Severe Hypercapnia Research Articles

Preliminary study of ventilation with 4 ml/kg tidal volume in acute respiratory distress syndrome: feasibility and effects on cyclic recruitment - derecruitment and hyperinflation

IntroductionCyclic recruitment-derecruitment and overdistension contribute to ventilator-induced lung injury. Tidal volume (Vt) may influence both, cyclic recruitment-derecruitment and overdistension. The goal of this study was to determine if decreasing Vt from 6 to 4 ml/kg reduces cyclic recruitment-derecruitment and hyperinflation, and if it is possible to avoid severe hypercapnia.MethodsPatients with pulmonary acute respiratory distress syndrome (ARDS) were included in a crossover study with two Vt levels: 6 and 4 ml/kg. The protocol had two parts: one bedside and other at the CT room. To avoid severe hypercapnia in the 4 ml/kg arm, we replaced the heat and moisture exchange filter by a heated humidifier, and respiratory rate was increased to keep minute ventilation constant. Data on lung mechanics and gas exchange were taken at baseline and after 30 minutes at each Vt (bedside). Thereafter, a dynamic CT (4 images/sec for 8 sec) was taken at each Vt at a fixed transverse region between the middle and lower third of the lungs. Afterward, CT images were analyzed and cyclic recruitment-derecruitment was determined as non-aerated tissue variation between inspiration and expiration, and hyperinflation as maximal hyperinflated tissue at end-inspiration, expressed as % of lung tissue weight.ResultsWe analyzed 10 patients. Decreasing Vt from 6 to 4 ml/kg consistently decreased cyclic recruitment-derecruitment from 3.6 (2.5 to 5.7) % to 2.9 (0.9 to 4.7) % (P <0.01) and end-inspiratory hyperinflation from 0.7 (0.3 to 2.2) to 0.6 (0.2 to 1.7) % (P = 0.01). No patient developed severe respiratory acidosis or severe hypercapnia when decreasing Vt to 4 ml/kg (pH 7.29 (7.21 to 7.46); PaCO2 48 (26 to 51) mmHg).ConclusionsDecreasing Vt from 6 to 4 ml/kg reduces cyclic recruitment-derecruitment and hyperinflation. Severe respiratory acidosis may be effectively prevented by decreasing instrumental dead space and by increasing respiratory rate.

3,4-Methylenedioxymethamphetamine induces a hyperthermic and hypermetabolic crisis in pigs with and without a genetic disposition for malignant hyperthermia

Clinical symptoms of acute 3,4-methylenedioxymethamphetamine (MDMA) intoxication and malignant hyperthermia have many similarities. At present, however, there is contradictory evidence concerning the malignant hyperthermia trigger potency of MDMA. This study was designed to investigate whether MDMA has malignant hyperthermia trigger potential and leads to malignant hyperthermia in pigs with or without a genetic predisposition to the condition. In addition, the therapeutic effectiveness of a new dantrolene sodium suspension was examined. Experimental study, using an animal model of Piétrain pigs. Institute for Research in Operative Medicine, University of Witten/Herdecke, Hospital Cologne Merheim, Cologne, Germany, October 2006 to February 2007. Trigger-free anaesthesia was performed on seven malignant hyperthermia-susceptible and six malignant hyperthermia-normal Piétrain pigs, and cumulative doses of MDMA were administered to each animal. After achieving predefined malignant hyperthermia criteria, standardised therapy was initiated; dantrolene sodium suspension (5 mg kg(-1)) was administered and the injection was repeated after 24 min. The malignant hyperthermia trigger potency of MDMA was analysed by monitoring pH, PaCO2 and temperature. In addition, concentrations of thyroid hormone, mitochondrial uncoupling protein 3, noradrenaline and free fatty acids during administration of MDMA and dantrolene sodium suspension were analysed. MDMA administration led to fulminant hypermetabolic and hyperthermic responses in malignant hyperthermia-susceptible and malignant hyperthermia-normal pigs, with significant decreases in pH (susceptible: pH 7.21 ± 0.11, normal: pH 7.21 ± 0.07), severe hypercapnia (susceptible: paCO2 10.3 ± 3.5 kPa, normal: paCO2 9.8 ± 1.7 kPa), and hyperthermia (susceptible: 40.6 ± 2.0°C, normal: 40.1 ± 0.4°C). There were no significant differences in changes in clinical and laboratory variables between groups. The dantrolene therapy regimen was effective in treating the MDMA-induced metabolic crises. MDMA is not a classic trigger for the development of malignant hyperthermia reactions in pigs. MDMA intoxication leads to severe, long-lasting hyperthermia and hypermetabolism in both malignant hyperthermia-susceptible and hyperthermia-normal pigs, with life-threatening malignant hyperthermia-like symptoms which are responsive to supportive treatment and dantrolene sodium suspension.

Deep-water prawn Pandalus borealis displays a relatively high pH regulatory capacity in response to CO2-induced acidosis

Deep-water prawn Pandalus borealis displays a relatively high pH regulatory capacity in response to CO2-induced acidosis

Postoperative delayed hypercapnia and respiratory failure after robot-assisted lower anterior resection

Postoperative delayed hypercapnia and respiratory failure after robot-assisted lower anterior resection

Influence of hypercapnia on the synthesis of neuropeptides and their receptors in murine brain

Sleep disorders are a complicated and major public health concern affecting millions of individuals. Obstructive sleep apnoea (OSA) is a common but still under-recognized disease which can cause intermittent nocturnal hypercapnia. Neuropeptides play critical roles in neurotransmission, acting as transmitters or modulators. Results from recent studies have implicated several neuropeptides in sleep and breathing regulation, including orexin, neuropeptides Y and galanin. Therefore, the present study aimed to evaluate the influence of hypercapnia on these neuropeptides and their receptors in order to assess their potential role in the pathogenesis of OSA. Fifteen C57BL/6J mice were randomly divided into three groups and exposed to moderate hypercapnia (5% CO(2) with balanced room air), or severe hypercapnia (10% CO(2) with balanced room air) or room air for 3 h (9:00-12:00 h), respectively. Immediately following exposure the brainstem and hypothalamus were excised for real-time reverse transcription polymerase chain reaction and western blot analyses. In the hypothalamus gene expression including galanin, orexin and neuropeptide Y receptor 1 (NPYR1) was downregulated by hypercapnia. However, protein and mRNA levels of orexin-A receptor were upregulated by severe hypercapnia. In the brainstem only NPYR1 mRNA expression was decreased in moderate hypercapnia compared with that in severe hypercapnia. These findings suggest that hypercapnia can affect these neuropeptides and their receptors, especially the orexin and orexin-A receptor. The potential relationships between these peptides and OSA are worthy of further investigation.

Lethal pneumonitis after docetaxel chemotherapy: Case report and review of the literature

Interstitial pneumonitis is a known, but uncommon adverse event during docetaxel therapy in cancer patients. We report the case of a patient with breast cancer who developed a severe, progressive pneu-monitis during dose-dense neoadjuvant chemother-apy with docetaxel. The condition was steroid resistant, and she died after 20 days on advanced ventilator therapy in the intensive care unit. The pneumonitis was complicated by reduced lung compliance, bilateral pneumothorax and severe hypercapnia and hypoxia. To our knowledge, this is the fi rst case of taxane-induced pneumonitis with a following autopsy report. We review the present lit-erature about the condition and discuss potential disease mechanisms.

Inhalational sevoflurane in severe bronchial obstruction unresponsive to multipharmacologic therapy: a case report

Introduction: Bronchial asthma with respiratory failure is a challenge for the intensivist as mechanical ventilation is often difficult due to bronchoconstriction and air-trapping. We describe a case of severe asthma with respiratory acidosis in a 10-year-old patient unresponsive to multipharmacologic broncholytic therapy. Only the initiation of sevoflurane inhalation resolved severe bronchoconstriction and dynamic hyperinflation, leading to complete recovery. Case presentation: A 10-year-old Caucasian boy was intubated and mechanically ventilated due to an asthmatic attack. Bronchoconstriction and dynamic hyperinflation were severe while multipharmacological broncholytic therapy was unsuccessful. Inhalation with sevoflurane via an anaesthesia machine was the key intervention leading to gradual resolving of severe hypercapnia and respiratory acidosis. Furthermore bilateral pupil dilation occurred during hypercapnia, but no intracranial pathology could be detected. The patient made an uneventful recovery. To our knowledge this is the first case where hypercapnia and respiratory acidosis were so profound and long lasting yet the patient survived without any damage. Conclusions: Inhalational anaesthetics must be considered as an early treatment option in ventilated asthmatic patients with bronchial obstruction unresponsive to conventional therapy even though their administration in intensive care units may be difficult.

Inhalational sevoflurane in severe bronchial obstruction unresponsive to multipharmacologic therapy: a case report

Introduction: Bronchial asthma with respiratory failure is a challenge for the intensivist as mechanical ventilation is often difficult due to bronchoconstriction and air-trapping. We describe a case of severe asthma with respiratory acidosis in a 10-year-old patient unresponsive to multipharmacologic broncholytic therapy. Only the initiation of sevoflurane inhalation resolved severe bronchoconstriction and dynamic hyperinflation, leading to complete recovery. Case presentation: A 10-year-old Caucasian boy was intubated and mechanically ventilated due to an asthmatic attack. Bronchoconstriction and dynamic hyperinflation were severe while multipharmacological broncholytic therapy was unsuccessful. Inhalation with sevoflurane via an anaesthesia machine was the key intervention leading to gradual resolving of severe hypercapnia and respiratory acidosis. Furthermore bilateral pupil dilation occurred during hypercapnia, but no intracranial pathology could be detected. The patient made an uneventful recovery. To our knowledge this is the first case where hypercapnia and respiratory acidosis were so profound and long lasting yet the patient survived without any damage. Conclusions: Inhalational anaesthetics must be considered as an early treatment option in ventilated asthmatic patients with bronchial obstruction unresponsive to conventional therapy even though their administration in intensive care units may be difficult.

Comparative effects of bronchoalveolar lavage with saline, surfactant, or perfluorocarbon in experimental meconium aspiration syndrome*

Today, in meconium aspiration syndrome, treatment focuses on bronchoalveolar lavage, because it removes meconium and proinflammatory factors from airways. This technique might be more effective if different solutions were used such as saline solution, a protein-free surfactant, or a perfluorocarbon, because these would be less inhibited by meconium proteins. Pulmonary physiology research unit, Cruces Hospital. Prospective, randomized study. We studied 24 lambs (<6 days) on mechanical ventilation for 180 mins. Catheters were placed and femoral and pulmonary arteries pressures registered (systemic and pulmonary arterial pressures). Lambs were instilled with 20% meconium (3-5 mL/Kg) and were randomly assigned to one of the following groups (n = 6): control: only continuous mechanical ventilation; saline bronchoalveolar lavage: bronchoalveolar lavage with 30 mL/kg of saline solution; dilute surfactant bronchoalveolar lavage: bronchoalveolar lavage with 32 mL/kg of diluted surfactant (lucinactant, 10 mg/mL); or perfluorocarbon bronchoalveolar lavage: bronchoalveolar lavage with 30 mL/kg of perfluorocarbon. Blood gases, cardiovascular parameters, and pulmonary mechanics were assessed. Meconium instillation produced severe hypoxia, hypercapnia, acidosis, and pulmonary hypertension with impairment of pulmonary mechanics (p < .05). Lung lavage with dilute surfactant resulted in the resolution of pulmonary hypertension as well as better gas exchange and pulmonary mechanics than the control group (p < .05). Bronchoalveolar lavage with perfluorocarbon produced a transient improvement in gas exchange and ventilatory indices in comparison with control and saline bronchoalveolar lavage groups. In lambs with meconium aspiration syndrome, bronchoalveolar lavage with diluted lucinactant is an effective therapy producing significant improvements in gas exchange, pulmonary hypertension, and pulmonary mechanics. In addition, bronchoalveolar lavage with perfluorocarbon appears to confer some advantages over lavage with equal volumes of saline or no lavage.

Characterization of the relationship between inspiratory neural discharges and the micturition reflex in decerebrate and urethane‐anesthetized adult in vivo rat

Previous studies have characterized respiratory neural outputs during the micturition reflex (MR). However, these studies primarily were conducted in cats, and it is not known if the relationship seen in the cat model is maintained in rodent models. To begin to address this issue, we recorded bladder pressure and phrenic (Phr), hypoglossal (XII) and pudendal motor nerve activity in decerebrate or urethane‐anesthetized vagi‐intact adult rats during passive bladder filling and active bladder contraction. Spontaneous MRs were elicited by slow infusion of saline into the bladder. The data show increased Phr post‐inspiratory activity and a transient increase followed by a transient decrease in burst frequency (due to changes in TE). Small XII neural discharges were observed during expiration while the bladder actively contracted. In contrast to cat data, no changes in Phr or XII amplitude were observed. Finally, while severe hypercapnia and hypocapnia affected respiratory patterns, they did not affect the MR. We conclude that, while there are some similarities to the cat model, a different relationship between respiration and micturition occurs in rat. Supported by HL63175

Activation of the Orexin 1 Receptor is a Critical Component of CO2-Mediated Anxiety and Hypertension but not Bradycardia

Acute hypercapnia (elevated arterial CO(2)/H(+)) is a suffocation signal that is life threatening and rapidly mobilizes adaptive changes in breathing and behavioral arousal in order to restore acid-base homeostasis. Severe hypercapnia, seen in respiratory disorders (eg, asthma or bronchitis, chronic obstructive pulmonary disease (COPD)), also results in high anxiety and autonomic activation. Recent evidence has demonstrated that wake-promoting hypothalamic orexin (ORX: also known as hypocretin) neurons are highly sensitive to local changes in CO(2)/H(+), and mice lacking prepro-ORX have blunted respiratory responses to hypercapnia. Furthermore, in a recent clinical study, ORX-A, which crosses blood-brain barrier easily, was dramatically increased in the plasma of patients with COPD and hypercapnic respiratory failure. This is consistent with a rodent model of COPD where chronic exposure to cigarette smoke led to a threefold increase in hypothalamic ORX-A expression. In the present study, we determined the role of ORX in the anxiety-like behavior and cardiorespiratory responses to acute exposure to a threshold panic challenge (ie, 20% CO(2)/normoxic gas). Exposing conscious rats to such hypercapnic, but not atmospheric air, resulted in respiratory, pressor, and bradycardic responses, as well as anxiety-like behavior and increased cellular c-Fos responses in ORX neurons. Systemically, pre-treating rats with a centrally active ORX1 receptor antagonist (30 mg/kg SB334867) attenuated hypercapnic gas-induced pressor and anxiety responses, without altering the robust bradycardia response, and only attenuated breathing responses at offset of the CO(2) challenge. Our results show that the ORX system has an important role in anxiety and sympathetic mobilization during hypercapnia. Furthermore, ORX1 receptor antagonists may be a therapeutic option rapidly treating increased anxiety and sympathetic drive seen during panic attacks and in hypercapnic states such as COPD.

Le syndrome d’hypoventilation alvéolaire central congénital (CCHS) : un cas de révélation tardive

The congenital central hypoventilation syndrome (CCHS) or Ondine's curse is a rare autosomal dominant disease, characterized by disorders of the autonomic nervous system, with abnormal ventilatory responses to hypercapnia and hypoxia. PHOX2B has been identified as the major gene causing CCHS. It results from polyalanine repeat expansion mutations. It typically presents in the newborn period but some cases have been described in adults (late onset CCHS) reflecting the variable penetrance of PHOX2B mutations. A 48 year-old woman presented, after ovarian cyst surgery, with severe hypoventilation requiring intubation. Arterial blood gases revealed a PaO2 of 6.6kPa (50mmHg), a PaCO2 of 10kPa (80mmHg) and a pH of 7.22. The past medical history revealed nocturnal symptoms for a few years. These included apnoeas, fitful sleep and awakening with headaches. Physical examination, pulmonary function tests, lung tomography and magnetic resonance imaging of the brainstem were all normal. Polysomnography revealed numerous central and obstructive apnoeas and hypopnoeas, with severe hypoxaemia and hypercapnia. Hypoxic and hypercapnic stimulation tests showed no adaptation of the ventilatory responses. Genetic analysis showed a heterozygous five alanine expansion mutation of the 20-residue polyalanine tract in exon 3 of the PHOX2B gene. The diagnosis of late onset CCHS should be considered in patients with unexplained hypoventilation, and physiological evaluation should be undertaken to document the abnormal ventilatory responses. The presence of a PHOX2B mutation confirms the diagnosis.

Rescue Therapy With a Pumpless Extracorporeal Lung Assist Device in a Patient With Acute Interstitial Lung Disease and Severe Refractory Hypercapnia

Idiopathic interstitial pneumonia frequently causes severe pulmonary restriction that in turn makes mechanical ventilation difficult. We report the case of a 44-year-old woman who developed a refractory severe hypercapnic respiratory failure (P(aCO(2)) 281 mm Hg, pH 6.77) despite mechanical ventilation with high inspiratory pressure and PEEP. A pumpless extracorporeal lung assist device, Novalung, was used as rescue therapy for carbon dioxide removal, enabling lung-protective ventilation and normalization of life-threatening acidosis. Open lung biopsy revealed an idiopathic interstitial pneumonia with histological features of a nonspecific interstitial pneumonia. Corticosteroid therapy led to progressive improvement of pulmonary function, soon permitting cessation of mechanical ventilation and extracorporeal therapy. The patient was discharged from the intensive care unit after 20 days. This case demonstrates the successful use of pumpless extracorporeal lung assist as an alternative device to pump-driven extracorporeal membrane oxygenation in severe hypercapnic respiratory failure secondary to nonspecific interstitial pneumonia.

Short-lived survival of severe hypercapnia from chronic respiratory failure in motor neuron disease

Surviving extreme hypercapnia from muscular respiratory failure has been only rarely reported. A 66-year-old male developed slowly progressive weakness of the lower limbs since one year resulting in recurrent falls and later dysarthria, weakness of the left intrinsic hand muscles, general wasting, brisk tendon reflexes, and symmetric stocking type pall-hypaesthesia. Electromyograms of various muscles were neurogenic. Cerebral MRI showed diffuse atrophy, leucaraiosis, spot-like hyperintensities subcortically and in the basal ganglia and a diffuse hypersignal in the pons. Probable amyotrophic lateral sclerosis (ALS) was diagnosed. Four months later he was admitted for respiratory insufficiency, impaired consciousness, exsiccosis, and cachexia. Blood pH was 6.9 and blood pCO2 was 235 mmHg (n, 35 - 45 mmHg). Within six hours under mechanical ventilation he recovered completely from hypercapnia and actively extubated himself two days after admission. This case shows that severe hypercapnia from weakness of the respiratory muscles may be survived if respiratory failure develops slowly, and if adequately treated.

Le pneumothorax tuberculeux (PT) : à propos de 29 cas

Background: Hypercapnic coma is a rare differential diagnosis in the unconscious patient. One underlying mechanism may be hypoventilation due to spontaneous pneumothorax. Although hypercapnia is not a typical finding in spontaneous pneumothorax in patients with otherwise healthy lungs, under certain circumstances, hypercapnia may readily develop. Objectives: We report a rare case of profound hypercapnic coma due to spontaneous pneumothorax after contralateral pneumonectomy. In addition, we review other causes of hypercapnic coma and its outcome and discuss the relationship between arterial carbon dioxide partial pressure and level of consciousness. Case Report: An 85-year-old man without evidence of trauma or intoxication presented unconscious to our Emergency Department. The physical examination and X-ray study revealed a left-sided spontaneous pneumothorax. A right-sided pneumonectomy 25 years earlier had promoted the development of profound hypercapnic coma. After insertion of a thoracic drain, the coma rapidly resolved without any neurological deficit. Conclusions: Although severe hypercapnia is usually due to decompensation of chronic lung disease, pneumothorax potentially may cause hypercapnic coma. Review of the literature suggests that there is no close correlation between arterial pCO2 (partial pressure of CO2) levels and the degree of impairment of consciousness; however, levels exceeding 80 mm Hg are likely associated with significantly impaired consciousness. Hypercapnic coma usually resolves without neurological deficit as arterial pCO2 tensions decline.

High-frequency oscillatory ventilation with and without arteriovenous extracorporeal lung assist in patients with severe respiratory failure

PurposeElimination of carbon dioxide by an arteriovenous extracorporeal lung assist (av-ECLA) can facilitate the lung protective capabilities of high-frequency oscillatory ventilation (HFOV). This case series describes patients treated with HFOV because of severe respiratory failure with and without additional av-ECLA. MethodsA retrospective analysis of 31 patients regarding patient characteristics, gas exchange, respirator settings, hemodynamics, and outcome. In 18 patients, av-ECLA was started before, together with, or during HFOV. ResultsThe initial arterial carbon dioxide tension before HFOV and av-ECLA was higher in patients who received av-ECLA compared with patients without (P = .043): 65 (48-84) mm Hg and 50 (44-60) mmHg (median and interquartile range). The initial arterial oxygen tension (Pao2)/inspiratory oxygen fraction (Fio2) index in patients who received av-ECLA was 79 (63-133) mm Hg. The Pao2/Fio2 index immediately before HFOV was 84 (65-124) mm Hg (av-ECLA) and 121 (68-150) mmHg (no av-ECLA) and improved to 149 (89-231) mm Hg and 200 (117-233) mmHg during HFOV. Similarly, the oxygenation index improved. No statistically significant differences among groups were detected for Pao2/Fio2 index, oxygenation index, and arterial carbon dioxide tension immediately before and during HFOV. The hospital mortality was 39% (av-ECLA) and 69% (no av-ECLA). ConclusionsHigh-frequency oscillatory ventilation improved the oxygenation in patients with severe respiratory failure. Additional av-ECLA may facilitate using lung protective HFOV settings in more severe lung injury and hypercapnia.

Metabolic changes associated with acid–base regulation during hypercarbia in the CO 2-tolerant chondrostean, white sturgeon ( Acipenser transmontanus)

CO 2 tolerance in white sturgeon is associated with the ability to tightly regulate intracellular pH (pHi) despite a large reduction in extracellular pH (pHe) termed preferential pHi regulation. How this regulatory response affects whole animal metabolic rate is unknown. Accordingly, we characterized oxygen consumption rate ( M ˙ O 2 ) and metabolically-relevant organismal and cellular responses in white sturgeon during exposure to hypercarbia. White sturgeon were able to protect intracellular pH (pHi) in liver and white muscle as early as 6 h (the earliest time period investigated) following exposure to severe (sub-lethal) hypercarbia (45 and 90 mmHg PCO 2). Sturgeon exposed to 15 and 30 mmHg PCO 2 exhibited pHe compensation and significant increases in M ˙ O 2 (up to 80% greater than control values). In contrast, severe hypercarbia (≥ 45 mmHg PCO 2) elicited an uncompensated reduction in pHe (up to ~ 1.0 pH units) and red blood cells (as great as ~ 0.5 pH units), and was accompanied by 30 and 60% reductions in M ˙ O 2 , respectively. While behavioral, respiratory and cellular responses to hypercarbia were observed, none corresponded well with the pattern or magnitude of changes in M ˙ O 2 . The findings of this research provide empirical support for the hypothesis that preferential pHi regulation is not metabolically costly, and thus may have been a strategy strongly selected for in fishes encountering short-term hypercarbia.

Very Low Tidal Volume Ventilation with Associated Hypercapnia - Effects on Lung Injury in a Model for Acute Respiratory Distress Syndrome

BackgroundVentilation using low tidal volumes with permission of hypercapnia is recommended to protect the lung in acute respiratory distress syndrome. However, the most lung protective tidal volume in association with hypercapnia is unknown. The aim of this study was to assess the effects of different tidal volumes with associated hypercapnia on lung injury and gas exchange in a model for acute respiratory distress syndrome.Methodology/Principal FindingsIn this randomized controlled experiment sixty-four surfactant-depleted rabbits were exposed to 6 hours of mechanical ventilation with the following targets: Group 1: tidal volume = 8–10 ml/kg/PaCO2 = 40 mm Hg; Group 2: tidal volume = 4–5 ml/kg/PaCO2 = 80 mm Hg; Group 3: tidal volume = 3–4 ml/kg/PaCO2 = 120 mm Hg; Group 4: tidal volume = 2–3 ml/kg/PaCO2 = 160 mm Hg. Decreased wet-dry weight ratios of the lungs, lower histological lung injury scores and higher PaO2 were found in all low tidal volume/hypercapnia groups (group 2, 3, 4) as compared to the group with conventional tidal volume/normocapnia (group 1). The reduction of the tidal volume below 4–5 ml/kg did not enhance lung protection. However, oxygenation and lung protection were maintained at extremely low tidal volumes in association with very severe hypercapnia and no adverse hemodynamic effects were observed with this strategy.ConclusionVentilation with low tidal volumes and associated hypercapnia was lung protective. A tidal volume below 4–5 ml/kg/PaCO2 80 mm Hg with concomitant more severe hypercapnic acidosis did not increase lung protection in this surfactant deficiency model. However, even at extremely low tidal volumes in association with severe hypercapnia lung protection and oxygenation were maintained.

Extracorporeal membrane oxygenation for refractory, life-threatening, and herpes simplex virus 1–induced acute respiratory distress syndrome. Our experience and literature review

We report our first experience of treating an immunocompetent adult patient with acute respiratory distress syndrome (ARDS) due to type 1 herpes simplex (HSV1) pneumonitis, using extracorporeal membrane oxygenation (ECMO). Similar cases reported in literature are reviewed as well. The therapeutic options for this particular complication are discussed. Pneumonia caused by HSV1 is a rare finding in immunocompetent individuals; it occurs more often in immunosuppressed and ventilated patients. It is a severe illness; therefore, early diagnosis and initiation of treatment are imperative. Diagnosis is based on cytologic and histologic findings, viral cultures, or serologic methods. This condition can be reversible; however, often, it can progress into refractory ARDS with limited therapeutic options available. We demonstrate the causative role of HSV1 in refractory ARDS of a previously healthy 18-year-old man who presented to the intensive care unit with acute respiratory distress after a week of flulike syndrome. Due to severe hypoxemia and hypercarbia, the patient required mechanical ventilation and later emergent blood oxygenation with extracorporeal support. For the first time in this condition, we used venovenous ECMO management, to rest the lung, sustain blood oxygenation and end-organ oxygen delivery, and promote potential lung recovery. During ECMO and after our etiologic diagnosis, specific therapy was introduced. After viral negativization, corticosteroid therapy (Meduri protocol) was initiated. Extracorporeal membrane oxygenation allowed us to initiate therapy while maintaining end-organ oxygenation and support the patient until lung recovery. After 18 days of ECMO, our patient recovered completely. Near-normal lung structures and functions were documented on a chest x-ray/computed tomography, thoracic ultrasonography, and pulmonary functional tests at hospital discharge and at a 1-year follow-up. Data suggest that severe pulmonary involvement in HVS1 infection associated with septicemia/shock is a rare but often fatal in immunocompetent adult as well. We suggest that ECMO might be the selected treatment for severe refractory ARDS in this clinical scenario. It seems to be an effective and useful ultimate therapeutic strategy for preventing death and furthermore permitting near-full pulmonary function recovery.

A coaxial breathing system may be faulty: Report of a case of severe hypercapnia after anesthesia induction

Makris, A.; Tsirigotis, A.; Gatos, N.; Rozakis, D.; Skarpa, N.; Mela, A. Author Information