Groupe Choc Contrat Avenir Inserm, U961, Faculte de Medecine, Nancy Universite, Nancy, France.
Anesthesiology. 2012 May;116(5):1083-91. doi: 10.1097/ALN.0b013e31824f9669.
Myocardial depression is a frequent event during septic shock and may mimic a cardiogenic shock state with decreased cardiac output. Nevertheless, data are scarce regarding the myocardial effects of vasopressors used to treat hypotension. In this study, the authors compared the effects of three commonly used vasopressors acting on different adrenergic receptors on myocardial function in a rodent model of septic shock, as explored with conductance catheter and positron emission tomography.
Septic shock was induced in rats by peritonitis. Eighteen hours after septic insult, vasopressors were titrated to increase mean arterial pressure by 20% compared with baseline values.
We observed that peritonitis was associated with arterial hypotension and systolodiastolic dysfunction. Norepinephrine and epinephrine improved mean arterial pressure, cardiac output, and preload recruitable stroke work, a load-independent measure of systolic function, as well as diastolic function and ventriculoarterial coupling. Heart rate, myocardial oxygen consumption, and arrhythmia incidence were furthermore increased in the epinephrine group. Conversely, phenylephrine, a peripheral α-agonist, exhibited deleterious effects on systolodiastolic function and ventriculoarterial coupling. Conductance catheter and positron emission tomography yielded identical results with regard to myocardial function evolution under vasopressor treatment.
Phenylephrine, a drug without β-1 effects, was associated with decreased ventricular performance and ventriculoarterial uncoupling, whereas epinephrine and norepinephrine improved global hemodynamics and myocardial function in severely hypokinetic and hypotensive experimental septic shock. Nevertheless, epinephrine was associated with increased myocardial oxygen consumption. Thus, norepinephrine appears to be a more reliable and safer strategy as a first-line therapy in this particular setting.
心肌抑制是感染性休克时常见的事件,可能会模仿心源性休克状态,导致心输出量降低。然而,关于用于治疗低血压的血管加压药对心肌的影响的数据很少。在这项研究中,作者使用心阻抗导管和正电子发射断层扫描比较了三种常用于治疗感染性休克的血管加压药对啮齿动物模型心肌功能的影响,这些药物作用于不同的肾上腺素能受体。
通过腹膜炎诱导感染性休克。在感染性损伤后 18 小时,通过滴定血管加压药将平均动脉压增加 20%,与基线值相比。
我们观察到腹膜炎与动脉低血压和收缩舒张功能障碍有关。去甲肾上腺素和肾上腺素改善了平均动脉压、心输出量和前负荷可诱导的工作,这是一种不依赖于负荷的收缩功能指标,以及舒张功能和心室血管耦联。肾上腺素组的心率、心肌耗氧量和心律失常发生率也增加。相反,苯肾上腺素,一种外周 α 激动剂,对收缩舒张功能和心室血管耦联有不良影响。心阻抗导管和正电子发射断层扫描在血管加压药治疗下心肌功能演变方面产生了相同的结果。
苯肾上腺素,一种没有 β1 作用的药物,与心室功能降低和心室血管解耦联有关,而肾上腺素和去甲肾上腺素改善了严重低动力和低血压的实验性感染性休克的整体血液动力学和心肌功能。然而,肾上腺素与心肌耗氧量增加有关。因此,去甲肾上腺素作为一线治疗在这种特殊情况下似乎是一种更可靠和更安全的策略。