Abstract 2643: Preservation of Left Ventricular Myocardial Distensibility Using a Novel Sodium-Hydrogen Exchanger Isoform-1 Inhibitor Markedly Enhances the Hemodynamic Efficacy of Chest Compression
Objective: We previously reported that inhibition of the sodium-hydrogen exchanger isoform-1 (NHE-1) preserves left ventricular (LV) myocardial distensibility, enabling higher LV preload to enhance the hemodynamic efficacy of chest compression. In the present study we examined the maximal hemodynamic benefit that could be obtained through this mechanism when maximal compression depth is used.
Methods: In two groups of 4 rats each, VF was electrically induced and left untreated for 10 mins. Closed-chest resuscitation was initiated and the depth of compression gradually increased to attain an aortic diastolic pressure between 26 and 28 mmHg at the end of 2 mins. Thereafter, the depth of compression was increased to a maximum of 17 mm. Defibrillation was attempted after 8 mins of chest compression. Resuscitated rats were monitored for 60 mins. Rats were randomized to receive a new NHE-1 inhibitor (BIX, 1-mg/kg) or vehicle control into the right atrium at the start of chest compression.
Results: Rats treated with BIX required less depth of compression during the initial 2 mins to attain the predetermined aortic diastolic pressure (Figure⇓). Rats treated with BIX demonstrated a markedly higher and stable coronary perfusion pressure (CPP) during chest compression whereas CPP continuously declined in control rats. The ratio between CPP and compression depth (an indirect measure of LV distensibility) was higher in BIX treated rats.
Conclusion: BIX improved the hemodynamic efficacy of chest compression by preserving left ventricular myocardial distensibility. Such effect, if translated clinically, could profoundly impact resuscitability given its critical dependency on CPP.