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Query: UMLS:C0012833 (dizziness)
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Two hours after taking 100 mg of flecainide, a patient developed gastrointestinal complaints, dizziness and shortness of breath. The ECG demonstrated novel prolonged JT interval with negative T wave in the precordial leads. During admission, several attacks of non-sustained ventricular tachycardia occurred. The plasma drug concentration was 814 mg/l. Although the tachycardia was non-sustained, cardiovascular collapse developed. Serum electrolytes were normal and myocardial infarction was excluded. The patient is now free of symptoms without medications.
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PMID:Flecainide-induced JT prolongation, T wave inversion and ventricular tachycardia during treatment for symptomatic atrial fibrillation. 807 75

Angiotensin converting enzyme inhibitors (ACEI) are established drugs for the treatment of congestive heart failure. Cases of symptomatic hypotension, especially on the first day of treatment, have been reported occasionally. The database we analysed consisted of 1,177 patients, mean age approximately 70 yrs, with congestive heart failure NYHA functional class II or III. These patients were treated and observed prospectively according to a uniform protocol, starting therapy with 2.5 mg enalapril and measuring blood pressure at hourly intervals for eight hours thereafter. 94.6% of the patients experienced no symptomatic hypotension, 4.75% moderate symptoms (e.g. dizziness, headache) and 0.59% severe symptoms (e.g. fainting, collapse, renal failure). For the analyses of risk factors a large number of baseline variables were analysed univariately to select those significant for inclusion in a multivariate stepwise logistic regression. Alternatively the CART-(classification and regression tree) technique was used. Both techniques showed diastolic blood pressure < or = 70 mmHg to be the single most significant risk factor. CART-analyses showed also pretreatment with nitrates and systolic blood pressure < or = 120 mmHg to be of prognostic relevance. Thus CART is a valuable complement when looking for prognostic factors.
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PMID:CART and logistic regression analyses of risk factors for first dose hypotension by an ACE-inhibitor. 814 29

Propionitrile, a substituted aliphatic nitrile commonly used in the chemical manufacturing industry, is capable of generating cyanide. However, there are few reports of human intoxication involving propionitrile. We report two workers at an organic chemical manufacturing plant who were overcome by fumes while treating a waste slurry into which unreacted propionitrile was discharged by mistake. One victim was comatose, acidotic, and hypotensive; his blood cyanide level was later measured at 5.0 micrograms/ml. He responded to sodium nitrite/sodium thiosulfate therapy by regaining consciousness. Continued symptoms were treated with hyperbaric oxygen at 2 atmospheres for a total of 4 hours. The second victim, who complained only of nausea, dizziness, and headache and who never lost consciousness, was treated with sodium nitrite/sodium thiosulfate. His measured blood cyanide concentration was 3.5 micrograms/ml. The ambient concentration of propionitrile in air samples at the work site shortly after the exposure was 77.5 mg/m3. In occupational situations in which workers exhibit rapidly progressive symptoms of headache, dizziness, collapse, and coma, and where substituted nitriles are known to be on site, acute cyanide poisoning should be strongly considered. Because of continued endogenous generation of cyanide from the metabolism of the parent compound, hyperbaric oxygen may be a valuable adjunctive therapy to consider, in addition to the immediate use of the cyanide antidote kit, in cases of poisoning by propionitrile or other substituted nitrile compounds. We urge the Occupational Safety and Health Administration to adopt workplace standards for the maximum ambient air concentrations for propionitrile.
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PMID:Successful treatment of life-threatening propionitrile exposure with sodium nitrite/sodium thiosulfate followed by hyperbaric oxygen. 788 67

We describe three typical consequences of chronic or subacute proximal vein obstruction: venous claudication, narrowing of the spinal canal by dilated veins that function as collaterals, and hypovolemia caused by trapping of blood in the periphery and slow return. Venous claudication is a well recognized clinical entity. We emphasize that the syndrome is often diagnosed in patients who do not remember acute thrombosis and that the signs on the skin of chronic venous insufficiency are typically absent in these patients. Venous drainage after proximal thrombosis often involves the veins of the spinal canal. Under the condition of sustained physical activity these veins become dilated and occupy space causing the syndrome of a narrow spinal canal. The clinical features differ from those encountered in other forms of a narrow spinal canal; the symptoms appear only after prolonged and strenuous exercise, do barely depend on the posture of the spine and do not disappear readily with cessation of the effort. In patients with bilateral pelvic vein occlusions we regularly found evidence for a shock-like syndrome that follows vigorous exercise. The patients experience sudden weakness and dizziness, with sweats, pallor and tachycardia and have to interrupt the effort to prevent collapse and fainting. The clinical features depend on the anatomical localisation of the obstruction as well as on the pathways of the collaterals. In patients with typical symptoms a venographic workup may be indicated to assess the possibility of recanalisation by endoluminal stenting. The presence of peripheral valve incompetence may be regarded as a contraindication to stenting since it may increase the volume overload and make the chronic venous insufficiency worse.
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PMID:[Sequelae of proximal venous stenosis]. 865 51

Sudden hemodynamic collapse occurred in a 20-year-old man after an Emergency Department visit with a complaint of dizziness and chest discomfort. A left atrial myxoma was demonstrated by echocardiography. Resuscitation procedures followed by surgical repair resulted in an excellent outcome. Although sudden death is a serious manifestation of cardiac myxoma, reports of survivors of near sudden death caused by this tumor have been rare.
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PMID:A survivor of near sudden death caused by giant left atrial myxoma. 1059 88

Isolated iliac artery aneurysm threatening to rupture is a rare condition with a poor prognosis if not dealt with by the physician in a brisk and effective manner. Symptoms from an iliac aneurysm can masquerade as a range of symptoms from neighbouring organs or be almost asymptomatic before rupturing. A case of a 81 year old man, with symptoms of dizziness, fatigue and light lower abdominal pain, who developed sudden cardiovascular collapse, is presented.
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PMID:[Rupture of an isolated iliac aneurysm]. 1068 Apr 75

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
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PMID:Carbon monoxide and the nervous system. 1266 97

When a disease process becomes life-threatening, it is termed to be malignant. Hyperthermia is a heat illness that arises from one of two basic causes: 1) the body's normal thermoregulatory mechanisms are overwhelmed by the environment (an exogenous heat load) or, more commonly, by excessive exercise in a moderate-to-extreme environment (an endogenous heat load); or 2) failure of the thermoregulatory mechanisms, such as those encountered in the elderly or debilitated patient. Either cause can lead to heat illnesses such as heat cramps, heat exhaustion or heatstroke. Heat cramps are brief, intermittent and often severe muscular cramps that frequently occur in muscles fatigued by heavy work or exercise. They are believed to be caused by a rapid change in the extracellular fluid osmolarity resulting from sodium and water loss. Heat exhaustion is a more severe form of heat illness characterized by minor changes in mental status (poor judgment, irritability), dizziness, nausea and headache. In severe cases, the patient may have an altered LOC. Just as with heat cramps, profuse sweating is present. Removing the patient from the hot environment and administering fluids will usually result in a rapid recovery. [table: see text] Left untreated, heat exhaustion may progress to heatstroke. Heatstroke results when there is a complete collapse of thermoregulatory mechanisms. This will lead to a rise in body core temperature in excess of 105.8 degrees F (41 degrees C), which will produce multisystem tissue damage and physiological collapse. Severe cases can cause death. The patient in this case had an axillary temperature taken and recorded at 101.4 degrees F. Typically, axillary temperatures are one degree cooler than oral temperatures, which are one degree cooler than core temperatures. This patient, then, had a core temperature of 103 degrees F or higher. There are two types of heatstroke: classic and exertional. Classic heatstroke occurs during periods of sustained high ambient temperatures and humidity. Exertional heatstroke more often occurs in athletes, military personnel and people who work strenuosly in the environment. In these situations, endogenous heat accumulates more rapidly than the body can dissipate it in the environment. Although sweating is usually absent in the classic form of heatstroke, 50% of exertional heatstroke cases have persistent sweating as a result of catecholamine release. The presence of sweating does not preclude the diagnosis of heatstroke, and cessation of sweating is not the cause of it. As the illness progresses, peripheral vasodilation occurs, resulting in hypotension and shunting. As internal temperatures rise, myocardial contractility begins to decrease, manifested by bradycardia and irritability of the myocardium. No matter the age group, the presence of hypotension and decreased cardiac output indicates a poor prognosis for the patient.
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PMID:Hot on the inside. 1288 21

Medical assistance by doctors on board an aircraft The number of in-flight medical emergencies continues to increase due to the rise in the number of (older) passengers, the greater capacity of new airplanes and the constant increases in the distances flown. The most common medical problems on board an aircraft are vasovagal collapse, dizziness, and gastro-intestinal and cardiac complaints. According to Dutch law, a physician on board an aircraft is obliged to deliver medical assistance in case of a medical emergency involving a passenger if requested by the cabin crew. The chances of being involved in a lawsuit afterwards are, however, very small because the usual medical standards do not apply and because the patient usually does not know the doctor that has assisted him. Even if it should come to a legal procedure, the chance that a physician will be found guilty of malpractice is very small because of the special circumstances and limitations in an airplane.
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PMID:[Medical assistance by doctors on board an aircraft]. 1696

Ropivacaine 1% 40 ml was mistakenly injected as part of an axillary plexus block in an 84-year-old woman. After 15 min the patient complained of dizziness and drowsiness and developed a generalised tonic-clonic seizure followed by an asystolic cardiac arrest. After 10 min of unsuccessful cardiopulmonary resuscitation, a bolus of 100 ml of Intralipid 20% (2 ml.kg(-1)) was administered followed by a continuous infusion of 10 ml.min(-1). After a total dose of 200 ml of Intralipid 20% had been given spontaneous electrical activity and cardiac output was restored. The patient recovered completely. We believe the cardiovascular collapse was secondary to ropivacaine absorption following the accidental overdose. This case shows that lipid infusion may have a beneficial role in cases of local anaesthetic toxicity when conventional resuscitation has been unsuccessful.
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PMID:Successful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion. 1722 38


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