Had a pt who was admitted for septic shock due to PNA. Initial ScVo2 was 89% and crept up to as high as 94%. Pt was on levo maxed at 30 and SBP was sustaining above 90 (goal SBP > 90). According to the MD, he wanted the pt to be on both levo & vasopressin even though levo in itself was sustaining pt's blood pressure.
Since we were using pressors on this pt, that may have been a contributing factor for why the pt's ScVo2 was high... since the body isn't able to properly utilize the O2. Just trying to get a rationale for why the MD prefers to have two pressors (btw, we're talking about a very potent pressor - Vaso) instead of just leaving the pt on levo.
Although this pt's ScvO2 was really high, lactate trended down after about 4L bolus. Is this because the bolus helped push O2 to the tissues? I know that lactate is a byproduct of anaerobic metabolism, but what exactly normalizes lactate?
Also, is So2 (on an i-STAT) the same as SaO2?
Thanks in advance for your help.
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Had a pt who was admitted for septic shock due to PNA. Initial ScVo2 was 89% and crept up to as high as 94%. Pt was on levo maxed at 30 and SBP was sustaining above 90 (goal SBP > 90). According to the MD, he wanted the pt to be on both levo & vasopressin even though levo in itself was sustaining pt's blood pressure.
Since we were using pressors on this pt, that may have been a contributing factor for why the pt's ScVo2 was high... since the body isn't able to properly utilize the O2. Just trying to get a rationale for why the MD prefers to have two pressors (btw, we're talking about a very potent pressor - Vaso) instead of just leaving the pt on levo.
Although this pt's ScvO2 was really high, lactate trended down after about 4L bolus. Is this because the bolus helped push O2 to the tissues? I know that lactate is a byproduct of anaerobic metabolism, but what exactly normalizes lactate?
Also, is So2 (on an i-STAT) the same as SaO2?
Thanks in advance for your help.