Study guide
9.3 Acute Aortic Dissection and Cardiac Ultrasound
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)
9.3 Acute Aortic Dissection and Cardiac Ultrasound
Key Takeaways Explain This Topic AI
Stanford type A dissection involves the ascending aorta and is an emergency surgical disease; type B spares the ascending aorta and is treated with anti-impulse medical therapy unless it is complicated by malperfusion, rupture, or refractory pain.
Reduce dP/dt first with an intravenous beta blocker (esmolol or labetalol) to a heart rate near 60 beats per minute, then add a vasodilator such as nicardipine or nitroprusside if systolic pressure remains high; a vasodilator given first causes reflex tachycardia and worse aortic shear.
AHA/ASA guidance classifies intravenous alteplase as harmful in acute ischemic stroke known or suspected to be associated with aortic arch dissection; look for chest or back pain, pulse deficit, inter-arm blood-pressure difference, aortic regurgitation, syncope, and hypotension.
Neurologic malperfusion includes carotid (often right-hemisphere) ischemic stroke and spinal cord infarction, typically an anterior spinal artery pattern: motor and pain/temperature loss with relatively spared dorsal-column sensation.
Bedside transthoracic echo answers four exam-ready questions—left-ventricular function, right-ventricular strain, pericardial tamponade physiology, and IVC size/collapsibility—and can suggest type A complications, but a normal TTE does not rule out dissection.
Last updated: September 2026
Why dissection is a stroke mimic that can kill twice
Quick answer: Stanford type A involves the ascending aorta and needs emergency surgery. Type B spares the ascending aorta and is managed with heart-rate and blood-pressure control unless complicated. Start an intravenous beta blocker to cut dP/dt, then a vasodilator if pressure remains high. Do not give intravenous alteplase or tenecteplase when stroke is known or suspected to come from aortic arch dissection . Bedside transthoracic echocardiography (TTE) assesses left-ventricular function, right-ventricular strain, tamponade, and the inferior vena cava (IVC); it cannot exclude dissection.
A patient can arrive with hemiparesis and no pain. Type A dissection extends into a carotid artery, occludes a true lumen, or embolizes. If you follow an ordinary lytic clock, you may convert a surgical disease into tamponade, extension of the flap, or fatal hemorrhage. Mortality in untreated type A dissection is often taught as about 1–2% per hour in the first 48 hours. The exam tests the classification, the drug sequence, the neurologic malperfusion patterns, and a short list of ultrasound findings—not a full echocardiography fellowship.
Stanford A versus B (and why the names matter)
The Stanford system asks one question: is the ascending aorta involved?
Feature Stanford type A Stanford type B
Anatomy Any dissection that involves the ascending aorta, regardless of where the intimal tear started Dissection that spares the ascending aorta (descending ± arch without ascending involvement in common teaching)
Default treatment Emergency open repair (replace the ascending aorta; address the aortic valve and coronaries as needed) Anti-impulse medical therapy in an ICU if uncomplicated
When to operate or stent Always involve cardiac surgery immediately Complicated type B: rupture, malperfusion, refractory pain or hypertension, rapid expansion → typically thoracic endovascular aortic repair
Neuro-ICU traps Carotid malperfusion, tamponade, acute AR, coronary ostial occlusion mimicking STEMI Spinal malperfusion, visceral or limb ischemia, delayed aneurysmal degeneration
The older DeBakey system (I = ascending plus distal; II = ascending only; III = descending) still appears in stems. A newer “non-A non-B” label is sometimes used for arch-entry tears that spare the ascending aorta; those patients still need aortic specialists, not a lytic checklist.
Pulse deficit (asymmetric pulses or a substantial inter-arm systolic difference, often taught around 20 mm Hg) supports the diagnosis and implies branch compromise. It is present in fewer than half of patients. Absence of a pulse deficit does not exclude dissection. Other bedside clues: abrupt tearing chest or interscapular pain, syncope, a new AR murmur, hypotension or tamponade, a widened mediastinum, and a neurologic deficit that does not match a typical lacunar story.
Neurologic malperfusion
The flap or false lumen can obstruct:
Carotid arteries , most often the innominate/right common carotid pathway, producing a right-hemisphere syndrome (left hemiparesis, aphasia if the patient has mixed or right-hemisphere language dominance is less typical—expect a large right MCA picture). Up to about two-thirds of dissection-related ischemic strokes in some series relate to supra-aortic extension rather than hypotension alone.
Left carotid or vertebral origins, producing left-hemisphere or posterior-circulation syndromes.
Anterior spinal artery supply, producing spinal cord infarction: bilateral motor loss, loss of pain and temperature, relatively preserved dorsal-column vibration and proprioception, often with a thoracic sensory level. Type B dissection is the classic aortic cause of this pattern.
Global hypoperfusion from tamponade, severe AR, or shock, which looks like coma or watershed injury rather than a single carotid.
Syncope in type A is not “vasovagal” until tamponade and carotid occlusion have been considered.
Anti-impulse therapy: beta block first, then vasodilate
Aortic wall stress tracks the product of pressure and the rate of pressure rise (dP/dt). The sequence is not optional:
Control pain and anxiety (they drive catecholamines).
Start a titratable intravenous beta blocker— esmolol or labetalol —and bring the heart rate to about 60 beats per minute (many protocols accept a range near 60–80 as long as shear is down and perfusion is intact).
If systolic blood pressure remains high, add a vasodilator: nicardipine , clevidipine , or nitroprusside . Typical systolic targets are 100–120 mm Hg provided the brain, cord, kidneys, and gut still perfuse. Complicated malperfusion may force a higher floor until the true lumen is restored.
If the patient cannot take a beta blocker, a nondihydropyridine calcium-channel blocker is the usual alternative for rate control before a pure vasodilator.
Never start nitroprusside or nicardipine first in an untreated, tachycardic dissection. Reflex tachycardia increases dP/dt and can extend the flap. Once the heart rate is controlled, vasodilators are appropriate. In type A with acute AR, remember that a very slow heart rate lengthens diastole and can worsen regurgitation—still start the beta blocker for shear, and move to the operating room rather than fine-tuning medical AR therapy.
Do not thrombolyse a stroke that is actually dissection
AHA/ASA eligibility language states that intravenous alteplase in acute ischemic stroke known or suspected to be associated with aortic arch dissection is potentially harmful and should not be administered (Class III: Harm). Case series of inadvertent lytics report very high mortality, on the order of 70% in compiled reports, from tamponade, rupture, and uncontrolled hemorrhage.
Clues that should stop the lytic hand: chest or back pain with the deficit, syncope, hypotension, pulse or blood-pressure asymmetry, a new AR murmur, a widened mediastinum, a dissection flap on carotid ultrasound or CTA of the neck, or a pericardial effusion on bedside echo. Cervical arterial dissection that is not an aortic arch dissection is a different entity; AHA/ASA language is more permissive for extracranial cervical dissection. The deadly mix-up is aortic dissection presenting as hemispheric stroke.
CTA from chest through neck and head is the practical single test when suspicion is more than trivial. D-dimer can support screening in some protocols but does not clear a high-probability patient. TTE may show a proximal flap, a dilated root, AR, or tamponade—useful to rule in complications, not to rule out the diagnosis. If the patient needs mechanical thrombectomy for a large-vessel occlusion caused by the flap, that is a surgical/endovascular aortic discussion, not a standard stroke-lytics pathway.
Bedside TTE: four questions, not a full echo course
You are not being tested as a level-III echocardiographer. You are being tested on whether you can use four views—parasternal long axis, parasternal short axis, apical four-chamber, and subcostal—to answer four management questions.
1. Left-ventricular function
Eyeball ejection fraction and look for regional wall-motion abnormalities. Global hypokinesis plus a modest troponin after SAH supports NSM. A territorial wall-motion abnormality plus ST elevation supports type 1 MI. Basal hyperkinesis with apical ballooning supports Takotsubo; look also for LVOTO and systolic anterior motion if the patient crashes after an inotrope. A hyperdynamic, underfilled cavity supports hypovolemia or vasoplegia.
2. Right-ventricular strain
Acute pressure overload (massive pulmonary embolism, hypoxia with high ventilator pressures) dilates the right ventricle, flattens the interventricular septum in short axis ( D-sign ), and can produce McConnell’s sign (mid-free-wall hypokinesis with apical sparing) in pulmonary embolism. A strained right ventricle plus a plethoric IVC argues against giving a large fluid bolus. This is how TTE separates obstructive shock from hypovolemic shock in a hypotensive stroke patient who cannot lie flat for a perfect study.
3. Pericardial tamponade
Tamponade is a clinical diagnosis helped by ultrasound. Findings that matter:
Pericardial effusion (size alone does not equal tamponade; a small acute postsurgical or dissection-related effusion can kill).
Right atrial systolic collapse and right ventricular diastolic collapse .
IVC plethora with little inspiratory collapse in a spontaneously breathing patient.
Exaggerated respirophasic variation of mitral and tricuspid inflows (ventricular interdependence).
In type A dissection, hemopericardium is an indication for surgery, not for percutaneous pericardiocentesis as destination therapy—draining the sac can restart bleeding from the false lumen. If the patient is in arrest, a drainage attempt may be a bridge to the operating room; that is salvage, not routine.
4. IVC as a right-atrial-pressure hint
In a spontaneously breathing patient, an IVC diameter less than 2.1 cm with greater than 50% inspiratory collapse is often taught as low right atrial pressure (about 0–5 mm Hg). A diameter greater than 2.1 cm with less than 50% collapse suggests higher pressure (about 10–20 mm Hg). Intermediate combinations sit in between. This estimate fails with high positive end-expiratory pressure, abdominal hypertension, and right-ventricular failure, and it is not a volume-responsiveness test by itself. On positive-pressure ventilation, look at distensibility rather than collapsibility, and only if the patient is fully adapted to the ventilator.
What TTE is not: a clearance test for dissection, a substitute for transesophageal echocardiography in the operating room, or a license to skip CTA when the chest-pain-plus-stroke story is sitting in front of you. Use it to find the complication that changes the next five minutes—tamponade, severe LV failure, massive RV strain—and then complete anatomic imaging.