Cavaliere F, Pennisi M A, La Mura F, Proietti R
Istituto di Anestesiologia e Rianimazione, Università Cattolica del Sacro Cuore, Roma.
Minerva Anestesiol. 2000 Sep;66(9):627-33.
Bicarbonate therapy for metabolic acidosis can cause tissue hypercapnia. We tested the hypothesis that CO2 retention is initially confined to blood and that tissue hypercapnia is consequent to blood hypercapnia.
prospective study.
general Intensive Care Unit in an University Hospital.
ten patients, aged 34-84, undergoing fixed mechanical ventilation for stroke, respiratory failure, polytrauma, or coma and presenting fairly stabilized circulatory condition were included in the study providing that definite exclusion criteria were absent. Sodium bicarbonate, 0.08, 0.17, and 0.25 mEq/kg, was infused in 5 minutes during stages A, B, and C. During each stage, before and after bicarbonate infusion, heart rate, arterial pressure, central venous pressure, and PetCO2 were registered and arterial and central venous haemogasanalysis were performed. CO2 output was measured during and after bicarbonate infusion and total CO2 output over basal values was calculated.
Heart rate, arterial pressure, central venous pressure did not change in any stage, while PetCO2 increased in all. Following bicarbonate infusion, pH increased more in venous than in arterial blood and was significantly affected by the amount of bicarbonate infused. In arterial blood both PCO2 and total CO2 content (TCO2) increased. In venous blood PCO2 did not change while TCO2 increased so that arterial-venous rl CO2 difference was unaffected. CO2 output changed in no patient but two during stage A, and increased by 0.54 +/- 0.16 mL/kg during stage B and by 1.18 +/- 0.26 mL/kg during stage C so that 14.5 +/- 4.3 and 21.2 +/- 4.7% of given bicarbonate was released as CO2 through the lungs. CO2 output increased after a latency that was significantly shorter during stage C (145 +/- 51 sec) than during stage B (226 +/- 53 sec).
Since arterial-venous TCO2 difference was unaffected and haemodynamic parameters were stable, the conclusion is drawn that CO2 and bicarbonate did not diffuse out of vascular compartment during this study. However CO2 and bicarbonate diffusion out of blood would have occurred if bicarbonate infusion had continued, because CO2 excess was released through the lungs after a latency and extended after the infusion. Consequently, tissue hypercapnia during bicarbonate infusion could probably be prevented by improving CO2 release through the lungs, i.e. by hyperventilating the patient.
代谢性酸中毒的碳酸氢盐治疗可导致组织高碳酸血症。我们检验了这样一个假设，即二氧化碳潴留最初局限于血液，而组织高碳酸血症是血液高碳酸血症的结果。
前瞻性研究。
一所大学医院的综合重症监护病房。
纳入10例年龄在34 - 84岁之间、因中风、呼吸衰竭、多发伤或昏迷接受固定机械通气且循环状况相当稳定的患者，前提是不存在明确的排除标准。在A、B、C三个阶段的5分钟内分别输注0.08、0.17和0.25 mEq/kg的碳酸氢钠。在每个阶段，在输注碳酸氢盐之前和之后，记录心率、动脉压、中心静脉压和呼气末二氧化碳分压（PetCO2），并进行动脉和中心静脉血气分析。在输注碳酸氢盐期间和之后测量二氧化碳排出量，并计算相对于基础值的总二氧化碳排出量。
在任何阶段，心率、动脉压、中心静脉压均未改变，而PetCO2在所有阶段均升高。输注碳酸氢盐后，静脉血pH值的升高幅度大于动脉血，且受输注碳酸氢盐量的显著影响。动脉血中二氧化碳分压（PCO2）和总二氧化碳含量（TCO2）均升高。静脉血中PCO2未改变，而TCO2升高，因此动静脉二氧化碳差值未受影响。在A阶段，除两名患者外，其他患者的二氧化碳排出量均未改变；在B阶段，二氧化碳排出量增加了0.54±0.16 mL/kg；在C阶段，增加了1.18±0.26 mL/kg，使得输注的碳酸氢盐中有14.5±4.3%和21.2±4.7%通过肺部以二氧化碳形式排出。二氧化碳排出量在延迟一段时间后增加，C阶段的延迟时间（145±51秒）明显短于B阶段（226±53秒）。
由于动静脉TCO2差值未受影响且血流动力学参数稳定，得出的结论是，在本研究期间，二氧化碳和碳酸氢盐未从血管腔室中扩散出来。然而，如果继续输注碳酸氢盐，二氧化碳和碳酸氢盐将会从血液中扩散出来，因为过量的二氧化碳在延迟一段时间后通过肺部排出，并在输注后持续排出。因此，在输注碳酸氢盐期间，通过改善肺部的二氧化碳排出，即让患者过度通气，可能预防组织高碳酸血症。
