A 48-year-old woman presented for surgical debridement of a sacral pressure ulcer. She had a medical history significant for Class D left-sided heart failure secondary to viral cardiomyopathy, implantation of a HeartMate II Left Ventricular Assist Device 5 months prior, and prolonged ventilatory support via a tracheostomy.
Preoperative transthoracic echocardiography revealed a severely dilated and hypertrophied left ventricle with severely depressed function, trace aortic insufficiency, pulmonary artery systolic pressure of 25 mm·Hg, normal right ventricular size and function, and a left VAD inflow cannula positioned in the left ventricular apex with laminar flow.
Inhalation induction with desflurane via tracheostomy was performed with standard American Society of Anesthesiologists monitors in place. The patient had diminished, yet palpable pulses, therefore a noninvasive arterial blood pressure cuff was used initially. Her PI was 4.8 to 5 after induction, consistent with preinduction values. With the assistance of the surgeon and perfusionist, the patient was turned prone onto a Wilson frame (OSI, Union City, CA), ensuring that the drive-line was not compressed. Shortly after the patient was positioned prone, the PI decreased to 2.8. Flow and pump speed were also diminished. Automatic blood pressure cuff measurements could no longer be obtained, and a right radial arterial catheter was immediately inserted with ultrasound guidance and revealed a MAP of 75 to 100 mm·Hg. Anesthesia was maintained with 0.5 minimum alveolar concentration of desflurane. One liter of 5% albumin, 1 unit packed red blood cells, and intermittent boluses phenylephrine were given that increased the PI to 3.4. On completion of the procedure, the patient was turned supine and the PI quickly returned to preoperative values. The patient was transported to the postanesthesia care unit spontaneously breathing without need of hemodynamic support.
The HeartMate II VAD is a second generation continuous flow mechanical assist device. The inflow cannula is placed in the left ventricle apex, and the outflow cannula is placed in the ascending aorta for systemic perfusion.1 Filling of the inflow cannula depends on right ventricular function, pulmonary vascular compliance, and a functional mitral valve.2 Because the left VAD requires adequate left ventricular filling to maintain a normal cardiac output, right ventricular cardiac output must be maintained. Positioning during surgery can affect intraoperative hemodynamics dramatically,3 and when substantial fluid shifts are anticipated, invasive monitoring of right ventricular and pump filling pressures may indicate the use of intraoperative TEE.4 TEE can also help guide clinical decision making, including the use of fluids, inotropic drugs, and vasoactive drugs. Cannula positioning and velocities, left ventricular decompression, thrombus formation, valve function, and right ventricular function are key examination findings on TEE.
Interpretation of left VAD data can provide valuable hemodynamic information to the anesthesiologist. The HeartMate II left ventricular-assist device console estimates 4 variables in real-time: pump speed in rotations per minute, pump flow in L/min, power consumption in watts (W), and PI. Pump speed is measured in revolutions per minute (RPMs) and is typically set at 9450 ± 490 RPMs with a range of 6000 to 15,000 RPMs. The pump flow is an estimate based on the pump speed and the power consumption, usually set between 4 and 6 L/min depending on the contribution of the native ventricle.5 Power refers to the number of watts the motor requires, typically 6.8 W.5
The PI is a dimensionless measurement of the flow pulse generated by the pump during the cardiac cycle, defined as PI = 10 × (Qmax − Qmin)/Qavg, where Qmax is the maximum of pump flow, Qmin is its minimum, and Qavg is the mean value of pump flow.3,6 Flow through the Heartmate II is augmented with each contraction of the native ventricle. The PI is determined by ventricular preload, myocardial contractility, and the contribution of the native ventricle to the total cardiac output. The PI should range between 3 and 4 (with a range of 1–10). A high PI indicates an increased ventricular filling, increased ventricular contribution, or decreased device contribution. A low PI indicates low ventricular filling, low ventricular contribution, increased device contribution, or inflow or outflow obstruction.5–7 During the intraoperative period, the PI should be readily visible to the anesthesiologist for trending.
Prone positioning may change the intraoperative management of a patient with a VAD. While the successful management of patients with a VAD without the use of intra-arterial blood pressure monitoring has been reported,8 the hemodynamic effects of the prone position may make it necessary. Although automatic blood pressure cuffs are able to accurately obtain a pressure 50% of the time in this patient population, the most reliable method is Doppler ultrasound that should be performed if invasive monitors cannot be placed.9 Decreased venous return due to the prone position may be hazardous to the patient with a VAD who requires adequate preload to maintain cardiac output. The Jackson Spine Table supports the legs at the level of the heart to avoid venous pooling in the lower extremities.10 The Wilson Frame supports the abdomen and pelvis with a convex saddle, allowing the legs to lie slightly below the heart.10 Both of these frames used for prone positioning can lead to increased intra-abdominal pressure and decreased venous return. This increase in intra-abdominal pressure can be transmitted to the thorax, leading to increased intrathoracic pressure, increased afterload, and decreased left ventricular compliance.10,11 In Case 1, right ventricular cardiac output significantly decreased when the patient was rotated into the prone position. This was likely a result of decreased venous return and compression of the RVOT by the left VAD outflow cannula, which anatomically is located anterior to the pulmonary artery (Fig. 1). Decreased RVOT velocity time integral reflected decreased right ventricular cardiac output (Fig. 3).
In Case 2, the PI was monitored throughout the case and immediately decreased after prone positioning. Without a concomitant increase in VAD flow and speed, low circulating volume was suspected. Both patients responded to fluid boluses in the form of colloid to augment venous return and stroke volume, which increased cardiac output of the right ventricle, and therefore left VAD output.
The management of VAD-supported patients for noncardiac surgery presents many challenges. Appropriate anesthetic planning and intraoperative monitoring may be supported by TEE. Proper hemodynamic trending of the PI, ongoing volume and right ventricular assessments, and understanding the influence of surgical positioning are all crucial to guide patient management.
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