CardiothoracicRight Ventricular Failure Resulting from Pressure Overload: Role of Intra-Aortic Balloon Counterpulsation and Vasopressor Therapy
Introduction
Sudden increases of right ventricular (RV) afterload result in acute right heart failure and are frequently observed in the adult or pediatric cardiac surgical population (i.e., heart transplantation, left-ventricular assist, postcardiotomy shock, sepsis) or after pulmonary embolism 1, 2. Several mechanisms have been hypothesized to account for the hemodynamic decompensation including decreased RV cardiac output (series circulatory connection) and altered RV-LV interactions mediated by pericardial constraint and leftward septal shift (ventricular interdependence) 3, 4. Together these changes lead to decreased LV filling, compromised LV contribution to RV performance, and subsequently low cardiac output 4, 5, 6. Ischemia has been demonstrated to be an important contributing factor for right heart failure in RV pressure overload (RVPO) 7, 8, 9, 10. RV ischemia has been attributed to systemic hypotension with decreased coronary driving pressure leading to inadequate coronary blood supply to meet the increased oxygen needs of the afterloaded RV 9, 10. In addition, coronary autoregulation fails to increase RV blood supply in severe pulmonary hypertension as right coronary vasomotor capacity is exhausted and increments in coronary blood flow through pressure-dependent mechanism is restricted due to hypotension 8, 10, 11. As a consequence, therapeutic strategies for pressure-induced RV failure are aimed towards restoring ventricular interactions and reversing RV ischemia. Experimentally, systemic hypertension after aortic constriction or vasopressors have been reported to optimize RV performance by maximizing ventricular interactions and increasing RV coronary driving pressure 5, 10. Conversely, others report no or even detrimental effects of systemic vasoconstriction for RV function during RVPO 12, 13, 14. More importantly, clinical application of these strategies is limited since relevant augmentation of coronary driving pressure with vasopressors may result in substantial increases of LV afterload and induce LV dysfunction 15, 16. In this context, intra-aortic balloon counterpulsation (IABP) seems to be a promising addition to systemic vasopressors as it unloads the LV and augments systemic and coronary driving pressure 17, 18. Supportive data for a stand-alone IABP therapy during RVPO arises from two reports 19, 20 that could demonstrate beneficial effects on cardiac output, but failed to clearly identify the underlying causes of their findings.
We tested in an acute model of RVPO whether IABP related augmentation of coronary perfusion pressure and presystolic LV unloading results in improved ventricular interactions and RV function in the presence of vasopressor-induced improvements of systemic and coronary perfusion pressure with phenylephrine. The effectiveness of this novel approach was analyzed using echocardiographic, systemic, and ventricular hemodynamic parameters and compared to IABP and phenylephrine treatment alone.
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Materials and Methods
All animals received humane treatment in compliance with the 1996 National Research Council Guide for the Care and Use of Laboratory Animals. Ten Yorkshire-Duroc pigs (39 ± 3 kg) were premedicated with ketamine hydrochloride (15 mg/kg, intramuscularly) and diazepam (0.5 mg/kg), and anesthesia was maintained with isoflurane 1%–2%. Bolus injections of fentanyl (5–10 mcg/kg) were used for analgesia, and pancuronium (0.1–0.2 mg/kg) was given for muscular relaxation. Respiratory support was started after
RVPO
Pulmonary artery constriction increased systolic RV pressure by ∼2-fold, and resulted in an elevation of RVPed (+66%; Table 1). LV filling was compromised with decreased LVPed (–25%) and accompanied by lower LVPsys (–27%) and LV peak (+)dPdt (-37%) compared with control. Hypotension with decreased diastolic AP resulted in subsequent lower RV (–30%) and LV CDP (–27%). RVPO lead to profound decreases of cardiac index (–51%) and SvO2 (–32%; P < 0.05 versus control).
Echocardiography confirmed RV
Discussion
This study determined the effects of a novel therapeutic approach consisting of IABP and systemic hypertension (phenylephrine) for the treatment of acute RVPO. We demonstrate that IABP alone failed to restore RV function and abnormal septal and ventricular interactions despite reversal of CDP to control values. Secondly, we confirmed that systemic hypertension with further increments in coronary driving pressures with phenylephrine resulted in significant RV decompression, reduction of TR, and
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