This study establishes that residual leaning of only 1.8 kg and 3.6 kg (approximately 10% and 20% of the force of the chest compressions) can substantially decrease CI and MBF during CPR. Surprisingly, the hemodynamic effects of 10% and 20% residual lean were similar, suggesting that the hemodynamic effects of leaning were primarily the result of the lack of full chest recoil. Furthermore, this study demonstrates that CI and MBF progressively decrease over time during prolonged CPR. Nevertheless, removal of leaning appeared to improve hemodynamics even after 16 mins of CPR.
The effects of leaning were demonstrable throughout 18 mins of CPR both during the first 9 mins (early) and the last 9 mins (later) (; ). For example, during the first 9 mins of CPR, the right atrial end-diastolic pressure increased from 9 ± 1 mm Hg with no lean to 11 ± 1 mm Hg and 13 ± 1 mm Hg with 10% and 20% lean, respectively, presumably because of transthoracic transmission of the leaning weight to the venous system. These higher venous pressures resulted in lower coronary perfusion pressure and the concomitant substantial decreases in MBF from 39 ± 7 mL · 100 g–1 · min–1 with no lean to 30 ± 10 mm Hg with 10% lean and 26 ± 10 mm Hg with 20% lean. In addition, the CI decreased from 1.9 ± 0.3 L · min–1 · M–2 with no lean to 1.2 ± 0.2 L · min–1 · M–2 with 10% lean and 1.0 ± 0.1 L · min–1 · M–2 with 20% lean. Interestingly, these seemingly modest changes in vascular pressures were associated with substantial changes in blood flows during the low-flow hemodynamic state of CPR. Although both 10% and 20% lean resulted in significantly different hemodynamics during CPR compared with no lean, they were not demonstrably different from one another. Both 10% and 20% leaning prevented full chest recoil and presumably impaired the generation of negative intrathoracic pressure, thereby limiting venous return and cardiac output. In this study, inhibiting the generation of negative intrathoracic pressure that would have been attained with full chest recoil was apparently a more important factor than the relative amount of leaning. Importantly, the adverse hemodynamic effects of 10% and 20% leaning remained significant after controlling for the expected hemodynamic deterioration during prolonged CPR ().
The American Heart Association Guidelines for Emergency Cardiovascular Care and Cardiopulmonary Resuscitation recommend target values for selected CPR parameters to optimize the effectiveness of CPR (1
). In the 2005 Guidelines, complete release of sternal pressure between chest compressions is specifically recommended with the intent to maximize venous return by allowing full chest recoil (1
). The 2005 Guidelines highlight data from Aufderheide et al (3
) showing that residual and continuous pressure on the chest wall was demonstrable during the decompression phase of CPR at some time in six of 13 patients during emergency medical services-provided out-of-hospital resuscitative efforts. In other data collected before 2005, Tomlinson et al (19
) documented that rescuers frequently do not allow full chest recoil. They showed that the average residual force, or “lean,” during adult out-of-hospital CPR was 1.7 ± 1.0 kg, corresponding to an average residual depth of 3 ± 2 mm. Interestingly, that average residual lean was quite similar to the 1.8-kg lean in our piglet investigation that corresponded to 10% of the force required to maintain 85 mm Hg aortic compression pressures. Recently, Niles et al (4
) showed that residual leaning of 2.5 kg was demonstrable in 50% of inhospital chest compressions for children 8 to 18 yrs old when automated feedback was not provided.
Yannopoulos et al (20
) have demonstrated that incomplete chest wall recoil during the decompression phase of CPR in adult pigs can increase endotracheal and right atrial pressure as well as decrease systolic, diastolic, and mean aortic pressures and coronary and cerebral perfusion pressures. In their model, CPR without “lean” was provided by a pneumatically driven automatic piston device compressing the chest wall 25% of the anteroposterior diameter. Residual lean was added by reducing the decompression distance to 75% of its full excursion in the decompression phase. These authors acknowledged that their definition of incomplete chest wall decompression (i.e., residual “leaning”) was an important limitation of their study because the decreases in hemodynamics may have resulted from the 25% decreased stroke length with their chest compressions and concomitant decrease in force of compressions rather than the residual lean per se
. We therefore chose to target the compression effort to attain aortic systolic pressures of 80–90 mm Hg during CPR rather than specifically limiting the force or depth of compressions. Furthermore, they reported the effect of reduced decompression distance only on hemodynamic pressures and not on blood flows. Our swine investigation is the first to specifically address the effects of residual leaning force on CPR hemodynamics without the confounding issue of a priori
prescriptive decreases in the amount of compression depth/force. More importantly, our investigation is the first to demonstrate that residual chest wall leaning decreases myocardial and systemic blood flows during CPR.
Novel methods and technology to monitor CPR quality have been recently developed that allow the quantification of the thoracic response to chest compressions. Specifically, a load cell and accelerometer sensor package has been integrated into a clinical monitor/defibrillator to track chest compression and applied force during CPR (21
). The sensor is interposed between the palms of the hands of the person administering CPR and the sternum of the patient. The accelerometer signal is processed with a double-integration algorithm, yielding deflection. These devices can measure and provide feedback on the rate, depth, force, and sternal pressure release during CPR. This automated directive and corrective feedback can improve the quality of CPR delivered during training and during actual CPR delivery (6
). Thus, the technology exists to provide feedback to providers when they are “leaning” on the chest during CPR.
There were several limitations with this model. This animal study used healthy young piglets, and the quality of CPR was excellent. The effects of residual leaning during CPR in sick children or when poor-quality CPR is administered may yield different results. Additional studies in humans are needed to evaluate the effects of residual leaning force on intrathoracic pressure, vascular pressures, venous return to the heart, and coronary and cerebral perfusion. In this experiment, hemodynamic parameters changed over time, consistent with previously well-documented changes in vascular pressures and blood flows with prolonged CPR (15
). Therefore, we accounted for this potentially confounding factor a priori
with a linear mixed-effect regression model. We evaluated five such models adjusting this time effect, and the model with the best fit was the log of time model used. This log model operates like an exponential decay (i.e., performance declines over time but at a decreasing rate).