Estimation of cardiac output in patients with congestive heart failure by analysis of right ventricular pressure waveforms

<p>Abstract</p> <p>Background</p> <p>Cardiac output (CO) is an important determinant of the hemodynamic state in patients with congestive heart failure (CHF). We tested the hypothesis that CO can be estimated from the right ventricular (RV) pressure waveform in CHF patients using a pulse contour cardiac output algorithm that considers constant but patient specific RV outflow tract characteristic impedance.</p> <p>Method</p> <p>In 12 patients with CHF, breath-by-breath Fick CO and RV pressure waveforms were recorded utilizing an implantable hemodynamic monitor during a bicycle exercise protocol. These data were analyzed retrospectively to assess changes in characteristic impedance of the RV outflow tract during exercise. Four patients that were implanted with an implantable cardiac defibrillator (ICD) implementing the algorithm were studied prospectively. During a two staged sub-maximal bicycle exercise test conducted at 4 and 16 weeks of implant, COs measured by direct Fick technique and estimated by the ICD were recorded and compared.</p> <p>Results</p> <p>At rest the total pulmonary arterial resistance and the characteristic impedance were 675 ± 345 and 48 ± 18 dyn.s.cm^-5, respectively. During sub-maximal exercise, the total pulmonary arterial resistance decreased (Δ 91 ± 159 dyn.s.cm^-5, p < 0.05) but the characteristic impedance was unaffected (Δ 3 ± 9 dyn.s.cm^-5, NS). The algorithm derived cardiac output estimates correlated with Fick CO (7.6 ± 2.5 L/min, R²= 0.92) with a limit of agreement of 1.7 L/min and tracked changes in Fick CO (R²= 0.73).</p> <p>Conclusions</p> <p>The analysis of right ventricular pressure waveforms continuously recorded by an implantable hemodynamic monitor provides an estimate of CO and may prove useful in guiding treatment in patients with CHF.</p

Electrical modalities beyond pacing for the treatment of heart failure

In this review, we report on electrical modalities, which do not fit the definition of pacemaker, but increase cardiac performance either by direct application to the heart (e.g., post-extrasystolic potentiation or non-excitatory stimulation) or indirectly through activation of the nervous system (e.g., vagal or sympathetic activation). The physiological background of the possible mechanisms of these electrical modalities and their potential application to treat heart failure are discussed