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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiopulmonary resuscitation does not end with restoration of spontaneous circulation; rather, it must be continued with the application of all the measures that allow organ function to be maintained. The initial goal of hemodynamic treatment is to achieve normal blood pressure for the patient's age by means of fluids and/or vasoactive drugs. The aim of respiratory treatment is to normalize ventilation and oxygenation without causing further lung injury, avoiding hyperoxia and hyperventilation as well as hypoxia and hypercapnia. Neurological stabilization aims to reduce secondary brain damage, by avoiding hypertension and hypotension, maintaining normal ventilation and oxygenation, and treating hyperglycemia, agitation and seizures. Although no specific studies in children are available, data from adults have shown that early moderate hypothermia attenuates brain damage secondary to cardiorespiratory arrest, without increasing complications. After the arrest, the need for analgesia and/or sedation must be considered. The process of transportation to the pediatric intensive care unit (PICU) requires the following steps: stabilizing the patient, checking for and stabilizing fractures and external wounds, ensuring a stable airway and intravenous lines, assessing the need for nasogastric and bladder tubes, taking blood samples for analyses, contacting the PICU and informing the staff about the child's condition, choosing the optimal vehicle for transportation according to the child's condition and the distance, checking pediatric equipment and medications, selecting experienced staff and, finally, maintaining close surveillance and monitoring during transportation.
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PMID:[Post-resuscitation stabilization and transportation]. 1734 Jul 87

Rapid, safe, and effective methods of anesthetic induction and recovery are needed for sea turtles, especially in cases eligible for immediate release. This study demonstrates that intravenous propofol provides a rapid induction of anesthesia in loggerhead (Caretta caretta) sea turtles and results in rapid recovery, allowing safe return to water shortly after the procedure. Forty-nine loggerhead sea turtles were recovered as local fishery by-catch in pound nets and transported to a surgical suite for laparoscopic sex determination. Treatment animals (n = 32) received 5 mg/kg propofol intravenously (i.v.) as a rapid bolus, whereas control animals (n = 17) received no propofol. For analgesia, all animals received a 4 ml infusion of 1% lidocaine, locally, as well as 2 mg/kg ketoprofen intramuscularly (i.m.). Physiologic data included heart and respiratory rate, temperature, and a single blood gas sample collected upon termination of the laparoscopy. Subjective data included jaw tone and ocular reflex: 3 (vigorous) to 0 (none detected). Anesthetic depth was scored from 1, no anesthesia, to 3, surgical anesthesia. Turtles receiving propofol became apneic for a minimum of 5 min with a mean time of 13.7 +/- 8.3 min to the first respiration. Limb movement returned at a mean time of 21.1 +/- 16.8 min. The treatment animals were judged to be sedated for approximately 30 min (mean anesthetic depth score > or = 1.5) when compared to controls. Median respiratory rates for treatment animals were slower compared to controls for the first 15 min, then after 35 min, they became significantly faster than the controls. Median heart rates of control animals became significantly slower than treatment animals between 40 and 45 min. Physiologic differences between groups persisted a minimum of 55 min. Possible explanations for heart rate and respiratory rate differences later in the monitoring period include a compensatory recovery of treatment animals from anesthesia-induced hypoxia and hypercapnia or, alternatively, an induced response of the nonsedated control animals. The animals induced with propofol were easier to secure to the restraint device and moved less during laparoscopy. In conclusion, propofol is a safe and effective injectable anesthetic for use in free-ranging loggerhead sea turtles that provides rapid induction and recovery.
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PMID:Propofol anesthesia in loggerhead (Caretta caretta) sea turtles. 1826 29

The management of critically ill children with traumatic brain injury (TBI) requires a precise assessment of the brain lesions but also of potentially associated extra-cranial injuries. Children with severe TBI should be treated in a pediatric trauma center, if possible. Initial assessment relies mainly upon clinical examination, trans-cranial Doppler ultrasonography and body CT scan. Neurosurgical operations are rarely necessary in these patients, except in the case of a compressive subdural or epidural hematoma. On the other hand, one of the major goals of resuscitation in these children is aimed at protecting against secondary brain insults (SBI). SBI are mainly because of systemic hypotension, hypoxia, hypercarbia, anemia and hyperglycemia. Cerebral perfusion pressure (CPP = mean arterial blood pressure - intracranial pressure: ICP) should be monitored and optimized as soon as possible, taking into account age-related differences in optimal CPP goals. Different general maneuvers must be applied in these patients early during their treatment (control of fever, avoidance of jugular venous outflow obstruction, maintenance of adequate arterial oxygenation, normocarbia, sedation-analgesia and normovolemia). In the case of increased ICP and/or decreased CPP, first-tier ICP-specific treatments may be implemented, including cerebrospinal fluid drainage, if possible, osmotic therapy and moderate hyperventilation. In the case of refractory intracranial hypertension, second-tier therapy (profound hyperventilation with P(a)CO(2) < 35 mmHg, high-dose barbiturates, moderate hypothermia, decompressive craniectomy) may be introduced, after a new cerebral CT scan.
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PMID:Management of critically ill children with traumatic brain injury. 1831 8

The presence of pulmonary arterial hypertension (PAH) is a significant predictor of major perioperative cardiovascular complications in patients undergoing cardiac diagnostic or interventional procedure or non cardiac surgery under sedation and/or anesthesia. Factors that precipitate a pulmonary hypertensive crisis include hypoxia, hypercarbia, acidosis, hypothermia, pain and airway manipulations. Pain management is challenging in patients with significant PAH. We report the use of dexmedetomidine for sedation and analgesia in a 16 year old patient with significant pulmonary hypertension, pneumonia and impending cardiorespiratory failure. This resulted in avoidance of endotracheal intubation and positive pressure ventilation, with subsequent recovery to discharge home.
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PMID:Novel use of dexmedetomidine in a patient with pulmonary hypertension. 1854 49

The ability of anesthetic agents to provide adequate analgesia and sedation is limited by the ventilatory depression associated with overdosing in spontaneously breathing patients. Therefore, quantitation of drug induced ventilatory depression is a pharmacokinetic-pharmacodynamic problem relevant to the practice of anesthesia. Although several studies describe the effect of respiratory depressant drugs on isolated endpoints, an integrated description of drug induced respiratory depression with parameters identifiable from clinically available data is not available. This study proposes a physiological model of CO2 disposition, ventilatory regulation, and the effects of anesthetic agents on the control of breathing. The predictive performance of the model is evaluated through simulations aimed at reproducing experimental observations of drug induced hypercarbia and hypoventilation associated with intravenous administration of a fast-onset, highly potent anesthetic mu agonist (including previously unpublished experimental data determined after administration of 1 mg alfentanil bolus). The proposed model structure has substantial descriptive capability and can provide clinically relevant predictions of respiratory inhibition in the non-steady-state to enhance safety of drug delivery in the anesthetic practice.
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PMID:On the modeling of drug induced respiratory depression in the non-steady-state. 1916 78

Respiratory depression limits provision of safe opioid analgesia and is the main cause of death in drug addicts. Although opioids are known to inhibit brainstem respiratory activity, their effects on cortical areas that mediate respiration are less well understood. Here, functional magnetic resonance imaging was used to examine how brainstem and cortical activity related to a short breath hold is modulated by the opioid remifentanil. We hypothesized that remifentanil would differentially depress brain areas that mediate sensory-affective components of respiration over those that mediate volitional motor control. Quantitative measures of cerebral blood flow were used to control for hypercapnia-induced changes in blood oxygen level-dependent (BOLD) signal. Awareness of respiration, reflected by an urge-to-breathe score, was profoundly reduced with remifentanil. Urge to breathe was associated with activity in the bilateral insula, frontal operculum, and secondary somatosensory cortex. Localized remifentanil-induced decreases in breath hold-related activity were observed in the left anterior insula and operculum. We also observed remifentanil-induced decreases in the BOLD response to breath holding in the left dorsolateral prefrontal cortex, anterior cingulate, the cerebellum, and periaqueductal gray, brain areas that mediate task performance. Activity in areas mediating motor control (putamen, motor cortex) and sensory-motor integration (supramarginal gyrus) were unaffected by remifentanil. Breath hold-related activity was observed in the medulla. These findings highlight the importance of higher cortical centers in providing contextual awareness of respiration that leads to appropriate modulation of respiratory control. Opioids have profound effects on the cortical centers that control breathing, which potentiates their actions in the brainstem.
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PMID:Opioids depress cortical centers responsible for the volitional control of respiration. 1955 57

This study evaluated the anesthetic and cardiorespiratory effects of a combination of intravenous propofol (2.2 mg/kg), intramuscular medetomidine (22.0 pg/kg), intravenous butorphanol (0.22 mg/kg), and intravenous atropine (0.022 mg/kg) in healthy dogs. Anesthesia was characterized by muscle relaxation and analgesia. Heart rate decreased after medetomidine and propofol administration (131 to 113 beats/min) but returned to baseline after intravenous atipamezole (110 microg/kg). Mild acidemia, hypercapnia, hypoxemia, and decreased SaO2 developed after premedication. PaO2 and SaO2 were further decreased by propofol injection. In conclusion, this combination proved to be an effective anesthetic protocol for healthy dogs and should be adequate for minor surgical procedures.
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PMID:Anesthetic and cardiopulmonary effects of propofol in dogs premedicated with atropine, butorphanol, and medetomidine. 1975 94

The precise definition of a severe asthmatic exacerbation is an issue that presents difficulties. The term 'status asthmaticus' relates severity to outcome and has been used to define a severe asthmatic exacerbation that does not respond to and/or perilously delays the repetitive or continuous administration of short-acting inhaled beta(2)-adrenergic receptor agonists (SABA) in the emergency setting. However, a number of limitations exist concerning the quantification of unresponsiveness. Therefore, the term 'acute severe asthma' is widely used, relating severity mostly to a combination of the presenting signs and symptoms and the severity of the cardiorespiratory abnormalities observed, although it is well known that presentation does not foretell outcome. In an acute severe asthma episode, close observation plus aggressive administration of bronchodilators (SABAs plus ipratropium bromide via a nebulizer driven by oxygen) and oral or intravenous corticosteroids are necessary to arrest the progression to severe hypercapnic respiratory failure leading to a decrease in consciousness that requires intensive care unit (ICU) admission and, eventually, ventilatory support. Adjunctive therapies (intravenous magnesium sulfate and/or others) should be considered in order to avoid intubation. Management after admission to the hospital ward because of an incomplete response is similar. The decision to intubate is essentially based on clinical judgement. Although cardiac or respiratory arrest represents an absolute indication for intubation, the usual picture is that of a conscious patient struggling to breathe. Factors associated with the increased likelihood of intubation include exhaustion and fatigue despite maximal therapy, deteriorating mental status, refractory hypoxaemia, increasing hypercapnia, haemodynamic instability and impending coma or apnoea. To intubate, sedation is indicated in order to improve comfort, safety and patient-ventilator synchrony, while at the same time decrease oxygen consumption and carbon dioxide production. Benzodiazepines can be safely used for sedation of the asthmatic patient, but time to awakening after discontinuation is prolonged and difficult to predict. The most common alternative is propofol, which is attractive in patients with sudden-onset (near-fatal) asthma who may be eligible for extubation within a few hours, because it can be titrated rapidly to a deep sedation level and has rapid reversal after discontinuation; in addition, it possesses bronchodilatory properties. The addition of an opioid (fentanyl or remifentanil) administered by continuous infusion to benzodiazepines or propofol is often desirable in order to provide amnesia, sedation, analgesia and respiratory drive suppression. Acute severe asthma is characterized by severe pulmonary hyperinflation due to marked limitation of the expiratory flow. Therefore, the main objective of the initial ventilator management is 2-fold: to ensure adequate gas exchange and to prevent further hyperinflation and ventilator-associated lung injury. This may require hypoventilation of the patient and higher arterial carbon dioxide (PaCO(2)) levels and a more acidic pH. This does not apply to asthmatic patients intubated for cardiac or respiratory arrest. In this setting the post-anoxic brain oedema might demand more careful management of PaCO(2) levels to prevent further elevation of intracranial pressure and subsequent complications. Monitoring lung mechanics is of paramount importance for the safe ventilation of patients with status asthmaticus. The first line of specific pharmacological therapy in ventilated asthmatic patients remains bronchodilation with a SABA, typically salbutamol (albuterol). Administration techniques include nebulizers or metered-dose inhalers with spacers. Systemic corticosteroids are critical components of therapy and should be administered to all ventilated patients, although the dose of systemic corticosteroids in mechanically ventilated asthmatic patients remains controversial. Anticholinergics, inhaled corticosteroids, leukotriene receptor antagonists and methylxanthines offer little benefit, and clinical data favouring their use are lacking. In conclusion, expertise, perseverance, judicious decisions and practice of evidence-based medicine are of paramount importance for successful outcomes for patients with acute severe asthma.
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PMID:Acute severe asthma: new approaches to assessment and treatment. 1991 54

Lung-protective ventilation with a low tidal volume, plateau pressure < 30 cm H(2)O. oxygen saturation > 90% and permissive hypercapnia results in reduction of the mortality rate in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The level of the positive end-expiratory pressure (PEEP) must be chosen in relation to oxygen requirement. High frequency oscillatory ventilation and neurally adjusted ventilatory assist are promising methods. However, further studies with firm end-points have to be awaited before a final judgment is possible. Veno-venous extracorporeal membrane oxygenation (ECMO) can ensure life-sustaining gas exchange in patients with severe vitally compromised pulmonary failure, to provide time for lung tissue to heal and reduce ventilatory stress. The latest guidelines for analgesia and sedation in intensive care medicine demand consistent monitoring of the level of sedation and the intensity of pain. The sedation should be interrupted daily, with phases of awakenings and, if possible, spontaneous breathing. Methods of supportive treatment: Positional treatment (prone position) and inhalation of vasodilators can improve ventilation/perfusion mismatch and thus oxygenation. However, administration of surfactant is currently not advised in adult respiratory failure.
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PMID:[Current approaches to the treatment of severe hypoxic respiratory insufficiency (acute lung injury; acute respiratory distress syndrome)]. 2127 78

Awake video-assisted thoracic surgery (VATS) has been increasingly employed in a variety of procedures involving pleura, lungs, and mediastinum. Adequate anesthesia and analgesia obtained from thoracic epidural anesthetic (TEA) allow VATS to be performed in awake patients. The potential general anesthesia-related adverse effects, such as intubation-related trauma, pneumonia, ventilator-associated lung injury, effects of neuromuscular blocking agents, and postoperative nausea and vomiting, can thus be avoided. Moreover, TEA holds the benefits of reducing pulmonary and cardiac morbidities and mortalities after noncardiac surgery. Patients who undergo awake VATS may also benefit from the efficient contraction of the dependent hemidiaphragm and preserved hypoxic pulmonary vasoconstriction during surgically-induced pneumothorax. Preliminary results from early case series have indicated certain benefits, including greater patient satisfaction, less nursing care, less sore throat, earlier resumption of oral intake, lower rate of morbidity, reduced perioperative pain, reduced cost, and shorter hospital stay. However, anesthesia for awake VATS presents a particular challenge to anesthesiologists and requires extra vigilance. Potential hazards include paradoxical respiration and mediastinum shift after surgery induced pneumothorax, which may cause progressive hypoxia, hypercapnia and hypotension. Anesthesiologists should be acquainted with the procedure to be performed, be knowledgeable on the physiological changes, be aware of the potential problems, and have good judgment on suitable timing for conversion of regional anesthesia to intubation general anesthesia in enforced circumstance.
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PMID:Anesthesia for awake video-assisted thoracic surgery. 2302 72


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