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Biomedical subjects

M T Naughton

Publications and source records attributed to M T Naughton.

At least 19 recordsLinked to original sources
PubMed2007

Non-invasive positive pressure ventilation for acute respiratory failure: justified or just hot air?

Non-invasive positive pressure ventilation (NIV) is the provision of mechanical positive airway pressure ventilatory support through the patient's upper airway through mask interface. Conditions in which it has been shown to be effective are acute cardiogenic pulmonary oedema and acute hypercapnic exacerbations of chronic obstructive pulmonary disease. In such conditions, NIV is associated with reduced intensive care unit demands, a reduction in intubation rates, reduced health-care expenditure and improved survival. Other conditions, such as hypercapnia of other cause, hypoxaemic respiratory failure and acute asthma, have supportive, but less conclusive data. Indications, contraindications and guidelines for the use of NIV are discussed.

Humans↗
PubMed2006

Marijuana lung.

Explore the source record for details and available documents.

Adult↗
PubMed2004

Obstructive sleep apnoea and cardiovascular disease.

Obstructive sleep apnoea (OSA) leads to both acute and chronic physiological effects on the cardiovascular system. There is now a large amount of evidence showing that OSA is independently associated with a wide spectrum of clinical cardiovascular disease (CVD). Evidence for a causative effect of OSA is strongest for hypertension, but is weaker for other cardiovascular disorders. Large prospective trials are ongoing and when results become available the link between OSA and CVD is likely to be strengthened. Treatment of OSA with continuous positive airway pressure has been shown to improve blood pressure, particularly in those with hypertension, and also left ventricular ejection fraction in those with congestive heart failure. Given the high prevalence of OSA in the community and its effects on the cardiovascular system, symptoms of this disorder should be sought in patients being investigated or treated for CVD.

Age Distribution↗
PubMed2004

Increased long-term mortality in heart failure due to sleep apnoea is not yet proven.

Previous small-scale studies of the effect of sleep-disordered breathing (SDB) on prognosis in congestive heart failure (CHF) are either lacking or conflicting. The aim of this study was to assess the impact of the presence and type of SDB on mortality in a patient group with severe CHF referred to a specialised heart failure centre. Out of 78 patients ((mean +/- SD) 53 +/- 9 yrs, left ventricular ejection fraction 19.9 +/- 7.2% and pulmonary capillary wedge pressure 16.5 +/- 8.3 mmHg) followed-up over a median period of 52 months, 29% had no apnoea (CHF-N), 28% had obstructive sleep apnoea (CHF-OSA) and 42% had central sleep apnoea (CHF-CSA). At 52 months, their overall mortality was 40%, and combined mortality and transplantation was 72%. Mortality rates were similar between the three apnoea groups. Survivors had a similar prevalence of SDB (71%) as the nonsurvivors (70%). Although a significant increase in mortality was evident at 500 days in those patients with either CHF-SDB or CHF-CSA as compared with CHF-N, this was not significant at final follow-up (52 months) using Kaplan Meier analysis. Multivariate analysis identified transplantation but not SDB type or severity as a significant predictor of survival. In conclusion, sleep-disordered breathing impacts upon early (500 day), but not long-term (52 month), mortality in a specialised heart failure centre.

Adult↗
PubMed2004

Sleep apnea and congestive heart failure.

Sleep apnea encompasses 2 forms of sleep disordered breathing, namely obstructive and central sleep apnea. Both these conditions are prevalent in patients with congestive heart failure (CHF) despite quite different etiology and pathogenesis. The last 15 years have seen the development of a large database of mechanistic data implicating both these conditions in the progression of cardiac dysfunction in patients with heart failure. Epidemiological data have also revealed that obstructive sleep apnea may be an independent risk factor for the development of cardiac diseases. Central sleep apnea, conversely, is more likely to emerge as a consequence of severe cardiac dysfunction, but through an elaborate vicious cycle could potentially lead to augmentation of sympathetic activity and contribute to further cardiac decline. In recent years a number of randomized controlled trials suggests secondary endpoints such as symptoms, sympatho-excitation and left ventricular function can be improved with the effective therapies available for both central and obstructive sleep apnea in patients in which these conditions co-exist. Mortality data is emerging also, and the first of a large scale mortality trial assessing the effect of attenuating central sleep apnea with continuous positive airway pressure in patients with moderate to severe CHF, is well underway. This review summarizes the important mechanistic, epidemiological and interventional studies in relation to sleep apnea and congestive heart failure with some commentary on the future direction of this rapidly growing field.

Blood Pressure↗
PubMed2003

Non-invasive ventilation assists chest physiotherapy in adults with acute exacerbations of cystic fibrosis.

BACKGROUND: Chest physiotherapy is essential to the management of cystic fibrosis (CF). However, respiratory muscle fatigue and oxygen desaturation during treatment have been reported. The aim of this study was to determine whether non-invasive ventilation (NIV) during chest physiotherapy could prevent these adverse effects in adults with exacerbations of CF. METHODS: Twenty six patients of mean (SD) age 27 (6) years and forced expiratory volume in 1 second (FEV1) 34 (12)% predicted completed a randomised crossover trial comparing standard treatment (active cycle of breathing technique, ACBT) with ACBT + NIV. Respiratory muscle strength (PImax, PEmax), spirometric parameters, and dyspnoea were measured before and after treatment. Pulse oximetry (SpO2) was recorded during treatment. Sputum production during treatment and 4 and 24 hours after treatment was evaluated. RESULTS: There was a significant reduction in PImax following standard treatment that was correlated with baseline PImax (r=0.73, p<0.001). PImax was maintained following NIV (mean difference from standard treatment 9.04 cm H2O, 95% confidence interval (CI) 4.25 to 13.83 cm H2O, p=0.006). A significant increase in PEmax was observed following the NIV session (8.04 cm H2O, 95% CI 0.61 to 15.46 cm H2O, p=0.02). The proportion of treatment time with SpO2 < or =90% was correlated with FEV1 (r=-0.65, p<0.001). NIV improved mean SpO2 (p<0.001) and reduced dyspnoea (p=0.02). There were no differences in FEV1, forced vital capacity (FVC) or sputum weight, but FEF(25-75) increased following NIV (p=0.006). CONCLUSION: Reduced inspiratory muscle strength and oxygen desaturation during chest physiotherapy are associated with inspiratory muscle weakness and severity of lung disease in adults with exacerbations of CF. Addition of NIV improves inspiratory muscle function, oxygen saturation and small airway function and reduces dyspnoea.

Acute Disease↗
PubMed2002

Measurement variability in sleep disorders medicine: the Victorian experience.

BACKGROUND: Surveys of laboratories in North America have documented significant diversity in the working definitions used for reporting respiratory events in sleep studies. AIM: To assess sources of variability in the measurement of sleep-disordered breathing (as defined by the Apnoea-Hypopnoea Index) between sleep laboratories in Victoria, Australia. METHODS: A self-complete written questionnaire was constructed following literature review and interviews with staff at three separate sleep laboratories. The survey was sent to all laboratories listed in Victoria by the Australasian Sleep Association. The first part of the survey related to the type of equipment used to record sleep and other variables during overnight polysomnography and the second part related to the definitions and methods used to report results. RESULTS: Seventeen out of 18 laboratories returned the surveys. There were variations identified in the types of sensors used to measure particular signals. There were also inconsistencies identified in the criteria used to score arousals, apnoeas and hypopnoeas by different laboratories. The variability was greatest for hypopnoea definitions. CONCLUSIONS: There is considerable variation in the methods used to measure and define sleep-disordered breathing between sleep laboratories in Victoria. The extent to which these variations influence the comparability of reported results between laboratories requires further evaluation. The survey findings may assist the process of developing and implementing local guidelines for the performance and reporting of polysomnography.

Clinical Laboratory Techniques↗
PubMed2002

The Victorian CPAP program: is there a need for additional education and support?

BACKGROUND: The Victorian Continuous Positive Airways Pressure (CPAP) Program provides CPAP services to financially disadvantaged individuals with moderate to severe sleep apnoea. AIMS: To evaluate health outcomes in patients referred to the pilot program in order to: (i) assess the magnitude of health benefit from treatment in this highly selected population and (ii) identify patient characteristics or factors related to service provision that may influence outcome. METHODS: We adopted a simple before-after research design. Patients who were referred to the program were recruited from five sleep centres. Questionnaires were administered at baseline and 1 and 3 months after commencing CPAP. Generic and disease-specific quality of life were assessed using the MOS 36-Item Short-form Health Survey and the Sleep Apnoea Quality-of-life Index, respectively. Subjective daytime sleepiness was measured using the Epworth Sleepiness Scale and the Sleep-Wake Activity Inventory. RESULTS: Of the 68 subjects enrolled in the study, 59 were available for follow up. There were significant improvements in daytime sleepiness (P < 0.0005). Treatment-related symptoms had a negative impact on overall disease-specific quality of life, however there were significant improvements in all other domains of disease-specific quality of life (P < 0.0005). Improvements in generic quality of life were small but statistically significant (P < 0.05). Hospital, disease severity, baseline sleepiness, gender and CPAP-machine type were not predictors of outcome (P > 0.05). CONCLUSION: This review of the Victorian CPAP Program identified significant improvements in subjective daytime sleepiness and quality of life, despite the negative impact of treatment-related symptoms. Future research should explore whether services can be modified to help reduce the impact of treatment-related side-effects.

Adolescent↗
PubMed2002

Cardiac diastolic function and hypercapnic ventilatory responses in central sleep apnoea.

Hyperventilation is the key factor contributing to the development of idiopathic nonhypercapnic central sleep apnoea (ICSA), where left ventricular systolic function is normal. ICSA is reported to occur in 20% of patients with left ventricular diastolic dysfunction, in whom elevated pulmonary vascular pressures and resultant increased pulmonary vagal afferent traffic may contribute to hyperventilation. The contribution of the two potential mechanisms responsible for the hyperventilation seen in the following ICSA was measured: 1) left ventricular diastolic dysfunction-induced pulmonary hypertension; and 2) increased peripheral and central hypercapnic ventilatory responses (HCVR). The pulmonary artery pressure, left ventricular diastolic function and chemosensitivity to hypercapnia were measured during wakefulness in 16 subjects with ICSA. All subjects had systolic pulmonary artery pressures <3.99 kPa (<30 mmHg) and only four had diastolic dysfunction. All subjects had elevated peripheral and central HCVR compared with historical normal control subjects. Diastolic dysfunction correlated with increasing age but not with HCVR or markers of central sleep apnoea severity. Idiopathic nonhypercapnic central sleep apnoea is likely to be dependent upon raised hypercapnic ventilatory responses, and not pulmonary hypertension due to left ventricular diastolic dysfunction.

Adolescent↗
PubMed2001

Acute effects of continuous positive airway pressure on cardiac sympathetic tone in congestive heart failure.

BACKGROUND: Depressed ventricular performance and neurohormonal activation are key pathophysiological features of congestive heart failure (CHF). Although angiotensin-converting enzyme inhibitors and beta-adrenoceptor blockers exert beneficial effects in CHF, mortality remains unacceptably high, and the development of further therapeutic approaches is warranted. Recent data suggest that continuous positive airway pressure (CPAP) may be of benefit in the treatment of CHF, although the mechanism for this action is incompletely understood. METHODS AND RESULTS: In the present study, we examined the effect of short-term CPAP (10 cm H(2)O for 10 minutes) on hemodynamics (Swan Ganz catheter) and total systemic and cardiac sympathetic activity (norepinephrine spillover method) in 14 CHF patients in New York Heart Association class III. The application of CPAP was associated with a fall in cardiac output (4.8+/-0.3 to 4.4+/-0.2 L/min; P<0.05) and a significant reduction in cardiac norepinephrine spillover (370+/-58 to 299+/-55 pmol/min; P<0.05), although total systemic norepinephrine spillover was unchanged. CONCLUSION: The short-term application of CPAP results in an inhibition of cardiac sympathetic nervous activity. Further investigation into the potential value of long-term CPAP in CHF patients is warranted.

Heart↗
PubMed2000

Peripheral and central ventilatory responses in central sleep apnea with and without congestive heart failure.

Given that the apnea-ventilation cycle length during central sleep apnea (CSA) with congestive heart failure (CHF) is approximately 70 s, we hypothesized that rapidly responsive peripheral CO(2) ventilatory responses would be raised in CHF-CSA and would correlate with the severity of CSA. Sleep studies and single breath and rebreathe hypercapnic ventilatory responses (HCVR) were measured as markers of peripheral and central CO(2) ventilatory responses, respectively, in 51 subjects: 12 CHF with no apnea (CHF-N), 8 CHF with obstructive sleep apnea (CHF-OSA), 12 CHF-CSA, 11 CSA without CHF ("idiopathic" CSA; ICSA), and 8 normal subjects. Single breath HCVR was equally elevated in CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (0.58 +/- 0.09 [mean +/- SE] and 0. 58 +/- 0.07 versus 0.23 +/- 0.06, 0.25 +/- 0.04, and 0.27 +/- 0.02 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Similarly, rebreathe HCVR was elevated in both CHF-CSA and ICSA groups compared with CHF-N, CHF-OSA, and normal groups (5.80 +/- 1.12 and 3.53 +/- 0. 29 versus 2.00 +/- 0.25, 1.44 +/- 0.16, and 2.14 +/- 0.22 L/min/PET(CO(2)) mm Hg, respectively, p < 0.001). Furthermore, in the entire CHF group, single breath HCVR correlated with central apnea-hypopnea index (AHI) (r = 0.63, p < 0.001) and percentage central/total apneas (r = 0.52, p = 0.022). Rebreathe HCVR correlated with awake Pa(CO(2)) (r = -0.61, p < 0.001), but not with central AHI or percentage central/total apneas independent of its relationship with single breath HCVR. In conclusion, in subjects with CHF, raised central CO(2) ventilatory response predisposes to CSA promoting background hypocapnia and exposing the apnea threshold to fluctuations in ventilation, whereas raised and faster-acting peripheral CO(2) ventilatory response determines the periodicity and severity of CSA.

Analysis of Variance↗
PubMed2000

Effect of moderate alcohol upon obstructive sleep apnoea.

Moderate-to-large quantities of alcohol are known to aggravate severe obstructive sleep apnoea (OSA), however, the reported effects of moderate alcohol consumption upon mild-to-moderate OSA are inconsistent. Given the reported benefits of moderate alcohol consumption on cardiovascular mortality, recommendations regarding the management of patients with OSA are difficult to formulate. The aim of this study was to evaluate the effects of moderate alcohol on sleep and breathing in subjects with mild-to-moderate OSA. Twenty-one male volunteers, who snored habitually, underwent polysomnography with and without 0.5 g alcohol x kg body weight (BW)(-1) consumed 90 min prior to sleep time, in random order. The mean blood alcohol concentration (BAC) following alcohol at the time of lights out was 0.07 g x dL(-1). The distribution amongst the various sleep stages was not significantly altered by alcohol. The mean apnoea/hypopnoea index rose from 7.1+/-1.9 to 9.7+/-2.1 events x h(-1) (mean+/-SEM, p=0.017); however, there was no significant change in the minimum arterial oxygen saturation measured by pulse oximetry Sp,O2, apnoea length or snoring intensity. Mean sleep cardiac frequency rose significantly from 53.9+/-1.4 to 59.9+/-1.9 beats x min(-1) (P<0.001) and overnight urinary noradrenalin increased from 14.9+/-2.3 to 18.8+/-2.3 nmol x mmol creatinine(-1) (p=0.061) on the alcohol night compared to the nonalcohol night. To conclude, modest alcohol consumption, giving a mean blood alcohol concentration of 0.07 g x dL(-1), significantly increases both obstructive sleep apnoea frequency and mean sleep cardiac frequency.

Adult↗
PubMed1999

Influence of pulmonary capillary wedge pressure on central apnea in heart failure.

BACKGROUND: Recent studies suggest that acute pulmonary congestion induces hyperventilation and that hyperventilation-related hypocapnia leads to ventilatory control instability and central sleep apnea. Whether chronic pulmonary congestion due to congestive heart failure (CHF) is associated with central apnea is unknown. We hypothesized that CHF patients with central apnea would have greater pulmonary capillary wedge pressure (PCWP) than patients without central apnea and that PCWP would correlate with central apnea severity. METHODS AND RESULTS: Seventy-five stable CHF patients underwent right heart catheterization and, on the basis of overnight sleep studies, were divided into central apnea (n=33), obstructive apnea (n=20), or nonapnea groups (apnea-hypopnea index [AHI] <5 events per hour). Mean PCWP was significantly greater in the central than in the obstructive and nonapnea groups (mean+/-SEM [range]: 22. 8+/-1.2 [11 to 38] versus 12.3+/-1.2 [4 to 21] versus 11.5+/-1.5 [3 to 28] mm Hg, respectively; P<0.001). Within the central apnea group, PCWP correlated with the frequency and severity of central apnea (AHI: r=0.47, P=0.006) and degree of hypocapnia (PaCO2: r=-0.42, P=0. 017). Intensive medical therapy in 7 patients with initially high PCWP and central apneas reduced both PCWP (29.0+/-2.6 [20 to 38] to 22.0+/-1.8 [17 to 27] mm Hg; P<0.001) and central apnea frequency (AHI) (38.5+/-7.7 [7 to 62] to 18.5+/-5.3 [1 to 31] events per hour; P=0.005). CONCLUSIONS: PCWP is elevated in CHF patients with central apneas compared with those with obstructive apnea or without apnea. Moreover, a highly significant relationship exists between PCWP, hypocapnia, and central apnea frequency and severity.

Adolescent↗
PubMed1999

Effects of continuous positive airway pressure on lung function in patients with chronic obstructive pulmonary disease and sleep disordered breathing.

OBJECTIVE: Sleep disordered breathing (SDB), namely hypoventilation and obstructive sleep apnoea, occur in about 50% of patients with severe chronic obstructive pulmonary disease (COPD). Previous studies that have investigated the reversal of SDB in such patients with nasally applied intermittent positive airway pressure have reported a fall in PaCO2 but little change in airflow obstruction. We reasoned that the lack of improvement in airflow obstruction may be due to insufficient expiratory pressure. Accordingly, we sought to determine the effects of chronic nasal continuous positive airway pressure (CPAP), at highest tolerable levels, upon blood gases and airflow obstruction in patients with severe COPD and SDB. METHODOLOGY: Fourteen patients were studied, ten of whom were able to tolerate CPAP (10.2 +/- 0.9 cmH2O) for at least 3 months. RESULTS: Within the CPAP compliant group, there was a fall in PaCO2 (58.0 +/- 3.5 to 48.0 +/- 0.9 mmHg, P = 0.015) associated with a rise in PaO2 (54.8 +/- 3.8 to 63.2 +/- 1.8 mmHg, P = 0.015) and forced expiratory volume in 1 s (0.95 +/- 0.13 to 1.10 +/- 0.13 L, P < 0.005). Concurrent with these improvements was a substantial fall in hospitalization rates (from 3.85 to 0.73 admissions per annum). CONCLUSION: Improvements in gas exchange, airflow obstruction and hospitalization rates were observed in patients with COPD and SDB treated with nasal CPAP during sleep.

Adult↗
PubMed1999

Hypoxemia and hypercapnia during exercise and sleep in patients with cystic fibrosis.

BACKGROUND: In patients with cystic fibrosis (CF), it has been proposed that hypoxemia and hypercapnia occur during episodes of stress, such as exercise and sleep, and that respiratory muscle weakness because of malnutrition may be responsible. METHODS: Pulmonary function, respiratory muscle strength, and nutrition were assessed and correlated with the degree of hypoxemia and hypercapnia during exercise and sleep in 14 patients with CF and 8 control subjects. RESULTS: Despite no differences in maximum static inspiratory pressure (PImax) between the two groups, the CF group developed more severe hypoxemia (minimum oxyhemoglobin saturation [SpO2], 89 +/- 5% vs 96 +/- 2%; p < 0.001) and hypercapnia (maximum transcutaneous CO2 tension [PtcCO2], 43 +/- 6 vs 33 +/- 7 mm Hg; p < 0.01) during exercise. Similarly, during sleep, the CF group developed greater hypoxemia (minimum SpO2, 82 +/- 8% vs 91 +/- 2%; p < 0.005), although CO2 levels were not significantly different (maximum PtcCO2, 48 +/- 7 vs 50 +/- 2 mm Hg). Within the CF group, exercise-related hypoxemia and hypercapnia did not correlate with FEV1, residual volume/total lung capacity ratio (RV/TLC), PImax, or body mass index (BMI). Hypoxemia and hypercapnia during sleep correlated with markers of gas trapping (RV vs minimum arterial oxygen saturation [r = -0.654; p < 0.05]), RV vs maximum PtcCO2 (r = 0.878; p < 0.001), and RV/TLC vs maximum PtcCO2 (r = 0.790; p < 0.01) but not with PImax or BMI. CONCLUSION: Patients with moderately severe CF develop hypoxemia and hypercapnia during exercise and sleep to a greater extent than healthy subjects with similar respiratory muscle strength and nutritional status. Neither respiratory muscle weakness nor malnutrition are necessary to develop hypoxemia or hypercapnia during exercise or sleep.

Adult↗
PubMed1998

Sleep apnea in congestive heart failure.

Sleep-related breathing disorders, including obstructive sleep apnea (OSA) and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA), commonly occur in patients with congestive heart failure (CHF). In this setting they can have adverse pathophysiologic effects on the cardiovascular system. OSA may lead to development or progression of left ventricular (LV) dysfunction by increasing LV afterload through the combined effects of elevations in systemic blood pressure and a generation of exaggerated negative intrathoracic pressure, and by activating the sympathetic nervous system through the influence of hypoxia and arousals from sleep. Abolition of OSA by continuous positive airway pressure (CPAP) can improve cardiac function in patients with CHF. In contrast to OSA, CSR-CSA is likely a consequence rather than a cause of CHF. Here, pulmonary congestion causes hyperventilation by stimulating pulmonary irritant receptors. This leads to reductions in PaCO2 below the apneic threshold during sleep, precipitating posthyperventilatory central apneas. CSR-CSA is associated with increased mortality in CHF, probably because of sympathetic nervous system activation caused by recurrent apnea-induced hypoxia and arousals from sleep. Treatment of CSR-CSA by supplemental O2, theophylline, and CPAP can alleviate central apneas. Of these treatments, however, only CPAP has been shown to improve cardiac function and symptoms of heart failure. We conclude that effective treatments of OSA and CSR-CSA may prove to be useful adjuncts to the standard pharmacologic therapy of patients with CHF.

Aged↗
PubMed1998

Heart failure and obstructive apnoea.

Obstructive sleep apnoea (OSA) may aggravate heart failure through the mechanisms of sleep related arousals, systemic hypertension (awake and asleep) and negative intrathoracic pressure which increase cardiac afterload at times of asphyxia and hypoxaemia. Reversal of OSA with nasal continuous positive airway pressure (CPAP), in the setting of heart failure, may return cardiac function to near normal values.

Journal Article↗