6.2 Non-Cardiogenic Shock: Hypovolemic, Distributive and Obstructive

Why Shock Categorization Is a High-Yield CMC Skill

Test-plan item II.F.2 Shock states sits inside Non-Cardiovascular Conditions, which carries 23% of the CMC blueprint. The exam rarely asks you to define a shock state in the abstract. It hands you a set of pulmonary artery (PA) catheter numbers, a physical exam, and a lactate, and asks what you do next. Because your patient already has a low-output substrate, the discriminating skill is separating non-cardiogenic shock from the cardiogenic shock covered elsewhere in this guide - and recognizing when both are running at once.

Every shock state is a mismatch between oxygen delivery and consumption. Oxygen delivery (DO2) is the product of cardiac output and arterial oxygen content, where arterial content = (1.34 x hemoglobin x SaO2) + (0.003 x PaO2). Only four levers exist: flow, hemoglobin, saturation, and the tissue's ability to extract. The four shock categories differ in which lever failed, and the hemodynamic profile tells you which one.

The Four Hemodynamic Profiles

Read the table as three questions in order: Is the tank empty? (CVP, PAOP), Is the pump failing? (CI), Is the pipe dilated? (SVR). The single most useful discriminator on the exam is the combination of a high CVP with a normal or low PAOP - that is right ventricular obstruction or failure, not left ventricular failure, and it means the answer is almost never more diuretic. In tamponade, every diastolic pressure equalizes: RA, RV end-diastolic, PA diastolic, and PAOP all land within about 5 mmHg of one another.

Mixed venous oxygen saturation (SvO2, drawn from the PA catheter distal port) is normally 60-80%; central venous saturation (ScvO2, from a superior vena cava line) runs roughly 5-8 points higher. A low SvO2 means delivery has fallen or extraction has risen. A high SvO2 in a patient who is clearly shocked is the fingerprint of failed extraction - septic microcirculatory shunting, cyanide toxicity from prolonged high-dose nitroprusside, a large left-to-right shunt such as a post-infarction ventricular septal rupture, or a permanently wedged catheter sampling arterialized blood.

Hypovolemic and Hemorrhagic Shock

Hypovolemic shock is a preload problem: reduced venous return lowers stroke volume, and compensatory catecholamine release raises heart rate and SVR. In the cardiac patient the compensation itself is dangerous, because tachycardia shortens diastole and raises myocardial oxygen demand in a heart that may already be ischemic.

The trap is Class II: the blood pressure is still normal, and the only early signals are a narrowing pulse pressure, tachycardia, and a rising base deficit. Waiting for hypotension means waiting for Class III.

Resuscitation. Start with a balanced crystalloid (lactated Ringer's or Plasma-Lyte) rather than 0.9% sodium chloride; large-volume normal saline produces hyperchloremic metabolic acidosis and is associated with more renal adverse events. Crystalloid is a bridge, not a treatment, for hemorrhage - once the loss is roughly 30% or the patient fails to respond to 1-2 L, switch to blood. A massive transfusion protocol delivers packed red cells, plasma, and platelets in a balanced 1:1:1 ratio, which reproduces whole blood more closely than red cells alone and reduces death from exsanguination. Give tranexamic acid within 3 hours of traumatic hemorrhage.

Citrate and calcium are the piece nurses own. Every unit of blood product carries citrate anticoagulant that chelates ionized calcium; in massive transfusion, citrate outstrips hepatic clearance and produces acute ionized hypocalcemia. Ionized calcium below about 1.0 mmol/L causes hypotension, negative inotropy, prolonged QT, and coagulopathy. Replace with calcium chloride 1 g IV (central line preferred) or calcium gluconate 2-3 g IV per 2-4 units transfused, guided by ionized calcium. The classic "lethal triad" of hypothermia, acidosis, and coagulopathy is now more accurately a diamond, with hypocalcemia as the fourth point. Use a fluid warmer and rapid infuser; a cold, acidotic cardiac patient will not clot and will not respond to catecholamines.

Distributive Shock

Septic shock is sepsis with vasopressor-requiring hypotension plus a lactate above 2 mmol/L after adequate fluid resuscitation. Surviving Sepsis Campaign 2021 practice:

• Measure lactate and repeat it if elevated; obtain blood cultures before antimicrobials whenever this does not meaningfully delay therapy.
• Antimicrobials immediately, ideally within 1 hour, for septic shock or a high likelihood of sepsis; within 3 hours for possible sepsis without shock.
• 30 mL/kg of IV crystalloid within the first 3 hours, using balanced crystalloid, then dynamic reassessment (stroke volume variation, passive leg raise, echocardiography) rather than fixed further boluses.
• Norepinephrine is first-line, titrated to a MAP of 65 mmHg. Start it peripherally rather than delay while a central line is placed.
• Add vasopressin 0.03 units/min rather than escalating norepinephrine indefinitely - typically when norepinephrine reaches 0.25-0.5 mcg/kg/min. Epinephrine is the next add-on; dobutamine is added for persistent hypoperfusion with cardiac dysfunction despite adequate MAP and volume.
• Hydrocortisone 200 mg/day (50 mg IV every 6 hours or a continuous infusion) for refractory shock - conventionally when norepinephrine or epinephrine is at or above 0.25 mcg/kg/min for at least 4 hours.

The 30 mL/kg number is the single most-tested trap in the cardiac patient. In a patient with an ejection fraction of 20%, severe aortic stenosis, or right ventricular infarction, a reflexive 2-liter bolus produces flash pulmonary edema. The defensible answer is smaller aliquots (250-500 mL) with reassessment after each, early norepinephrine, and invasive or echocardiographic guidance.

Anaphylactic shock. First-line treatment is epinephrine 0.3-0.5 mg of the 1 mg/mL concentration intramuscularly into the anterolateral thigh, repeated every 5-15 minutes; an IV infusion at 0.05-0.1 mcg/kg/min is reserved for refractory cases. Antihistamines and corticosteroids are adjuncts that treat hives, not shock, and must never delay epinephrine. Volume shifts are enormous - up to 35% of intravascular volume can leave the circulation within 10 minutes - so aggressive crystalloid is required. The beta-blocked cardiac patient is the exam scenario: chronic carvedilol or metoprolol blunts the beta response to epinephrine, leaving relatively unopposed alpha stimulation, refractory hypotension, and refractory bronchospasm. The antidote is glucagon 1-5 mg IV over 5 minutes followed by an infusion of 5-15 mcg/min, because glucagon activates adenylate cyclase downstream of the beta receptor. Anticipate vomiting and protect the airway. Observe for a biphasic reaction, which can occur hours after apparent resolution.

Neurogenic shock follows loss of sympathetic outflow after spinal cord injury at or above roughly T6. It is the one shock state with hypotension plus bradycardia, and the skin is warm, dry, and pink below the level of injury with poikilothermia. Treat with fluid plus a vasopressor that has both alpha and beta activity (norepinephrine), not phenylephrine, whose reflex bradycardia worsens the problem; atropine or temporary pacing for symptomatic bradycardia; MAP goal of 85-90 mmHg for the first 7 days to preserve cord perfusion. Do not confuse it with spinal shock, which is the flaccid areflexia of the injured cord and is a neurologic, not hemodynamic, phenomenon.

Obstructive Shock: Four Mechanical Problems With Four Mechanical Fixes

Obstructive shock is the category where pharmacology fails and a procedure succeeds. Each entity has one intervention that actually reverses it.

Two nursing points carry disproportionate exam weight. In tamponade, preload is the only thing keeping the ventricle filling: diuretics, nitrates, and the drop in venous return that accompanies intubation and positive-pressure ventilation can precipitate arrest, so the fluid bolus goes up and the sedation goes down until the pericardium is drained. In auto-PEEP, the patient who becomes profoundly hypotensive within minutes of intubation is being ventilated faster than they can exhale; the answer is to disconnect the ventilator and reduce the respiratory rate, not to give fluid and start a pressor.

In massive PE the instinct to fluid-load is also wrong. The overdistended right ventricle bows the septum leftward and further impairs left ventricular filling, so volume beyond about 500 mL worsens output. Norepinephrine is the pressor of choice because it supports RV coronary perfusion pressure while providing modest inotropy.

Mixed Shock in the Cardiac Patient

Septic shock superimposed on cardiomyopathy does not look like textbook septic shock. The SVR falls, but the ventricle cannot raise cardiac index to compensate, so the "warm and bounding" phase never appears. Expect a low-normal CI with a low SVR, a low rather than high SvO2, and a lactate out of proportion to the blood pressure. Sepsis also produces its own reversible sepsis-induced cardiomyopathy - global hypokinesis with ventricular dilation that typically recovers over 7-10 days. Management requires a vasopressor and an inotrope, and the fixed 30 mL/kg becomes actively harmful.

Endpoints of Resuscitation and Nursing Priorities

Blood pressure alone is a poor endpoint. Track a bundle:

• Lactate clearance of at least 10-20% every 2 hours, targeting normalization below 2 mmol/L.
• Capillary refill time of 3 seconds or less - reassessed every 30 minutes early in resuscitation, and at least as good a target as lactate.
• Urine output of 0.5 mL/kg/h or more.
• ScvO2 of 70% or more / SvO2 of 65-75%, interpreted alongside lactate.
• MAP 65 mmHg, individualized upward to 80-85 mmHg in chronic uncontrolled hypertension or in spinal cord injury.
• Mental status, base deficit, and narrowing of the anion gap.

The nurse's priorities are recognition and sequence: obtain the lactate and cultures before antibiotics, establish two large-bore peripheral lines or an introducer sheath before the patient becomes unresuscitatable, warm every fluid, replace ionized calcium during massive transfusion, and reassess after every intervention rather than after every hour. When the numbers do not fit one profile, say so out loud - a rising CVP with a falling PAOP during resuscitation is the earliest signal that you have moved from hypovolemia into right ventricular failure, and it changes the plan from volume to inotropy and pulmonary vasodilation.