Showing papers on "Hypoventilation published in 2004"

Respiratory and haemodynamic effects of acute postoperative pain management: evidence from published data

Abstract: Background. This study examines the evidence from published data concerning the adverse respiratory and haemodynamic effects of three analgesic techniques after major surgery; i.m. analgesia, patient-controlled analgesia (PCA), and epidural analgesia. Methods. A MEDLINE search of the literature was conducted for publications concerned with the management of postoperative pain. Information relating to variables indicative of respiratory depression and of hypotension was extracted from these studies. Over 800 original papers and reviews were identified. Of these papers, 212 fulfilled the inclusion criteria but only 165 provided usable data on adverse effects. Pooled data obtained from these studies, which represent the experience of a total of nearly 20 000 patients, form the basis of this study. Results. There was considerable variability between studies in the criteria used for defining respiratory depression and hypotension. The overall mean (95% CI) incidence of respiratory depression of the three analgesic techniques was: 0.3 (0.1–1.3)% using requirement for naloxone as an indicator; 1.1 (0.7–1.7)% using hypoventilation as an indicator; 3.3 (1.4–7.6)% using hypercarbia as an indicator; and 17.0 (10.2–26.9)% using oxygen desaturation as an indicator. For i.m. analgesia, the mean (95% CI) reported incidence of respiratory depression varied between 0.8 (0.2–2.5) and 37.0 (22.6–45.9)% using hypoventilation and oxygen desaturation, respectively, as indicators. For PCA, the mean (95% CI) reported incidence of respiratory depression varied between 1.2 (0.7–1.9) and 11.5 (5.6–22.0)%, using hypoventilation and oxygen desaturation, respectively, as indicators. For epidural analgesia, the mean (95% CI) reported incidence of respiratory depression varied between 1.1 (0.6–1.9) and 15.1 (5.6–34.8)%, using hypoventilation and oxygen desaturation, respectively, as indicators. The mean (95% CI) reported incidence of hypotension for i.m. analgesia was 3.8 (1.9–7.5)%, for PCA 0.4 (0.1–1.9)%, and for epidural analgesia 5.6 (3.0–10.2)%. Whereas the incidence of respiratory depression decreased over the period 1980–99, the incidence of hypotension did not. Conclusions. Assuming a mixture of analgesic techniques, Acute Pain Services should expect an incidence of respiratory depression, as defined by a low ventilatory frequency, of less than 1%, and an incidence of hypotension related to analgesic technique of less than 5%.

PHOX2B mutations and polyalanine expansions correlate with the severity of the respiratory phenotype and associated symptoms in both congenital and late onset Central Hypoventilation syndrome

Abstract: Congenital Central Hypoventilation syndrome (CCHS (MIM 209880)) is a rare disorder, with fewer than 200 patients currently reported worldwide, characterised by absence of adequate autonomic control of respiration with decreased sensitivity to hypercapnia and hypoxia, in the absence of neuromuscular or lung disease, or an identifiable brain stem lesion.1 Children with CCHS show an adequate ventilation while awake but hypoventilate during sleep. More severely affected children hypoventilate both when awake and during sleep.1 CCHS has been reported in association with several disorders, among which aganglionic megacolon (Hirschsprung disease, HSCR) and tumours of neural crest origin, reflecting a common molecular pathogenesis sustained by defects of one or more genes that control the correct development of neural crest derived cell lineages.1–3 A genetic aetiology has long been hypothesised for CCHS based on recurrence reported in siblings, in half siblings and in affected children born to women with CCHS.2–6 More recently, a generalised autonomic nervous system (ANS) imbalance has been observed among children with CCHS and an increased incidence of ANS dysfunctions (ANSD) reported among relatives of 56 patients with CCHS, as against relatives of 56 matched controls.7 A family transmission study has shown that the risk of developing an ANSD symptom including CCHS, regarded as the most severe expression of ANS imbalance, mainly depends on the genotype at a major locus, while significant residual variants could be due to additional minor genes, modifying loci effects or environmental factors.8 Genes involved in the ANS development, like the RET proto-oncogene, its ligand GDNF , the Endothelin 3 gene, the Brain Derived Neurotrophic Factor ( BDNF ) and the RNX genes, have been tested and a few mutations found, showing no cosegregation with the disease phenotype in CCHS families.9–13 The PHOX2B gene encodes a 314 amino acids …

Prader-Willi syndrome: causes of death in an international series of 27 cases.

Abstract: Prader-Willi syndrome (PWS) is a complex condition with many medical and psychological features. In individuals with this syndrome, causes of death were studied. Data of 27 case reports were collected. Ages at death ranged from neonatal to 68 years. None of the individuals were treated with growth hormone (GH). Most cases were not completely documented and autopsy was performed in a minority of cases only. In five cases, death was considered not to be causally related to PWS. Hypotonia with hypoventilation was noted in the babies, and acute respiratory illness with unexpected sudden death was experienced in young children with PWS. Two young children died after a short period of fever and gastroenteritis. Obesity and its complications leading to death were pronounced in the adult group. One (possibly two) adult(s) died from gastric dilatation and shock. Based on these data, some cautious conclusions can be drawn. In babies with PWS hypoventilation is a risk factor; upper airway infection may be more serious than anticipated and any other clinical features pointing to an infection should be taken very seriously. Therefore, young infants with PWS hospitalized with an upper airway infection and/or hypoventilation or gastroenteritis symptoms, should be closely monitored. Early diagnosis and prevention of overweight is a major factor in preventing early causes of death in individuals with PWS. In the adult group, weight reduction is important but difficult to manage. Sleep apnea should be recognized and treated. Pain in the upper stomach and/or vomiting should be taken as a possible sign of acute intestinal dilatation; intravenous support may be life saving.

Epidemiologic survey of 196 patients with congenital central hypoventilation syndrome

Abstract: This study examined the cross-sectional medical and social characteristics of children diagnosed with congenital central hypoventilation syndrome (CCHS). A detailed questionnaire was mailed to all families with a child with CCHS who are affiliated with a family network or support group. The questionnaire response rate was >75% (n=196). Mean age was 10.22 years +/- 6.6 years (SD) (range, 0.4-38 years), with a 1:1 sex ratio. Multisystem involvement was almost universal among the cohort, with Hirschsprung's disease (HD) present in 16.3%; 61.7% of the children had a tracheotomy, but 14.3% were never tracheotomized, with 77 subjects (39.3%) not having a tracheostomy tube at time of survey. Respiratory support approaches varied but clearly reflected the trend towards earlier and more widespread transition to noninvasive ventilatory modalities. Significant developmental problems were noted, but attendance in regular classes occurred in the majority. Significant deficiencies in routine periodic evaluation and management were reported. In addition, the presence of CCHS was associated with a significant financial and psychosocial burden to the families. In conclusion, a comprehensive survey of 196 CCHS children and their families revealed a cross-sectional picture of substantial medical and psychosocial complexities associated with this disorder, and pointed out substantial inadequacies in routine preventive care that appear to impose stress on the families. The emerging trend of earlier transition to noninvasive ventilatory support warrants future studies. Implementation of recommended guidelines for diagnosis and multidisciplinary follow-up of CCHS should ultimately ameliorate the long-term outcome of this lifelong condition.

Poisoning Due to Chlorophenoxy Herbicides

Abstract: Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.

The influence of gender and upper airway resistance on the ventilatory response to arousal in obstructive sleep apnoea in humans.

Abstract: The termination of obstructive respiratory events is typically associated with arousal from sleep. The ventilatory response to arousal may be an important determinant of subsequent respiratory stability/instability and therefore may be involved in perpetuating obstructive respiratory events. In healthy subjects arousal is associated with brief hyperventilation followed by more prolonged hypoventilation on return to sleep. This study was designed to assess whether elevated sleeping upper airway resistance (RUA) alters the ventilatory response to arousal and subsequent breathing on return to sleep in patients with obstructive sleep apnoea (OSA). Inspired minute ventilation (VI), RUA and end-tidal CO2 pressure (PET,CO2) were measured in 22 patients (11 men, 11 women) with OSA (mean ±s.e.m., apnoea–hypopnoea index (AHI) 48.9 ± 5.9 events h−1) during non-rapid eye movement (NREM) sleep with low RUA (2.8 ± 0.3 cmH2O l−1 s; optimal continuous positive airway pressure (CPAP) = 11.3 ± 0.7 cmH2O) and with elevated RUA (17.6 ± 2.8 cmH2O l−1 s; sub-optimal CPAP = 8.4 ± 0.8 cmH2O). A single observer, unaware of respiratory data, identified spontaneous and tone-induced arousals of 3–15 s duration preceded and followed by stable NREM sleep. VI was compared between CPAP levels before and after spontaneous arousal in 16 subjects with tone-induced arousals in both conditions. During stable NREM sleep at sub-optimal CPAP, PET,CO2 was mildly elevated (43.5 ± 0.8 versus 42.5 ± 0.8 Torr). However, baseline VI (7.8 ± 0.3 versus 8.0 ± 0.3 l min−1) was unchanged between CPAP conditions. For the first three breaths following arousal, VI was higher for sub-optimal than optimal CPAP (first breath: 11.2 ± 0.9 versus 9.3 ± 0.6 l min−1). The magnitude of hypoventilation on return to sleep was not affected by the level of CPAP and both obstructive and central respiratory events were rare following arousal. Similar results occurred after tone-induced arousals which led to larger responses than spontaneous arousals. VI for the first breath following arousal under optimal CPAP was greater in men than women (11.0 ± 0.4 versus 7.6 ± 0.6 l min−1). These results demonstrate that the ventilatory response to arousal is influenced by pre-arousal airway resistance and gender. Whether this contributes to the perpetuation of respiratory events and the pathogenesis of OSA is unclear.

Congenital hypoventilation and impaired hypoxic response in Nurr1 mutant mice.

Abstract: Nurr1, a transcription factor belonging to the family of nuclear receptors, is expressed at high levels immediately after birth. Gene-targeted mice lacking Nurr1 fail to develop midbrain dopaminergic neurones and do not survive beyond 24 h after birth. Dopamine (DA) levels may be regulated by Nurr1, and as DA is involved in both central and peripheral respiratory control, we hypothesized that lack of Nurr1 may impair breathing and cause death by respiratory failure. We demonstrate herein that Nurr1 newborn knockout mice have a severely disturbed breathing pattern characterized by hypoventilation, numerous apnoeas and failure to increase breathing when challenged with hypoxia. In heterozygote Nurr1 mice the response to hypoxia is also altered. Furthermore, the central respiratory rhythm, generated from isolated brainstem–spinal cord preparations, exhibits impaired response to hypoxia in mice lacking Nurr1. Moreover, Nurr1 is expressed in several respiratory-related regions of the nervous system, including the nucleus of the solitary tract, the nucleus ambiguus and the dorsal motor nucleus of the vagus nerve, and in the carotid bodies. The prominent Nurr1 expression in these areas, involved in respiratory control, along with the severe respiratory phenotype, indicates that Nurr1 plays a major role in the extrauterine adaption of respiratory control and the response to hypoxia.

Prevalence of pulmonary hypertension and its association with respiratory disturbances in obese patients living at moderately high altitude

Abstract: OBJECTIVE: To determine the point prevalence of pulmonary hypertension (PH) and its relationship with respiratory disturbances in obese patients living at moderate altitude. SUBJECTS: A total of 57 obese patients comprised the final sample and consisted of 34 women and 23 men, with a mean age of 42.7±12.1 ys and a mean body mass index (BMI) 47.1±10.6 kg/m2 (range from 30.1 to 76.1). The mean living altitude was 2248.7 m, range 2100–2400 m above sea level. MEASUREMENTS: Doppler echocardiography, pulmonary function tests, arterial blood gas analysis, and polysomnography were performed. RESULTS: Data showed that 96.5% of the studied sample had daytime PH defined as calculated systolic pulmonary artery pressure (PSAP) >30 mmHg (mean PSAP=50, s.d.=13 mmHg). The severity of diurnal PH was found to be related to the presence of alveolar hypoventilation and BMI. The main risk factor for severity of diurnal PH was hypoventilation with a significant odds ratio (OR) 7.96, 95% CI 1.35–46.84, BMI was (OR 1.12, 95% CI 1.02–1.25) and apnea/hypopnea index was not a predictor of pulmonary hypertension severity (OR 0.99, 95% CI 0.97–1.02). CONCLUSION: We concluded that prevalence of diurnal PH is high in obese patients living at moderate altitude, and that hypoventilation is the main risk factor associated with the severity of pulmonary hypertension.

Predictive factors of oxygen desaturation of patients submitted to endoscopic retrograde cholangiopancreatography under conscious sedation

Abstract: BACKGROUND AND AIMS: Hypoxemia can occur during endoscopic retrograde cholangiopancreatography probably induced by the analgesia and sedation done. Moreover the patient’s prone position difficults the adequate ventilation. The hypoxemia and hypoventilation may not be noticed by nursing staff. A transversal study was used to investigate possible predictive factors of oxygen desaturation in sedated patients with midazolam associated to meperidine undergoing endoscopic retrograde cholangiopancreatography. PATIENTS AND METHODS: A total of 186 patients were monitored with continuous pulse oximetry. Poisson regression was used to measure the independent effect of each factor adjusted for effects of each of the other factors. The variables studied were: age, gender, hematocrit and hemoglobin levels, scopolamine use, diagnostic or therapeutic exam, American Society of Anesthesiologists Scores (ASA), duration time of exam, sedative used midazolam in the average of 0.07 mg/kg and analgesic drug meperidine in the average of 0.7 mg/kg that was titrated according patient’s reaction. RESULTS: No desaturation was found in 113 (60.8%) patients, mild desaturation (SpO2 60 years old and ASA score III. The duration of exam was barely significant for desaturation. CONCLUSIONS:The variables of age of 60 years old or more, and ASA III score are identified as increased risk for desaturation for patients who undergo endoscopic retrograde cholangiopancreatography under conscious sedation. Long time of exam suggests the patient oxygen desaturate. Such patients require very close monitoring to desaturation and hypoventilation by the assistants and nursing staff alerting to respiratory depression. The use of pulse oximeter and asking for deep breaths during the exam helps to diminish such risks.

Chronic obstructive pulmonary disease and sleep. Discussion

Abstract: The control of breathing in patients with chronic obstructive pulmonary disease (COPD) follows the same basic principles as in normal subjects, both awake and asleep, with an expected lower feedback response during sleep.This impacts nocturnal gas exchange and sleep quality most profoundly in patients with more severe COPD, as multiple factors come into play. Hypoventilation causes the most important gas-exchange alteration in COPD patients, leading to hypercapnia and hypoxemia, especially during rapid-eye-movement sleep, when marked respiratory muscle atonia occurs. The hypoxia leads to increased arousals, sleep disruption, pulmonary hypertension, and higher mortality. The primary mechanisms for this include decreased ventilatory responsiveness to hypercapnia, reduced respiratory muscle output, and marked increases in upper airway resistance. In the presence of more profound daytime hypercapnia, polysomnography should be considered (over nocturnal pulse oximetry) to rule out other co-existing sleep-related breathing disorders such as obstructive sleep apnea (overlap syndrome) and obesity hypoventilation syndrome. Present consensus guidelines provide insight into the proper use of oxygen, continuous positive airway pressure, and nocturnal noninvasive positive-pressure ventilation for those conditions, but several issues remain contentious. In order to provide optimal therapy to patients, the clinician must take into account certain reimbursement and implementation-process obstacles and the guidelines for treatment and coverage criteria.

Rapidly progressive fatal respiratory failure (Ondine’s curse) in the lateral medullary syndrome

Abstract: A 70-year-old man presented with unilateral lateral medullary infarction, and then died of rapidly progressive respiratory failure within a day. The clinical manifestations were hiccups, hoarseness, dysarthria, nystagmus, left central facial paralysis, paralysis of the left soft palate, dysphagia, decreased superficial sensation over the right face and upper limb, and cerebellar ataxia in the left upper and lower limbs. The arterial blood gas analysis revealed mild hypoventilation. Soon thereafter, an apneic episode occurred during a sleep and advanced to ataxic respiration, and the patient died. Pathologically, there were fresh ischemic infarction localized to the left dorsolateral area of the upper medulla, caused by atherothrombotic occlusion of the left vertebral artery. These foci were in the areas including the medullary reticular formation, the solitary nucleus, the intramedullary fibers of the vagus nerve, and the nucleus ambiguus on the left side. We attributed the fatal acute progressive respiratory impairment in the present case to impairment of the automatic respiratory system (Ondine's curse) rather than the voluntary respiratory system.

Classification and definition of respiratory disorders during sleep.

Abstract: Growing interest in sleep disorders has led to increased research in this direction. Increasingly sophisticated instrumental tests have disclosed new breathing patterns and complex syndromes. The initial identification of obstructive apneas was followed by studies characterizing snoring, hypopneas, respiratory effort-related arousal and flow limitation events. Since Pickwickian syndrome, an historical term currently deemed obsolete and confusing, sleep investigations have differentiated secondary hypoventilation, central hypoventilation and syndromes resulting from narrowing of the upper airways (snoring, upper airway resistance syndrome, obstructive sleep apnea-hypopnea syndrome). Inevitably, this has given rise to some confusion in the classification of events and syndromes which recent studies have attempted to clarify.

Guidelines for the Transport of Critically Ill Patients

Abstract: Hypotension and arrhythmias occur predominantly in mechanically ventilated patients (2, 3). Events being closely related to periods of hypoventilation or hyperventilation with changes of pCO2 of up to 27 mm Hg. Respiratory complications include changes in respiratory rate, fall in PaO2 (4). In patients with head injury, adverse effects include hypotension, hypoxia and increased intracranial pressure.

Respiratory failure in tuberculosis: a modern perspective.

Abstract: Acute respiratory failure is more common in miliary tuberculosis than in tuberculous bronchopneumonia and also has a worse prognosis. Chronic hypercapnic respiratory failure is frequent after both spinal tuberculosis and surgical treatments for pulmonary tuberculosis. It may develop insidiously or present acutely, for instance, during a chest infection. Hypoventilation appears during REM sleep before non-REM sleep or wakefulness and is readily treatable with non-invasive ventilation. The prognosis is good even if initially tracheostomy ventilation is required temporarily.

A modified monobloc for treatment of young children with obstructive sleep apnea.

Abstract: The polysomnographic features of child-hood OSA also differ from those of adults. Theoverall obstructive apnea indices are lower, andinstead of repetitive discrete obstructive apneas,children often exhibit a pattern of partial obstruc-tive hypoventilation, characterized by snoring,paradoxical rib-cage motion, phasic oxyhemo-globin desaturation, and hypercapnia.

Uncompensated metabolic acidosis: an underrecognized risk factor for subsequent intubation requirement.

Abstract: Background: There are no published reports identifying an inadequate ventilatory response to metabolic acidosis as a predictor of impending respiratory failure. Metabolic acidosis should induce a respiratory alkalosis in which the partial pressure of carbon dioxide (Paco 2 ) is (1.5 [HCO 3 - ] + 8) ± 2. This study examined the relation between inadequate ventilatory compensation and intubation among trauma patients. Methods: A retrospective chart review was performed for trauma patients admitted between January 1999 and December 2000. Age, gender, Injury Severity Score and combined Trauma and Injury Severity Score, chest injury, history of cardiac or pulmonary disease, partial pressure of oxygen (Pao 2 ), Paco 2 , Glasgow Coma Score, respiratory rate, systolic blood pressure, base deficit, and ability to compensate were analyzed with respect to intubation and need for ventilator support. Results: Of 140 patients with metabolic acidosis, 45 ultimately were intubated. The mean Paco 2 for the unintubated patients was 34 ± 7 mm Hg, as compared with 41 ± 11 mm Hg for the intubated patients (p < 0.001). Only injury severity and ability to compensate for metabolic acidosis were independent predictors of intubation. Patients with inadequate compensation were 4.2 times more likely to require intubation when control was used for the Injury Severity Score (95% confidence interval, 1.8-9.7; p < 0.001). Conclusions: Inability to mount an adequate hyperventilatory response to metabolic acidosis is associated with an increased likelihood of respiratory failure and a need for ventilatory support. Recognition of this relation should lead to closer monitoring of patients with this condition, and could help to avert unforeseen crisis intubations. This observation needs to be validated in a prospective study.

Non-invasive Mechanical Ventilator Care for the Patients with Advanced Neuromuscular Disease

Abstract: Objective: The usage of mechanical ventilator has been an issue in advanced stage of most neuromuscular diseases. The patients experience hypoventilation symptoms and usually die from pulmonary complications at last. Besides traditional invasive mechanical ventilation, non-invasive intermittent positive pressure ventilation (NIPPV) has provided an alternative treatment option. We evaluated the effects of NIPPV. Method: We applied NIPPV method to the patients with advanced neuromuscular disease who were hospitalized due to ventilatory failure, who visit our outpatient clinic due to hypercapnic symptoms, or who showed hypercapnia on a routine follow-up. To evaluate ventilatory status, blood gas tensions were analyzed by the arterial blood gas analysis and/or pulse-oxymeter and capnometer. Overnight pulseoxymeter monitorings were done whenever necessary. Results: Thirty patients were managed with NIPPV successfully. In five cases, invasive IPPV with tracheostomy at admission was switched to NIPPV. Three patients who had been intubated to receive IPPV were transferred to NIPPV without being tracheostomized. Conclusion: NIPPV can be used safely and effectively as an alternative method of ventilatory support for the patients with advanced neuromuscular disease who show ventilatory failure. It would relieve symptoms and signs of hypoventilation and prevent the acute respiratory muscle decompensation, if applied before overt ventilatory failure.

A Case of Myxedema Coma with Severe Hypoventilation

Abstract: A myxedema coma, representing the extreme feature of hypothyroidism is rare. Despite early vigorous treatment, a myxedema coma is associated with a mortality rate as high as 60%. Herein, a case of a myxedema coma, with severe hypoventilation, is described. When the patient arrived at the emergency room, she complained of dyspnea and general weakness, and was of a drowsy mental status. 7 days after admission, she was more confused and disoriented, and respiratory insufficiency had developed. Although levothyroxine was continued and her respiration improved, she still had a confused mentality and seizure developed. Despite medication her consciousness did not improve, so was discharged in despair by her family members. The respiratory abnormality with a myxedema coma is a depressed ventilatory response to hypercapnea, resulting in a decrease in alveolar ventilation, with progressive retention. An upper airway obstruction, especially during sleep, and neuromuscular dysfunction in breathing may be shown in hypothyroidism. Therefore, a myxedema coma, accompanied by severe hypoventilation, should be intensively treated with thyroid hormone replacement therapy and mechanical ventilatory support.

Post-hyperventilation hypoxaemia is due to alteration of ventilation and perfusion matching.

Abstract: Objective: The aim of this study was to investigate the mechanisms of post-hyperventilation hypoxia. Methodology: Seven healthy male volunteers, aged 29.1 ± 1.4 years, underwent two 10-min periods of voluntary hyperventilation to pulmonary end tidal CO2 values of 20 mmHg (severe hyperventilation), or 30 mmHg (moderate hyperventilation). Post-hyperventilation, the arterial oxygen saturation, VE and arterial blood gas values were measured. Sleep was excluded by EEG monitoring. Results: Maximal hypoxaemia occurred in proportion to severity of hyperventilation; at approximately 5 min post-hyperventilation Pao2 fell to 64 ± 7 mmHg (severe hyperventilation) and 72 ± 6 mmHg (moderate hyperventilation) from 97 ± 3 mmHg at baseline. Hypoxaemia persisted beyond the time of normalization of Paco2 and HCO3. On another occasion, a N2 washout test was performed after severe hyperventilation, which excluded bronchoconstriction. Conclusion: Relative hypoventilation may partly explain post-hyperventilation hypoxaemia, but by excluding bronchoconstriction and periodic breathing, we have demonstrated that most of the hypoxaemia must have been due to alteration of pulmonary blood flow distribution causing a fall in V/Q ratio.

Hypoventilation and hypoxia in reversal of cardiogenic shock in an infant with congenital heart disease.

Abstract: The case is presented of a child in cardiogenic shock in whom oxygen administration exacerbated a systemic to pulmonary shunt that caused a critical deterioration in his cardiovascular status requiring hypoventilation and restoration of baseline hypoxia for reversal.

The effect of infestation with the Australian paralysis tick, Ixodes holocyclus, on thermoregulation and respiration in the dog

Abstract: Tick paralysis is a disease prevalent along the eastern seaboard of Australia affecting an estimated 20 000 domestic animals each year. The disease is caused by adult female Ixodes holocyclus secreting toxin while feeding on the host. Early investigations of the disease relied mainly on observations of affected animals with naturally acquired disease. More recently, specific investigations of experimentally induced and naturally acquired disease has elucidated the effect of the toxin on the neuromuscular and cardiovascular systems.The toxin has been demonstrated to cause temperature-dependent skeletal muscle paralysis and cardiac dysfunction. Extrapolation of these findings to the treatment of dogs with tick paralysis has lead to the active cooling of animals and the awareness that pulmonary oedema may be a feature of respiratory dysfunction. The aims of this study were to investigate the effects of the tick toxin and treatment practices on thermoregulation and to classify and investigate possible causes of the respiratory dysfunction.Thermoregulation was investigated in dogs before and after the onset of paralysis by the measurement of rectal, oesophageal and skin gradient temperatures. The technique of measuring the skin temperature gradient of the hind limb to determine the presence of vasodilation was established. Respiratory dysfunction of dogs with tick paralysis was classified into three distinct respiratory patterns based on respiratory rate and character. TI and TE, oxygen saturation, expired carbon dioxide and audible and auscultated respiratory sounds of the upper and lower respiratory tract were measured. The response of each respiratory pattern to breathing a mixture of helium and oxygen was also determined.Rectal and oesophageal temperatures decreased with the progression of paralysis with oesophageal temperature being significantly lower than rectal temperature in the later stage of the disease. Thermoregulation was compromised by the inability to conserve heat, by vasoconstriction, and the inability to generate heat, by shivering and muscle movement. Vasodilation, as measured by skin temperature gradient of the hind limb, increased as paralysis progressed, despite the presence of low oesophageal temperature to stimulate vasoconstriction. The very nature of appendicular paralysis limited limb muscle tone and movement to generate heat. The decrease in muscle tone was assessed by the ability to shiver, which was lost as paralysis progressed, though the two stimuli for shivering, low skin temperature and low oesophageal temperature, were present. With the decrease in limb movement, movement of other muscle groups in the generation of heat increased in importance. In dogs with severe respiratory dysfunction, movement of the respiratory muscles, as identified by respiratory rate, was a key factor in influencing rectal temperature. Hydration of the coat in dogs with severe paralysis and body weight and body surface area in dogs with mild paralysis appeared to also influence thermoregulation.Respiratory dysfunction in dogs with tick paralysis is well documented with a number of suggested causes. Tachypnea has recently been attributed to pulmonary oedema resulting from cardiac dysfunction, and packed cell volume percentages in dogs with rapid respiratory rates in this investigation support that hypothesis.In this study, respiratory dysfunction was classified into three patterns; slow, deep respiration, rapid, shallow respiration and rapid, deep respiration. The first two patterns were present in dogs with no inspiratory crackles, and all three respiratory patterns occurred in dogs with inspiratory crackles. Grunts and stridors, which have been previously reported as common features of tick paralysis, were either absent or uncommon, while sighs were associated with slow, deep respiration. Inspiratory time (corrected for respiratory rate) was prolonged in dogs with marked bradypnea and tachypnea signifying the imminent development of or the presence of respiratory muscle fatigue. Decreased oxygen saturation was a feature of all of the respiratory patterns while expired carbon dioxide levels were below the level signifying hypoventilation. Auscultated respiratory sounds were influenced by respiratory effort and the presence of alveolar disease.The effect of breathing a helium-oxygen mixture on the breathing patterns was assessed. Respiratory effort, inspiratory and expiratory times (corrected for respiratory rate), oxygen saturation, expired carbon dioxide, audible and auscultated respiratory sounds, rectal temperature and gait score were measured. The response to breathing a less dense gas, by assessing the change in respiratory effort, demonstrated the presence of respiratory muscle fatigue in dogs with a slow, deep respiratory pattern. The administration of Heliox to dogs with a rapid, shallow respiratory pattern was beneficial in some individuals but further study of a larger number of dogs is required to determine its importance in this respiratory presentation. Changes in audible and auscultated respiratory sounds were due to the change in the density of inspired gas. Inspiratory and expiratory times, oxygen saturation, expired carbon dioxide levels, rectal temperature and gait score were either minimally or not affected. The response to breathing the heliumoxygen mixture in dogs with inspiratory crackles, was variable and its detrimental effect in two dogs warrants caution in its use in such cases.Important clinical and therapeutic implications regarding thermoregulation and respiratory dysfunction can be drawn from this study. Clinicians need to be aware that thermoregulation may become compromised as the disease progresses. The inability to conserve heat by vasoconstriction of arteriovenous anastomoses and to generate heat by muscle movement of the limbs and shivering results in a decrease in core temperature that is not accurately reflected by rectal temperature measurement. Common nursing practices such as bathing animals and administration of vasodilator drugs can exacerbate the situation. As hypothermia mimics and compounds the clinical signs of tick paralysis, hypothermia may go undetected and contribute to mortality.The development and change in respiratory dysfunction can be easily categorised by respiratory rate and character into three distinct patterns to aid therapeutic decisions and alert the clinician to response to therapy. Respiratory muscle fatigue was demonstrated in dogs with slow, deep respiration and resting of the respiratory muscles by administrating Heliox was shown to be beneficial in these cases.