SNACC Medically Challenging Case: Recalcitrant Hypotension in a Patient with Heart Failure Undergoing Intracranial Resection of a Meningioma

By: Emmad Kabil MD and Lauren K. Dunn MD, PhD

Emmad Kabil MD1
1Medical University of South Carolina

Lauren K. Dunn MD, PhD1,2
1Department of Anesthesiology
2Neurological Surgery, University of Virginia, Charlottesville, VA

The authors have no conflicts to disclose.


A 68-year-old man presented for modified left orbitozygomatic craniotomy for resection of left parasellar sphenoid meningioma. Three months prior, he presented to the emergency department after a grand-mal tonic clonic seizure.  Neuroimaging revealed a left sphenoid mass, likely meningioma.  Cardiac history was notable for nonischemic cardiomyopathy, chronic heart failure with reduced ejection fraction (HFrEF), paroxysmal atrial fibrillation, left bundle branch block, hypertension, hyperlipidemia, and a biventricular implantable cardiac defibrillator with cardiac resynchronization capability. Other medical history included obstructive sleep apnea, chronic obstructive pulmonary disease (COPD), tobacco use, and insulin-dependent diabetes. Medications included amiodarone, apixaban, aspirin, carvedilol, famotidine, furosemide, gabapentin, insulin glargine and lispro, ipratropium/albuterol nebulizer, levetiracetam, metformin, rosuvastatin, and sacubitril-valsartan. Transthoracic echocardiography from two years prior was notable for an ejection fraction of 30-35%, improved from 5-10% prior to pacer/ICD placement. The last cardiac device interrogation was pre-MRI four weeks prior to surgery and was notable for DDD pacing with 96% ventricular pacing and 6 defibrillation shocks.

Preoperative Assessment

Preoperative assessment was as follows: weight 114.3 kg (BMI 36.2), blood pressure 122/69, pulse 54 BPM with wide-complex paced rhythm, respirations 19 RPM, SpO2 in room air 97%, temperature 36.8 C; airway: Mallampati II, edentulous; cardiopulmonary: normal heart and breath sounds, pitting edema to the knee. Laboratory values were unremarkable except for blood glucose 177 mg/dL and trace proteinuria. It was thought that the patient was optimized as much as possible and could proceed with surgery.

Due to pacemaker dependence and history of defibrillation, the implantable cardiac device was reprogrammed to asynchronous biventricular pacing (DOO) at 80 BPM and ICD was disabled and defibrillator pads placed on the patient prior to induction of anesthesia.

Intraoperative Management

Induction of Anesthesia

Standard ASA monitors were attached. Noninvasive blood pressures were recorded every minute. Anesthesia was induced with lidocaine, ketamine, propofol, remifentanil and succinylcholine and the patient was intubated successfully. Preinduction blood pressure was 180/79. The patient was hemodynamically stable throughout induction and intubation. Additional peripheral intravenous access and a right radial arterial catheter were placed without complication. Electrodes were placed for motor and sensory evoked potential monitoring.

Maintenance of Anesthesia

Anesthesia was maintained with intravenous infusions of propofol and remifentanil and one-half minimum alveolar concentration (MAC) sevoflurane to facilitate neuromonitoring. Propofol and remifentanil were chosen because they decrease cerebral metabolic oxygen consumption with minimal effects on cerebral blood flow (CBF) or intracranial pressure and allow for rapid and smooth emergence from anesthesia. Sevoflurane was administered at less than one-half MAC to avoid increasing CBF. Adequacy of baseline neuromonitoring signals was confirmed prior to the start of surgery. A norepinephrine infusion was titrated to maintain a mean arterial blood pressure within 20 mmHg of baseline.

The anesthetic was deepened for skull pinning with remifentanil.  Dexamethasone and 0.5 g/kg 20% mannitol were given for brain relaxation and levetiracetam was administered for seizure prophylaxis. An insulin infusion was started to maintain blood glucose < 180 mg/dL.  Norepinephrine was titrated to MAP > 75, which was within 20% of the patient’s baseline.

Several hours post-induction, the patient’s blood pressure began to decrease.  The differential for hypotension was broad and included vasodilation secondary to anesthetic infusions, hypovolemia, anemia, vasoplegia secondary to inflammatory response to surgery, myocardial infarction, pulmonary embolus, failure of his cardiac resynchronization device, hypocalcemia, or other electrolyte disturbance.  Anesthetic infusion rates were reduced and norepinephrine was increased to 10 mcg/min to keep MAP > 75mmHg.  Anemia and electrolyte derangements were ruled out with arterial blood gas analysis.

Albumin was chosen for volume resuscitation given the patient’s history of heart failure, lower extremity edema, and COPD.  The norepinephrine requirement decreased only minimally and alternative causes of hypotension were considered, including inhibition of the renin-angiotensin pathway by sacubitril-valsartan. A vasopressin infusion was added and an additional liter of sodium chloride was infused with no change in pressor requirement. Notably, blood gasses during this period were unremarkable despite the pressor requirement.

At the conclusion of surgery, final neuromonitoring signals were unchanged from baseline, and intravenous anesthetics were discontinued. Vasopressin and norepinephrine infusions were weaned. Hydromorphone was given for analgesia, and the patient was extubated uneventfully. Estimated blood loss was 300 mL.

Postoperative Course

The patient was transferred to the neurointensive care unit for postoperative monitoring. He was alert and following commands with a normal neurological exam. The patient continued to recover uneventfully and was discharged from the ICU to step-down on postoperative day 1, and discharged home on postoperative day 8.

Case Discussion

Perioperative Management of Pacemaker and Internal Cardiac Defibrillators

Cardiac devices capable of pacing (PPM) and/or defibrillating (ICD) are becoming more prevalent.  Electromagnetic interference from surgical electrocautery or other intraoperative sources may result in inappropriate activation or withholding of pacing and cardioversion/defibrillation therapies. Patients at higher risk for cardiac arrest in the event of device failure include those with complete heart block dependent on device pacing and those with a high burden of ventricular tachycardia.  Surgeries taking place in the close proximity to the device may have higher risk of interference, and care should be taken when placing grounding pads to ensure current does not pass through the device.1

Identification of the device brand and function is the first step and may provide some clues as to the indication for the device, cardiac resynchronization therapy (CRT) is indicated for HFrEF with EF < 35%, sinus rhythm with LBBB, symptomatic heart failure despite appropriate medical therapy, QRS > 149 msec, and atrial fibrillation requiring ventricular pacing.2 The location and number of leads can be determined by chest x-ray. Defibrillator leads appear thicker than pacer leads, and the devices themselves are larger. Often there is a pattern or number visible by chest x-ray to help identify the precise model. An app available may help identify the device from an x-ray photograph.3

Records should be reviewed to determine functionality, underlying rhythm, frequency of discharges, and current mode of operation. If interrogation data are unavailable or outdated, the device should be interrogated preoperatively.

Pacer dependence also determines the need for reprogramming. If dependent, the device should be programmed to asynchronously pace prior to surgery.4 If the device cannot be reprogrammed, a magnet can be used. The effect of the magnet can vary, but in most cases the device will be placed in an asynchronous pacing mode and ICD functionality disabled. Defibrillator pads and a defibrillator should be available, and the device reactivated after surgery.

Fluid Resuscitation for the Neurosurgical Patient with Heart Failure

Isotonic crystalloid fluids are considered the fluid of choice for neurosurgery.  There is evidence to suggest increased mortality in traumatic brain injury (TBI) patients resuscitated with 4% albumin versus normal saline5, although the difference was only present in severe TBI. Albumin crosses the blood-brain barrier (BBB) and may increase vasogenic edema.6 Local surgical trauma disrupts the BBB, increasing permeability to osmotically active molecules such as mannitol, leading to increased edema.

Buffered crystalloid solutions are generally preferred over normal saline (NS) to avoid hyperchloremic metabolic acidosis7 without affecting brain relaxation in elective craniotomies.8 Lactated Ringer’s (LR) may be suboptimal due to its hypotonicity and lower sodium content causing worsened surgical visualization.9 Plasmalyte demonstrates an improved metabolic profile over NS with no adverse effect on surgical visualization.8

Albumin has been shown to increase osmotic pressure and improve hemodynamics versus normal saline in patients undergoing dialysis.10 Increased osmotic pressure theoretically avoids interstitial edema (“third-spacing”) associated with crystalloid administration. Albumin may be of theoretical benefit for hypovolemic patients with heart failure; however, randomized controlled trials comparing albumin 4% and normal saline for resuscitation in critically ill patients have shown no mortality benefit.11,12 A retrospective analysis of inpatients with heart failure, in which 25% had surgery, demonstrated no increased or decreased risk of intubation, new renal replacement therapy, or mortality in the 45% of patients that received albumin.13

Perioperative Management of Hypotension in Patients on Renin-Angiotensin Inhibitors

          It is recommended to withhold angiotensin-converting-enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs) during the 24 hours preceding surgery to avoid refractory hypotension in the perioperative period.14 Vascular tone is dependent upon the sympathetic nervous system, the renin-angiotensin system (RAS), and the hypothalamus-vasopressin axis. Anesthesia inhibits sympathetic tone, leaving vascular tone dependent upon the RAS and vasopressin axis. Further inhibition of the RAS with an ACEI or ARB can result in hypotension refractory to sympathomimetic drugs.14 Vasopressin and analogs improve hemodynamic parameters in patients with ACEI- or ARB-related refractory hypotension.15 The vasopressin prodrug terlipressin is more effective than norepinephrine at treating hypotension refractory to phenylephrine and ephedrine in patients with recent ACEI or ARB use.16 However, terlipressin may increase MAP while decreasing tissue perfusion.17 Therefore, a balanced-pressor approach may be the ideal treatment for refractory intraoperative hypotension.


Patients with heart failure presenting for intracranial surgery present unique challenges. Patients with PPMs should have their device interrogated and placed in an asynchronous mode, while ICDs should be turned off prior to surgery. Isotonic fluids are recommended for volume resuscitation in neurosurgical patients with hypovolemic blood loss. Patients taking renin-angiotensin inhibitors prior to surgery may experience hypotension unresponsive to phenylephrine and norepinephrine and may benefit from treatment with vasopressin.


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