[High altitude pulmonary edema misdiagnosed as pneumonia].

High altitude pulmonary edema (HAPE) is a relatively rare form of high altitude illness. However, without immediate treatment, HAPE is fatal. Furthermore, HAPE is characterized by non-specific signs and symptoms, and many clinical conditions may mimic it. In the present article, we report a case of HAPE misdiagnosed as pneumonia. We also discuss the issues of prevention and early treatment options in this illness.

[Diagnosis and treatment of pulmonary hypertension: from the point of view of 2017]. / Diagnostika i lechenie legochnykh gipertonii: vzgliad s pozitsii 2017 g.

Pulmonary hypertension (PH) is a group of diseases characterized by increased pulmonary vascular resistance (PVR). Regardless of its cause, PH leads to right ventricular failure and premature death. Recent advances in the diagnosis and treatment of PH have prompted the elaboration of new guidelines for the diagnosis and treatment of PH. This paper provides a brief overview of major achievements in diagnostic and treatment approaches in patients PH.

Sildenafil inhibits hypoxia-induced pulmonary hypertension.

BACKGROUND: This study investigated the effect of the phosphodiesterase 5 inhibitor sildenafil on the pulmonary vascular response to hypoxia in humans and mice. METHODS AND RESULTS: In a randomized, double-blind study, sildenafil 100 mg or placebo was given orally to 10 healthy volunteers 1 hour before breathing 11% O(2) for 30 minutes. Pulmonary artery pressure (PAP) was measured with an indwelling right heart catheter. The acute 56% increase in mean PAP produced by hypoxia during placebo treatment (mean PAP [mean+/-SD mm Hg]: normoxia 16.0+/-2.1 versus hypoxia 25.0+/-4.8) was almost abolished by sildenafil (normoxia 16.0+/-2.1 versus hypoxia 18.0+/-3.6), with no significant effect on systemic blood pressure. In the isolated perfused lung of wild-type and endothelial nitric oxide synthase (eNOS)-deficient mice, sildenafil markedly blunted acute hypoxic pulmonary vasoconstriction. Wild-type mice dosed orally with the drug (25 mg. kg(-1). d(-1)) throughout 3 weeks of exposure to hypoxia (10% O(2)) exhibited a significant reduction in right ventricular systolic pressure (placebo versus sildenafil: 43.3+/-9.9 versus 29.9+/-9.7 mm Hg, P<0.05) coupled with a small reduction in right ventricular hypertrophy and inhibition of pulmonary vascular remodeling. In eNOS mutant mice, sildenafil attenuated the increase in right ventricular systolic pressure but without a significant effect on right ventricular hypertrophy or vascular remodeling. CONCLUSIONS: Sildenafil attenuates hypoxia-induced pulmonary hypertension in humans and mice and offers a novel approach to the treatment of this condition. The eNOS-NO-cGMP pathway contributes to the response to sildenafil, but other biochemical sources of cGMP also play a role. Sildenafil has beneficial pulmonary hemodynamic effects even when eNOS activity is impaired.