No abstract available.
Hirschsprung Disease* ; Hypoventilation*

BACKGROUND: There are many factors such as diffusion abnormality, V/Q mismatch, intrapulmonary shunt, alveolar hypoventilation and FIO2 in reducing arterial hypoxemia. Intrapulmonary shunting can be due to blood going from the right to the left side of the heart without respiring with alveolar gas(true shunt mechanism) or blood that respires but achieves a PaO2 less than the ideal (shunt effect mechanism). Understanding the portion of true shunt in patients with hypoxemia is very important indicator to analyze the effects of oxygen therapy. Several equations are used for calculation of physiologic shunt. The aim of this study was to calculate and compare shunts derived from four shunt equations; classic physiologic, estimated, modified clinical and simple equations. METHOD: After cardiovascular stability following open heart surgery, 40 patients were mechanically ventilated with an FIO2=1.0. Arterial and mixed blood gases were measured. We calculated and compared shunts by classic physiologic [S/T=(CcO2 CaO2)/(CcO2 CO2)], estimated [S/T=(CcO2 CaO2)/ (3.5 CcO2 CO2)], modified clinical [S/T= AaDO2 0.0031/(AaDO2 0.0031 CcO2 CaO2)], and simple equations [S/T=AaDO2/20]/ RESULTS: Shunts by classic physiologic, estimated, and modified clinical shunt equation were 26.9 8.5%, 25.1 7.1%, and 26.3 8.2%, respectively and did not differ one another significantly. Shunts by simple shunt equations was 18.8 6.2% and significantly lower than those by other 3 equations(P<0.05). CONCLUSIONS: It is reasonable to conclude that in post-open heart patients with stable cardiovascular function and mechanically ventilated with an FIO2=1.0, classic physiologic, estimated, and modified clinical shunt equations show a reliable reflection of the physiologic shunt. But simple equation (AaDO2/20) might be used as a simple estimate.
Anoxia ; Diffusion ; Gases ; Heart ; Humans ; Hypoventilation ; Oxygen ; Thoracic Surgery

BACKGROUND AND PURPOSE: Cerebrovascular reactivity (CVR) can be estimated by measuring the change of cerebral blood flow that occurs during vasostimulation. To estimate the cerebrovascular reactivity, we investigated the change of flow velocity of the internal carotid artery (ICA) and the middle cerebral artery (MCA) during hyperventilation and hypoventilation with the transcranial doppler. So we studied whether the CVR measured by this method could show a significant difference between the normal and the atherosclerotic subjects and whether the CVR may decrease with age in normal gubjects. METHODS: Using transcranial doppler, we measured the mean velocity (Vm), the pulsatility index (P.I.) at the resting state, the end of breath-holding and the end of hyperventilation in 30 normal and 10 atherosclerotic subjects, so we calculated the percentile change of mean velocity (% Vm) and P.I. (% P.I.) after the vasostimulation. We estimated the change of Vm, P.I., % Vm and % P.I. By the age group and compared those parameters between the age-matched normal control and atherosclerotic subjects. RESULTS: The Vm in ICA and MI significantly decreased with age (p<0.01), but there was no significant difference in Vm and P. I. Between normal and atherosclerotic subjects. The % Vm and % P.I. In response to hyperventilation significantly decreased with age in ICA, M1, M2 and there was significant difference in % Vm of ICA and M1 after breath-holding and % Vm of ICA after hyperventilation between the normal and atherosclerotic subjects. CONCLUSION: The breath-holding and hyperventilation tests could be non-invasive and useful methods in estimation of the cerebrovascular reactivity and could be applied in the basal and follow-up evaluation of the cerebrovascular reserve of the ischemic stroke patients.
Carotid Artery, Internal ; Humans ; Hyperventilation ; Hypoventilation ; Middle Cerebral Artery ; Stroke

Child, Preschool ; Humans ; Male ; Obesity Hypoventilation Syndrome ; diagnosis ; therapy

Humans ; Sleep Apnea, Central/therapy* ; Hypoventilation/congenital* ; Homeodomain Proteins

Obesity-Hypoventilation syndrome (OHS) is characterized by morbid obesity, hypoxia, and hypercapnea during wakefulness without parechymal lung disease or severe obstructive sleep apnea. A woman was admitted because of mental deterioration and diagnosed as OHS on the basis of obesity and hypoventilation, while awake, after ruling out other causes. By bilevel positive airway pressure (BiPAP) therapy, hypercapnea and hypoxia were resolved. We report that BiPAP can be an effective treatment for severe hypercapnea and hypoxia in OHS, which obviate the need for invasive endotracheal intubation.
Anoxia ; Female ; Humans ; Hypoventilation ; Intubation, Intratracheal ; Lung Diseases ; Obesity ; Obesity Hypoventilation Syndrome* ; Obesity, Morbid ; Sleep Apnea, Obstructive ; Wakefulness

Congenital central hypoventilation syndrome (CCHS) is a disorder of the autonomic nervous system characterized by a decreased response to hypercarbia. CCHS is frequently associated with congenital megacolon; the combination is called Haddad syndrome. CCHS is associated with dysfunction in respiratory features of the autonomic nervous system and with other disorders, including facial deformities, cardiovascular symptoms, and tumors. Patients with CCHS frequently have a mutation in the homeobox protein 2b (PHOX2B) gene. Most mutations involve heterozygous expansion of alanine repeats (GCN). Interestingly, a higher polyalanine repeat number is associated with a more severe clinical phenotype. To clarify the role of PHOX2B in disease pathogenesis, we introduce and review the clinical and molecular features of CCHS and Haddad syndrome.
Alanine ; Autonomic Nervous System ; Congenital Abnormalities ; Genes, Homeobox ; Hirschsprung Disease ; Humans ; Hypoventilation* ; Molecular Biology* ; Phenotype

PURPOSE: Imploding antrum (silent sinus) syndrome has clinical features of enophthalmos and hypoglobus after a downward collapse of inferior orbital wall with an ipsilateral volume decrease of maxillary sinus. We present a case of imploding antrum syndrome after an orbital decompression surgery. CASE SUMMARY: A 26-year-old female underwent inferomedial wall orbital decompression surgery through a caruncular approach to reduce exophthalmos. At 14 months after surgery, her right eye showed 2 mm of enophthalmos and orbital CT scan revealed both maxillary sinusitis. At 28 months after surgery, 3 mm of enophthalmos and hypoglobus of the right were observed, and an orbital CT scan was taken. Orbital CT scan showed a downward collapse of inferior orbital wall, a volume decrease and inward bowing of the maxillary sinus, and a maxillary opacification on the right side, which are typical findings of imploding antrum (silent sinus) syndrome. CONCLUSIONS: Imploding antrum (silent sinus) syndrome after orbital decompression surgery is a rare complication. Considering that any prolapsed orbital fat after orbital decompression surgery could result in imploding antrum syndrome with hypoventilation of a maxillary sinus, care should be taken to keep the maxillo-ethmoidal interface (bony strut) intact, which helps maintain maxillary aeration.
Adult ; Decompression ; Enophthalmos ; Exophthalmos ; Eye ; Female ; Humans ; Hypoventilation ; Maxillary Sinus ; Maxillary Sinusitis ; Orbit

BACKGROUND: The purpose of this study was to define morphine's effects on resting ventilation and the ventilatory response to hypoxia and hypercarbia. METHODS: Six healthy nonsmoking young adult males were tested for the respiratory effects of intravenous morphine (0.15 mg/kg). Test began with baseline measurement of resting ventilation, isocapnic hypoxic ventilatory response (HVR), and normoxic hypercapnic ventilatory response (HCVR). After baseline measurement, morphine was administered and ventilatory responses were determined 20 and 40 min postinfusion. RESULTS: Morphine significantly decreased resting ventilation, hypoxic ventilatory response, and hypercarbic ventilatory response. Resting hypoventilation manifested as a peak rise in PETCO2 from 38.0+/-1.4 to 42.8+/-1.0 mmHg ( SEM) at 20 min (p<0.05). Hypoxic ventilatory response, measured as the slope of the ventilatory response to hypoxia, decreased from a control of 20.7+/-3.8 to 14.5+/-7.2 at 20 min after morphine (p<0.05). Hypercapnic ventilatory response, measured as the slope of the ventilatory response to hypercarbia, also decreased from 34.9+/-7.5 to 11.1+/-4.9 (p<0.05) 20 min after morphine. CONCLUSION: These decreased responsiveness to the chemical stimuli to breathing may contribute to the ventilatory depression frequently seen after administration of morphine.
Anoxia* ; Humans ; Hyperventilation* ; Hypoventilation ; Male ; Morphine* ; Respiration ; Respiratory Insufficiency ; Ventilation ; Young Adult

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