Refractory Hypotension and Intraoperative Cardiac Arrest in a Patient with Severe Aortic Insufficiency: A Case of Physiology-Guided Crisis Management
Casey E. Hofstaedter, PhD1,2, Justin Zhang, BS1, Reney Henderson, MD1, Emily Bergbower, MD, PhD1
1Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD; 2Medical Scientist Training Program, University of Maryland School of Medicine, Baltimore, MD
Learning Objective
•Refractory hypotension is defined as low blood pressure that is not responsive to fluid resuscitation or vasopressor therapy.1,2
•Refractory hypotension can be caused by several underlying pathologies.1,2
•A strong foundation in physiologic reasoning is important when approaching refractory hypotension in the operating room.
Case Description
•52-year-old male with a history of asthma and CHF presents with several days of dyspnea on exertion and mild cough
- Patient was admitted 3 weeks prior with these symptoms and improved with diuresis.
•Blood pressure was 170/63 on admission and oxygen saturation was 89% on room air
-LVEDP severely elevated (52mmHg)
•Dyspnea acutely worsened overnight, leading to an emergency diagnosis of severe AI with a bicuspid aortic valve
•Surgical plan: CABG 3x and Aortic Valve Replacement
•Day of surgery, patient acutely desaturated to 65% O2 on room air despite steroids and albuterol. Rushed to OR. Bag mask ventilation improved O2 saturation to 100%.
•Induction and Intubation: Ketamine (20mg) and Etomidate (8mg), central line (Right internal jugular vein), pre-induction arterial line (in place from CSICU, left radial), intubation uneventful,
•Post-operative care: extubated POD1, discharged POD20
•Key Intraoperative events: Performed coronary artery bypass graft (CABG) 3x and aortic valve replacement
•20 minutes post-induction: Patient’s systolic pressure had started declining. Pressor boluses administered with minimal effect. TEE did not show pericardial effusion, and breath stacking was not present. Allowing full exhale did not improve hemodynamics.
•28 minutes post-induction: Arterial line flattened. CPR initiated, sternotomy made immediately after, and direct-on-heart CPR was performed.
•Pressor doses continually administered: 4x 1mg epinephrine doses, 2g calcium, 1 ampoule HCO3.
•35 minutes after induction: Aorta cannulated, progressed to the bypass.
Discussion
•Aortic insufficiency, although common, can have routine or complicated presentations (4.9% are complicated)3
•Induction-related drops in SVR and bradycardia can worsen aortic regurgitation, increasing regurgitant volume and reducing forward flow, making patients highly sensitive to abrupt anesthetic changes.
•Maintaining preload, moderate tachycardia, and adequate afterload is essential, as controlled induction and sympathetic tone help limit diastolic regurgitation and support hemodynamic stability.