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What intra-anesthetic monitoring might be required for patients with LVADs?
Electrocardiography, pulse oximetry, end-tidal carbon dioxide, temperature, and blood pressure are standard for patients undergoing general anesthesia, and the LVAD-supported patient is no exception. LVAD command consoles offer continuous digital readouts of the effective cardiac output (VAD-output).
Invasive hemodynamic pressure monitoring is not mandatory for all procedures. Blood pressure can be monitored noninvasively, at the anesthesiologist’s discretion. Arterial pressure monitoring catheters are generally inserted for procedures anticipated to produce large swings in blood pressure or for frequent arterial blood sampling.
Central venous pressure (CVP) monitoring is used when large fluid shifts are anticipated. As explained above, opti-mal LVAD function depends on adequate intravascular vol-ume. However, LVADs increase the risk of RV failure. High output from an LVAD will increase RV preload. Sometimes, this alone is enough to cause RV failure in patients with moderate-to-severe RV dysfunction. Decompression of the LV by an LVAD causes a leftward shift of the interventricu-lar septum, resulting in altered RV geometry, increased RV compliance, and decreased RV contractility. While an opti-mally functioning LVAD will reduce RV afterload and often improve RV function in patients with normal pulmonary vascular resistance (PVR), patients with fixed, elevated PVR may actually experience an increased RV afterload, due to increased right-sided and PA flows. Finally, moderate-to-severe tricuspid regurgitation occasionally results from dilation of the tricuspid annulus during LVAD support. In addition to monitoring CVP to detect developing RV failure and guide fluid management, central access is useful for drug infusions and the potential introduction of a transve-nous pacing wire. Additionally, one can calculate SVR in the LVAD-supported patient with an indwelling CVP monitor by substituting the VAD output for the cardiac output in the hemodynamic formula. The calculation would then be as follows:
SVR = [(MAP − CVP)/LVAD output] x 80 dynes-sec/cm5
Central catheters are a potential source of sepsis, and should be avoided when not absolutely necessary.
Pulmonary artery catheters (PACs) are a “double edged sword.” Generally, they provide no useful information in LVAD-supported patients. The LVAD console offers a continuous cardiac output display. PACs pose an increased risk of PA rupture in the patient with pulmonary hyper-tension. PACs can be of some help in the pharmacologic management of pulmonary hypertension. If the patient has a CVP catheter, SVR can be calculated without a PAC as outlined above. Further, though it is not quantitative, one can tell that the SVR has abruptly increased in the LVAD-supported patient when the residual volume in the pump abruptly increases. Transesophageal echocar-diography (TEE) is the intraoperative monitor of choice if there is concern about failure of an unassisted ventricle.
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