Subclinical pulmonary edema in endurance athletes

Strenuous exercise may cause progressive and proportional haemodynamic overload damage to the alveolar membrane, even in athletes. Despite the high incidence of arterial desaturation reported in endurance athletes has been attributed, into other factors, also to the damage of the alveolar-capillary membrane this evidence is equivocal. Some studies demonstrated flood of the interstitial space and consequent increase in pulmonary water content, but most of them were able to show this through indirect signs of interstitial oedema. The present review illustrates the literature's data in favour or against pulmonary interstitial edema due to intense exercise in athletes

Noninvasive estimation of the lactate threshold in a subject with dissociated ventilatory and pulmonary gas exchange indices : a case report

This case report describes the responses to incremental work-rate exercise in a healthy subject (with normal pulmonary function), for whom the pulmonary gas exchange (V-slope) and ventilatory-related indexes (ie, ventilatory equivalents and end-tidal partial pressures for O2 and CO 2) uncharacteristically do not occur at the same metabolic rate. Based on the results of additional constant-work-rate exercise tests, we propose that in the (occasional) event of such a dissociation between the V-slope and ventilatory-related responses normally associated with the lactate threshold (\u3b8L), then the V-slope index should take priority as the \u3b8L estimator

Case report: Aspirin and concomitant drug choice in congestive heart failure

This case report provided by the authors of 'Comparing Losartan with Enalapril in Congestive Heart Failure' demonstrates a clinical approach to treating a patient with congestive heart failure in whom aspirin therapy is also indicated

Hemodynamic response to oral prenalterol in dilated decompensated cardiomyopathy as a result of cardiac and vascular effects

The initial antifailure efficacy of beta-adrenergic agonists is generally lost during prolonged treatment. The reasons are not fully understood. In 11 patients with advanced cardiac decompensation due to dilated cardiomyopathy, prenalterol, a selective beta1 adrenergic agonist, improved the left ventricular contractility after acute intravenous and during prolonged oral administration. However, after periods of treatment ranging from 2 to 18 weeks, blood pressure and systemic vascular resistance were raised in each patient. These changes resulted in an increase of the left ventricular afterload which was such as to overwhelm the effects of the enhanced contractility, and to extinguish the initial improvement of the cardiac function and of the clinical condition. Stimulation of the presynaptical beta-receptors facilitating norepinephrine release or of the renin secretion by this beta1 agonist, may be the causes of the systemic vasoconstriction and of the loss of effectiveness in the long run