Showing papers on "Hypoventilation published in 2011"

Obesity hypoventilation syndrome: mechanisms and management.

Abstract: Obesity hypoventilation syndrome describes the association between obesity and the development of chronic daytime alveolar hypoventilation. This syndrome arises from a complex interaction between sleep-disordered breathing, diminished respiratory drive, and obesity-related respiratory impairment, and is associated with significant morbidity and mortality. Therapy directed toward reversing these abnormalities leads to improved daytime breathing, with available treatment options including positive pressure therapy, weight loss, and pharmacological management. However, a lack of large-scale, well-designed studies evaluating these various therapies has limited the development of evidence-based treatment recommendations. Although treatment directed toward improving sleep-disordered breathing is usually effective, not all patients tolerate mask ventilation and awake hypercapnia may persist despite effective use. In the longer term, weight loss is desirable, but data on the success and sustainability of this approach in obesity hypoventilation are lacking. The review outlines the major mechanisms believed to underlie the development of hypoventilation in this subgroup of obese patients, their clinical presentation, and current therapy options.

Nocturnal monitoring of home non-invasive ventilation: the contribution of simple tools such as pulse oximetry, capnography, built-in ventilator software and autonomic markers of sleep fragmentation

Abstract: Complex respiratory events, which may have a detrimental effect on both quality of sleep and control of nocturnal hypoventilation, occur during sleep in patients treated with non-invasive ventilation (NIV). Among these events are patient-ventilator asynchrony, increases in upper airway resistance (with or without increased respiratory drive) and leaks. Detection of these events is important in order to select the most appropriate ventilator settings and interface. Simple tools can provide important information when monitoring NIV. Pulse oximetry is important to ensure that adequate oxygen saturation is provided and to detect either prolonged or short and recurrent desaturations. However, the specificity of pulse oximetry tracings during NIV is low. Transcutaneous capnography helps discriminate between hypoxaemia related to ventilation/perfusion mismatch and hypoventilation, documents correction of nocturnal hypoventilation and may detect ventilator-induced hyperventilation, a possible cause for central apnoea/hypopnoea and glottic closure. Data provided by ventilator software help the clinician by estimating ventilation, tidal volume, leaks and the rate of inspiratory or expiratory triggering by the patient, although further validation of these signals by independent studies is indicated. Finally, autonomic markers of sympathetic tone using signals such as pulse wave amplitude of the pulse oximetry signal can provide reliable information of sleep fragmentation.

Rapid-Onset Obesity With Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation: Analysis of Hypothalamic and Autonomic Candidate Genes

Abstract: Rapid-onset Obesity with Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation (ROHHAD) is a rare and complex pediatric disorder. Despite increased identification and advancing knowledge of the disease course, the variable onset and timing of phenotypic features in ROHHAD often result in delayed or missed diagnosis, potentially leading to fatal central hypoventilation, cardiorespiratory arrest, and impaired neurocognitive development. The 5-hydroxytryptamine receptor 1A (HTR1A), orthopedia (OTP), and pituitary adenylate cyclase activating polypeptide (PACAP) genes were targeted in the etiology of ROHHAD based on their roles in the embryologic development of the hypothalamus and autonomic nervous system. We hypothesized that variations of HTR1A, OTP, and/or PACAP would be associated with ROHHAD. All coding regions and intron-exon boundaries of the HTR1A, OTP, and PACAP genes, in addition to the promoter region of the HTR1A gene, were analyzed by standard sequencing in 25 ROHHAD cases and 25 matched controls. Thirteen variations, including six protein-changing mutations, were identified. None of these variations were significantly correlated with ROHHAD. This report provides evidence that variation of the HTR1A, OTP, and PACAP genes are not responsible for ROHHAD. These results represent a further step in the investigation of the genetic determinants of ROHHAD.

Monozygotic Twins Discordant for ROHHAD Phenotype

Abstract: Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) falls within a group of pediatric disorders with both respiratory control and autonomic nervous system dysregulation. Children with ROHHAD typically present after 1.5 years of age with rapid weight gain as the initial sign. Subsequently, they develop alveolar hypoventilation, autonomic nervous system dysregulation, and, if untreated, cardiorespiratory arrest. To our knowledge, this is the first report of discordant presentation of ROHHAD in monozygotic twins. Twin girls, born at term, had concordant growth and development until 8 years of age. From 8 to 12 years of age, the affected twin developed features characteristic of ROHHAD including obesity, alveolar hypoventilation, scoliosis, hypothalamic dysfunction (central diabetes insipidus, hypothyroidism, premature pubarche, and growth hormone deficiency), right paraspinal/thoracic ganglioneuroblastoma, seizures, and autonomic dysregulation including altered pain perception, large and sluggishly reactive pupils, hypothermia, and profound bradycardia that required a cardiac pacemaker. Results of genetic testing for PHOX2B (congenital central hypoventilation syndrome disease-defining gene) mutations were negative. With early recognition and conservative management, the affected twin had excellent neurocognitive outcome that matched that of the unaffected twin. The unaffected twin demonstrated rapid weight gain later in age but not development of signs/symptoms consistent with ROHHAD. This discordant twin pair demonstrates key features of ROHHAD including the importance of early recognition (especially hypoventilation), complexity of signs/symptoms and clinical course, and importance of initiating comprehensive, multispecialty care. These cases confound the hypothesis of a monogenic etiology for ROHHAD and indicate alternative etiologies including autoimmune or epigenetic phenomenon or a combination of genetic predisposition and acquired precipitant.

Rapid-onset obesity with hypothalamic dysfunction, hypoventilation and autonomic dysregulation (ROHHAD): a case with additional features and review of the literature.

Abstract: A rare syndrome of rapid-onset obesity with hypothalamic dysfunction, hypoventilation and autonomic dysregulation (ROHHAD) has been recently described. We report the first patient with this syndrome in Southeast Asia and review reported cases to date. Our patient was good health with normal development until the age of 2. He then developed hyperphagic obesity, hypersomnolence, seizures, alveolar hypoventilation, central hypothyroidism, sodium and water dysregulation, gastrointestinal dysmotility, strabismus, disordered temperature and irregular heart rate, altered sweating, delayed puberty, mental retardation and recurrent respiratory tract infections. The cardiomyopathy with heart failure and abnormal cerebral spinal fluid (CSF) neurotransmitter analysis present in our patient have not been reported previously. Tumours of the sympathetic nervous system are known to be associated with this syndrome but had not been found in our patient at the time of reporting. We highlight the difficulty of achieving the diagnosis of ROHHAD syndrome and its overlap with other well-established disease entities. The mortality and morbidity resulting from the high incidence of cardiorespiratory arrest may be prevented by early ventilatory support.

Respiratory complications of obesity.

Abstract: Obesity, well known as a cardiovascular risk factor, can also lead to significant respiratory complications. The respiratory changes associated with obesity extend from a simple change in respiratory function, with no effect on gas exchange, to the more serious condition of hypercapnic respiratory failure, characteristic of obesity hypoventilation syndrome. More recently, it has been reported that there is an increased prevalence of asthma which is probably multifactorial in origin, but in which inflammation may play an important role. Hypoventilation in the obese subject is the result of complex interactions that involve changes in the ventilatory mechanics and anomalies in breathing control. Two other conditions (COPD and sleep apnea-hypopnea syndrome [SAHS], often present in obese patients, can trigger or aggravate it. The prevalence of hypoventilation in the obese is under-estimated and the diagnosis is usually established during an exacerbation, or when the patient is studied due to suspicion of SAHS. Ventilatory management of these patients includes either CPAP or NIV. The choice of one or another will depend on the underlying clinical condition and whether or not there is another comorbidity. Both NIV and CPAP have demonstrated their effectiveness, not only in the control of gas exchange, but also in improving the quality of life and survival of these patients.

Coagulation Changes to Systemic Acidosis and Bicarbonate Correction in Swine

Abstract: : Background: As part of our overall interest in the mechanisms and treatment related to the development of the lethal triad of hypothermia, acidosis, and coagulopathy seen in trauma patients, the purpose of this study was to determine whether acidosis, inducible either by HCl infusion or hemorrhage/hypoventilation, leads to coagulopathy, and if correction of the acidosis will alleviate this coagulopathy. Methods: In two separate experiments, acidosis was induced in anesthetized swine by (1) HCl infusion (n 10) or (2) hemorrhage/hypoventilation (n 8). Arterial blood samples were taken before HCl infusion or hemorrhage (arterial pH 7.4), after HCl infusion or hemorrhage (pH 7.1), and after bicarbonate infusion to return pH to 7.4. Arterial pH and blood gases were measured every 15 minutes. Results: Acidosis (arterial pH 7.1) led to a hypocoagulation as measured by several coagulation parameters. In both experiments, acidosis was associated with a significant decrease in the maximum strength of the clot and the rate at which the clot formed. There was a significant decrease in endogenous thrombin potential and maximum thrombin concentration after acidosis in both groups (thrombin generation assay). However, the activated clotting time, prothrombin time, and activated partial thromboplastin time were significantly elevated only in the HCl-infused group. Fibrinogen concentration and platelet count were significantly reduced in both groups after acidosis. The hypocoagulation that was induced by either hemorrhage/hypoventilation or HCl infusion was not immediately corrected after returning pH to 7.4 with bicarbonate injection. Conclusions: These data suggest that acidosis induced by HCl infusion or by hemorrhage/hypoventilation leads to hypocoagulation. Simple correction of the arterial pH with bicarbonate is not sufficient to correct this coagulopathy.

Respiratory rates and arterial blood-gas tensions in healthy rabbits given buprenorphine, butorphanol, midazolam, or their combinations.

Abstract: Companion animal practitioners and academic anesthesiologists advocate many different combinations of sedatives and opioids to achieve balanced anesthesia. The benefits of premedicating with an opioid–sedative combination is that patient stress is reduced, animal handling is easier, preemptive analgesia can be attained, and inhalant anesthetic requirements are reduced, resulting in less cardiovascular and respiratory depression. In laboratory animals and pet exotic animals, such as rabbits, balanced anesthesia is often foregone in preference to simple mask induction with inhalant agents. In addition, analgesia in these species is often inadequate due to concern about adverse respiratory effects of opioids. Because obtaining a controlled airway in these species can be challenging, pronounced respiratory depression from opioids is an even greater concern. As such, the mixed agonist–antagonist opioids (for example, butorphanol) or partial-agonist opioids (for example, buprenorphine) are often chosen as analgesics or premedications in laboratory animal species, because these classes of opioids may induce less respiratory depression than others. The majority of the medical literature, both human and veterinary, points to a ‘ceiling effect’ in respiratory depression with agonist–antagonist or partial-agonist opioid drugs as compared with the dose-dependent respiratory depression that may be observed with pure μ-agonist opioids, such as hydromorphone.6,7,24,26,27 There are conflicting data in the literature, however, regarding the clinical significance of respiratory depression associated with the partial-agonist and mixed agonist–antagonist opioids. One study that examined the respiratory and cardiovascular effects of buprenorphine in rabbits reported mild hypoxemia associated with its administration.22 Another study similarly found that administration of buprenorphine to anesthetized rabbits resulted in hypoventilation but no change in the ventilatory response to hypoxia.8 Buprenorphine caused a moderate decrease in respiratory rate in rabbits, but significant respiratory depression as evidenced by respiratory rate was apparent only at dosages higher than those used clinically.11 Butorphanol has not been as extensively studied as a sole agent in rabbits. However, butorphanol and butorphanol combinations are known to result in statistically significant respiratory depression in rabbits, dogs, sheep, horses, and humans.15,23-25,27,28 In another study, dogs given butorphanol postoperatively had no change in pO2 or pCO2.5 Discrepancies in the literature regarding buprenorphine's and butorphanol's effects on respiratory drive likely relate to differences in methodology, sampling, and doses studied. The clinical significance of any changes in blood-gas tensions that occur after buprenorphine or butorphanol in most species is questionable in healthy animals, and most studies conclude that these 2 opioid drugs do not result in clinically unacceptable respiratory depression in most species. To our knowledge, no studies have examined the concurrent use of opioids and benzodiazepines and their effects on arterial blood gases in rabbits, despite the fact that, when premedication is used, benzodiazepines and butorphanol or buprenorphine are often combined for use in these animals.9 Various studies show that benzodiazepines, such as midazolam, cause mild to moderate hypoxemia in rabbits and humans,5,13,18 but the clinical significance of any additive effect of benzodiazepine-induced respiratory depression when these drugs are combined with butorphanol or buprenorphine is unknown. The combination of benzodiazepines and opioids in rabbits can cause significant sedation.17 The purpose of the current study was to assess changes in arterial blood-gas values in healthy rabbits given midazolam, butorphanol, or buprenorphine, alone or in combination. We hypothesized that administration of butorphanol, buprenorphine, midazolam, or midazolam–opioid combinations would cause statistically significant changes in respiratory rate and arterial blood gases.

Detection of hypoventilation by capnography and its association with hypoxia in children undergoing sedation with ketamine.

Abstract: Objectives: Hypopneic hypoventilation, a decrease in tidal volume without a change in respiratory rate, is not easily detected by standard monitoring practices during sedation but can be detected by capnography. Our goal was to determine the frequency of hypopneic hypoventilation and its association with hypoxia in children undergoing sedation with ketamine. Methods: Children who received intravenous ketamine with or without midazolam for sedation in a pediatric emergency department were prospectively enrolled. Heart rate, respiratory rate, pulse oximetry, and end-tidal carbon dioxide (ETco 2 ) levels were recorded every 30 seconds. Results: Fifty-eight subjects were included in this study. Fifty percent of subjects had recorded ETco 2 values less than 30 mm Hg without a rise in respiratory rate. Twenty-eight percent of subjects experienced a decrease in pulse oximetry less than 95%. Patients who experienced a persistent decrease in ETco 2 at least 30 seconds in length were much more likely to have a persistent decrease in pulse oximetry than those with normal or transient decreases in ETco 2 (relative risk, 6.6; 95% confidence interval, 1.4-30.5). Decreases in ETco 2 occurred on an average of 3.7 minutes before decreases in pulse oximetry. Conclusions: Hypopneic hypoventilation as detected by capnography is common in children undergoing sedation with ketamine with or without midazolam. Hypoxia is frequently preceded by low ETco 2 levels. Further studies are needed to determine if the addition of routine monitoring with capnography can reduce the frequency of hypoxia in children undergoing sedation.

Capnography for assessing nocturnal hypoventilation and predicting compliance with subsequent noninvasive ventilation in patients with ALS.

Abstract: Background Patients with amyotrophic lateral sclerosis (ALS) suffer from hypoventilation, which can easily worsen during sleep. This study evaluated the efficacy of capnography monitoring in patients with ALS for assessing nocturnal hypoventilation and predicting good compliance with subsequent noninvasive ventilation (NIV) treatment. Methods Nocturnal monitoring and brief wake screening by capnography/pulse oximetry, functional scores, and other respiratory signs were assessed in 26 patients with ALS. Twenty-one of these patients were treated with NIV and had their treatment compliance evaluated. Results Nocturnal capnography values were reliable and strongly correlated with the patients' respiratory symptoms (R2 = 0.211–0.305, p = 0.004–0.021). The duration of nocturnal hypercapnea obtained by capnography exhibited a significant predictive power for good compliance with subsequent NIV treatment, with an area-under-the-curve value of 0.846 (p = 0.018). In contrast, no significant predictive values for nocturnal pulse oximetry or functional scores for nocturnal hypoventilation were found. Brief waking supine capnography was also useful as a screening tool before routine nocturnal capnography monitoring. Conclusion Capnography is an efficient tool for assessing nocturnal hypoventilation and predicting good compliance with subsequent NIV treatment of ALS patients, and may prove useful as an adjunctive tool for assessing the need for NIV treatment in these patients.

Effects of breathing training on voluntary hypo- and hyperventilation in patients with panic disorder and episodic anxiety.

Abstract: Anxiety disorders are associated with respiratory abnormalities. Breathing training (BT) aimed at reversing these abnormalities may also alter the anxiogenic effects of biological challenges. Forty-five Panic Disorder (PD) patients, 39 Episodic Anxiety patients, and 20 non-anxious controls underwent voluntary hypoventilation and hyperventilation tests twice while psychophysiological measures were recorded. Patients were randomized to one of two BT therapies (Lowering vs. Raising pCO(2)) or to a waitlist. Before treatment panic patients had higher respiration rates and more tidal volume instability and sighing at rest than did non-anxious controls. After the Lowering therapy, patients had lower pCO(2) during testing. However, neither reactivity nor recovery to either test differed between patients and controls, or were affected by treatment. Although the two treatments had their intended opposite effects on baseline pCO(2), other physiological measures were not affected. We conclude that baseline respiratory abnormalities are somewhat specific to PD, but that previously reported greater reactivity and slower recovery to respiratory challenges may be absent.

Causes of and Compensations for Hypoxemia and Hypercapnia

Abstract: By far the commonest cause of impaired gas exchange in patients with lung disease is ventilation-perfusion inequality. This is a complicated topic and much can be learned from computer models. Ventilation-perfusion inequality always causes hypoxemia, that is, an abnormally low PO2 in arterial blood. However, it is also the commonest cause of an increased arterial PCO2, or hypercapnia, in patients with chronic obstructive pulmonary disease (COPD). There is often confusion in this area with some people attributing the CO2 retention to "hypoventilation" when in fact these patients are usually moving much more air into their lungs than normal subjects. A patient with COPD can often return the arterial PCO2 to normal by increasing the ventilation. However, this does not return the arterial PO2 to normal because of the different shapes of the oxygen and carbon dioxide dissociation curves. Increasing pulmonary blood flow in the presence of ventilation-perfusion inequality usually raises the arterial PO2 but much less than increasing ventilation. Raising the inspired oxygen concentration is typically very effective in increasing the arterial PO2. Ventilation-perfusion inequality interferes with the transfer of all gases by the lung including the anesthetic gases. The gas exchange behavior of a lung depends greatly on the pattern of ventilation-perfusion inequality. It is theoretically possible to find a distribution that improves the transfer of some gases but this requires bizarre conditions that can never occur in practice.

Pseudo-piano playing motions and nocturnal hypoventilation in anti-NMDA receptor encephalitis: response to prompt tumor removal and immunotherapy.

Abstract: Tumor resection is recommended in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, however it is often difficult during an early stage of the disease. We report here the efficacy of early tumor removal in a patient with anti-NMDAR encephalitis. This 21-year-old woman was admitted to another hospital with rapidly progressive psychiatric symptoms, a decreased level of consciousness, and seizures. Abdominal CT showed a pelvic mass. On day 1 of admission to our center, she developed hypoventilation requiring mechanical support. She had orofacial dyskinesias with well-coordinated, pseudo-piano playing involuntary finger movements. Based on these clinical features, she was immediately scheduled for tumor resection on day 3. While awaiting surgery, she began to receive high-dose intravenous methylprednisolone. After tumor removal, she received plasma exchange, followed by intravenous immunoglobulin and additional high-dose methylprednisolone. Two weeks after tumor removal, she started following simple commands and progressive improvement, although she remained on mechanical ventilation for 10 weeks due to nocturnal central hypoventilation. Anti-NMDAR antibodies in serum/CSF were detected. Pathological examination showed immature teratoma with foci of infiltrates of B- and T-cells. Early tumor resection with immunotherapy facilitates recovery from this disease, but central hypoventilation may require long mechanical support. Non-jerky elaborate finger movements suggest antibody-mediated disinhibition of the cortico-striatal systems.

Late onset congenital central hypoventilation syndrome after exposure to general anesthesia.

Abstract: Purpose Prolonged postoperative hypoventilation presents a challenge to anesthesiologists with regard to assessing etiology and related treatment. We present a case of recurrent episodes of postoperative hypoventilation in a previously asymptomatic child after uneventful general anesthesia. In this case, the child eventually required lifelong ventilatory support during sleep.

Congenital central hypoventilation syndrome: four families.

Abstract: Background Congenital central hypoventilation syndrome (CCHS) is a rare condition that usually presents soon after birth and is potentially life-shortening if not treated. The defining abnormality is hypoventilation during sleep which requires life-long treatment with artificial ventilation. This syndrome may also be associated with generalised dysfunction of the autonomic nervous system and a sub-group with associated Hirschsprung’s disease. The genetic basis of CCHS has been identified as mutations in the PHOX2B gene.

Predicting nocturnal hypoventilation in hypercapnic chronic obstructive pulmonary disease patients undergoing long-term oxygen therapy.

Abstract: Background: Chronic obstructive pulmonary disease (COPD) patients are very sensitive to changes in pulmonary mechanics and central ventilation control during sleep and may develop significant gas exchange alterations with increased hypoxemia and hypercapnia. Oxygen therapy improves nocturnal desaturation but can worsen hypoventilation. Objectives: To analyze the prevalence of nocturnal hypoventilation (NHV) in hypercapnic COPD patients and to determine predictive factors for this phenomenon. Methods: This was a prospective multicenter study which enrolled 80 clinically stable COPD patients with hypercapnic respiratory failure who fulfilled the conventional criteria for long-term oxygen therapy (LTOT). All patients had undergone pulmonary function testing, blood gas analysis, and respiratory polygraphy. Arterial blood gas samples were obtained while patients were awake and during sleep. NHV was considered when an increase in PaCO2 >10 mm Hg was observed in any nocturnal arterial blood gas sample as compared to the awake levels. Results: Seventeen patients (21%) developed NHV. NHV was associated with the values of BMI, hemoglobin, hematocrits, DLCO, and PaO2 reached after oxygen administration. In the logistic regression analysis BMI (OR 1.26, 95% CI 1.068–1.481; p = 0.006) and the diurnal increase of PaO2 after O2 (OR 0.89, 95% CI 0.807–0.972; p = 0.010) were the variables that best discriminated with a sensitivity of 82% and a specificity of 78%. Conclusions: NHV is a relatively common finding in stable hypercapnic COPD patients undergoing LTOT and it is related to a higher BMI and lower PaO2 after oxygen administration.

Clinical Management of One-Lung Ventilation

Abstract: One-lung ventilation (OLV) is a recognized and modifiable risk factor for acute lung injury. OLV needs to be individualized to the patient’s predicted body weight and their particular lung mechanics. Protective OLV is a combination of small, physiologic tidal volumes with consequently low ventilating pressures and routine, individualized PEEP to facilitate open lung ventilation. Ventilator-induced lung injury is preventable by minimizing driving pressure, which is a direct correlate of transpulmonary stress and strain. In patients at particular risk of lung injury, the use of permissive hypercapnia may facilitate a decrease in the mechanical strain onto the lung. Hypoxemia during one-lung ventilation is now rare and often secondary to alveolar de-recruitment in the face of hypoventilation. Management of hypoxemia requires a structured treatment algorithm.

Ondine's curse: anesthesia for laparoscopic implantation of a diaphragm pacing stimulation system.

Abstract: Central alveolar hypoventilation syndrome (CAHS) is a rare disease characterized by the loss of autonomic control of breathing. This condition causes hypoventilation and obstruction during sleep. Throughout their lives, these patients require ventilatory assistance by means of positive pressure ventilation to their lungs via mask, tracheotomy, or other means, such as phrenic nerve pacers. The diaphragm pacing stimulation system (DPSS) is a new treatment where electrodes are implanted into the diaphragm and cause contraction on stimulation. The DPSS has been used successfully in tetraplegic patients and patients suffering from amyotrophic lateral sclerosis (ALS). It has been shown to improve quality of life and to extend survival in patients with advanced respiratory muscle weakness. In our case, we describe the perioperative management of an adult patient with acquired CAHS who presented for laparoscopic DPSS insertion. Our patient was a 50-yr-old female who developed CAHS at age thirteen after contracting encephalitis. Since the onset of her disease, she had been managed with positive pressure ventilation to her lungs via mask. Due to her longstanding disease, she presented with pulmonary hypertension and cor pulmonale and was scheduled for laparoscopic DPSS implantation. Our anesthetic technique included a total intravenous technique with remifentanil and propofol, and her trachea was intubated without the use of muscle relaxants. The pacemakers were switched on when the patient emerged from anesthesia, which provided her with ventilatory support and allowed us to extubate her trachea. We present the successful anesthetic management of an adult patient with CAHS undergoing laparoscopic DPSS insertion.

Presentation and Treatment of Monozygotic Twins with Congenital Central Hypoventilation Syndrome

Abstract: Congenital central hypoventilation syndrome is a rare genetic disorder characterized by hypoventilation during sleep secondary to a blunted response to hypercapnia and hypoxia The current case report describes developmentally normal four-year-old monozygotic twin boys who presented in infancy with variable presentations and clinical severity of congenital central hypoventilation syndrome Both were managed with noninvasive positive pressure ventilation

Cardiorespiratory and blood gas alterations during laparoscopic surgery for intra-uterine artificial insemination in dogs

Abstract: Cardiorespiratory and blood gas alterations were evaluated in 6 healthy dogs that underwent a laparoscopic procedure using isoflurane anesthesia and carbon dioxide (CO2) pneumoperitoneum for 30 min. Heart rate, respiratory rate, body temperature, venous blood pH, partial pressure of CO2 and oxygen, oxygen saturation, total carbon dioxide (TCO2) and bicarbonate were monitored. Significant alterations were hypercapnia, hypoventilation, and respiratory acidosis.

Alteration in blood gases in cats naturally infected with Aelurostrongylus abstrusus.

Abstract: Four cats were presented with respiratory signs and first-stage larvae of Aelurostrongylus abstrusus were found in faecal samples. Anthelmintic treatment was given to the infected cats and venous blood gases were analysed during the treatment period. Blood gas analysis suggested hypoventilation and respiratory acidosis in infected cats. Hypoventilation may be the result of airway obstruction by adults and larvae in respiratory bronchioles and the alveolar canals. The blood gas values had returned close to the physiological range by two months after treatment. Assessment of respiratory acidosis may aid development of additional treatment methods in cats infected with A. abstrusus.

Congenital central hypoventilation syndrome and the PHOX2B gene mutation.

Abstract: Congenital central hypoventilation syndrome (CCHS) is a rare syndrome of dysfunction of the autonomic nervous system characterized by a decreased response to hypercarbia. It is a disorder in which affected individuals fail to breathe during sleep despite progressive hypercapnia and hypoxia. Infants simply fall asleep and quit breathing. They are found by their parents or caregivers blue and lifeless. CCHS is an autosomal dominant disease. It has been linked with tumors of neural crest origin, segmental aganglionosis of the colon, and diffuse autonomic dysregulation but can occur alone. Discovery of the genetic link between the paired-like homeobox 2B (PHOX2B) genetic mutations and CCHS represents a breakthrough in the diagnosis of CCHS, association of mutated alleles with disease severity, and clues to the pathophysiology responsible for the disorder. Early genetic screening and intervention can provide the families of these infants with hope for achieving a normal life.

Sleep hypoventilation syndrome and respiratory failure due to multifocal motor neuropathy with conduction block.

Abstract: Sleep hypoventilation syndrome and respiratory failure have been reported in association with a diverse spectrum of neuromuscular disorders. We report a patient with multifocal motor neuropathy with conduction block who presented with sleep hypoventilation, presumably due to bilateral phrenic neuropathy and was initially diagnosed to have obstructive sleep apnea syndrome. Once the correct diagnosis was made the patient was treated successfully with a combination of regular immunoglobulin and bilevel nocturnal ventilation. Delay in the administration of intravenous immunoglobulin resulted in respiratory failure. Muscle Nerve, 2011