Study guide
8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
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)
8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
Key Takeaways Explain This Topic AI
Auto-PEEP is incomplete emptying: flow has not reached zero before the next breath; treat it by lengthening expiratory time (lower rate, shorter inspiratory time), not by raising rate to “blow off CO2.”
Permissive hypercapnia protects the obstructed or ARDS lung but is limited or contraindicated when high ICP or a threatened herniation physiology needs a controlled PaCO2.
Status asthmaticus combines bronchodilators, steroids, and a slow ventilator (low rate, long expiratory time); a sudden arrest is often auto-PEEP — disconnect the circuit and compress the chest.
PAH crises worsen with hypoxia, hypercarbia, acidosis, high PEEP, and systemic hypotension; support the RV by keeping SVR up and avoiding those PVR triggers.
Neuro ICU bronchoscopy is for secretion plugs, lobar atelectasis, and BAL; coughing, hypoventilation, hypercapnia, and hypoxia during the procedure can spike ICP, so keep it brief on FiO2 1.0 with a secured airway and monitored CPP.
Last updated: September 2026
Obstructive lung disease, pulmonary arterial hypertension, and bronchoscopy share a theme in the neuro ICU: maneuvers that look lung-protective or diagnostic can still raise PaCO2, drop venous return, or spike ICP. This section covers auto-PEEP, the ICP limit on permissive hypercapnia, status asthmaticus, pulmonary arterial hypertension pitfalls, and why a “quick scope” is not neurologically free.
Auto-PEEP and dynamic hyperinflation
Auto-PEEP (intrinsic PEEP) is alveolar pressure that remains positive at end-expiration because the next breath starts before the lung has emptied. Causes are high airway resistance (COPD, asthma), high minute ventilation, a short expiratory time, and early airway collapse. Detection:
Expiratory flow on the ventilator graphic does not return to zero before the next breath.
An end-expiratory pause (passive patient) reveals a pressure above the set PEEP; that difference is auto-PEEP.
Rising plateau and peak pressures, progressive hypotension, and a rising PaCO2 despite a high set rate are late clues.
In a spontaneous patient, auto-PEEP is an inspiratory threshold load: the patient must generate enough negative pleural pressure to overcome trapped pressure before the ventilator triggers.
- Lever Effect on auto-PEEP Comment
- Lower respiratory rate More expiratory time First and best lever in asthma and COPD
Shorter inspiratory time / lower I:E (e.g., 1:4 or 1:5) More time to empty Watch for incomplete inspiration if too extreme
- Modest tidal volume (about 6–8 mL/kg PBW) Less volume to empty Do not chase a normal PaCO2 with 10–12 mL/kg
- Treat bronchospasm and secretions Lower resistance Nebulizers, steroids, suction, consider a larger ETT
Applied PEEP in COPD (often ~80% of measured auto-PEEP) Can ease triggering Do not routinely add high external PEEP in pure asthma; airways collapse dynamically
Raise the set rate to “blow off CO2” Worsens trapping Classic exam trap
If a ventilated asthmatic or COPD patient arrests or loses a pulse with high airway pressures , disconnect the ventilator, allow a long passive exhale, and manually compress the chest to empty the lungs. That is auto-PEEP tamponade of venous return, not primary cardiogenic shock.
Permissive hypercapnia — and its ICP ceiling
Permissive hypercapnia means accepting a PaCO2 above 45 mm Hg (often with pH down toward ~7.20 if hemodynamics allow) so that you do not use injurious tidal volumes or respiratory rates. It is a standard tool in status asthmaticus, severe COPD, and ARDS.
It is not a free variable when the brain is tight. Hypercapnia dilates cerebral arterioles, increases cerebral blood volume, and can raise ICP. Relative or absolute limits include:
- Uncontrolled intracranial hypertension or an evolving herniation syndrome
- Large mass lesions, especially in the posterior fossa, where small volume changes matter
- Acute ICH or SAH with a labile ICP tracing
In those patients, keep tidal volume lung-protective and look for other CO2 tools (treat auto-PEEP so effective alveolar ventilation actually rises, reduce circuit dead space, treat fever and shivering, consider deeper sedation only if the examination can be spared). Do not return to 12 mL/kg tidal volumes to decorate an ABG, and do not use prolonged hyperventilation to PaCO2 < 25 mm Hg as daily ICP control. If both the lung and the brain are refractory, that is an ECMO / rescue conversation, not a reason to abandon either organ.
Status asthmaticus
Status asthmaticus is an asthma exacerbation that does not respond to initial bronchodilators and threatens respiratory failure. Medical therapy is continuous nebulized beta-agonists, ipratropium, systemic corticosteroids, and magnesium sulfate (typically 2 g IV) in severe obstruction. Adjuncts include ketamine for intubation sedation (bronchodilation), and, in extreme cases, inhaled anesthetics or ECMO. Heliox can buy time in selected non-intubated patients but cannot be delivered easily on every ICU ventilator.
If intubation is required, the ventilator strategy is slow and empty :
- Respiratory rate often 10–14 /min, not 20+
- Tidal volume ~6–8 mL/kg PBW
- Long expiratory time; tolerate hypercapnia if ICP allows
Peak pressure will be high from resistance; believe the plateau — if plateau is modest, the problem is airway resistance, not baby-lung overdistention
Deep sedation to prevent stacking; neuromuscular blockade briefly if needed to measure plateau and empty the lung
Never “fix” hypercapnia by cranking rate in a still-tight chest
Neuro overlap: a patient intubated for convulsive status epilepticus may also have severe bronchospasm from aspiration or from a beta-blocker given for hypertension. Treat both. Permissive hypercapnia after a seizure is in tension with ongoing ICP risk; check the examination, imaging, and, if an EVD is present, the tracing before you decide that a pH of 7.18 is acceptable.
Pulmonary arterial hypertension in the ICU
Pulmonary arterial hypertension (PAH) (WHO Group 1) is a pulmonary vascular disease with high pulmonary vascular resistance (PVR) and a pressure-overloaded right ventricle. Group 2 is left-heart disease, Group 3 chronic lung disease/hypoxia, Group 4 chronic thromboembolic disease; the ICU crash physiology is similar: the RV fails when PVR jumps or systemic pressure falls.
PVR rises with hypoxia, hypercarbia, and acidosis — the three ventilator sins. High PEEP and high tidal volume overdistend alveoli and also raise PVR. Systemic hypotension cuts the RV coronary perfusion gradient (aortic pressure minus RV intramural pressure). Volume overload dilates the RV, flattens the septum, and starves the LV.
- Pitfall Why it crashes the RV Better move
- Hypoxia Hypoxic pulmonary vasoconstriction raises PVR Adequate FiO2; treat atelectasis without extreme PEEP
Hypercarbia / acidosis Independent PVR increase; combined effect is worse Ventilate enough to keep pH and PaCO2 reasonable
High PEEP / high VT West Zone 1, high afterload Modest PEEP, 6 mL/kg PBW
Intubation without a plan Apnea, hypoxia, loss of sympathetic tone Push-dose vasopressors ready; experienced airway; avoid long apnea
Phenylephrine as the only pressor Can raise PVR; pure vasoconstriction without inotropy Norepinephrine or vasopressin to keep SVR; dobutamine or milrinone if more inotropy is needed (watch the SVR drop with milrinone)
Stopping chronic PAH infusions Rebound pulmonary hypertensive crisis Continue epoprostenol/treprostinil; add inhaled nitric oxide or inhaled epoprostenol for acute V/Q-selective vasodilation
Fluid boluses for every hypotension RV dilation and septal shift Use echo; small aliquots only if the RV is underfilled
Intubation in decompensated PAH has a grim reputation for peri-intubation arrest. Avoid it if noninvasive support and pulmonary vasodilators can close the gap. If you must intubate, preoxygenate, keep the first bagged breaths small, start a vasopressor before the propofol, and do not permit a hypoxic/hypercapnic apnea. VA-ECMO is a rescue bridge in selected refractory RV failure.
Bronchoscopy in the neuro ICU
Flexible bronchoscopy is both diagnostic and therapeutic. Typical indications :
- Secretion plugging and lobar or whole-lung atelectasis that does not recruit with suction and physiotherapy
- BAL when VAP organisms or unusual pathogens (immunocompromised, atypical) will change therapy
- Airway inspection for blood, a malpositioned tube, or suspected obstruction
- Guidance for percutaneous tracheostomy (a different procedure with its own ICP literature)
It is not first-line for every dirty-looking film. A brief, well-sedated suction and a recruitment-aware ventilator adjustment often suffice.
The neuro cost is real. The bronchoscope occupies the endotracheal tube, so alveolar ventilation falls and PaCO2 rises . Coughing, light sedation, hypoxia, and increased intrathoracic pressure all impede cerebral venous drainage and raise cerebral blood volume. Prospective work in brain-injured patients has shown ICP increases during fiberoptic bronchoscopy , sometimes by more than 10–20 mm Hg, even when CPP is later restored. Patients with a baseline ICP already > 15 mm Hg are at particular risk of pathologic peaks (the same pattern is reported during percutaneous tracheostomy).
- Step Purpose
- ETT large enough (often ≥ 8.0 mm ID in adults) Leave an annular channel for ventilation
- FiO2 1.0 for several minutes before and during the procedure Blunt hypoxia
- Head of bed up, neck neutral Jugular drainage
- Deep sedation ± brief neuromuscular blockade Stop cough and ventilator dyssynchrony
- Topical lidocaine Less airway reactivity
- Limit scope time; suction in short bursts Limit CO2 rise
- Monitor SpO2, ETCO2 or transcutaneous CO2, MAP, and ICP/CPP if a monitor is present Treat a spike in real time
- Hold the EVD at a defined level; do not let it dangle or clot unseen Avoid unrecognized ICP or overdrainage
Uncontrolled ICP, refractory hypoxia on FiO2 1.0, and an undersized tube are reasons to defer or to use a rigid, planned approach with anesthesia rather than a casual bedside look. After BAL, expect a transient oxygenation dip; warn the team before a trip to CT or a prone turn.
Putting the three problems on one ventilator
A single neuro ICU patient can have COPD auto-PEEP, a P/F ratio that tempts high PEEP, and an ICP of 25 mm Hg. Rank the immediate threats: empty the lung if auto-PEEP is tamponading the circulation, protect the brain from hypercapnia and hypoxia, then titrate PEEP. Bronchoscopy, if needed for a plug, waits until ICP is treated and the tube and sedation are ready. That ordering — circulation, brain gases, then procedures — is the practical exam answer when the stem piles on comorbidities.