Study guide
16.2 Transcranial Doppler (02.D)
ABIM Neurocritical Care Subspecialty Certification Exam
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1 Introduction & Exam Overview
1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide
2 ICU Neurologic Exam, Cerebral Physiology, and CSF
2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology
3 Core Neuropharmacology
3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes
4 Reperfusion Drugs, Airway, and Ventilation
4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation
5 Hemodynamics and Shock
5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock
6 Nutrition, Temperature, and ICU Prophylaxis
6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)
7 General Trauma
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation
8 Pulmonary Critical Care
8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
9 Cardiovascular Critical Care
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound
10 Renal and Infectious Disease
10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed
11 Endocrine and Salt-Water Disorders
11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
12 Gastrointestinal Critical Care
12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)
13 Hematologic Disorders
13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)
14 Neuroimaging
14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography
15 EEG, EMG, and CSF Analysis
15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)
16 ICP, TCD, and Multimodality Monitoring
16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)
17 Brain Death and Bedside Procedures
17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)
18 Coma, Anoxia, and Intracranial Hypertension
18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)
19 Acute Ischemic Stroke
19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)
20 Intraparenchymal Hemorrhage
20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)
21 SAH, CVST, and Spinal Cord Infarction
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)
22 Vascular Anomalies and Traumatic Brain Injury
22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)
23 Spine, Hydrocephalus, and CNS Infection
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)
24 Seizures and Neuromuscular Emergencies
24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)
25 Inflammatory Disease, Neuro-Oncology, and Special Populations
25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)
26 Neurosurgical and Perioperative Complications
26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)
27 Ethics, Prognostication, and Organ Donation
27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)
16.2 Transcranial Doppler (02.D)
Key Takeaways Explain This Topic AI
MCA mean flow velocity ≥120 cm/s raises concern for vasospasm; ≥200 cm/s is the commonly taught severe-spasm velocity when the Lindegaard ratio is also high.
Lindegaard ratio is MCA mean velocity divided by extracranial ICA mean velocity: >3 supports vasospasm and >6 is commonly taught as severe spasm.
High MCA velocity with a Lindegaard ratio <3 favors hyperemia (or high flow) rather than isolated angiographic vasospasm.
Oscillating (to-and-fro) flow and systolic spikes can support death by neurologic criteria only as ancillary data; they do not replace the clinical examination and apnea test.
Temporal-window failure is common, especially in older patients with cranial hyperostosis; absent signal is not the same as absent flow.
Last updated: September 2026
Transcranial Doppler (TCD) is pulsed-wave ultrasound of the large intracranial arteries through relatively thin bone windows. On the exam it appears as a surveillance tool after aneurysmal subarachnoid hemorrhage, a way to separate vasospasm from hyperemia , a detector of microemboli, and—carefully—an ancillary pattern in death by neurologic criteria. Independent ExamFinch teaching covers TCD as listed under diagnostic studies (02.D). It does not replace catheter angiography, the clinical diagnosis of delayed cerebral ischemia, or the full brain-death chapter.
What the probe actually measures
TCD reports peak systolic , end-diastolic , and mean flow velocity (MFV) , usually in centimeters per second, plus derived indices. Mean velocity in the middle cerebral artery (MCA) is the workhorse number after subarachnoid hemorrhage because the MCA is the easiest large vessel to insonate and because MCA spasm is common.
The Gosling pulsatility index (PI) is (peak systolic − end-diastolic) / mean velocity. A rising PI can accompany high distal resistance, including high ICP or distal vasospasm, but PI is not a substitute for an ICP catheter. Direction of flow (toward or away from the probe) and depth of insonation tell you which vessel you think you are in; guessing the vessel from velocity alone is a common error.
- Vessel (typical window) Approximate depth Typical flow relative to probe
- MCA (transtemporal) About 45–55 mm Toward the probe
- ACA (transtemporal) About 60–75 mm Away from the probe
- Terminal ICA (transtemporal) About 60–65 mm Toward the probe
- PCA (transtemporal) About 55–70 mm Variable by P1 versus P2
- Ophthalmic / siphon (transorbital) Shallower / deeper Ophthalmic toward; siphon variable
- Vertebral (suboccipital) About 60–80 mm Away from the probe
- Basilar (suboccipital) About 80–100+ mm Away from the probe
- Extracranial ICA (submandibular) Along the neck Used for the Lindegaard ratio
- Windows and technical failure
Four windows matter:
Transtemporal — MCA, ACA, PCA, terminal ICA. This is the daily SAH study.
Transorbital — ophthalmic artery and carotid siphon; reduce power because of the eye.
Suboccipital / transforaminal — vertebrals and basilar.
Submandibular — extracranial ICA for the Lindegaard ratio .
Technical failure is not rare. About 10–20% of adults, disproportionately older patients and people with thicker temporal bone (hyperostosis), have inadequate temporal windows. Absent Doppler signal then means you could not insonate, not that the MCA is occluded. Confirm with another window, a different operator, or a different modality (CT angiography, catheter angiography, or perfusion imaging) before you treat absent TCD as absent flow. Poor angle of insonation, restless movement, and surgical dressings also degrade studies. TCD is operator-dependent; a single high number on one shift should be compared with the patient's baseline velocities from earlier days, not with a textbook in isolation.
Vasospasm surveillance after subarachnoid hemorrhage
Angiographic vasospasm and delayed cerebral ischemia (DCI) are related but not identical. TCD detects velocity changes that often accompany large-vessel narrowing. DCI remains a clinical diagnosis (a new focal deficit or a drop in consciousness not explained by hemorrhage, hydrocephalus, seizure, or infection). Do not start intra-arterial therapy from a velocity alone in a well patient, and do not dismiss DCI because yesterday's TCD was reassuring.
Commonly taught MCA MFV bands (always interpret with the Lindegaard ratio and the examination):
- MCA mean flow velocity Common teaching
- <120 cm/s Unlikely significant MCA spasm (high negative predictive value)
- 120–149 cm/s Mild spasm if the ratio is also elevated
- 150–199 cm/s Moderate spasm if the ratio is also elevated
- ≥200 cm/s Severe spasm if the ratio is also elevated (high specificity when both are high)
Daily studies from roughly day 4 through day 14 after aneurysm rupture catch the usual spasm window. A rising trend is more informative than one isolated value. Anterior cerebral and basilar spasm are harder to catch; the Sviri ratio (basilar MFV / extracranial vertebral MFV) is sometimes used for the posterior circulation, but MCA plus Lindegaard is the exam's core pair.
Lindegaard ratio: spasm versus hyperemia
High velocity is not automatically spasm. Fever, anemia, hypercarbia, induced hypertension, and global hyperemia all raise flow. The Lindegaard ratio is:
- Lindegaard ratio = MCA MFV / extracranial ICA MFV
- (the extracranial ICA sampled in the submandibular window)
Common teaching:
- Lindegaard ratio Interpretation with high MCA velocity
- <3 Hyperemia or high flow; not isolated MCA spasm
- >3 Consistent with vasospasm (mild when the ratio is in the 3–6 band)
- >6 Commonly taught severe vasospasm
Worked example: MCA MFV 210 cm/s and extracranial ICA MFV 30 cm/s give a ratio of 7 , which is severe-spasm teaching territory. MCA MFV 180 cm/s and extracranial ICA MFV 90 cm/s give a ratio of 2 , which is hyperemia despite the impressive MCA number. Treating the second patient with balloon angioplasty as if the artery were string-like is the classic error.
TCD sensitivity versus digital subtraction angiography is only moderate and is best for the MCA; specificity is higher at extreme velocities. A normal TCD does not exclude distal or small-vessel spasm. Catheter angiography remains the anatomic reference when endovascular treatment is on the table.
Emboli detection
High-intensity transient signals (HITS) or microembolic signals are brief, unidirectional intensity spikes in the Doppler spectrum. They appear in carotid stenosis, after carotid or cardiac procedures, with mechanical valves, and in some dissection or vasculitis cases. Counting emboli is a specialized monitoring mode (often with a headset for a set time), not a 30-second bedside sweep. A few signals do not by themselves prove an indication for anticoagulation; they add a mechanism when the clinical question is artery-to-artery embolization versus hemodynamic failure.
Ancillary patterns in death by neurologic criteria
When the clinical examination and apnea test cannot be completed, some jurisdictions accept ancillary tests of cerebral blood flow. TCD patterns that support circulatory arrest include:
- Oscillating / to-and-fro flow (anterograde systole, retrograde diastole)
- Short systolic spikes without diastolic flow
- Eventually, no demonstrable flow if windows are adequate
These patterns are ancillary . They do not replace prerequisites, a complete brainstem examination, or apnea testing as taught in the brain-death chapter. Inadequate windows make TCD unusable as an ancillary test. Do not pronounce death by neurologic criteria from a single TCD screenshot, and do not confuse a high-resistance waveform in a living patient with intracranial hypertension for a death study.
What to do with a concerning study
If velocities and the Lindegaard ratio climb and the patient is worse, look for a treatable cause of DCI: hypovolemia, hypotension, anemia, hypoxia, fever, hyponatremia, hydrocephalus, and seizure. Nimodipine 60 mg orally every 4 hours for 21 days remains standard for aneurysmal SAH as a DCI-outcome drug; it is not a TCD-triggered rescue. Induced hypertension (not classic triple-H therapy) is the usual hemodynamic step for symptomatic DCI after the aneurysm is secured. Endovascular angioplasty or intra-arterial vasodilators are reserved for selected patients with clinical and imaging evidence of large-vessel spasm, not for hyperemia.
TCD is a trend tool. Pair it with the examination, ICP/CPP when a monitor is in place, and vessel or perfusion imaging when the story does not fit.