Cardiac metastasis: a cause of recurrent pulmonary emboli.

Intracavitary cardiac metastasis is rare. Apart from causing intracardiac obstruction, this type of metastasis can present as pulmonary emboli. It is important to suspect this diagnosis in an oncology patient with recurrent pulmonary emboli, particularly in the setting of a negative venous Doppler ultrasound of the lower limbs and pelvis. Early recognition may help in improving the prognosis. We present a case of intracavitary cardiac metastasis arising from a squamous carcinoma of the cervix, in a patient with recurrent pulmonary tumour emboli.

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.

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.

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.

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.

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.

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.

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.

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.

Lung volume reduction surgery for emphysema.

OBJECTIVE: To report the results of lung volume reduction surgery (LVRS) for severe emphysema in Australia. SETTING: A tertiary teaching hospital. DESIGN: A prospective study of a consecutive case series. PARTICIPANTS: 20 patients (mean age, 56 years) with severe emphysema--mean forced expiratory volume in one second (FEV1), 0.72 L (28% of predicted) and severe gas trapping (mean residual volume, 286% of predicted). INTERVENTION: Bilateral apical LVRS was performed via a median sternotomy with a linear stapler; bovine pericardial strips were used to reinforce the staple line. RESULTS: There was a 95% survival, and a mean (range) inpatient stay of 17 (8-45) days. No complications occurred in nine patients; a further six patients had only minor complications. Five patients had major complications (sputum retention requiring reintubation, persistent air leak requiring reoperation, duodenal perforation, and epidural haemorrhage); one patient died from multiorgan failure at 28 days. Intercostal drainage was left in situ for a mean of eight days. The results of FEV1, Medical Research Council (MRC) Dyspnoea Score and six-minute walk test improved in more than 90% of patients. FEV1 improved an average of 0.35 L (54% over baseline) (P < 0.001). Mean MRC Dyspnoea Score decreased from 3.4 to 2.1 (P < 0.001). Mean distance for the six-minute walk test increased from 306 to 431 metres (P < 0.001). CONCLUSION: Our experience confirms that LVRS produces worthwhile early outcomes for a subgroup of patients with severe emphysema. The clinical, economic and ethical questions raised by this new therapy will need to be assessed.