effective circulatory blood volume. It is sometimes difficult to determine the type of fluid loss. Therefore, it is prudent to start with a warm isotonic crystalloid solution of 30 ml/kg body weight, infused rapidly to restore tissue perfusion quickly. This blouse can be repeated more than once.[13] Effective resuscitation can be monitored by heart rate, blood pressure, urine output, mental status, and peripheral edema. As described above, multiple modalities exist for measuring fluid responsiveness, such as ultrasound to assess IVC compressibility, central venous pressure monitoring, and pulse pressure fluctuation. Vasopressors should not be used for hypovolemic shock because they can worsen tissue perfusion.[12][14] However, it can be used to catch up with volume resuscitation in the initial resuscitation phase. 

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 patient's lab values, estimated resuscitation volume, acid/base status, and physician or institutional preferences. Isotonic saline is hyperchloremic relative to blood plasma, and resuscitation with large amounts can lead to hyperchloremic metabolic acidosis. Several other isotonic fluids with lower chloride concentrations exist, such as lactated Ringer's solution or commercially available IV electrolyte replacement solutions.[10] These solutions are often referred to as buffered or balanced crystalloids. Some evidence suggests that patients who need large volume resuscitation may experience less renal injury with restrictive chloride strategies and the 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.[15]

Differential Diagnosis

Distributive shock: This is a vasoplegic (vasodilatory) type of shock. It is the most common type of shock, septic shock. The presence of a source of infection usually differentiates from hypovolemic shock with reduced peripheral vascular resistance.[16] Another type of distributive shock is neurogenic shock seen after a high cervical spine fracture with reduced sympathetic outflow.[17] The main difference between hypovolemic shock is the increased peripheral vascular resistance, which usually increases in hypovolemic shock.

Obstructive shock: This is due to an obstructive pathology that impedes cardiac output. An example of this type of shock is cardiac tamponade and tension pneumothorax. In trauma patients, the differentiation from hypovolemic hemorrhagic shock can be challenging, given the high probability of concomitant shock types. Increased CVP usually differentiates it.[18]

Cardiogenic shock: This is caused by primary pump failure due to various etiologies, commonly due to coronary ischemia or blunt cardiac injury. It is usually differentiated from hypovolemic shock by increased CVP with increased peripheral vascular resistance.[19]

Undifferentiated shock is when the cause of shock is unknown. The type of shock could be a combination of all the above types.

Prognosis

The prognosis depends on the etiology and severity of hypovolemic shock. Early bleeding source control and effective early goal-directed volume resuscitation have improved outcomes for the hemorrhagic type. Once patients with hypovolemic shock get into MOF, the prognosis worsens, and mortality increases. Older patients and those with underlying comorbid conditions have worse outcomes. 

Complications

As mentioned above, one of the most feared complications of hypovolemic shock is circulatory failure leading to MOF and death. However, other complications result primarily from treatment, such as circulatory overload, abdominal compartment syndrome, and transfusion-related reactions.; this is in addition to complications from surgical and radiology interventions.

Deterrence and Patient Education

Loss of total circulating blood volume due to both and/or fluids loss causes hypovolemic shock. If the lost volume doesn't get replenished in a timely fashion, this will lead to a lack of oxygen delivery and transport to vital cells and organs in the body, which might lead to the failure of these organs and, ultimately, death.

Pearls and Other Issues

  • In patients with hemorrhagic hypovolemic shock, prompt bleeding source control with early balanced blood product resuscitation are key.
  • In patients with non-hemorrhagic hypovolemic shock, the etiology of fluid loss must be promptly identified and treated.
  • Monitoring electrolytes and acid/base status in patients in hypovolemic shock are of utmost importance.
  • Determining a patient's response to fluid resuscitation should rely on various assessments, including ultrasound, pulse pressure wave variation, passive leg raises, or central venous pressure, in addition to relying on clinical presentation and laboratory values such as lactate.
  • For replacement fluids, we recommend isotonic crystalloids over colloids.

Enhancing Healthcare Team Outcomes

The management of hypovolemic shock requires an interprofessional team, including ICU clinicians and ICU nurses, EMTs/paramedics, and pharmacists. For patients with hypovolemic shock due to fluid loss, the crystalloid solution is preferred over colloid. These patients need monitoring of their fluid input and output and should be in an ICU setting. The outcomes depend on the cause of shock, the patient's age, comorbidities, and the presence of renal failure.

All interprofessional team members must react promptly and maintain accurate records of any interventions they initiate; this allows all team members to accurately assess what has been done for the patient and quickly decide the way forward. Pharmacists must prepare the required IV solutions immediately. Clinicians and nurses will address active bleeding to help return hemodynamic stability. Everyone must play their part in the team approach to care and exercise open communication with the rest of the team to ensure rapid assessment and intervention, which can be life-saving. This interprofessional approach will result in the best possible patient outcomes. [Level 5]


Article Details

Article Author

Sharven Taghavi

Article Author

Aussama k. Nassar

Article Editor:

Reza Askari

Updated:

10/4/2022 5:31:37 PM

PubMed Link:

Hypovolemic Shock

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