No abstract available.
Hypercapnia* ; Respiratory Insufficiency*

No abstract available.
Hypercapnia* ; Respiratory Insufficiency*

No abstract available.
Hypercapnia* ; Respiration, Artificial*

Malfunction of the unidirectional valve in a breathing circuit system may cause hypercapnia from the rebreathing of expired gas, ventilation failure, and barotrauma. Capnography is a useful method for monitoring the integrity of the unidirectional valve. We experienced two cases of malfunction of a unidirectional valve which caused leakage and reverse flow, diagnosed early as a change of the capnographic waveform. One case was caused by expiratory unidirectional valve breakage. The other was caused by an incorrectly-assembled inspiratory unidirectional valve.
Barotrauma ; Capnography ; Hypercapnia ; Respiration ; Ventilation

Interventional lung assist (iLA) effectively reduces CO2 retention and allows protective ventilation in cases of life-threatening hypercapnia. Despite the clinical efficacy of iLA, there are a few major limitations associated with the use of this approach, such as bleeding, thrombosis, and catheter-related limb ischemia. We presented two cases in which thrombotic complications developed during iLA. We demonstrated the two possible causes of thrombotic complications during iLA; stasis due to low blood flow and inadequate anticoagulation.
Extremities ; Hemorrhage ; Hypercapnia ; Ischemia ; Lung* ; Thrombosis ; Ventilation

No abstract available.
Continuous Positive Airway Pressure* ; Hypercapnia* ; Pneumonia* ; Pulmonary Edema*

No abstract available.
Continuous Positive Airway Pressure ; Hypercapnia ; Pneumonia ; Pulmonary Edema

A 35 year old male patient with inhalation injury including 45% body surface area burn was transferred to the hospital. After 2 days of hospitalization lung protective ventilation was supported due to acute respiratory distress occurrence. Fifth day the patient suffered hypercapnea which was uncontrollable with mechanical ventilators. Interventional lung assist (iLA) was proceeded on the tenth day, and the patients hypercapnia symptom was compatible with lung protective ventilation at the time, but the patient eventually suffered death after 12 days of treatment and care in the hospital.
Body Surface Area ; Burns ; Hospitalization ; Humans ; Hypercapnia ; Inhalation ; Lung ; Male ; Ventilation ; Ventilators, Mechanical

The purpose of this study is to verify severity of asthma in asthmatic patients through through the arterial blood gas analysis. Subjects were consisted of 103 patients (74 boys and 29 girls), between 2~13 years of ages. Clinically, asthmatic patients were classified into 6 groups, i, e., group 0(no rhonchi), group 1(rhonchi only), group 2(mild attack), group 3(moderate attack), group 4(severe attack), group 5(respiratory failure with disturbance of consciousness). PH kept normal range in the group 0, group 1, group 1 and group 3,but began decrease in the group 4.There was linear fall in Po2 and began decrease in the group 3. HCO3- maintained normal level through the whole range. BE showed acidemia on the whole, and began distinctive decrease in the group 4 and group 5, especially. Hypoxemia, hypercapnia and acidemia were common in patients in severe attacks with disturbance of consciousness.
Anoxia ; Asthma ; Blood Gas Analysis* ; Child* ; Consciousness ; Humans ; Hydrogen-Ion Concentration ; Hypercapnia ; Reference Values

To evaluate the regulation of and in the CSF during respiratory acidosis, the changes in cisternal CSF and arterial plasma acid-base status were asaessed in anesthetized, paralyzed, mechanically ventilated dogs rendered hypercapneic (PaCO2 of 60~70 mmHg) by hypoventilation. The electrochemical potential difference (u) between the CSF and blood for H+ and HCO2- was calculated from values for and in CSF and arterial plasma, and CSF/plasma DC potential difference was calculated. Simultaneously arterial blood and the CSF samples were drawn at 0, 1, 2, 3, 4, 6, 8 hours after hypercapnia. After 8 hours of respiratory acidosis, the arterial pH declined 0.09 units to 7.26 whereas the CSF pH fell by 0.07 units to 7.29. The CSF rose to 34 mEq/L whereas arterial plasma increased to 29 mEq/L. Therefore, increase of the CSF was almost 11 mEq/L, while the arterial plasma HCO, had increased 7 mE/L. So, much increase in CSF bicarbonate maintained the spinal fluid significantly less acidic than the blood during sustained hypercapnia. CSF/plasma PD was not only increased during acute respiratory acidosis, but also remained high as long as the plasma pH was acid. Values of p for H+ and HCO at 8 hours had returned to +1.1 and -0.1 mV of the control value. The attainment of steady-state values for u close to the control value may be compatible with passive distribution of these ions between the CSF and blood. But active mechanism can not be ruled out, because CSF/plasma PD remained high during the study.
Acidosis, Respiratory ; Animals ; Dogs ; Hydrogen-Ion Concentration ; Hypercapnia ; Hypoventilation* ; Ions ; Plasma