International journal of cardiology · 2018
Midazolam addition to analgosedation for pulmonary vein isolation may increase risk of hypercapnia and acidosis.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Kaess Bernhard M, Feurich Florian, Bürkle Gerd, Ehrlich Joachim R
Аннотация
BACKGROUND: Pulmonary vein isolation (PVI) is generally performed under analgosedation, but sedation protocols vary and no optimal protocol has been defined. We investigated procedural, respiratory and hemodynamic parameters in patients undergoing PVI using analgosedation either with or without midazolam.
METHODS: In a prospective observational study, we compared n = 43 consecutive patients (54% male, mean age 62 years) undergoing PVI using analgosedation either with or without midazolam added to propofol and fentanyl. A priori defined outcome measures were propofol dose, hypotension (systolic blood pressure <100 mm Hg or >30 mm Hg drop from baseline), acidosis (pH < 7.30), hypercapnia (pC02 > 55 mm Hg) and hypoxemia (transdermal oxygen saturation < 90%).
RESULTS: Patients in the midazolam group (n = 22) received a mean dose of 3 ± 1.5 mg midazolam and required less propofol than those in the no-midazolam group (n = 21, 473 ± 189 mg vs. 618 ± 219 mg, p = .03). Incidence of hypotension did not differ between groups (54.5% vs. 61.9%, p = .63). Acidosis was more frequent in the midazolam group (63.6% vs. 28.6%, p = .03), as was hypercapnia (50% vs. 14.3%, p = .03) while occurrence of hypoxemia did not differ between groups (22.7 vs. 33.3%, p = .5).
CONCLUSION: Patients receiving midazolam had a more than doubled risk of respiratory depression as mirrored by hypercapnia and acidosis, but not hypoxemia. These observations may help in choosing an analgosedation and monitoring protocol for PVI.
METHODS: In a prospective observational study, we compared n = 43 consecutive patients (54% male, mean age 62 years) undergoing PVI using analgosedation either with or without midazolam added to propofol and fentanyl. A priori defined outcome measures were propofol dose, hypotension (systolic blood pressure <100 mm Hg or >30 mm Hg drop from baseline), acidosis (pH < 7.30), hypercapnia (pC02 > 55 mm Hg) and hypoxemia (transdermal oxygen saturation < 90%).
RESULTS: Patients in the midazolam group (n = 22) received a mean dose of 3 ± 1.5 mg midazolam and required less propofol than those in the no-midazolam group (n = 21, 473 ± 189 mg vs. 618 ± 219 mg, p = .03). Incidence of hypotension did not differ between groups (54.5% vs. 61.9%, p = .63). Acidosis was more frequent in the midazolam group (63.6% vs. 28.6%, p = .03), as was hypercapnia (50% vs. 14.3%, p = .03) while occurrence of hypoxemia did not differ between groups (22.7 vs. 33.3%, p = .5).
CONCLUSION: Patients receiving midazolam had a more than doubled risk of respiratory depression as mirrored by hypercapnia and acidosis, but not hypoxemia. These observations may help in choosing an analgosedation and monitoring protocol for PVI.