[Acute dyspnea--what should I not forget?]. / Akute Dyspnoe--was darf ich nicht vergessen?

Acute dyspnea represents a diagnostic challenge even for the experienced physician. There are no prospectively evaluated diagnostic algorithms dealing with this frequent clinical problem. First of all, the emergency has to be assessed and life supporting measures have to be considered. In addition to a thorough medical history and clinical examination, chest X-ray, spirometry, ECG, hemoglobin measurement, BNP and D-dimer testing represent valuable diagnostic tools and are available to GP's. Most commonly, acute dyspnoea is pulmonary or cardiac in origin. Up to one third of all cases will have several causes. Functional dyspnea is difficult to diagnose but should be taken into consideration after excluding any somatic cause. Hyperventilation is found in both, organic and non organic diseases, and is therefore an inappropriate criterion to differentiate between the two. The mainstay in the management of any symptom is to primarily treat the underlying disease. A significant hypoxemia (SO2 < 90%, pO2 < 60 mmHg) ought to be corrected by supplemental oxygen. It is inappropriate to withhold oxygen from patients with COPD and severe hypoxemia just to avoid hypercapnia. Besides oxygen, opiates efficiently relief dyspnoea but harbour the risk of respiratory depression, altered mental status or aspiration.

Intravenous iloprost bridging to orthotopic liver transplantation in portopulmonary hypertension.

Portopulmonary hypertension (PPHTN) is associated with poor prognosis and high perioperative mortality after orthotopic liver transplantation. This study documents the first case of a patient with PPHTN who was successfully bridged to orthotopic liver transplantation with i.v. iloprost, a stable prostacyclin analogue. The PPHTN had resolved completely 4 months after successful transplantation. In conclusion, portopulmonary hypertension is a relative contraindication to orthotopic liver transplantation, which should be attempted only if pulmonary haemodynamics improve with prostanoids. In this context, iloprost may be a valuable alternative to epoprostenol.

Adipose tissue storage of drugs as a function of binding competition. In-vitro studies with distribution dialysis.

Distribution dialysis was used to study binding competition between homogenates of adipose tissue and of lean tissues. The concentration ratios adipose/X (X = blood, muscle, lung, liver) of eight lipophilic drugs were determined in the absence and in the presence of a competing binding system X. With drugs which do not undergo storage in adipose tissue in-vivo, yet have a high volume of distribution, such as imipramine or desipramine, there was strong binding competition, and the balance of distribution was shifted from adipose to lean tissues. In the case of indomethacin with a low volume of distribution this shift was from adipose tissue to blood. With diazepam there was a marked binding competition which was not, however, sufficient to shift the balance of distribution away from adipose tissue. Binding competition was negligible with thiopentone. In contrast, with the equally lipophilic hexethal a moderate binding competition was observed. This is consistent with a decreased adipose tissue storage of the latter barbiturate. It is concluded that binding competition exists not only between blood and tissues but also among individual tissues. It is suggested that occurrence and extent of adipose tissue storage of drugs are determined by binding competition between lean and adipose tissues and, more generally, that distribution of lipophilic drugs is largely a function of binding competition.