Study guide
5.2 IABP, Temporary VADs, LVAD, and ECMO
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)
5.2 IABP, Temporary VADs, LVAD, and ECMO
Key Takeaways Explain This Topic AI
Intra-aortic balloon pump counterpulsation is contraindicated in moderate-to-severe aortic regurgitation and in aortic dissection because diastolic inflation worsens regurgitant volume and can extend a dissection flap.
DanGer Shock (NEJM 2024) found that Impella CP plus standard care reduced 180-day death versus standard care in STEMI-related cardiogenic shock (45.8% vs 58.5%), at the cost of more bleeding, limb ischemia, and renal-replacement therapy.
VV-ECMO supports gas exchange when cardiac output is adequate; VA-ECMO supports both perfusion and gas exchange in refractory cardiogenic shock or extracorporeal CPR, but raises left-ventricular afterload.
LVAD neurologic injury clusters around pump thrombosis, ischemic versus hemorrhagic stroke, device-related infection, and the antithrombotic dilemma of a circuit that clots if you stop warfarin and a brain that bleeds if you do not.
After ECMO-associated intracranial hemorrhage, stop systemic anticoagulation immediately; VV-ECMO can often run heparin-free for more than two days, whereas VA-ECMO off anticoagulation carries a higher circuit and arterial thromboembolism risk.
Last updated: September 2026
Why these devices belong on a neurocritical care exam
Quick answer: An intra-aortic balloon pump (IABP) is contraindicated in severe aortic regurgitation and aortic dissection . Veno-venous ECMO (VV-ECMO) treats refractory hypoxemic or hypercapnic respiratory failure with adequate cardiac output; veno-arterial ECMO (VA-ECMO) treats refractory cardiogenic shock or cardiac arrest. After intracranial hemorrhage on ECMO , stop heparin now; VV circuits can often remain off anticoagulation longer than VA circuits.
Patients arrive in the neuro ICU on pumps after cardiac arrest, after massive pulmonary embolism, after infarction-related shock with a large hemispheric stroke, or as destination left ventricular assist device (LVAD) recipients who then bleed or infarct. You will be asked to recognize device-specific contraindications, to distinguish ischemic from hemorrhagic stroke in an anticoagulated pump patient, and to know when the circuit itself is embolizing the brain.
Intra-aortic balloon pump
The IABP sits in the descending thoracic aorta, typically via the femoral artery, with the tip just distal to the left subclavian artery. Helium inflation in diastole raises aortic diastolic pressure and coronary perfusion. Rapid deflation in systole lowers afterload and myocardial work. On an arterial tracing you should see diastolic augmentation higher than unassisted systolic pressure when the balloon is timed to the dicrotic notch. Weaning usually steps from 1:1 to 1:2 to 1:3 counterpulsation.
Classic indications include cardiogenic shock as a bridge to recovery or revascularization, mechanical complications of infarction (acute mitral regurgitation, ventricular septal defect), and selected high-risk percutaneous coronary intervention. IABP-SHOCK II showed no 30-day mortality benefit for routine IABP in infarct-related shock, so do not treat the balloon as proven mortality therapy; still know the physiology and the contraindications, because those remain testable and clinically decisive.
Absolute or near-absolute contraindications include moderate-to-severe aortic regurgitation (diastolic inflation worsens regurgitant volume, raising left-ventricular preload and wall stress) and aortic dissection (the balloon can enter the false lumen, extend the flap, or rupture the aorta). Severe peripheral arterial disease, an untreated abdominal aortic aneurysm, and uncontrolled bleeding are additional reasons to stay out of the aorta. After a surgically repaired type A dissection, rare salvage IABP use has been reported; that exception does not make unrepaired dissection an acceptable insertion setting.
Complications the neurointensivist sees include ipsilateral limb ischemia, cholesterol or thrombus emboli to brain or viscera, balloon rupture with helium embolus, and thrombocytopenia. An IABP also invalidates many pulse-contour cardiac-output algorithms (Section 5.1).
Temporary ventricular support
Temporary ventricular assist devices unload a failing ventricle more than an IABP. The Impella family is a microaxial pump sitting across the aortic valve, drawing blood from the left ventricle and expelling it into the ascending aorta (Impella RP or a ProtekDuo cannula can support the right ventricle). Contraindications include left-ventricular thrombus, a mechanical aortic valve, and severe aortic stenosis or regurgitation that prevents safe crossing or creates a closed-loop regurgitant circuit.
DanGer Shock (Møller and colleagues, New England Journal of Medicine 2024) randomized patients with ST-elevation myocardial infarction and cardiogenic shock to Impella CP plus standard care versus standard care. Death at 180 days was 45.8% versus 58.5% (hazard ratio 0.74). A composite of severe bleeding, limb ischemia, hemolysis, device failure, or worsening aortic regurgitation was much higher with the pump (24.0% versus 6.2%), and renal-replacement therapy was more common (41.9% versus 26.7%). The trial supports selected use in infarct-related shock; it does not make Impella a default for every hypotensive neuro ICU patient, and older patients may not share the mortality benefit.
Other temporary configurations include TandemHeart (transseptal left-atrial drainage to a femoral arterial return) and surgically placed Impella 5.5 via the axillary artery when longer support or ambulation is planned. Escalation from IABP to a temporary VAD to VA-ECMO follows the amount of flow and the degree of biventricular or respiratory failure, not a fixed ladder you must climb in every case.
Durable LVAD: the antithrombotic dilemma
Continuous-flow LVADs (HeartMate 3 is the contemporary durable device; HeartMate II and HVAD are historical but still appear in stems) require anticoagulation, typically warfarin plus aspirin, because blood contacts a spinning rotor. Neurologic complications cluster in four exam-ready patterns:
Pump thrombosis. Power spikes, a low pulsatility index, dark urine from hemolysis, a rising lactate dehydrogenase, and recurrent heart failure suggest thrombus in the pump. Device exchange is definitive; intravenous heparin or thrombolysis can be attempted but trades one stroke risk for another.
Ischemic stroke. Emboli from the pump, the aortic root, or atrial appendage, plus low pulsatile flow and hypertension, drive infarction. Continuous-flow MAP is often kept in a mid-70s to low-90s mm Hg range in chronic support; ENDURANCE-era HVAD data linked higher MAP to more strokes. Intravenous thrombolysis is usually off the table because the patient is already anticoagulated; large-vessel occlusion may still go to mechanical thrombectomy after a multidisciplinary discussion.
Hemorrhagic stroke. Warfarin, antiplatelet therapy, and acquired von Willebrand syndrome from shear of high-molecular-weight multimers produce intracerebral hemorrhage, subdural hematoma, and subarachnoid blood. Reverse warfarin with four-factor prothrombin complex concentrate plus vitamin K when the bleed is life-threatening, then plan a restart because a dry pump thromboses. Observational series often restart warfarin around 1–2 weeks if imaging is stable; antiplatelet timing is individualized. Inadequate reversal is common and associated with hematoma growth.
Device-related infection. Driveline infection seeds bacteremia, septic emboli, and mycotic aneurysms. New headache or a focal deficit in a febrile LVAD patient is infection-related cerebrovascular disease until proven otherwise.
The antithrombotic dilemma is the exam phrase: stopping anticoagulation risks pump thrombosis and ischemic stroke; continuing it risks hematoma expansion. There is no protocol that erases both risks. Pair the VAD team with neurology, reverse coagulopathy for expanding hemorrhage, and resume anticoagulation only after stable imaging and a documented risk discussion.
VV versus VA ECMO
Mode Circuit What it supports Typical indication What it does not do
VV-ECMO Venous drain → oxygenator → venous return Gas exchange Refractory hypoxemic or hypercapnic respiratory failure with adequate cardiac output (severe ARDS) Raise blood pressure or cardiac output
VA-ECMO Venous drain → oxygenator → arterial return Perfusion and gas exchange Refractory cardiogenic shock, extracorporeal CPR, massive PE with obstructive shock Unload the left ventricle; peripheral VA actually increases LV afterload
V-AV / hybrid Extra return limb Both when lungs and heart fail in sequence Harlequin physiology, combined failure Eliminate embolic risk
Neurologic complications of ECMO are common enough to expect on the exam:
Ischemic stroke from circuit thrombus, aortic atheroma, or low native flow.
Intracranial hemorrhage on systemic heparin plus circuit-induced platelet dysfunction and fibrinolysis.
Harlequin syndrome (also called north-south syndrome or differential hypoxia ) in femoral VA-ECMO: as the native heart recovers while the lungs remain sick, poorly oxygenated blood is ejected antegrade to the arch, coronaries, and brain, while bright ECMO blood perfuses the lower body. The patient can have pink legs and a cyanotic right arm and brain.
Differential hypoxia is detected on a right radial arterial blood gas or saturation (pre-mixing with femoral ECMO return) and with cerebral near-infrared spectroscopy. Left radial or femoral gases can look falsely reassuring.
Circuit-related emboli include thrombus, air, and fibrin debris; a sudden pupil change on ECMO is a head CT until a reversible cause is proven.
Management of Harlequin physiology: improve native lung function, increase ECMO flow, reduce native cardiac output if safe, add a venous return limb (V-AV), relocate the arterial cannula more centrally, or convert configurations. Adding an Impella (ECPELLA) unloads the left ventricle but can worsen differential hypoxia by increasing antegrade poorly oxygenated ejection—monitor the right radial gas even more closely.
The Extracorporeal Life Support Organization neurologic consensus (2024) recommends against intravenous tPA during ECMO because of bleeding risk, supports thrombectomy for eligible large-vessel occlusion, and supports early cessation of anticoagulation after intracranial hemorrhage. Prolonged cessation (more than about two days) is recommended for ICH on VV-ECMO ; VA-ECMO can run without anticoagulation but with a higher thromboembolism risk. Data on pharmacologic reversal of heparin in this setting are limited; the practical first move is to stop the infusion, control blood pressure, obtain serial non-contrast head CT, and involve neurosurgery. Do not restart heparin the same hour as a new ICH “because the circuit requires it.” The circuit can often wait; an expanding hematoma cannot.