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Increased Intrathoracic Impedance May Predict Adverse Events in LVAD Patients Carlo R. Bartoli, M.D., Ph.D,* Kimberly M. Vessels, R.N.,y and Kelly C. McCants, M.D.y *Division of Cardiovascular Surgery, University of Pennsylvania, Philadelphia, Pennsylvania; and yDivision of Cardiovascular Medicine, University of Louisville, Louisville, Kentucky ABSTRACT We describe a 36-year-old male with a HeartWare LVAD and a Medtronic Virtuoso DR pacemaker in whom increased intrathoracic impedance preceded suction events, low LVAD flows, symptoms of a heart failure exacerbation, and hospitalization. Measurement of intrathoracic impedance may identify fluid shifts prior to symptoms and predict adverse events in patients with an LVAD. doi: 10.1111/jocs.12191 (J Card
In patients with advanced heart failure, new pacemaker technology permits continuous outpatient measurement of intrathoracic impedance, an indicator of R interstitial fluid content. For example, OptiVol technology (Medtronic, Inc., Minneapolis, MN, USA) has been validated to predict heart failure exacerbations.1 Yet the utility of monitoring intrathoracic impedance in patients with an LVAD is unknown. We describe a patient in whom changes in intrathoracic impedance preceded suction events, low LVAD flows, symptoms of a heart failure exacerbation, and hospitalization. Intrathoracic impedance measurements may identify fluid shifts prior to symptoms and predict adverse events in LVAD patients. Patient Profile Institutional Review Board (IRB) approval was obtained through Jewish Hospital, Louisville Kentucky (IRB#11.0147). A 36-year-old white male with an eightyear history of nonischemic cardiomyopathy and a Virtuoso DR dual-chamber pacemaker (Medtronic, Inc.) underwent elective implantation of an HVAD continuous-flow LVAD (HeartWare Inc., Framingham, MA, USA) for destination therapy. The postoperative course was uneventful. Prior to discharge on postoperative day 13, the patient weighed 76 kg.
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Kelly C. McCants, M.D. Division of Cardiovascular Medicine Jewish Hospital 200 Abraham Flexner Way, Suite 1001 Louisville, KY 40202. E-mail: [email protected]
After 25 days of support, the patient was admitted for suction events, low LVAD flows, dyspnea, and lightheadedness from orthostatic hypotension. Interrogation of the LVAD controller demonstrated a nonpulsatile flow waveform with frequent suction events. Transthoracic echocardiography demonstrated complete left ventricular unloading without opening of the aortic valve. On readmission, the patient weighed 73 kg. The patient was given one liter of intravenous normal saline, and the LVAD speed was decreased. Suction events and low LVAD flows ceased. A repeat echocardiogram demonstrated good left-ventricular filling and intermittent opening of the aortic valve. Symptoms resolved, and the patient was discharged on hospitalday one. During admission, interrogation of the pacemaker revealed recent, large fluctuations in intrathoracic impedance (Fig. 1). Prior to LVAD implantation, baseline impedance was approximately 80 V. After LVAD implantation, impedance decreased from 80 to 55 V, likely from perioperative fluid accumulation with cardiopulmonary bypass. At discharge, impedance was 60 V. In the three weeks preceding admission, intrathoracic impedance progressively increased from 60 to 75 V. In parallel, the patient lost 3 kg. The relative increase in impedance and decrease in body weight indicated decreased interstitial fluid content and relative hypovolemia. As a result, intravascular volume depletion limited LVAD preload, and excessive left ventricular unloading produced suction events and low LVAD flows. Upon admission, intravascular volume repletion and adjustment of the LVAD settings corrected the
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BARTOLI, ET AL. INTRATHORACIC IMPEDANCE AND LVAD MANAGEMENT
Figure 1. A progressive increase in intrathoracic impedance preceded intravenous volume depletion and consequent left ventricular assist device (LVAD) dysfunction. Over the course of the three weeks prior to admission, intrathoracic impedance steadily increased from 60 to 75 V as body water content decreased. As a result, hypovolemia produced suction events, low LVAD flows, and hospitalization. Intravenous volume repletion and adjustment of the LVAD settings corrected the LVAD dysfunction.
LVAD dysfunction. After discharge, the patient maintained a new baseline intrathoracic impedance of 70 V. DISCUSSION We report the potential utility of intrathoracic impedance measurements in a patient with an LVAD. In this case study, increased intrathoracic impedance preceded intravascular volume depletion and dangerous LVAD dysfunction. The history and presentation of our patient suggests that early postoperative monitoring and remote surveillance of intrathoracic impedance may serve an adjunctive role in monitoring fluids and predicting adverse events in LVAD patients. Tissue impedance reflects the relative extracellular fluid content within a tissue of interest. Specifically, intrathoracic impedance quantifies the interstitial fluid content within the lungs. Recently, next generation pacemakers and automated implantable cardioverter defibrillators (AICDs) have the ability to continuously measure electrical impedance across the chest wall and indirectly quantify pulmonary interstitial fluid. Fluid accumulation in the lungs over weeks typically precedes an episode of overt heart failure decompensation.2 As such, some1 but not all3 clinical trials have validated this technology to predict impending volume overload and heart failure exacerbations. Yet intrathoracic impedance is not routinely measured in LVAD patients to optimize device settings or manage fluids. Importantly, intrathoracic impedance measurements are available in many LVAD patients. Most candidates for an LVAD have an AICD or pacemaker in situ prior to LVAD implantation. These patients are referred for mechanical circulatory support after they have received an AICD for high risk of sudden death or have failed cardiac resynchronization therapy.
Postoperative intrathoracic impedance data may assist to optimize settings during the programming of an LVAD. During cardiopulmonary bypass and the perioperative period, fluids accumulate in peripheral tissues. Postoperative mobilization of interstitial fluids may rapidly increase intravenous volume. If this occurs, new preload and afterload conditions may necessitate adjustment of LVAD settings. Routine intrathoracic impedance monitoring in the postoperative period may demonstrate these changes for timely intervention prior to discharge from the hospital. Indeed, in multiple patients (data not shown), we have observed the same rapid decrease and slow, progressive increase in thoracic impedance after the implantation of an LVAD as demonstrated in Figure 1. Remote surveillance of fluid status may also detect early signs of circulatory compromise prior to an adverse event and serve an ancillary role in outpatient management of patients with an LVAD. In ambulatory patients, many factors such as medicine noncompliance, dietary indiscretions, changes in the level of activity, and non-cardiovascular illness trigger fluid shifts. Signs of deterioration are often nonspecific and may not be recognized by the patient for early intervention. In heart failure patients, intrathoracic impedance may be monitored to predict impending volume overload. Conversely, in patients with an LVAD, the utility of intrathoracic impedance may be the opposite—to predict intravascular volume depletion. If LVAD settings are not adjusted appropriately, adverse events such as suction events and low LVAD flows may occur. As such, during outpatient therapy, intrathoracic impedance monitoring may objectively track fluid status independent of patient compliance and identify subtle changes in body fluid content before LVAD function is affected. Early identification of impending events and timely intervention may decrease hospitalizations and reduce the cost of LVAD support. Intrathoracic impedance measurements may also facilitate mechanistic studies of LVAD physiology. Evaluation of diurnal and nocturnal changes in intravascular volume may assist to elucidate the mechanisms of circadian hemodynamics with continuous-flow LVADs.4 This is the first report to demonstrate that intrathoracic impedance measurements may detect subtle fluid shifts in patients with an LVAD. Early postoperative monitoring and remote outpatient surveillance of intrathoracic impedance may predict volume depletion, impending adverse events, decrease hospitalizations, and reduce the cost of prolonged mechanical circulatory support. Further investigation is warranted. Acknowledgments: The authors acknowledge and thank the University of Louisville VAD coordinators for their support.
AUTHOR CONTRIBUTIONS C.R.B., K.C.M., and K.M.V. participated in the clinical management of the patient. C.R.B. drafted the manuscript. K.C.M. and K.M.V. edited the manuscript.
BARTOLI, ET AL. INTRATHORACIC IMPEDANCE AND LVAD MANAGEMENT
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