Anesthesia Management of a Geriatric Patient with a Left Ventricular Ejection Fraction of 15% with Multiple Comorbidities for Spine Fixation

Dear Editor, We describe our anesthetic approach for an 80-year-old man who was posted for spine fixation and had a 15% left ventricular (LV) ejection fraction (EF), diabetes mellitus, hypertension, asthma, interstitial lung disease, ischemic heart disease, and L1-L5 prolapsed disk (FNAC: tuberculosis). The patient was on T. linagliptin (5 mg), T. dapagliflozin (5 mg), T. metoprolol (25 mg), T. sacubitril (24 mg), T. valsartan (26 mg), T. eplerenone (25 mg), T. atorvastatin (10 mg), T. aspirin (75 mg), and T. haloperidol (0.5 mg), on antitubercular treatment and formoterol inhaler. On examination, vitals were normal. SpO2 was 93% on room air. The electrocardiogram (ECG) showed intraventricular conduction delay, and two-dimensional (2D) echo revealed EF 15%, global LV hypokinesia, severely depressed LV systolic function, and grade 1 diastolic dysfunction with multivalvular involvement. Chest X-ray and high-resolution computed tomography (HRCT) chest showed left pleural effusion and interstitial lung disease [Figure 1]. Blood investigations including electrolytes (Na—135 mmol/L; K—4.19 mmol/L) were within normal limits except for hemoglobin of 9 gram/dL.Figure 1: X-ray of the patient showing left costophrenic angle blunting and features of interstitial lung diseaseChallenges anticipated were poor fluid tolerance; selection of vasopressor; ventilatory settings related to interstitial lung disease, asthma, and compromised cardiac function; the detrimental effect of prone position on an already compromised cardiac function; and complications of diabetes, hypertension, and old age. Given poor tolerance to even minimal blood loss, we optimized hemoglobin to 12.3 gram/dl by transfusing 2 packed cell volume (PCV), each on a separate day with a gap of 48 hours, each over a period of 6 hours along with inj. furosemide 20 mg intravenously to prevent volume overload. The patient was nebulized with salbutamol sulfate + ipratropium bromide and budesonide. All medications except oral hypoglycemic drugs and T. valsartan were continued on the morning of surgery. Fasting blood glucose was 110 mg/dL. Arterial and central lines were secured. The necessary monitors were connected. The lower limbs were wrapped with an elastocrepe bandage to avoid deep vein thrombosis and hypotension. The patient was premedicated with inj. midazolam (1 mg), inj. fentanyl (100 μg), inj. lignocaine (50 mg), and inj. ondansetron (4 mg); preoxygenated for 3 min, induced with inj. etomidate (30 mg) and inj. succinylcholine (100 mg); intubated with 8.5 oral, cuffed, flexometallic tube; and maintained with O2, N2O, sevoflurane, and intermittent inj. cisatracurium. Due to asthma, low cardiac output, and pulmonary fibrosis, expiratory time was kept longer (I: E ratio = 1:3) with low tidal volume, respiratory rate 18/min, and positive end-expiratory pressure (PEEP) zero. The patient was made prone with due precaution to prevent inferior vena cava compression. The patient was kept warm by warm blankets. Intraoperatively, pulse, blood pressure, end-tidal carbon dioxide (CO2), oxygen saturation, and temperature were monitored [Figure 2]. As the patient was intolerant to even minimal loss, we started infusion of norepinephrine (0.05 μg/Kg/min), minute-to-minute monitoring, and balancing of input–output. Infusion of norepinephrine was only required for initial 45 min.Figure 2: Intraoperative monitoring chart showing heart rate (HR), blood pressure (BP), temperature (Temp), end-tidal CO2 (EtCO2) and SpO2There was a difference in opinion about the choice of vasopressor. In a trial comparing epinephrine vs norepinephrine, the occurrence of organ dysfunction and mortality in cardiogenic shock was lower with norepinephrine. It also improved shock resolution and balance between oxygen delivery and oxygen consumption in the splanchnic area.[1] The hemodynamic effect of norepinephrine is beyond an increase in blood pressure. One may expect a decreased cardiac output due to increased blood pressure and thus afterload but it increases cardiac output as it acts on all determinants of cardiac output, that is, preload, afterload, contractility, and heart rate.[2] The study by Monnet et al.[3] showed that noradrenaline increased central venous pressure (CVP), LV end-diastolic area, global end-diastolic volume, and cardiac index, the reason being noradrenaline increases preload due to venoconstriction causing redistribution of blood from unstressed to stressed volume. Norepinephrine reserves vascular tone capacitance of vein, thus decreasing the amount of fluid needed to restore venous return gradient. Milrinone causes vasodilatation which increases capacitance, and so, more fluid is required.[4] Further, most stroke volume could be used up to accommodate increased capacitance in an already compromised ejection fraction. The beauty of the combination of a rise in arterial pressure, contractility, and improved coronary perfusion improving ventriculoarterial coupling with noradrenaline supported our choice to use this drug.[5] Intraoperatively, input was 760 ml (300 ml ringer lactate + 200 ml voluven [6% hydroxyethyl starch in 0.9% normal saline] + 160 ml fresh frozen plasma + 100 ml PCV), and output was 600 ml (blood loss 400 ml and urine output 200 ml). After reversal, the patient was awake with normal tone and reflexes and shifted for observation after extubation. In conclusion along with adequate preoperative optimization, application of elastocrepe bandage, appropriate ventilatory setting, minute-to-minute monitoring, and balancing of input–output, we suggest optimization of hemoglobin and choice of vasopressor as norepinephrine in such cases. Data availability statement The data that support the findings of this study are available from the corresponding author, Jain R, upon reasonable request. Author contribution The authors confirm their contribution to the case report as follows: Conception: Baheti S; Design: Baheti S, Jain R; Definition of intellectual content: Baheti S; Literation search, draft manuscript preparation and editing: Baheti S, Jain R. All authors reviewed the results and approved the final version of the manuscript. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.