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Autor: anton 12 April 2011
Words: 979 | Pages: 4
Running head: SHOCK VS. SHOCK
Septic Shock Vs. Cardiogenic Shock
In APA Style
Rio Hondo College
Septic Shock Vs. Cardiogenic Shock
Septic shock is an extreme immune system response to an infection that has spread throughout the blood and tissues. Severe septic shock often causes extremely low blood pressure, which limits blood flow to the body and can result in organ failure and death.
Septic shock is most often the result of a bacterial infection, but it can also be caused by other types of infection. While septic shock can occur in people of any age, it is more common in infants, older adults, and people who have compromised immune systems. Respiratory failure, cardiac failure, or any other organ failure can occur.
Symptoms of Septic Shock
Symptoms of Septic shock include either fever, malaise, chills, and nausea. The first sign of shock is often confusion and decreased consciousness. In this beginning stage, the extremities are usually warm. Later, they become cool, pale, and bluish. Other symptoms include: shallow, rapid breathing, rapid heartbeat, delirium, palpitations, restlessness, agitation, lethargy, low blood pressure, especially when standing, reddish patches in the skin, lightheadedness, shortness of breath. Septic shock may progress to cause "adult respiratory distress syndrome," in which fluid collects in the lungs, and breathing becomes shallow and labored. This condition may lead to ventilatory collapse, in which the patient can no longer breathe adequately without assistance.
Cause of Septic Shock
Septic shock is seen most often in patients with suppressed immune systems, and is usually due to bacteria acquired during treatment at the hospital. The immune system is suppressed by drugs used to treat cancer, autoimmune disorders, organ transplants, and diseases of immune deficiency such as AIDS. Malnutrition, chronic drug abuse, and long-term illness increase the likelihood of succumbing to bacterial infection. Bacteremia is more likely with preexisting infections such as urinary or gastrointestinal tract infections, or skin ulcers, but can be introduced to the blood stream by surgical procedures, catheters, or intravenous equipment. Menstruating women using highly absorbent tampons are also at risk for Ð’â€˜toxic shock syndrome'. The incidence of toxic shock syndrome has declined markedly since this type of tampon was withdrawn from the market.
Diagnosis of septic shock is made by measuring blood pressure, heart rate, and respiration rate, as well as by a consideration of possible sources of infection. Blood pressure may be monitored with a catheter device inserted into the pulmonary artery supplying the lungs (Swan-Ganz catheter). Blood cultures are done to determine the type of bacteria responsible. The levels of oxygen, carbon dioxide, and acidity in the blood are also monitored to assess changes in respiratory function.
Signs and tests
Ð’Â· Blood gases revealing low oxygen concentration and acidosis
Ð’Â· Blood cultures or blood count detecting infection
Ð’Â· Low blood pressure
Ð’Â· Chest x-ray revealing pneumonia or pulmonary edema
Ð’Â· Blood tests detecting poor organ function or organ failure
Treatment of Septic Shock
Septic shock is a medical emergency, and patients are usually admitted to intensive care. Septic shock is treated with antibiotics, fluids, and medications to support blood pressure and prevent organ damage. The antibiotic is chosen based on the bacteria present, although two or more types of antibiotics may be used initially until the organism is identified. Intravenous fluids, either blood or protein solutions, replace the fluid lost by leakage. Coagulation and hemorrhage may be treated with transfusions of plasma or platelets. Dopamine may be given to increase blood pressure further if necessary. Respiratory distress is treated with mechanical ventilation and supplemental oxygen, either using a nosepiece or a tube into the trachea through the throat.
Hemodynamic monitoring -- the evaluation of the pressures in the heart and lungs -- may be required. There are new drugs that act against the hyperinflammatory response seen in septic shock. These may help limit the damage to vital organs.
Identification and treatment of the primary infection site is important to prevent ongoing proliferation of bacteria.
Prognosis of Septic Shock
Septic shock is most likely to develop in the hospital, since it follows infections, which are likely to be the objects of treatment. Because of this, careful monitoring and early, aggressive therapy can minimize the likelihood of progression. Nonetheless, death occurs in at least 25% of all cases. The likelihood of recovery from septic shock depends on many factors, including the degree of immunosuppression of the patient, underlying disease, promptness of treatment, and type of bacteria responsible. Mortality is highest in the very young and the elderly, those with persistent or recurrent infection, and those with compromised immune systems. Septic shock has a high death rate, exceeding 50%, depending on the type of organism causing the infection and the degree of organ failure.
Prevention of Septic Shock
The risk of developing septic shock can be minimized through treatment of underlying bacterial infections, and prompt attention to signs of bacteremia. In the hospital, scrupulous aseptic technique on the part of medical professionals lowers the risk of introducing bacteria into the bloodstream.
Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state. It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI). Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mental status, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min) with evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure (Hochman, 1999). Tissue hypoperfusion was defined as cold peripheries (extremities colder than core), oliguria (
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