Cardiac Ultrasound-Guided Hemodynamic Management to Augment Cerebral Perfusion

First Author(s)

• BA

  Beddome Allen

  Wake Forest School of Medicine

  Disclosure information not submitted.

  Slides and Audio

Co-Author(s)

• CO

  Chesney Oravec, MD

  House Officer IV, Neurosurgery
  Wake Forest Baptist Health, United States

  Disclosure information not submitted.
• DS

  Dan Silaghi, MD

  Assistant Instructor, Neurology
  Wake Forest Baptist Health
  Winston-Salem, North Carolina, United States

  Disclosure information not submitted.
• SW

  Stacey Wolfe, MD

  Associate Professor, Neurosurgery
  Wake Forest School of Medicine, United States

  Disclosure information not submitted.
• 

  Aarti Sarwal, MD, FAAN, FNCS,FCCM

  Medical Director, Neurocritical Care
  Wake Forest Baptist Health Center
  Winston-Salem, North Carolina

  Disclosure information not submitted.

Title: Cardiac Ultrasound Guided Hemodynamic Management to Augment Cerebral Perfusion

Case Report Body:

Introduction: Cardiac ultrasound (CUS) can guide hemodynamic management in critically-ill patients by assessing parameters like inferior vena cava diameter, left ventricle (LV) end-diastolic area, and LV outflow tract velocity time integer. Neurocritically-ill patients may need vasopressors for induced hypertension (HTN) to maintain cerebral perfusion pressure (CPP). This can be complicated in hypertrophic obstructive cardiomyopathy (HOCM) physiology where vasopressors may reduce cardiac output (CO) due to tachycardia or increased peripheral vascular resistance (PVR). We used CUS parameters to guide systolic blood pressure (SBP) targets to optimize CPP in a patient requiring induced HTN due to an occluded external–internal carotid (EC-IC) bypass to encourage cerebral collateralization.

Description: A 70-year-old male with multiple TIAs per day due to left internal carotid occlusion despite permissive HTN and antiplatelets underwent EC-IC bypass. The bypass occluded within 24 hours of surgery and he developed paraphasic speech errors and right-sided weakness corresponding to left MCA territory, with penumbra in the region of the bypass on CT perfusion. Induced HTN of 160-180 mmHg via norepinephrine infusion normalized these neurologic deficits. However, he developed episodes of neurologic deterioration with SBPs >180, similar to the episodes at SBP < 140, which prompted echocardiogram that showed increased aortic outflow gradient of 53 mmHg and reduced CO with underlying HOCM physiology. We decreased target SBP sequentially to 140-160 to prevent worsening of the LV outflow tract obstruction, confirmed by aortic outflow gradient improving to 19 mmHg on reduced SBP goal. The patient remained asymptomatic and was transitioned from norepinephrine to midodrine prior to discharge with SBP goal 140-160. He has been maintained on midodrine with only 1 subsequent TIA at home in the ensuing 3 months while dehydrated with an SBP drop to 120s.

Discussion: Induced HTN is used in several scenarios in neurocritically-ill patients with flow limiting cerebral hemodynamic pathology. Concomitant HOCM physiology may impair CO at higher blood pressures due to vasopressors increasing PVR and cardiac afterload. Use of serial CUS parameters can be useful in such scenarios to guide optimal range of blood pressures.