Left ventricular assist device

Over the 2-year period of 2009–2011, implantation of left ventricular assist devices (LVADs) in the United States increased ten-fold when selected for destination therapy.^[1] LVADs can be utilized in three clinical scenarios: (1) acute ventricular failure as a bridge to recovery; (2) chronic ventricular failure as a bridge to heart transplant; or (3) permanent implantation in those not suitable for heart transplantation. All LVADs fall into one of two physiological categories: pulsatile or non-pulsatile devices. Non-pulsatile, or continuous-flow, LVADs are smaller in size, operate silently, and have proven more durable when compared with pulsatile flow LVADs.^[2] In patients selected for destination therapy, the continuous-flow Heartmate II device has demonstrated improved patient survival when compared with the pulsatile LVAD Heartmate XVE (58% vs. 24%, 2-year survival).^[3] Thus, continuous-flow LVADs are more common and practitioners in the Post-Anesthesia Care Unit (PACU) setting are likely to encounter a continuous-flow VAD.

The VAD is implanted during a surgical procedure utilizing cardiopulmonary bypass. The left ventricle is emptied by a cannula located at the apex. This cannula delivers blood into a sub-diaphragmatic pre-peritoneal or intra abdominal pump. The rotary pump is capable of generating flow, a surrogate of cardiac output, of up to 10 l/min. Blood is returned from the device to the ascending aorta. LVADs are sensitive to changes in both preload (volume status) and afterload (systemic vascular resistance). LVAD patients will either have a weak or non-palpable pulse. The failing left ventricle cannot generate sufficient intrinsic contractile strength to create pulsatile flow beyond the continuous flow of the device.

Vital sign monitoring: The non-pulsatile flow of an LVAD can create difficulty in measuring basic vital signs in the PACU. Pulse oximetry estimates the percentage of oxygenated hemoglobin in arterial blood based upon characteristic light absorption of oxygenated and deoxygenated hemoglobin. Arterial saturation is differentiated from the “background” oxygen saturation of venous blood by detecting arterial pulsations. In the absence of pulsatile flow, standard pulse oximetry will be unreliable. In this situation it is best to confirm clinical signs of tissue oxygenation such as mental status, capillary refill, and skin pallor. If concern exists regarding a patient’s oxygenation, arterial blood gas analysis is indicated. In addition to pulse oximetry, automatic non-invasive blood pressure cuffs require pulsatility to generate accurate blood pressure measurements. A trial of a non-invasive cuff is warranted, however, as a mean blood pressure may be detected in those with weak pulsatility. In the absence of pulsatility, an alternative method for blood pressure measurement involves using a manual blood pressure cuff and an audible Doppler. The Doppler probe is placed over a distal artery as the manual cuff is slowly deflated. The blood pressure cuff reading when audible flow is heard by Doppler should be considered in the range of the patient’s mean blood pressure.^[2] In the absence of consistent blood pressure monitoring, mental status, urine output, and tissue oxygenation should be monitored as clinical signs of normotension. If concern exists regarding the patient’s blood pressure, an arterial line should be considered. The use of ultrasound or Doppler can be of assistance in cannulating an artery with little or no palpable pulse.

LVAD console: A mechanical circulation coordinator or nurse who is familiar with the patient’s assist device settings will accompany the majority of patients with a VAD. Should a specialized nurse not be available, standard VAD systems include a monitor that displays the pump speed (RPM), power (watts), flow (l/min), and pulsatility index (PI). The pump is run in a fixed speed mode in the range of 8,000 to 10,000 revolutions per minute (RPM).^[4] The fixed speed is determined shortly after device placement and is based upon both optimal emptying of the left ventricle and right ventricular function. The pump power is a direct measurement of power output and self-adjusts to maintain pump speed based upon changes in afterload and viscosity. When evaluating the patient’s VAD settings, a continual increase in power, or an absolute power value greater than 10–12 watts may indicate the presence of a thrombus inside the LVAD.^[4] PI represents the contribution of the native left ventricle to cardiac output.^[4] The PI ranges from 1 to 10 and is averaged every 15 seconds. The higher the PI, the more the left ventricle is contributing to flow through the VAD. A progressively lower PI often represents a decrease in left ventricular preload as the native heart can no longer augment flow through the LVAD.

Hypotension: LVAD patients are sensitive to changes in preload owing to the fixed cardiac output generated by the device. PI can be used as a surrogate for preload; however, it will not differentiate true hypovolemia from decreased device inflow secondary to right ventricular failure. The evaluation of severe hypotension in the PACU should include an emergent transthoracic or transesophageal echocardiogram to determine right ventricular function, volume status, and inflow or outflow problems intrinsic to the device.^[5] Treatment should be tailored based on the echocardiographic findings with volume resuscitation for hypovolemia and inotropic therapy for progressive right ventricular failure.

Suction event: A significant drop in left ventricular preload can result in suction of the ventricular wall, most often the intraventricular septum, into the inflow cannula, as the pump continues to rotate at a set speed. A suction event will often trigger ventricular arrhythmias and can result in profound hypotension and circulatory collapse. Treatment of a suction event includes immediate restoration of left ventricular preload and treatment of malignant arrhythmias to restore biventricular function. Suction events are sensed by the LVAD system when there is an acute and severe decrease in the PI.^[4] In this instance, the LVAD will automatically drop its speed to a previously set low limit to temporize the problem and minimize suction forces against the ventricular wall. This temporary decrease in RPM allows the clinician a window to restore circulating volume and maintain normal device function. After the suction event has resolved, the LVAD will slowly increase its speed, in 100 RPM intervals, until it reaches the standard RPM setting.

Other concerns for LVAD patients: Careful consideration of the LVAD patient’s anticoagulation status is important in their PACU management. VAD patients are anticoagulated with a regimen consisting of antiplatelet agents and warfarin. Some centers use a target INR (international normalized ratio) of 2.0 to 3.0 whereas others use 1.5 to 2.5.^[2] The antiplatelet agent also varies, but may include aspirin 81 mg daily with or without dipyridamole 75 mg. Although the etiology is not yet completely understood, many continuous-flow LVAD patients demonstrate reduced levels of von Willebrand factor, which may further increase their bleeding diathesis.^[6]

Right ventricular output is not supported by an LVAD, and rhythms such as sustained ventricular tachycardia and ventricular fibrillation can quickly lead to hemodynamic compromise. A patient with an LVAD can safely receive cardioversion or defibrillation. Caution is advised in performing chest compressions on a VAD patient owing to the risk of dislodging or damaging the inflow and outflow grafts. In a situation where augmented circulation is necessary, abdominal compressions may be performed.^[4] VADs contain ferromagnetic components, and these patients should not be subjected to an MRI.