Hypovolemia and Hypovolemic Shock

Etiology

Shock is defined as a state of global tissue hypoperfusion, leading to cellular hypoxia and dysfunction. Experts generally classify shock into 4 types according to etiology.[4] 

Distributive Shock

Severe peripheral dilation causes distributive shock. Sepsis is the most common cause of distributive shock.[4] Additional examples of distributive shock are anaphylactic shock, neurogenic shock due to a traumatic brain or spinal cord injury, and transfusion reactions.

Cardiogenic Shock 

Intracardiac causes of reduced cardiac output cause cardiogenic shock. Potential causes are myocardial infarction, an exacerbation of congestive heart failure, hypotension due to ventricular tachyarrhythmias and bradyarrhythmias, valvular disease, ventricular septal defects, and ruptured ventricular wall aneurysms.[5]  

Obstructive Shock

Extracardiac causes of decreased cardiac output cause obstructive shock. The most common causes are pulmonary embolism or severe pulmonary hypertension, where the right heart fails due to the inability to generate enough pressure to overcome high pulmonary vascular resistance. Mechanical causes are tension pneumothorax, cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. 

Hypovolemic shock

Hypovolemic shock can result from both hemorrhagic and nonhemorrhagic causes. Hemorrhagic shock most commonly arises from trauma, followed by gastrointestinal bleeding, but can also result from intraoperative or postoperative bleeding, ruptured aneurysms, postpartum hemorrhage, or vaginal and uterine bleeding.

Nonhemorrhagic hypovolemic shock stems from significant body fluid losses that reduce effective circulating volume. Gastrointestinal causes include severe vomiting, diarrhea, or excessive losses through stomas or fistulas, where fluid loss exceeds the usual resorption of the gut's 3 to 6 L secreted daily.

Renal causes involve excessive sodium and water loss, which can occur with the use of diuretics, osmotic diuresis from hyperglycemia, or salt-wasting nephropathies. The skin is another key site of fluid loss, particularly in individuals exercising in hot environments, where patients may lose 1 to 2 L/h or in patients with burns or compromised skin barriers.[3][6]

Fluid sequestration, or third-spacing, occurs when fluid shifts from the intravascular space into the interstitial or third space, resulting in intravascular volume depletion and potential hypovolemic shock. Third-spacing of fluid can occur in intestinal obstruction, pancreatitis, burns, postoperatively, obstruction of a major venous system, or any other pathological condition that results in a massive inflammatory response.[3]

Epidemiology

Recent studies show that septic shock is the most common form of shock in patients admitted to the intensive care unit, accounting for approximately 62% of cases, followed by cardiogenic shock (16%), hypovolemic shock (16%), distributive shock (4%), and obstructive shock (2%).[1][7] An Australian study of emergency medical services (EMS)-treated prehospital nontraumatic shock reports similar findings, with septic shock leading at 31%, followed by cardiogenic shock at 28%, and hypovolemic shock at 11.5%. The study notes a 30-day mortality rate of 32%, with increased risk associated with female sex, older age, elevated heart rate, prehospital intubation, and comorbidities such as chronic kidney disease. Higher initial systolic blood pressure and better socioeconomic standing correlate with lower mortality. In the patient population with EMS-treated prehospital nontraumatic shock, shock occurs more frequently in men, older adults, rural populations, and those with lower socioeconomic status.

In emergency departments, the most common types of shock vary depending on the facility type and patient demographics. Septic and hypovolemic shock are the most frequently encountered overall.[4] However, hemorrhagic shock is more prevalent at level-1 trauma centers, which treat a higher volume of major injuries. A study finds that 62.2% of massive transfusions in these centers result from trauma, accounting for 75% of total blood product use.[3]

Pathophysiology

Cardiac output (CO) and systemic vascular resistance (SVR) are key determinants of tissue perfusion, with blood pressure reflecting their interaction (BP = CO × SVR). CO itself depends on heart rate and stroke volume (CO = HR x SV).[2]

Hypovolemia reduces CO, impairing tissue perfusion and oxygen delivery. This results in tissue hypoxia, which disrupts cellular function, causes acidosis, and impairs endothelial-dependent vasodilation, partly due to decreased nitric oxide (NO) production. Inadequate perfusion also activates inflammatory and anti-inflammatory mediators, further contributing to systemic dysfunction. If uncorrected, the resulting oxygen and nutrient deprivation leads to progressive cellular damage, systemic acidosis, and endothelial dysfunction. Tissue hypoxia triggers a shift to anaerobic metabolism and elevated lactate levels, which are often used to assess the severity of shock and response to treatment.

Shock progresses through a series of stages. In the initial phase, associated with a 10% reduction in total effective arterial blood volume, known as pre-shock or compensated shock, the body responds to the decreased CO associated with hypovolemia by increasing the SVR to maintain perfusion to vital organs. The body redistributes blood to the brain, heart, and kidneys and away from the skin, muscle, and gastrointestinal tract. The heart rate and myocardial contractility increase, and peripheral blood vessels constrict, primarily through sympathetic stimulation regulated by cardiac and vasomotor centers in the lower pons and medulla oblongata. These centers influence heart rate via parasympathetic vagal input and control vascular tone through sympathetic spinal pathways.

The kidneys stimulate renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by the lungs and liver. Angiotensin 2 acts to vasoconstrict arteriolar smooth muscle and stimulate aldosterone secretion by the adrenal cortex. Aldosterone causes sodium reabsorption and water conservation. The neuroendocrine system helps respond to hypovolemia by increasing the secretion of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH also promotes salt and water resorption.

The second phase, shock, corresponds to a 20% to 25% fall in arterial blood volume and occurs when the compensatory mechanisms become overwhelmed.[8] Patients exhibit signs and symptoms of end-organ dysfunction. The final phase, end-organ dysfunction, results in irreversible organ damage, multiorgan failure (MOF), and death.[9]

Clinicians can measure hemodynamic profiles on pulmonary artery catheters. Measured parameters include pulmonary capillary wedge pressure (PCWP), an indicator of left atrial pressure; cardiac output; systemic vascular resistance; and mixed venous oxygen saturation, which assesses the oxygen content of blood returning to the heart. The mixed venous oxyhemoglobin provides insight into the balance between oxygen delivery and oxygen use in the body. The value reflects the amount of oxygen in the blood after tissues have extracted oxygen. A low value may indicate tissue hypoxia, while an elevated value suggests poor oxygen extraction or cardiac output. 

Classic Physiological Parameters Associated with the Various Types of Shock

Hypovolemic: Decreased PCWP, decreased CO, increased SVR, decreased mixed venous oxyhemoglobin concentration

Obstructive due to pericardial tamponade: Increased PCWP, decreased CO, increased SVR, decreased mixed venous oxyhemoglobin concentration

Obstructive due to pulmonary embolism and pulmonary hypertension: Decreased PCWP, decreased CO, increased SVR, increased mixed venous oxyhemoglobin concentration

Distributive: Decreased PCWP, increased CO, decreased SVR, increased mixed venous oxyhemoglobin concentration

Cardiogenic: Increased PCWP, decreased CO, increased SVR, decreased mixed venous oxyhemoglobin concentration

History and Physical

Patients with hypovolemic shock can present with various signs and symptoms based on the underlying cause. Typically, in patients who have hypovolemia, the source is evident through the patient's history. However, the source may not be easily identifiable in patients presenting with other forms of shock or in older patients. Potential causes of hypovolemia are hemorrhage, gastrointestinal, renal, and skin losses, along with third-space sequestration. A history of trauma, overt bleeding, or recent surgery is often present in patients with hemorrhagic shock. Common places for hemorrhage in patients who experience trauma are external sources, like scalp lacerations and open fractures, the thoracic and peritoneal cavities, the retroperitoneal space due to a pelvic fracture, and muscle or subcutaneous tissue due to a long bone fracture. 

Patients with gastrointestinal losses may present with nausea, vomiting, diarrhea, fevers, melena, hematochezia, hematemesis, external drainage, abdominal pain, edema due to third-spacing, and high ostomy output. They may report recent travel, ill contacts with similar symptoms, immunocompromising conditions, a history of pancreatitis, alcohol use disorder, or recent antibiotic use. Patients with burns and exudative skin lesions will also present with pain and symptoms related to the specific skin condition.[6] 

Along with osmotic diuresis due to glucosuria and diuretic use, hypoaldosteronism and salt-wasting nephropathy are additional potential causes of renal losses. Patients with hypoaldosteronism may present with the following symptoms: 

• Dizziness
• Headache
• Salt craving
• Nausea and vomiting
• Lethargy
• Dehydration
• Hypotension
• Arrhythmia
• Muscle weakness [10]

Additionally, patients with salt-wasting nephropathy, like Bartter syndrome, may have the following symptoms:

• Polyuria
• Hypotension
• Muscle cramps and weakness
• Constipation
• Poor growth
• Kidney stones
• Salt craving
• Fatigue [11]

The typical symptoms of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid-base disorders that accompany hypovolemic shock.[2] Early symptoms of hypovolemia are sluggishness, easy fatigability, increased thirst, muscle cramps, decreased urinary output, and postural dizziness. As hypovolemia worsens, patients can experience abdominal pain, chest pain, lethargy, and mental status changes due to hypoxia of the mesenteric, coronary, or cerebral vasculature. Symptoms due to electrolyte abnormalities may include the following findings:

• Muscle weakness due to hyperkalemia or hypokalemia
• Tachypnea due to acidosis
• Lethargy, seizure, or coma due to hypernatremia or hyponatremia 
• Salt craving due to adrenal insufficiency
• Neuromuscular irritability and confusion due to metabolic alkalosis caused by prolonged vomiting or diuretic use

Physical examination findings suggestive of volume depletion include dry mucous membranes, decreased skin turgor, cold, prolonged capillary refill, clammy skin, cyanosis, decreased urinary output, tachycardia, hypotension, and low jugular venous pressure (JVP). The normal height of the JVP is 3 cm or less above the sternal notch. When determining JVP, clinicians must add 5cm to the measured height above the sternal angle, as the sternal angle is approximately 5 cm above the right atrium. Increased skin pigmentation suggests primary adrenal insufficiency.[12]

Patients in pre-shock may have normal or slightly elevated blood pressure. As effective circulating blood volume is further reduced, hypotension and tachycardia ensue. As hypovolemia progresses, the blood pressure decreases in the upright position, followed by hypotension in any position. 

Clinicians should recognize that the presentation of hypovolemia can vary significantly in older adults and children. Older adults often exhibit nonspecific symptoms, making early diagnosis more challenging. Due to a higher proportion of body fat and lower muscle mass, older adults have less total body water than younger individuals. Consequently, fluid losses in older adults result in a disproportionately greater reduction in extracellular fluid volume. Among this population, acute weight loss is the most specific indicator of hypovolemia. In contrast, hypotension is typically a late finding in children. Once it occurs, hypovolemic shock in pediatric patients can rapidly deteriorate into cardiovascular collapse and cardiac arrest.

Estimating the Degree of Hypovolemia in Children

Clinicians categorize hypovolemia in children as mild, moderate, or severe based on the history and clinical findings.

Mild hypovolemia

Mild hypovolemia in children is characterized by a 3% to 5% volume loss. Clinical signs may be absent or minimal. Decreased urine output may be present, but it is often not appreciated. 

Moderate hypovolemia

Moderate hypovolemia in children characterizes a 6% to 9% volume loss. Typical findings include tachycardia, orthostatic changes in blood pressure, prolonged capillary refill time (2 to 3 seconds), tachypnea, decreased urinary output, tears, and a sunken fontanelle on physical examination.

Severe hypovolemia 

Children with severe hypovolemia have a 10% or more volume depletion. Classic findings are cool, mottled skin, prolonged capillary refill time, lethargy, tachycardia, hypotension, tachypnea, or deep or absent respirations. 

Four Classes of Hemorrhagic Shock

In addition to the above symptoms and clinical findings, the Advanced Trauma Life Support (ATLS) curriculum outlines 4 classes of hemorrhagic shock. The ability to recognize the early signs of shock before hypotension develops helps clinicians reverse end-organ hypoxia.[13]  

Class I

Class I corresponds to a loss of up to 15% of blood volume. The patient's heart rate is minimally elevated or normal, and there is no change in blood pressure, pulse pressure, or respiratory rate. 

Class II

Class II hemorrhage occurs with a 15% to 30% blood volume loss. Patients present with a heart rate of 100 to 120 beats per minute (bpm), a respiratory rate of 20 to 24 breaths per minute, and a decreased pulse pressure, although the change in systolic blood pressure is minimal. Additional findings may be cool, clammy skin and poor skin turgor.

Class III

Class III hemorrhage involves a 30% to 40% blood volume loss, hypotension, mental status changes, delayed capillary refill, decreased urinary output, heart rate of 120 bpm or more, and respiratory rate greater than 24 breaths/min. 

Class IV

Class IV hemorrhage involves greater than 40% blood volume loss. Affected patients are hypotensive, with a systolic blood pressure of less than 90 mm Hg, a heart rate greater than 120 bpm, and a narrowed pulse pressure of 25 mm Hg or less. Affected patients exhibit markedly decreased or absent urine output, delayed capillary refill, and pale, cold skin.

Evaluation

The evaluation of patients with hypovolemia begins with a thorough history and physical examination to identify the source of volume loss. The source may not be evident in older patients with cognitive impairment or mental status changes. Key physical examination features to determine volume status are skin turgor, mucous membranes, blood pressure, heart rate, body weight, respiratory rate, capillary refill, and jugular venous pressure.[14] Irritability, lethargy, weight loss, and decreased urinary output are important clinical clues when assessing volume status in children.[15]

Recommended laboratory tests include the following:

• Serum electrolytes
• Blood glucose 
• Blood urea nitrogen (BUN) and creatinine
• Urine osmolarity
• Urine sodium
• Serum lactate
• Complete blood count 
• Blood type and crossmatch for patients with acute hemorrhage or severe anemia
• Prothrombin time for patients with acute hemorrhage or severe anemia
• International normalized ratio for patients with acute hemorrhage or severe anemia
• Activated partial thromboplastin time for patients with acute hemorrhage or severe anemia

While hypovolemia is primarily a clinical diagnosis, clinicians can confirm the diagnosis with a low urinary sodium concentration.[16] With hypovolemia, the kidneys conserve sodium and water to expand the extracellular volume. The urine sodium concentration should be less than 20 meq/L in patients with hypovolemia. Exceptions to this finding include patients with salt-wasting states, such as those on diuretics or with underlying kidney disease, kidney ischemia associated with acute glomerulonephritis or bilateral renal artery stenosis, or those on a very low-sodium diet. Additional scenarios where the urine sodium may exceed 20 meq/L despite volume depletion are a high rate of water resorption and sodium excretion with another anion, as in metabolic alkalosis. Urine sodium can also be low in patients who are euvolemic with heart failure, cirrhosis, or nephrotic syndrome. 

A fractional excretion of sodium (FENa) of less than 1% also suggests volume depletion. However, the FENa is most useful for patients with an oliguric acute kidney injury and a decreased glomerular filtration rate (GFR) to determine if the oliguria is due to hypovolemia or acute tubular necrosis.[17] In this setting, a FENa of less than 1% suggests hypovolemia, and a FENa greater than 1% suggests acute tubular necrosis. In patients with a normal GFR, a FENa of less than 0.1% to 0.2% indicates hypovolemia due to the higher filtered sodium load in these patients. Likewise, an elevated urine osmolality can also suggest hypovolemia. However, an elevated urine osmolality also occurs in the setting of impaired concentrating ability by the kidneys, osmotic diuresis, or if the patient receives diuretics. Additional potential commonly encountered laboratory abnormalities are as follows:

• Elevated BUN and creatinine
• Hypernatremia
• Hyponatremia
• Hyperkalemia
• Hypokalemia
• Elevated specific gravity above 1.015 
• Metabolic acidosis due to diarrhea, intestinal losses, or diabetic ketoacidosis
• Metabolic alkalosis due to vomiting, nasogastric suction, or diuretics 
• Relative polycythemia due to volume constriction
• Elevated serum albumin due to volume constriction
• Anemia due to hemorrhage

Clinicians often measure central venous pressure 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 the accuracy of central venous pressure as a measure of volume status. Pulse pressure variation measurements using various commercial devices assess volume responsiveness with varying effectiveness. However, pulse pressure variation, as a measure of fluid responsiveness, is only valid in patients without spontaneous breathing or arrhythmias. Right heart failure, decreased lung or chest wall compliance, and high respiratory rates can compromise the accuracy of pulse pressure variation.

Like 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.[18] Measuring the effect of passive leg raises on cardiac contractility using echocardiography appears to be the most accurate method for assessing volume responsiveness, although it is also subject to limitations.[19]

The underlying cause of bleeding must guide the evaluation of patients with hemorrhagic shock, as different sources require distinct diagnostic approaches. In trauma cases, such as blunt or penetrating injuries from motor vehicle collisions or gunshots, rapid imaging, such as a Focused Assessment with Sonography for Trauma (FAST) ultrasound or computed tomography, is often necessary to identify internal bleeding. Surgical complications may require re-exploration or imaging to locate active bleeding, especially after procedures involving major vessels or organs. Gastrointestinal bleeding typically warrants endoscopy to identify the sources, such as ulcers or varices. Obstetric emergencies, such as postpartum hemorrhage or ectopic pregnancy, demand prompt bedside assessment and often an ultrasound. A ruptured aneurysm requires immediate imaging and surgical consultation. Laboratory testing to evaluate clotting function is essential in patients with coagulopathies, such as hemophilia or disseminated intravascular coagulation. Internal bleeding into body cavities may be occult and necessitate imaging to localize the source. In contrast, external bleeding from wounds or amputations is more apparent and managed with direct pressure and surgical control. Please see StatPearls' companion topic, "Hemorrhagic Shock," for an in-depth discussion of evaluating patients presenting with hemorrhagic shock.

Treatment / Management

Identifying the type of shock before initiating specific management is crucial, though determining the exact cause can be challenging. When the specific type is unclear, the condition is referred to as undifferentiated shock. The initial step in managing hypovolemic shock is to differentiate between hemorrhagic and nonhemorrhagic causes. Early resuscitation with prompt bleeding source control is crucial for hemorrhagic hypovolemic shock to improve survival and reduce blood product transfusion. Clinicians achieve bleeding source control through direct pressure, fracture stabilization, endoscopic or surgical interventions, or with the assistance of interventional radiology.

Volume resuscitation begins with a warm isotonic crystalloid solution (30 mL/kg) like normal saline or lactated Ringers (LR) in rapidly infused 500 mL boluses for adult patients. Clinicians should monitor the patient’s response to each bolus by assessing vital signs, urine output, mental status, and signs of pulmonary edema.[20][21] Clinicians do not generally utilize vasopressors like norepinephrine to manage hypovolemic shock, as they can worsen tissue perfusion unless patients fail to improve despite adequate volume resuscitation.[22][23](A1)

Current guidelines recommend crystalloid fluids over colloid solutions for resuscitating patients with severe volume depletion not caused by hemorrhage. Healthcare professionals tailor the choice of crystalloid solution to the individual patient. Isotonic saline contains a higher chloride concentration than plasma and may cause hyperchloremic metabolic acidosis when administered in large volumes. LR is also isotonic but has a lower chloride content.[24] Evidence suggests that using balanced crystalloids, such as LR solution, in large-volume resuscitation may reduce the risk of renal injury, particularly when a restrictive chloride strategy is employed. However, the lactate in the LR solution converts to bicarbonate and can worsen metabolic alkalosis. Crystalloids are equally effective and significantly less costly than colloid solutions. Commonly used colloids include albumin and hyperoncotic starch, though studies have not shown improved outcomes with albumin. Clinicians should avoid hyperoncotic starch, as studies associate it with increased risks of renal failure and mortality.[25] For a detailed comparison of fluid types and their clinical indications, please see StatPearls' companion topic, "Fluid Management."(A1)

Fluid administration should be kept to a minimum and used only in patients who are hypotensive until blood products are available, or to achieve a systolic blood pressure of 80 to 90 mm Hg in patients with hemorrhagic hypovolemic shock.[19] Administration of crystalloid solutions in volumes greater than 1 L results in increased morbidity and mortality due to hypothermia and consumption of coagulation factors. Balanced transfusion using 1:1:1 of plasma to platelets to packed red blood cells results in better hemostasis.[20] 

Clinicians must remember that hypotension is a late finding in pediatric patients. They can maintain blood pressure despite losing 35% to 45% of their total blood volume. Tachycardia and poor skin perfusion should alert healthcare professionals to the potential for shock in pediatric patients and prompt the administration of isotonic fluids. Pediatric patients with severe volume depletion should receive a 20 mL/kg bolus, and those with moderate volume depletion a 10 mL/kg bolus within the first 5 minutes. After the initial bolus, clinicians reassess the child to determine whether an additional bolus is necessary. Patients with severe hypovolemia should receive 60 mL/kg within the first 15 minutes. Patients who are lethargic or have altered mental status should undergo bedside glucose testing with rapid administration of glucose in those with hypoglycemia. Pediatric patients with hypovolemia due to hemorrhage who do not respond to 3 boluses or 60 mL/kg of fluid should undergo a blood transfusion. Pediatric Advanced Life Support defines hypotension in pediatric patients as a blood pressure reading below the fifth percentile, which varies by age. The following parameters indicate a blood pressure less than the fifth percentile based on age:

• Term neonate 0 to 28 days: Systolic blood pressure less than 60 mm Hg 
• Infants 1 to 12 months: Systolic blood pressure less than 70 mm Hg 
• Children 1 to 10 years: Systolic blood pressure less than (70 mm Hg + [age in years x 2]) 
• Children older than 10: Systolic blood pressure less than 90 mm Hg

Neonates who require blood transfusions should receive units of red blood cells that are leukoreduced and cytomegalovirus seronegative. The normal transfusion rate for neonates, infants, and children is 10 to 20 mL/kg over 2 to 4 hours. However, in pediatric patients who are hemodynamically unstable, red blood cells are often administered more rapidly at 10 mL/kg over 1 to 2 hours. As with adults, administering red blood cells, platelets, and fresh frozen plasma in a 1:1:1 ratio has been shown to improve outcomes.[21] 

Once the vital signs are stable, clinicians can switch to administering maintenance fluids plus enough fluids to cover any continued losses. Please see StatPearls' companion topic, "Fluid Management," for a detailed description of calculating maintenance fluid requirements for adult and pediatric patients.  A fluid change may be necessary based on the patient's electrolyte levels, blood glucose levels, clinical condition, and renal function. If maintenance fluids are not required, then fluids are discontinued. 

According to the Clinical Randomization of Antifibrinolytic in Significant Hemorrhage (CRASH-2) trial, patients with moderate to severe active hemorrhage who are within 3 hours of their injury and receive tranexamic acid, an antifibrinolytic agent, have a lower incidence of all-cause mortality.[22] Further studies are necessary to determine the safety in pediatric patients.[23] Research continues on oxygen-carrying red blood cell substitutes as an alternative to packed red blood cells. However, no blood substitutes are currently licensed in the United States.[20]

Parameters to monitor during the resuscitation of adult patients with hemorrhagic shock are as follows:

• The goal blood pressure is a mean arterial pressure (MAP) above 65 mm Hg or above 85 mm Hg in patients with blunt trauma who may also have a spinal cord or traumatic brain injury.
• Maintain an oxygen saturation of 94% or higher.
• Maintain a heart rate between 60 and 100 bpm.
• Maintain urine output of more than 0.5 mL/h.
• Maintain a serum lactate of less than 2 mmol/L.

The MAP should be individualized based on the patient's age, history of hypertension, and presence of additional injuries. Recent evidence suggests that the goal of early fluid resuscitation should be to achieve minimally tolerable organ perfusion and continue only to a MAP of 50 to 60 mm Hg. This "permissive hypotension" appears to be beneficial to patients who experience hemorrhagic shock due to torso injuries from gunshot or stab wounds. However, such hypotension is harmful to patients with spinal cord injuries and traumatic brain injuries. European guidelines recommend maintaining a MAP of 50 to 60 mm Hg until active hemorrhage stops.[24] Clinicians should use caution in older patients and those with a history of hypertension.

Differential Diagnosis

Hypovolemic Shock

The potential underlying causes of hypovolemic shock are:

• Trauma
• Gastrointestinal bleeding like varicies, peptic ulcers, and diverticula 
• Intraoperative and postoperative hemorrhage
• Retroperitoneal bleeding due to conditions like a ruptured aortic aneurysm or renal and adrenal malignancies
• Aortic-enteric fistula
• Hemorrhagic pancreatitis
• Tumor or abscess erosion into major vessels
• Ruptured ectopic pregnancy
• Postpartum hemorrhage
• Uterine or vaginal hemorrhage 
• Spontaneous hemorrhage from bleeding diathesis
• Diarrhea
• Vomiting
• Burns
• Various skin conditions
• Drug-induced or osmotic diuresis
• Salt-wasting nephropathies
• Hypoaldosteronism
• Third space losses

Distributive Shock

Distributive shock is a vasoplegic (vasodilatory) type of shock.[26][27] The primary difference between hypovolemic shock and distributive shock is the increased peripheral vascular resistance associated with hypovolemic shock.

The potential causes of distributive shock are:

• Sepsis
• Pancreatitis
• Post-myocardial infarction
• Post-coronary bypass
• Post-cardiac arrest
• Viscus perforation
• Amniotic fluid embolism
• Fat embolism
• Idiopathic systemic capillary leak syndrome
• Neurogenic shock due to traumatic brain injury, spinal cord injury (quadriparesis with bradycardia or paraplegia with tachycardia), or neuraxial anesthesia
• Liver failure
• Transfusion reactions
• Toxic shock syndrome
• Heavy metal toxicity
• Beriberi
• Anaphylaxis
• Inflammatory shock due to burns or trauma
• Endocrine shock due to Addison disease or thyrotoxicosis [26][27][28][29] 

Obstructive Shock

Obstructive shock is due to an obstructive pathology that impedes cardiac output. Examples of this type of shock are cardiac tamponade and tension pneumothorax. Differentiating obstructive and hypovolemic hemorrhagic shock can be challenging, given the high probability of concomitant shock types in patients who experience trauma. An increased central venous pressure is typically a distinguishing feature of obstructive shock.[30]

Potential causes of obstructive shock are:

• Pulmonary embolus
• Severe pulmonary hypertension
• Severe or acute obstruction of the pulmonic or tricuspid valve
• Venous air embolus
• Tension pneumothorax
• Hemothorax 
• Pericardial tamponade
• Constrictive pericarditis
• Restrictive cardiomyopathy
• Severe dynamic hyperinflation due to mechanical ventilation
• Left or right ventricular outflow tract obstruction
• Abdominal compartment syndrome 
• Aorto-caval compression due to positioning or surgical retraction [31][32]

Cardiogenic Shock

Primary pump failure causes cardiogenic shock. Clinicians differentiate cardiogenic shock from hypovolemic shock by the presence of increased central venous pressure and peripheral vascular resistance.[33] Potential causes of cardiogenic shock are:

• Myocardial infarction
• Severe right ventricular infarction
• Acute exacerbation of severe heart failure from dilated cardiomyopathy
• Takesubo cardiomyopathy or other stress-induced cardiomyopathies, like cardiomyopathy due to sepsis
• Severe septic shock
• Myocarditis
• Myocardial contusion
• Drug-induced (eg, β-blockers)
• Tachyarrhythmia
• Bradyarrhythmia
• Severe valvular insufficiency
• Acute valvular rupture
• Critical valvular stenosis
• Acute or severe ventricular septal wall defect
• Ruptured ventricular wall aneurysm
• Atrial myxoma [31][34]

 Undifferentiated or Mixed Shock 

Some patients may have an unknown form of shock or a combination of the different classifications. Potential etiologies include the following:

• Multiple traumas involving more than 1 shock type
• Shock in the presence of preexisting cardiovascular or pulmonary disease 

Prognosis

The prognosis for hypovolemic shock depends on its cause and severity. Clinicians improve outcomes in hemorrhagic shock by controlling bleeding early and initiating effective, goal-directed volume resuscitation. Once patients progress to multiorgan failure, their prognosis worsens, and mortality rises. Older adults and those with preexisting comorbidities tend to experience poorer outcomes. 

Complications

As mentioned above, 1 of the most feared complications of hypovolemic shock is circulatory failure, leading to multiorgan failure and death. However, additional complications occur both as a result of hypovolemia and as a result of treatment. Potential complications of hypovolemic shock are: 

• Abdominal compartment syndrome
• Coagulopathy
• Hypothermia
• Sheehan syndrome or postpartum hypopituitarism due to infarction secondary to hypovolemic shock
• Asherman syndrome due to uterine curettage following postpartum hemorrhage
• Transfusion reactions
• Transfusion-related infections
• Fluid overload
• Acute respiratory distress syndrome
• Myocardial infarction
• Depression
• Anxiety
• Myocardial infarction
• Stroke
• Renal failure
• Cognitive dysfunction
• Posttraumatic stress disorder
• Limb amputation
• Complications due to surgical and radiological interventions [35][36][37]