[Management of sleep-related abnormal breathing by cardiologists and hospital departments of cardiology]. / Versorgung von Patienten mit obstruktiver Schlafapnoe in kardiologischen Praxen und Kliniken.

BACKGROUND AND OBJECTIVES: In the general population there is a high prevalence of sleep-related disorders of breathing (sleep apnea). In addition to being leading symptom of excessive day-time sleepiness they are also important predictors are cardiovascular disease such as arterial hypertension, heart failure, cardiac arrhythmias and stroke. Are the cardiologists the specialists who recognize such patients and refer them to diagnostic procedures and treatment? METHODS: We sent out a questionnaires to cardiologists in private practice, to hospitals with cardiology departments and to cardiology rehabilitation units in Germany in order to assess the knowledge about sleep apnea and of the current diagnostic and therapeutic procedures in patients with suspected sleep apnea. All cardiology rehabilitation units and every other practice and cardiology department listed in the reference book 'Medführer' were approached. RESULTS: 98% of 388 cardiologists with private practice were found to know about the disorder sleep apnea. 94.3% routinely asked their patients about any sleep disorder and specifically about excessive day-time sleepiness. More than half of the cardiologists (59.3%) questioned patients about possible sleep apnea as part of their interview, but only 32.7% carried out tests with a portable sleep apnea monitor. Most patients were referred to a sleep center. In 60% of the cardiology departments a portable sleep apnea monitor was used. Further diagnostic investigation followed in collaborating sleep centers (66.4%), because only 22.4% of the departments had a sleep laboratories. The main focus was on the diagnosis of abnormal sleep due to central or obstructive disorders of breathing. More than two thirds of the cardiology departments initiate nocturnal ventilation treatment. CONCLUSION: Cardiologists in private practice and cardiologists in hospital departments know about sleep-related abnormal breathing. The use of portable sleep apnea monitors and of polysomnography in special as parts of sleep centers within cardiology departments should be improved.

Therapeutic electrical stimulation of the hypoglossal nerve in obstructive sleep apnea.

BACKGROUND: Hypoglossal nerve stimulation has been demonstrated to relieve upper airway obstruction acutely, but its effect on obstructive sleep apnea is not known. OBJECTIVE: To determine the response in obstructive sleep apnea to electrical stimulation of the hypoglossal nerve. METHODS: Eight patients with obstructive sleep apnea were implanted with a device that stimulated the hypoglossal nerve unilaterally during inspiration. Sleep and breathing patterns were examined at baseline before implantation and after implantation at 1, 3, and 6 months and last follow-up. RESULTS: Unilateral hypoglossal nerve stimulation decreased the severity of obstructive sleep apnea throughout the entire study period. Specifically, stimulation significantly reduced the mean apnea-hypopnea indices in non-rapid eye movement (mean +/- SD episodes per hour, 52.0 +/- 20.4 for baseline nights and 22.6 +/- 12.1 for stimulation nights; P<.001) and rapid eye movement (48.2 +/- 30.5 and 16.6 +/- 17.1, respectively; P<.001) sleep and reduced the severity of oxyhemoglobin desaturations. With improvement in sleep apnea, a trend toward deeper stages of non-rapid eye movement sleep was observed. Moreover, all patients tolerated long-term stimulation at night and did not experience any adverse effects from stimulation. Even after completing the study protocol, the 3 patients who remained free from stimulator malfunction continued to use this device as primary treatment. CONCLUSION: The findings demonstrate the feasibility and therapeutic potential for hypoglossal nerve stimulation in obstructive sleep apnea.

Expiratory flow limitation and intrinsic positive end-expiratory pressure in obesity.

Breathing at very low lung volumes might be affected by decreased expiratory airflow and air trapping. Our purpose was to detect expiratory flow limitation (EFL) and, as a consequence, intrinsic positive end-expiratory pressure (PEEPi) in grossly obese subjects (OS). Eight OS with a mean body mass index (BMI) of 44 +/- 5 kg/m2 and six age-matched normal-weight control subjects (CS) were studied in different body positions. Negative expiratory pressure (NEP) was used to determine EFL. In contrast to CS, EFL was found in two of eight OS in the upright position and in seven of eight OS in the supine position. Dynamic PEEPi and mean transdiaphragmatic pressure (mean Pdi) were measured in all six CS and in six of eight OS. In OS, PEEPi increased from 0.14 +/- 0.06 (SD) kPa in the upright position to 0.41 +/- 0.11 kPa in the supine position (P < 0.05) and decreased to 0.20 +/- 0.08 kPa in the right lateral position (P < 0.05, compared with supine), whereas, in CS, PEEPi was significantly smaller (<0.05 kPa) in each position. In OS, mean Pdi in each position was significantly larger compared with CS. Mean Pdi increased from 1.02 +/- 0.32 kPa in the upright position to 1.26 +/- 0.17 kPa in the supine position (not significant) and decreased to 1. 06 +/- 0.26 kPa in the right lateral position (P < 0.05, compared with supine), whereas there were no significant changes in CS. We conclude that in OS 1) tidal breathing can be affected by EFL and PEEPi; 2) EFL and PEEPi are promoted by the supine posture; and 3) the increased diaphragmatic load in the supine position is, in part, related to PEEPi.

Electric stimulation of the upper airway muscle.

In various studies, it has been postulated that pharyngeal collapse occurring during sleep in obstructive sleep apnea may be alleviated by stimulating the genioglossus muscle. Basic experiments have demonstrated that neuromuscular stimulation applied intraorally via electrodes or by direct neural stimulation of the hypoglossal nerve might improve upper airway and respiratory function. An increase of maximal inspiratory airflow, an improvement of upper airway collapsibility and a decrease in respiratory events during sleep were observed. An impairment of sleep quality during electric stimulation has been excluded simultaneously. Considering clinical aspects, anatomical properties and long-term experience in electric stimulation it might be possible to develop full implantable devices as an alternative treatment for patients with obstructive sleep apnea.

Electrical stimulation of upper airway musculature.

Investigators have postulated that pharyngeal collapse during sleep in patients with obstructive sleep apnea (OSA) may be alleviated by stimulating the genioglossus. The effect of electrical stimulation (ES) of the genioglossus on pharyngeal patency was examined in an isolated feline upper airway preparation and in apneic humans during sleep. We found that stimulation of the genioglossus (n = 8) and of the hypoglossal nerve (n = 1) increased maximum airflow through the isolated feline upper airway in humans during sleep. Additional findings in the isolated feline upper airway suggest that such increases in airflow were due to decreases in pharyngeal collapsibility. The evidence suggests that improvements in airflow dynamics with electrical stimulation are due to selective recruitment of the genioglossus, rather than due to nonspecific activation of the pharyngeal musculature or arousal from sleep. The implications of these results for future therapy with ES are discussed.

Manifestations and consequences of obstructive sleep apnoea.

Over the last two decades the diagnostic tools used in sleep medicine have developed enormously, making it possible to study the interaction of sleep-related breathing disorders (SRBD) with cardiovascular function and the autonomic nervous system, as well as the effects of SRBD on a variety of physiological processes during wakefulness. Different modes of nasal ventilation are now available, allowing all forms of SRBD to be treated. If early diagnosis and treatment are provided, the acute and long-term sequelae of SRBD can be prevented. In addition to the care and treatment of patients with severe obstructive sleep apnoea syndrome (OSAS), future patient management will need to focus on patients with milder forms of obstructive sleep apnoea (OSA). In particular, the consequences of SRBD on cardiac arrhythmias, arterial hypertension and hypersomnolence are discussed, considering epidemiological, clinical, diagnostic and therapeutic aspects. Some economical issues arising from SRBD are also discussed, and the authors conclude that a Europewide programme for early detection, treatment and prevention of SRBD is required. This could make a large contribution to the reduction of cardiovascular morbidity and mortality and also reduce the incidence of "human error catastrophes" due to hypersomnolence.

Intrathoracic pressure changes and cardiovascular effects induced by nCPAP and nBiPAP in sleep apnoea patients.

The effect of nasal continuous positive airway pressure (nCPAP) and nasal bi-level positive airway pressure (nBiPAP) on intrathoracic pressure and haemodynamics during wakefulness was studied in a group of nine patients with severe sleep apnoea. No patient took cardiovascular medication. Patients were studied with a Swan Ganz catheter, an arterial line and an oesophageal balloon. nCPAP and nBiPAP were applied in the following pressure sequence: 5, 10 and 15 cm H2O of CPAP and 10/5 and 15/10 cm H2O of nBiPAP. Measurements were made at the end of a 5-min period at each pressure level. Intrathoracic pressure was noted to increase to a level of approximately 50% of the pressure delivered at the mask. At a CPAP of 10 cm H2O and above, as well as at BiPAP of 10/5 or higher, there was a decrease in cardiac output (CO) and cardiac index (CI). CI fell below the normal value in two of the patients. Transmural pulmonary artery pressure (PPAtm) decreased at a CPAP of 15 cm H2O and at both BiPAP levels. Transmural right atrial pressure (PRAtm) decreased at both BiPAP levels. There were no differences in CO, CI, PPAtm and PRAtm between nCPAP and nBiPAP at equal inspiratory pressures. SaO2 increased during BiPAP 15/10 cm H2O, whereas heart rate and arterial blood pressure did not change significantly. The data presented here are consistent with the literature on positive end-expiratory pressure (PEEP) applied via intratracheal tube and are likely to be due to a reduced venous return. It is concluded that nasally applied positive pressure may have acute negative effects on cardiac function in patients with sleep apnoea.

Clinical and haemodynamic effects of long-term treatment with torasemide in congestive heart failure.

The clinical and haemodynamic effects of 12 weeks of treatment with torasemide, 5 mg/day, were measured in 24 men aged 51-60 years with symptoms of mild, chronic, congestive heart failure. Clinical status was assessed by NYHA functional class and haemodynamic effects were measured at rest and during supine bicycle exercise at the beginning and end of the 12-week period of study. Torasemide was well tolerated and there was no significant change in any of the measured safety variables. Clinical status was improved in 16 of the 23 patients assessed after 12 weeks of treatment and none experienced symptomatic deterioration. Compared with pretreatment haemodynamic measurements, right atrial and pulmonary vascular pressures were significantly decreased both at rest and during exercise after torasemide. Systemic arterial pressure was reduced at rest, but there were no significant changes in cardiac output, heart rate, or systemic and pulmonary vascular resistances either at rest or during exercise, neither were there any significant changes in systemic arterial blood oxygen saturation, pulmonary arterial blood pH, gas tensions, or bicarbonate concentration either at rest or during exercise at 12 weeks. The results of these studies indicate that the clinical and haemodynamic benefits of torasemide are not subject to the development of tolerance during sustained treatment.

[Inspiratory intrathoracic pressure changes in obstructive and mixed sleep apnea]. / Inspiratorische intrathorakale Druckschwankungen bei obstruktiver und gemischter Schlafapnoe.

Oesophageal pressure swings were analysed during complete occlusion of the upper airways in 8 patients with obstructive sleep apnoea. We hypothesed that in dependence of the apnoea type, there is a significant decrease in oesophageal inspiratory effort in REM vs. NREM that is caused by a decrease of the respiratory drive. We analysed in each patient 40 apnoeas in which the respiratory timing (Ti) and the inspiratory effort (Pin) were calculated and compared with the type of apnoea and the degree of oxygen desaturation. A significant decrease in inspiratory effort in REM vs NREM occurred only in mixed apnoeas but not in patients with mainly obstructive apnoeas. Additionally, all apnoeas with a decrease of inspiratory effort at the end of apnoea during NREM were seen in obstructive apnoeas only, whereas none occurred in mixed apnoeas. Due to the significant lower inspiratory timing during obstructive apnoeas vs mixed apnoeas we assume a decrease in respiratory drive in the patients suffering mainly from obstructive apnoeas.

[Effect of obstructive sleep apnea on preload of the right heart]. / Der Einfluss der obstruktiven Schlafapnoe auf die Vorlast des rechten Herzens.

Obstructive sleep apnea (OSA) is characterized by a total inspiratory occlusion of the extrathoracic airways with persisting respiratory effort. During obstructive breathing efforts the intrathoracic pressure (ITP) falls below-20 Torr. This should augment venous return by depleting the blood from the extrathoracic veins into the thoracic veins, thus pre- and afterload of the right heart rises. Until now preload of the right heart during OSA was not measured. This study shows the filling pressures (tmPRA) of the right heart during OSA. In five patients the in- and expiratory right atrial pressure and the intrathoracic pressure were measured, beat by beat, during the non REM hour in which the most apnea episodes occurred. The tmPRA values were calculated as follows: tmPRA = PRA-ITP. The rising tmPRA with falling ITP shows that the venous return, during apnea episodes, rises mostly unhampered. Only in one patient did a cut-off of the increasing tmPRA occur. This patient showed a flow limitation of venous return. Two more patients developed different trends. One part of the measurements led to a linear increase of tmPRA, the other part shows a plateau up from a certain ITP. In two patients tmPRA increases linearly, in the extreme, with decreasing ITP. This indicates no flow limitation of venous return. The results of this investigation suggest that the protective mechanism of the limitation of venous return, occurring under artificial conditions, does not regularly appear in patients with OSA. This leads to repetitive volume overloads of the right heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous non-invasive blood pressure monitoring in patients with sleep disorders.

Sleep related breathing disorders are of high prevalence and are often associated with essential hypertension. It is therefore necessary to study blood pressure continuously in all patients with sleep related breathing disorders and arterial hypertension as well as in all patients with essential hypertension and suspected sleep apnoea. To investigate the usefulness of a non-invasive continuous volume-clamp method during sleep we used this technique in parallel with 130 sleep recordings and performed a validation study of the Finapres instrument on a subgroup where continuous invasive blood pressure recordings were available. Absolute pressure values of Finapres are valid when the position and the movement of the sensor were carefully observed and only appropriate segments of the recordings were taken for further evaluation. The high beat to beat resolution of the systolic and diastolic pressure is the main advantage of this non-invasive technique because it reflects rapid blood pressure variations as they occur in sleep related breathing disorders. This could be investigated only invasively until now.

[Combination therapy in chronic heart failure. Hemodynamic effects with a calcium antagonist-diuretic combination]. / Kombinationstherapie bei chronischer Herzinsuffizienz. Hämodynamische Wirkungen unter einer Kalziumantagonist-Diuretikum-Kombination.

In twelve patients with chronic cardiac insufficiency (NYHA II-III), the effect of a fixed combination of drugs (160 mg verapamil/50 mg triamterene/25 mg hydrochlorothiazide) on cardiac hemodynamics was studied over a period of four weeks. During the course of treatment, the arterial blood pressure decreased from 145 +/- 16/93 +/- 9 mmHg to 133 +/- 18/86 +/- 14 mmHg, and the heart rate from 79 +/- 13 to 75 +/- 12 beats/min. Exercise blood pressure (900 watts) decreased from 180 +/- 22/104 +/- 14 mmHg to 158 +/- 25/96 +/- 17 mmHg and the heart rate from 104 +/- 14 to 100 +/- 16 beats per min. After treatment, a decrease in pulmonary arterial pressure and resting pulmonary capillary wedge pressure (PPA:-2.3 mmHg, PPC:-1.4 mmHg) and in exercise pressure (PPA:-8.5 mmHg, PPC:-6.6 mmHg) was established. Clinically relevant changes in cardiac output and cardiac index were not observed. The subjective symptoms (NYHA stage) were improved in eight patients. Combination treatment would appear suitable for patients with mild-to-moderate cardiac insufficiency.

[Pulmonary artery blood pressure and snoring]. / Pulmonalarterieller Blutdruck und Schnarchen.

Snoring is an extrathoracic inspiratory airway obstruction during sleep, accompanied by more or less intense noise. The inspiration volume being limited at the same time, this can produce additional blood gas changes. Epidemiological studies have shown an increased risk of myocardial infarction or cerebral ischaemia during night for snorers. Little is known, however, about acute effects of snoring on the haemodynamics of heart and circulation. The present study presents data of the pulmonary artery blood pressure during sleep-related upper airway obstruction. Pulmonary arterial pressure during sleep was examined with five patients via Swan-Ganz catheter. When an upper airway obstruction occurred, the inspiratory pulmonary arterial pressures rose in all the five patients. Two patients showed a clinically significant decrease in arterial oxygen saturation during snoring so that in these cases, a hypoxic vasoconstriction can be discussed as a possible cause. The other three patients did not produce significant decreases in oxygen saturation, so that in these cases mechanical factors (negative inspiratory intrathoracic pressure oscillations) should be regarded as the most probable cause for increases in the pulmonary arterial blood pressure.

[Which factors promote chronic alveolar hypoventilation in patients with obstructive sleep apnea?]. / Welche Faktoren begünstigen die chronische alveoläre Hypoventilation bei Patienten mit obstruktiver Schlafapnoe?

The pathogenesis of obesity hypoventilation is incompletely understood. We investigated 505 patients with sleep apnoea in respect of determinants that correlate with chronic hypercapnia. 14 patients (2.8 per cent) exhibited daytime hypercapnia (PCO2 greater than or equal to 45 mmHg). Compared with the entire group of patients, these patients showed heavier overweight (p less than 0.001) and their nightly respiratory dysregulation defined by the apnoea index was more severe (p less than 0.001). If these patients were compared with 14 normocapnic controls matched for apnoea index, weight and age, there was no difference in respect of lung function data. We conclude that overweight and the severity of sleep apnoea are determinants that predispose to chronic alveolar hypoventilation.