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

The complex pathophysiology of adult respiratory distress syndrome (ARDS) makes preventive and therapeutic concepts difficult. Ample experimental evidence indicates that ARDS can be prevented by blocking systemic inflammatory agents. Clinically, only heparin, for inhibition of coagulation phenomena, is presently used among this array of approaches. Corticosteroids have not proven to be beneficial in ARDS. Alternative antiinflammatory agents are being proposed and are under current clinical investigation (e.g. indomethacin, acetylcysteine, alpha 1-proteinase inhibitor, antitumor necrosis factor, interleukin 1 receptor antagonist, platelet-activating factor antagonists). Symptomatic therapeutic strategies in early ARDS include selective pulmonary vasodilation (preferably by inhaled vasorelaxant agents) and optimal fluid balance. Transbronchial surfactant application, presently tested in pilot studies, may be available for ARDS patients in the near future and may have acute beneficial effects on gas exchange, pulmonary mechanics, and lung hemodynamics; its impact on survival cannot be predicted at the present time. Strong efforts should be taken to reduce secondary nosocomial pneumonia in ARDS patients and thus avoid the vicious circle of pneumonia, sepsis from lung infection, and perpetuation of multiple organ dysfunction syndrome. Optimal respirator therapy should be directed to ameliorate gas-exchange conditions acutely but at the same time should aim at minimizing potentially aggravating side effects of artificial ventilation (barotrauma, O2 toxicity). Several new techniques of mechanical ventilation and the concept of permissive hypercapnia address these aspects. Approaches with extracorporeal CO2 removal and oxygenation are being used in specialized centers.
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PMID:Prevention and therapy of the adult respiratory distress syndrome. 761 57

The prevention and treatment of secondary insults to the brain of systemic origin in severely head injured patients remain of utmost importance. Head injury remains the leading cause of traumatic death, being responsible for 50-60% of fatalities. Head-injured patients not only suffer from the primary injury at the time of trauma, but also from the secondary, largely ischaemic, brain damage that occurs later. Some of these insults are of extracranial origin (or systemic), such as arterial hypotension, hypoxaemia, hypercarbia and anaemia. Their impact on mortality and morbidity is extremely high and requires greater efforts in improving the care of head-injured patients. Systemic insults occur either before the patient reaches hospital or during interfacility transfer or, in a surprisingly large number of cases, within hospital during emergency procedures, intrahospital transport or during their stay in intensive care units. Hypoxaemia, although quite easy to treat, is still common. This calls for better and earlier protection of the airway, more systematic administration of oxygen to trauma patients and wider use of pulse oximetry. Arterial hypotension has even more dramatic consequences in severe head injury. Recent studies indicate that short episodes of hypotension may induce severe brain ischaemia, that will be present even after complete systemic haemodynamic restoration. The treatment of hypotensive episodes should be immediate and aggressive. In some circumstances, restoration of an adequate cerebral perfusion pressure may not be obtained sufficiently rapidly with fluids alone and may require early use of vasopressors. Optimal haemodynamic resuscitation of the trauma patient with haemorrhagic hypotension and severe head injury remains a special challenge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Concept of secondary cerebral injury of systemic origin]. 767 75

A key element of neonatal regionalization is the establishment of transport links between centres of tertiary care and subregional centres. During the 11-year period 1982-92, 186 transports were undertaken from the neonatal unit, Vestfold Central Hospital, for a total of 180 patients, or 0.8% of all live born infants (n = 23,652). 64 patients (36%) were referred for prematurity/respiratory distress syndrome (IRDS), 81 (45%) for congenital malformations, and 35 (19%) for other conditions. Transports for prematurity/IRDS declined significantly from the the first 6-year period 1982-87 to the last 5-year period 1988-92 (3.6 vs. 1.8 per 1,000 live born infants; p < 0.01), owing to the establishment of a local respirator treatment programme for severe IRDS. In 71 (38%) transports the infants were mechanically ventilated. Seven (10%) suffered in-transport complications related to the endotracheal tube. At arrival, significantly more patients were anaemic (Hb < 14 g%; transports before 48 hours after birth), alcalotic (pH > 7.50), hypocapnic (PCO2 < 4 kPa) or had a base excess < -10 mmol/l than before transportation (p < 0.05). There was a tendency towards more patients with hypothermia (tp < 36 degrees C), acidosis (pH (< 7.20) and hypercapnia (PCO2 > 10 kPa) at arrival than before transportation (p > 0.05). No deaths occurred during transport. However, two infants died within two hours after arrival, giving a transport-related mortality rate of 1%. Transporting critically ill neonates implies discontinuity of treatment and monitoring of these infants. Optimal stabilization before transportation, and scrupulous work on technical details are of utmost importance.
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PMID:[Transport from a subregional neonatal unit. Experiences from Vestfold Central Hospital during an 11-year period 1982-92]. 825 80

There is a growing body of evidence suggesting that high levels of inflation pressure and high levels of PEEP may be injurious to lung tissue and other organ systems. Limiting peak alveolar pressures below 35 cm H2O may help in avoiding these injuries. The findings have led to the development of a lung-protective strategy that is based on physiologic parameters. This strategy, often using permissive hypercapnia and pressure-limited modes of ventilation, may gain widespread use in the near future. If this strategy reduces barotrauma, a reduction in the length of time on mechanical ventilation and mortality rates can be anticipated. At our center we routinely initiate mechanical ventilation in patients with acute lung injury, using tidal volumes of approximately 6 mL/kg. This may be decreased further if peak alveolar pressures exceed 30 to 35 cm H2O. PEEP is added to maximize alveolar recruitment and oxygenation. Optimal PEEP is located at the inflection point of the respiratory compliance curve. Usually a PEEP of 8 to 12 cm H2O is sufficient. Although we usually initiate mechanical ventilation with a volume-cycled mode, we are not hesitant to switch rapidly to a pressure-limited mode if results are unsatisfactory. We believe that more attention to the potential harmful effects of pressure and volume on lung architecture may result in further improvement of survival in patients with acute respiratory failure.
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PMID:High-inflation pressure and positive end-expiratory pressure. Injurious to the lung? Yes. 883 94

Anaesthesiologists must be familiar with the particularities of the respiratory physiology of newborns and infants when providing perioperative care to these patients. Even brief periods of inadequate respiratory support can cause atelectatrauma and volutrauma which in turn can have deleterious cardiorespiratory consequences and accentuate pre-existing lung disease. A variety of respirators and respiratory support strategies are available and should be selected to meet a patient's particular needs. Optimal PEEP and normal tidal volumes during conventional ventilation, high volume strategy during high frequency ventilation, and permissive hypercapnia are the corner stones of a lung protective strategy. Using an interdisciplinary approach, surgery in the intensive care unit using total intravenous anaesthesia with the uninterrupted use of the ICU equipment is an attractive option for the most vulnerable patients in this age group.
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PMID:[Ventilation of newborns and infants]. 1522 Nov 19

The presence of pulmonary dysfunction after brain injury is well recognized. Acute lung injury (ALI) occurs in 20% of patients with isolated brain injury and is associated with a poor outcome. The "blast injury" theory, which proposes combined "hydrostatic" and "high permeability" mechanisms for the formation of neurogenic pulmonary edema, has been challenged recently by the observation that a systemic inflammatory response may play an integral role in the development of pulmonary dysfunction associated with brain injury. As a result of the primary cerebral injury, a systemic inflammatory reaction occurs, which induces an alteration in blood-brain barrier permeability and infiltration of activated neutrophils into the lung. This preclinical injury makes the lungs more susceptible to the mechanical stress of an injurious ventilatory strategy. Tight CO2 control is a therapeutic priority in patients with acute brain injury, but the use of high tidal volume ventilation may contribute to the development of ALI. Establishment of a therapeutic regimen that allows the combination of protective ventilation with the prevention of hypercapnia is, therefore, required. Moreover, in patients with brain injury, hypoxemia represents a secondary insult associated with a poor outcome. Optimal oxygenation may be achieved by using an adequate FiO2 and by application of positive end-expiratory pressure (PEEP). PEEP may, however, affect the cerebral circulation by hemodynamic and CO2-mediated mechanisms and the effects of PEEP on cerebral hemodynamics should be monitored in these patients and used to titrate its application.
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PMID:Acute lung injury in patients with severe brain injury: a double hit model. 1954 20

Sulfur mustard (SM) inhalation causes the rare but life-threatening disorder of plastic bronchitis, characterized by bronchial cast formation, resulting in severe airway obstruction that can lead to respiratory failure and death. Mortality in those requiring intubation is greater than 80%. To date, no antidote exists for SM toxicity. In addition, therapies for plastic bronchitis are solely anecdotal, due to lack of systematic research available to assess drug efficacy in improving mortality and/or morbidity. Adult rats exposed to SM analog were treated with intratracheal tissue plasminogen activator (tPA) (0.15-0.7 mg/kg, 5.5 and 6.5 h), compared with controls (no treatment, isoflurane, and placebo). Respiratory distress and pulse oximetry were assessed (for 12 or 48 h), and arterial blood gases were obtained at study termination (12 h). Microdissection of fixed lungs was done to assess airway obstruction by casts. Optimal intratracheal tPA treatment (0.7 mg/kg) completely eliminated mortality (0% at 48 h), and greatly improved morbidity in this nearly uniformly fatal disease model (90-100% mortality at 48 h). tPA normalized plastic bronchitis-associated hypoxemia, hypercarbia, and lactic acidosis, and improved respiratory distress (i.e., clinical scores) while decreasing airway fibrin casts. Intratracheal tPA diminished airway-obstructive fibrin-containing casts while improving clinical respiratory distress, pulmonary gas exchange, tissue oxygenation, and oxygen utilization in our model of severe chemically induced plastic bronchitis. Most importantly, mortality, which was associated with hypoxemia and clinical respiratory distress, was eliminated.
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PMID:Tissue plasminogen activator prevents mortality from sulfur mustard analog-induced airway obstruction. 2325 28

Obstructive sleep apnoea (OSA) is characterised by repetitive compromise of the upper airway, causing impaired ventilation, sleep fragmentation, and daytime functional impairment. It is a heterogeneous condition encompassing different phenotypes. The prevalence of OSA among patients presenting for elective surgery is growing, largely attributable to an increase in age and obesity rates, and most patients remain undiagnosed and untreated at the time of surgery. This condition is an established risk factor for increased perioperative cardiopulmonary morbidity, heightened in the presence of concurrent medical comorbidities. Therefore, it is important to perform preoperative OSA screening and risk stratification - using the STOP-Bang screening questionnaire, nocturnal oximetry, and ambulatory and in-laboratory polysomnography, for example. Postoperative risk assessment is an evolving process that encompasses evaluation of upper airway compromise, ventilatory control instability, and pain-sedation mismatch. Optimal postoperative OSA management comprises continuation of regular positive airway pressure, a multimodal opioid-sparing analgesia strategy to limit respiratory depression, avoidance of supine position, and cautious intravenous fluid administration. Supplemental oxygen does not replace a patient's regular positive airway pressure therapy and should be administered cautiously to avoid risk of hypoventilation and worsening of hypercapnia. Continuous pulse oximetry monitoring with specified targets of peripheral oxygen saturation measured by pulse oximetry is encouraged.
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PMID:Perioperative considerations in the management of obstructive sleep apnoea. 3152 64

Pulmonary hypertension (PH) is a condition of raised pulmonary artery pressure (PAP), which may be secondary to a number of causes, one of which is sleep disordered breathing (SDB). When PH complicates SDB, it carries a significant burden of morbidity and mortality due to the risk of progression to right ventricular failure over time. This narrative review will cover the definition and classification of PH, and explore the epidemiology of PH in SDB. The mechanisms by which the two conditions are linked will be reviewed. Repetitive hypoxia with or without hypercapnia alongside frequent arousals can result in important metabolic and pulmonary vascular consequences for the left and right heart. MEDLINE was used to search for all relevant articles and abstracts published from January 1960 to October 2019 inclusive (in all languages). Current best practice in the investigation and management of PH complicating SDB will be reviewed. Important diagnostic investigations and when to consider and screen further for PH in patients with SDB will be discussed. Optimal disease management must include control of SDB with therapy. Additional treatment options will be reviewed. Areas for further research will be highlighted.
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PMID:Narrative review of sleep and pulmonary hypertension. 3321 23