Circulatory collapse shock

Signs and symptoms of inhalational anthrax follow a biphasic course. The initial phase is characterized by fever, malaise, and unproductive cough characteristic of an upper respiratory infection. Following this flu-like phase, the patient will typically recover after 2-4 days. The second phase proceeds rapidly with the following constellation of signs and symptoms acute dyspnea, pleural effusion, fever, progressively worsening respiratory failure, cyanosis, circulatory collapse, shock, and death, if left untreated. 

One of the most catastrophic accidents occurring after delivery is DIG related to amniotic fluid embolism (AFE). This condition manifests with an acute onset of respiratory failure, circulatory collapse, shock, and thrombohemorrhagic syndrome. In the United States, DIG accounts for about 10% of all maternal deaths. Exaggerated uterine contraction caused by oxytocin, caesarean section, uterine rupture or premature separation of the placenta are risk factors for AFE. Pathophysiology of AFE may be related to lacerations on the membrane from the placenta that provides a portal entry for amniotic fluid into the maternal venous sinuses in the uterus [16]. 

Severe dehydration leading to hypotension and shock (circulatory collapse). Hypovolemia may not be responsive to intravenous hydration and may require the use of vasopressors. 

As a bacterial protein, streptokinase is viewed by the human immune system as an antigenic substance. In some cases, its administration has elicited allergic responses that have ranged from mild rashes to more serious anaphylactic shock (an extreme and generalized allergic response characterized by swelling, constriction of the bronchioles, circulatory collapse and heart failure). 

In a study of the mechanism whereby BordeteUa pertussis vaccine increased acute ozone toxicity in rats, Thompson ascribed the effects to /3-adrenergic blockade, and not to an immune-mediated response. It was further noted that both atropine and reserpine reduced mortality, whidi suggested that the acute lethal effects of ozone were due to shock and circulatory collapse, rather than pulmonary edema. 

The absorption of drugs in solution from intramuscular and subcutaneous sites of injection is limited by the perfusion rate. Failure to recognize this important concept has resulted in patient death. For example, morphine sulfate is often administered subcutaneously in a dose of 10 mg per 70 kg of body weight. This dose is sufficient to produce analgesia in 70% of patients with moderate to severe pain. However, in the setting of circulatory collapse and shock (e.g., septic shock in bacteremia due to release of endotoxin) in which the peripheral circulation may be impaired, morphine is not absorbed. Cases have been reported in which the lack of analgesia prompted the additional injection of morphine, all of which remained at the injection site and in the subcutaneous capillary bed. When the peripheral circulation improved, the massive amount of morphine that had collected became absorbed and death ensued, which was primarily due to respiratory depression. 

During acute stress, such as in shock or with septicemia, there is a rapid rise in circulating HA.69-72 Such HA may function as a volume expander, as a survival mechanism to prevent circulatory collapse. Some of this rapid rise in HA represents HA recruited from interstitial stores and from lymphatics, and not entirely a reflection of increased synthesis or decreased degradation.73 However, higher plasma levels of HA do correlate with decreased turnover rates, the ty2 reaching 20 to 45 min in situations of acute stress. 

Severe immediate hypersensitivity reactions (tjrpe 1), sometimes accompanied by anaphylactic shock and circulatory collapse, have been described very rarely (1). AUergic reactions of the Arthus phenomenon type, characterized by local swelling and necrosis following less than 24 hours after immunization, have occurred in rare instances. Some of these cases have been fatal. 

Under conditions of severe stress, such as extensive blood loss, bums [182], massive trauma or surgery, shock, and septicemia [183], HA levels in the circulation increase dramatically. The HA may function as an emergency molecule, a naturally occurring volume expander to prevent or delay circulatory collapse. 

Small children treated with topical lidocaine 2% for teething five to six times daily for a week developed seizures. Patients being managed for several days with lidocaine for control of acute arrhythmias may accumulate lidocaine and its metabolites if they have changes in blood flow (e.g., shock, circulatory collapse). Decreased clearance and accumulation of lidocaine and desmethyllidocaine may result in the development of drowsiness, tinnitus, muscle twitching, and may eventually lead to seizures, coma, and arrhythmias. 

Do not give IM or IV. Violent cholinergic reaction (circulatory collapse severe hypotension, bloody diarrhea, shock, cardiac arrest) will occur. Antidote 0-0.6-1.2 mg atropine sulfate Give 1 hour before or 2 hour after meals. If patient complains of gastric pain, the drug may be given with meals. 

Acute myocardial infarction Congestive heart failure Shock and circulatory collapse... 

Selective loss of fluid from each of these compartments gives rise to distinct signs and symptoms. Intracellular lluid loss, for example, causes cellular dysfunction which is most notably evident as lethargy, confusion and coma. Loss of blood, an ECF fluid, leads to circulatory collapse, renal shutdown and shock. Loss of total body water will eventually produce similar effects. However, the signs of lluid depletion are not seen at first since the water loss, albeit substantial, is spread across both ECF and ICF compartments. 

Laboratory tests are important, but not more important than preventing circulatory collapse, which is inevitable in a client in hypovolemic shock, as this client is. 

Chronic exposure to low levels of inor-gaiuc mercuric compounds produces tremors, excess salivation, and psychological changes characterized by irritability and excitement. Collectively, this is often described as the mad hatter syndrome. Mercuric mercury (Hg +) is a potential toxic chemical, although it is poorly absorbed by the GI tract and other body parts. Accidental or suicidal ingestion of mercuric chloride or other mercuric salts produces corrosive ulceration, bleeding, necrosis of the intestinal tract, and are usually accompanied by shock and circulatory collapse. If the patient... 

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