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Since 2005, invasive long-term ventilation in Germany has increased significantly from around 1000 to 20 000 patients in Germany. Due to complex home care, the health care system incurs additional costs of around 4 billion euros per year. In addition, in the last 2 - 3 years more tracheostomized patients have been discharged home without ventilation (usually after stroke), and they receive the same complex home care. These patients have almost never been given the chance of a professional weaning trial by a weaning center. They are discharged from hospitals directly into the care. As a result, the quality of care is significantly worse than traditional care with structured discharge management via a weaning center. The solutions are difficult to find due to the interface problems between inpatient and outpatient care and the different organizational structures with different delivery systems. Possible solutions are shown, but most of them require a change in the law.

Regional weaning centers play a more and more important role in the weaning process of long-term ventilated patients. The medical center Kloster Grafschaft is one of the oldest and largest centers in Germany. There is very little published data from larger weaning centers in Europe.From 2007 to 2011 all weaning patients were registered in a database. Additional information of the transferring hospitals was inquired. Prolonged weaning was defined by a period of at least 7 days of mechanical ventilation as well as three unsuccessful weaning trials.Data from 867 of 916 registered patients could be analyzed. 71.1% could be successfully weaned from mechanical ventilation. All patients were suffering from a hypercapnic insufficiency as well as a variety of secondary diagnoses, on average 15.1 per patient. The median of age was 70 years, 62 % were male. Prior to hospital transfer patients had been ventilated for a median of 41 days. Time to successful removal of the artificial airway was 8 days according to the DRG code directive and 13.4 days when non-invasive ventilation (NIV) time was included. Of the 616 patients who could be successfully weaned, 42 % were discharged on NIV. Out of the 251 patients who could not be weaned, 107 were discharged. The remaining 144 (16.7 %) patients died, 33 % due to the primary underlying disease or a complication. 66 % of the deceased patients received palliative care. Patients with successful and unsuccessful weaning did not differ by age, by duration of mechanical ventilation or time until tracheostomy. Postoperative patients could be weaned more often than medical patients (p 0.05). Discrimination between patients with successful and unsuccessful weaning was not possible by the point in time of the first spontaneous breathing trial in regard to the duration of ventilation but only by the duration of this trial after transfer to our unit (150 vs. 60 min; p 10-6). The TISS-28 and the SAPS-II-Score did not differ between the two groups. Patients with successful weaning had less agitation according to the RASS-Score (0.47 vs. 0.15; p 0.005).It becomes apparent that in a specialized weaning center the majority of difficult to wean patients can be liberated in short time from mechanical ventilation.

Polycythemia is defined by the increase of hematocrit and haemoglobin respectively. Possible causes might be neoplastic diseases like polycythemia vera with proliferation of a cell clone. More often one will find reactive forms resulting from chronic hypoxemia. A physiologic form of polycythemia can be found in highlanders and athletes training at high altitude. With increasing frequency erytrhopoetin and it's analoga are being used as doping substances to induce Polycythemia. Red cell proliferation induced by chronic hypoxemia is the most common form in patients. In this instance the lung itself can be the cause (hypoxemia with hypocapnea in blood gas analysis) or hypoventilation caused by an insufficient respiratory pump (hypercapnea with hypoxemia in blood gas analysis) induces a compensatory Polycythemia. The former form can be treated with long term oxygen therapy and the latter by non-invasive ventilation, either approach corrects hypoxemia and reduces Polycythemia within some weeks.

According to the literature, hypoxemia is considered to be severe when oxygen saturation (Sa O(2)) falls below 90 %. Frequently one can discover lower values without impairment of the patient. Especially patients with the obesity hypoventilation syndrome (OHS) will have frequent night time desaturations of significant duration below 50 % Sa O(2), but do still cope with their daytime jobs. This discrepancy can only be explained by the fact, that hypoxemia is not equivalent to tissue hypoxia. The latter is mainly being determined by oxygen delivery (DO2) which is being calculated by multiplying cardiac output (CO) and oxygen content (CaO2). Ca O(2) is determined by the product of Sa O(2) and haemoglobin (Hb) times 1.35. From this context it becomes evident, that assessing hypoxemia without considering oxygen content will frequently be misleading. The human organism has several possible ways of compensation in order to avoid tissue hypoxia. In case of acute hypoxemia that evolves within minutes the organism can shift the oxygen binding curve by changing 2 - 3-DGP erythrocytic activity. Additionally non vital organ systems might reduce their oxygen uptake. During sustained hypoxia (lasting 2 - 3 days) the Krebs cycle and the respiratory chain will express hypoxia-resistant iso-enzymes. Long lasting hypoxia can be compensated by polycythemia. Indirect data suggest, that the critical number for the oxygen content is rather low and is estimated to be somewhere around 33 % of the normal value. These mechanism of hypoxia-resistance are hardly ever maxed out in patients on critical care units.Lack of knowledge of the above described mechanisms does frequently result in diseases like ARDS which frequently develops due to excessive ventilatory pressures and excessive inspired O(2) concentrations.

Heart failure is an established diagnosis. Respiratory muscle or ventilatory pump failure, however, is less well known. The latter becomes obvious through hypercapnia, caused by hypoventilation. The respiratory centre tunes into hypercapnea in order to prevent the danger of respiratory muscle overload (hypercapnic ventilatory failure). Hypoventilation will consecutively cause hypoxemia but this will not be responsible for performance limitation. One therefore has to distinguish primary hypoxemia evolving from diseases in the lung parenchyma. Here hypoxemia is the key feature and compensatory hyperventilation usually decreases PaCO2 levels. The cardiac as well as the respiratory pump adapt to an inevitable burden caused by chronic disease. In either case organ muscle mass will increase. If the burden exceeds the range of possible physiological adaptation, compensatory mechanisms will set in that are similar in both instances. During periods of overload either muscle system is mainly fueled by muscular glycogen. In the recovery phase (e. g. during sleep) stores are replenished, which can be recognized by down-regulation of the blood pressure in case of the cardiac pumb or by augmentation of hypercapnia through hypoventilation in case of the respiratory pump. The main function of cardiac and respiratory pump is maintenance of oxygen transport. The human body has developed certain compensatory mechanisms to adapt to insufficient oxygen supply especially during periods of overload. These mechanisms include shift of the oxygen binding curve, expression of respiratory chain isoenzymes capable of producing ATP at lower partial pressures of oxygen and the development of polyglobulia. Medically or pharmacologically the cardiac pump can be unloaded with beta blockers, the respiratory pump by application of inspired oxygen. Newer forms of therapy augment the process of recovery. The heart can be supported through bypass surgery or intravascular pump systems, while respiratory muscles may be supported through elective ventilatory support (mainly non-invasive) in the patient's home. The latter treatment in particular will increase patient endurance and quality of life and decrease mortality. Heart and respiratory pump failure share many common features. Since both take care of oxygen supply to the body, their function and compensatory mechanisms are closely related and linked.

The prevalence of difficult or prolonged weaning from mechanical ventilation is increasing because of a growing number of elderly patients with multiple diseases and pulmonary problems requiring mechanical ventilation. Intensive care units (ICU) are inclined to refer to specialized unit those patients who are difficult to wean. A nationwide survey of German facilities was conducted and this article reports the current state of weaning centers staffed by chest physicians.38 centers participated in the survey, which was divided into 10 items, covering characteristics of the hospital, weaning strategies, patients and outcomes during 2006. The survey included 2718 patients in whom weaning was difficult or prolonged. Almost three quarters of patients were transferred to one of the weaning centers from the ICU of another hospital.The weaning success rate was 66.4%. In 31,9 % of patients home mechanical ventilation was started after they had been weaned. The overall hospital mortality rate was 20.8%. There were major differences between individual centres concerning the number of patients, organization of the weaning unit and weaning strategies.Weaning was successful in two thirds of patients who had been on prolonged mechanical ventilation and had then been transferred to weaning facilities staffed by chest physicians. These centres effectively improved the quality of care of patients on prolonged mechanical ventilation by avoiding long-term invasive ventilation and sparing cost-intensive ICU resources. The problems that still exist may be overcome by a network of weaning facilities.

Inhalation of bronchodilators and corticosteroids is the mainstay treatment for patients with obstructive lung diseases. Many dry powder inhaler devices and drug combinations are now available, and competing promotional claims can confuse both prescribers and patients. The appropriate dose of a given drug may be different for a pressurized metered dose inhaler (pMDI) and a dry powder inhaler (DPI). DPIs create aerosols by drawing air through an aliquot of dry powder. The powder contains either micronized (5 micro m in diameter) drug particles bound into loose aggregates, or micronized drug particles that are loosely bound to large (30 micro m in diameter) lactose or glucose particles. Usually, the drug particles are bound to carrier particles and are stripped form the carrier particles by the energy provided by the patientacute;s inhalation. The release of respirable particles of the drug requires inspiration at relatively high flow rates (30 - 120 L/min). Other important factors influencing aerosol generation and lung deposition are device design (resistance to airflow) and environmental conditions (humidity, temperature). Preferably, patients should employ only one type of aerosol-generating device for inhalation therapy. The technique of use varies among devices, and repeated instruction is highly advisable, to ensure that the patient uses the device appropriately. At present, DPIs are recommended for prophylactic and maintenance therapy in patients with asthma and chronic obstructive pulmonary disease, but not for patients with acute severe bronchoconstriction or children less than 5 years of age.

Patients subjected to an increased load and with a decreased capacity of their respiratory muscles may be difficult to wean from mechanical ventilation. Using a weaning strategy with a focus on unloading respiratory muscles may be successful even after long-term mechanical ventilation. In a prospective uncontrolled study, we examined the outcome of our weaning protocol.Under prolonged mechanical ventilation in outlying intensive care units (44.3 +/- 38.1 days) 232 patients (64.8 +/- 12.7 years, 149 males, 83 females) with the following underlying diagnoses were investigated: chronic obstructive pulmonary disease (54.3%), neuromuscular diseases (16%), thoracic restriction (10.8%), chronic left heart failure (7.3%), postsurgical ventilatory failure (6.9%) and miscellaneous conditions (4.7%). Our weaning strategy was focused on type of mechanical ventilation, endotracheal tubes, non-invasive interface, oxygen supply and transport capacity, body position and home mechanical ventilation, if an increased load or a decreased capacity of the respiratory muscles remained after weaning.Altogether 65% of the patients (n = 152) were weaned in a mean duration of 7.5 days. Intermittent home mechanical ventilation followed in 45 patients (19.4%). In our hospital died 64 patients (27.6%). After a stay of 19.7 +/- 12.2 days in our hospital 72.4% of the patients (n = 168) were discharged. The postdischarge 3-month mortality of the cohort was 36.5%.Applying our weaning strategy about 65% of the patients requiring long-term mechanical ventilation were successfully weaned. Weaning was achieved in approximately one fifth of the time previously spent on mechanical ventilation. However, the 3-month mortality of the investigated cohort was 36.3%.

In severe "pink puffer" emphysema the patients' physical capacity is limited by dyspnoea despite maximal application of established treatment. This pilot study investigated the effect of retarded morphine, taken orally for 10 days, on ventilation, dyspnoea, walking capacity and wakefulness.Twenty clinically stable patients (11 men, 9 women, mean age 68.5 [50-81] years) with "pink puffer" emphysema were studied over a period of 10 days in a prospective, non-controlled trial of cross-over design. Criteria for inclusion in the study were: 1-second forced expiratory volume (FEV1)1 I, vital capacity50% and normocapnia. In addition to their existing therapy patients received either no further therapy or retarded morphine. Morphine dosage was increased to maximally 3 x 30 mg daily, depending on effectiveness and side effects, dyspnoea at rest and immediately after a 6-min walk (assessed with Borg's visual analog scale), maximal walking capacity were determined, as well as blood gases, respiratory minute volume and the respiratory drive (airway occlusion pressure [P0.1]), responsiveness of the respiratory pathways to CO2 and wakefulness (concentration, fatigue, interest in surroundings).Twelve patients completed the study (group A). In the remaining patients (group B) the test had to be stopped prematurely because of undesirable side effects or an exacerbation of the underlying infection. In group A, morphine (mean dosage: 49.2 +/- 28.4 mg/d) caused a reduction of PaO2, dyspnoea on activity, the resting minute respiratory volume, respiratory drive and CO2 response, and an increase in PaCO2, HCO3- and the 6-min walking distance. Morphine did not produce a change in subjectively evaluated vigilance and the blood pH.After strict patient selection oral morphine produced a reduction of exercise dyspnoea and an increase in walking capacity in half of the patients with severe pulmonary emphysema. There also occurred a slight rise in PaCO2 without any relevant respiratory acidosis or significant decrease in wakefulness.

Of 129 patients with an acute lumbar root compression syndrome due to disc herniation 21, who were symptom-free, were examined by computed tomography (CT) on average 276 days after a three-step regimen of conservative treatment. In no instance had there been a deterioration of the original findings. In 14 patients the CT picture continued to demonstrate disc herniation, although the patients were without symptoms. In two patients a moderate, in five a marked regression of herniation was demonstrated by CT. Clinical improvement without change in the CT picture points to the compression syndrome not being explainable solely in mechanical terms. As a matter of fact, a possible cause may be a disturbance of radicular blood supply resulting in oedematous root swelling which is usually masked in the CT by prolapsed disc tissue. There is as yet no easy explanation for regression in case of prolapsed, perhaps even sequestered, disc tissue. It is possible that there have been reparative processes, such as have been described histopathologically in form of ingrown vessels. More plausibly would be a separation of the herniated and/or sequestered disc tissue in form of an asymptomatic sliding into the terminal caudal region.