Huberfeld S I, Genovese J, Patel U, Scharf S M
Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New Hyde Park, NY, USA.
Crit Care Med. 1996 Dec;24(12):2027-34. doi: 10.1097/00003246-199612000-00016.
To test the hypothesis that increased cardiac output with continuous positive airway pressure (CPAP) leads to increased myocardial metabolic cost.
Prospective, repeated-measures, laboratory studies.
University-affiliated hospital animal research laboratory.
Eight sedated pigs that had been previously instrumented for collection of hemodynamic data.
Application of CPAP at 0, 5, 10, and 15 cm H2O and recovery under conditions of normal blood volume (normovolemia) and after administration of hetastarch 35 mL/kg (hypervolemia).
We measured mean arterial pressure, cardiac output, systemic vascular resistance index, the first derivative of the left ventricular pressure at a left ventricular pressure of 50 mm Hg, rate-pressure product, left ventricular tension-time index, stroke work index, myocardial pressure-myocardial segment length area, coronary artery blood flow and coronary vascular resistance, and myocardial oxygen consumption (four pigs). With normovolemia, cardiac output decreased with CPAP (4.9 +/- 1.2 L/min at CPAP of 0 cm H2O to 4.5 +/- 1.3 L/min at CPAP of 15 cm H2O, p < .005) and systemic vascular resistance index increased (2509 +/- 702 to 3095 +/- 1080 dyne.sec/cm5.m2, p < .01). With hypervolemia, cardiac output increased at low-level CPAP (5.7 +/- 1.4 L/min at CPAP of 0 cm H2O to 6.4 +/- 1.6 L/min at CPAP of 5 cm H2O, p < .05) and systemic vascular resistance index decreased (2412 +/- 552 to 2033 +/- 436 dyne.sec/cm5.m2, p < .01). There were no associated significant changes in myocardial oxygen consumption, or its major correlates when cardiac output increased with CPAP (hypervolemic conditions).
In normal pigs, there is no change in myocardial oxygen demand with CPAP, whatever the change in cardiac output. Thus, increased cardiac output with CPAP carries little extra metabolic cost. Increased cardiac output with low-level CPAP in hypervolemia is associated with systemic vasodilation.
检验持续气道正压通气(CPAP)使心输出量增加会导致心肌代谢成本增加这一假设。
前瞻性、重复测量的实验室研究。
大学附属医院动物研究实验室。
八只先前已植入仪器以收集血流动力学数据的镇静猪。
分别以0、5、10和15 cm H₂O的压力应用CPAP,并在正常血容量(血容量正常)条件下以及给予35 mL/kg羟乙基淀粉(高血容量)后进行恢复。
我们测量了平均动脉压、心输出量、全身血管阻力指数、左心室压力为50 mmHg时左心室压力的一阶导数、心率 - 血压乘积、左心室张力 - 时间指数、每搏功指数、心肌压力 - 心肌节段长度面积、冠状动脉血流量和冠状动脉血管阻力以及心肌耗氧量(四只猪)。在血容量正常时,随着CPAP的应用心输出量降低(CPAP为0 cm H₂O时为4.9±1.2 L/min,CPAP为15 cm H₂O时为4.5±1.3 L/min,p<.005),全身血管阻力指数升高(2509±702至3095±1080达因·秒/厘米⁵·平方米,p<.01)。在高血容量时,低水平CPAP下心输出量增加(CPAP为0 cm H₂O时为5.7±1.4 L/min,CPAP为5 cm H₂O时为6.4±1.6 L/min,p<.05),全身血管阻力指数降低(2412±552至2033±436达因·秒/厘米⁵·平方米,p<.01)。当CPAP使心输出量增加(高血容量情况)时,心肌耗氧量及其主要相关指标无显著变化。
在正常猪中,无论心输出量如何变化,CPAP均不会改变心肌需氧量。因此,CPAP使心输出量增加几乎不会带来额外的代谢成本。高血容量时低水平CPAP使心输出量增加与全身血管扩张有关。