Department of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.
Division of Cardiovascular Surgery, Department of Surgery, Cathay General Hospital, Taipei, Taiwan.
Physiol Rep. 2022 May;10(10):e15136. doi: 10.14814/phy2.15136.
Pulmonary arterial hypertension (PAH) increases right ventricular (RV) workload and decreases myocardial oxygen reserve, eventually leading to poor cardiac output. This study created and assessed a novel model of RV work output based on RV hemodynamics and oxygen supply, allowing new insight into causal mechanisms of RV dysfunction.
The RV function model was built upon an earlier, left ventricular model and further adjusted for more accurate clinical use. The model assumes that RV total power output (1) is the sum of isovolumic and stroke power and (2) is linearly related to its right coronary artery oxygen supply. Thus, when right coronary artery flow is limited or isovolumic power is elevated, less energy is available for producing cardiac output. The original and adjusted models were validated via data from patients with idiopathic PAH (n = 14) and large animals (n = 6) that underwent acute pulmonary banding with or without hypoxia.
Both models demonstrated strong, significant correlations between RV oxygen consumption rate and RV total power output for PAH patients (original model, R = 0.66; adjusted model, R = 0.78) and sheep (original, R = 0.85; adjusted, R = 0.86). Furthermore, the models demonstrate a significant inverse relationship between required oxygen consumption and RV efficiency (stroke power/total power) (p < 0.001). Lastly, higher NYHA class was indicative of lower RV efficiency and higher oxygen consumption (p = 0.013).
Right ventricular total power output can be accurately estimated directly from pulmonary hemodynamics and right coronary perfusion during PAH. This model highlights the increased vulnerability of PAH patients with compromised right coronary flow coupled with high afterload.
肺动脉高压 (PAH) 增加右心室 (RV) 的工作量并降低心肌氧储备，最终导致心输出量降低。本研究创建并评估了一种基于 RV 血液动力学和氧供应的 RV 工作输出新模型，为 RV 功能障碍的因果机制提供了新的见解。
RV 功能模型建立在早期的左心室模型基础上，并进一步进行了调整，以更准确地用于临床。该模型假设 RV 总功率输出 (1) 是等容和射血功率的总和，(2) 与右冠状动脉氧供应呈线性相关。因此，当右冠状动脉流量受限或等容功率升高时，产生心输出量的能量就会减少。原始和调整后的模型通过特发性 PAH 患者 (n = 14) 和大型动物 (n = 6) 的数据进行了验证，这些患者或动物经历了急性肺动脉结扎术，并伴有或不伴有缺氧。
两个模型都显示了 PAH 患者 (原始模型，R = 0.66；调整模型，R = 0.78) 和绵羊 (原始模型，R = 0.85；调整模型，R = 0.86) 的 RV 耗氧量与 RV 总功率输出之间具有很强的显著相关性。此外，这些模型还表明，所需的耗氧量与 RV 效率 (射血功率/总功率) 之间存在显著的反比关系 (p < 0.001)。最后，较高的 NYHA 分级表明 RV 效率较低且耗氧量较高 (p = 0.013)。
PAH 期间可以直接从肺血液动力学和右冠状动脉灌注准确估计 RV 总功率输出。该模型强调了与高后负荷相关的右冠状动脉流量受损的 PAH 患者的脆弱性增加。
