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Related to secondary shock: primary shock
Shock may be caused by dehydration, hemorrhage, sepsis, myocardial infarction, valvular heart disease, cardiac tamponade, adrenal failure, burns, trauma, spinal cord injury, hypoxia, anaphylaxis, poisoning, and other major insults to the body.
Shock results in failure of multiple organ systems, including the brain, heart, kidneys, lungs, skin, and gastrointestinal tract. Common consequences of shock are confusion, agitation, anxiety, or coma; syncope or presyncope; increased work of breathing; respiratory distress; pulmonary edema; decreased urinary output; and/or acute renal failure. Signs of shock include tachycardia, tachypnea, hypotension, and cool, clammy, or cyanotic skin.
Attempts to restore normal blood pressure and tissue perfusion include fluid resuscitation (in hypovolemic shock); control of hemorrhage (in shock caused by trauma or bleeding); administration of corticosteroids (in adrenal failure); pressor support (in cardiogenic or septic shock); the administration of epinephrine (in anaphylaxis); antibiotic administration with the drainage of infected foci (in sepsis); pericardiocentesis (in cardiac tamponade); transfusion; and oxygenation. Oral or parenterally administered sugars (typically glucose) can treat hypoglycemia caused by insulin, oral hypoglycemic drugs, or insulinomas.
The shock syndrome is a life-threatening medical emergency and requires very careful therapy and monitoring. If the patient does not respond at once, treatment and monitoring in the best facility available (such as intensive care unit) are essential. It is important that the ECG, arterial and central venous blood pressures, blood gases, core and skin temperatures, pulse rate, blood volume, blood glucose, hematocrit, cardiac output, urine flow rate, and neurological status be monitored on an ongoing basis (for example, hourly).
Patients at risk for shock include, but are not limited to, those with severe injuries, external or suspected internal hemorrhage, profound fluid loss or sequestration (severe vomiting, diarrhea, burns), allergen exposures, sepsis, impaired left ventricular function, electrical and thermal injuries (including lightning strikes), and diabetes (if receiving supplemental insulin).
One, two, or more large-bore intravenous catheters are inserted, and prescribed fluid therapy is initiated. External monitoring of vital signs is instituted; a pulmonary artery catheter may be placed or impedance cardiography instituted for precise hemodynamic monitoring; and an indwelling urinary catheter is inserted to track urine output hourly. Prescribed oxygen therapy is provided; SaO2, arterial blood gas levels (ABGs), and ventilatory function are monitored to determine the need for ventilatory support. If occult bleeding is suspected, stools and gastric fluids are tested, and injured tissues and spaces are carefully assessed or imaged. Routine measures are taken to reduce the risk of decubitus ulcers, muscular atrophy, deep venous thrombosis, delirium, and contractures. The patient is maintained in a normothermic environment for comfort. Radiant warmers are useful in preventing hypothermia in patients who cannot be kept clothed or covered during assessment and treatment. The environment is kept as calm and controlled as possible. Procedures and treatments are explained to the patient in a simple, clear, easily understandable manner.
Positioning is based on the particular shock type. Although hypovolemic shock states respond best to supine positioning, or even elevation of the feet and lower legs, cardiac and anaphylactic shock states require head elevation to ease ventilatory effort. Correct body alignment should be maintained, whatever the necessary position. Oral fluids are often withheld to prevent vomiting and aspiration. Oral care and misting are provided frequently to prevent dryness, stomatitis, sordes, and salivary obstructions. The patient's sensorium is closely assessed, and sensory overload is prevented as much as possible. Regular assessments are conducted for acute organ dysfunction, e.g., urine output below 0.5 ml/kg/hr, hypotension, hypoxemia, lactic acidosis, and low platelet count. While providing comfort measures and emotional support, the health care professional acts as a liaison to family members or significant others, providing them with information about the patient's status and the treatment regimen. If shock is irreversible, the family must prepare for the patient's death; family members are encouraged to be with, talk to, and touch the patient, and social work and mental health consultations or spiritual measures may be obtained for the patient and family as determined by their beliefs and desires.
The condition is the result of a type I allergic or hypersensitivity reaction during which the allergen is absorbed into the blood directly or through the mucosa. The most common agents are bee or wasp venoms, drugs (such as penicillins), and radiographic contrast media. It also can be triggered by severe food allergies (shellfish, peanuts) and by latex exposure. Individuals with a history of asthma, eczema, or hay fever are at increased risk. Chemical mediators released during the reaction cause constriction of the bronchial smooth muscle, vasodilation, and increased vascular permeability.
Initial symptoms include anxiety, tingling, itching, or warm feelings and skin rash, a metallic taste, swelling of lips and tongue, dyspnea, wheezing, vomiting, abdominal cramps, diarrhea, light-headedness, dizziness, and chest pain. Severe symptoms include acute respiratory distress, hypotension, edema, rash, tachycardia, pale cool skin, convulsions, and cyanosis. If no treatment is received, unconsciousness and death may result. Tissue swelling can be life-threatening if the larynx is involved, since air flow is obstructed with even minimal swelling.
A history of past allergic reactions, particularly to bee stings, drugs, blood products, or contrast media, is obtained. The at-risk patient is observed for reaction during and immediately after administration of any of these agents.
At the first sign of life-threatening respiratory distress, an airway is established, the appropriate physician is notified, and oxygen is administered by non–rebreather mask. Venous access is established. Epinephrine is administered, and diphenhydramine and corticosteroids are administered per protocol. Drugs should be administered intravenously if the patient is unconscious or hypotensive, and subcutaneously or intramuscularly if the patient is conscious and normotensive. Airway patency is maintained, and the patient should be observed for early signs of laryngeal edema, e.g., stridor, hoarseness, and dyspnea. Endotracheal intubation or a surgical airway may be necessary. In addition to high-concentration oxygen for all patients in shock, cardiopulmonary resuscitation and defibrillation, as indicated, are initiated if the patient becomes pulseless. The patient is assessed for hypotension and shock; circulatory volume is maintained with prescribed volume expanders, and blood pressure is stabilized with prescribed vasopressors. Blood pressure, central venous pressure, and urinary output are monitored in the hospital setting. Once the initial emergency has subsided, prescribed drugs for long-term management and inhaled bronchodilators for bronchospasm may be considered. The patient is taught to identify and avoid common allergens and to recognize an allergic reaction. Sensitivity testing may be advised to help determine offending allergens. If a patient is unable to avoid exposure to allergens and requires medication, an emergency kit should be kept readily available. Typically, this contains epinephrine in an auto-injector and liquid diphenhydramine. Both patient and family are instructed in its use. The patient with known serious allergies should wear an identifying bracelet or carry a card in his/her wallet. Patients with food allergies should be advised to read labels and to ask about food preparation and content when eating out. Individuals with insect sting allergies should avoid wearing bright-colored clothing, scented cosmetics, hairsprays, or perfumes that attract insects and should use insect repellant and wear closed shoes outdoors.
The patient is assessed for a history of any cardiac disorder that severely decreases left ventricular function, for anginal pain, dysrhythmias, reduced urinary output, respiratory effort and rate, blood pressure, pulse, dizziness, alterations in mental status, and perfusion of the skin. Signs of poor tissue perfusion include cold, pale, clammy skin; cyanosis; restlessness, mental confusion and obtundation; tachycardia; tachypnea; systolic blood pressure 30 mm Hg below baseline or below 80 mm Hg; and oliguria (urine output below 20 ml/hr). Heart sounds are auscultated for a gallop rhythm and murmurs, the lungs are checked for crackles and wheezes, and neck veins are assessed for distention.
Arterial blood gas values, electrolyte levels, cardiac rhythms, and hemodynamic values (pulmonary artery pressures, wedge pressures, and cardiac output) are monitored intensively. Echocardiography helps to determine left ventricular function and valve abnormalities. Treatment goals include enhancing cardiovascular status by increasing cardiac output, improving myocardial perfusion, and decreasing cardiac workload. Combinations of various cardiovascular drugs and mechanical assist techniques are used. Prescribed intravenous fluids are administered via a large-bore intravenous catheter (14 G to 18 G) according to hemodynamic patterns and urine output. Oxygen is administered by face mask or artificial airway to ensure adequate tissue oxygenation. Prescribed inotropic agents and vasopressors are administered and evaluated for desired effects and any adverse reactions.
Some patients will undergo emergent cardiac catheterization, coronary angioplasty, coronary stents, bypass surgery, or placement of intra-aortic balloon pumps, turbine pumps, or temporary or permanent ventricular assist devices. The ICU setting, special procedures, and equipment are explained to the patient and family to reduce their anxiety; a calm environment with as much privacy as possible and frequent rest periods are provided; and frequent family visits are permitted. All invasive sites are assessed for infection and/or hematomas. When the patient’s hemodynamic stability is restored, he/she is gradually weaned from supportive mechanical devices and drug therapies. The family is prepared for the possibility of a fatal outcome and assisted to find effective coping strategies.
Whether or not an electric shock will cause death is influenced by the pathway the current takes through the body, the amount of current, and the skin resistance. Thus, a very small amount of electrical energy applied directly to the heart may be enough to stop it from beating or to trigger ventricular fibrillation.
Burns, loss of consciousness, and/or cardiac arrest are symptoms of electrical injury.
The patient should be freed carefully from the current source by first shutting off the current. Prolonged support in a critical care unit may be needed.
All unconscious patients should be treated for presumptive hypoglycemia with an injection of D50. Once the patient is conscious, glucose is given by mouth to attain the desired glucose level. The rescue therapy is followed by a carbohydrate and protein snack to maintain the desired level.
The stabilized patient's immediate past history should be reviewed, looking for triggering factors. The patient and family can then be taught ways to avoid such situations in the future or to manage them before hypoglycemia again becomes this serious. If insulin levels need to be adjusted, the patient's preprandial glucose levels for the preceding 24 hr must be reviewed. The patient and family are assisted in processing the event. Their treatment actions are given positive reinforcement, correcting any errors such as inability to recognize early symptoms of insulin shock, overcorrection of insulin deficiency, or use of food products that are absorbed too slowly.
insulin shockHypoglycemic shock.
oligemic shockHypovolemic shock.
secondary shockDeferred shock.
Organisms and released endotoxins or exotoxins initiate a systemic inflammatory response. Chemical mediators of inflammation and the cell-mediated immune response (esp. tumor necrosis factor and interleukin 1) cause the physiological changes to septic shock. Initially, vasodilation, increased capillary permeability, and movement of plasma out of blood vessels produce hypovolemia and hypotension. Compensatory vasoconstriction occurs in an effort to maintain blood flow to vital organs. As sepsis progresses, secondary inflammatory mediators are released, increasing vascular endothelial damage.
Selective vasoconstriction produces tissue hypoxia and single or multiple organ dysfunction. Tissue hypoxia is increased by abnormal stimulation of the coagulation and kinin cascades in the capillaries, which produce microthrombi. Within the lung, damage to the capillary endothelium may cause adult respiratory distress syndrome. Septic shock often progresses to multiple organ dysfunction syndrome (MODS), which is the most common cause of death in surgical intensive care units.
Confusion and other alterations of consciousness are common symptoms. Signs include hypotension, fever, tachypnea, tachycardia, decreased urinary output, and cold, clammy skin. Laboratory studies reveal acidosis and, sometimes, renal failure or coagulopathies.
Empiric therapy with an extended-spectrum penicillin (such as ticarcillin/clavulanate, piperacillin/tazobactam) or third-generation cephalosporin (such as ceftriaxone), plus clindamycin or metronidazole, provide antibiotic coverage until an organism from the primary site of infection is positively identified. Intravenous resuscitation and if necessary, vasopressors such as dopamine or norepinephrine are used to stabilize blood pressure. Activated drotecogin alfa, a recombinant form of human activated protein C (Xigris) is occasionally effective. Oxygen and other supportive interventions are used to minimize organ damage. Maintaining blood glucose levels between 80 and 110 mg/dl improves chances of survival significantly. Use of corticosteroids is not supported by research.
Intensive care measures are instituted to monitor blood pressure, fluid and electrolyte balance, renal function, and changes in neurological status. Assessment of progressive agitation or confusion should emphasize the possibility of hypoxia. Routine measures to reduce the risk of decubitus ulcers, muscle atrophy, and contractures are needed. Repeated teaching is necessary for family members to understand the severity of the infection, the purpose of interventions, signs of improvement, and the possibility of death.
Cerebral injury: Shock from concussion of the brain secondary to cranial contusion or fracture or spontaneous hemorrhage. The shock may be evident immediately or later due to edema or delayed intracranial hemorrhage. Chemical injury: Shock due to physiological response to tissue injury, such as fluid mobilization, toxicity of the agent, and reflexes induced by pain due to the effect of chemicals, esp. corrosives. Crushing injury: Shock caused by disruption of soft tissue with release of myoglobulins, hemorrhage, and so forth, generally proportional to the extent of the injury. Fracture (esp. open fracture): Shock due to blood loss, fat embolism, and the physiological effects of pain. Heart damage: Shock caused by myocardial infarction, myocarditis, pericarditis, pericardial tamponade, or direct trauma with ensuing cardiovascular effects. Inflammation: Shock caused by severe sepsis, for example, peritonitis due to release of toxins affecting cardiovascular function and significant fluid mobilization. Intestinal obstruction: Shock caused by respiratory compromise due to distention, fluid mobilization, release of bacterial toxins, and pain. Nerve injury: Shock caused by injury to the area controlling respirations (e.g., high cervical cord injury) or to highly sensitive parts, such as the testicle, solar plexus, eye, and urethra, or secondary to cardiovascular reflexes stimulated by pain. Operations: Shock that may occur even after minor operations and paracentesis or catheterization due to rapid escape of fluids resulting in abrupt alteration of intra-abdominal pressure dynamics and hemorrhage. Perforation or rupture of viscera: Shock resulting from acute pneumothorax, ruptured aneurysm, perforated peptic ulcer, perforation of appendicial abscess or colonic diverticulum, or ectopic pregnancy. Strangulation: Shock resulting from strangulated hernia, intussusception, or volvulus. Thermal injury: Shock caused by burn, frostbite, or heat exhaustion secondary to fluid mobilization due to the physiological effects of pain. Torsion of viscera: Shock caused by torsion of an ovary or a testicle secondary to the physiological effects of pain.