Study guide
5.3 Diagnosis and Management of Shock
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)
5.3 Diagnosis and Management of Shock
Key Takeaways Explain This Topic AI
Classify shock by the dominant physiology: distributive (low SVR), cardiogenic (low cardiac output, high filling pressures), hypovolemic (low preload), or obstructive (blocked flow), using exam, lactate, ultrasound, and invasive numbers together.
Neurogenic shock is distributive hypotension with bradycardia after high spinal cord injury from loss of sympathetic tone; it is not the same as spinal shock (areflexia) and is not the default diagnosis in a tachycardic, bleeding trauma patient.
Surviving Sepsis Campaign 2021 priorities for septic shock are immediate resuscitation, cultures without delaying antimicrobials, source control, crystalloid, and norepinephrine as the first-line vasopressor with an initial MAP of 65 mm Hg—raise that floor when CPP or cord perfusion requires it.
After aneurysmal SAH, neurogenic stunned myocardium produces a cardiogenic (sometimes mixed) picture with regional wall-motion abnormalities that do not follow a coronary territory; it can block induced hypertension for delayed cerebral ischemia.
A single patient can stack phenotypes: hemorrhage plus neurogenic shock after polytrauma, or vasoplegia plus cardiogenic failure after SAH. Treat the dominant limiter of oxygen delivery first.
Last updated: September 2026
Name the physiology before you name the pressor
Quick answer: Distributive shock is low systemic vascular resistance (sepsis, anaphylaxis, neurogenic shock , adrenal crisis). Cardiogenic shock is a pump problem. Hypovolemic shock is missing preload. Obstructive shock is blocked flow (tamponade, tension pneumothorax, massive pulmonary embolism). Neurogenic shock is hypotension plus bradycardia after a high cord injury—not tachycardia and cool skin from bleeding.
Shock is inadequate tissue oxygen delivery or utilization. In the neuro ICU the brain and cord are the organs that declare failure first as a pupil change, a new deficit, or a rising ICP, so you cannot wait for anuric kidneys to prove the point. Start with the bedside: skin temperature, capillary refill, heart rate, pulse pressure, urine output, mentation, and lactate. Then confirm with ultrasound and, when needed, the monitors from Section 5.1.
Four families, with the numbers you should expect
Type Cardiac output SVR Filling pressures SvO2 / ScvO2 Bedside clues
Distributive (septic, anaphylactic, neurogenic, adrenal) Normal or high (neurogenic may be relatively low if bradycardic) Low Low or normal Often high in pure vasoplegia (shunting); can fall if myocardial depression coexists Warm skin (classic); bounding pulses; in neurogenic shock: bradycardia, warm dry skin below the lesion
Cardiogenic Low High High (PCWP or LVDA high in LV failure; RA high in RV failure) Low Cool skin, pulmonary edema, S3, congested IVC, hypokinetic ventricle
Hypovolemic (hemorrhage, GI losses, cerebral salt wasting with profound volume loss) Low High Low Low Cool clammy skin, flat veins, collapsing IVC, tachycardia
Obstructive Low High High and unequal (RA >> left in tamponade/PE; airway pressures in tension pneumothorax) Low Distended neck veins, RV strain, absent lung sliding, equalization of diastolic pressures in tamponade
Do not memorize the table as destiny. Early septic shock can look hypovolemic until the tank is filled. Epinephrine and high-dose norepinephrine confuse lactate. A PAC occlusion pressure is not a substitute for looking at the ventricle.
Neurogenic shock: classify it here
Neurogenic shock is a distributive state from sudden loss of sympathetic outflow, typically after a cervical or high thoracic cord injury (often T6 and above). Unopposed vagal tone produces hypotension and bradycardia . The skin below the lesion is often warm and dry because cutaneous vasoconstriction is lost. Priapism can appear with complete cervical injuries. This chapter only needs you to classify it and not to confuse it with the other hypotensive trauma phenotypes; later spine chapters cover autonomic hyperreflexia, chronic cardiovascular care, and steroid evidence (NASCIS high-dose methylprednisolone is not standard).
Spinal shock is a different term: temporary loss of reflexes and motor function below the injury, including a flaccid bladder. A patient can have spinal shock without hemodynamic neurogenic shock, and vice versa. Do not use the words interchangeably on a multiple-choice stem.
First-line hemodynamic care after you have stopped bleeding and opened the airway is volume to euvolemia, then a vasopressor with both α and some chronotropic support. Norepinephrine is a practical first agent in many ICUs; phenylephrine can worsen bradycardia; atropine or glycopyrrolate treats symptomatic vagal bradycardia; pacing is reserved for refractory bradycardia that threatens perfusion. MAP targets for cord perfusion were covered in Section 5.1.
Surviving Sepsis-style bundles without inventing unpublished cutoffs
The Surviving Sepsis Campaign 2021 adult guideline is the document exam writers still reach for. Treat sepsis and septic shock as emergencies. Obtain cultures before antimicrobials when that does not cause a substantial delay, then give antimicrobials immediately and pursue source control . For sepsis-induced hypoperfusion or septic shock the guideline suggests at least 30 mL/kg of intravenous crystalloid within the first 3 hours (weak recommendation, low-quality evidence) and recommends crystalloid as first-line fluid , with a preference in practice for balanced crystalloids. That 30 mL/kg figure is published; it is also a poor automatic order in a patient with high ICP, neurogenic stunned myocardium, or oliguric right-heart failure—give volume as a series of assessed boluses rather than as a mandatory dump.
For adults with septic shock, norepinephrine is the first-line vasopressor (strong recommendation). Target an initial MAP of 65 mm Hg . If MAP remains inadequate, add vasopressin rather than endlessly escalating norepinephrine (in many ICUs that add-on occurs around 0.25–0.5 μg/kg/min of norepinephrine, a practice remark rather than a hard published universal dose). If cardiac dysfunction with persistent hypoperfusion remains after preload and MAP are addressed, add dobutamine or switch to epinephrine. Peripheral norepinephrine is acceptable for a short period in a proximal vein while central access is obtained. In the neuro ICU, MAP 65 mm Hg is a starting floor for septic shock without intracranial hypertension; if ICP is 25 mm Hg, a MAP of 65 mm Hg yields a CPP of 40 mm Hg and is not acceptable.
Mixed shock after SAH: neurogenic stunned myocardium
Aneurysmal subarachnoid hemorrhage dumps catecholamines onto the myocardium. Neurogenic stunned myocardium (overlap with takotsubo-like cardiomyopathy) produces troponin leak, electrocardiographic deep T-wave inversions or ST changes, and wall-motion abnormalities that follow a nerve-innervation pattern rather than a single coronary territory—apical ballooning or a basal (inverted) pattern with apical sparing. Cardiac output falls, filling pressures rise, and the patient develops pulmonary edema. This is cardiogenic physiology, sometimes mixed with a systemic inflammatory, low-SVR state in high-grade SAH.
It usually declares within 48 hours and often improves over days to two weeks. The practical collision with Section 5.1 is delayed cerebral ischemia : induced hypertension for symptomatic DCI can drown a stunned left ventricle. Use echocardiography before you chase a systolic of 180 mm Hg. Inotropes (dobutamine or milrinone) may restore both blood pressure and brain flow better than pure vasoconstriction. Mechanical support (IABP, Impella, VA-ECMO) is rare but appears when stunned myocardium becomes true refractory cardiogenic shock; apply the contraindications from Section 5.2.
Do not assume every hypotensive SAH patient on day 8 has stunned heart. Day-8 hypotension with fever, a rising white count, warm extremities, and a new infiltrate is distributive septic shock until you prove otherwise—and SAH patients get both pneumonia and catheter infections. Nimodipine-related hypotension is another mimic: the outcome benefit of nimodipine is not an excuse to leave the patient at a MAP of 55 mm Hg; split the dose or infuse vasopressors rather than silently stopping the drug without a plan.
Worked scenario: three hypotensive patients, three physiologies
Patient A. A 28-year-old helmetless motorcyclist has a complete C5 injury. Blood pressure is 78/42 mm Hg, heart rate is 48 beats/min, skin is warm and dry, the abdomen is soft, FAST is negative, hemoglobin is 13.8 g/dL, and lactate is 2.1 mmol/L. This is neurogenic shock . Fill to euvolemia, start norepinephrine, treat bradycardia if it limits output, and set a cord-perfusion MAP target. Do not assume occult hemorrhage solely because the patient is a trauma activation.
Patient B. The same mechanism, but now the heart rate is 128 beats/min, skin is cool and clammy, the abdomen is distending, FAST shows fluid, hemoglobin is 8.1 g/dL, and lactate is 6.4 mmol/L. This is hypovolemic (hemorrhagic) shock , possibly stacked with a cord injury. Operate and transfuse first. Vasopressors without a volume and surgical plan will hide ongoing bleeding. Bradycardia would have argued for a neurogenic contribution; tachycardia argues against isolated neurogenic shock.
Patient C. A 58-year-old on day 2 after aneurysmal SAH has pulmonary edema, cool extremities, blood pressure 88/64 mm Hg, heart rate 110 beats/min, an electrocardiogram with deep T inversions, troponin elevation, and echo showing apical ballooning with ejection fraction 25% in a non-coronary pattern. This is cardiogenic shock from neurogenic stunned myocardium . Avoid a 30 mL/kg sepsis fluid dump. Support with inotropes, cautious afterload reduction if MAP allows, and delay induced hypertension for DCI until the ventricle can tolerate it. Catheterize the coronaries only if the wall-motion pattern or electrocardiogram suggests a true plaque rupture you cannot afford to miss.
If Patient C instead presents on day 8 with fever, a new dense hemiparesis, warm skin, lactate 4.8 mmol/L, and a normal ejection fraction, shift to distributive septic shock plus a DCI work-up: cultures, source, crystalloid in assessed aliquots, norepinephrine, and a MAP high enough for the brain—not a medical-ICU MAP of 65 mm Hg if that starves a vasospastic hemisphere.
Putting a first hour together
Airway, oxygen, access, arterial line if vasoactive drugs or CPP titration are coming.
Point-of-care glucose, hemoglobin, lactate, blood gas, electrocardiogram, and a focused echo/IVC/lung view.
Name the dominant shock family; treat hemorrhage and obstruction immediately.
For suspected sepsis: cultures when they do not delay drugs, antimicrobials, source, fluids, norepinephrine.
Recalculate CPP or cord perfusion after every MAP change.
If SAH and pulmonary edema coexist, think stunned myocardium before you induce hypertension.
The exam reward is the distinction, not the brand of norepinephrine. Hypotension plus bradycardia after a high cord is neurogenic until bleeding is excluded. Hypotension plus tachycardia and a collapsing IVC is hypovolemia. Hypotension plus a territorial-sparing, severely hypokinetic left ventricle after SAH is cardiogenic stunning. Hypotension plus fever and vasoplegia is distributive sepsis. Mixed pictures are allowed—your job is to identify which limiter you must fix first.