Adenosine as pulmonary vasodilator in ARDS

Background

Pulmonary hypertension plays a major role in the physiopathology of ARDS. Because some studies report a predictive value of increased pulmonary vascular resistances on mortality in patients with ARDS, treatment of this pulmonary hypertension seems to be justified. However, traditional intravenous vasodilators agents have both pulmonary and sistemics effects. Adenosine, a new agent, has been shown to have potent selective pulmonary vasodilator actions in patients with primary pulmonary hypertension when is infused directly in pulmonary artery.

Objectives

To assess the vasodilator pulmonary effects of adenosine and its consecuences on cardiac performance and gas exchange, in patients with ARDS-induced pulmonary hypertension.

Methods

Patients with ARDS admitted to the ICU were included in this prospective study. All of them received mechanical ventilation (PCV-IRV). Haemodynamic monitoring was made by Swan-Ganz catheter. Arterial pressure was monitored in an invasive mode and mixed venous saturation was recorded too. Cardiac output was measured with thermodilution method. Haemodynamic stability in the last 12 h regardless the use of inotropic drugs, a pO₂ ≥ 100 mmHg and a pH≥ 7.2, were goals to achieve before entering in the study. Variables not measured directly, were calculated with standar formulae. Transthoracic echocardiography was used to assess systolic and diastolic function of both ventricles, by calculating left ventricular ejection fraction (LVEF) and right ventricular shortening fraction (RVSF) in the assessment of systolic function and measuring maximal flow velocities of E and A waves in the case of diastolic function. Continuous intravenous infusion of adenosine was performed by a central venous line with increasing doses of 0.001, 0.01, 0.03 and 0.05 mg/kg per min. Haemodynamic and oxymetric parameters and echocardiographic measurements were recorded before the start of adenosine infusion and after each increase in the dose. Statistical analysis was made with ANOVA and Student's T tests, considering P ≤ 0.05 as significance level.

Conclusions

Adenosine decreases pulmonary hypertension in ARDS only in high doses, but producing systemic effects too, decreasing cardiac output and mean arterial pressure. Gas exchange is impaired because inhibiton of hypoxic pulmonary vasoconstriction. Diastolic function is improved but systolic one is impaired in both ventricles after the use of adenosine.

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