Study guide
9.2 Arrhythmias and Pacing
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)
9.2 Arrhythmias and Pacing
Key Takeaways Explain This Topic AI
Atrial fibrillation with rapid ventricular response after stroke or SAH is treated first as a cerebral-perfusion problem: restore an adequate MAP, slow the rate with a blood-pressure–tolerant agent, and cardiovert immediately if the patient is unstable.
Anticoagulation after ICH is individualized: AHA/ASA 2022 guidance finds early resumption reasonable for mechanical valves and LVADs, and considers later restart (often discussed around 7–8 weeks) for nonvalvular AF; after craniotomy, therapeutic anticoagulation waits on a stable scan and the surgeon.
QTc above about 500 ms, or a large interval increase, plus hypokalemia, hypomagnesemia, bradycardia, and ICU drugs (haloperidol, methadone, ondansetron, many fluoroquinolones and macrolides) sets up torsades de pointes; give intravenous magnesium even if the serum magnesium is in the ‘normal’ range.
Cushing bradycardia is treated by lowering ICP, not by making atropine the primary therapy; high cervical spinal cord injury causes unopposed vagal bradycardia and asystole, especially with suctioning or hypoxia.
Transcutaneous pacing is an emergency bridge; transvenous pacing is temporary when a reliable capture is needed; a permanent pacemaker is for bradycardia expected to persist after reversible causes are treated. Beta blockers after SAH can worsen hypotension and delayed cerebral ischemia.
Last updated: September 2026
Why rhythm control is a CPP problem
Quick answer: Atrial fibrillation (AF) with rapid ventricular response (RVR) after stroke or SAH cuts diastolic filling and MAP. Slow the rate without causing hypotension; cardiovert if unstable. Therapeutic anticoagulation after ICH or craniotomy is delayed and individualized—mechanical valves restart earlier than nonvalvular AF. Torsades de pointes (TdP) is pause-dependent polymorphic ventricular tachycardia in a long-QT setting; give intravenous magnesium and stop culprits. Cushing bradycardia means treat ICP. High cervical spinal cord injury (SCI) causes unopposed vagal asystole that may need pacing if medicines fail.
The same 140-beats-per-minute run that a medical ICU might watch on telemetry can drop stroke volume enough to lose the CPP floor after TBI or to lose induced hypertension during delayed cerebral ischemia. The exam tests whether you pick a rate-control drug that the blood pressure can tolerate, whether you know conceptually when anticoagulation restarts after intracranial bleeding or a craniotomy, and whether you can tell an ICP-driven bradycardia from a cord-driven one.
AF with RVR after stroke or SAH
New or recurrent AF is common after ischemic stroke, ICH, and aneurysmal SAH. Mechanisms include catecholamine surge, atrial stretch from volume, inflammation, and pre-existing atrial disease unmasked by the acute illness. RVR (typically ventricular rates sustained above about 110–120 beats per minute, and certainly rates above 150) shortens diastole, reduces left-ventricular filling, raises myocardial oxygen demand, and can precipitate type 2 MI or pulmonary edema in a stunned ventricle.
Unstable RVR —shock, pulmonary edema, or ongoing myocardial ischemia—gets immediate synchronized cardioversion. Do not wait for a therapeutic anticoagulant in a crashing patient; the unstable brain needs MAP now. If the AF has lasted more than 48 hours and the patient is stable enough to wait, consider a transesophageal echocardiogram to look for left-atrial appendage thrombus before elective cardioversion; that luxury disappears when CPP is falling.
Stable RVR is a rate-control problem first. Choose the agent by ventricular function and blood pressure:
Situation Prefer Avoid as first-line
Preserved ejection fraction, MAP comfortable Short-acting intravenous beta blocker (esmolol) or diltiazem, titrated Bolus diltiazem that drops MAP below the CPP target
Reduced ejection fraction or NSM without LVOTO Amiodarone; cautious beta blocker if MAP allows Large diltiazem or verapamil boluses
LVOTO from Takotsubo basal hyperkinesis Short-acting beta blocker plus phenylephrine if hypotensive Inotropes and arterial vasodilators
Borderline MAP needed for delayed cerebral ischemia Amiodarone or a very cautious esmolol titration; add a vasopressor if you must Any agent that trades a prettier ECG for a CPP of 45 mm Hg
Digoxin may slow the resting rate but is a weak acute agent when catecholamines are high. Correct hypokalemia, hypomagnesemia, hypoxia, fever, and pain—those are reversible drivers of RVR.
Anticoagulation timing after ICH, ischemic stroke, and craniotomy
Know the concept, not a fake universal day number that erases hematoma size and surgical detail.
After ICH , AHA/ASA 2022 guidance stops and reverses anticoagulation immediately. Restart is a risk–benefit decision. Early resumption is reasonable when thrombotic risk is very high (mechanical heart valve, left ventricular assist device). For nonvalvular AF, resumption may be reasonable ; many teaching summaries discuss considering initiation around 7–8 weeks, tailored to hematoma size, location (lobar cerebral amyloid angiopathy bleeds recur more than deep hypertensive bleeds), age, and CHA2DS2-VASc-type thromboembolic risk. Antiplatelet agents may be reasonable to restart when atherosclerotic benefit outweighs re-bleed risk; RESTART did not show a surge in recurrent ICH, but the median time to restart was 76 days.
After AF-related ischemic stroke , older teaching used a 1–3–6–12-day scheme (TIA, small, moderate, large infarct). Contemporary practice, including ELAN (2023), supports earlier oral anticoagulation in milder infarcts and more delay when the infarct is large or already shows hemorrhagic transformation. Bridging with full-dose heparin is generally not helpful and increases hemorrhage. After intravenous thrombolysis, still wait for the ~24-hour scan before starting anticoagulation (Section 9.1).
After craniotomy , therapeutic anticoagulation waits for hemostasis, a stable postoperative scan, and the operating surgeon. Pharmacologic venous-thromboembolism prophylaxis often begins about 24–48 hours after a stable scan. A mechanical valve may force an earlier, monitored restart (sometimes a heparin infusion with serial imaging) because valve thrombosis can be fatal within days; nonvalvular AF almost never requires that urgency in the first postoperative week.
QTc prolongation and torsades de pointes
Corrected QT (commonly Bazett QTc = QT / √RR) lengthens when delayed rectifier potassium current is blocked. Risk concentrates when QTc exceeds about 500 ms , when QTc has increased by more than about 60 ms from baseline, and when several insults stack: female sex, heart failure, congenital long-QT syndrome, bradycardia, pauses, hypokalemia, hypomagnesemia, hypocalcemia, and drug combinations.
- Common neuro-ICU culprit Why it matters
- Intravenous haloperidol , droperidol High TdP risk among antipsychotics, especially intravenous
- Methadone IKr block; risk rises with dose, bradycardia, and other QT drugs
- Ondansetron Additive QT effect, especially intravenous and with other risk factors
- Fluoroquinolones, macrolides, azole antifungals Stacked IKr block with antiemetics and antipsychotics
- Sotalol , procainamide, quinidine Marked QT drugs; amiodarone prolongs QT but TdP is less common
- Citalopram / escitalopram at high dose Dose-related QT effect
TdP is polymorphic ventricular tachycardia that twists around the baseline, usually launching after a pause (short–long–short sequence). Unstable or pulseless TdP is defibrillated. For recurrent pause-dependent TdP with a pulse, give intravenous magnesium sulfate (typically 1–2 g, repeat as needed) even if the serum magnesium is numerically normal, stop every culprit drug, replete potassium toward the high-normal range (many labs use a target around 4.5 mEq/L in this setting), and accelerate the heart rate with isoproterenol or temporary overdrive pacing to shorten the QT and abolish pauses. Do not give a class Ia or III agent “for ventricular tachycardia” when the rhythm is pause-dependent TdP.
Bradyarrhythmias: high ICP versus cervical SCI
Cushing bradycardia is reflex vagal slowing from intracranial hypertension, often paired with hypertension and irregular respiration (Cushing triad). The heart is a messenger. Treat ICP—airway and oxygenation, head position, osmotherapy, cerebrospinal fluid drainage, surgical decompression—rather than chasing every low heart-rate number with atropine while the brain herniates. Atropine may raise heart rate transiently; it does not replace CPP restoration.
High cervical SCI (especially C5 and above, complete injuries) interrupts descending sympathetic fibers and leaves unopposed vagal tone. Bradycardia and asystole cluster in the first 1–2 weeks, classically triggered by tracheal suctioning, turning, hypoxia, or tracheal stimulation. Keep atropine at the bedside. Oxygen, atropine, vasopressors with chronotropy (dopamine, norepinephrine, epinephrine), and methylxanthines (aminophylline or theophylline) are the usual medical ladder. Recurrent asystole despite those measures is the usual indication to pace.
Other reversible bradycardias in this unit include beta-blocker or calcium-channel-blocker overdose, high-dose dexmedetomidine, hypothyroidism, inferior ischemia, and severe hyperkalemia. Reverse those before declaring a need for a lifelong generator.
Transcutaneous, transvenous, and permanent pacing
Mode Role Neuro-ICU pearls
Transcutaneous pacing Immediate bridge for unstable bradycardia or asystole while you prepare a better solution Painful; capture is unreliable; sedate if the patient is conscious; confirm mechanical capture with a pulse, not only with pacing spikes
Temporary transvenous pacing Hours to days of reliable ventricular (or AV sequential) capture Use for high-grade AV block, recurrent SCI asystole, or pause-dependent TdP that needs overdrive; balloon-tipped catheters can cause ventricular perforation or infection
Permanent pacemaker Bradycardia expected to persist after reversible causes are treated ACC/AHA indications include symptomatic sinus-node dysfunction and high-grade or complete AV block not expected to recover; in SCI, implant when life-threatening bradyarrhythmias persist despite medicines, not prophylactically in every C5 injury
Do not implant a permanent pacemaker for Cushing bradycardia. Do not leave a patient with recurrent SCI asystole on transcutaneous pads for days because “the cord might wake up tomorrow.”
Beta blockers after SAH: theoretical protection, practical hypotension
Catecholamine toxicity is the rationale for beta blockade after SAH, and some observational series associated pre-admission beta blockers with less stress cardiomyopathy. Prospective proof that starting a beta blocker in the ICU improves neurologic outcome is lacking. The practical harm is obvious: nimodipine already lowers blood pressure, stunned myocardium may not tolerate negative inotropy, and hypotension undercuts CPP and the induced-hypertension strategy for delayed cerebral ischemia.
Use a short-acting agent (esmolol) if you need a beta blocker for LVOTO, for aortic-dissection anti-impulse therapy (Section 9.3), or for ischemic coronary disease with a MAP that can spare the milligrams. Do not start a long-acting beta blocker in a hypotensive, vasospasm-prone SAH patient “for neuroprotection.” If heart failure with recovered or recovering stunning needs chronic neurohormonal therapy, start it after the patient is euvolemic and no longer pressor-dependent.