Hypotensive shock

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

Anaphylaxis is the most dramatic and potentially catastrophic manifestation of allergic disorders. It can affect virtually any organ including the cardiovascular system. Cardiovascular collapse and hypotensive shock in anaphylaxis have been attributed to peripheral vasodilation, enhanced vascular permeability and plasma leakage, rather than any direct effect on the myocardium. However, there is increasing experimental and clinical evidence that the human heart is a site and target of anaphylaxis. 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

TNF (17.5) Monocyte/macrophage, lymphocyte, neutrophil, endothelium, fibroblast, keratinocyte Activation of T and B cells, natural killer cells, neutrophils, and osteoblasts. Stimulation of endothelial cells to release chemotactic proteins, NO and PGI2. Tumoricidal activity. Induces fever, sleep, hepatic acute phase protein synthesis, catabolism, ACTH release. Lead to myocardial depression, hypotension/shock, hypercoagulability, and death. Stimulates production of IL-1, IL-6, IL-8, IFN-y, and H202. Suppression of cytochrome P-450, thyroglobulin, and lipoprotein lipase. Induces complement activation, release of eicosanoids, including PAF. Procoagulant activity. 

There is evidence that y-aminobutyric acid A receptors may be modified during SE and become less responsive to endogenous agonists and antagonists. Two phases of GCSE have been identified. During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, and hypotension, shock, rhabdomyolysis, secondary hyperkalemia, and acute tubular necrosis may ensue. 

Hypertensive crisis Patients recovering from hypotension/shock Hypertension... 

It is used in hypotensive shock for the purpose of elevating blood pressure, which can result from spinal anesthesia, surgical complications, and head trauma. Synonyms of metaraminol are aramine, isophenylephrin, metaradine, and others. 

Other adverse events may include pancytopenia, aplastic anemia, neutropenia, leukopenia, thrombocytopenia, lymphopenia, leukocytosis, lymphadenopathy, coagulation disturbances, hypotension/shock, heart failure, angina/MI, tachycardia, bradycardia, tachypnea/hyperventilation, abnormal chest sounds, pneumonia/pneumonitis, rash, urticaria, pruritus, erythema, flushing, diaphoresis, diarrhea, bowel infarction, arthralgia, arthritis, blindness, blurred vision, diplopia, hearing loss, otitis media, tinnitus, vertigo, photophobia, conjunctivitis, nasal/ear stuffiness, and anuria/oliguria. 

Treatment and prevention of acute hypotension shock (associated with cardiac decompensation, Ml, open heart surgery, renal failure, or trauma), treatment of low cardiac output, treatment of CHF IV 1 mcg/kg/min up to 50 mcg/kg/min titrated to desired response. 

NO also seems to play a role in the hypotension of septic shock. Septic shock is a life-threatening clinical condition occurring as a complication of bacterial infections and characterized by hypotension, shock, organ failure, and death. In severe Gramnegative bacterial infections, increased urinary excretion of nitrates, an oxidative byproduct of NO, has been described bacterial wall lipopolysaccharides activate the NOS enzyme. 

Adverse effects include flushing, urticaria, hypotension, shock, tachypnoea, hypoxaemia, tachycardia, cardiac arrhythmias, convulsions, erythema, swelling, GIT disturbances, dysuria, fever, allergic skin rashes. Leg cramps on long term therapy and reversible ocular and auditory disturbances have also been reported. 

Nitroprusside Releases nitric oxide Powerful vasodilation Hypertensive emergencies Parenteral short duration Toxicity Excessive hypotension, shock... 

Beta blockers Bradycardia, hypotension, shock, Szs, bronchospasm (rare)... 

Embolism associated with long flights is generally due to thrombus formation in deep leg veins (deep-vein thrombosis, or DVT). The thrombus may move to the pulmonary circulation, where effects on lung function depend on the extent of the blockage produced. A massive embolus may occlude the main pulmonary artery, resulting in hypotension, shock and possibly death multiple small emboli cause little problem and are lysed by the fibrinolytic system. Sometimes surgical removal of the embolus is necessary, but in Pats/s case clot lysis was successful and she made an uneventful recovery. 

Q12 Stable angina usually subsides over several minutes when exercise is stopped and the patient s usual medication, such as GTN, is taken. Pain which does not diminish, accompanied by pallor, hypotension, shock, nausea and sweating, suggests there may be a coronary occlusion. 

Sedation, convulsions, extrapyramidal symptoms, coma, hypotension, shock, hypo/hyperthermla... 

Aspirin hypersensitivity is also a potential concern and can occur in two ways (1) a respiratory reaction, which is more profitimd in patients with rhinitis, asthma, or nasal polyps, or (2) a typical type I hypersensitivity reaction, including urticaria, wheals, angioedema, itching, rash, bronchospasm, laryngeal edema, hypotension, shock, or syncope. This latter response generally occurs within 1 hour of aspirin ingestion. Such aspirin intolerance may manifest itself in 4% to 19% of patients with asthma and may approach 40% of steroid-dependent asthmatics. 

The initial clinical review should include a search for known consequences of poisoning, which include impaired consciousness with flacddity (benzodiazepines, alcohol, trichloroethanol) or with hypertonia (tricyclic antidepressants, antimuscaiinic agents), hypotension, shock, cardiac arrhythmia, evidence of convulsions, behavioural disturbances (psychotropic drugs), hypothermia, aspiration pneumonia and cutaneous blisters, burns in the mouth (corrosives). 

After rapid intravenous administration hypotension, shock, and atrioventricular block can occur and can be fatal (2). The rate of infusion should not exceed 5 mg/minute. Qther adverse effects reported during intravenous infusion include sinus bradycardia (236), facial flushing, and thrombophlebitis (236-239). The risk of this last complication can be reduced by infusing the drug into as large a vein as possible and preferably via a central venous catheter, or perhaps by using a very dilute solution of the drug (240). 

In severe reactions, intravenous glucocorticoids are usually given on an empirical basis, with oxygen as required. Non-cardiogenic hypotensive shock usually responds best to fluid replacement, but vasopressors are occasionally required. Adrenaline is primarily... 

Most severe reactions to contrast media are associated with cardiovascular manifestations, causing hypotensive shock and in some cases ventricular fibrillation and cardiac arrest these events are reversible in most cases in which prompt treatment is given. In a case of hypotensive collapse reported in 1977, and followed by a small number of others, there was disseminated intravascular coagulation (50). In milder cases there is only hypotension, which can be transient and symptomless in some cases there is bradycardia (due apparently to vagal overactivity) rather than tachycardia. 

Acute intoxication with phenylbutazone is dominated by metabolic acidosis, which can progress to coma, seizures, hypotension, shock, and oliguria. Kidney and liver reactions, acute bone marrow depression, and acute perforation of peptic ulcer have all been described (5,11,35). 

Severe anaphylaxis has been reported in two patients with infected wounds that had been treated with topical rifamycin for several months (82). There was urticaria, angioedema, and hypotension in one case, and urticaria, wheezing, dyspnea, and hypotensive shock in the other. In both cases, prick tests with 10% rifamycin solution were positive, while there were no positive reactions in 20 controls. 

Vaccines administered parenterally are not weU tolerated. Severe local pain and/or swelling occurred in 6-40% of vaccinees systemic reactions have been reported in 9-30% (headache), and in 14-29% (fever) 13-24% of vaccinees missed work or school due to adverse effects. More severe reactions (hypotension, shock) have been reported sporadically (1). 

Initial pain at the site of the bite may be followed with a metallic sensation in the mouth. Victims may become weak, and experience nausea, diarrhea, diaphoresis, and chills. Edema may begin around the bite area or may be delayed. Observation of the site for edema is a clue as to whether or not a dry bite has occurred that is, that no venom was injected into the site. Envenomation is most serious if venom is injected directly into joints, muscles, or veins. Hemorrhagic blisters and tissue destruction are possible. Neurotoxicity from rattlesnakes (but generally not from cottonmouths or copperheads) may be manifested as fasciculations, which are fine continuous contractions. In some cases, systemic neurotoxicity may involve respiratory failure. In the most serious cases, massive envenomation may lead to serious bleeding, hypotension, shock, multiple organ failure, and a high incidence of mortality. 

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