Showing papers on "Hypoventilation published in 1998"

Congenital central hypoventilation syndrome and Hirschsprung’s disease

Abstract: Five cases of the Hirschsprung's disease-congenital central hypoventilation syndrome (CCHS) association are presented and 41 other published cases reviewed. These children have a distinct pattern of associated features, an equal sex incidence, and a characteristic spectrum of disease severity which suggests that the condition is genetically distinct from other cases of Hirschsprung's disease. While approximately 1.5% of Hirschsprung's disease patients, and 10% of those with total colonic aganglionosis, will have CCHS, up to 50% of CCHS patients will have Hirschsprung's disease. Approximately 20% of CCHS/Hirschsprung patients will also have neuroblastoma or ganglioneuroma, usually multiple. Abnormalities of the eye and autonomic nervous system are also common. The ventilatory abnormality is usually evident on the first day of life. The aganglionosis is also severe, with more than half (59%) of the patients having aganglionosis extending into the small bowel.

Loss of catecholaminergic neurons in the medullary reticular formation in myotonic dystrophy

Abstract: Objective: To clarify the possible relation between the extent of involvement of catecholaminergic neurons and the presence of alveolar hypoventilation in patients with myotonic dystrophy (MyD). Background: Respiratory insufficiency has been reported frequently in MyD patients. Recent data support the hypothesis that this respiratory failure results from a primary dysfunction of the CNS. Methods: The authors performed a quantitative immunoreactive study of tyrosine hydroxylase immunoreactive (TH+) neurons linked to hypoventilation in the dorsal central medullary nucleus (DCMN), the ventral central medullary nucleus (VCMN), and the subtrigeminal medullary nucleus (SMN)-where the automatic respiratory center is thought to be located-in eight MyD patients and in 10 age-matched control subjects. Alveolar hypoventilation of the central type was present in three of the MyD patients but not in the remaining MyD patients or the control subjects. Results: The densities of TH+ neurons of the DCMN, the VCMN, and the SMN in MyD patients with hypoventilation were significantly lower than in those without hypoventilation ( p p p p p p Conclusions: These data suggest that the loss of TH+ neurons of the DCMN, the VCMN, and the SMN is associated with the presence of hypoventilation in MyD and may be an important feature of MyD.

Effects of hyperventilation and hypoventilation on PaCO2 and intracranial pressure during acute elevations of intraabdominal pressure with CO2 pneumoperitoneum: large animal observations

Abstract: Background: The side effects of acute elevations in intraabdominal pressure (IAP) are related to a multifactorial etiology. Previous studies have reported that acute elevations in IAP produce an immediate increase in intracranial pressure (ICP). This study was designed to analyze the reasons for increased ICP during acute elevations of IAP and to determine the combined effects of IAP and changes in ventilation indices on ICP and hemodynamic indices. Study Design: Five pigs were studied. A subarachnoid screw was placed for ICP monitoring. The jugular vein, femoral vein, and femoral artery were cannulated. Mean arterial pressure (MAP), central venous pressure (CVP), ICP, and arterial pressure of carbon dioxide (PaCO 2 ) were monitored before and after carbon dioxide pneumoperitoneum was established at 0, 10, and 20 mmHg of IAP. Effects of hyperventilation and hypoventilation were recorded and compared with baseline ventilation. Cavography was performed to evaluate the morphology of the inferior vena cava (IVC) at different levels of IAP. Multiple regression and Student's t -test were used to examine the effects of IAP and ventilation on dependent variables. Results: The IVC showed a progressive narrowing at the level of the diaphragm as IAP was increased. There was a simultaneous increase in CVP, MAP, and ICP. The mean changes in ICP with hypoventilation were significantly larger than with hyperventilation. Conclusions: Acutely increased IAP displaces the diaphragm cranially, narrowing the IVC and increasing intrathoracic pressure. This increases CVP and increases ICP by venous stasis and increased pressure in the sagittal sinus with decreased resorption of cerebrospinal fluid. Hemodynamic changes are directly related to the rise in ICP. Hypoventilation and hypercarbia significantly increase ICP when compared with hyperventilation and hypocarbia. Hyperventilation does not significantly decrease ICP during acute elevations of IAP.

Abnormal respiratory patterns in childhood cerebral malaria.

Abstract: Of 295 children with cerebral malaria, 117 (40%) had an abnormal respiratory pattern; 15 children exhibited more than one pattern during their clinical course. Four distinct patterns were seen. (i) Deep breathing (80 children); this was associated with severe metabolic acidosis, and resolved following treatment with intravenous fluids and/or blood. (ii) Hypoventilation with nystagmus and salivation (18 children); simultaneous electroencephalographic recording revealed continuous electrical seizure activity, demonstrating that these children were in subtle status epilepticus; anticonvulsant treatment resulted in return to normal of blood gases and recovery of consciousness. (iii) Hyperventilation with extensor posturing (20 children), which was associated with varying degrees of intracranial hypertension. (iv) Periodic respiration (14 children); all had clinical features suggestive of transtentorial herniation, and died following a respiratory arrest. Abnormal respiratory patterns can alert the clinician to complications of cerebral malaria that require treatment. Recognition of these patterns and rapid initiation of appropriate supportive therapy may help to reduce the high mortality rate of this disease.

Respiratory insufficiency due to high anterior cervical cord infarction

Abstract: OBJECTS AND METHODS—Respiratory dysfunction may occur as a result of lesions in the upper cervical spinal cord disturbing the descending pathways subserving automatic and volitional ventilatory control. Four patients are described who presented with acute respiratory insufficiency caused by infarction of the anterior portion of the upper cervical cord due to presumed anterior spinal artery occlusion. RESULTS—Two patients presented after respiratory arrests; they were ventilated and there was no automatic or volitional respiratory effort. Both had signs of an extensive anterior spinal cord lesion at the C2 level and this was confirmed by MRI. One patient presented with a C4 infarction and required ventilation for three months. Ventilatory recovery was characterised by the development of an automatic respiratory pattern. The fourth patient required ventilation for two months after infarction at the C3 level. On attempted weaning he had prolonged periods of hypoventilation and apnoea during inattention and sleep indicating impairment of automatic respiratory control. CONCLUSION—Infarction of the spinal cord at high cervical levels may be due to fibrocartilaginous embolism and involvement of the descending respiratory pathways may occur. Extensive lesions at C1/2 cause complete interruption of descending respiratory control leading to apnoea. Partial lesions at C3/4 cause selective interruption of automatic or voluntary pathways and give rise to characteristic respiratory patterns. The prognosis depends on the level and extent of the lesion.

Extreme hypoventilation reduces ventilator-induced lung injury during ventilation with low positive end-expiratory pressure in saline-lavaged rabbits

Abstract: ObjectiveTo compare the degrees of ventilator-induced lung injury caused by two ventilation protocols.DesignRandomized trial.SettingUniversity animal laboratory.SubjectsSixteen New Zealand white rabbits.InterventionsAfter five sequential saline lung lavages, eight pairs of anesthetized rabbits were

Treatment of central sleep apnoea in congestive heart failure with nasal ventilation.

Abstract: Cheyne-Stokes respiration (CSR) is common in patients with congestive heart failure (CHF).1 This characteristic crescendo-decrescendo pattern of breathing is often seen during sleep in patients with CHF and is a form of central sleep apnoea.2 Disordered nocturnal breathing leads to oxygen desaturation, poor sleep quality, and altered sleep architecture.3 These features may lead to complaints of daytime somnolence, fatigue, insomnia, and many of the symptoms typical of sleep disordered breathing. It has been proposed that CSR during sleep in patients with heart failure is an indicator of a poor prognosis.4 5 The likely adverse effects of CSR on daytime performance and myocardial function have resulted in the introduction and evaluation of a range of treatments aimed at reducing CSR. These include low flow oxygen,6 theophylline,7 and nasal continuous positive airways pressure (nCPAP).8 In one controlled study nCPAP was shown to improve both sleep quality and daytime myocardial function.8 Other groups have found nCPAP to be ineffective in controlling CSR.9-11 Nocturnal nasal intermittent positive pressure ventilation (nIPPV) is the accepted treatment for patients with chronic respiratory failure due to hypoventilation during sleep.12 13 We hypothesised that nIPPV may also effectively treat central sleep apnoea in heart failure by controlling ventilation and carbon dioxide in patients whose disordered breathing has been linked to fluctuating carbon dioxide levels, relative hyperventilation, and hypocapnia.14 15Nasal IPPV was administered in an attempt to mechanically ventilate the patient through the apnoeic portion of the Cheyne-Stokes cycle, thereby preventing fluctuations in carbon dioxide levels and consequently abolishing CSR. This study describes the use of nocturnal nIPPV in a group of patients with heart failure and Cheyne-Stokes respiration during sleep. The effects of this therapy on respiratory disturbance and sleep quality following an in-hospital acclimatisation period are …

Respiratory failure and hypoventilation secondary to neurosarcoidosis.

Abstract: We report a patient manifesting severe hypoventilation resulting from diaphragmatic paresis secondary to sarcoid. A 34yr-old female presented with chest pain. Chest radiograph revealed hilar adenopathy and left pleural effusion; computed tomography scan showed a 2-cm solid lesion in the aorto-pulmonary window. Bronchoscopy and thoracentesis failed to further identify the nature of the lesion. An episode of aspiration resulted in cardiopulmonary arrest, necessitating cardiopulmonary resuscitation. Electrodiagnostic findings were consistent with bilateral phrenic neuropathy with axon loss, suggesting a poor prognosis. Biopsy via mediastinoscopy revealed noncaseating confluent granulomas with many multinucleated epithelioid histiocytes consistent with the diagnosis of sarcoidosis. Eight months after initial diagnosis and immunosuppressive treatment, the patient was successfully extubated and became ambulatory. Upon tapering her prednisone, however, she became dyspneic and manifested hypoventilation secondary to muscle weakness. Her corticosteroids were increased, but she eventually died of an opportunistic lung infection 2 yr later. This case establishes phrenic neuropathy and peripheral polyneuropathy secondary to neurosarcoidosis as a cause of respiratory failure. It also illustrates the utility of phrenic and diaphragmatic electrodiagnosis in the evaluation as well as prognostication of such lesions.

Hyper- and hypoventilation affects spinal motor neuron excitability during isoflurane anesthesia.

Abstract: Increasing evidence indicates that the spinal cord is an important site of anesthetic action necessary for surgical immobility.Whether clinical hyper- or hypoventilation affects motor neuron excitability during general anesthesia is unknown. To clarify this issue, we studied seven adult ASA physical

Assessment of ventilation during the performance of a percutaneous dilatational tracheostomy: hypoventilation is not a common complication.

Abstract: Percutaneous dilatational tracheostomy (PDT) is becoming an accepted cost-effective alternative to surgical tracheostomy. PDT is performed by progressive dilatation of a tracheal opening placed under bronchoscopic guidance. Case reports of hypoventilation with associated hypercarbia during the performance of PDT have raised concerns about the utility of this procedure in patients in whom hypercarbia is problematic (e.g., patients with closed head injury). In a prospective cohort analysis of 11 critically ill patients, we evaluated the effect of PDT on ventilation during and after the procedure using end tidal capnography. We found that hypercarbia does not occur during or after the performance of PDT as compared to baseline levels.

Sleep-related disorders and chronic obstructive pulmonary disease.

Abstract: Sleep-disordered breathing is ubiquitous in COPD. Sleep-related hypoxemia results from hypoventilation attributable to reduced respiratory drive and abnormal mechanics, and from probable changes in V/Q matching. An overlap syndrome combining COPD and OSA also has been described. Disturbances in cardiac, hematologic, and pulmonary function, as well as sleep complaints, are common when COPD is complicated by nocturnal hypoxemia, and these sequelae are even more common when COPD and OSA coexist. Treatment with oxygen is the mainstay for COPD and sleep desaturation alone, whereas combined nasal CPAP and oxygen are most frequently used for the overlap syndrome.

Insuficiência respiratória na criança Respiratory failure in the child

Abstract: Objetive: To describe the main physiopathologic mechanism of the respiratory failure in the child, as well as to discuss some aspects of the differential diagnosis and treatment. Source of data: The main national and international textbooks and articles about respiratory failure in the child were used as sources of data for this research. Results: Respiratory failure is defined as the incapacity to maintain a paO 2 over 50 mmHg associated or not to a paCO 2 over 50 mmHg in children breathing ambient air at sea level. This failure may be classified as hypoxemic or hypercapnic, or even as acute or chronic. The main alterations may be hypoventilation, ventilation perfusion mismatch and diffusion defect. It may be secondary to a central origin, upper or lower airway compromise, parenchyma disease, or due to pleural or thorax wall affection. The hypoxemia evaluation may be done by hemoglobin saturation, alveolar capillary gradient of oxygen (D[A-a]O 2 ) or by the paO 2 / FiO 2 index. Comments: The knowledge of the physiopathologic mechanisms that cause respiratory failure in the child is important to define the more efficient therapeutic strategy for each cause.

Respiratory failure in the child

Abstract: OBJECTIVE: To describe the main physiopathologic mechanism of the respiratory failure in the child, as well as to discuss some aspects of the differential diagnosis and treatment. SOURCE OF DATA: The main national and international textbooks and articles about respiratory failure in the child were used as sources of data for this research. RESULTS: Respiratory failure is defined as the incapacity to maintain a paO(2) over 50 mmHg associated or not to a paCO(2) over 50 mmHg in children breathing ambient air at sea level. This failure may be classified as hypoxemic or hypercapnic, or even as acute or chronic. The main alterations may be hypoventilation, ventilation perfusion mismatch and diffusion defect. It may be secondary to a central origin, upper or lower airway compromise, parenchyma disease, or due to pleural or thorax wall affection. The hypoxemia evaluation may be done by hemoglobin saturation, alveolar capillary gradient of oxygen (D[A-a]O(2)) or by the paO(2) / FiO(2) index. COMMENTS: The knowledge of the physiopathologic mechanisms that cause respiratory failure in the child is important to define the more efficient therapeutic strategy for each cause.

A 60-year-old woman with weakness, fatigue, and acute respiratory failure: case report and discussion of the differential diagnosis

Abstract: A 60-year-old woman with chronic progressive fatigue, diurnal somnolence, proximal muscle weakness, and dyspnea developed acute respiratory failure when given supplemental oxygen. Hypoventilation secondary to neuromuscular dysfunction was suspected by the critical care specialist. Neurologic consultation and supportive laboratory evaluations led to the diagnosis of acid maltase deficiency, which was confirmed by muscle biopsy. The discussion includes a literature review that describes the pathophysiology and treatment of this rare muscle enzyme deficiency disorder. Acid maltase deficiency should be suspected in any adult presenting with hypoxemia, fatigue, and acute respiratory failure.

Critical care management of the asthmatic patient.

Abstract: The incidence and severity of asthma continue to increase despite advances in therapy. Two types of severe asthma exacerbations have been described: "sudden onset" and "slow onset." Beta-adrenergic agonists and corticosteroids are still the mainstay of therapy in the intensive care unit. Hypercapnic hypoventilation is advocated as a mode of mechanical ventilation to maintain oxygenation while minimizing barotrauma. Sedating and paralytic agents must be used with caution to prevent complications such as myopathy, which may occur with prolonged use of these agents. Future avenues of study could include the use of leukotriene and platelet-activating factor inhibitors. Asthma management guidelines should be practiced to prevent worsening of bronchospasm to the point of severe exacerbation.

Estimated numbers of patients with intractable respiratory diseases

Abstract: To estimate the number of patients with intractable respiratory diseases, we conducted a two-stage nationwide epidemiological survey in 1997. The first survey was performed at randomly sampled hospitals to identify the number of patients treated. The second survey sought detailed clinico-epidemiological data on the patients reported in the first survey. The response rates were 54% for the first survey and 62% for the second. Based on the survey findings, we derived the following nationwide estimates: 450 patients (95% confidence interval: 360-530) with chronic thromboembolic pulmonary hypertension; 230 (200-260) with primary pulmonary hypertension; 180 (150-210) with obesity-associated hypoventilation syndrome; 40 (30-50) with primary alveolar hypoventilation syndrome; 160 (140-180) with histiocytosis X; and 190 (150-230) with juvenile pulmonary emphysema.

The control of breathing with reference to congenital central hypoventilation syndrome.

Abstract: The aims of respiration are to provide the body with oxygen and relieve it of carbon dioxide in the most efficient way possible. We seldom make a conscious effort to control our breathing yet our respiratory pattern always matches our requirements. Even in health, the rate and depth of breathing can vary enormously from person to person and within the same person at different times. For example, during strenuous exercise, the demands of the body for oxygen uptake and carbon dioxide elimination can be 10 times those during sleepl. Despite this, the body maintains levels of oxygen, carbon dioxide and arterial pH within a remarkably small range. Normal activities such as talking, eating and coughing also require specially coordinated patterns of breathing. For this to be possible a series of complex and incompletely understood control mechanisms exist to regulate ventilationl4. The failure of these mechanisms in some disease states can help us to appreciate the normal physiology more fully. Congenital central hypoventilation syndrome, a rare but important disorder of ventilatory control, provides us with some insight into the automatic and voluntary influences on breathing during both sleep and wakefulness.

Sleep disordered breathing in patients with chronic obstructive pulmonary disease

Abstract: Nocturnal hypoxia often occurs in patients with chronic obstructive pulmonary disease (COPD) In a group of 60 patients with an FEV1 below 65% of the reference value, we found episodes of desaturation in 47 patients (78%)1 Control of breathing during sleep depends highly on the sleep-stage In non-REM sleep (nREM; no rapid eye movements) the ‘metabolic’ control of breathing is intact: ventilation (VI) is regulated to a level where the need of oxygen uptake and the elemination of carbon dioxide is met There is an absence of the ‘wakefullness drive’, which leads to some hypoventilation and lowered responsiveness to hypoxia, and especially to hypercapnia (fig 1) The arterial Pco2 is usually increased by 05 to 10 kPa, as compared to the awake state2 Nevertheless, the major ventilatory drive in slow wave sleep is the CO2 drive

Right-to-Left Shunt Through a Ventricular Septal Defect During Sedated Sleep.

Abstract: A 10-month-old infant with Down's syndrome developed cyanosis due to a right-to-left shunt through a ventricular septal defect during sedated sleep induced for echocardiography. During cardiac catheterization, arterial oxygen saturation decreased, and arterial carbon dioxide concentration increased. Various echocardiographic parameters during sedated and natural sleep were compared. It was considered that hypoventilation caused by the narrowed upper airway was induced by sedated sleep. We conclude that the influence of sedatives should be considered in the estimation of echocardiographic data if an infant with Down's syndrome has a ventricular septal defect with pulmonary hypertension.