Study guide
8.1 Pulmonary Physiology and ARDS (01.N.1–2)
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)
8.1 Pulmonary Physiology and ARDS (01.N.1–2)
Key Takeaways Explain This Topic AI
Berlin ARDS is acute (≤1 week) bilateral opacities not fully explained by heart failure, with PEEP or CPAP ≥5 cm H2O: mild P/F 201–300, moderate 101–200, severe ≤100 mm Hg.
The ARDS Network ARMA trial cut death before home unassisted breathing from 39.8% to 31.0% using 6 mL/kg predicted body weight and plateau pressure ≤30 cm H2O, not actual weight.
PROSEVA used ≥16-hour prone sessions in P/F ≤150 mm Hg ARDS and lowered 28-day mortality from 32.8% supine to 16.0% prone in experienced centers.
ROSE found no 90-day mortality difference for early continuous cisatracurium versus lighter sedation (42.5% versus 42.8%); early neuromuscular blockade is not automatic.
In neuro ICU patients, prone positioning and permissive hypercapnia can raise ICP; carbon dioxide is a cerebral vasodilator, and hardware or an unstable spine may preclude proning.
Last updated: September 2026
Pulmonary failure is a daily problem in the neuro ICU. Arterial oxygen and carbon dioxide set cerebral blood flow, intracranial pressure (ICP), and secondary ischemic risk, so a ventilator change is also a brain change. This section covers the gas-exchange physiology that makes those trade-offs predictable, then the ARDS bundle that still drives most exam items: the Berlin definition , low tidal volume, plateau-pressure limits, PEEP/FiO2 tables used as titration recipes, prone positioning from PROSEVA, and the ROSE nuance that early neuromuscular blockade is not automatic.
West zones of the lung
John B. West described regional pulmonary blood flow as the interaction of alveolar pressure (Palv) , pulmonary arterial pressure (Part) , and pulmonary venous pressure (Pven) . In an upright person the gradient runs from apex to base. In a supine ICU patient the same physics runs from nondependent (ventral) to dependent (dorsal) lung — which is why prone positioning recruits dorsal units rather than “the bases.”
Zone Pressure ranking Blood flow Clinical meaning
1 (nondependent) Palv > Part > Pven None Alveolar dead space . Rare in health; appears with hypotension, hypovolemia, or high Palv from PEEP or tidal overdistention.
2 Part > Palv > Pven Intermittent (“waterfall”) Flow during systole; more recruitment as Part rises.
3 (dependent) Part > Pven > Palv Continuous Most of a normal lung; extra-alveolar vessels held open.
4 High interstitial / extra-alveolar pressure Reduced Very dependent lung; edema and airway closure cut flow.
Raising PEEP or dropping cardiac output can convert Zone 3 into Zone 1: more dead space, a higher PaCO2 for the same minute ventilation, and a lower mixed-venous PO2 if stroke volume falls. An “oxygenation win” from PEEP can still harm the brain if PaCO2 rises or mean arterial pressure falls and cerebral perfusion pressure (CPP) follows it down.
Shunt versus dead space
Ventilation–perfusion (V/Q) mismatch is a spectrum, not two diseases. Shunt is perfusion without ventilation (V/Q → 0). Dead space is ventilation without perfusion (V/Q → ∞). Low-but-not-zero V/Q units behave like shunt for oxygen but still exchange some CO2; high-but-not-infinite V/Q units waste ventilation.
- Feature Shunt (low V/Q → 0) Dead space (high V/Q → ∞)
- Physiology Blood skips ventilated alveoli Gas skips perfused capillaries
Classic causes Atelectasis, pneumonia, ARDS flooding, intracardiac right-to-left shunt Pulmonary embolism, Zone 1 from high PEEP, low cardiac output, emphysema
- PaO2 and A-a gradient PaO2 falls; A-a gradient widens PaO2 may stay near normal until mixed-venous O2 falls
- 100% oxygen True shunt does not fully correct Low V/Q units usually improve
- PaCO2 Often normal or low if minute ventilation rises Rises unless minute ventilation increases
Bedside therapy Recruit: PEEP, prone positioning, drainage, treat pneumonia Restore perfusion: treat PE, avoid overdistention, support cardiac output
The shunt fraction is Qs/Qt = (CcO2 − CaO2) / (CcO2 − CvO2). Dead-space fraction by the Bohr equation is Vd/Vt = (PaCO2 − PECO2) / PaCO2; a normal value is about 0.30 and it climbs in PE and in overdistended ARDS. Exam items usually ask you to match the pattern (hypoxemia that ignores oxygen versus hypercapnia after a PE or a PEEP jump), not to grind the algebra.
Berlin definition of ARDS
The 2012 Berlin definition remains the diagnostic frame most vignettes still use. ARDS is acute hypoxemic respiratory failure with four required pieces:
Timing — within 1 week of a known clinical insult or of new or worsening respiratory symptoms.
Chest imaging — bilateral opacities not fully explained by effusions, lobar collapse, or nodules.
Origin of edema — respiratory failure not fully explained by cardiac failure or fluid overload. Use echocardiography when there is no clear risk factor.
Oxygenation — PaO2/FiO2 ( P/F ) measured on at least 5 cm H2O of PEEP (CPAP is allowed for mild disease).
- Severity P/F ratio (mm Hg) Minimum PEEP/CPAP Approximate mortality in the Berlin derivation
- Mild 200 < P/F ≤ 300 PEEP or CPAP ≥ 5 ~27%
- Moderate 100 < P/F ≤ 200 PEEP ≥ 5 ~32%
- Severe P/F ≤ 100 PEEP ≥ 5 ~45%
A 2024 global definition expanded ARDS to include patients on high-flow nasal oxygen, allowed SpO2/FiO2 criteria, and described resource-limited settings without a PEEP requirement. Board-style stems still typically hand you a P/F ratio on PEEP ≥ 5 and expect Berlin severity. Common neuro ICU precipitants are aspiration at intubation, pneumonia, transfusion, sepsis, and neurogenic or mixed pulmonary edema that then meets Berlin criteria if it persists.
Low tidal volume and plateau pressure
The ARDS Network ARMA trial ( NEJM 2000) randomized 861 adults with early ALI/ARDS to a starting tidal volume of 6 mL/kg predicted body weight (PBW) with a plateau-pressure ceiling of 30 cm H2O , versus 12 mL/kg PBW with a 50 cm H2O ceiling. Death before discharge home breathing unassisted was 31.0% versus 39.8% (P = 0.007), and ventilator-free days improved. That is the strongest mortality evidence in ARDS ventilation.
Tidal volume is not based on actual body weight. ARDSNet PBW:
- Men: 50 + 0.91 × (height in cm − 152.4)
- Women: 45.5 + 0.91 × (height in cm − 152.4)
Worked example: a 170 cm woman has PBW ≈ 45.5 + 0.91 × 17.6 ≈ 61.5 kg . Target tidal volume at 6 mL/kg is about 370 mL . If she weighs 90 kg, 6 mL/kg actual weight is 540 mL — enough to overdistend the small remaining “baby lung.” Measure plateau pressure with an end-inspiratory pause on a passive patient. If plateau exceeds 30 cm H2O, reduce tidal volume toward 4 mL/kg PBW . Driving pressure (plateau − PEEP) near or below 15 cm H2O tracks mortality in observational work (Amato, NEJM 2015); it supplements, rather than replaces, the 6 mL/kg starting rule.
The FACTT trial showed that a conservative fluid strategy increased ventilator-free days in ARDS once shock was resolving — relevant when osmotherapy, SAH euvolemia, and lung water compete in the same patient.
PEEP and FiO2 tables, conceptually
ARDSNet published lower-PEEP / higher-FiO2 and higher-PEEP / lower-FiO2 tables. They are matched titration recipes, not proofs that one PEEP is “correct.” You move PEEP and FiO2 together to keep oxygenation in a protocol band (classically PaO2 55–80 mm Hg or SpO2 88–95%) while watching plateau pressure, dead space, blood pressure, and RV function.
- Concept Lower-PEEP table Higher-PEEP table
- FiO2 0.30–0.40 PEEP often 5–8 cm H2O PEEP already ~8–14 cm H2O
- FiO2 0.60–0.70 PEEP ~10–14 PEEP ~14–20
- FiO2 1.0 PEEP 18–24 PEEP 18–24
- Trade-off Less hemodynamic hit, more oxygen toxicity More recruitment, more Zone 1 dead space and RV afterload
Pick a table and stay on it; do not mix rows from both. High PEEP can flatten the right ventricle, raise Vd/Vt, and drop CPP if MAP falls. The ART trial of aggressive stepwise recruitment plus high PEEP increased mortality — recruitment maneuvers are not routine rescue.
Prone positioning: PROSEVA
PROSEVA ( NEJM 2013) enrolled intubated patients with P/F ≤ 150 mm Hg , FiO2 ≥ 0.60, and PEEP ≥ 5, and used prone sessions of at least 16 consecutive hours . Twenty-eight-day mortality was 16.0% prone versus 32.8% supine in experienced European centers that also used low tidal volume (and, in most patients, neuromuscular blockade during the turn). Proning recruits dorsal lung, improves V/Q matching, and can unload the right ventricle.
Neuro ICU constraints are the exam twist:
Uncontrolled ICP, an unstable cervical or thoracolumbar spine, an unprotected craniectomy bone flap, a tenuous airway, and EVD, bolt, or lumbar-drain hardware that cannot be secured are relative or absolute barriers.
The turn itself can spike ICP via abdominal pressure, neck rotation that impairs jugular drainage, and coughing.
If you prone a monitored patient, keep the neck neutral , raise the head as much as the position allows, lock the EVD to a stated reference, and watch ICP and CPP through the turn — not only after it.
Neuromuscular blockade: ACURASYS versus ROSE
ACURASYS (2010) reported a 90-day mortality benefit from 48 hours of cisatracurium in early severe ARDS (P/F ≤ 150), with both groups deeply sedated. ROSE (PETAL Network, NEJM 2019) compared early continuous cisatracurium plus deep sedation with a lighter-sedation usual-care strategy in moderate-to-severe ARDS. Ninety-day in-hospital mortality was 42.5% versus 42.8% (stopped early for futility), and the cisatracurium group had more cardiovascular adverse events. Contemporary teaching: early neuromuscular blockade is not automatic . Use it when severe asynchrony, double-triggering, or prone positioning cannot be managed with sedation and ventilator adjustment. Paralysis erases the neurologic examination and can mask seizures — a high price in the neuro ICU.
Hypercapnia versus the injured brain
Lung-protective ventilation often raises PaCO2. Carbon dioxide is a potent cerebral vasodilator ; hypercapnia increases cerebral blood flow and can raise ICP. Permissive hypercapnia that is acceptable in a medical ICU ARDS patient may be unacceptable after TBI, ICH, or a tight posterior fossa. Do not treat herniation with prolonged hypocapnia: the Brain Trauma Foundation 4th edition reserves brief hyperventilation as a bridge and warns against PaCO2 < 25 mm Hg . Keep tidal volume at 6 mL/kg PBW and look for other ways to control CO2: modest respiratory-rate increases if auto-PEEP allows, reduced circuit dead space, treating shock, and, in refractory hypoxemic/hypercapnic ARDS, extracorporeal support rather than 12 mL/kg volumes. Oxygen targets still matter: hypoxia also increases cerebral blood flow and can worsen ICP, so the goal is lung protection without abandoning the brain.