5.3 Diagnosis and Management of Shock

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

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

1. Airway, oxygen, access, arterial line if vasoactive drugs or CPP titration are coming.
2. Point-of-care glucose, hemoglobin, lactate, blood gas, electrocardiogram, and a focused echo/IVC/lung view.
3. Name the dominant shock family; treat hemorrhage and obstruction immediately.
4. For suspected sepsis: cultures when they do not delay drugs, antimicrobials, source, fluids, norepinephrine.
5. Recalculate CPP or cord perfusion after every MAP change.
6. 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.