Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The minimum alveolar concentration (MAC) of aliflurane was measured in ten dogs. A value of 1.84 volumes per cent was determined, which correlates well with predictions based on lipid solubility. Induction of anesthesia and recovery were rapid, as would be anticipated with an agent of relatively low solubility in blood (blood-gas partition coefficient = 1.7). Circulatory responses over a relatively narrow range of aliflurane concentrations (0.8 to 1.4 MAC) remained stable, but the development of tachypnea, irregular ventilatory patterns, and increased muscle tone were frequently encountered during aliflurane anesthesis.
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PMID:Determination of the minimum alveolar concentration (MAC) of aliflurane in dogs. 4 31

Infants born to opiate-dependent women frequently have low birth weights and low 1- and 5-min Apgar scores. Significant postnatal problems, excluding neonatal withdrawal, can include jaundice, infection, aspiration pneumonia, transient tachypnea, and hyaline membrane disease. Neonatal abstinence may be severe and persist for as long as 3 months. Abstinence symptoms can include central nervous system hyperirritability, gastrointestinal dysfunction, respiratory distress, tremors, fever, high-pitched cry, increased muscle tone, uncoordinated sucking and swallowing reflexes, dehydration, and possible electrolyte imbalance. During the first week of life, increased respirations associated with hypocapnia and alkalosis may occur. The Brazelton Neonatal Behavioral Assessment Scale has been used to quantify the neurobehavioral effects on neonates of narcotics administered prenatally. A marked decline in mortality rates of infants born to opiate-dependent mothers is evident. In Philadelphia, infant morbidity has been related not only to the type of maternal narcotic dependence, but also to the amount of prenatal care. Infants whose mothers received prenatal care have been found to have higher birth weights similar to infants of control mothers. Although the newborn with intrauterine exposure to narcotic agents may appear normal at birth, the effects of the pharmacologic agent may not become apparent until later in development. To obtain a more favorable outcome for the high-risk mother and child involved in the problems of perinatal addiction, several recommendations are proposed.
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PMID:Effects of maternal opiate abuse on the newborn. 388 86

Six cases of PCP intoxication in young children age 5 years and younger seen at UCLA Medical Center recently and 10 other cases from the literature are described and their clinical findings summarized. PCP intoxication should be suspected in young children and infants presenting with rapid onset of lethargy or coma, strange behavior, staring spells, ataxia, and nystagmus. Other findings less frequent but still suspect are opisthotonos, hypertension, tachypnea or hyperpnea, miosis, hyperreflexia, hypertonia, and rigidity. Once suspected, the diagnosis is most easily made by finding PCP in the urine. Proper diagnosis of PCP intoxication is important to ensure that rapid, appropriate treatment is given, costly diagnostic workups are avoided, and family evaluations are instituted. One case strongly suggests that intoxication in infants may result from accidental inhalation when near individuals who are smoking PCP.
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PMID:PCP intoxication in young children and infants. 738 38

Holocarboxylase synthetase deficiency is typically a biotin responsive disorder that presents with lactic acidosis, tachypnea, temperature instability, and shock in neonates (Briones et al.1989 and Fuchshuber et al. 1992). The primary defect in cases studied to date appears to be the decreased affinity of HCS for its substrate, biotin (Gompertz et al. 1971). Supplemental biotin can provide sufficient substrate to increase HCS enzymatic function and thereby permit biotinylation of the four carboxylase apoenzymes (Briones et al. 1989). We report an infant with HCS deficiency who presented with lactic acidosis, shock, and hypertonia. Subependymal cysts were identified on cranial ultrasound and subsequently confirmed by MRI. Six months following biotin supplementation, she is developmentally normal and MRI of the brain shows complete resolution of the cysts.
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PMID:Resolution of subependymal cysts in neonatal holocarboxylase synthetase deficiency. 918 68

Mechanical ventilation is a well-established strategy in intensive care medicine. ICU trauma patients require analgesia, and sedation mostly consists of benzodiazepines and opioids with increasing doses over time. The weaning period is complicated by the withdrawal syndrome, showing tachycardia, hypertonia, tachypnea and restlessness. Although treatment with clonidine can influence these symptoms, tachypnea still remains the main problem in weaning patients from mechanical ventilation. Adding sufentanil, an opioid with greater effects on analgesia than on respiratory depression compared with fentanyl, tachypnea can be reduced to normal frequency. In this way weaning management can be managed more easily for the benefit of both, the patient and physician. In comparison with a group of 50 patients treated with clonidine alone, 72 patients treated with clonidine/sufentanil showed a shorter period from the start of spontaneous ventilation until extubation (4.8 vs 7.6 days) and until discharge from the ICU (7.7 vs 12.4 days). The number of reintubations caused by respiratory exhaustion decreased from 16.0 to 2.8%.
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PMID:[In Process Citation] 1006 33

Paroxysmal autonomic instability with dystonia (PAID) is a rare complication of brain injury. Symptoms of PAID include diaphoresis, hyperthermia, hypertension, tachycardia, and tachypnea accompanied by hypertonic movement. Herein, we present the case of a 44-year-old female patient, who was diagnosed with paraneoplastic limbic encephalopathy caused by thyroid papillary cancer. The patient exhibited all the symptoms of PAID. On the basis that the symptoms were unresponsive to antispastic medication and her liver function test was elevated, we performed alcohol neurolysis of the musculocutaneous nerve followed by botulinum toxin type A (BNT-A) injection into the biceps brachii and brachialis. Unstable vital signs and hypertonia were relieved after chemodenervation. Accordingly, alcohol neurolysis and BNT-A injection are proposed as a treatment option for intractable PAID.
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PMID:Paroxysmal autonomic instability with dystonia managed using chemodenervation including alcohol neurolysis and botulinum toxin type a injection: a case report. 2593 29

Dysautonomia is a potentially life-threatening syndrome seen in many different types of brain injuries. It involves paroxysmal sympathetic hyperactivity and typically includes a constellation of symptoms, including: tachycardia, tachypnea, hyperthermia, hypertension, diaphoresis, hypertonia, and/or decerebrate or decorticate posturing. It is a clinical diagnosis of exclusion. A multimodal treatment approach is necessary including environmental modifications along with pharmacotherapy. Early management can help prevent comorbidities including secondary brain injury while also improving patient outcomes. This discussion serves as an overview of dysautonomia with a focus on management in the pediatric population including an example of a clinical algorithm and a review of the commonly used medications.
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PMID:Calming the Storm: Dysautonomia for the Pediatrician. 2871 15

Paroxysmal sympathetic hyperactivity (PSH) has predominantly been described after traumatic brain injury (TBI), which is associated with hyperthermia, hypertension, tachycardia, tachypnea, diaphoresis, dystonia (hypertonia or spasticity), and even motor features such as extensor/flexion posturing. Despite the pathophysiology of PSH not being completely understood, most researchers gradually agree that PSH is driven by the loss of the inhibition of excitation in the sympathetic nervous system without parasympathetic involvement. Recently, advances in the clinical and diagnostic features of PSH in TBI patients have reached a broad clinical consensus in many neurology departments. These advances should provide a more unanimous foundation for the systematic research on this clinical syndrome and its clear management. Clinically, a great deal of attention has been paid to the definition and diagnostic criteria, epidemiology and pathophysiology, symptomatic treatment, and prevention and control of secondary brain injury of PSH in TBI patients. Potential benefits of treatment for PSH may result from the three main goals: eliminating predisposing causes, mitigating excessive sympathetic outflow, and supportive therapy. However, individual pathophysiological differences, therapeutic responses and outcomes, and precision medicine approaches to PSH management are varied and inconsistent between studies. Further, many potential therapeutic drugs might suppress manifestations of PSH in the process of TBI treatment. The purpose of this review is to present current and comprehensive studies of the identification of PSH after TBI in the early stage and provide a framework for symptomatic management of TBI patients with PSH.
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PMID:Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury. 3216 63