Hypovolemic shock

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Hypovolemic shock
Capillary microcirculation.svg
A diagram showing the formation of interstitial fluid from the bloodstream.
Specialty Emergency care
Symptoms anxiety, confusion, decreased or no urine output, cool and clammy skin, sweating, weakness, pallor, rapid breathing, unconsciousness [1]
Causessevere dehydration or blood loss
Treatmentreplacement of fluids, surgery to repair cause of bleeding

Hypovolemic shock is a form of shock caused by severe hypovolemia (insufficient blood volume or extracellular fluid in the body). [1] [2] It could be the result of severe dehydration through a variety of mechanisms or blood loss. [3] [2] Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failure. [4]

Contents

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 losses. To minimize ischemic damage to tissues, treatment involves quickly replacing lost blood or fluids, with consideration of both rate and the type of fluids used. [4]

Tachycardia, a fast heart rate, is typically the first abnormal vital sign. [3] 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. [3] The body in hypovolemic shock prioritizes getting oxygen to the brain and heart, which reduces blood flow to nonvital organs and extremities, causing them to grow cold, look mottled, and exhibit delayed capillary refill. [3] The lack of adequate oxygen delivery ultimately leads to a worsening increase in the acidity of the blood (acidosis). [3] The "lethal triad" of ways trauma can lead to death is acidosis, hypothermia, and coagulopathy. [3] It is possible for trauma to cause clotting problems even without resuscitation efforts. [3]

Damage control resuscitation is based on three principles:

Signs and symptoms

Symptoms of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid–base disorders that accompany hypovolemic shock. [4]

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 characterize brain mal-perfusion. [4]

Dry mucous membranes, decreased skin turgor, low jugular venous distention, tachycardia, and hypotension can be seen along with decreased urinary output. [4] Patients in shock can appear cold, clammy, and cyanotic. [4]

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. [6] 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. [6]

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. [6] Echocardiography in such case may be helpful to distinguish cardiac failure from other diseases. [6] Cardiac failure manifests a weak contractibility myocardium; treatment with an inotropic drug such as dobutamine may be appropriate. [6]

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. [4]

Hypovolemic shock occurs as a result of either blood loss or extracellular fluid loss. [4]

Blood loss

Hemorrhagic shock is hypovolemic shock from blood loss. Traumatic injury is by far the most common cause of hemorrhagic shock, [4] particularly blunt and penetrating trauma, [3] followed by upper and lower gastrointestinal sources, [3] such as gastrointestinal (GI) bleed. [4] Other causes of hemorrhagic shock include bleed from an ectopic pregnancy, bleeding from surgical intervention, vaginal bleeding [4] , and splenic rupture. [7]

Obstetrical, vascular, iatrogenic, and even urological sources have all been described. [3] Bleeding may be either external or internal. [3] A substantial amount of blood loss to the point of hemodynamic compromise may occur in the chest, abdomen, or the retroperitoneum. [3] The thigh itself can hold up to 1 L to 2 L of blood. [3]

Localizing and controlling the source of bleeding is of utmost importance to the treatment of hemorrhagic shock. [3]

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. [8]

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. [9]

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. [1] Hypovolemic shock as a result of extracellular fluid loss can be of the 4 etiologies. [4]

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. [4]

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. [4]

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. [4]

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. [4]

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 [10] or any other pathological condition that results in a massive inflammatory response. [4]

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. [3]

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. [3]

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. [3]

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. [3]

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. [3]

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. [3]

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. [4]

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. [4]

Diagnosis

Shock index (SI) has been defined as heart rate / systolic blood pressure  ; SI≥0.6 is a clinical shock.

Such ratio value is clinically employed to determine the scope or emergence of shock. [11] 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. [12] [13]

Patients classified by Shock Index: traditional vital signs presented at the emergency department (ED) admission and at first scene.
Group I (SI <0.6, no shock)Group II (SI ≥0.6 to <1.0, mild shock)Group III (SI ≥1.0 to <1.4, moderate shock)Group IV (SI ≥1.4, severe shock)
SBP at scene (mmHg)
Mean ± standard deviation136.8 (32.8)121.9 (29.4)105.2 (33.1)92.9 (34.4)
Median (IQR)138 (120 to 160)120 (105 to 140)100 (90 to 120)90 (70 to 110)
SBP at ED (mmHg)
Mean ± standard deviation148.4 (25.6)124.1 (20.2)96.9 (16.8)70.6 (15.7)
Median (IQR)147 (130 to 160)120 (110 to 138)98 (86 to 108)70 (60 to 80)
HR at scene (beats/minute)
Mean ± standard deviation83.0 (19.2)94.0 (20.6)103.7 (26.6)110.5 (31.3)
Median (IQR)80 (70 to 95)94 (80 to 105)105 (90 to 120)115 (100 to 130)
HR at ED (beats/minute)
Mean ± standard deviation73.7 (13.6)91.3 (15.1)109.1 (17.9)122.7 (19.5)
Median (IQR)74 (65 to 80)90 (80 to 100)110 (100 to 120)120 (110 to 135)
SI at scene (beats/minute)
Mean ± standard deviation0.6 (0.2)0.8 (0.3)1.1 (0.4)1.3 (0.5)
Median (IQR)0.6 (0.5 to 0.7)0.8 (0.6 to 0.9)1.0 (1.0 to 1.0)1.2 (0.9 to 1.6)

Data presented as n (%), mean ± standard deviation or median (interquartile range (IQR)). n = 21,853; P <0.001 for all parameters. ED Emergency department, GCS Glasgow coma scale, HR Heart rate, SBP Systolic blood pressure, SI = Shock index.

[13]

Bleeding

Recognizing the degree of blood loss via vital sign and mental status abnormalities is important. The American College of Surgeons Advanced Trauma Life Support (ATLS) hemorrhagic shock classification links the amount of blood loss to expected physiologic responses in a healthy 70 kg patient. As total circulating blood volume accounts for approximately 7% of total body weight, this equals approximately five liters in the average 70 kg male patient. [3]

Again, the above is outlined for a healthy 70 kg individual. Clinical factors must be taken into account when assessing patients. For example, elderly patients taking beta blockers can alter the patient's physiologic response to decreased blood volume by inhibiting mechanism to increase heart rate. As another, patients with baseline hypertension may be functionally hypotensive with a systolic blood pressure of 110 mmHg. [3]

Non-bleeding

Various laboratory values can be abnormal in hypovolemic shock. Patients can have increased BUN and serum creatinine as a result of pre-renal kidney failure. Hypernatremia or hyponatremia can result, as can hyperkalemia or hypokalemia. [4]

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. [4]

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. 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. [4]

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. [4]

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. [4]

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. [4]

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. [4] 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. [4]

Although relatively nonsensitive and nonspecific, physical exam can be helpful in determining the presence of hypovolemic shock. [4] 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. [4]

Differential diagnosis

While hemorrhage is the most common cause of shock in the trauma patient, other causes of shock are to remain on the differential. Obstructive shock can occur in the setting of tension pneumothorax and cardiac tamponade. These etiologies should be uncovered in the primary survey. [3] In the setting of head or neck trauma, an inadequate sympathetic response, or neurogenic shock, is a type of distributive shock that is caused by a decrease in peripheral vascular resistance. [3] This is suggested by an inappropriately low heart rate in the setting of hypotension. [3] Cardiac contusion and infarctions can result in cardiogenic shock. [3] Finally, other causes should be considered that are not related to trauma or blood loss. In the undifferentiated patient with shock, septic shock and toxic causes are also on the differential. [3]

Management

The first step in managing hemorrhagic shock is recognition. Ideally, This should occur before the development of hypotension. Close attention should be paid to physiological responses to low-blood volume. [3] Tachycardia, tachypnea, and narrowing pulse pressure may be the initial signs. Cool extremities and delayed capillary refill are signs of peripheral vasoconstriction. [3]

Bleeding

In the setting of trauma, an algorithmic approach via the primary and secondary surveys is suggested by ATLS. Physical exam and radiological evaluations can help localize sources of bleeding. A trauma ultrasound, or Focused Assessment with Sonography for Trauma (FAST), has been incorporated in many circumstances into the initial surveys. The specificity of a FAST scan has been reported above 99%, but a negative ultrasound does not rule out intra-abdominal pathology. [3]

With a broader understanding of the pathophysiology of hemorrhagic shock, treatment in trauma has expanded from a simple massive transfusion method to a more comprehensive management strategy of "damage control resuscitation". The concept of damage control resuscitation focuses on permissive hypotension, hemostatic resuscitation, and hemorrhage control to adequately treat the "lethal triad" of coagulopathy, acidosis, and hypothermia that occurs in trauma. [3]

Hypotensive resuscitation has been suggested for the hemorrhagic shock patient without head trauma. The aim is to achieve a systolic blood pressure of 90 mmHg in order to maintain tissue perfusion without inducing re-bleeding from recently clotted vessels. Permissive hypotension is a means of restricting fluid administration until hemorrhage is controlled while accepting a short period of suboptimal end-organ perfusion. Studies regarding permissive hypotension have yielded conflicting results and must take into account type of injury (penetrating versus blunt), the likelihood of intracranial injury, the severity of the injury, as well as proximity to a trauma center and definitive hemorrhage control. [3]

The quantity, type of fluids to be used, and endpoints of resuscitation remain topics of much study and debate. For crystalloid resuscitation, normal saline and lactated ringers are the most commonly used fluids. Normal saline has the drawback of causing a non-anion gap hyperchloremic metabolic acidosis due to the high chloride content, while lactated ringers can cause a metabolic alkalosis as lactate metabolism regenerates into bicarbonate. [3]

Recent trends in damage control resuscitation focus on "hemostatic resuscitation" which pushes for early use of blood products rather than an abundance of crystalloids in order to minimize the metabolic derangement, resuscitation-induced coagulopathy, and the hemodilution that occurs with crystalloid resuscitation. The end goal of resuscitation and the ratios of blood products remain at the center of much study and debate. A recent study has shown no significant difference in mortality at 24 hours or 30 days between ratios of 1:1:1 and 1:1:2 of plasma to platelets to packed RBCs. However, patients that received the more balanced ratio of 1:1:1 were less likely to die as a result of exsanguination in 24 hours and were more likely to achieve hemostasis. Additionally, reduction in time to first plasma transfusion has shown a significant reduction in mortality in damage control resuscitation. [3]

In addition to blood products, products that prevent the breakdown of fibrin in clots, or antifibrinolytics, have been studied for their utility in the treatment of hemorrhagic shock in the trauma patient. Several antifibrinolytics have been shown to be safe and effective in elective surgery. The CRASH-2 study was a randomized control trial of tranexamic acid versus placebo in trauma has been shown to decrease overall mortality when given in the first three hours of injury. [3] Follow-up analysis shows additional benefit to tranexamic acid when given in the first three hours after surgery. [3]

Damage control resuscitation is to occur in conjunction with prompt intervention to control the source of bleeding. [3] Strategies may differ depending on proximity to definitive treatment. [3]

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. [4]

Fluid loss

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. [4] Vasopressors may be used if blood pressure does not improve with fluids.

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. [4]

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 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 hyper-oncotic starch leads to increased mortality rate and renal failure. [4] Patients in shock can appear cold, clammy, and cyanotic. [4]

Hypothermia increases the mortality rate of patients with hypovolemic shock. It is advised to keep the patient warm for the sake of maintaining the temperatures of all kinds of fluids inside the patient. [6]

Monitoring parameters

Prognosis

If the vital organs are deprived of perfusion for more than just a short time, the prognosis is generally not good. Shock is still a medical emergency characterized by a high mortality rate. Early identification of patients who are likely to succumb to their illness is of utmost importance. [14]

Epidemiology

Blood loss

Trauma remains a leading cause of death worldwide with approximately half of these attributed to hemorrhage. In the United States in 2001, trauma was the third leading cause of death overall, and the leading cause of death in those aged 1 to 44 years. While trauma spans all demographics, it disproportionately affects the young with 40% of injuries occurring in ages 20 to 39 years by one country's account. Of this 40%, the greatest incidence was in the 20 to 24-year-old range. [3]

The preponderance of hemorrhagic shock cases resulting from trauma is high. During one year, one trauma center reported 62.2% of massive transfusions occur in the setting of trauma. The remaining cases are divided among cardiovascular surgery, critical care, cardiology, obstetrics, and general surgery, with trauma utilizing over 75% of the blood products. [3]

As patients age, physiological reserves decrease the likelihood of anticoagulant use increases and the number of comorbidities increases. Due to this, elderly patients are less likely to handle the physiological stresses of hemorrhagic shock and may decompensate more quickly. [3]

Fluid loss

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 the blood products used were related to traumatic injury. Elderly patients are more likely to experience hypovolemic shock due to fluid losses as they have less physiologic reserve. [4]

Hypovolemia secondary to diarrhea and/or dehydration is thought to be predominant in low-income countries. [15]

See also

Related Research Articles

<span class="mw-page-title-main">Shock (circulatory)</span> Medical condition of insufficient blood flow

Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.

<span class="mw-page-title-main">Bleeding</span> Loss of blood escaping from the circulatory system

Bleeding, hemorrhage, haemorrhage or blood loss is blood escaping from the circulatory system from damaged blood vessels. Bleeding can occur internally, or externally either through a natural opening such as the mouth, nose, ear, urethra, vagina or anus, or through a puncture in the skin. Hypovolemia is a massive decrease in blood volume, and death by excessive loss of blood is referred to as exsanguination. Typically, a healthy person can endure a loss of 10–15% of the total blood volume without serious medical difficulties. The stopping or controlling of bleeding is called hemostasis and is an important part of both first aid and surgery.

<span class="mw-page-title-main">Fluid replacement</span>

Fluid replacement or fluid resuscitation is the medical practice of replenishing bodily fluid lost through sweating, bleeding, fluid shifts or other pathologic processes. Fluids can be replaced with oral rehydration therapy (drinking), intravenous therapy, rectally such as with a Murphy drip, or by hypodermoclysis, the direct injection of fluid into the subcutaneous tissue. Fluids administered by the oral and hypodermic routes are absorbed more slowly than those given intravenously.

<span class="mw-page-title-main">Hypotension</span> Abnormally low blood pressure

Hypotension, also known as low blood pressure, is a cardiovascular condition characterized by abnormally reduced blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood and is indicated by two numbers, the systolic blood pressure and the diastolic blood pressure, which are the maximum and minimum blood pressures within the cardiac cycle, respectively. A systolic blood pressure of less than 90 millimeters of mercury (mmHg) or diastolic of less than 60 mmHg is generally considered to be hypotension. Different numbers apply to children. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

<span class="mw-page-title-main">Hypovolemia</span> Low blood volume

Hypovolemia, also known as volume depletion or volume contraction, is a state of abnormally low extracellular fluid in the body. This may be due to either a loss of both salt and water or a decrease in blood volume. Hypovolemia refers to the loss of extracellular fluid and should not be confused with dehydration.

<span class="mw-page-title-main">Internal bleeding</span> Medical condition

Internal bleeding is a loss of blood from a blood vessel that collects inside the body, and is not usually visible from the outside. It can be a serious medical emergency but the extent of severity depends on bleeding rate and location of the bleeding. Severe internal bleeding into the chest, abdomen, pelvis, or thighs can cause hemorrhagic shock or death if proper medical treatment is not received quickly. Internal bleeding is a medical emergency and should be treated immediately by medical professionals.

<span class="mw-page-title-main">Traumatic cardiac arrest</span> Medical condition

Traumatic cardiac arrest (TCA) is a condition in which the heart has ceased to beat due to blunt or penetrating trauma, such as a stab wound to the thoracic area. It is a medical emergency which will always result in death without prompt advanced medical care. Even with prompt medical intervention, survival without neurological complications is rare. In recent years, protocols have been proposed to improve survival rate in patients with traumatic cardiac arrest, though the variable causes of this condition as well as many coexisting injuries can make these protocols difficult to standardize. Traumatic cardiac arrest is a complex form of cardiac arrest often derailing from advanced cardiac life support in the sense that the emergency team must first establish the cause of the traumatic arrest and reverse these effects, for example hypovolemia and haemorrhagic shock due to a penetrating injury.

<span class="mw-page-title-main">Neurogenic shock</span> Insufficient blood flow due to autonomic nervous system damage

Neurogenic shock is a distributive type of shock resulting in hypotension, often with bradycardia, caused by disruption of autonomic nervous system pathways. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting from loss of sympathetic tone, which in turn causes blood pooling within the extremities rather than being available to circulate throughout the body. The slowed heart rate results from a vagal response unopposed by a sympathetic nervous system (SNS) response. Such cardiovascular instability is exacerbated by hypoxia, or treatment with endotracheal or endobronchial suction used to prevent pulmonary aspiration.

<span class="mw-page-title-main">Beck's triad (cardiology)</span> Medical condition

Beck's triad is a collection of three medical signs associated with acute cardiac tamponade, a medical emergency when excessive fluid accumulates in the pericardial sac around the heart and impairs its ability to pump blood. The signs are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.

Pulseless electrical activity (PEA) is a form of cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not. Pulseless electrical activity is found initially in about 20% of out-of-hospital cardiac arrests and about 50% of in-hospital cardiac arrests.

<span class="mw-page-title-main">Ringer's lactate solution</span> Fluid used for resuscitation after blood loss

Ringer's lactate solution (RL), also known as sodium lactate solution,Lactated Ringer's, and Hartmann's solution, is a mixture of sodium chloride, sodium lactate, potassium chloride, and calcium chloride in water. It is used for replacing fluids and electrolytes in those who have low blood volume or low blood pressure. It may also be used to treat metabolic acidosis and to wash the eye following a chemical burn. It is given by intravenous infusion or applied to the affected area.

<span class="mw-page-title-main">Amniotic fluid embolism</span> Potentially fatal complication of pregnancy

An amniotic fluid embolism (AFE) is a life-threatening childbirth (obstetric) emergency in which amniotic fluid enters the blood stream of the mother, triggering a serious reaction which results in cardiorespiratory collapse and massive bleeding (coagulopathy). The rate at which it occurs is 1 instance per 20,000 births and it comprises 10% of all maternal deaths.

In medicine, intravascular volume status refers to the volume of blood in a patient's circulatory system, and is essentially the blood plasma component of the overall volume status of the body, which otherwise includes both intracellular fluid and extracellular fluid. Still, the intravascular component is usually of primary interest, and volume status is sometimes used synonymously with intravascular volume status.

Pediatric advanced life support (PALS) is a course offered by the American Heart Association (AHA) for health care providers who take care of children and infants in the emergency room, critical care and intensive care units in the hospital, and out of hospital. The course teaches healthcare providers how to assess injured and sick children and recognize and treat respiratory distress/failure, shock, cardiac arrest, and arrhythmias.

A volume expander is a type of intravenous therapy that has the function of providing volume for the circulatory system. It may be used for fluid replacement or during surgery to prevent nausea and vomiting after surgery.

Obstructive shock is one of the four types of shock, caused by a physical obstruction in the flow of blood. Obstruction can occur at the level of the great vessels or the heart itself. Causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. These are all life-threatening. Symptoms may include shortness of breath, weakness, or altered mental status. Low blood pressure and tachycardia are often seen in shock. Other symptoms depend on the underlying cause.

The Hs and Ts is a mnemonic used to aid in remembering the possible reversible causes of cardiac arrest. A variety of disease processes can lead to a cardiac arrest; however, they usually boil down to one or more of the "Hs and Ts".

Orthostatic syncope refers to syncope resulting from a postural decrease in blood pressure, termed orthostatic hypotension.

Permissive hypotension or hypotensive resuscitation is the use of restrictive fluid therapy, specifically in the trauma patient, that increases systemic blood pressure without reaching normotension. The goal blood pressure for these patients is a mean arterial pressure of 40-50 mmHg or systolic blood pressure of less than or equal to 80. This goes along with certain clinical criteria. Following traumatic injury, some patients experience hypotension that is usually due to blood loss (hemorrhage) but can be due to other causes as well. In the past, physicians were very aggressive with fluid resuscitation to try to bring the blood pressure to normal values. Recent studies have found that there is some benefit to allowing specific patients to experience some degree of hypotension in certain settings. This concept does not exclude therapy by means of i.v. fluid, inotropes or vasopressors, the only restriction is to avoid completely normalizing blood pressure in a context where blood loss may be enhanced. When a person starts to bleed the body starts a natural coagulation process that eventually stops the bleed. Issues with fluid resuscitation without control of bleeding are thought to be secondary to dislodgement of the thrombus that is helping to control further bleeding. Thrombus dislodgement was found to occur at a systolic pressure greater than 80mm Hg. In addition, fluid resuscitation will dilute coagulation factors that help form and stabilize a clot, hence making it harder for the body to use its natural mechanisms to stop the bleeding. These factors are aggravated by hypothermia.

Damage control surgery (DCS) is surgical intervention to keep the patient alive rather than correct the anatomy. It addresses the "lethal triad" for critically ill patients with severe hemorrhage affecting homeostasis leading to metabolic acidosis, hypothermia, and increased coagulopathy.

References

  1. 1 2 3 "Hypovolemic shock: MedlinePlus Medical Encyclopedia". MedlinePlus. 2019-01-28. Retrieved 2019-02-21.
  2. 1 2 McGee, Steven (2018). Evidence-based physical diagnosis. Philadelphia, PA: Elsevier. ISBN   978-0-323-39276-1. OCLC   959371826. The term hypovolemia refers collectively to two distinct disorders: (1) volume depletion, which describes the loss of sodium from the extracellular space (i.e., intravascular and interstitial fluid) that occurs during gastrointestinal hemorrhage, vomiting, diarrhea, and diuresis; and (2) dehydration, which refers to the loss of intracellular water (and total body water) that ultimately causes cellular desiccation and elevates the plasma sodium concentration and osmolality.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 Hooper, Nicholas; Armstrong, Tyler J. (2018-10-27). "Shock, Hemorrhagic". NCBI Bookshelf. PMID   29262047 . Retrieved 2019-02-21.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 Taghavi, S; Askari, R (2018), "article-28977", Hypovolemic Shock, Treasure Island (FL): StatPearls Publishing, PMID   30020669 , retrieved 2019-02-20
  5. ↑ Cap, Andrew P.; Gurney, Jennifer M.; Meledeo, Michael A. (2020). "Hemostatic Resuscitation". Damage Control Resuscitation. pp. 117–144. doi:10.1007/978-3-030-20820-2_7. ISBN   978-3-030-20819-6. S2CID   242142361.
  6. 1 2 3 4 5 6 7 Nolan, J. P.; Pullinger, R. (2014-03-07). "Hypovolaemic Shock". BMJ. 348 (mar07 1): bmj.g1139. doi:10.1136/bmj.g1139. ISSN   1756-1833. PMID   24609389. S2CID   45691590.
  7. ↑ Akoury, T; Whetstone, DR (January 2021). "Splenic Rupture". PMID   30247826.{{cite journal}}: Cite journal requires |journal= (help)
  8. ↑ "Definition, classification, etiology, and pathophysiology of shock in adults". UpToDate. Retrieved 2019-02-22.
  9. ↑ "definition-classification-etiology-and-pathophysiology-of-shock-in-adults". UpToDate. Retrieved 2019-02-21.
  10. ↑ Gulati, A (2016). "Vascular Endothelium and Hypovolemic Shock". Current Vascular Pharmacology. 14 (2): 187–95. doi:10.2174/1570161114666151202210221. ISSN   1570-1611. PMID   26638794.
  11. ↑ Berger, Tony; Green, Jeffrey; Horeczko, Timothy; Hagar, Yolanda; Garg, Nidhi; Suarez, Alison; Panacek, Edward; Shapiro, Nathan (2013-03-01). "Shock Index and Early Recognition of Sepsis in the Emergency Department: Pilot Study". Western Journal of Emergency Medicine. 14 (2): 168–174. doi:10.5811/westjem.2012.8.11546. ISSN   1936-900X. PMC   3628475 . PMID   23599863.
  12. ↑ Fröhlich, M; Driessen, A; Böhmer, A; Nienaber, U; Igressa, A; Probst, C; Bouillon, B; Maegele, M; Mutschler, M (2016-12-12). "Is the shock index based classification of hypovolemic shock applicable in multiple injured patients with severe traumatic brain injury?—an analysis of the TraumaRegister DGU®". Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 24 (1): 148. doi: 10.1186/s13049-016-0340-2 . PMC   5153863 . PMID   27955692.
  13. 1 2 Mutschler, M; Nienaber, U; Münzberg, M; Wölfl, C; Schoechl, H; Paffrath, T; Bouillon, B; Maegele, M (2013-08-12). "The Shock Index revisited - a fast guide to transfusion requirement? A retrospective analysis on 21,853 patients derived from the TraumaRegister DGU". Critical Care. 17 (4): R172. doi: 10.1186/cc12851 . ISSN   1364-8535. PMC   4057268 . PMID   23938104.
  14. ↑ Tuchschmidt, JA; Mecher, CE (1994). "Predictors of outcome from critical illness. Shock and cardiopulmonary resuscitation". Critical Care Clinics. 10 (1): 179–95. doi:10.1016/S0749-0704(18)30155-6. ISSN   0749-0704. PMID   8118727.
  15. ↑ Mbevi, G; Ayieko, P; Irimu, G; Akech, S; English, M (2016-11-16). "Prevalence, aetiology, treatment and outcomes of shock in children admitted to Kenyan hospitals". BMC Medicine. 14 (1): 184. doi: 10.1186/s12916-016-0728-x . PMC   5111353 . PMID   27846837.
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