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

This article reviews adult respiratory distress syndrome as it is associated with multiple organ dysfunction and systemic inflammatory response. The pathophysiology of adult respiratory distress syndrome is discussed and related to the clinical presentation. Included in the clinical presentation is a discussion of respiratory and hemodynamic alterations, lung mechanics, and oxygen delivery and consumption alterations. Conventional therapeutic modalities for treatment of adult respiratory distress syndrome are reviewed in addition to new ventilatory approaches. New approaches to ventilation and oxygenation included in this article are pressure control ventilation, inverse ratio ventilation, permissive hypercapnia, and extracorporeal therapy. New pharmacologic therapy for the treatment of adult respiratory distress syndrome is also reviewed in this article.
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PMID:Respiratory consequences of multisystem crisis: the adult respiratory distress syndrome. 811 38

Present evidence demonstrates that mechanical ventilation in patients with adult respiratory distress syndrome (ARDS) contributes to the ongoing pulmonary damage, a condition known as "ventilator lung". Data from various animal studies indicate that volume, rather than pressure, is probably the main culprit. Accordingly, clinicians should use tidal volumes smaller than those usually recommended. This approach leads to hypercapnia (i.e. so-called "permissive hypercapnia"), which seems to have very few adverse effects and might even be beneficial. Moreover, there is an added risk of atelectasis, which can be prevented by the application of positive end-expiratory pressure (PEEP). The present study reviews the pathophysiological mechanisms by which mechanical ventilation is injurious to the lung, and attempts to outline an approach aimed at minimizing such damage.
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PMID:[ARDS and mechanical ventilation--"primum nil nocere"]. 821 Oct 22

Many experimental studies have shown that mechanical ventilation with high tidal volumes (Vt) or with a low end-expiratory volume allowing repeated end-expiratory collapse, can result in acute parenchymal lung injury and probably an inflammatory response. Low volume ventilation with permissive hypercapnia has been used in an attempt to avoid such injury in ARDS. Such management can affect oxygenation in many complex ways. The right-shift of the haemoglobin-oxygen dissociation curve during acute respiratory acidosis may increase venous oxygen tension (PvO2) which could allow increased O2 uptake in ischaemic tissues. Acidosis may reduce intrapulmonary shunt (Qs/Qt) by potentiating hypoxic pulmonary vasoconstriction, and there may also be direct and autonomically mediated effects of hypercapnia both on the lung vasculature and on the airways. Cardiac output usually increases as a consequence of hypercapnia and perhaps as a result of reduced intrathoracic pressure, further increasing PvO2 and CvO2, but the increase in cardiac output (CO) may tend to increase Qs/Qt as flow increases preferentially in unventilated lung. The reduction of mean airway pressure may directly increase Qs/Qt. Hypercapnia may affect the distribution of systemic blood flow both within organs and between organs. Limited clinical studies suggest that tissue oxygenation is usually unchanged or improved during permissive hypercapnia with increased CO, reduced arterio-venous O2 content difference and reduced blood lactate concentration. However, acute hypercapnia per se can reduce lactate production. Further studies are required of this complex issue.
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PMID:Permissive hypercapnia in ARDS and its effect on tissue oxygenation. 859 78

The respiratory management strategy of small tidal volume with permissive hypercapnia has been adopted to avoid further aggravation of lung injury due to high airway pressure with some impressive success (1). No consensus, however, has been established in terms of the rate of increase in PaCO2 and its upper limit. Recently, our colleague in the intensive care unit experienced a severe case of ARDS successfully treated with the above strategy despite of the fact that during the course of treatment, the highest PaCO2 reached 177 mmHg and the lowest pH, 7.03 (2). The fact that PaCO2 may reach a very high level in the clinical setting and the well-known role of haemoglobin (Hb) in buffering CO2 led us to study effects of different Hb levels on pH and haemodynamic changes in response to acute CO2 loading in the blood. We will summarize the case report first with permission of authors (the case report was published in Japanese) (2) and then discuss the studies conducted in our animal laboratory.
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PMID:How far can we go with permissive hypercapnia? A case presentation and some biased comments with emphasis on maintaining normal haemoglobin level. 859 79

Acute respiratory distress syndrome (ARDS) is rare but beset with a high mortality rate. In recent years, however, a trend towards higher survival rates has been observed. High inspiratory oxygen concentrations, large tidal volumes, and high peak inspiratory airway pressures applied during mechanical ventilation have been identified as harmful to the lung and can contribute to the progression of ARDS. This had led to reconsideration of the sequelae of ventilatory therapy. Mechanical ventilation and other adjunctive strategies in ARDS have changed from the conventional approach aiming at normalisation of physiological ventilatory parameters to an elaborated approach that intends to protect the ventilated lung, prevent oxygen toxicity, recruit the infiltrated atelectatic and consolidated lung and reduce the anatomical and alveolar dead space. This new approach consists of various forms of pressure-controlled mechanical ventilation with PEEP and permissive hypercapnia, body position changes, and inhalation of nitric oxide. Should these procedures fail to improve impaired gas exchange, extracorporeal membrane oxygenation is an additional therapeutic option. None of these therapeutic procedures, however, has been tested against traditional standard treatment in a classical randomised controlled trial. The following review focuses on the latest insights into the pathophysiology, diagnosis, and treatment of ARDS.
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PMID:[Clinical aspects of acute lung failure in adults (ARDS)]. 867 73

ARDS remains a syndrome which despite all efforts poses problems in exact definition (cause, course and severity). Most of the existing information comes from clinical observations and uncontrolled studies and is therefore of limited value. Despite the advent of new treatment modalities mortality from ARDS has remained high and is influenced or caused by several factors like underlying disease, previous health status, presence of MOSF, complications of therapy or ultimate failure of gas exchange. Therapy is directed at elimination of the cause of ARDS if possible, but then mainly supportive, considering all organs and systems. With the introduction of gentler respiratory support techniques (small tidal volumes and pressure limitation, permissive hypercapnia and HFO) and appropriate measures to reduce oxygen toxicity (titration of PEEP, possibly NO), iatrogenic lung injury, indistinguishable from ARDS, can be reduced, and this might improve survival rates. For the future, modulation of the host's inflammatory response may hold great promises for prevention and treatment of ARDS, but such strategies need to be explored with well controlled clinical trials, respecting the complexity of the issue.
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PMID:Acute respiratory distress syndrome (ARDS) in neonates and children. 873 7

In the fluid-filled lungs of early adult respiratory distress syndrome (ARDS) the dependent parts are compressed and atelectatic; whereas, the nondependent areas remain aerated and functional. Ventilating these considerably restricted lungs carries the risk of overinflation and ventilatory-induced lung injury (baro-volutrauma). The consequences for adjusting mechanical ventilation are: 1) reducing tidal volumes in order to avoid alveolar hyperinflation and excessive alveolar pressures; 2) considering permissive hypercapnia if adequate CO2 elimination cannot be maintained; 3) keeping open the unstable alveoli by positive end-expiratory pressure (PEEP) (external or intrinsic). However, the large variations in regional lung compliance make it improbable that an optimal external PEEP level beneficial for the whole lung will be found; 4) using intrinsic PEEP in the inverse ratio ventilation (IRV) mode which varies with differences in regional ventilatory kinetics. No clinical study has yet convincingly demonstrated the benefit of IRV compared to conventional ventilation, controlled clinical long-term trials are not yet available; and 5) using superimposed spontaneous breathing which may be considerably more effective in opening up collapsed alveoli, combined with intentional intrinsic PEEP this is achieved in airway pressure release ventilation (APRV). Other new principles of mechanical ventilation, such as "proportional assist ventilation" or "tracheal gas insufflation" must still be considered as experimental.
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PMID:New strategies in mechanical ventilation for acute lung injury. 879 70

Acute respiratory distress syndrome is a common cause of morbidity and mortality in intensive care units. For the most part, the mortality of this syndrome has arguably not decreased since the syndrome was originally described. One of the major reasons for this lack of reduction in mortality may be related to adherence to more traditional ventilatory strategies that have the potential to cause ventilator-induced lung injury. Ventilator strategies that attempt to limit ventilator-induced lung injury and accept permissive hypercapnia have successfully demonstrated a marked reduction in mortality in uncontrolled settings. So encouraging are these reductions that there has been a subtle shift in philosophy of mechanical ventilation toward using lung-protective ventilatory strategies at all times. With broad acceptance of this shift in philosophy, and the use of recently standardized clinical definitions for controlled studies, we optimistically anticipate improved mortality rates for acute respiratory distress syndrome.
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PMID:Strategies of invasive ventilatory support in ARDS. 882 93

A case of severe accidental hypercapnia during anesthesia is presented. A 44-year-old woman underwent laparotomy under general anesthesia. Forty minutes after the start of the operation, BP rose slightly and HR increased from 110 to 140 x min-1. Then ST segment depression was noted on ECG monitor. Therefore, nitrous oxide was discontinued for 20 minutes. Frequent oxygen supply with oxygen flush was needed to inflate the collapsed bag. The operation was concluded without additional clinical problems. The patient remained unconscious after the anesthetics were discontinued. Cyanosis was observed despite the delivery of 100% oxygen. Cardiac arrest occurred following abrupt bradycardia, but she responded immediately to resuscitation. She was in a deep comatose state and did not respond to painful stimuli. The pupils were fully dilated with absent light reflex. Arterial blood gas analysis revealed; pH 6.720, PaCO2 277 mmHg, PaO2 159 mmHg, and BE-16.2. Disconnection of anesthetic circuit was noted, thereafter, and hyperventilation was performed. Then, the pupils became promptly constricted and the response to painful stimuli appeared within 30 minutes. Her level of consciousness recovered completely after 4.5 hours of hyperventilation. She suffered from refractory hypotension (BP70-85 mmHg in systolic pressure) in spite of catecholamine administration, tachycardia (HR 140-160 x min-1) and ARDS in the ICU, but all the symptoms disappeared by the 16 hours after ICU admission.
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PMID:[A patient who manifested various symptoms following severe accidental hypercapnia]. 899 34

Acute respiratory distress syndrome is a response of the lung to both direct and indirect insults. Although much knowledge has been gained in understanding the pathophysiology of the syndrome, overall mortality in the past 25 years remains unchanged. Application of scientific knowledge to present-day technology has yielded advances in ventilator and pharmacological support for the patient with ARDS. Emphasis is now made on the prevention of iatrogenic lung injury with the use of pressure-limited mechanical ventilation, permissive hypercapnia, and artificial means of gas exchange (discussed in the chapter by Dr Furukawa). The role of INO and surfactant, as well as antimediator therapy, in the armamentarium against ARDS appears promising but awaits definitive clinical trials. Only with progress and newer therapies will we be able to improve the outlook for patients and families in the future.
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PMID:Mechanical ventilation and adjuncts in acute respiratory distress syndrome. 911 24


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