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Introduction: Despite a decreasing incidence, sudden infant death syndrome (SIDS) is still the most frequent cause of death in industrial nations during the first year of life. Hypoxia plays a major role in the pathogenesis, but the exact mechanism is not fully understood., Methods: This study was based on personal considerations and a selective online literature search., Hypothesis: SIDS is the result of a frequently protracted ATP-depletion., Discussion: Especially in combination, all risk factors for SIDS favour an ATP-deficiency by increasing ATP-catabolism and/or by diminishing ATP-synthesis. Prenatal chronic hypoxaemia and an insufficient supply with nutrients lead to low birth-weight, reduced adipose tissue, elevated haemoglobin F, increased sympathetic activity, hypermetabolism, and diminished hypoxia tolerance in the neonates. Because of reduced adipose tissue, more energy for thermogenesis is needed after birth. In reaction to hypoxaemia, infants with risk factors show hyperventilation instead of hypoxic hypometabolism and respiratory depression. Enhanced breathing, however, requires additional ATP and causes increasing oxygen affinity, which is elevated physiologically during the first months of life. Thereby, tissue-hypoxia and diminished ATP-synthesis may arise. Besides, enhanced sympathetic activity leads to hypermetabolism and increased ATP-catabolism. While innate risk factors may reduce ATP-production in burdening situations, like food deprivation, postnatal hyperthermia and stress augment ATP-catabolism by hyperventilation and hypermetabolism and empty energy stores. For term newborns, the peak incidence of SIDS might be explained by the haemoglobin nadir of physiological anaemia and by the therefore reduced capacity for oxygen transport. Thereby, the risk of tissue-hypoxia, which follows increased oxygen affinity and vanishing ability to hypoxic hypometabolism, is further enhanced. The almost identical symptoms of SIDS and ATP-deficiency diseases like hypophosphataemia, heat stroke, and carbon monoxide poisoning support the presented hypothesis., (Georg Thieme Verlag KG Stuttgart.New York.)

We report about a 49 year old woman with repeated chest pain at rest. During hyperventilation significant ST-segment elevation in leads V1-V5 appeared. Bicycle stress test did not provoke any ECG changes. Coronary angiography showed a significant stenosis of the left anterior descending coronary artery. Successful balloon angioplasty followed by stent implantation was performed. After an uneventful course of twelve months, hyperventilation could provoke neither chest pain nor ECG changes again without any antispastic medical treatment. Impact of fixed atherosclerotic lesions for the occurrence of coronary vasospasm, usefulness of hyperventilation as a non-invasive provocation test and therapy are discussed.

Hyperventilation syndrome is considered an established diagnosis if it is confirmed that the patient's complaints correlate with arterial hypocapnia. In the diagnostic criteria set up by a group in Nijmegen, paCO2 is determined indirectly by measuring the end tidal CO2. Values below 4 kPa measured at rest and 10 or more minutes after deliberate hyperventilation are classified positive diagnostic criteria for hyperventilation syndrome. However, it has not been proven that end tidal pCO2 agrees well with paCO2 during the entire manoeuvre. We performed simultaneous measurements of both parameters in 10 healthy non-smokers, before, during and after 3 minutes of deliberate hyperventilation. A comparison of the values employed for diagnosing a hyperventilation syndrome (during normal respiration before and 10 and more minutes after hyperventilation) yields a mean difference of 0.39 kPa according to the statistical computation described by Bland and Altman (limits of the range of agreement between 0.98 and -0.18). The end tidal CO2 values measured during the normal respiratory phase as well as 10 and more minutes after hyperventilation, agree well with the arterial values (the arterial values being slightly higher). During and shortly after hyperventilation the values obtained by both methods differ from one another, so that the exact degree of hypocapnia during a hyperventilation period cannot be assessed by measuring the end tidal CO2.

Prinzmetal's angina is a variant of the classic exertion dependent angina pectoris. Typical is the appearance of the symptoms at rest during early morning hours. It is due to spasms in the coronary arteries. Various provocation tests may be used to trigger spasms, among others hyperventilation which leads to vasoconstriction of coronary arteries. The case of a 53-year-old patient with Prinzmetal's angina is described in whom spasms of the right coronary artery could be evoked by hyperventilation. The following pathogenetic mechanisms may be possible in Prinzmetal's angina: disturbed endothelial permeability, endothelial dysfunction, or secretion of vasoconstrictive substances as well as local hypersensitivity of segments disturbed by atherosclerotic lesions to circulating vasoconstrictors.

Background: The reported incidence of neonatal acidosis varies++ significantly in different obstetrical departments. We wanted to investigate to which extend neonatal acidosis is depended on maternal respiration patterns during the third stage of labor., Methods: Maternal arterial blood gas analysis was performed in 101 term pregnancies. Fetal acid-base parameters from arterial and venous umbilical blood were assessed simultaneously. SPEARMAN rank correlation (rs) was used to investigate the statistical relationship of maternal and fetal blood gas parameters and pH-values. Moreover a computer model was developed to describe the influence of maternal respiration on neonatal acidotic risk figures., Results: A highly significant correlation was established between corresponding variables in maternal arterial blood and in venous umbilical blood (rs > or = 0.500, 2P < 0.001). These correlations were not as striking when comparing maternal parameters with corresponding variables in arterial umbilical blood. The partial oxygen pressure in arterial and venous umbilical blood did not show any correlation with the variables of the maternal acid-base status. In the computerized simulation model mild maternal hyperventilation during the third stage of labor decreased the risk of neonatal acidosis (pH, UA < 7.100%) by approximately 25% without evidence of lack of fetal oxygen supply., Conclusions: A mild maternal hyperventilation synchronized with uterine contractions during the third stage of labor in combination with rapid breathing when delivering the fetal head has a favourable influence on the neonatal acid-base balance. In this study there is no indication that such an obstetrical management results merely in a laboratory artifact, because according to our data there was indeed no indication of compromised fetal oxygen supply. Routine fetal blood sampling also from venous umbilical blood appears to be useful in differentiating between combined feto-maternal and isolated fetal variations in actual pH-values.

Physical exercise can induce an acute attack in most asthmatics. Exercise-induced asthma (EIA) is therefore a common clinical presentation of bronchial asthma. EIA is likely a consequence of bronchial hyperreactivity whereby alterations in bronchial osmolarity, heat-loss by hyperventilation and physical activity per se are discussed as pathogenic triggers. Clinical presentation, pathogenesis and diagnosis of exercise-induced asthma are summarized. Pharmacologic and non-pharmacologic possibilities are covered in some depth. In this context the value of sports-therapy in treatment of asthma is redefined. The possibilities and limitations for this form of treatment are explained.

The clinical classification, pathophysiology and often difficult diagnosis of acute pulmonary embolism are reviewed. The diagnostic power of subjective and objective clinical symptoms and the diagnostic procedures (electrocardiogram, chest X-ray, echocardiography, pulmonary arteriography, pulmonary scintigraphy, determination of arterial blood gases) are evaluated and an actual investigative plan outlined. Diagnostic problems and frequent pitfalls are discussed. The often non characteristic and masked course in acute and chronically recurrent pulmonary embolism is emphasized.

In the search for methods which might increase the discrimination of the EEG, the power density spectra of a random sample of patients during different conditions were analysed. Power density spectra were made during eyes closed, eyes open, after hyperventilation, during photic stimulation, and during auditory stimulation. It proved that the spectra may change under different provocation tests, sometimes in a rather peculiar way. The conclusion was, that these analyses improve explicit the EEG diagnosis, a problem however is the time required for spectra interpretation.

1. Voluntary hyperventilation during rest in the recumbent position induces a fall in H+ concentration, PCO2 and PO2 in mixed venous blood and in the blood of the coronary sinus. 2. If the breathing volume is increased during voluntary hyperventilation between 2- and 2.5 fold above the volume at rest, O2 uptake increases by only 6% but CO2 excretion rises by 66%. 3. Cardiac output decreases by 8% and the O2 extraction of the myocard increases by 12%. There is a quantitative relationship between arterial pH or PCO2 and changes in the systemic and coronary circulation. Blood pressure decreases in the pulmonary circulation. 4. Nitroglycerin during hyperventilation produces an additional reduction in cardiac output but no effect on the O2 extractions of the myocard. 5. With dipyridamol, the O2 extraction of the myocard is reduced and the PO2 in the blood of the coronary sinus increases. 6. In the case of severe coronary obstruction, the effect of dipyridamol can cause acute angina pectoris and left heart insufficiency due to poststenotic ischemis (steal syndrome).

The sensation of dyspnea is related to pathologically increased breathing work as a result of hyperventilation and/or increased airway resistance. Low cardiac output resulting in tissue hypoxia provokes hyperventilation. In diffuse interstitial lung diseases, hyperventilation is combined with severely reduced lung compliance. In severe airway obstruction, hypoventilation is the result of excessively enhanced breathing work. Habituation and acute changes of situation have an important bearing on the subjective sensation of dyspnea.

Subjective differences in EEG evaluation are demonstrated by means of a seven step scale for grading the unspecific hyperventilation effect in 3263 EEG of children. Intermediate steps of this scale allow to minimize such unavoidable differences.

CBF decreases when arterial PCO2 is lowered by physiological, pathological or therapeutically induced hyperventilation. This is accompanied by an undelayed compensatory increase of oxygen-av-differences. Continuous monitoring of enzymatically determined glucose-av-differences of the brain during hyperventilation has for the first time shown that there is an undelayed fall of the cerebral venous glucose content, too. This indicates that the brain cells extract an augmented amount of glucose per ml blood during decreased CBF. Therefore glucose metabolism of the brain is not impaired during non-critical CBF reduction. However, when arterial PCO2 falls below 25 mmHg a detrimental effect on CBF and cerebral metabolism has to be expected. CBF will then decrease below the critical threshold for an undisturbed oxygen supply, and the respiratory alcalosis will lead to a disturbed oxygen delivery due to the Bohr-effect. As a consequence both of these factors will reduce the energy-yielding oxydative glycolysis and augment the little energy producing anaerobic glycolysis with a concomitant increase of lactate formation, resulting in a tissue and spinal fluid lactate acidosis. From our results it is therefore concluded that induced hyperventilation should be avoided, and that central hyperventilation in diseased states has to be considered as an additional threat to the brain.

The most important adaptive mechanism to acute hypoxia is alveolar hyperventilation which improves the oxygen uptake in the lung. The delivery of oxygen to the particular organs is regulated according to their vital function. An essential adaptive mechanism can not be observed above an inspiratory O2 partial pressure of 100 mm mercury, corresponding to an altitude of about 3000 m in normals. In contrast, in patients with cardio-pulmonary disturbances adaptive mechanisms take place at far lower altitudes. Especially in patients with arterial hypoxemia, pulmonary hypertension and occlusive vascular disease moderate hypoxia may lead to decompensation of an a priori unstable equilibirum.

The amplitude of the volume pulse in relation to transmural pressure and the compliance as a viscoelastic property of the digital arteries were determined noninvasively in 9 male subjects (mean age 16 years). The amplitude of the volume pulse was measured impedance-plethysmographically and the amplitude of the pressure pulse sphygmomanometrically. The registration of the pulses was performed under different conditions (sitting-control), lying, 3-min forearm ischaemia, concentration-performance test, hyperventilation, 0.8 mg Nitrangin sublingual) to provoke different states of the vessel wall. The amplitude of the volume pulse under concentration-performance test (0.054 +/- 0.015 ml), hyperventilation (0.045 +/- 0.015 ml) and Nitrangin (0.142 +/- 0.034 ml) is significantly (p = 0.025) different from control (0.086 +/- 0.016 ml). The amplitude of the volume pulse and the compliance increase with decreasing transmural pressure.

An investigation of certain electroencephalographic parameters recorded during 19 psychomotor attacks was made. Each attack had been recorded in full. Fourteen of the attacks were preceded by a temporal focus, 13 were provoked by hyperventilation, 18 were initiated focally, 9 were accompanied by seizure potentials, 7 revealed primary or secondary delta rhythms, and 8 were followed by temporal delta focus.

In experimental and clinical studies the effect of Acetazolamide (Diamox) on acute mountain sickness was investigated. It could be established that Acetazolamide does influence the symptoms, the man effect seems to be a reduction of the respiratory alkalosis, which is found in control persons in high altitudes. Observations made with a group of 25 tourists mountaineering in the Cordilleras (South America) over 24 days in altitudes between 3200 and 6000 m are described. In accordance with other published data the favorable influence of Acetazolamide on acute mountain sickness could be confirmed. Persons taking Acetazolamide were more efficient and better prepared to cope with the extreme situations in high altitude. They also showed to be more resistent to other diseases, which are following the stress in high altitude and are caused by the different climate and food.

In 10 cats anaesthetized using chloralose and with muscular relaxation by gallamine and continuous artificial ventilation in acute experiments photically evoked potentials (PEP) were recorded from the visual area of the cortex under different intragastric pressures and varying tidal volumes. It was the aim of this study to examine whether an exteroceptive stimulus (light flash) in the visual analyzer, which is influenced by an interoceptive stimulation (gastric pressure), may also be modified by different tidal volumes. Times, amplitudes and slope parameters, blood pressure and heart rate of the animals were studied. The PEP of the visual cortex was modified under the influence of the interoceptive stimuli. It could, however, be shown that already hypo- and hyperventilation alone may cause alterations in the latency period of the PEP. They arise in a different manner in individual parts of the measured parameters of the PEP and do not change these values in a typical manner. Additional dilatation of the stomach may suppress the phenomena caused by alterations in the tidal volume. Thus, attention should be paid to both blood gases and acid base balance in animals in studies on viscero-cerebral interrelationships as well as to interactions between different analyses using the method of evoked potentials.