SHOCK Shock is a life-threatening medical condition as a result of insufficient blood flow throughout the body.

. Shock often accompanies severe injury or illness. Medical shock is a medical emergency and can lead to other conditions such as lack of oxygen in the body's tissues (hypoxia), heart attack (cardiac arrest) or organ damage. It requires immediate treatment as symptoms can worsen rapidly. Medical shock is different than emotional, or psychological, shock that can occur following a traumatic or frightening emotional event.

Septic shock results from bacteria multiplying in the blood and releasing toxins. Common causes of this are pneumonia, intra-abdominal infections (such as a ruptured appendix) and meningitis. Anaphylactic shock is a type of severe hypersensitivity or allergic reaction. Causes include allergy to insect stings, medicines or foods (nuts, berries, seafood), etc. Cardiogenic shock happens when the heart is damaged and unable to supply sufficient blood to the body. This can be the end result of a heart attack or congestive heart failure. Hypovolemic shock is caused by severe blood and fluid loss, such as from traumatic bodily injury, which makes the heart unable to pump enough blood to the body. Neurogenic shock is caused by spinal cord injury, usually as a result of a traumatic accident or injury.

What are the causes of shock? There are several main causes of shock: Heart conditions (heart attack, heart failure) Heavy internal or external bleeding, such as from a serious injury Dehydration Infection (septic shock) Severe allergic reaction (anaphylactic shock) Spinal injuries (neurogenic shock) Burns Persistent vomiting or diarrhea

What are the signs and symptoms of shock? Low blood pressure and rapid heart rate (tachycardia) are the is the key signs of shock. Symptoms of all types of shock include: Rapid, shallow breathing Cold, clammy skin Rapid, weak pulse

Dizziness or fainting Weakness

Depending on the type of shock the following symptoms may also be observed: Eyes appear to stare Anxiety or agitation Seizures Confusion or unresponsiveness Low or no urine output Bluish lips and fingernails Sweating Chest pain

1. 2. 3. 4.

Hypovolemic shock is an emergency condition in which severe blood and fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working. Hypovolemic shock reduces CO and causes inadequate tissue perfusion from loss of circulating blood volume. Inadequate tissue perfusion resulting from markedly reduced circulating volume. Surgical patients are at high risk because of blood loss intraoperatively and trauma from the manipulation of body tissue.

B. Causes 1. Hemorrhage 2. Burns 3. Dehydration 4. Trauma C. Assessment findings 1. Systolic blood pressure less than 90 mm Hg or 30 mm Hg less than baseline values 2. Rapid weak pulse 3. Dyspnea 4. Tachypnea 5. Cool, clammy skin 6. Pallor 7. Extreme thirst 8. Irritability 9. Urine output less than 30mL/hr D. Diagnostic test findings 1. Chest X-ray: pulmonary lesions and areas of atelectasis 2. ABG measurements: respiratory alkalosis progressing to combined respiratory and metabolic acidosis; hypoxemia

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Serum chemistries: increased BUN, alkaline phosphatase, creatinine, lactate, and potassium levels; decreased HCO3, and albumin levels 4. CBC: increased hematocrit (HCT) levels E. Patient care management goal: restore the circulating blood volume 1. Assess and document continuous ECG rhythm; vital signs; mental status; heart, lung, and bowel sounds; urine output; and any signs and symptoms indicating changes in these parameters 2. Administer fluids (lactated Ringers solution or normal saline solution) to correct fluid deficit 3. Obtain ABG measurements and monitor for hypoxemia and acid-base imbalance; monitor SaO2 with a pulse oximeter 4. If a pulmonary artery catheter is in place, assess the patients fluid volume and document CVP, PAP, PAWP, CO, and SVR as ordered 5. Weigh the patient daily, at the same time and on the same scale with patient wearing the same amount of clothing, to evaluate fluid balance 6. Administer oxygen at a flow rate based on the patients clinical condition to relieve ischemia 7. If gas exchange is inadequate, prepare the patient and equipment for intubation

Hemorrhage is a major cause of hypovolemic shock. However, plasma loss/ dehydration and interstitial fluid accumulation (third spacing) adversely reduce circulating volume by decreasing tissue perfusion. The primary defect is decreased preload. Four classifications of hypovolemic shock based on the amount of fluid and blood loss: Class I: <750 ml, or ? 15% total circulating volume. Class II: 750 to 1000 ml, 05 15% to 30% total circulating volume Class III: 1500 to 2000 ml, or 30% to 40% total circulating volume Class IV: >2000 ml, or > 40% total circulating volume. The patients compensatory response intensifies as the percent of blood loss is increases. Signs And Symptoms Depends on the degree of blood loss and compensatory response. Physical Examination Appearance Anxiety progressing to coma Vital signs Blood pressure normal to unobtaionable Palpable radial pulse reflects systolic blood pressure of 80 mm Hg Palpable femoral pulse reflects systolic blood pressure of 70 mm Hg Palpable carotid pulse reflects systolic blood pressure of 60 mm Hg HR normal to > 140 beats/min RR normal to > 35 breaths/ min Cardiovascular Weak Thready pulse Pulmonary Deep or shallow rapid respirations Lungs usually clear Skin Cool, clammy skin, pale color Delayed/ absent capillary refill

Lips cyanotic (late sign)

Acute Care Patient Management Nursing Diagnosis: Ineffective tissue perfusion related to blood loss and hypotension. Outcome Criteria Patient alert and oriented Skin warm and dry Peripheral pulses strong Urine output 30 ml/hr or 0.5 to 1 ml/kg/hr Hct 32% Systolic blood pressure 90 to 120 mm Hg Mean arterial pressure 70 to 105 mm Hg Cardiac index 2.5 to 4 l/min/m2 O2 sat ?95 % Patient Monitoring 1. Monitor BP continuously via arterial cannulation because cuff pressures are less accurate in shock states. 2. Obtain cardiac output and cardiac index at least every 8 hours or more frequently to evaluate the patients response to changes in therapy. 3. Monitor peripheral artery pressures and central venous pressure hourly or more frequently to evaluate the patients response to treatment. 4. Continuously monitor ECG to detect life-threatening dysrythmias of HR > 140 beats/min, which can adversely affect SV. 5. Monitor hourly urine output to evaluate renal perfusion. 6. Measure blood loss if possible. Patient Assessment 1. Obtain vital signs every 15 minutes to evaluate the patients response to therapy and to detect cardiopulmonary deterioration. 2. Assess level of consciousness, mentation, skin temperature, and peripheral pulses to evaluate tissue perfusion. 3. Assess for pressure ulcer development. Diagnostic Assessment 1. Review Hgb and Hct levels and note trends. Decreased RBCs can adversely affect oxygen carrying capacity. 2. Review lactate levels, an indicator of reduced tissue perfusion and anaerobic metabolism. 3. Review ABGs for hypoxemia and respiratory or metabolic acidosis. 4. Review BUN, creatinine, and electrolytes and more trends to evaluate renal function. Patient Management 1. Use a large bore (16 to 18 gauge) cannula for intravenous lines to replace volume rapidly. 2. Administer blood products or autotranfuse as ordered. 3. Administer colloids and crytalloids in addition to blood products as ordered. 4. Pharmacologic agents may be used to improve hemodynamic parameters if intravascular volume is replaced. 5. Provide oxygen as ordered. 6. Prepare the patient for surgical intervention is required. 7. Institute pressure ulcer prevention strategies.

Cardiogenic shock is the inability to meet the metabolic needs due to severely impaired contractility of either ventricle. That leads to decreased tissue perfusion and a shock like state. Risk factor includes prior myocardial infarction, advanced age, female, diabetes, or anterior wall myocardial infarction. The most common cause of cardiogenic shock are acute Myocardial infarction, ventricular septal defect, acute mitral regurgitation, cardiac tamponade,aortic dissection, massive pulmonary infarct, and severe dysrhythmias. Signs and Symptoms Pale, cool and clammy skin Pulmonary congestion and hypoxemia worsen as the ventricles fail to eject adequate volume and the blood backs up into the lung. Tissue hypoperfusion continues because the oxygen does not meet the metabolic needs. Physical Examination Appearance Restlessness progressing to unresponsiveness Chest pain Dysrhythmias Vital signs HR: >100 beats/min BP: <80 mm Hg RR: > 20 breaths/min Neurologic Agitation Restlessness progressing to unresponsiveness, and changes in level of consciousness. Cardiovascular Weak thready pulses Rhythm may be irregular Pulmonary Orthopnea Crackles Cough with increased secretions. Acute Care Patient Management Nursing Diagnosis: Impaired gas exchange related to increased left ventricular diastolic pressure (LVEDP) and pulmonary edema associated with severe left ventricular (LV) dysfunction. Outcome Criteria Patient alert and oriented Pao2 80 to 100 mm Hg pH 7.35 to 7.45 Paco2 35 to 45 mm Hg O2 sat ?95 % RR 12 to 20 breaths/min, eupnea Lungs clear to auscultation Nursing Interventions Patient Monitoring 1. Continuously monitor oxygenation status with pulse oximetry. 2. Monitor for desaturation in response to nursing intervention. 3. Monitor ECG for dysrhythmias caused by hypoxemia, electrolyte imbalances, or ventricular dysfunction.

4. Monitor fluid volume status. Patient Assessment 1. Obtain HR, RR, and BP every 15 minutes to evaluate the patients response to therapy and detect cardiopulmonary deterioration. 2. Assess the patients respiratory status. The use of accessory muscles and inability to speak suggest worsening pulmonary congestion. 3. Assess for excess fluid volume, which can further compromise myocardial function. Diagnostic Assessment 1. Review ABGs for decreasing trend in Pao2 (hypoxemia) or pH (acidosis). These conditions can adversely affect myocardial contractility. 2. Review serial chest radiographs to evaluate the patients progress or a worsening lung condition. Patient Management 1. Provide supplemental oxygen as ordered. If the patient develops respiratory distress, be prepared for intubation and mechanical ventilation. 2. Administer low-dose morphine sulfate as ordered to reduce preload in an attempt to decrease pulmonary congestion. 3. Minimize oxygen demand by maintaining bed rest and decreasing anxiety, fever, and pain. 4. Position the patient for maximum chest excursion and comfort. 5. Administer diuretics and /or vasodilators as ordered to reduce circulating volume and decrease preload.

Septic shoc Septic shock is a serious condition that occurs when an overwhelming infection leads to life-threatening low blood pressure. Causes Septic shock occurs most often in the very old and the very young. It also occurs in people who have other illnesses. Any type of bacteria can cause septic shock. Fungi and (rarely) viruses may also cause the condition. Toxins released by the bacteria or fungi may cause tissue damage, and may lead to low blood pressure and poor organ function. Some researchers think that blood clots in small arteries cause the lack of blood flow and poor organ function. The body also produces a strong inflammatory response to the toxins. This inflammation may contribute to organ damage. Risk factors for septic shock include: Diabetes Diseases of the genitourinary system, biliary system, or intestinal system Diseases that weaken the immune system such as AIDS Indwelling catheters (those that remain in place for extended periods, especially intravenous lines and urinary catheters and plastic and metal stents used for drainage) Leukemia Long-term use of antibiotics Lymphoma

Recent infection Recent surgery or medical procedure Recent use of steroid medications

Symptoms Septic shock can affect any part of the body, including the heart, brain, kidneys, liver, and intestines. Symptoms may include: Cool, pale extremities High or very low temperature, chills Lightheadedness Low blood pressure, especially when standing Low or absent urine output Palpitations Rapid heart rate Restlessness, agitation, lethargy, or confusion Shortness of breath Skin rash or discoloration

Exams and Tests Blood tests may be done to check for infection, low blood oxygen level, disturbances in the body's acid-base balance, or poor organ function or organ failure. A chest x-ray may show pneumonia or fluid in the lungs (pulmonary edema). A urine sample may show infection. Additional studies, such as blood cultures, may not become positive for several days after the blood has been taken, or for several days after the shock has developed. Treatment Septic shock is a medical emergency. Patients are usually admitted to the intensive care unit of the hospital. Treatment may include: Breathing machine (mechanical ventilation) Drugs to treat low blood pressure, infection, or blood clotting Fluids given directly into a vein (intravenously) Oxygen Surgery

There are new drugs that act against the extreme inflammatory response seen in septic shock. These may help limit organ damage.

Hemodynamic monitoring -- the evaluation of the pressures in the heart and lungs -- may be required. This can only be done with special equipment and intensive care nursing

Neurogenic shock occurs after an injury to the spinal cord. Sympathetic outflow is disrupted resulting in unopposed vagal tone. The major clinical signs are hypotension and bradycardia. Acute spinal cord injury is most commonly seen with blunt trauma accounting for approximately 85 to 90 percent of cases. The most commonly affected area is the cervical region, followed by the thoracolumbar junction, the thoracic region, and the lumbar region. Neurogenic shock must be differentiated from spinal shock. Spinal shock is defined as temporary loss of spinal reflex activity occurring below a total or near-total spinal cord injury. CLINICAL FEATURES

Patients are generally hypotensive with warm, dry skin. The loss of sympathetic tone may impair the ability to redirect blood flow from the periphery to the core circulation leading to excessive heat loss and hypothermia. Bradycardia is a characteristic finding of neurogenic shock; however, it is not universally present. These symptoms can be expected to last from one to three weeks.

The anatomic level of the injury to the spinal cord impacts the likelihood and severity of neurogenic shock. Injuries above the T1 level have the capability of disrupting the spinal cord tracts that control the entire sympathetic system. Injuries occurring in the levels from T1 to L3 may only partially interrupt the sympathetic outflow. The higher the level of injury the more likely it is for the patient to exhibit severe symptoms. Neurogenic shock may be present with both complete and incomplete spinal cord lesions. The initial presentation represents the acute traumatic injury to the cord. However, a secondary cord injury may evolve over the first few days to weeks following the initial injury. The secondary cord injury is thought to be a result of ischemia to the spinal cord and may lead to a higher level of dysfunction than originally present or to an incomplete injury becoming a complete lesion. DIAGNOSIS AND DIFFERENTIAL

The diagnosis of neurogenic shock should be one of exclusion. Neurogenic shock must be differentiated from other types of shock, particularly hypovolemic. When dealing with a trauma patient, one must always assume that any hypotension is a result of ongoing blood loss. A patient suffering from neurogenic shock may also have concomitant injuries which may contribute to hemodynamic instability. Clinical clues such as hypotension, bradycardia, neurologic dysfunction, and warm, dry skin may lead the clinician to suspect neurogenic shock;

however, only after other injuries have been identified and treated can the diagnosis of neurogenic shock safely be made.

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The initial evaluation and care of the patient with potential neurogenic shock is the same as for all trauma patients, that is, rapid identification and stabilization of life-threatening injuries. 1. 2. Airway control should be insured with spinal immobilization and protection. Crystalloid IV fluids should be infused to maintain a mean arterial blood pressure above 70 torr. To prevent excessive fluid administration, a pulmonary artery catheter may be placed to monitor hemodynamic response. If fluid resuscitation is inadequate to insure organ perfusion, inotropic agents such as dopamine 2.5 to 20.0 g/kg per min and dobutamine 2.0 to 20.0 g/kg per min may be added to improve cardiac output and perfusion pressure. The doses should be titrated to the appropriate clinical response. 3. If necessary, severe bradycardia may need to be treated with atropine 0.5 to 1.0 mg IV (every 5 min for a total dose of 3.0 mg) or with a pacemaker. 4. In the presence of neurologic deficits, high-dose methylprednisolone therapy should be instituted within 8 h of injury. A 30 mg/kg bolus should be administered over 15 min followed by a continuous infusion of 5.4 mg/kg per h for the next 23 h. 5. Trauma surgery, neurosurgery, and orthopedic consultation should be obtained and arrangement made for transfer if necessary. ANAPHYLACTIC SHOCK Anaphylaxis is a severe allergic reaction that occurs rapidly and causes a life-threatening response involving the whole body. This reaction can lead to difficultybreathing and shock ultimately leading to death. For an anaphylactic reaction to occur, you must have been exposed in the past to the substance that causes the reaction, called the antigen. This is called "sensitization." A bee sting, for example, may not cause an allergic reaction the first time. Another bee sting may produce a sudden, severe allergic reaction known as anaphylaxis or anaphylactic shock. These reactions usually occur within seconds to minutes of exposure. Occasionally, they are delayed. You may develop sensitivity and anaphylaxis to a substance that you have been exposed to many times in the past without a reaction, and often people don't recall the previous exposure. Severe Allergic Reaction Causes

An anaphylactic reaction occurs when the body's immune system overreacts to an antigen, which it recognizes as an "invader" or foreign substance. The body's white blood cells produce substances called antibodies as a reaction to that antigen. The antibodies circulate in the bloodstream and attach themselves to certain cells in the body. o o In an allergic reaction, the antibody is called immunoglobulin E, or IgE. When the antibodies come in contact with the antigen, they signal other cells to produce certain chemicals called "mediators." Histamine is an example of a mediator. The effects of these mediators on organs and tissues of the body cause the symptoms of the reaction. Triggers of anaphylaxis include many substances. Only a trace amount of thetrigger may be needed to cause a severe reaction. Triggers of allergic reactions, including anaphylaxis, may include: o o Prescription and over-the-countermedications (see Drug allergy) Venom of stinging insects such as yellow jackets, bumble bees, honey bees, wasps, fire ants(see Allergy: Stinging Insect Venom) Foods, especially high-protein foods - most commonly, shellfish, fish, nuts, fruit, wheat, milk, eggs, soy products (see Food allergy) Food additives, such as sulfites Transfusion of blood or blood products Numerous other substances such as latex (natural rubber) Dyes and contrast materials used during radiologic procedures or tests Sometimes the trigger of the reaction is obvious--a bee sting, or a newprescription drug. Often, however, the trigger is unknown. People with asthma, eczema, or hay fever are slightly more likely to have an anaphylactic reaction than people who do not have these conditions. The first priority in the emergency department is to protect the airway (breathing) and maintain adequate blood pressure. The emergency team will make sure that your airway is open and that you are getting adequate oxygen. Oxygen may be given through tubes into the nose or by face mask.

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In severe respiratory distress, mechanical ventilation may be required. In this situation, a tube is placed via the mouth into the air passages to keep the airway open. The tube is connected to a ventilator( providing oxygen directly into the lung )

In rare cases, a simple surgery is performed to open an airway. If blood pressure is dangerously low, medication to increase blood pressure will be given.

An intravenous (IV) catheter may be inserted This is used to give saline solution to help boost blood pressure. The IV line may also be used to give medication. You may need to be admitted to the hospital for further monitoring and treatment. Medications

Epinephrine - Given in severe allergic reactions, epinephrine is extremely effective and fast-acting; it acts by constricting blood vessels, which increases blood pressure, and widening the airway. Epinephrine is given by injection into themuscle, through an IV line, or by injection under the skin. H1-receptor blockers/antihistamines - Usually diphenhydramine (Benadryl); these drugs do not stop the reaction but relieve some of the symptoms. They may be given by IV, by injection in the muscle, or by mouth Inhaled beta-agonists (albuterol) - Used to treat bronchospasm (spasms in the lung) and dilate the airways; inhaled H2-receptor blockers - Usually cimetidine(Tagamet); given by IV or by mouth Corticosteroids (examples are prednisone, Solu-Medrol) - These drugs help decrease the severity and recurrence of symptoms; may be given orally, injected in muscle, or by IV line If low blood pressure does not improve, additional medications, such as dopamine, may be given.