Permissive hypercapnia is a well-accepted ventilator strategy for the management of acute respiratory distress syndrome as well as other causes of respiratory failure, such as the respiratory distress syndrome seen in premature infants. Multiple studies have demonstrated that both myocardial contractility and systemic vascular resistance (SVR) decrease with hypercapnic acidosis, the ultimate effect being that cardiac function is maintained or even augmented. The effects of hypercapnic acidosis on cardiac function in the preterm infant have not been elucidated. In a prospective observational study, published in the May issue of The Journal of Pediatrics, the authors analyzed paired blood gases and echocardiograms from 29 hemodynamically stable preterm infants at 30 weeks’ gestation or less.
Samples were taken within the first two weeks of life, either during the transitional period (days 1-3) or post-transitional period (days 4-14). In all, there were 103 paired blood gases and echocardiograms from 21 subjects in the transitional period and 44 paired studies from 15 subjects in the post-transitional period. Each echocardiographic examination included measurements for shortening fraction (which is a load-dependent measure of contractility), stress-velocity index (which is a load-independent measure of contractility), left and right ventricular output, assessment of the ductus arteriosus, myocardial performance index, and SVR.
The results of the study demonstrated differences in the way the older infants responded to acidosis and hypercapnia. During the transitional period, pH and Paco2 had no effect on any of the hemodynamic measures, including shortening fraction, stress velocity index, and SVR. However, during the post-transitional period, the infants’ hemodynamics resembled those seen in adult patients. In this set of subjects, SVR dropped as the infants became more acidotic and had higher Pco2 levels. Unlike in the adult population, no relationship was demonstrated between the shortening fraction and stress velocity index and pH or Pco2.
This study has some limitations. Echocardiography in itself is limited in its ability to assess SVR, and the authors assumed a right atrial pressure of 4 mm HG in performing the calculations. Also, as the authors noted, distribution of subjects in the two groups was unbalanced. Finally, all subjects were hemodynamically stable, so the results may not apply to infants in shock.
Importantly, the authors raise a question that is clinically relevant, as it is still common to have buffers rapidly administered to infants who are acidotic and have myocardial dysfunction. This study would suggest that, other than providing more fluid, this therapy is not warranted. In conclusion, more studies are needed to demonstrate the relationship between acidosis (both metabolic and respiratory) and hemodynamics in children.
This Concise Critical Appraisal is authored by SCCM member Daniel E. Sloniewsky, MD. Each installment highlights journal articles most relevant to the critical care practitioner.