NO VENTILATION CPR IN SYSTOLIC HEART FAILURE PATIENTS

No Ventilation CPR in Systolic Heart Failure Patients

ABSTRACT

Ventilatory effectiveness, right ventricular (RV) function, and secondary pulmonary hypertension are each prognostic indicators in patients with heart failure due to left ventricular systolic dysfunction, but the connections amidst these variables have not been comprehensively investigated. In this study, we hypothesized that inefficient ventilation throughout exercise, as defined by an abnormally vertical relationship between ventilation and carbon dioxide output (Ve/Vco2 slope), may be a marker of lesser pulmonary hypertension and RV dysfunction in heart failure. A cohort of patients with systolic heart failure (mean±SD age, 58±13 years; left ventricular ejection fraction, 0.27±0.05; peak oxygen uptake, 11.2±3.2 mL kg-1 min-1) underwent incremental cardiopulmonary exercise testing with simultaneous hemodynamic monitoring and first-pass radionuclide ventriculography before and after 12 weeks of treatment with sildenafil, a selective pulmonary vasodilator, or placebo. Ve/Vco2 gradient was positively associated to rest and workout pulmonary vascular resistance (R=0.39 and R=0.60, respectively) and rest pulmonary capillary wedge force (R=0.49, P<0.005 for all) and weakly indirectly related to peak workout RV ejection part (R=-0.29, P=0.03. Over the 12-week study time span, Ve/Vco2 slope dropped 8±3% (P=0.02) with sildenafil and was unchanged with placebo. Changes in Ve/Vco2 slope correlated with changes in exercise pulmonary vascular resistance (R=0.69, P<0.001) and rest and exercise RV ejection fraction (R=-0.58 and -0.40, respectively, both P<0.05). In patients with systolic heart failure and lesser pulmonary hypertension, ventilatory efficiency is closely associated to RV function and pulmonary vascular pitch throughout exercise.

No Ventilation CPR in Systolic Heart Failure Patients

Introduction

The relationship between minute ventilation and the rate of CO2 elimination during incremental exercise (Ve/VCO2 slope) is a noninvasive, reproducible measurement that is strongly related to mortality and the need for cardiovascular hospitalization in heart failure (HF) patients.1-5 However, the pathophysiologic mechanisms underlying impaired ventilatory efficiency are incompletely understood.

Clinical Perspective

According to the alveolar ventilation equation, Ve/VCO2 is determined by 2 variables: dead space ventilation relative to tidal volume (Vd/Vt) and arterial Paco2.6 In patients with HF, inefficient ventilation (as indicated by high Ve/VCO2 slope) has been ascribed to the increased ventilation required to overcome a large dead space and an increased central drive to ventilation, which results in lowering of arterial partial pressure of carbon dioxide (Paco2).6,7 Although Vd/Vt is higher in patients with worsening HF, there are conflicting reports as to the degree to which increased ventilatory drive (independent of higher dead space fraction) lowers Paco2 in patients with HF.8,9 High Vd/Vt in the absence of concomitant primary lung disease reflects ventilation-perfusion (V/Q) mismatch characteristic of pulmonary hypertension (PH).

Methods

Study Design

Patients mentioned to the Massachusetts General Hospital Heart Failure Center 18 years of age or older with left ventricular ejection part (LVEF) <0.40, lesser PH (mean pulmonary arterial force >25 mm Hg), and New York Heart Association class II to IV chronic HF regardless of standard treatment were eligible for study, as previously described.20 topics were randomized to an primary dose of 25 mg of sildenafil or placebo administered 3 times every day, ...