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      Suction Due to Left Ventricular Assist: Implications for Device Control and Management

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          Abstract

          Left ventricular assist device (LVAD) overpumping is associated with hemolysis, thrombus release, and tissue damage at the pump inlet. However, the impact of LVAD suction on pulmonary circulatory function remains unknown. We investigated LVAD suction as induced by pulmonary artery banding and overpumping in experimental animals and in a computer model. In six sheep, a rotary LVAD was implanted. Before inducing suction, partial support (40-60% of cardiac output) was established and characterized by measuring pressures and flows. In the animals, pulmonary artery occlusion (PAOC) elicited LVAD suction (left ventricular pressure was from -10 to -20 mm Hg) within 5-10 heartbeats. During suction, aortic pressure dropped to 50% and LVAD flow decreased significantly. After releasing the occlusion (20 s), the collapsed state persisted for another 20 s. A similar trend was obtained by simulating PAOC in the computer model. Additional simulations showed that pulmonary vascular resistance (PVR), volume status, and right ventricular (RV) contractility are exponentially related to the persistence of collapse after a suction event. Even modest increases in predisposing factors (elevated PVR, RV dysfunction, hypovolemia) caused sustained hemodynamic collapse lasting in excess of 15 min. Both in selected animals and the computer model, comparable suction-induced collapse was obtained by increasing LVAD speed by about 33%. Attempted compensation by simply decreasing speed was not effective, but temporarily shutting down the LVAD caused rapid reversal of collapse. In conclusion, rotary LVAD suction causes unfavorable conditions for effective unloading. The use of pump interventions appears a promising tool to detect suction and to avoid the associated hemodynamic depression.

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          Most cited references25

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          Acute right ventricular failure--from pathophysiology to new treatments.

          The right ventricle (RV) provides sustained low-pressure perfusion of the pulmonary vasculature, but is sensitive to changes in loading conditions and intrinsic contractility. Factors that affect right ventricular preload, afterload or left ventricular function can adversely influence the functioning of the RV, causing ischaemia and right ventricular failure (RVF). As RVF progresses, a pronounced tricuspid regurgitation further decreases cardiac output and worsens organ congestion. This can degenerate into an irreversible vicious cycle. The effective diagnosis of RVF is optimally performed by a combination of techniques including echocardiography and catheterisation, which can also be used to monitor treatment efficacy. Treatment of RVF focuses on alleviating congestion, improving right ventricular contractility and right coronary artery perfusion and reducing right ventricular afterload. As part of the treatment, inhaled nitric oxide or prostacyclin effectively reduces afterload by vasodilating the pulmonary vasculature. Traditional positive inotropic drugs enhance contractility by increasing the intracellular calcium concentration and oxygen consumption of cardiac myocytes, while vasopressors such as norepinephrine increase arterial blood pressure, which improves cardiac perfusion but increases afterload. A new treatment, the calcium sensitiser, levosimendan, increases cardiac contractility without increasing myocardial oxygen demand, while preserving myocardial relaxation. Furthermore, it increases coronary perfusion and decreases afterload. Conversely, traditional treatments of circulatory failure, such as mechanical ventilation and volume loading, could be harmful in the case of RVF. This review outlines the pathophysiology, diagnosis and treatment of RVF, illustrated with clinical case studies.
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            The pulmonary manifestations of left heart failure.

            Determining whether a patient's symptoms are the result of heart or lung disease requires an understanding of the influence of pulmonary venous hypertension on lung function. Herein, we describe the effects of acute and chronic elevations of pulmonary venous pressure on the mechanical and gas-exchanging properties of the lung. The mechanisms responsible for various symptoms of congestive heart failure are described, and the significance of sleep-disordered breathing in patients with heart disease is considered. While the initial clinical evaluation of patients with dyspnea is imprecise, measurement of B-type natriuretic peptide levels may prove useful in this setting.
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              Normalization of high pulmonary vascular resistance with LVAD support in heart transplantation candidates.

              Pulmonary hypertension (PH) and elevated pulmonary vascular resistance (PVR) lead to poor outcome after heart transplantation due to postoperative failure of the non-conditioned right ventricle. The role of continuous flow left ventricular assist device (LVAD) support in the reduction of elevated PVR was evaluated in a series of clinical implants. Among 17 patients with terminal heart failure receiving a MicroMed DeBakey LVAD as bridge to transplant, there were six patients with pulmonary hypertension (mean systolic PAP 47 mmHg) and high PVR (398 dynes/cm5), previously not considered suitable for heart transplantation, who underwent serial right heart catheters during their LVAD support period. In these patients mean systolic pulmonary pressure dropped to 29 mmHg and PVR decreased to a mean 167 dynes/cm5 under LVAD support. Clinical improvement was significant in all patients. Four patients were successfully transplanted without major postoperative difficulties (mean duration 130 days support) and all are doing well to date. Post-transplant-PVR remained in the normal range in all transplanted patients. Elevated PVR and severe PH were both previously considered as contraindication for heart transplantation. A period of LVAD pumping leads to a progressive decrease of PVR and normalization of pulmonary pressures, making these patients amenable for heart transplantation. LVAD as bridge to heart transplantation is safe and highly beneficial for terminal heart failure patients with severe PH.
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                Author and article information

                Journal
                Artificial Organs
                Artificial Organs
                Wiley
                0160-564X
                1525-1594
                July 2007
                July 2007
                : 31
                : 7
                : 542-549
                Article
                10.1111/j.1525-1594.2007.00420.x
                17584479
                7623565f-f9b2-4927-8238-d3f02bf6d0b9
                © 2007

                http://doi.wiley.com/10.1002/tdm_license_1.1

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