Hypovolemic shock is a life-threatening condition that results when you lose more than 15 percent of your body’s blood or fluid supply and your heart function is impaired. It can occur due to any type of fluid loss, for example, as a result of dehydration or diarrhea. Show Severe fluid loss makes it difficult for the heart to pump enough blood to your body. As the fluid loss increases, hypovolemic shock can lead to organ failure. This requires immediate emergency medical attention. The symptoms of hypovolemic shock vary with the severity of the fluid loss. However, all symptoms of shock are life-threatening and need emergency medical treatment. Generally, symptoms may include:
You may experience pain in your abdomen or your chest. You may also experience some neurological symptoms like confusion, agitation, or lethargy (drowsiness), which occur due to decreased blood flow to the brain. Older adults are highly susceptible to shock, and children may not show symptoms of shock until they reach a more severe stage. Hypovolemic shock occurs in stages, and the symptoms may change as the condition progresses. The stages of the condition are: Class 1At this stage, you would be losing less than 15 percent of your blood volume, which is about 750 milliliters (mL). Your blood pressure and breathing will still appear normal, but you may begin to suddenly feel anxious and your skin may look pale. Class 2The blood volume loss in this stage ranges between 15 and 30 percent, which is typically 750 to 1,500 mL. Your heart rate and breathing may get faster. Your blood pulse pressure may narrow. Your systolic blood pressure (the top number in a blood pressure measurement) may still be normal. Your blood pressure at the beginning of this stage may still be normal, though the bottom number of the measurement, the diastolic pressure, may be high. Class 3At this stage, you lose 30 to 40 percent of your blood volume, which is between 1,500 and 2,000 mL. You’ll experience a major drop in your blood pressure and begin to see changes to your mental status. Your heart rate will rise above 120 beats per minute (bpm), your breathing will become faster, and you’ll see a decrease in the amount you urinate. Class 4Once you’ve experienced blood volume loss of more than 40 percent, your condition becomes critical. Your pulse pressure will be really low, and your heart will beat faster at more than 120 bpm. You may experience: Your mental status will be obviously abnormal, and you’ll stop urinating almost completely. You may experience external and internal bleeding from areas in your body. When the fluid loss occurs exclusively as a result of severe blood loss, a more specific term is used to describe the condition. This is called “hemorrhagic shock.” Depending on the location of the bleeding inside the body, the signs and symptoms may include: If you have any signs of hemorrhaging, you or someone near you must seek medical attention immediately. While some symptoms like abdominal pain and sweating can point to something less urgent like a stomach virus, you should seek immediate medical attention when seeing groupings of these symptoms together. This is especially true for the more serious symptoms. The longer you wait, the more damage can be done to your tissues and organs. Blood carries oxygen and other essential substances to your organs and tissues. When heavy bleeding or fluid loss occurs, there’s not enough blood in circulation for the heart to be an effective pump. This is hypovolemic shock. As you lose more fluid, you no longer have enough blood to effectively supply oxygen to your tissues. To make up for this, your body sends the remaining blood supply to the most important organs: the brain and the heart. This means the rest of the body is even more in need of oxygen, and your tissues respond by producing lactic acid. As a result, the body enters acidosis, which is when your body fluid contains too much acid. Without timely treatment, this can lead to death. If you are near someone else who is experiencing shock symptoms, do the following until first responders arrive:
Click here for information on how to perform CPR. Do not elevate their head. Remove any visible dirt or debris from the injury site. Do not remove embedded:
If the area is clear of debris and no visible object is sticking out from it, tie fabric, such as a shirt, towel, or blanket, around the site of injury to minimize blood loss. Apply pressure to the area. If you can, tie or tape the fabric to the injury. A lack of blood and fluid in your body can lead to the following complications: The effects of hypovolemic shock depend on the speed at which you’re losing blood or fluids and the amount of blood or fluids you’re losing. The extent of your injuries can also determine your chances of survival. Certain chronic medical conditions can increase the likelihood that you’ll experience more complications from hypovolemic shock. These may include: There are often no advance warnings of shock. Instead, symptoms tend to arise only when you’re already experiencing the condition. A physical examination can reveal signs of shock, such as low blood pressure and rapid heartbeat. A person experiencing shock may also be less responsive when asked questions by the emergency room doctor. Heavy bleeding is immediately recognizable, but internal bleeding sometimes is not found until you show signs of hemorrhagic shock. In addition to physical symptoms, your doctor may use a variety of testing methods to confirm that you’re experiencing hypovolemic shock. These include:
Your doctor may order other tests based on your symptoms. Once at a hospital, a person suspected of having hypovolemic shock will receive fluids or blood products via an intravenous (IV) line, to replenish the blood loss and improve circulation. Treatment revolves around:
Treatments may include: Doctors may also administer medications that increase the heart’s pumping strength to improve circulation and get blood where it’s needed. These include:
Antibiotics may be administered to prevent septic shock and bacterial infections. Close cardiac monitoring will determine the effectiveness of the treatment you receive. Hypovolemic shock is dangerous for everyone, but it can be particularly dangerous in older adults. Older adults tend to experience hypovolemic shock more commonly than their younger counterparts. As people age, they may have more health conditions that can reduce their tolerance to shock. Older people are also more likely to take anticoagulants, which are medications that help prevent blood clots. This means that if they go into hypovolemic shock, which then develops into hemorrhagic shock, they are at a higher risk of serious complications and even death. Recovery from hypovolemic shock depends on factors like the patient’s prior medical conditions and the degree of the shock itself. Those with milder degrees of shock may have an easier time recovering. If you progress to the third or fourth stage, severe organ damage can result. This makes it much harder to recover, and continued medical interventions may be needed. In severe cases, organ damage may be irreversible. Overall, your outlook will depend on the amount of blood you lost and the type of injury you sustained. The outlook is best in patients with good overall health who haven’t had severe blood loss.
Cardiogenic shock may also be observed during pregnancy. [34] The major cause of cardiogenic shock is severe valvular disease. In cardiogenic shock, the left ventricle is not able to pump sufficient blood to meet the metabolic demands of the tissues. The compensatory response is tachycardia, but eventually, hypervolemia, pulmonary venous congestion, and generalized edema occur. Inadequate oxygen delivery leads to cellular damage, multiorgan failure, and death. The clinical signs of cardiogenic shock are distended neck veins, dyspnea, tachypnea, the presence of a third heart sound, systolic or diastolic murmurs, and generalized edema. Peripartum cardiomyopathy is an idiopathic disorder that occurs during the last month of pregnancy and up to 6 months postpartum. The incidence of this disease is 1 case in 1500-4000 deliveries. The risk factors include old age, multiparity, twin gestation, and preeclampsia. Upon presentation, these patients have signs and symptoms of congestive heart failure. The mortality associated with peripartum cardiomyopathy is 25-50%. [35] This disease tends to recur in subsequent pregnancies. A small percentage of these patients are found to have inflammatory myocarditis after analysis of endomyocardial biopsy specimens. The treatment consists of diuretics, vasodilators for afterload reduction, digoxin, and careful follow-up. Inflammatory myocarditis may respond to immunosuppressive therapy. Postpartum patients may have a localized abscess, resistant organism, or septic pelvic thrombophlebitis. Patients with septic pelvic thrombophlebitis usually develop persistent fever; the diagnosis may be suggested by findings from a CT scan of the pelvis. Treatment consists of a broad spectrum of antibiotics and standard anticoagulation. Coronary artery disease is uncommon in reproductive-aged women, but myocardial infarction has occurred because of the excessive hemodynamic stress of pregnancy. Management of coronary artery disease in a pregnant patient is similar to that in a nonpregnant patient. Spontaneous coronary artery dissection, a rare event, causes myocardial ischemia and sudden death in younger age groups and especially postpartum women. The clinical presentation includes angina, myocardial infarction, cardiogenic shock, and death. No specific cardiac risk factors have been associated with its occurrence. In postpartum patients, the possible mechanism for dissection is thought to be pregnancy-induced degeneration of collagen and the additional stresses of parturition. The treatment is usually tailored to the individual patient's needs. Amniotic fluid embolism (AFE) is a catastrophic peripartum syndrome that manifests as a sudden onset of severe dyspnea, hypoxemia, hemodynamic collapse, coagulopathy, and seizures. AFE is a rare disorder, occurring in 1 case in 20,000-30,000 pregnancies, but it accounts for 10% of all maternal deaths. [36] AFE may occur at any point during pregnancy, labor, or delivery. Uterine manipulation or trauma may often precede AFE. Whether the pathogenesis occurs secondary to embolization of particulate cellular contents or secondary to humoral factors has not been established. An analysis of 46 verified cases of AFE had none of the previously cited predisposing factors: 12% of the cases occurred in women with intact membranes, 70% during labor, 11% after vaginal delivery, and 19% during cesarean delivery with or without labor. The fetal substance may initiate an anaphylactoid reaction, resulting in endogenous mediator release and causing hypotension, tachycardia, hypoxemia, and seizures. This may lead to pulmonary arterial vasospasm and transient pulmonary hypertension, followed by left ventricular failure, decreased cardiac output, and hydrostatic pulmonary edema. The acute left ventricular dysfunction may be caused by humoral mediators or cytokines contained in amniotic fluid released during the anaphylactoid reaction. AFE is extremely difficult to predict or prevent. Although most cases occur after the onset of labor, some may occur outside of labor. Respiratory distress and cyanosis occur suddenly within the first few minutes and are quickly followed by hypotension, pulmonary edema, shock, and neurologic manifestations, such as confusion, loss of consciousness, and seizures. More than 80% of patients experience cardiorespiratory arrest at the outset. Approximately 50% of patients do not survive this cardiopulmonary catastrophe, but of those who do, 40-50% develop coagulopathy and hemorrhage up to 4 hours later, and this may well be the first indication of AFE. Seizure activity may, at times, be the first manifestation. The diagnosis of AFE is based on a characteristic clinical picture. Treatment consists of oxygenation and hemodynamic support. Patients often require invasive monitoring to assess the adequacy of intravascular volume status and to guide inotropic therapy. Corticosteroids have been used, but their benefit has not been established. The mortality rate for AFE is high: 86% of patients may succumb to this disorder. Approximately 40% of cases have fetal death at the time of presentation, and placental abruption occurs in 50% of the cases. Management includes supportive measures and should begin emergently. The initial principles of dealing with obstetric emergencies include airway, breathing, and circulation. The 3 main goals of treatment are (1) oxygenation, (2) maintaining cardiac output and blood pressure, and (3) correcting coagulopathy. The fetus should be monitored continuously for signs of compromise. To ensure optimal uterine perfusion, the mother should be placed in the left lateral position. The first priority is resuscitation of the mother and administration of oxygen (100% concentration). The patient may need to be intubated and ventilated. The initiation of fluid therapy and the administration of pharmacologic agents to maintain optimal blood pressure and cardiac output is the next step. Volume replacement and therapy for left ventricular dysfunction should be directed toward improving inotropy. A clinical guideline is to maintain the systolic blood pressure at 90 mm Hg or higher, with acceptable organ perfusion, as indicated by a urine output of 25 mL/hr or more. Administration of blood transfusions and blood components is considered the first line of treatment for correcting coagulopathy associated with AFE. Intravenous steroids to treat underlying inflammatory response and similarities of AFE to anaphylaxis may be helpful. The risk of developing deep venous thrombosis (DVT) and pulmonary embolism (PE) increases markedly during the advanced stages of pregnancy and is greatest during postpartum. Rates of maternal mortality from PE have been reported at 2.6 cases per 100,000 live births in white females and 2.5-fold higher in black females. Incidence increases markedly following cesarean delivery, as compared to vaginal delivery. [37] The signs and symptoms of PE are more problematic because dyspnea and tachypnea are common in pregnancy. In nonpregnant patients, tachypnea, dyspnea, chest pain (pleuritic), apprehension, and crackles are present in only 50% or more of patients. Chest radiographic findings are abnormal in 80% or more of patients with PE, and the findings are nonspecific. Electrocardiographic findings are abnormal in 70% of patients with PE, but they are nonspecific. Arterial oxygen tension is low in most patients with PE. Objective diagnostic testing As with DVT, PE requires objective diagnostic testing to confidently confirm or exclude the diagnosis. This is particularly true in pregnancies, because the diagnosis of DVT or PE requires the following:
The first objective diagnostic test should be compression ultrasonography; if it is not available, impedance plethysmography is adequate. If findings from the noninvasive leg studies are negative, proceed to ventilation-perfusion lung scanning. Perfusion scanning alone is recommended initially, adding ventilation scanning when perfusion defects are noted. Pulmonary angiography might be necessary if lung scan findings are of low probability or indeterminate but clinical evidence is strong. Several studies show no increased risk of teratogenicity in patients undergoing radiologic procedures for the diagnosis of maternal venous thromboembolic disease. A complete and adequate evaluation to document the presence or absence of PE requires less than 0.005 Gy. Obtaining the appropriate diagnostic study in pregnancies is mandatory. Management Immediately treat patients, pregnant or not, in whom PE is strongly considered. Treatment is with intravenous unfractionated heparin, unless the patient has a high risk or contraindication to the use of any anticoagulants. Extensive clinical experience and cohort studies have established that heparin is the safest anticoagulant to use during pregnancy, because it does not cross the placenta. The initial loading dose should be 5000-10,000 U. Following loading, an infusion of 18 U/kg is started. Monitor and keep the activated partial thromboplastin time in the therapeutic range, which is 1.5-2 times the baseline value. Although data are relatively modest, low-molecular-weight heparin (LMWH), which does not cross the placenta, can be administered once a day and does not require monitoring. LMWH has not been shown to have an increased risk of bleeding with surgical procedures, including cesarean deliveries, in a small number of patients. In one report, dalteparin was used safely and effectively for prophylaxis in 47 women throughout their pregnancies. The recommended dose was 5000 U, once or twice daily, with a target trough plasma heparin level of 0.1-0.2 U/mL. However, data on the use of LMWH during pregnancy are limited; most come from diverse case series involving prophylaxis rather than therapy. These data provide no clear conclusions as to the efficacy and adverse effects of LMWH; no optimal dose regimen; and insufficient information on risks of obstetric, fetal, or neonatal problems. Additionally, cases of epidural hematoma have occurred after epidural anesthesia. Warfarin should be avoided throughout pregnancy because it can cause embryopathy characterized by mental retardation, optic atrophy, cleft lip, cleft palate, cataracts, and hemorrhage. The teratogenic effects are particularly common during the first trimester. Warfarin crosses the placenta; it can cause fetal and neonatal hemorrhage and placental abruption. Vena cava filters (Greenfield, stainless steel or titanium; bird's nest; Simon-Nitinol) are positioned within the infrarenal inferior vena cava to trap thrombi arising from the lower extremities. Patients with documented venous thromboembolic disease who have contraindications to anticoagulation therapy or in whom conventional therapy has failed are candidates for inferior vena cava filter placement. Vena cava filters and filter placement are associated with a favorable safety profile; however, both fatal and nonfatal complications have been reported. Fatal complications are rare, and most nonfatal complications are of minimal clinical significance. Duration of anticoagulation Patients who develop DVT or PE antepartum should receive anticoagulation therapy with heparin throughout pregnancy. After delivery, warfarin should be started; the heparin can be discontinued once an adequate international normalized ratio (INR) is achieved. Continue the warfarin for at least 6 weeks postpartum or until at least 3 months of anticoagulant therapy have been completed. Complications of treatment Osteopenia has been reported with unfractionated heparin administered for more than 6 months. No information is available about the beneficial effects of concomitant multivitamins, calcium, or vitamin D supplementation. The problem of osteopenia and osteoporosis might be less severe if LMWH is used, but providing optimum calcium and vitamin D supplementation to all patients receiving long-term heparin administration during pregnancy is reasonable. |