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Biomedical subjects

J H Peter

Publications and source records attributed to J H Peter.

At least 127 records · Page 7Linked to original sources
PubMed1992

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.

Blood Pressure Determination↗
PubMed1991

Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease.

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.

Aged↗
PubMed1991

[Combination therapy in chronic heart failure. Hemodynamic effects with a calcium antagonist-diuretic combination].

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.

Adult↗
PubMed1991

Reduction of nocturnal diuresis and natriuresis during treatment of obstructive sleep apnea (OSA) with nasal continuous positive air pressure (nCPAP) correlates to cGMP excretion.

In ten patients with severe obstructive sleep apnea (OSA) profound changes in renal function could be demonstrated at night during nCPAP therapy. Natriuresis and diuresis decreased by about 50% while creatinine excretion rate and urinary osmolality did not change. We found parallel changes in the excretion of ANP's second messenger cyclic guanosine monophosphate (cGMP) in a dose-response-related manner to natriuresis respectively diuresis. These data are in agreement with recently demonstrated decrease of nocturnal plasma levels of atrial natriuretic peptide (ANP) during nCPAP therapy in apneic patients. This may be an indicator for an increased cardiac volume load during obstructive apnea. The decrease of diuresis, natriuresis and cGMP excretion demonstrate the beneficial effects of nCPAP treatment on the cardiovascular system. Therefore measurements of cGMP excretion may be a useful parameter to assess the cardiovascular function of apneic patients before and during treatment.

Adult↗
PubMed1991

Influence of antihypertensive drug therapy on sleep pattern and sleep apnea activity.

Sleep apnea, which affects 10% of men in the mean age group, is a common illness, and arterial hypertension one of its early symptoms. For the large group of, mainly young, patients with mild to moderate sleep apnea and arterial hypertension it is important to have a drug treatment available which will effectively control blood pressure without exacerbating symptoms of sleep apnea. We studied the effects of antihypertensive agents on blood pressure, sleep and sleep apnea in a randomized double-blind study of 24 patients with a sleep apnea activity of more than 10 apnea phases per hour of sleep and arterial hypertension with diastolic blood pressure values in the sitting position greater than or equal to 95 mm Hg. Mean age was 51 (range: 33-69) years, mean body mass index 31.4 (24.9-40.6) kg/m2. The study protocol envisaged two baseline measurements in the sleep laboratory, after which the medication was administered for 8 days. On the last 2 days of the treatment, polysomnographic leads were once again recorded in the sleep laboratory. The patients received either the beta-blocker metoprolol (1 x 100 mg/day) or the angiotensin-converting enzyme inhibitor cilazapril (1 x 2.5 mg/day). Systolic and diastolic blood pressure were decreased by both substances as expected. Total sleep time was 358 (233-425) min vs. 332 (255-383) min in the metoprolol group and 368 (295-424) min vs. 341 (265-434) min in the cilazapril group which is statistically not different between the two groups nor between the proportions of non-REM and REM sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy.

Arterial blood pressure patterns in 12 men with sleep apnea and arterial hypertension were studied at baseline and after 6 months' therapy with nasal continuous positive airway pressure (nCPAP). Preexisting antihypertensive medication was discontinued 1 week before baseline measurements. Weight did not change during the study period; body mass index was 29.3 (range, 25.4-38.5) vs. 29.3 (25.0-38.5). During therapy the apnea index decreased from 58 (range 30-73) to 2 (range 0-7) apneic episodes per hour (p less than 0.01). Intra-arterial systolic (BP sys.) and diastolic (BP dias.) blood pressure and heart rate decreased during therapy (p less than 0.001). Mean values +/- 95% confidence intervals were as follows: BP sys., 147.1 (+/- 1.6) mm Hg vs. 126.4 (+/- 1.5) mm Hg; BP dias., 81.6 (+/- 0.8) mm Hg vs. 69.4 (+/- 0.6) mm Hg; heart rate, 68.8 (+/- 0.7) beats/min vs. 65.4 (+/- 0.7) beats/min. Furthermore, the variability of these parameters decreased during therapy: variability BP sys., 53.8 (+/- 1.1) mm Hg vs. 25.6 (+/- 1.1) mm Hg; variability BP dias., 35.6 (+/- 0.7) mm Hg vs. 17.9 (+/- 0.7) mm Hg; variability of heart rate, 28.1 (+/- 0.7) beats/min vs. 14.9 (+/- 0.7) beats/min (p less than 0.001). During treatment we found that blood pressure scores already dropped during the awake phase, with a further decrease during non-REM and REM sleep (p less than 0.001). Our results, which demonstrate the reversibility of high blood pressure upon treatment of sleep apnea, indicate that sleep apnea can be an etiological factor in hypertension. Sleep apnea should therefore be considered in the differential diagnosis of arterial hypertension.

Adult↗
PubMed1991

First experience with cilazapril in the treatment of sleep apnoea-related hypertension.

Sleep-related breathing disorders are associated with considerably impaired vitality and reduced life expectancy. In this respect, a particularly important role is played by obstructive snoring and obstructive or mixed sleep apnoea. Because of the often underestimated prevalence of sleep-related breathing disorders and their association with hypertension in greater than 50% of patients, it is important to introduce antihypertensive drug therapy that does not exacerbate the effects and the degree of these disorders, and that above all produces an adequate lowering of blood pressure by night. In the present study in 12 patients, it has been shown that the new ACE inhibitor, cilazapril, achieves a good reduction in blood pressure over 24 hours and during all stages of sleep, without any negative influence on the ratio of REM: nonREM sleep. The apnoea index was reduced from 40 (range 12 to 84) to 27 (range 0 to 72) apnoeas per hour of sleep (p less than 0.01). It will be increasingly important to take into account the effects of antihypertensive therapy on other clinical parameters, especially the nocturnal blood pressure profile and its association with sleep-related breathing disorders.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Disturbances in volume regulating hormone system--a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome?

Recent studies about renal function and volume regulating hormones in obstructive sleep apnea (oSAS) indicate complex disturbances in volume homeostasis. Increased nocturnal secretion of atrial natriuretic peptide (ANP) and decreased renin secretion during apnea looks similar to a situation seen during hypervolemia or increased cardiac volume load. Increased venous return induced by pathologically high negative intrathoracic pressure during obstructive apnea may be the cause. Since during wakefulness no true hypervolemia is present, a "pseudohypervolemia" or "central hypervolemia" must exist caused by volume shift from the peripheral to the central compartment during apnea. Since volume homeostasis and blood pressure regulation are complexly connected the question arises whether disturbances in volume homeostasis play a role in the pathogenesis of arterial hypertension in sleep apnea. In a subgroup of hypertensive patients hypertension is salt-sensitive and volume dependent; it is called volume-expanded or low-renin hypertension. An inhibitor of the Na+/K(+)-ATPase acting via the digitalis receptor - called digitalis like factor (DLF) - is regarded as the causative agent for the development of hypertension in these cases. From this background, we were interested in the question whether DLF may be the linkage between disturbances in volume homeostasis and the pathogenesis of hypertension in sleep apnea. We could demonstrate a decrease of nocturnal urinary excretion of DLF during nasal continuous positive air pressure (nCPAP) therapy. Since a positive correlation between changes in diuresis respectively natriuresis and DLF excretion was found, we suggested DLF to be involved in changes of renal function in sleep apnea besides ANP. In 3 patients we measured nocturnal plasma levels of DLF and renin.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1991

[Computer analysis of disturbed respiration in patients with sleep apnea].

In patients with sleep related breathing disorders parallel evaluation of respiration, blood gases and the EEG are indispensible. Computerized methods can provide a detailed analysis of the interrelation of these parameters to enlighten the disturbed central regulation of respiration in these patients. These methods also can help to achieve a better differential diagnosis in routine clinical work. A new method is presented here which evaluates the signals of nasal airflow, thoracic and abdominal movements together with oxygen saturation and heart rate in parallel. The new method is validated using a detailed visual analysis. Results prove the usefulness of the new method. To apply the method the relationship between length of apnea and oxygen desaturation is evaluated for different sleep stages separately.

Blood Gas Analysis↗
PubMed1991

[Assessment of the MESAM and Biox 3700 early warning methods for the diagnosis of sleep-related respiratory disorders in young men].

We can use pulse oximetry as a method for diagnosis of the sleep apnoea syndrome, as well as L-EKG, MESAM II and the actigraph. In this study MESAM II and pulse oximetry were combined for finding out discrete sleep-related breathing disorders. The results were compared with polysomnography. 5 (15.1%) of 32 patients had an index of apnoea (AI) greater than 10, whereas 4 (12.1%) patients showed an AI greater than 5. All of the patients with positive signs in MESAM II/pulse oximetry had an AI greater than 5 in polysomnography, whereas non of the patients with negative signs in MESAM II/pulse oximetry had an AI greater than 5 in polysomnography.

Adult↗
PubMed1991

[SIDAS 2010: mobile 10-channel unit for the diagnosis of sleep-related respiratory disorders].

At the moment diagnosis of sleep related breathing disorders (SRBD) is carried out in specialised clinical centres with well-equipped sleep laboratories. Since there are only few of these in Germany, medical care in this field is not sufficient at all even if applied only to high-risk patients. To cope with the large number of patients with severe SRBD we developed a mobile 10-channel unit (SIDAS 2010) designed for diagnosing SRBD even outside the conventional sleep laboratories. In this study we investigated 108 patients who after using the 4-channel recorder presented signs and symptoms suggesting SRBD. After evaluating the tracings in 53 patients a distinct obstructive sleep apnoea (OSA) (AI 10) could be diagnosed; in 55 patients the signs remained indistinguishable. In 2 recordings with SIDAS in 74 patients, a distinct OSA was diagnosed, 34 patients had an AI less than 10; these patients underwent renewed polysomnographic recordings with EEG in addition. The polysomnographic recordings revealed 5 patients with an AI between 5 and 10.3 with primary and secondary alveolar obstructive hypoventilation due to excessive snoring. The comparison of SIDAS recordings with recordings made by polysomnography proved SIDAS to be valuable in respect of diagnosing type of SRBD (obstructive/central) and amount of respiratory events (apneas/hypopnoeas). In this study only 13 patients with SRBD (14.9%) need further diagnostic procedures. We conclude that with SIDAS most of the SRBD can be diagnosed sufficiently even outside conventional sleep laboratories.

Adult↗
PubMed1991

[Pulmonary artery blood pressure and snoring].

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.

Blood Gas Analysis↗
PubMed1991

[Which factors promote chronic alveolar hypoventilation in patients with obstructive sleep apnea?].

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.

Adult↗
PubMed1991

[Sleep-related respiratory disorders and coronary heart disease].

A review of the literature shows that more than 50% of examined patients suffering from coronary heart disease were also suffering from sleep-related apnea. We were able to diagnose a pathological sleep apnea in 9 out of 25 patients (36%) suffering from an angiographically confirmed coronary 2-vessel and 3-vessel disorder. Patients with this combination--this is the hypothesis derived from our study--are at risk due to nocturnal apnea-induced myocardial ischaemia and rhythmic disorders. In 15 patients with sleep apnea and coronary heart disease or small vessel disease, nocturnal polysomnography was conducted, in parallel a 6-channel ECG was recorded. The apnea index (second night) was on the average 33 phases/h, the maximal duration of an apnea phases being 120 seconds. The minimal blood gas saturation recorded during sleep was between 46 and 89% (median 76.0%). In 4 of the 15 patients it was possible to confirm myocardial ischaemia (correlated via REM and also via NREM) with a maximum duration of 60 seconds, mainly during the phases of maximal apnea activity and blood gas desaturation. On comparing the ventricular arrhythmias waking/sleep, the Lown class did not change in 12 patients; there was deterioration in 2 patients and in one patient a qualitative improvement during the sleep phase. Patients suffering from sleep-related respiratory disorders and coronary heart disease are at cardiac risk, the more so since long-lasting apneas can lead to conditions of hypoxia at the heart in pre-existing changes in the coronary arteries, restricted coronary reserves and reduced tolerance to hypoxia. Such hypoxia can in turn induce enhanced electrical instability and a disturbance of the contractile function.

Arrhythmias, Cardiac↗
PubMed1991

[Risk of accidents in patients with nocturnal respiration disorders].

Excessive daytime sleepiness is one of the main symptoms of sleep apnoea, which can, especially in monotonous situations, lead to real nodding off. Since driving a motor vehicle can also be monotonous, patients suffering from untreated sleep apnoea may be a possible traffic risk. Before undergoing a polysomnographic examination, 123 patients filled in a questionnaire inquiring about fatigue and sleepiness while driving a vehicle as well as accidents during the past three years. Five groups were formed according to severity of sleep apnoea. Right through these groups, the increase in heavy fatigue during driving (median) was significant: from "seldom" (AI less than 5) via "sometimes" to "often" (AI greater than or equal to 35). Occurrences of short periods of falling asleep (means) were practically not reported (0.02) by the group without sleep apnoea but increased considerably to 3.37 times per 1000 km for the group with an AI greater than or equal to 35. The frequency of accidents due to sleepiness rises significantly in concurrence with the seriousness of sleep apnoea. Besides, patients with an AI greater than or equal to 5 attribute 23 out of 28 accidents to sleepiness, whereas patients without sleep apnoea attribute all four accidents to other reasons (p = .0035). These findings emphasise the importance of an early diagnosis and effective therapy of sleep apnoea - which is available as nasal continuous positive airway pressure ventilation (nCPAP). Sleep medicine can thus not only help patients suffering from sleep apnoea but may also reduce the health risk of other traffic participants and be cost-saving.

Accidents, Traffic↗
PubMed1991

[Treatment of primary and secondary therapy failure in patients with sleep apnea treated with nasal CPAP].

Two forms of treatment failure of nCPAP therapy should be distinguished: 1. Primary treatment failure: the reversal of apnoeas and hypopnoeas cannot be achieved due to central SA or a combination of MSA and central hypoventilation. In 10 patients who did not respond to nCPAP (7 patients with purely central SA and 3 patients with MSA who still demonstrated long phases of central hypoventilation during nCPAP) we performed a nasal intermittent positive pressure ventilation (nIPPV) during at least 3 treatment nights. In all patients a reversal of apnoeas and hypopnoeas could be achieved, despite a few phases of mask leakage. Due to possibly life threatening side effects continuous monitoring is required during the initial treatment phase. 8 patients who reported a reduction of symptoms have been successfully using the treatment at home for up to 22 months. 2. Secondary treatment failure: nCPAP leads to a normalisation of breathing pattern but patients refuse nCPAP or discontinue treatment. Besides patients who are poorly motivated there are four major side effects of nCPAP as a reason for non-compliance: a) drying out of the nasopharyngeal mucosa or rhinitis; b) pressure marks caused by the nose mask; c) intolerance to the high expiratory pressure; d) noise. Drying out of the mucosa and rhinitis are the most important side effects. If an increase of room temperature and humidity, nasal cream and small amounts of mint-oil as well as a heat-moisture exchanger (HME) prove inadequate, we use a heated humidifier (Dräger, Aquapor).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗