Innovative treatment of hypercapnia with soda lime in COVID-19: a case report.

One of the rare consequences of COVID-19 is increasing blood carbon dioxide, which can lead to unconsciousness, dysrhythmia, and cardiac arrest. Therefore, in COVID-19 hypercarbia, non-invasive ventilation (with Bi-level Positive Airway Pressure, BiPAP) is recommended for treatment. If CO2 does not decrease or continues rising, the patient's trachea must be intubated for supportive hyperventilation with a ventilator (Invasive ventilation). The high morbidity and mortality rate of mechanical ventilation is an important problem of invasive ventilation. We launched an innovative treatment of hypercapnia without invasive ventilation to reduce morbidity and mortality. This new approach could open the window for researchers and therapists to reduce COVID death. To investigate the cause of hypercapnia, we measured the carbon dioxide of the airways (mask and tubes of the ventilator) with a capnograph. Increased carbon dioxide inside the mask and tubes of the device was found in a severely hypercapnic COVID patient in the Intensive Care Unit (ICU). She had a 120kg weight and diabetes disease. Her PaCO2 was 138mmHg. In this condition, she had to be under invasive ventilation and accept its complication or lethal risk but we decreased her PaCO2 with the placement of a soda lime canister in the expiratory pathway to absorb CO2 from the mask and ventilation tube. Her PaCO2 dropped from 138 to 80, and the patient woke up from drowsiness completely without invasive ventilation, the next day. This innovative method continued until PaCO2 reached 55 and she was discharged home 14 days later after curing her COVID. Soda lime is used for carbon dioxide absorption in anesthesia machines and we can research its application in hypercarbia state in ICU to postpone invasive ventilation for treatment of hypercapnia.

Hypercapnia in COPD Patients Undergoing Endobronchial Ultrasound under Local Anaesthesia and Analgosedation: A Prospective Controlled Study Using Continuous Transcutaneous Capnometry.

BACKGROUND: Flexible bronchoscopy (FB) in analgosedation causes alveolar hypoventilation and hypercapnia, the more so if patients suffer from COPD. Nonetheless, neither is capnometry part of standard monitoring nor is there evidence on how long patients should be monitored after sedation. OBJECTIVES: We investigated the impact of COPD on hypercapnia during FB with endobronchial ultrasound (EBUS) in sedation and how the periprocedural monitoring should be adapted. METHODS: Two cohorts of consecutive patients - with advanced and without COPD - with the indication for FB with EBUS-guided transbronchial needle aspiration in analgosedation received continuous transcutaneous capnometry (ptcCO2) before, during, and for 60 min after the sedation with midazolam and alfentanil. MAIN RESULTS: Forty-six patients with advanced COPD and 44 without COPD were included. The mean examination time was 26 ± 9 min. Patients with advanced COPD had a higher peak ptcCO2 (53.7 ± 7.1 vs. 46.8 ± 4.8 mm Hg, p < 0.001) and mean ptcCO2 (49.5 ± 6.8 vs. 44.0 ± 4.4 mm Hg, p < 0.001). Thirty-six percent of all patients reached the maximum hypercapnia after FB in the recovery room (8 ± 11 min). Patients with COPD needed more time to recover to normocapnia (22 ± 24 vs. 7 ± 11 min, p < 0.001). They needed a nasopharyngeal tube more often (28 vs. 11%, p < 0.001). All patients recovered from hypercapnia within 60 min after FB. No intermittent ventilation manoeuvres were needed. CONCLUSION: A relevant proportion of patients reached their peak-pCO2 after the end of intervention. We recommend using capnometry at least for patients with known COPD. Flexible EBUS in analgosedation can be safely performed in patients with advanced COPD. For patients with advanced COPD, a postprocedural observation time of 60 min was sufficient.

Unusual case of central alveolar hypoventilation.

Central alveolar hypoventilation is rarely encountered. This case report describes a young woman who was recently diagnosed with hypertension and ischemic heart disease. She presented to the emergency room with hypercapnic respiratory failure, for which she was mechanically ventilated. This was preceded by an acute upper respiratory tract infection. She was initially suspected to have Guillain-Barré syndrome, but further investigations ruled out neuromuscular or autoimmune disorders. Sleep-related hypoventilation was suspected after she experienced recurrent apneas at night that resulted in re-intubation. Polysomnographic studies confirmed episodes of central apnea and hypopnea during sleep, with significant carbon dioxide retention and oxygen desaturations. She required nocturnal ventilation via a tracheostomy tube until a diaphragmatic pacer could be placed. Using bi-level positive airway pressure and average volume-assured pressure support together with the diaphragmatic pacer, adequate ventilation during sleep was achieved.

Protective effect of Dl-3n-butylphthalide on learning and memory impairment induced by chronic intermittent hypoxia-hypercapnia exposure.

Cognitive impairment is a common finding in patients with chronic obstructive pulmonary disease (COPD), but little attention has been focused on therapeutic intervention for this complication. Chronic intermittent hypoxia hypercapnia (CIHH) exposure is considered to be responsible for the pathogenesis of COPD. Dl-3n-Butylphthalide (NBP), extracted from Apium graveolens Linn, has displayed a broad spectrum of neuroprotective properties. Our study aimed to investigate the potential of NBP on CIHH-induced cognitive deficits. The cognitive function of rats after CIHH exposure was evaluated by the Morris water maze, which showed that the NBP treated group performed better in the navigation test. NBP activated BDNF and phosphorylated CREB, the both are responsible for neuroprotection. Additionally, NBP decreased CIHH induced apoptosis. Moreover, NBP further induced the expression of HIF-1α, accompanied by the up-regulation of the autophagy proteins Bnip3, Beclin-1 and LC3-II. Finally, NBP also reversed the decreased expression of SIRT1 and PGC-1α, but the expression of Tfam, Cox II and mtDNA remained unchanged. These results suggested that the neuroprotective effects of NBP under CIHH condition possibly occurred through the inhibition of apoptosis, promotion of hypoxia-induced autophagy, and activation of the SIRT1/PGC-1α signalling pathway, while stimulation of mitochondrial biogenesis may not be a characteristic response.

Evaluation of a respiratory rehabilitation program in children with scoliosis.

BACKGROUND: Thoracic scoliosis is a lateral curvature of the spine associated with restrictive lung defects, manifested by a decrease in respiratory function tests. We undertook this study to evaluate the effect of a respiratory rehabilitation program over lung function in children with scoliosis. METHODS: We carried out a prospective and deliberate intervention study including 25 consecutive patients, aged 6 to 18 years, diagnosed with thoracic scoliosis. The respiratory rehabilitation program was structured into two phases: institutional and private residence. Statistical analysis was carried out using descriptive parameters and paired t-test and Wilcoxon signed-ranks test. Spearman correlation was used to measure intensity of association among variables. Statistical significance was considered when p <0.05. RESULTS: Idiopathic scoliosis was present in 52% of patients, with right dorsal curvature in 72%. Cobb angle average was 50.6° ± 29.7°. Most importantly, we found a negative correlation between this angle on left curvature and lung function. Initially, the main respiratory symptoms were dyspnea with poor effort tolerance in 52%. After treatment, 88% of patients were asymptomatic and only 4% presented poor effort tolerance. Oxygen saturation and forced vital capacity percentage had a significant increment after the program. CONCLUSION: Respiratory rehabilitation has a positive effect on increasing pulmonary function of children with scoliosis.

Effects of loading on upper airway and respiratory pump muscle motoneurons.

The functional outcomes of respiratory muscle loading by chemical (e.g. hypercapnia), mechanical (i.e. external mechanical loading) or ventilatory (e.g. exercise) factors can be either positive, such as through an increase in pressure-generating capacity of the inspiratory muscles or detrimental, such as by fatigue. Neurophysiological responses to respiratory muscle loading can occur at one or more points along the pathway from motor cortex to muscle. This paper describes the respiratory pump and upper airway motoneuron responses to the imposition of acute loads including processes of pre-activation, respiratory reflexes, potentiation and fatigue. It also considers changes suggestive of adaptation to chronic loading either from specific respiratory muscle training programs or as part of disease processes such as chronic obstructive pulmonary disease or obstructive sleep apnoea.

Atrial electrophysiology is altered by acute hypercapnia but not hypoxemia: implications for promotion of atrial fibrillation in pulmonary disease and sleep apnea.

BACKGROUND: Chronic pulmonary disease and sleep apnea have been associated with the development of atrial fibrillation (AF). OBJECTIVE: The purpose of this study was to characterize the atrial electrical changes that occur with hypercapnia and hypoxemia and to determine their role in AF development. METHODS: Seventeen sheep (6 control, 5 hypercapnia, 6 hypoxemia) underwent open chest electrophysiologic evaluation under autonomic blockade. A 64-electrode endocardial basket catheter was positioned in the right atrium, and 2 x 128 electrode epicardial plaques were sutured to the right atrial and left atrial appendages to determine atrial refractoriness (effective refractory period [ERP]) at 9 sites and 5 cycle lengths, conduction time to fixed points on each plaque, and AF vulnerability. RESULTS: Hypercapnia was associated with a 152% lengthening of ERP from baseline and increased conduction time. ERPs rapidly returned to baseline, but recovery of conduction was delayed at least 117 +/- 24 minutes following resolution of hypercapnia. AF vulnerability was reduced during hypercapnia (with increased ERP) but increased significantly with subsequent return to eucapnia (when ERP normalized but conduction time remained prolonged). No significant changes in ERP, atrial conduction time, or AF vulnerability occurred in hypoxemic or control groups. CONCLUSION: Differential recovery of ERP and conduction that occurs following hypercapnia might account for the increased vulnerability to AF observed in the phase after return to eucapnia. This may explain in part the increased prevalence of AF in pulmonary disease and sleep apnea.

[Salbutamol improves diaphragmatic contractility in chronic airway obstruction]. / El salbutamol mejora la contractilidad diafragmática en la obstrucción crónica de la vía aérea.

INTRODUCTION: Chronic airflow obstruction in conditions such as chronic obstructive pulmonary disease is associated with respiratory muscle dysfunction. Our aim was to study the effects of salbutamol-a beta-adrenergic agonist known to improve muscle strength in physiologic and pathologic conditions-on diaphragm contractility in an animal model of chronic airway obstruction achieved by tracheal banding. MATERIALS AND METHODS: Twenty-four Sprague-Dawley rats were randomized into a control group and 3 tracheal banding groups, 1 that received acute salbutamol treatment, 1 that received chronic salbutamol treatment, and 1 that received nothing. Arterial blood gases, acid-base balance, and in vitro diaphragmatic contractility were evaluated by measuring peak twitch tension, contraction time, contraction velocity, half-relaxation time, relaxation velocity, and force-frequency curves. RESULTS: The 3 study groups had significantly reduced arterial pH and increased PaCO2 and bicarbonate levels compared to the control group (P<.05). The untreated tracheal banding group had significantly reduced peak twitch tension and contraction velocity, and a significantly lower force-frequency curve in comparison with the other groups (P<.05). The chronic treatment group had a higher relaxation velocity than the untreated study group (P<.05). The mean (SE) peak twitch tension values were 6.46 (0.90)N/cm(2) for the control group, 3.28 (0.55)N/cm(2) for the untreated tracheal banding group, 6.18 (0.71)N/cm(2) for the acute treatment group, and 7.09 (0.59)N/cm(2) for the chronic treatment group. CONCLUSIONS: Diaphragmatic dysfunction associated with chronic airflow obstruction improves with both the acute and chronic administration of salbutamol. The mechanisms involved in respiratory muscle dysfunction warrant further study.

Extramedullary hematopoiesis-related pleural effusion: the case of beta-thalassemia.

BACKGROUND: Thalassemia intermedia has a later clinical onset and a milder anemia than thalassemia major, characterized by high output state, left ventricle remodeling, and age-related pulmonary hypertension. Bone deformities, extramedullary hematopoiesis (EMH), and spleen and liver enlargement are the consequences of hypoxia and enhanced erythropoiesis. The EMH-related pleural effusion is rarely referred to in the literature of thalassemia. METHODS: We reviewed the thalassemia patients' medical records hospitalized for pleural effusion in our Department, within the last 6 years. RESULTS: Eight (4 men) thalassemia intermedia patients admitted for symptomatic pleural effusion were identified. Common clinical findings on admission were dyspnea and apyrexia. Their mean hemoglobin level was 7.15 +/- 0.64 g/dL. Radiology revealed intrathoracic EMH and pleural effusion in all patients: exudative in seven patients and massive hemothorax in one. Cytologic fluid analysis was negative for malignancy. Fluid and serum cultures, antibodies, and stains were negative for viral, bacterial, and fungal infection. The hemothorax case was successfully treated with repeated aspirations, transfusions, and hydroxyurea. Although repeated thoracentesis and radiation could not control the effusions in the rest of the cases, pleurodesis was successful in 5 patients, without serious adverse events. Treatment was further accomplished with hydroxyurea. No relapses were observed in the mean 30 month follow-up period. CONCLUSIONS: Afebrile, EMH-related pleuritis represents a potentially life-threatening complication in thalassemia. Therapy should be individualized and treatment is emerging. Pleurodesis seems to be an effective and safe therapeutic option for exudative effusions, while transfusion-chelation therapy combined with hydroxyurea may be helpful in suppressing increased erythropoiesis.

Tube breathing as a new potential method to perform respiratory muscle training: safety in healthy volunteers.

Normocapnic hyperpnea has been established as a method of respiratory muscle endurance training (RMET). This technique has not been applied on a large scale because complicated and expensive equipment is needed to maintain CO(2)-homeostasis during hyperpnea. This CO(2)-homeostasis can be preserved during hyperpnea by enlarging the dead space of the ventilatory system. One of the possibilities to enlarge dead space is breathing through a tube. If tube breathing is safe and feasible, it may be a new and inexpensive method for RMET, enabling its widespread use. The aim of this study was to evaluate the safety of tube breathing and investigate the effect on CO(2)-homeostasis in healthy subjects. A total of 20 healthy volunteers performed 10 min of tube breathing (dead space 60% of vital capacity). Oxygen-saturation, PaCO(2), respiratory muscle function, hypercapnic ventilatory response and dyspnea (Borg-score) were measured. Tube breathing did not lead to severe complaints, adverse events or oxygen desaturations. A total of 14 out of 20 subjects became hypercapnic (PaCO(2)>6.0 kPa) during tube breathing. There were no significant correlations between PaCO(2) and respiratory muscle function or hypercapnic ventilatory responses. The normocapnic versus hypercapnic subjects showed no significant differences between decrease in oxygen saturation (-0.7% versus -0.2%, respectively, P=0.6), Borg score (4.3 versus 4.7, P=0.9), respiratory muscle function nor hypercapnic ventilatory responses. Our results show that tube breathing is well tolerated amongst healthy subjects. No complaints, nor desaturations occurred. Hypercapnia developed in a substantial number of subjects. When tube breathing will be applied as respiratory muscle training modality, this potential development of hypercapnia must be considered.

Endogenous adenosine and secondary injury after chest trauma.

BACKGROUND: No previous studies have examined actions of adenosine or related compounds after blunt chest trauma, but we have shown that the prototype adenosine-regulating agent, acadesine (aminoimidazole carboxamide ribonucleotide [AICAR]), has multiple favorable anti-inflammatory actions after other forms of trauma, ischemia, hemorrhage, and sepsis; and that a progressive inflammatory response in the contralateral (uninjured) lung after unilateral blunt chest trauma is caused (in part) by activation and sequestration of circulating leukocytes (white blood cells [WBCs]). Thus, we hypothesized that AICAR would ameliorate WBC-dependent, secondary pathophysiologic changes after blunt chest trauma. METHODS: Mongrel pigs (28+/-1 kg, n = 21) were anesthetized, mechanically ventilated, and injured on the right chest (pulmonary contusion) with a captive bolt gun. Either AICAR (1 mg/kg + 0.2 mg/kg/min) or its saline vehicle were administered for a 12-hour period, beginning 15 minutes before injury. RESULTS: Injury caused a three- to fourfold increase in bronchoalveolar lavage (BAL) WBC counts, 10- to 20-fold increases in BAL protein, and 200% increases in lung edema as measured by wet-dry ratio (all p < 0.05), in both the injured (right) and the noninjured (left) lungs. With AICAR versus saline, BAL WBC counts, lung myeloperoxidase levels, and systemic hemodynamics were similar. However, the increases in BAL protein were attenuated by 30% to 50% (p < 0.14, NS) and edema was reduced (p < 0.05) in both lungs. Furthermore, oxygenation, hypercapnia, acidosis (all p < 0.05), and survival were improved (9 of 10 vs. 4 of 11, p < 0.04). CONCLUSION: Pretreatment with AICAR before experimental pulmonary contusion ameliorates the trauma-induced destruction of the alveolar capillary membrane, and attenuates the delayed secondary injury in the contralateral uninjured lung, by a mechanism that may be independent of leukocytes. Endogenous adenosine could have a role in the pathophysiologic response after blunt chest injury, with potential sites of action including the endothelium and alveolar macrophage. Adenosine-regulating agents may have therapeutic potential after blunt chest injury, but further studies are needed in clinically relevant models, with administration begun at the time of resuscitation.

Acute effects of deep diaphragmatic breathing in COPD patients with chronic respiratory insufficiency.

This study investigated the impact of deep diaphragmatic breathing (DB) on blood gases, breathing pattern, pulmonary mechanics and dyspnoea in severe hypercapnic chronic obstructive pulmonary disease (COPD) patients recovering from an acute exacerbation. Transcutaneous partial pressure of carbon dioxide (Ptc,CO2) and oxygen (Ptc,O2) and arterial oxygen saturation (Sa,O2), were continuously monitored in 25 COPD patients with chronic hypercapnia, during natural breathing and DB. In eight of these patients, breathing pattern and minute ventilation (V'E) were also assessed by means of a respiratory inductance plethysmography. In five tracheostomized patients, breathing pattern and mechanics were assessed by means of a pneumotachograph/pressure transducer connected to an oesophageal balloon. Subjective rating of dyspnoea was performed by means of a visual analogue scale. In comparison to natural breathing deep DB was associated with a significant increase in Ptc,O2 and a significant decrease in Ptc,CO2, with a significant increase in tidal volume and a significant reduction in respiratory rate resulting in increased V'E. During DB, dyspnoea worsened significantly and inspiratory muscle effort increased, as demonstrated by an increase in oesophageal pressure swings, pressure-time product and work of breathing. We conclude that in severe chronic obstructive pulmonary disease patients with chronic hypercapnia, deep diaphragmatic breathing is associated with improvement of blood gases at the expense of a greater inspiratory muscle loading.

Correction of blood pH attenuates changes in hemodynamics and organ blood flow during permissive hypercapnia.

OBJECTIVES: To determine whether changes in cardiac output, regional blood flow, and intracranial pressure during permissive hypercapnia are blood pH-dependent and can be attenuated by correction of intravascular acidemia. DESIGN: Prospective, controlled study. SETTING: Research laboratory. SUBJECTS: Female Marino ewes. INTERVENTIONS: Animals were instrumented with a pulmonary artery catheter, femoral arterial and venous catheters, a catheter in the third cerebral ventricle, and ultrasonic flow probes on the left carotid, superior mesenteric, and left renal arteries 1 wk before experimentation. At initiation of the protocol, ewes underwent endotracheal intubation and mechanical ventilation under general anesthesia. Minute ventilation was reduced to induce hypercapnia with a target PaCO2 of 80 torr (10.7 kPa). In the pH-uncorrected group (n = 6), arterial blood pH was allowed to decreased without treatment. In the pH-corrected group (n = 5), 14.4 mEq/kg of sodium bicarbonate was given intravenously as a bolus to correct arterial blood pH toward a target arterial pH of 7.40 (dose calculated by the Henderson-Hasselbalch equation). MEASUREMENTS AND MAIN RESULTS: Arterial blood pH, PCO2, cardiac output, intracranial pressure, and carotid, superior mesenteric, and renal artery blood flow rates were measured at normocapnic baseline and at every hour during hypercapnia for 6 hrs. In the pH-uncorrected group, arterial blood pH decreased from 7.41 +/- 0.03 at normocapnia to 7.14 +/- 0.01 (p < .01 vs. normocapnia) as blood PCO2 increased to 81.2 +/- 1.8 torr (10.8 +/- 0.2 kPa). In the pH-corrected group, arterial blood pH was 7.42 +/- 0.02 at normocapnia and was maintained at 7.37 +/- 0.01 while PaCO2 was increased to 80.3 +/- 0.9 torr (10.7 +/- 0.1 kPa). Significant increases in cardiac output occurred with the initiation of hypercapnia for both groups (pH-uncorrected group: 4.3 +/- 0.6 L/min at normocapnia vs. 6.8 +/- 1.0 L/min at 1 hr [p < .05]; pH-corrected group: 4.1 +/- 0.4 at normocapnia vs. 5.7 +/- 0.4 L/min at 1 hr [p < .05]). However, this increase was sustained only in the uncorrected group. Changes in carotid and mesenteric artery blood flow rates, as a percent of baseline values, showed sustained significant increases in the pH-uncorrected groups (p < .05) and only transient (carotid at 1 hr) or no (superior mesenteric) significant change in the pH-corrected groups. Conversely, significant increases in renal artery blood flow were seen only in the pH-uncorrected group during the last 2 hrs of the experiment (p < .05). Organ blood flow, as a percent of cardiac output, did not change significantly in either group. Intracranial pressure increased significantly in the pH-uncorrected group (9.0 +/- 1.5 mm Hg at normocapnia vs. 26.8 +/- 5.1 at 1 hr, p < .05), and remained increased, while showing no significant change in the pH-corrected group (8.5 +/- 1.6 mm Hg at normocapnia to 7.7 +/- 4.2 at 1 hr). CONCLUSIONS: Acute hypercapnia, induced within 1 hr, is associated with significant increases in cardiac output, organ blood flow, and intracranial pressure. These changes can be significantly attenuated by correction of blood pH with the administration of sodium bicarbonate, without adverse effects on hemodynamics.

Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest.

OBJECTIVE: To compare three endotracheal epinephrine instillation techniques in a pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest model. DESIGN: Prospective, randomized, laboratory comparison of three instillation techniques. SETTING: Large animal research facility at a children's hospital. SUBJECTS: Thirty-six preadolescent anesthetized and paralyzed Yucatan swine (mean weight 10.0 +/- 1.9 kg) with apnea-induced hypoxic and hypercarbic cardiopulmonary arrest. INTERVENTIONS: After 8 mins of cardiopulmonary arrest and 1 min of cardiopulmonary resuscitation (CPR), 500 micrograms (51 +/- 9 micrograms/kg) of radiolabeled endotracheal epinephrine was administered by direct injection (n = 17), injection via feeding catheter (n = 10), or via monitoring lumen built into the sidewall of the endotracheal tube (n = 9). CPR was resumed and continued for 5 mins. If resuscitation occurred, monitoring was continued for 1 hr. Outcome variables included successful resuscitation, pulmonary distribution, heart rate, mean arterial pressure, plasma radiolabeled epinephrine counts, and total plasma epinephrine concentrations. Analysis by Fisher's exact test, one-way analysis of variance and Pearson's phi coefficient was performed. MEASUREMENTS AND MAIN RESULTS: Successful resuscitation occurred in 31% of all pigs with no difference between groups (p = .69). Bilateral distribution occurred in 39% with no difference between groups (p = .25). No correlation was noted between successful resuscitation and distribution (p = .65). HR, mean arterial pressure, plasma radiolabeled epinephrine counts, and total plasma epinephrine concentrations showed significant changes over time within groups, but no difference between groups at any time point. Adherence of the epinephrine dose to the endotracheal tube was < or = 1.5% in all cases. CONCLUSIONS: Instillation of 50 micrograms/kg of endotracheal epinephrine by three different techniques during pediatric porcine asphyxial arrest does not affect resuscitation rate, pulmonary distribution, hemodynamic response, or plasma exogenous and total epinephrine concentrations. No correlation was found between successful resuscitation and bilateral distribution. Therefore, currently recommended cumbersome endotracheal epinephrine instillation techniques may offer no resuscitation advantage over commonly used direct injection in this setting.

[Hypercapnea during facial surgery under local anesthesia].

We examined the ventilation of patients whose faces were draped during facial surgery under local anesthesia. Ten patients who underwent eye surgery received hydroxyzine 25 mg and pentazocine 15 mg i.m. before local anesthesia. Arterial blood samples and end-tidal respiratory gases from nasal cannulae were collected at the following selected times: before draping their faces, 10 min, 30 min, 60 min after draping, and after the drapes were removed. Both arterial carbon dioxide tension (42 +/- 1 mmHg before draping and 46 +/- 1 mmHg at 10 min) and end-tidal carbon dioxide tension (33 +/- 2 mmHg before draping and 36 +/- 1 mmHg at 10 min) were elevated significantly after their faces were draped. Hypercapnea was completely eliminated by suctioning the expired gases. It is concluded that hypercapnea is inevitable during face or neck surgery under local anesthesia, and that the expired gases should be monitored and removed.

[Control of respiration in patients with respiratory insufficiency in chronic obstructive lung disease]. / Kontrola oddychania u chorych z niewydolnoscia oddychania w przebiegu przewleklej obturacyjnej choroby pluc.

Twenty eight COPD patients with respiratory insufficiency were studied. These included: 12 hypoxemic and normocapnic patients, 16 hypoxemic and hypercapnic patients, and 22 healthy volunteers. During at rest respiration both COPD groups differed from the control group--demonstrating a higher respiratory incidence, VT/Ti and PO2 values. During hypercapnic stimulation using the rebreathing method the ventilatory response to CO2 in the COPD patients was lowered in comparison with the control. Increase of occlusion pressure as a response to the increasing hypercapnia was lowered in both groups, significantly in patients with hypercapnia.

[Correction of hypocapnia in hypoxic humans using biofeedback of alveolar carbon dioxide pressure]. / Ustranenie gipokapnii u cheloveka v gipoksicheskikh usloviiakh s pomoshch'iu bioupravleniia al'veoliarnym napriazheniem dvuokisi ugleroda.

Reactions of the respiratory system to the inhalation of a hypoxic gas mixture were compared when the test subjects (young healthy men) practised normal breathing or breathing with a stable alveolar PCO2. In the latter case the test subjects controlled their lung ventilation using the biofeedback technique. In this manner hyperventilation and related hypocapnia were eliminated. The possibility of practical application of biofeedback to the control of man's respiration in situations that may cause hypocapnia is discussed.