Department of Cardiovascular, Neural and Metabolic Sciences, Istituto Auxologico Italiano IRCCS, Ospedale San Luca, Milan, Italy.
Department of Management, Information and Production Engineering, University of Bergamo, Dalmine (BG), Italy.
Eur J Heart Fail. 2020 Dec;22(12):2228-2237. doi: 10.1002/ejhf.2058. Epub 2020 Dec 7.
Interstitial pneumonia due to coronavirus disease 2019 (COVID-19) is often complicated by severe respiratory failure. In addition to reduced lung compliance and ventilation/perfusion mismatch, a blunted hypoxic pulmonary vasoconstriction has been hypothesized, that could explain part of the peculiar pathophysiology of the COVID-19 cardiorespiratory syndrome. However, no invasive haemodynamic characterization of COVID-19 patients has been reported so far.
Twenty-one mechanically-ventilated COVID-19 patients underwent right heart catheterization. Their data were compared both with those obtained from non-mechanically ventilated paired control subjects matched for age, sex and body mass index, and with pooled data of 1937 patients with 'typical' acute respiratory distress syndrome (ARDS) from a systematic literature review. Cardiac index was higher in COVID-19 patients than in controls [3.8 (2.7-4.5) vs. 2.4 (2.1-2.8) L/min/m , P < 0.001], but slightly lower than in ARDS patients (P = 0.024). Intrapulmonary shunt and lung compliance were inversely related in COVID-19 patients (r = -0.57, P = 0.011) and did not differ from ARDS patients. Despite this, pulmonary vascular resistance of COVID-19 patients was normal, similar to that of control subjects [1.6 (1.1-2.5) vs. 1.6 (0.9-2.0) WU, P = 0.343], and lower than reported in ARDS patients (P < 0.01). Pulmonary hypertension was present in 76% of COVID-19 patients and in 19% of control subjects (P < 0.001), and it was always post-capillary. Pulmonary artery wedge pressure was higher in COVID-19 than in ARDS patients, and inversely related to lung compliance (r = -0.46, P = 0.038).
The haemodynamic profile of COVID-19 patients needing mechanical ventilation is characterized by combined cardiopulmonary alterations. Low pulmonary vascular resistance, coherent with a blunted hypoxic vasoconstriction, is associated with high cardiac output and post-capillary pulmonary hypertension, that could eventually contribute to lung stiffness and promote a vicious circle between the lung and the heart.
由 2019 年冠状病毒病(COVID-19)引起的间质性肺炎常伴有严重的呼吸衰竭。除了肺顺应性降低和通气/血流不匹配外,还假设存在缺氧性肺血管收缩减弱,这可以部分解释 COVID-19 心肺综合征的特殊病理生理学。然而,迄今为止尚未报道对 COVID-19 患者进行有创血流动力学特征描述。
21 名需要机械通气的 COVID-19 患者接受了右心导管检查。将他们的数据与非机械通气配对的对照组进行比较,对照组按年龄、性别和体重指数匹配,并与系统文献综述中 1937 名“典型”急性呼吸窘迫综合征(ARDS)患者的数据进行了汇总。COVID-19 患者的心指数高于对照组[3.8(2.7-4.5)比 2.4(2.1-2.8)L/min/m 2 ,P<0.001],但略低于 ARDS 患者(P=0.024)。COVID-19 患者的肺内分流和肺顺应性呈负相关(r=-0.57,P=0.011),与 ARDS 患者无差异。尽管如此,COVID-19 患者的肺血管阻力正常,与对照组相似[1.6(1.1-2.5)比 1.6(0.9-2.0)WU,P=0.343],且低于 ARDS 患者(P<0.01)。76%的 COVID-19 患者和 19%的对照组患者存在肺动脉高压(P<0.001),且均为毛细血管后高压。COVID-19 患者的肺动脉楔压高于 ARDS 患者,与肺顺应性呈负相关(r=-0.46,P=0.038)。
需要机械通气的 COVID-19 患者的血流动力学特征表现为心肺合并改变。低肺血管阻力与缺氧性血管收缩减弱一致,与心输出量高和毛细血管后肺动脉高压相关,这可能最终导致肺僵硬,并促进肺与心脏之间的恶性循环。