Cerebral desaturation during cardiac arrest: Its relation to arrest duration and left ventricular pump function*
2009; Lippincott Williams & Wilkins; Volume: 37; Issue: 2 Linguagem: Inglês
10.1097/ccm.0b013e3181953d4c
ISSN1530-0293
AutoresKeso Skhirtladze, Beatrice Birkenberg, Bruno Mora, Andrea Moritz, Ismail Ince, Hendrik Jan Ankersmit, Barbara Szeinlechner, Martin Dworschak,
Tópico(s)Cardiac, Anesthesia and Surgical Outcomes
ResumoObjective: To determine the impact of brief periods of cardiac arrest (CA) on regional cerebral oxygen saturation (rSo2) in patients with low left ventricular ejection fraction (LVEF 50%), moderately impaired (LVEF 30%–50%), or severely reduced (LVEF <30%). Interventions: None. Measurements and Main Results: rSo2 was determined during threshold testing with concomitant induction of CA. In patients with LVEF <30%, mean baseline rSo2 (59%) was already below the lower range of normal despite normal arterial blood pressure, heart rate, and arterial oxygen saturation. rSo2 increased by 6% after 6 L/min oxygen insufflation (p < 0.05) and dropped again in each group after CA, reaching a nadir after successful defibrillation. Patients with LVEF 20% drop from baseline or rSo2 value <50%). rSo2 in patients with LVEF 30% (p < 0.05). There was a strong correlation between rSo2 values before CA and rSo2 nadir (p < 0.05). The drop in rSo2 was only moderately related to the brief CAs (p < 0.05). Conclusion: These findings demonstrate that severely compromised left ventricular pump function is associated with diminished rSo2. As these patients seem to be more susceptible to critical desaturations, they may be prone to severe tissue hypoxemia unless adequate oxygen delivery is reestablished rapidly. This may contribute to the poor neurologic outcome after successful resuscitation in patients with LVEF <30%.
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