Schou H, Perez de Sá V, Larsson A, Roscher R, Kongstad L, Werner O
Department of Anesthesia and Intensive Care, University Hospital, Lund, Sweden.
Acta Anaesthesiol Scand. 1997 Feb;41(2):218-28. doi: 10.1111/j.1399-6576.1997.tb04669.x.
Hemodilution is used to reduce the need for allogenic blood transfusion. The aim of this study was to evaluate to what extent acute extreme normovolemic hemodilution affects the circulatory response to isoflurane.
Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to isoflurane at end-tidal concentrations of 0, 0.5, 1.0, 1.5 and 2%, before and after extreme normovolemic hemodilution (hematocrit 33 +/- 3% and 11 +/- 1%, respectively). Systemic and myocardial hemodynamics and oxygen delivery and consumption were measured.
At zero end-tidal isoflurane concentration, hemodilution caused an increase in cardiac output (from 157 +/- 12 to 227 +/- 39 ml kg min-1, P < 0.01) a decrease in systemic vascular resistance (from 39 +/- 7 to 18 +/- 5 mmHg.L-1.min-1, P < 0.01) a decrease in mean arterial blood pressure (MAP) (from 130 +/- 13 to 91 +/- 13 mmHg, P < 0.01) and a decrease in systemic oxygen delivery (from 23.1 +/- 2.7 to 11.8 +/- 1.7 ml.kg-1.min-1, P < 0.01). When the end-tidal isoflurane concentration was increased from 0 to 2% after hemodilution, cardiac output decreased by 86 +/- 37 ml.kg-1.min-1, as compared with 36 +/- 20 ml.kg-1.min-1 (P < 0.01) before hemodilution. Likewise, systemic vascular resistance decreased with increasing isoflurane concentrations; at 2%, the decrease was 7 +/- 4 mmHg.L-1.min-1 after hemodilution and 18 +/- 5 mmHg.L-1.min-1 before hemodilution (P < 0.01). At an end-tidal isoflurane concentration of 2%, MAP had decreased to 43 +/- 6 mmHg after hemodilution, and to 61 +/- 15 mmHg before hemodilution (P < 0.01). After hemodilution, isoflurane concentrations above 1% decreased systemic oxygen delivery enough to cause delivery-dependent oxygen consumption and hyperlactemia; and at 2% isoflurane, myocardial blood flow became insufficient, as indicated by myocardial lactate production.
isoflurane-induced cardiovascular depression had adverse effects on cardiac output and oxygen delivery during extreme hemodilution because: 1) The vasodilatory effect of isoflurane was insufficient to compensate for the myocardial depression, and also contributed to a critically low arterial blood pressure; 2) A decrease in cardiac output produced delivery-dependent oxygen consumption and hyperlactemia; and 3) A decrease in myocardial blood flow caused myocardial ischemia which may have exacerbated the myocardial depression.
血液稀释用于减少异体输血的需求。本研究的目的是评估急性极重度等容血液稀释在多大程度上影响对异氟烷的循环反应。
10只接受咪达唑仑 - 芬太尼 - 潘库溴铵麻醉的猪，在极重度等容血液稀释前后（血细胞比容分别为33±3%和11±1%），分别接受呼气末浓度为0、0.5、1.0、1.5和2%的异氟烷。测量全身和心肌血流动力学以及氧输送和消耗情况。
在呼气末异氟烷浓度为零时，血液稀释导致心输出量增加（从157±12增至227±39 ml·kg⁻¹·min⁻¹，P<0.01），全身血管阻力降低（从39±7降至18±5 mmHg·L⁻¹·min⁻¹，P<0.01），平均动脉血压（MAP）降低（从130±13降至91±13 mmHg，P<0.01），全身氧输送降低（从23.1±2.7降至11.8±1.7 ml·kg⁻¹·min⁻¹，P<0.01）。血液稀释后呼气末异氟烷浓度从0增至2%时，心输出量降低86±37 ml·kg⁻¹·min⁻¹，而血液稀释前为36±20 ml·kg⁻¹·min⁻¹（P<0.01）。同样，随着异氟烷浓度增加全身血管阻力降低；在2%时，血液稀释后降低7±4 mmHg·L⁻¹·min⁻¹，血液稀释前为18±5 mmHg·L⁻¹·min⁻¹（P<0.01）。在呼气末异氟烷浓度为2%时，血液稀释后MAP降至43±6 mmHg，血液稀释前为61±15 mmHg（P<0.01）。血液稀释后，异氟烷浓度高于1%时全身氧输送降低到足以导致氧消耗依赖于输送并出现高乳酸血症；在异氟烷浓度为2%时，心肌乳酸生成表明心肌血流不足。
异氟烷诱导的心血管抑制在极重度血液稀释期间对心输出量和氧输送产生不利影响，原因如下：1）异氟烷的血管舒张作用不足以补偿心肌抑制，且还导致动脉血压极低；2）心输出量降低产生氧消耗依赖于输送并出现高乳酸血症；3）心肌血流减少导致心肌缺血，这可能加剧了心肌抑制。
