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Biomedical subjects

M T Naughton

Publications and source records attributed to M T Naughton.

33 records · Page 2Linked to original sources

Heart failure and central apnoea.

Central sleep apnoea with a Cheyne-Stokes pattern of respiration is a disorder commonly observed in patients with established symptomatic congestive heart failure (CHF). It is associated with hyperventilation and hypocapnia which are likely to result from either increased pulmonary vagal afferent nerve stimulation due to pulmonary oedema or from upregulation of chemoreceptors induced by increased sympathoneural activity. Treatment should be aimed at improving underlying cardiac function which may include angiotensin-converting enzyme inhibitors, nasal continuous positive airway pressure (CPAP) or possibly supplemental oxygen.

Journal Article↗

The prevalence of obstructive sleep apnea in hypertensives.

This study was designed to measure the prevalence of obstructive sleep apnea in untreated and treated hypertensive patients by comparing them with normotensive subjects, taking into account the possible confounding variables body mass index, age, sex, and alcohol consumption. Subjects with no known sleep disorders were recruited, had full polysomnography, and had their blood pressure assessed with a 24-h ambulatory monitor. Subjects with a mean 24-h blood pressure greater than 140/90, and receiving no treatment for, or with no history of, hypertension were classified as untreated hypertensives; those receiving antihypertension medication were classified as treated hypertensives; those with a mean 24-h blood pressure less than 140/90 and no history of hypertension were classified as normotensives. Thirty-eight percent of the 34 untreated and 38% of the 34 treated hypertensives, and 4% of the 25 normotensives had apnea-hypopnea indexes greater than 5. Logistic regression analysis showed that body mass index (p = 0.001), age (p = 0.07), sex (p = 0.07), treated hypertension (p = 0.05), and untreated hypertension (p = 0.06) were associated with the presence of sleep apnea, but that alcohol consumption (p = 0.82) was not. It is concluded that there is a relationship between sleep apnea and hypertension that, although partially explained by the confounding variables body mass index, age, and sex, persists when these are allowed for.

Age Distribution↗

Central sleep apnoea in congestive heart failure despite vagal denervation after bilateral lung transplantation.

Nonhypercapnic central sleep apnoea is a disorder of respiratory control characterized by hyperventilation previously attributed to the stimulation of either pulmonary vagal afferent nerve fibres or respiratory chemoreceptors. This report describes central sleep apnoea in a patient with congestive heart failure following bilateral lung transplant in whom pulmonary vagal afferent nerve activity was absent.

Heart Failure↗

Effects of cardiac dysfunction on non-hypercapnic central sleep apnea.

INTRODUCTION: Non-hypercapnic central sleep apnea (CSA) commonly occurs during nonrapid eye movement (non-REM) sleep in adults with congestive heart failure (CHF) and in some subjects without signs or symptoms of CHF. Hyperventilation, reduced lung volume, and circulatory delay are known to contribute to CSA, but to differing degrees depending on presence or absence of CHF. AIM: To determine whether the pattern of ventilation during sleep could be used to determine the presence of CHF. METHODS: Full polysomnographs demonstrating CSA were examined in 10 consecutive subjects with CHF and in 10 without CHF. Ventilatory, apnea, and cycle lengths, and circulation time (from the onset of ventilatory effort to the nadir of oximeter trace) were measured from cyclic apneas during non-REM sleep. RESULTS: The non-CHF group had a greater left ventricular ejection fraction (LVEF) (59.7+/-1.9% vs 19.2+/-2.2%). Circulation time (11.8+/-0.5 s vs 24.9+/-1.7 s; p < 0.001) and cycle length (35.1+/-2.8 s vs 69.5+/-4.5 s; p < 0.001) were significantly greater in the CHF group compared with the non-CHF group, but not apnea length (21.3+/-1.8 s vs 26.8+/-2.0 s; p=0.06). Ventilatory length to apnea length ratio (VL:AL) was uniformly > 1.0 in the CHF group (mean, 1.65; range, 1.02 to 2.33), and in the non-CHF group < 1.0 (mean, 0.66; range, 0.54 to 0.89). LVEF correlated negatively with both circulation time (r=-0.86; p < 0.001) and cycle length (r=-0.79; p < 0.001). CONCLUSION: The VL:AL ratio > 1.0, as well as both circulation time > 15 s and cycle length > 45 s, can be used to recognize the presence of CHF in subjects with CSA.

Adolescent↗

Respiratory correlates of muscle sympathetic nerve activity in heart failure.

1. Sympathetic activation in congestive heart failure indicates a poor prognosis. Haemodynamic correlates of increased sympathetic nerve traffic to muscle (MSNA) and to the heart have been well characterized, but these account for only 50 to 60% of the variance in sympathetic activity between patients.2. In healthy subjects, breathing pattern modulates MSNA and positive airway pressure consistently increases MSNA. However, in patients with heart failure, the influence of spontaneous breathing pattern and of short-term application of nasal continuous positive airway pressure on MSNA have not been described.3. Spontaneous breathing frequency, tidal volume, end-expiratory lung volume, PCO2 and MSNA were recorded, along with blood pressure, heart rate and stroke volume in 14 men with congestive heart failure of idiopathic or ischaemic origin (left ventricular ejection fraction <35%). Measurements were made during baseline rest, followed by 45 min of either nasal continuous positive airway pressure applied at 10 cmH2O (n=9), or spontaneous breathing, in the absence of nasal continuous positive airway pressure (time control; n=6).4. At baseline, there was a significant positive correlation between MSNA burst frequency and breathing frequency (r=0.758, P=0.001), and an inverse correlation between MSNA burst incidence and tidal volume (r=-0.705, P=0.005). These relationships were independent of left ventricular ejection fraction, stroke volume or cardiac output.5.Nasal continuous positive airway pressure increased end-expiratory lung volume, but had no effect on breathing frequency, tidal volume or MSNA.6. In patients with congestive heart failure, there is a significant independent and previously unrecognized correlation between spontaneous breathing pattern and MSNA; patients with rapid shallow breathing exhibit the highest degree of sympathetic activation. In distinct contrast to healthy subjects, the short-term application of nasal continuous positive airway pressure at 10 cmH2O does not increase MSNA in congestive heart failure.

Heart Failure↗

Effect of continuous positive airway pressure on mitral regurgitant fraction and atrial natriuretic peptide in patients with heart failure.

OBJECTIVES: We sought to determine the effects of continuous positive airway pressure (CPAP) on mitral regurgitant fraction (MRF) and plasma atrial natriuretic peptide (ANP) concentration in patients with congestive heart failure (CHF). BACKGROUND: In patients with CHF, elevated plasma ANP concentration is associated with elevated cardiac filling pressures. Secondary mitral regurgitation may contribute to elevation in plasma ANP concentration in patients with CHF. Because CPAP reduces transmural cardiac pressures and left ventricular (LV) volume, we hypothesized that long-term CPAP application would decrease the MRF and plasma ANP concentration in patients with CHF and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). METHODS: Seventeen patients with CHF and CSR-CSA underwent baseline assessments of plasma ANP concentration and left ventricular ejection fraction (LVEF) and MRF by radionuclide angiography. They were then randomized to receive nocturnal CPAP plus optimal medical therapy (n = 9) or optimal medical therapy alone (n = 8) for 3 months and were then reassessed. RESULTS: In the CPAP-treated group, LVEF increased from (mean +/-SEM) 20.2 +/- 4.2% to 28.2 +/- 5.3% (p < 0.02); MRF decreased from 32.8 +/- 7.7% to 19.4 +/- 5.5% (p < 0.02); and plasma ANP concentration decreased from 140.9 +/- 20.8 to 103.9 +/- 17.0 pg/ml (p < 0.05). The control group experienced no significant changes in LVEF, MRF or plasma ANP concentration. Among all patients, the change in plasma ANP concentration from baseline to 3 months correlated significantly with the change in MRF (r = 0.789, p < 0.0002). CONCLUSIONS: In patients with CHF, CPAP-induced reductions in MRF and plasma ANP concentration in association with improvements in LVEF indicate improved cardiac mechanics. Our findings also suggest that reductions in plasma ANP concentration were at least partly due to reductions in MRF.

Atrial Natriuretic Factor↗

CPAP improves inspiratory muscle strength in patients with heart failure and central sleep apnea.

Patients with congestive heart failure (CHF) suffer from respiratory muscle weakness which may contribute to dyspnea. Nasal continuous positive airway pressure (NCPAP) can improve left ventricular ejection fraction (LVEF) and reduce dyspnea in patients with CHF and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) but its effects on respiratory muscle strength are not known. We therefore studied the effects of NCPAP on maximal inspiratory and expiratory pressures (MIP and MEP, respectively), LVEF, dyspnea, and fatigue in patients with chronic CHF and CSR-CSA over 3 mo. Eight patients were randomized to control and nine to nightly NCPAP. There were no significant changes in any of these factors in the control group during the study. In contrast, among the NCPAP group, MIP increased from 79.3 +/- 8.1 to 90.7 +/- 10.4 cm H2O (mean +/- SEM; p < 0.02), LVEF increased from 24.0 +/- 4.0 to 32.6 +/- 6.6% (p < 0.02) and symptoms of dyspnea and fatigue were alleviated. However, MEP did not change. In addition, the number of apneas and hypopneas decreased from 49 +/- 11 to 17 +/- 7 per hour of sleep (p < 0.001) and mean low Sao2 during sleep increased from 87.9 +/- 1.0 to 93.0 +/- 1.0% (p < 0.01). Our data indicate that nightly application of NCPAP in patients with CHF and CSR-CSA improves inspiratory muscle strength and LVEF, and relieves dyspnea and fatigue.

Aged↗

Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure.

BACKGROUND: Continuous positive airway pressure (CPAP) can improve cardiac function in patients with congestive heart failure (CHF). We hypothesized that this effect might be related to CPAP-induced increases in intrathoracic pressure, which would reduce left ventricular transmural pressure (LVPtm) during systole, thereby decreasing left ventricular afterload. METHODS AND RESULTS: The effect of graduated CPAP from 0 to 10 cm H2O on the above variables was examined over a 75-minute period and compared with a 75-minute time control period without CPAP in two groups of subjects: 15 patients with CHF and 9 healthy subjects. Intrathoracic pressure was estimated from esophageal pressure (Pes), and systolic LVPtm, a determinant of left ventricular afterload, was assessed by subtracting Pes during systole from systolic blood pressure. Cardiac index (CI) was assessed by Doppler echocardiography. At baseline, inspiratory Pes amplitude, which reflects inspiratory muscle force generation, was greater in the patients with CHF than in the healthy group (9.9 +/- 0.8 versus 5.5 +/- 0.4 mm Hg, P < .001). In addition, systolic Pes, which represents the relative contribution of intrathoracic pressure to LVPtm, was more negative in the patients with CHF than in the healthy group (-4.1 +/- 0.3 versus -2.2 +/- 0.1 mm Hg, P < .001). While on CPAP of 10 cm H2O, inspiratory Pes amplitude decreased and systolic Pes increased significantly in the group with CHF (from 11.1 +/- 1.1 to 7.5 +/- 1.1 mm Hg, P < .025 and from -4.7 +/- 0.6 to 0.6 +/- 0.6 mm Hg, P < .001, respectively), but CPAP had no effect on these variables in the healthy subjects. Compared with the equivalent time control period, Pes amplitude x respiratory rate decreased significantly while on CPAP in both the group with CHF (from 188 +/- 22 to 112 +/- 17 mm Hg x breaths per minute, P < .005) and the healthy group (from 82 +/- 8 to 60 +/- 6 mm Hg x breaths per minute, P < .05). Compared with time control, systolic LVPtm decreased significantly while on CPAP, from 116.0 +/- 5.3 to 110.3 +/- 4.5 mm Hg (P < .025) in the group with CHF, but did not change in the healthy group. Moreover, systolic LVPtm x heart rate decreased significantly in the group with CHF (from 80.55 +/- 5.27 to 71.83 +/- 4.73 mm Hg x beats per minute/100, P < .005) but not in the healthy group. CI decreased significantly while on CPAP in the healthy group (P < .025) but did not change in the group with CHF. CONCLUSIONS: In patients with CHF, the inspiratory muscles generate greater force per breath and systolic Pes contributes more to LVPtm than in healthy subjects. By increasing intrathoracic pressure in patients with CHF, CPAP unloaded inspiratory muscles and reduced left ventricular afterload without compromising CI.

Adult↗

Continuous positive airway pressure increases heart rate variability in congestive heart failure.

OBJECTIVES: Our objective was to determine whether continuous positive airway pressure augments the low heart rate variability of congestive heart failure, a marker of poor prognosis. BACKGROUND: Nasal continuous positive airway pressure improves ventricular function in selected patients with heart failure. METHODS: In 21 sessions in 16 men (mean [+/- SE] age 56 +/- 2 years) with New York Heart Association functional class II to IV heart failure, we assessed the effects of 45 min with (n = 14) and without (as a time control, n = 7) nasal continuous positive airway pressure (10 cm of water) on heart rate variability and end-expiratory lung volume. Coarse-graining spectral analysis was used to derive total spectral power (PT), its nonharmonic component (fractal power [PF]) and the low (0.0 to 0.15 Hz [PL]) and high (0.15 to 0.50 Hz [PH]) frequency components of harmonic power. Standard deviation of the RR interval, high frequency power and the PH/PT ratio were used to estimate parasympathetic activity in the time and frequency domains, and the PL/PH ratio was used to estimate cardiac sympathetic activity in the frequency domain. RESULTS: Use of continuous positive airway pressure increased end-expiratory lung volume by 445 +/- 82 ml (p < 0.01) and both time (p < 0.006) and frequency domain indexes of heart rate variability: Total spectral power (p < 0.01), nonharmonic power (p < 0.023) and low (p < 0.04) and high (p < 0.05) frequency components of harmonic power all increased. Time alone had no effect on these variables. By comparison, the PH/PT ratio increased during nasal continuous positive airway pressure (p < 0.004), whereas the PL/PH ratio was unchanged. Breathing rate remained constant in both groups. CONCLUSIONS: Short-term application of nasal continuous positive airway pressure increases heart rate variability and time and frequency domain indexes of parasympathetic activity without influencing cardiac sympathetic activity. This increase may occur reflexively, through stimulation of pulmonary mechanoreceptor afferents.

Adult↗

Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure.

A previous uncontrolled study suggested that nasal continuous positive airway positive airway pressure (NCPAP) may improve left ventricular ejection fraction (LVEF) in patients with congestive heart failure (CHF) and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In order to more critically evaluate the effects of NCPAP on cardiac function, we undertook a randomized, controlled trial of NCPAP in 29 patients with heart failure and CSR-CSA over a 3-mo period, with LVEF as the primary outcome measure. Patients with CHF and associated CSR-CSA who were receiving optimal medical therapy were randomly assigned to a control group (n = 15) or a group receiving nightly NCPAP (n = 14). Twelve patients in each group completed the study. There was a greater improvement of LVEF in the NCPAP group than in the control group during the study (mean +/- SEM = 7.7 +/- 2.5 versus - 0.5 +/- 1.5%, p = 0.019). In addition, there was a significantly greater reduction in the number of apneas and hypopneas (-28.5 +/- 3.9 versus -6.1 +/- 7.0 per hour of sleep, p = 0.012) in the NCPAP group than in the control group. Significantly greater improvements in symptoms of fatigue (5.6 +/- 1.2 versus 0.8 +/- 0.7, p = 0.005) and disease mastery (3.6 +/- 1.1 versus -0.7 +/- 0.7, p = 0.031) were also observed in the NCPAP group. We conclude that in patients with chronic heart failure and CSR-CSA, nightly administration of NCPAP can attenuate CSR-CSA, improve cardiac function, and alleviate symptoms of heart failure.

Analysis of Variance↗

Effects of nasal CPAP on sympathetic activity in patients with heart failure and central sleep apnea.

We hypothesized that (1) patients with congestive heart failure (CHF) and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) would have greater nocturnal urinary and daytime plasma norepinephrine concentrations (UNE and PNE, respectively) than those without CSR-CSA because of apneas, hypoxia and arousals from sleep and (2) attenuation of CSR-CSA by nasal continuous positive airway pressure (NCPAP) would reduce UNE and PNE concentrations. Eighteen patients with and 17 without CSR-CSA (Non-CSR-CSA group) were studied. Left ventricular ejection fraction was similar in the two groups, but overnight UNE and awake PNE concentrations were greater in the CSR-CSA group (30.2 +/- 2.5 nmol/mmol creatinine and 3.32 +/- 0.29 nmol/L) than in the Non-CSR-CSA group (15.8 +/- 2.1 nmol/mmol creatinine, p < 0.005, and 2.06 +/- 0.56 nmol/L, p < 0.05, respectively). Patients with CSR-CSA were randomized to a control group or to nightly NCPAP for 1 mo. CSR-CSA was attenuated in the NCPAP but not in the control group. The NCPAP group experienced greater reductions in UNE and PNE concentrations (-12.5 +/- 3.3 nmol/mmol creatinine and -0.74 +/- 0.40 nmol/L) than did the control group (-1.3 +/- 2.8 nmol/mmol creatinine, p < 0.025 and 1.16 +/- 0.66 nmol/L, p < 0.025, respectively). In conclusion, in patients with CHF, CSR-CSA is associated with elevated sympathoneural activity, which can be reduced by NCPAP.

Adolescent↗

Is normobaric simulation of hypobaric hypoxia accurate in chronic airflow limitation?

Hypobaric hypoxemia is experienced by passengers during commercial aircraft flight. In order to assess the extent of hypoxemia and to test whether hypobaric hypoxia can be accurately estimated at sea level, the results of the normobaric hypoxia altitude simulation test (N-HAST) were compared with those of the hypobaric hypoxia altitude simulation test (H-HAST) in six normal control subjects and nine patients with chronic airflow limitation (CAL) at simulated cabin altitudes of 6,000 ft (1,829 m) and both at rest and during exercise at 8,000 ft (2,438 m). Serial arterial blood samples were drawn during the breathing of 15.1 and 16.3% inspired oxygen at sea level (N-HAST) at rest and during light exercise, and during the breathing of room air at simulated cabin altitudes (H-HAST) of 609 mm Hg (6,000 ft) and 565 mm Hg (8,000 ft) at rest and during light exercise. As measured with the H-HAST technique, the mean (+/- SD) PaO2 of the normal group fell from 96.2 +/- 6.2 mm Hg (sea level) to 70.1 +/- 6.0 mm Hg (6,000 ft), and to 61.7 +/- 1.6 mm Hg (8,000 ft at rest) and 54.8 +/- 7.1 mm Hg (8,000 ft during exercise) (p < 0.005 by analysis of variance [ANOVA]). In the CAL group, the mean (+/- SD) PaO2 fell from 75.8 +/- 8.2 mm Hg (sea level) to 57.0 +/- 6.3 mm Hg (6,000 ft), and 49.5 +/- 6.1 mm Hg (8,000 ft at rest), and 38.6 +/- 7.5 mm Hg (8,000 ft during exercise) (p < 0.005 by ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure.

We have previously shown that hypocapnia triggers Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). Nasal continuous positive airway pressure (NCPAP) may attenuate CSR-CSA in patients with CHF and CSR-CSA. Accordingly, we hypothesized that attenuation of CSR-CSA by NCPAP would be related to an increase in PCO2. Therefore, we examined the effect of NCPAP on the frequency of apneas and hypopneas, transcutaneous PCO2 (PtcCO2), and minute volume of ventilation (VI) in 12 consecutive patients with CHF and CSR-CSA during stage 2 sleep. A control group of six patients, who did not receive NCPAP, was also studied. In the control group, there were no changes from baseline to 1 mo in the frequency of central apneas and hypopneas, mean PtcCO2, mean VI, or mean SaO2 during stage 2 sleep. In contrast, from baseline to 1 mo the NCPAP group experienced a decrease in the frequency of apneas and hypopneas (58.7 +/- 5.2 to 23.2 +/- 6.0/h of sleep, p < 0.001), an increase in mean PtcCO2 (34.6 +/- 1.4 to 40.8 +/- 1.1 mm Hg, p < 0.001), a reduction in mean VI (8.1 +/- 1.0 to 5.2 +/- 0.5 L/min, p < 0.01) and an increase in mean SaO2 (91.6 +/- 1.1 to 95.0 +/- 0.5%, p < 0.025) during stage 2 sleep while on 10.2 +/- 0.5 cm H2O nasal CPAP. We conclude that likely mechanisms through which NCPAP reduces CSR-CSA are by increasing SaO2 and raising PaCO2 during sleep toward or above the apneic threshold.

Blood Gas Monitoring, Transcutaneous↗