Hypovolemic shock is a form of shock caused by severe hypovolemia (insufficient blood volume or fluid outside of cells in the body). It can be caused by severe dehydration or blood loss. Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failures.
In treating hypovolemic shock, it is important to determine the cause of the underlying hypovolemia, which may be the result of bleeding or other fluid loss. To minimize damage to tissues from insufficient blood flow, treatment involves quickly replacing lost blood or fluids, with consideration of both rate and the type of fluids used.
Tachycardia, a fast heart rate, is typically the first abnormal vital sign. When resulting from blood loss, trauma is the most common root cause, but severe blood loss can also happen in various body systems without clear traumatic injury. The body in hypovolemic shock prioritizes getting oxygen to the brain and heart, which reduces blood flow to nonvital organs and the limbs, causing them to grow cold, look mottled, and exhibit delayed capillary refill. The lack of adequate oxygen delivery causes the blood to become more acidic (acidosis). The "lethal triad" of ways trauma can lead to death is acidosis, hypothermia, and coagulopathy. It is possible for trauma to cause clotting problems even without resuscitation efforts.
Damage control resuscitation is based on three principles: permissive hypotension: tries to balance temporary suboptimal perfusion to organs with conditions for halting blood loss by setting a goal of 90 mmHg systolic blood pressure hemostatic resuscitation: restoring blood volume in ways (with whole blood or equivalent) that interfere minimally with the natural process of stopping bleeding. damage control surgery.
Signs and symptoms
Symptoms of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid–base disorders that accompany the condition.
Patients with volume depletion may complain of thirst, muscle cramps, and/or orthostatic hypotension. Severe hypovolemic shock can result in insufficient blood flow to the heart and to the mesentery in the abdomen, which can cause or chest pain or abdominal pain. Agitation, lethargy, or confusion may characterize brain mal-perfusion.
Dry mucous membranes, decreased skin turgor, low jugular venous distention, tachycardia, and hypotension can be seen along with decreased urinary output. Patients in shock can appear cold, clammy, and cyanotic.
Early signs and symptoms include tachycardia given rise to by catecholamine release; skin pallor due to vasoconstriction triggered by catecholamine release; hypotension followed by hypovolaemia and perhaps arising after myocardial insufficiency; and confusion, aggression, drowsiness and coma caused by cerebral hypoxia or acidosis. Tachypnoea owing to hypoxia and acidosis, general weakness caused by hypoxia and acidosis, thirst induced by hypovolaemia, and oliguria caused by reduced perfusion may also arise.
Abnormal growing central venous pressure indicates either hypotension or hypovolemia. Tachycardia accompanied by declined urine outflow implies either tension pneumothorax, cardiac tamponade or cardiac failure which is thought secondary to cardiac contusion or ischaemic heart disease. Echocardiography in such case may be helpful to distinguish cardiac failure from other diseases. Cardiac failure manifests a weak contractibility myocardium; treatment with an inotropic drug such as dobutamine may be appropriate.
Cause
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.
Blood loss
Hemorrhagic shock is hypovolemic shock from blood loss. Traumatic injury is by far the most common cause of hemorrhagic shock, particularly blunt and penetrating trauma, followed by upper and lower gastrointestinal sources, such as gastrointestinal (GI) bleed. Other causes of hemorrhagic shock include bleed from an ectopic pregnancy, bleeding from surgical intervention, vaginal bleeding, and splenic rupture.
Obstetrical, vascular, iatrogenic, and even urological sources have all been described. Bleeding may be either external or internal. A substantial amount of blood loss to the point of hemodynamic compromise may occur in the chest, abdomen, or the retroperitoneum. The thigh itself can hold up to 1 L to 2 L of blood.
Localizing and controlling the source of bleeding is of utmost importance to the treatment of hemorrhagic shock.
The sequence of the most-commonly-seen causes that lead to hemorrhagic type of hypovolemic shock is given in order of frequencies: blunt or penetrating trauma including multiple fractures absent from vessel impairment, upper gastrointestinal bleeding e.g., variceal hemorrhage, peptic ulcer., or lower GI bleeding e.g., diverticular, and arteriovenous malformation.
Except for the two most common causes, the less common causes are intra-operative and post-operative bleeding, abdominal aortic rupture or left ventricle aneurysm rupture, aortic–enteric fistula, hemorrhagic pancreatitis, iatrogenic e.g., inadvertent biopsy of arteriovenous malformation, severed artery., tumors or abscess erosion into major vessels, post-partum hemorrhage, uterine or vaginal hemorrhage owing to infection, tumors, lacerations, spontaneous peritoneal hemorrhage caused by bleeding diathesis, and ruptured hematoma.
Fluid loss
In spite of hemorrhage, the amount of circulating blood in the body may drop as well when one loses excessive body fluid owing to non-hemorrhagic reasons. Hypovolemic shock as a result of extracellular fluid loss can be of the 4 etiologies.
Gastrointestinal
Gastrointestinal (GI) losses can occur via many different etiologies. The gastrointestinal tract usually secretes between 3 and 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.
Kidneys
Renal losses of salt and fluid can lead to hypovolemic shock. The kidneys usually excrete sodium and water in a manner that matches sodium intake and water 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
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-spacing
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, vascular endothelium or any other pathological condition that results in a massive inflammatory response.
Pathophysiology
Blood loss
Hemorrhagic shock is due to the depletion of intravascular volume through blood loss to the point of being unable to match the tissues' demand for oxygen. As a result, mitochondria are no longer able to sustain aerobic metabolism for the production of oxygen and switch to the less efficient anaerobic metabolism to meet the cellular demand for adenosine triphosphate. In the latter process, pyruvate is produced and converted to lactic acid to regenerate nicotinamide adenine dinucleotide (NAD+) to maintain some degree of cellular respiration in the absence of oxygen.
The body compensates for volume loss by increasing heart rate and contractility, followed by baroreceptor activation resulting in sympathetic nervous system activation and peripheral vasoconstriction. Typically, there is a slight increase in the diastolic blood pressure with narrowing of the pulse pressure. As diastolic ventricular filling continues to decline and cardiac output decreases, systolic blood pressure drops.
Due to sympathetic nervous system activation, blood is diverted away from noncritical organs and tissues to preserve blood supply to vital organs such as the heart and brain. While prolonging heart and brain function, this also leads to other tissues being further deprived of oxygen causing more lactic acid production and worsening acidosis. This worsening acidosis along with hypoxemia, if left uncorrected, eventually causes the loss of peripheral vasoconstriction, worsening hemodynamic compromise, and death.
The body's compensation varies by cardiopulmonary comorbidities, age, and vasoactive medications. Due to these factors, heart rate and blood pressure responses are extremely variable and, therefore, cannot be relied upon as the sole means of diagnosis.
A key factor in the pathophysiology of hemorrhagic shock is the development of trauma-induced coagulopathy. Coagulopathy develops as a combination of several processes. The simultaneous loss of coagulation factors via hemorrhage, hemodilution with resuscitation fluids, and coagulation cascade dysfunction secondary to acidosis and hypothermia have been traditionally thought to be the cause of coagulopathy in trauma. However, this traditional model of trauma-induced coagulopathy may be too limited. Further studies have shown that a degree of coagulopathy begins in 25% to 56% of patients before initiation of the resuscitation. This has led to the recognition of trauma-induced coagulopathy as the sum of two distinct processes: acute coagulopathy of trauma and resuscitation-induced coagulopathy.
Trauma-induced coagulopathy is acutely worsened by the presence of acidosis and hypothermia. The activity of coagulation factors, fibrinogen depletion, and platelet quantity are all adversely affected by acidosis. Hypothermia (less than 34 C) compounds coagulopathy by impairing coagulation and is an independent risk factor for death in hemorrhagic shock.
Fluid loss
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 the oxygen needs of the cells. 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.
Diagnosis
Shock index (SI) has been defined as ; SI≥0.6 is a clinical shock.
Such ratio value is clinically employed to determine the scope or emergence of shock. The SI correlates with the extent of hypovolemia and thus may facilitate the early identification of severely injured patients threatened by complications due to blood loss and therefore need urgent treatment, i.e. blood transfusion.
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