Study guide
Acute Coronary, Valvular, Rhythm & Aortic Emergencies
ABPN Neurocritical Care Study Guide Exam
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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU
Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU
2 Chapter 2: Cerebral Physiology & Intracranial Dynamics
Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes
3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management
Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions
4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management
Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy
5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management
Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury
6 Chapter 6: Neuropharmacology, Analgesia & Sedation
ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU
7 Bleeding, Thrombosis & Hematologic Emergencies
Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine
Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention
9 Systemic Trauma & Environmental Injury
Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging
10 Cardiac Emergencies & Mechanical Support
IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies
11 Kidney Injury, Acid–Base & Renal Replacement
Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement
12 Systemic Infection & Endocrine Emergencies
Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies
13 Gastrointestinal & Hepatic Emergencies
Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects
14 Chapter 9: Neuroimaging in the Neuro-ICU
Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness
15 Chapter 10: Electrophysiology & Neuromonitoring
Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler
16 Angiography, Electrodiagnosis & CSF Analysis
Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage
17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria
Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria
18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies
Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction
19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage
Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH
20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia
Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations
21 Venous, Spinal & Traumatic Vascular Disease
Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury
22 Chapter 15: Traumatic Brain & Spinal Cord Injury
Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes
23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies
Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure
24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis
Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies
25 Neuroinflammation & Neurooncology
Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies
26 Pregnancy, Transplantation & Pediatric Care
Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care
27 Chapter 18: Neurosurgical & Perioperative Emergencies
Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies
28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU
Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor
Acute Coronary, Valvular, Rhythm & Aortic Emergencies
Key Takeaways Explain This Topic AI
Cerebral T waves and elevated troponin do not exclude an acute coronary occlusion.
Unstable tachyarrhythmia or severe bradycardia requires immediate hemodynamic management while the cause is investigated.
Acute severe valve dysfunction can cause shock without the loud murmur expected in chronic disease.
Acute aortic dissection can present with focal neurologic deficits; antithrombotic or thrombolytic treatment can be hazardous.
Last updated: October 2026
Cardiac Physiology as a Clinical Decision Tool
Cardiac output equals heart rate multiplied by stroke volume. Stroke volume depends on preload, contractility, afterload, and valve function. A higher arterial pressure after a pure vasoconstrictor does not necessarily mean that cardiac output or tissue oxygen delivery improved. Conversely, reducing excessive afterload can improve forward flow in selected patients but may sacrifice cerebral perfusion if systemic pressure falls too far.
The outline includes acute coronary syndromes, valvular disorders, arrhythmias, pacing, and aortic dissection. In a neurologically impaired patient, ischemic chest pain may be unreportable. New pulmonary edema, unexplained shock, ventricular arrhythmia, ECG changes, or regional wall motion abnormalities may therefore be the presenting clues. Evaluate the cardiac problem in parallel with the neurologic diagnosis rather than assuming that all abnormalities result from sympathetic stress.
Acute Coronary Syndrome and Its Mimics
Stress cardiomyopathy can produce marked ventricular dysfunction with relatively modest troponin elevation and wall motion abnormalities extending beyond one coronary territory. These findings raise suspicion but do not reliably exclude a concurrent coronary lesion. Obtain serial ECGs and biomarkers and assess echocardiography in context. Persistent ischemic changes, shock, or malignant arrhythmias may require urgent coronary evaluation.
Type 1 myocardial infarction reflects an acute coronary atherothrombotic event. Type 2 infarction involves ischemia from a supply-demand imbalance; elevated troponin without clinical evidence of ischemia is myocardial injury rather than automatically either type of infarction. Hypoxemia, anemia, tachycardia, hypotension, renal dysfunction, and systemic inflammation complicate interpretation in the ICU.
Antiplatelet and anticoagulant treatment can conflict with an active intracranial hemorrhage. The correct response is an urgent joint decision among cardiology and neurologic teams, considering the immediate threats and potential interventions. Neither automatic administration nor indefinite withholding of every antithrombotic is a universal answer. A recent coronary stent adds a specific risk of stent thrombosis if therapy is stopped.
Valvular and Mechanical Causes of Shock
Problem Physiologic consequence Important diagnostic clue
Acute severe mitral regurgitation Abrupt elevation of left atrial pressure and pulmonary edema New shock or edema with acute ischemia or endocarditis
Acute aortic regurgitation Ineffective forward flow and elevated LV filling pressure Dissection, endocarditis, or acute valve injury
Severe aortic stenosis Fixed outflow limitation and vulnerability to hypotension Valve imaging, limited stroke-volume reserve
Prosthetic valve dysfunction Obstruction, regurgitation, or embolism New valve findings, altered anticoagulation, infection, or hemolysis
Acute regurgitation may have a short or relatively soft murmur because pressures equalize rapidly. A reassuring auscultation does not substitute for echocardiography. TTE is the initial bedside study; TEE can be needed for prosthetic valves, suspected endocarditis, or anatomy not resolved by TTE, after considering procedural risks. Treat cardiogenic shock and obtain urgent structural or surgical assessment when a correctable lesion is suspected.
Tachyarrhythmia, Bradycardia, and Pacing
First ask whether the rhythm is causing instability: hypotension, altered consciousness, ischemia, or acute heart failure. Unstable organized tachyarrhythmias generally require synchronized cardioversion; pulseless VT or VF requires defibrillation and resuscitation. Polymorphic rhythms may require an unsynchronized shock when synchronization is impossible. Correct hypoxemia and electrolyte abnormalities and review QT-prolonging or conduction-slowing drugs.
Atrial fibrillation in critical illness can reflect infection, adrenergic stress, or fluid and cardiac disease. Rate or rhythm treatment depends on pressure, ventricular function, onset, and the risk of treatment. Avoid reflex administration of a negative inotrope in decompensated shock. Anticoagulation decisions require separate assessment of embolic and intracranial bleeding risks.
Symptomatic severe bradycardia or high-grade AV block may need medication and transcutaneous pacing while transvenous support is arranged. Confirm mechanical capture with a perfusion signal, not pacing spikes alone. Persistent high-grade block without a reversible cause can require a permanent pacemaker. If bradycardia accompanies new pupillary changes and severe hypertension, treat the intracranial emergency promptly; if it independently compromises circulation, manage both problems simultaneously.
Aortic Dissection and the Neurologic Presentation
Acute aortic dissection may involve carotid branches, spinal arteries, coronary ostia, the aortic valve, or the pericardium. A patient can present with stroke, spinal cord ischemia, syncope, limb ischemia, tamponade, or shock, sometimes without a classic pain description. Pulse or pressure asymmetry, a new regurgitant murmur, or an appropriate imaging finding heightens concern but absence of these signs does not exclude disease.
When dissection is suspected, obtain urgent appropriate aortic imaging and surgical or vascular consultation. Thrombolysis for a presumed ordinary ischemic stroke can be dangerous in this setting. In a hypertensive patient, impulse control commonly begins with rate control and then additional pressure control, while preserving organ perfusion. Hypotension demands investigation for rupture, tamponade, severe regurgitation, or malperfusion rather than routine escalation of antihypertensive drugs. Type A dissection generally requires emergency surgical evaluation.
Sources checked October 17, 2026: AHA 2025 adult advanced life support and ACC/AHA aortic disease guideline .