Study guide
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves
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)
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves
Key Takeaways Explain This Topic AI
Neurogenic stunned myocardium and Takotsubo syndrome after aneurysmal SAH are catecholamine-mediated: wall-motion abnormalities (apical ballooning or an inverted basal/midventricular pattern) that extend beyond one coronary territory, modest troponin rise, ECG ST-T and QTc changes, and recovery over days to weeks.
The Fourth Universal Definition (2018) defines type 1 MI as acute atherothrombosis from plaque rupture or erosion and type 2 MI as ischemic injury from supply–demand mismatch without acute plaque rupture; an isolated troponin rise without ischemic evidence is myocardial injury, not MI.
After intravenous alteplase or tenecteplase, AHA/ASA early-management guidance (2019 update) is to obtain follow-up CT or MRI at about 24 hours before starting antiplatelets or anticoagulants unless a separate, documented indication forces an earlier exception.
Severe aortic stenosis is preload-dependent with a fixed obstruction: avoid hypotensive arterial vasodilators and tachycardia; phenylephrine or norepinephrine supports blood pressure when left-ventricular function is preserved.
Severe aortic regurgitation wants afterload reduction and a relatively faster heart rate; severe mitral stenosis needs a slow ventricular rate so diastolic filling time is preserved.
Last updated: September 2026
Why the heart is a cerebral-perfusion organ
Quick answer: After aneurysmal subarachnoid hemorrhage (SAH) , neurogenic stunned myocardium (NSM) and Takotsubo syndrome produce transient wall-motion abnormalities (classically apical ballooning ), a modest troponin rise, and electrocardiogram (ECG) changes that recover over days to weeks. Type 1 myocardial infarction (MI) is plaque rupture with coronary thrombosis; type 2 MI is supply–demand mismatch without acute atherothrombosis. After intravenous thrombolysis, hold antiplatelets and anticoagulants until about 24-hour imaging excludes hemorrhage. In severe aortic stenosis (AS) , avoid hypotensive arterial vasodilators and tachycardia.
The neuro ICU lives at the intersection of cardiac output (CO) and cerebral perfusion pressure (CPP) . CO equals heart rate times stroke volume. Stroke volume is set by preload, afterload, and contractility. CPP equals mean arterial pressure (MAP) minus intracranial pressure (ICP), or minus right atrial pressure if that value is higher. A stunned ventricle, a stenotic valve, or a tachyarrhythmia that steals diastolic filling time will drop MAP and therefore CPP even if the intracranial vault has not changed.
Acute brain injury—especially high-grade SAH, large intracerebral hemorrhage (ICH) , and severe ischemic stroke—triggers a catecholamine storm via the insular cortex, hypothalamus, and brainstem. Circulating epinephrine and norepinephrine produce contraction-band necrosis, coronary microvascular spasm, and wall-motion abnormalities that do not follow a single epicardial artery. That shared mechanism explains NSM and Takotsubo syndrome. This exam asks whether you recognize the phenotype and protect the brain, not whether you send every elevated troponin to the catheterization laboratory while an unsecured aneurysm is still at risk of rerupture.
Physiology you actually use at the bedside
Preload is wall stretch at end-diastole. After SAH the fluid prescription is euvolemia: too little preload collapses CO; too much preload in a stunned left ventricle produces pulmonary edema and hypoxemia that then injure the brain. Afterload is the impedance to ejection. A stunned ventricle is afterload-sensitive; a severely stenotic aortic valve is a fixed obstruction, so dropping systemic vascular resistance may drop coronary and cerebral perfusion without raising stroke volume. Contractility falls in NSM, septic cardiomyopathy, and type 1 infarct; it is not interchangeable with a high lactate, which has many noncardiac causes (seizure, liver failure, epinephrine, β2-agonists).
Heart rate matters because of diastolic filling time. Atrial fibrillation (AF) with rapid ventricular response (RVR) shortens diastole, cuts left-ventricular filling, and is especially dangerous in mitral stenosis (MS) and severe AS. Conversely, severe aortic regurgitation (AR) worsens with bradycardia because a longer diastole means more regurgitant volume back into the left ventricle.
Coronary perfusion of the left ventricle occurs mainly in diastole and depends on the gradient between aortic diastolic pressure and left-ventricular end-diastolic pressure. Hypotension, severe AR with a very low diastolic pressure, and extreme tachycardia all steal coronary flow and can convert stunning into true ischemia.
Neurogenic stunned myocardium and Takotsubo after SAH
NSM is transient left-ventricular dysfunction, ECG change, and biomarker leak after acute brain injury, classically aneurysmal SAH. Takotsubo syndrome (stress cardiomyopathy, apical ballooning syndrome) is the overlapping phenotype: hypokinesis of mid and apical segments with basal hyperkinesis, wall-motion abnormalities extending beyond one coronary territory, and recovery over days to weeks (sometimes longer if the initial ejection fraction is very low). In SAH, inverted basal or midventricular patterns are also common; you do not need a classic octopus-pot apex to make the diagnosis.
Typical bedside cluster:
Modest troponin rise that is small relative to the wall-motion abnormality. An older conventional-assay series (Bulsara and colleagues, 2003) found peak cardiac troponin I often far below values seen in MI with a similar ejection fraction; a historical teaching cut of less than 2.8 ng/mL with ejection fraction under 40% favored stunning on those assays. Do not treat that number as a modern high-sensitivity troponin rule-out.
ECG: deep T-wave inversions, ST depression or elevation, QTc prolongation, and occasionally Q waves that later resolve. The ECG territory often disagrees with the echocardiogram.
N-terminal pro–B-type natriuretic peptide (NT-proBNP) may be disproportionately high compared with the modest troponin.
Recovery of wall motion over days to a few weeks in most patients; delayed recovery is more often reported with lower initial ejection fraction and ongoing acute neurologic illness.
Incidence depends on definition. ECG changes are very common after SAH. Troponin elevation occurs in roughly one-fifth to two-fifths of patients in many series. Regional wall-motion abnormalities appear in about 10–30%. Frank Takotsubo is a smaller subset. Higher clinical grade, female sex, and more severe hemorrhage appear more often in series of cardiac injury.
Distinguishing NSM from type 1 infarction
Take the reperfusion pathway when the story is type 1 acute coronary syndrome: ischemic chest pain, regional wall motion in a single coronary territory, a rising-and-falling troponin typical of coronary occlusion, ST-elevation MI criteria, or instability you cannot attribute to neurogenic stunning. Coronary computed tomographic angiography is a lower-risk alternative when the aneurysm is unsecured and the pretest probability of plaque rupture is intermediate. Do not delay aneurysm securement solely to “clear the coronaries” if the echo–ECG–troponin mismatch is classic NSM.
Management of NSM is supportive: euvolemia, treat pulmonary edema without drying the patient into delayed cerebral ischemia, and phenotype the shock. If there is left ventricular outflow tract obstruction (LVOTO) from basal hyperkinesis and systolic anterior motion of the mitral valve, avoid inotropes and arterial vasodilators; use cautious volume, a pure vasopressor (phenylephrine or vasopressin), and a short-acting beta blocker only if blood pressure allows. If the problem is pump failure without LVOTO, a non-catecholamine inotrope such as milrinone may raise CO for cerebral perfusion, but milrinone vasodilates—expect hypotension and have a vasopressor ready. Repeat echocardiography in days to document recovery.
Type 1 versus type 2 MI in the ICU
The Fourth Universal Definition of Myocardial Infarction (2018) separates myocardial injury (troponin above the 99th percentile upper reference limit) from MI (injury plus evidence of acute ischemia: symptoms, new ischemic ECG change, new Q waves, or new regional wall-motion abnormality). Isolated troponin leak in sepsis, NSM, or chronic kidney disease is injury, not MI.
Category Mechanism Typical neuro-ICU example Immediate implication
Myocardial injury without ischemia Myocyte damage without an ischemic syndrome Sepsis, NSM without ischemic ECG, chronic kidney disease Treat the cause; do not reflexively start dual antiplatelet therapy
Type 1 MI Acute atherothrombosis from plaque rupture or erosion STEMI or NSTEMI from coronary occlusion Reperfusion pathway, antithrombotics, catheterization laboratory
Type 2 MI Supply–demand mismatch without acute plaque rupture Shock, hypoxia, severe anemia, sustained RVR, extreme hypertension Fix the imbalance; angiography only if type 1 cannot be excluded or the patient remains unstable
Type 3–5 MI Death before biomarkers, or MI related to PCI or CABG Peri-procedural injury Context-specific; not the usual SAH troponin stem
Type 2 MI is common in the neuro ICU because fever, neurogenic pulmonary edema, AF with RVR, and induced hypertension for delayed cerebral ischemia all raise demand or cut supply. Treatment is oxygen, transfusion if severely anemic, rate control, and blood-pressure hygiene—not automatic heparin plus a P2Y12 inhibitor while a fresh hematoma is still expanding.
Antithrombotic conflict after brain bleed or thrombolysis
This is the daily negotiation between myocardium and brain parenchyma.
After intravenous alteplase or tenecteplase for ischemic stroke, AHA/ASA early-management guidance (2019 update) is to obtain follow-up CT or MRI at about 24 hours before starting anticoagulants or antiplatelet agents, unless a separate indication (for example an endovascular stent) forces an earlier, documented exception. Aspirin for ischemic stroke otherwise starts within 24–48 hours of onset when lytics were not given.
After spontaneous ICH , stop the offending antithrombotic and reverse it (warfarin: four-factor prothrombin complex concentrate plus vitamin K; dabigatran: idarucizumab; factor Xa inhibitors: andexanet alfa, with the ANNEXA-I NEJM 2024 finding of better hematoma-expansion control versus usual care but more thrombotic events including ischemic stroke). AHA/ASA 2022 ICH guidance: early resumption of anticoagulation is reasonable for very high thrombotic-risk hardware (mechanical valve, left ventricular assist device); for nonvalvular AF, resumption may be reasonable , and many summaries discuss considering initiation around 7–8 weeks, individualized by hematoma size, location, age, and thromboembolic risk. Antiplatelet resumption may be reasonable when ischemic benefit outweighs bleed risk; RESTART’s median restart was 76 days, so “restart aspirin tomorrow after every ICH” is not what that trial proved.
After craniotomy , therapeutic anticoagulation is a surgeon-timed decision. Pharmacologic venous-thromboembolism prophylaxis often starts about 24–48 hours after a stable postoperative scan; full-dose anticoagulation for AF is usually delayed days to weeks unless a mechanical valve forces an earlier, monitored restart.
Acute coronary syndrome needing dual antiplatelet therapy (DAPT) after recent ICH or after thrombolysis is not solved by a single recipe. Options include delaying non-emergent catheterization, using a brief parenteral anticoagulant without a P2Y12 load until imaging is stable, preferring radial access, and sitting cardiology with neurosurgery. Do not start DAPT the same night as a large unsecured ICH because a troponin is 0.08 ng/mL from NSM.
Severe valvular disease: ICU pearls
Lesion Hemodynamic logic Do Do not
Severe AS Fixed obstruction; the left ventricle is preload-dependent and coronary flow is tenuous Maintain sinus rhythm and avoid tachycardia; phenylephrine or norepinephrine for hypotension if left-ventricular function is preserved; cautious diuresis for frank edema Routine nitroglycerin or other hypotensive vasodilators; uncontrolled AF with RVR; hypovolemia
Severe AR Afterload-sensitive regurgitant leak; bradycardia lengthens diastole and increases regurgitant volume Afterload reduction (nitroprusside) if not hypotensive; relatively faster heart rate; urgent surgery for acute severe AR (often from type A dissection or endocarditis) Intra-aortic balloon pump (diastolic inflation worsens regurgitation); pure vasoconstrictors as first-line; relying on medical therapy in acute severe AR
Severe MS Filling across a stenotic mitral valve needs diastolic time Slow the ventricular rate; restore sinus rhythm if possible; vasopressin or phenylephrine if a pressor is required Tachycardic inotropes as first-line; afterload reduction that drops coronary and cerebral perfusion
Nitroprusside exception in AS: Khot and colleagues ( New England Journal of Medicine 2003) showed that in monitored, nonhypotensive patients with severe AS, reduced ejection fraction, and high systemic vascular resistance, nitroprusside can raise cardiac index. That is not permission to give nitroglycerin to a hypotensive older adult with a loud murmur and a neurogenic stunned ventricle.
Acute AR from type A aortic dissection is a surgical emergency. Beta blockade for the dissection (to cut dP/dt) conflicts with the faster heart-rate preference of isolated AR—treat dissection physiology first and get the patient to the operating room.
The usual exam stem is an SAH patient with apical ballooning, a troponin of 0.4 ng/mL, and T-wave inversions. Support blood pressure for the brain, secure the aneurysm, repeat the echocardiogram, and do not start DAPT as if this were a type 1 non–ST-elevation MI.