National Survey Regarding Motivation and Conditions of Physicians Working in a Pediatric Cardiac Intensive Care Unit.

BACKGROUND: The professional demands on the expertise in pediatric intensive care have continuously increased in recent years. Due to a lack of applicants, the staffing of a continuous shift service with qualified medical staff poses major challenges to the hospitals. METHODS: A web-based questionnaire with 27 predominantly matrix questions on working conditions and motivation for working in this area was sent to pediatric hospitals throughout Germany. RESULTS: 165 doctors responded to the survey. The average age of the participants was 35.2 years. The average weekend work load reported by 79% of the respondents was 2 weekends per month, 70% of the study participants performed five to seven night shifts per month. 92% of the respondents stated that they basically enjoyed working in the intensive care unit (ICU). When asked to prioritize the working conditions, an appreciative working atmosphere in the team was named as priority 1 by 57%, followed by good guidance in the independent performance of interventions (25%) and good working conditions (19%). DISCUSSION: The survey result shows that neither aspects of work-life balance nor payments are the key issues selecting the interesting, but physically and emotionally demanding job in pediatric ICU. CONCLUSION: When evaluating vocational training in pediatric intensive care medicine, the immediate working atmosphere in the team with mutual respect and understanding and the guidance in training are more important than the general conditions.

Altitude exposure in pediatric pulmonary hypertension-are we ready for (flight) recommendations?

Patients with congenital heart disease are surviving further into adulthood and want to participate in multiple activities. This includes exposure to high altitude by air travel or recreational activities, such as hiking and skiing. However, at an altitude of about 2,500 m, the barometric environmental pressure is reduced and the partial pressure of inspired oxygen drops from 21% to 15% (hypobaric hypoxia). In physiologic response to high-altitude-related hypoxia, pulmonary vasoconstriction is induced within minutes of exposure followed by compensatory hyperventilation and increased cardiac output. Even in healthy children and adults, desaturation can be profound and lead to a significant rise in pulmonary pressure and resistance. Individuals with already increased pulmonary pressure may be placed at risk during high-altitude exposure, as compensatory mechanisms may be limited. Little is known about the physiological response and risk of developing clinically relevant events on altitude exposure in pediatric pulmonary hypertension (PAH). Current guidelines are, in the absence of clinical studies, mainly based on expert opinion. Today, healthcare professionals are increasingly faced with the question, how best to assess and advise on the safety of individuals with PAH planning air travel or an excursion to mountain areas. To fill the gap, this article summarises the current clinical knowledge on moderate to high altitude exposure in patients with different forms of pediatric PAH.

The ß2 agonist terbutaline specifically decreases pulmonary arterial pressure under normoxia and hypoxia via α adrenoceptor antagonism.

Pulmonary hypertension is a severe, incurable disease with a poor prognosis. Although treatment regimens have improved during the last 2 decades, current pharmacologic strategies are limited and focus on the modulation of only a few pathways related to endothelin, NO, and prostacyclin signaling. Therefore, the identification of novel molecular targets is urgently needed. We found that the ß2 adrenoceptor (AR) agonists terbutaline (TER) and salbutamol induced a dose-dependent vasorelaxation in large pulmonary arteries but not aortas of mouse. This effect was found to be independent of ß ARs and the endothelium but was determined by the type of the preconstrictor. Vasodilation by ß2 AR agonists occurred after pretreatment of pulmonary arteries with phenylephrine and serotonin, both agonists of α1 ARs, but was absent after preconstriction with the thromboxane analog U46619. These data indicated α-adrenolytic activity of ß2 AR agonists, which was confirmed by a right shift of the phenylephrine dose-response curve by TER. This effect was physiologically relevant because TER also relaxed small intrapulmonary arteries in lung slices and diminished pulmonary arterial pressure in an isolated perfused lung model under normoxia and hypoxia. Finally, TER applied as an aerosol also selectively decreased pulmonary arterial pressure without effects on systemic blood pressure and heart rate in mouse in vivo. Thus, ß2 AR agonists display α-adrenolytic activity in pulmonary arteries ex vivo and in vivo, and may provide a novel option to reduce pulmonary arterial pressure in pulmonary hypertension.-Neumann, V., Knies, R., Seidinger, A., Simon, A., Lorenz, K., Matthey, M., Breuer, J., Wenzel, D. The ß2 agonist terbutaline specifically decreases pulmonary arterial pressure under normoxia and hypoxia via α adrenoceptor antagonism.

beta(2)-adrenoceptor antagonist ICI 118,551 decreases pulmonary vascular tone in mice via a G(i/o) protein/nitric oxide-coupled pathway.

beta(2)-adrenoceptors are important modulators of vascular tone, particularly in the pulmonary circulation. Because neurohormonal activation occurs in pulmonary arterial hypertension, we have investigated the effect of different adrenergic vasoactive substances on tone regulation in large and small pulmonary arteries, as well as in systemic vessels of mice. We found that the beta(2)-adrenoceptor antagonist ICI 118,551 (ICI) evoked a decrease of vascular tone in large pulmonary arteries and reduced the sensitivity of pulmonary arteries toward different contracting agents, eg, norepinephrine, serotonin, or endothelin. ICI proved to act specifically on pulmonary vessels, because it shifted the dose-response curve of norepinephrine to the right in pulmonary arteries, whereas there was no effect in the aorta. Pharmacological experiments proved that the right shift of the norepinephrine dose-response curve by ICI was mediated via a beta(2)-adrenoceptor/G(i/o) protein-dependent pathway enhancing NO production in the endothelium; these results were corroborated in beta-adrenoceptor and endothelial NO synthase knockout mice where ICI had no effect. ICI increased vascular lumen diameter in lung sections and reduced pulmonary arterial pressure under normoxia and under hypoxia in the isolated perfused lung model. These effects were found to be physiologically relevant, because ICI specifically decreased pulmonary but not systemic blood pressure in vivo. Thus, the beta(2)-adrenoceptor antagonist ICI is a pulmonary arterial-specific vasorelaxant and, therefore, a potentially interesting novel therapeutic agent for the treatment of pulmonary arterial hypertension.