Қан көлдемі және гиповолемиялық шок: себептері, белгілері және емдеуі

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. 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:
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.

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

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. or any other pathological condition that results in a massive inflammatory response.

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.

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.

Oxygen saturation by pulse oximetry (SpO2). Respiratory rate. Pulse rate. Arterial blood pressure. Pulse pressure. Central venous pressure. Urine output. Base deficit and/or lactic acid. Temperature. Mental state. Changes in the electrocardiogram.

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. 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.

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