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Hypovolemic shock is a form of shock caused by severe hypovolemia (insufficient blood volume or extracellular fluid in the body). It can be caused by severe dehydration or blood loss. Hypovolemic shock is a medical emergency; if left untreated, the Ischemia can cause damage to organs, leading to multiple organ failure.
In treating hypovolemic shock, it is important to determine the cause of the underlying hypovolemia, which may be the result of hemorrhage or other . 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.
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 extremities, causing them to grow cold, look mottled, and exhibit delayed capillary refill. The lack of adequate oxygen delivery ultimately leads to a worsening increase in the acidity of the blood (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:
Patients with volume depletion may complain of thirst, , and/or orthostatic hypotension. Severe hypovolemic shock can result in mesenteric and coronary ischemia that can cause abdominal pain or chest pain. Agitation, lethargy, or confusion may characterize brain mal-perfusion.
Dry , 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.
Hypovolemic shock occurs as a result of either blood loss or extracellular fluid loss.
Obstetrical, Blood vessel, 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 Bone fracture 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., or abscess erosion into major vessels, post-partum hemorrhage, uterine or vaginal hemorrhage owing to infection, , lacerations, spontaneous peritoneal hemorrhage caused by bleeding diathesis, and ruptured hematoma.
Diuretics and osmotic diuresis from hyperglycemia can lead to excessive renal sodium and volume loss. In addition, there are several tubular disease and interstitial diseases beyond the scope of this article that cause severe salt-wasting nephropathy.
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.
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.
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.
| + Patients classified by Shock Index: traditional vital signs presented at the emergency department (ED) admission and at first scene. | |
| 92.9 (34.4) | |
| 90 (70 to 110) | |
| 70.6 (15.7) | |
| 70 (60 to 80) | |
| 110.5 (31.3) | |
| 115 (100 to 130) | |
| 122.7 (19.5) | |
| 120 (110 to 135) | |
| 1.3 (0.5) | |
| 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.
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 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.
Lactic acidosis can result from increased anaerobic metabolism. However, the effect of acid–base balance can be variable as patients with large GI losses can become alkalotic.
In cases of hemorrhagic shock, hematocrit and hemoglobin can be severely decreased. However, with a reduction in plasma volume, hematocrit and hemoglobin can be increased due to hemoconcentration.
Low urinary sodium is commonly found in hypovolemic patients as the kidneys attempt to conserve sodium and water to expand the extracellular volume. However, sodium urine can be low in a euvolemic patient with heart failure, cirrhosis, or nephrotic syndrome. Fractional excretion of sodium under 1% is also suggestive of volume depletion. Elevated urine osmolality can also suggest hypovolemia. However, this number also can be elevated in the setting of impaired concentrating ability by the kidneys.
Central venous pressure (CVP) is often used to assess volume status. However, its usefulness in determining volume responsiveness has recently come into question. Ventilator settings, chest wall compliance, and right-sided heart failure can compromise CVPs accuracy as a measure of volume status. Measurements of pulse pressure variation via various commercial devices has also been postulated as a measure of volume responsiveness. However, pulse pressure variation as a measure of fluid responsiveness is only valid in patients without spontaneous breaths or arrhythmias. The accuracy of pulse pressure variation also can be compromised in right heart failure, decreased lung or chest wall compliance, and high .
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.
History and physical can often make the diagnosis of hypovolemic shock. For patients with hemorrhagic shock, a history of Injury or recent surgery is present. For hypovolemic shock due to fluid losses, history and physical should attempt to identify possible GI, renal, skin, or third-spacing as a cause of extracellular fluid loss.
Although relatively nonsensitive and nonspecific, physical exam can be helpful in determining the presence of hypovolemic shock. Physical findings suggestive of volume depletion include dry , decreased skin turgor, and low jugular venous distention. Tachycardia and hypotension can be seen along with decreased urinary output.
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.
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.
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.
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.
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. Follow-up analysis shows additional benefit to tranexamic acid when given in the first three hours after surgery.
Damage control resuscitation is to occur in conjunction with prompt intervention to control the source of bleeding. Strategies may differ depending on proximity to definitive treatment.
For patients in hemorrhagic shock, early use of 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. Antifibrinolytic 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.
Crystalloid fluid resuscitation is preferred over for severe volume depletion not due to bleeding. The type of crystalloid used to resuscitate the patient can be individualized based on the patients' chemistries, estimated volume of resuscitation, acid/base status, and physician or institutional preferences.
Isotonic saline is hyperchloremic relative to blood plasma, and resuscitation with large amounts can lead to 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. Patients in shock can appear cold, clammy, and cyanotic.
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.
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.
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.
Hypovolemia secondary to diarrhea and/or dehydration is thought to be predominant in low-income countries.
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