By Eleanor McDermid, Senior medwireNews Reporter
Researchers have published a protocol for use of inotropic agents during initiation of epoprostenol therapy in patients with severe pulmonary arterial hypertension (PAH).
Satoshi Akagi (National Hospital Organization Okayama Medical Center, Japan) and colleagues report their experiences using dobutamine and dopamine for haemodynamic support of 46 patients undergoing epoprostenol therapy for World Health Organization functional class IV PAH.
The team initiated epoprostenol in 71 patients in total, 24 of whom also received dobutamine because of critically low mixed venous oxygen saturation (<60%) or cardiac index (<2.0 L/min per m2) or clinical evidence of right ventricular failure. A further eight patients received dopamine because of hypotension (systolic blood pressure <90 mmHg) or oliguria (<20 mL/hr). Fourteen patients received both treatments.
Because epoprostenol can affect the systemic circulation even more than the pulmonary circulation, these patients would be in danger of severe hypotension and haemodynamic collapse, explain the researchers, which is why they initiated a protocol for use of inotropic agents.
They administered dobutamine and dopamine, where indicated, at a starting dose of 3 μg/kg per minute and titrated the dose up when needed.
By the time of right heart catheter removal, haemodynamic parameters did not differ between patients who did and did not receive inotropic agents, with the exception of heart rate, which was significantly increased in the dobutamine group.
Inotropic agent support also had no adverse effect on survival during hospitalisation. In all, 62 patients survived and were discharged to receive home epoprostenol infusion, eight died and one underwent lung transplantation. Patients who died had an increased likelihood of receiving maximal doses of dobutamine and dopamine, relative to those who died. However, on multivariate analysis, only the need for treatment with noradrenaline (norepinephrine) and mechanical support were significantly associated with mortality.
“In our study, non-survivors during hospitalization had low cardiac output that required progressive increases in dobutamine and dopamine doses and treatment with norepinephrine and mechanical supports”, comment the researchers in the Annals of the American Thoracic Society. “These patients were severely decompensated at baseline.”
They stress: “It is important to initiate epoprostenol therapy before deterioration of the patient’s clinical condition because initiation of epoprostenol therapy is difficult in severely ill patients.”
Akagi et al conclude that their protocol for inotropic support “may be a reasonable approach” to protect against haemodynamic compromise caused by epoprostenol therapy. “Testing of this protocol is called for at other institutions to validate or further refine the approach presented here.”
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