猪心源性休克模型中动脉血压和心输出量变化的比较。

IF 2.8 Q2 CRITICAL CARE MEDICINE
Laura Svanekjaer, Jeppe K P Larsen, Peter H Frederiksen, Louise Linde, Emilie Gregers, Nanna L J Udesen, Ole K Helgestad, Ann Banke, Lisette O Jensen, Jens F Lassen, Amalie L Povlsen, Henrik Schmidt, Jacob E Møller, Hanne B Ravn
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引用次数: 0

摘要

背景:低收缩压(SBP)是诊断由卒中量和心输出量(CO)减少引起的心源性休克(CS)的关键标准。在CS的发展中,压力和流量变化之间的时间相互作用尚未得到很好的描述。在大型动物模型中,我们评估了CS诱导过程中收缩压、一氧化碳和颈动脉血流的时间关系。方法:15头成年丹麦长白猪(平均体重71 kg)每3 min向左冠状动脉注射聚乙烯醇微球,诱导微血管阻塞。每次注射后,同时记录颈动脉脑室鞘和右颈内静脉肺动脉导管的CO、SBP和混合静脉饱和度(SvO2)。多普勒血流探头测量左颈动脉的血流。CS被定义为CO或SvO2比基线减少≥50%,或绝对SvO2。结果:CS发生在平均8(范围5至19)剂微球后。收缩压从99(±15)mmHg下降到74(±6)mmHg,相当于基线值的74(±13)%。CO从5.8(±0.7)L/min降至2.2(±1.3)L/min,相当于基线值的38(±23)%,SvO2从63(±7)%降至37(±7)%,相当于基线值的60(±13)%。在心率保持不变的情况下,CO的减少是由于卒中容量减少了43(±26)%。颈动脉血流量从285(±50)mL/min降至155(±56)mL/min,相当于基线值的54%。SvO2和CO的下降在收缩压降低之前,给予25%的栓子后,CO下降了24%,而收缩压不变。结论:在猪缺血性心肌损伤模型中,血流量和脑卒中量的减少先于收缩压的下降,提示在低灌注的情况下发生了压力保存。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Comparison of changes in arterial blood pressure and cardiac output during cardiogenic shock development in a porcine model.

Comparison of changes in arterial blood pressure and cardiac output during cardiogenic shock development in a porcine model.

Comparison of changes in arterial blood pressure and cardiac output during cardiogenic shock development in a porcine model.

Comparison of changes in arterial blood pressure and cardiac output during cardiogenic shock development in a porcine model.

Background: Low systolic blood pressure (SBP) is a key criterion for diagnosing cardiogenic shock (CS) caused by a reduction in stroke volume and cardiac output (CO). The temporal interaction between changes in pressure and flow has not been well described in the development of CS. In a large animal model, we assessed the temporal relationships of SBP, CO, and blood flow in the carotid artery during induction of CS.

Methods: Fifteen adult Danish landrace pigs (median weight 71 kg) underwent CS induction by stepwise injection of polyvinyl alcohol microspheres into the left main coronary artery every 3 min to induce microvascular obstruction. After each injection, CO, SBP, and mixed venous saturation (SvO2) were recorded simultaneously from a ventricle sheath in the carotid artery and a pulmonary artery catheter in the right internal jugular vein. A Doppler flow probe measured blood flow in the left carotid artery. CS was defined as a ≥ 50% reduction in CO or SvO2 from baseline, or absolute SvO2 < 30%.

Results: CS occurred after a mean of 8 (range 5 to 19) boluses of microspheres. SBP declined from 99 (± 15) mmHg to 74 (± 6) mmHg, equal to 74 (± 13)% of the baseline value. CO was reduced to 5.8 (± 0.7) L/min to 2.2 (± 1.3) L/min, equal to 38 (± 23)% and SvO2 from 63 (± 7)% to 37 (± 7)%, equal to 60 (± 13)% of baseline values. The decrease in CO was due to a reduction to 43 (± 26)% in stroke volume, as heart rate remained unchanged. The carotid artery blood flow was reduced from 285 (± 50) mL/min to 155 (± 56) mL/min, equal to 54% of baseline values. The decline in SvO2 and CO preceded a reduction in SBP, and after 25% of emboli were given, CO decreased by 24% while SBP was unchanged.

Conclusion: In a porcine model of ischemic myocardial injury, the decrease in blood flow and stroke volume preceded a decline in SBP, suggesting pressure preservation occurs in the presence of hypoperfusion.

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来源期刊
Intensive Care Medicine Experimental
Intensive Care Medicine Experimental CRITICAL CARE MEDICINE-
CiteScore
5.10
自引率
2.90%
发文量
48
审稿时长
13 weeks
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