Percutaneous Right Ventricular Assist via the Internal Jugular Vein in Cardiogenic Shock Complicating (FULL TITLE BELOW)

ABSTRACT: Management of right heart failure in acute myocardial infarction (AMI) includes emergent reperfusion of the infarct-related artery, fluid resuscitation, vasopressor and inotropic support, and trans-venous pacing in the presence of high-grade atrio-ventricular conduction block. Historically, mechanical support for right ventricular failure after an AMI has been limited to intra-aortic balloon pump (IABP) counterpulsation or surgically placed ventricular assist devices. Recently, a percutaneous right ventricular assist device (pRVAD, TandemHeart; CardiacAssist Inc., Pittsburgh, Pennsylvania) has offered an intermediate alternative for patients with refractory right heart failure in the setting of AMI. We describe a novel approach to pRVAD implantation via the right internal jugular vein in the setting of cardiogenic shock secondary to an acute inferior myocardial infarction.

J INVASIVE CARDIOL 2010;22:E23–E26

Key words: acute coronary syndrome, right ventricle, cardiomyopathy

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The incidence of cardiogenic shock following acute myocardial infarction (AMI) is 8.6%.¹ While, the right ventricle (RV) is involved in greater than one-third of all inferior myocardial infarctions, right ventricular myocardial infarction (RVMI) accounts for 2.8% of patients presenting with cardiogenic shock in the setting of AMI.² Mortality after RVMI approaches 60%; equal to that of shock due to MI-associated left ventricular (LV) failure.³ Management of right heart failure in AMI includes emergent reperfusion of the infarct-related artery, fluid resuscitation, vasopressor and inotropic support, and trans-venous pacing in the setting of high-grade atrio-ventricular conduction block.⁴ Historically, mechanical support for RV infarction has been limited to intra-aortic balloon pump (IABP) counterpulsation or surgically placed ventricular assist devices. Recently, a percutaneous RV assist device (pRVAD, TandemHeart; CardiacAssist Inc., Pittsburgh, Pennsylvania) has offered an intermediate alternative for patients with refractory right heart failure in the setting of AMI. The standard approach to pRVAD cannulation is via the femoral vein and artery. We describe the technical approach to pRVAD implantation via the right internal jugular vein and discuss the hemodynamic effect of pRVAD support in the setting of cardiogenic shock after AMI. Case Report. A 50-year-old man with long-standing Type II diabetes presented to a community hospital after one hour of sudden onset, crushing, sub-sternal chest pain at rest. Upon arrival, the patient was hypotensive and bradycardic with intermittent Type 1 second degree AV-nodal heart block. Admission electrocardiogram (ECG) revealed an infero-posterior ST-segment elevation myocardial infarction (STEMI). Right-sided ECG showed ST-segment elevation in lead rV4 consistent with RV involvement. The patient was emergently transferred for percutaneous coronary revascularization after receiving unfractionated heparin (5000 unit bolus), aspirin 325 mg, and clopidogrel 300mg. Left heart catheterization revealed moderate disease in the left anterior descending and circumflex arteries, and a 90% stenosis due to a ruptured plaque in the proximal right coronary artery (RCA). A single bare-metal stent (Medtronic, 3.5 x 16 mm) was successfully deployed and restored Thrombolysis in Myocardial Infarction (TIMI) III flow without any residual stenosis (Figure 1). Time from initial presentation at the referring hospital to balloon inflation was 126 minutes. Despite successful reperfusion, fluid resuscitation, and vasopressor support, the patient remained hypotensive and bradycardic. An IABP and percutaneous temporary pacing wire were placed. Over the next 12 hours, worsening renal and hepatic function ensued with a marked reduction in urine output. The patient was transferred to our tertiary care facility for further management. Upon transfer, serum creatinine was 3.mg/dL, with levels of aspartate aminotranferase (AST) of 14,830 IU/L and alanine aminotranferase (ALT) of 8970 IU/L. Biomarkers of myocardial necrosis peaked with a Troponin-I greater than 50 ng/ml and CK-Mb of 2000 ng/ml (Table 1). A transthoracic echocardiogram estimated a LV ejection fraction of 40% and severe inferoposterior hypokinesis. The RV was severely depressed and moderately dilated with flattening of the intraventricular septum, indicative of right-sided pressure and volume overload. No significant valvulopathy was identified. Despite maximal pharmacologic therapy (including dobutamine, milrinone, norepinephrine and vasopressin) and IABP support, the patient developed worsening multisystem organ failure, depressed mental status, and anuria. Pulmonary artery (PA) catheterization revealed massively elevated right and left heart filling pressures (right atrial pressure (RAP): 25 mmHg; pulmonary artery pressure (PAP): 35/30 mmHg; pulmonary capillary wedge pressure (PCWP): 27 mmHg) and severely depressed cardiac output (mixed venous oxygen saturation (MVO2): 31.5%; calculated Fick CI: 1.1 L/min/m2). Right ventricular stroke work was 110 mmHg.mL. The patient was then intubated and the decision made to proceed with pRVAD support as a bridge to recovery. TandemHeart RVAD Insertion. For LV support, the TandemHeart pVAD requires placement of a 62 cm, 21 Fr inflow cannula (CardiacAssist, Inc.) extending from the femoral vein, across the inter-atrial septum, into the left atrium. A second 15 to 17 Fr outflow cannula is placed into a femoral artery. For RV support, the 21 Fr inflow cannula is positioned in the RA with a second 21 Fr outflow cannula inserted into the main pulmonary artery (MPA). The standard approach for pRVAD support has been via both femoral veins. In this case, the distance from the right femoral access site to the 5th intercostal space (ICS) was 64 cm, exceeding the length of the standard 21Fr 62 cm cannula. For this reason, we placed the outflow cannula via the right internal jugular (IJ) vein, thereby ensuring adequate length to reach the MPA. Prior to sheath insertion, ultrasound showed a widely patent right IJ vein with maximum luminal diameter of 2.3 cm. A 0.035 exchange length J-wire (Cook, Bloomington, Indiana) was advanced into the RA via an 8 Fr sheath. To place the pRVAD outflow cannula in the main PA, a 7 Fr, 110 cm Berman end-hole wedge catheter (Arrow International, Reading, Pennsylvania) was placed inside the 21 Fr cannula. The dermotomy was dilated and the 8 Fr introducing sheath was removed with the J-wire remaining in the RA. Both the Berman catheter and outflow cannula were then advanced into the right PA over the J-wire. With the tip of the Berman catheter in the right PA, the outflow cannula was advanced into the MPA (Figure 2, Panels A and B). Transesophageal echocardiography (TEE) confirmed placement of the PA outflow cannula distal to the pulmonic valve with mild pulmonic regurgitation only (Figure 2, Panel C). The Berman catheter and exchange wire were withdrawn into the outflow cannula and removed. We then clamped the IJ outflow cannula and positioned a second 21 Fr inflow cannula in the RA via the right femoral vein. The Tandem system was primed and activated at 6800 rotations per minute (rpm), which yielded an estimated flow of 4.0 L/min via a flow-probe attached to the outflow cannula. Cardiac function improved within minutes of pRVAD activation (MVO2: 69%). Over the next 96 hours, the patient remained hemodynamically stable with increasing urine output, normalization of liver transaminases, and significant improvement in RVSW. Due to evidence of biventricular dysfunction, the IABP was continued for 24 hours after pRVAD placement with gradual weaning of inotropic therapy. Once tolerating diuresis, the patient’s central filling pressures declined and pRVAD support was slowly weaned. On hospital day three, pRVAD support was reduced to 4500 rpm, which yielded a MVO2 of 59% and RVSW of 1146 mmHg.mL, suggesting improved RV function. The pRVAD was successfully explanted after 4 days of mechanical support. Hemostasis was achieved with manual compression after removal of both venous cannulae. Within 6 hours of pRVAD removal, remaining vasopressors were discontinued. The patient was extubated on hospital day ten and discharged to rehabilitation on day fourteen. At 6 months follow-up the patient remained asymptomatic with normal biventricular size and function by transthoracic echocardiogram. Discussion. Management of RV failure in AMI is largely empiric and aimed at reversing the underlying cause, while RV specific therapy remains largely unexplored.^4–7 Fluid resuscitation, vasopressors, inotropes, and IABP therapy are designed to support RV preload, contractility, while maintaining coronary perfusion and reducing LV afterload. Despite aggressive medical therapy, the onset of multisystem organ failure following AMI heralds a poor prognosis with increased mortality. In 2006, Atiemo and colleagues reported the first successful pRVAD implantation in the setting of RV failure after AMI.⁸ Since their introduction, 120 pRVADs have been implanted world-wide for several indications including RV failure in the setting of: AMI,^8,9 post-left ventricular assist device,¹⁰ severe pulmonary hypertension,¹¹ and cardiac rejection after orthotopic heart transplantation.¹² The RV ejects blood into a highly complaint, low-resistance circulation, therefore a much lower proportion of RV stroke work goes to pressure generation and is directed towards generating antegrade momentum.^13,14 As a centrifugal pump that generates continuous flow with a minimal, low-amplitude pulsatile component, the TandemHeart pRVAD more closely approximates native RV function and may have hemodynamic benefits over more common used surgically-placed, pulsatile RVADs. Unlike conventional therapy for cardiogenic shock in acute RVMI with an IABP, the TandemHeart pRVAD provides centrifugal flow up to 5.0 L/min from the RA to main PA, thereby bypassing a poorly functioning right ventricle. In the majority of cases, pRVAD are implanted via both femoral veins. In individual with a measured distance greater than 58 cm from the femoral vein to the 5th ICS, either access from the right IJ vein or femoral cannulation with a 72 cm 21 Fr outflow cannula (CardiacAssist, Inc.) is recommended. Furthermore, right IJ insertion may be considered when femoral venous access is limited by infection, thrombosis, or inferior vena caval filters. Close monitoring for evidence of cannula migration is essential. Antegrade migration into a secondary branch of the pulmonary arteries could present as hypoxic respiratory failure, hemothorax, hemoptysis, decreased cardiac output, and an acute decrease in pRVAD flows. Retrograde migration into the right ventricle may result in decreased cardiac output due to tricuspid regurgitation, reduced pRVAD flows, or ventricular arrhythmia. Cannula migration can be prevented by: 1) meticulous attention to cannula depth at the dermotomy site, 2) stabilization of both cannulae during patient movement in the intensive care unit, and 3) echocardiographic documentation of cannula placement in the MPA. As pRVADs are increasingly applied in the management of right heart failure, weaning parameters will also be necessary to determine the optimal time for device explantation. In the case described above, RVSW closely correlated with clinical improvement and provided an index by which to measure the patient’s response to pRVAD support. Furthermore, we used pulmonary artery pulse pressure (PAPP) to gauge RV recovery. With full pRVAD support, the PAPP narrowed and flow was laminar, consistent with full centrifugal flow in a poorly functioning RV. As the RV recovered, PA pulsatility improved and PAPP increased during reducing pRVAD support, thereby indicating RV improvement. (Figure 3). As experience with pRVADs increases, the development of guidelines to aid device selection, cannula stabilization, and weaning parameters will be required. Acknowledgment. We wish to acknowledge Carey D. Kimmelstiel, MD and Brian Cross, MD for contributing their assistance with preparation of this manuscript. References

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_________________________________________ From the Tufts Medical Center, Division of Cardiology, Boston, Massachusetts. The authors report no conflicts of interest regarding the content herein. Manuscript submitted July 6, 2009, provisional acceptance August 26, 2009, final version accepted September 22, 2009. Address for correspondence: Navin K. Kapur, MD, Tufts Medical Center, Division of Cardiology, 800 Washington Street, Box# 80, Boston, MA 02111. E-mail: nkapur@tuftsmedicalcenter.org