In population-based study heart transplant recipients have a significantly higher risk of any "de novo" cancer due to immunosuppressive therapy [1]. The incidence of post transplant malignancy ranged from 4.1–16.3%, and a 2-fold to 4-fold overall increased risk of cancer over the general population was observed. Carcinoma of lung represents one of the five most common malignancies in these transplant populations [2]. Therefore, is not uncommon for these patients undergoing oncologic surgery after transplant. The main worries are risks of infection and impairment of other organs, particularly those that may be compromised due to either immunosuppressive therapy or dysfunction of the transplanted organ itself [3]: diabetes, hypertension, coronary disease, osteoporosis, neurological impairment. Patients' comorbidities may request high invasive intraoperative monitoring, as well as neuraxial analgesia to avoid acute pain stress response, exposing patients to iatrogenic nosocomial infection.

The traditional invasive hemodynamic monitoring like pulmonary artery catheter (PAC) has the same risk associated with central venous catheterization. These risks include arrhythmias, pulmonary infarction, infection, pulmonary embolus, and rupture of the pulmonary artery to name just a few [4]. The minimally invasive monitoring devices are enable to measure pressures in the central circulation but their use in the assessment of global tissue perfusion is necessary to the goal directed therapy [5].

A 41-year-old female, 67 kg of body weight, 1.68 m tall, was admitted to thoracic surgery ward for lung adenocarcinoma diagnosis and a video assisted upper left lobectomy was planned. She received heart transplantation 15 years before due to idiopathic dilatative cardiomyopathy and she had chronic rejection six years after transplant treated with corticosteroid therapy. Echocardiogram showed adequate systolic function with mild tricuspid regurgitation. No evidence of graft rejection was documented by regular myocardial biopsies. She had an impaired glycemic tolerance and fasting hyperglycemia at 8.9 mmol/L. No kidney pathologies and mild anemia was referred. She was in treatment with cyclosporine, mycophenolate mofetil, corticosteroids, B-blocker, diuretics and antiplatelet drug. Preoperative respiratory values were forced expiratory volume in the 1st second (FEV1) 104%, diffusion lung carbon monoxide (DLCO) 79% and maximal oxygen consumption (VO2 max) 17 ml/kg/min with physiological arterial blood pressure (AP) and heart rate (HR) rising pattern during cardiopulmonary exercise test; metabolic equivalents of task (METs) >> 4. Predicted postoperative values (ppo) were: ppoFEV1 77%, ppoDLCO 58%, and ppoVO2max 12.5 ml/kg/min.

Vascular access included a 16-G and a 14-G intravenous catheters. Monitoring consisted of American Society of Anesthesiologist standard monitors, train of four (TOF-Watch®, Organon Ltd., Dublin, Ireland) and Bispectral Index Spectroscopy (BIS Covidien, Mansfield, Massachusetts, USA). After light intravenous sedation with midazolam 0.03 mg/kg and sufentanil 10 mg, achieving observer's assessment of alertness/sedation (OAA/S) Scale score 4, right radial artery incannulation was performed to assess cardiovascular status (Figure 1) and (Figure 2): heart rate 99 bpm; AP 136/81 mmHg; C.I. 4,7 l/min/m2; SVV 4%. The hemodynamics parameters were assessed with a self-calibrating arterial pulse contour cardiac output monitoring system (FloTrac/VigileoTM, Edwards Lifesciences, Irvine, California, U.S.A.). Induction of general anesthesia was performed with intravenous propofol 1 mg/kg and remifentanil 0,15 mg/kg/min until BIS < 60 and intravenous rocuronium 0.6 mg/kg was administered to perform tracheal intubation (TOF < 2).

One lung ventilation (OLV) was obtained using a left side double-lumen bronchial PVC tube 37 F (RÜSCH, Wien, Austria) and bronchoscopic control. Mechanical ventilation settings were: tidal volume 4 ml/kg; respiratory rate 16; minute ventilation 4 l; fraction of inspired oxygen 65%; positive end expiratory pressure 4 cmH2O. Hemodynamics values just after induction were: heart rate 90 bpm; AP 129/79 mmHg; C.I. 3 l/min/m2 and SVV 5%. Anesthesia depth was guaranteed by BIS value of 47; Pulse oximetry (SpO₂) 98% was firm even in OLV.

Forty-five minutes after anesthesia induction, an hypotension episode occurred: HR 100 bpm, AP 80/50 mmHg, SpO₂ 98%, C.I. 2.5 l/min/m², SVV 9% and BIS 60. Crystalloids bolus (300 ml) was administered obtaining a fast recovery from hypotension until getting HR 93 bpm; AP 113/75 mmHg; C.I. 2.5 l/min/m² and SVV 4%. After 75 minutes of OLV the arterial blood gas (ABG) showed: pH 7.33, PaCO₂ 49 mmol/L, PaO₂ 93 mmol/L, Lactate 0,7 mmol/l and Base Excess, 0.1 mmol/l. An antalgic elastomeric pump was prepared with morphine 0.2 mg/kg. Antalgic transition was obtained with intravenous sufentanil 20 mg and acetaminophen 1 g, 20 minute before ending surgery. After chest drainage positioning, surgeons made an internal video assisted intercostal blockade using 20 ml of ropivacaine 0.5% at 4th and 6th intercostal space, covering the thoracic trocar access and mini-thoracotomy. Programmed upper left lobectomy was performed in 210 minutes without complications.

Proprofol infusion was stopped and remifentanil infusion decreased at 0.05 mg/kg/min, patient awake after few minutes, returning to BIS value > 80. The reversal of neuromuscular block, according to TOF, was obtained with sugammadex 2 mg/kg. The tracheal tube was removed after patient spontaneous breathe recovery. Heart rate 89 bpm; AP 115/66; SpO₂ 98%; C.I. 3.2 l/min/m2; SVV 13%. Pain control was adequate with visual analogue scale < 3. The patient was transferred to intensive care unit (ICU) to perform postoperative surveillance. Before leaving operating room one of the venous access (16 G) and arterial catheter were removed. After 18 hours in ICU, spent in isolation room to prevent any infection, without any complications, patient came back to thoracic surgery ward and five days later she was discharged from the hospital.

The patient had no clinical markers of heart impairment or functional capacity decrease, the only risk factors were anemia and specific surgery risk, ECG and echocardiogram revealed no cardiac impairment and cardiopulmonary exercise test revealed a physiological response to maximal physical stress without ischemic signs [6]. We did not need further investigation according to 2014 ACC/AHA guidelines for perioperative cardiovascular evaluation for noncardiac surgery-executive summary [7].

To prevent any kind of iatrogenic infection a central venous catheter was not inserted, preferring peripheral approach to arterial and venous catheterizations. Dynamic arterial pulse monitoring was enough to check heart activity, and patient respiratory status did not require strict central venous oxygen saturation (ScvO2) monitoring. Massive blood loss could be managed with two large bore (14–16 G) intravenous catheters using blood warmer and rapid infusion device. Patient heart status was good and there was no need for inotropic support, unless unpredictable eventualities. The only hypotension episode was reverted, reading the raise in SVV, with fast crystalloids administration. Goal-directed fluid therapy guided by functional parameters of preload, such as SVV, is believed to be rather fluid aggressive since in clinical studies the goal-directed groups received more fluids than the control group [8] and a volume restrictive regime is usually recommended for lung surgery [9] but SVV-guided fluid management, in specific thoracic surgery study, does not result in pulmonary fluid overload [10]. Furthermore, after thoracotomy with open chest conditions, SVV is not without controversy regarding prediction of volume responsiveness [11] but the VATS-approach is "close chest" procedure, so no major confounding factors but side position could interfere with our parameters.

Even not admitting the absolute precision of arterial pulse contour CO monitoring in thoracic surgery, due to side position and OLV, its relative modifications are still a measure of hemodynamic pattern; also anesthesia induction is one of the more critical moment in a cardiac patient and position and mechanical ventilation is quite the same in every surgery specialties, so we can obtain significant information during induction and early phases of anesthesia.

Video assisted surgery granted patient less intense postoperative pain [12] [13] so thoracic epidural analgesia could be considered overtreatment and too invasive exposing patient to dangerous hypotension, compared to intravenous morphine and remifentanil infusion during ICU staying. Hypotension in heart transplant patients is worrying due to their "preload dependence" [14], so, to prevent acute vasodilatation, hypotension and hypovolemia, central neuraxial blockade was avoided. Internal intercostal blockade and sufentanil bolus granted adequate analgesia during the critical first hours after surgery. Every invasive device was placed under strictly aseptic conditions and removed before entering ICU, to minimize infective risk. The theory behind using the arterial pulse wave form to measure CO is based on the model that describes the loads faced by the heart when pumping against the pulmonary or systemic circulation and the relationship between the arterial blood pressure and flow in the systemic and pulmonary arteries. Particular algorithms can be used to define an area under the systemic arterial pulse waveform, available to establish CO and SV [15]. Changes in the systolic pressure between the inspiratory and expiratory phase during mechanical ventilation can be used to ascertain intravascular volume status and, by calculating the systolic pressure variation and the SV variation (SVV), the pulse contour systems can also function as volume status monitors [16]. Pulse contour devices have some advantages over other devices used to measure CO. They require little training, are simple to calibrate and provide an estimation of intravascular volume status [5]. Several studies show a good correlation between pulse contour devices and traditional invasive hemodynamic monitoring both during cardiac surgery and no cardiac surgery [17] [18] [19].

Pulse contour devices have some advantages over other devices used to measure CO. They require little training, are simple to calibrate and provide an estimation of intravascular volume status. Several studies show a good correlation between pulse contour devices and traditional invasive hemodynamic monitoring both during cardiac surgery and no cardiac surgery.

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