Types of Shock: A Nursing Guide

MAP = (SBP + 2 × DBP) ÷ 3. Example: BP 90/50 gives a MAP of (90 + 100) ÷ 3 = about 63.

Why 65 matters: below a MAP of about 65 mmHg, most organs (especially the kidneys and brain) can no longer keep their own blood flow steady. A MAP of 65 or higher is the standard minimum target in shock unless the provider orders a different goal.

Tachycardia plus a narrowing pulse pressure with a "normal" BP is shock until proven otherwise. Example: BP drops from 128/78 (pulse pressure 50) to 112/90 (pulse pressure 22) while HR climbs from 84 to 118. The systolic still looks fine. The patient is not. Hypotension is a late sign. By the time the BP falls, compensation is already failing.

Initial

What the body is doing: oxygen delivery starts to fall and cells begin shifting to anaerobic metabolism. The damage is at the cellular level.

What you see: often very little. HR and BP near baseline, maybe a slight rise in HR. Mentation normal. Lactate may begin to rise. This stage is usually caught only by labs or by knowing your patient is at risk.

Compensatory

What the body is doing: the sympathetic nervous system kicks in (epinephrine and norepinephrine), the renin-angiotensin-aldosterone system holds sodium and water, and ADH holds more water. Blood is shunted away from the skin, gut, and kidneys to protect the heart and brain.

• HR: up (often over 100)
• BP: normal or near normal; pulse pressure narrowing as the diastolic rises
• RR: up and deeper; may cause respiratory alkalosis
• Mentation: anxious, restless, "something is wrong"
• Urine output: starting to drop, urine more concentrated
• Skin: cool and pale (except early distributive shock, which is warm)
• Lactate: rising, often over 2 mmol/L

Progressive

What the body is doing: compensation is failing. Vessels leak, acidosis worsens, and organs start to fail (acute kidney injury, ARDS, liver injury, DIC).

• HR: very fast, pulses weak and thready
• BP: falling; SBP under 90 or MAP under 65
• RR: rapid and shallow; crackles if fluid is leaking into the lungs
• Mentation: confused, lethargic
• Urine output: under 0.5 mL/kg/hr
• Skin: cold, clammy, mottled; capillary refill over 3 seconds
• Lactate: high, often 4 mmol/L or more, with metabolic acidosis on the ABG

Refractory (irreversible)

What the body is doing: cell death and organ failure are so widespread that the body no longer responds to fluids, vasopressors, or other treatment. MODS is established.

• HR: may drop to bradycardia before arrest
• BP: severe hypotension despite high-dose vasopressors
• RR: respiratory failure, usually needing mechanical ventilation
• Mentation: unresponsive
• Urine output: little to none (anuria)
• Skin: cold, mottled, cyanotic; bleeding from DIC
• Lactate: very high and not clearing; severe acidosis

What is failing: there is not enough circulating volume, so less blood returns to the heart (low preload) and less goes out (low cardiac output). The vessels clamp down to compensate.

Hemorrhagic causes: trauma, GI bleed, ruptured aortic aneurysm, postpartum hemorrhage, surgical bleeding, ruptured ectopic pregnancy.
Non-hemorrhagic causes: vomiting and diarrhea, burns, DKA and other causes of heavy urination, diuretics, third spacing (pancreatitis, bowel obstruction), heat and poor intake.

Key clues: HR up, skin cool, pale, and clammy, flat neck veins, clear lungs, normal temperature (may be low in trauma), thirst, dry mucous membranes, low urine output, and a source of loss.

Hemodynamics: CVP ↓, CO ↓, SVR ↑, PCWP ↓.

Priority interventions:

• Stop the loss: direct pressure, tourniquet for a limb bleed, prepare for surgery or endoscopy.
• Two large-bore IVs (16 to 18 gauge).
• Hemorrhagic: replace with blood products (packed RBCs, plasma, platelets, often through a massive transfusion protocol). Limit large volumes of crystalloid, which dilute clotting factors.
• Non-hemorrhagic: isotonic crystalloid (balanced solution such as lactated Ringer's, or 0.9% saline) as ordered.
• Keep a trauma patient warm. Hypothermia worsens bleeding.

Monitor: HR, BP, MAP, urine output, H&H, lactate, coags, temperature, and any ongoing bleeding or drain output.

NCLEX trap: a normal hemoglobin right after an acute bleed does not rule out hemorrhage. The patient loses whole blood, so the H&H can look normal until fluids dilute it. Trust the vitals.

What is failing: the heart muscle cannot pump enough blood forward. Blood backs up into the lungs and veins, while the organs downstream starve.

Common causes: acute MI (most common, especially a large anterior MI), end-stage heart failure, severe dysrhythmias, acute valve rupture, myocarditis, cardiomyopathy.

Key clues: HR usually up (can be slow with heart block), skin cool, pale, and clammy, JVD, crackles in the lungs, new S3, chest pain, dyspnea, normal temperature, low urine output.

Hemodynamics: CVP ↑, CO ↓, SVR ↑, PCWP ↑.

Priority interventions:

• Oxygen to keep SpO2 at goal; prepare for noninvasive or mechanical ventilation if pulmonary edema worsens.
• Fix the cause: for an MI, rapid reperfusion (cardiac cath and PCI).
• Inotropes (such as dobutamine or milrinone) to strengthen contraction, and a vasopressor (norepinephrine is commonly first) for hypotension, as ordered.
• Fluids only cautiously and only as ordered. Diuretics once the BP can tolerate them.
• Prepare for mechanical support (intra-aortic balloon pump, Impella, ECMO) if ordered.
• Continuous cardiac monitoring; 12-lead ECG.

Monitor: lung sounds, SpO2, work of breathing, rhythm, MAP, urine output, daily weight, troponin, BNP, lactate, mentation.

NCLEX trap: do not give a large fluid bolus to a patient with crackles and JVD. The tank is already full. More fluid floods the lungs.

What is failing: the pipes. A dysregulated immune response to infection releases inflammatory mediators that dilate vessels, make capillaries leaky, and damage organs.

Common causes: pneumonia, urinary tract infection, abdominal infection, skin and wound infections, central line infections. Higher risk: older adults, immunocompromised patients, recent surgery, invasive devices.

Key clues: HR up, RR up, fever (or hypothermia, especially in older adults), warm, flushed skin early that becomes cool and mottled late, flat neck veins, new confusion, low urine output, and a source of infection.

Hemodynamics: CVP ↓ or ↔, SVR ↓, PCWP ↓ or ↔. CO is ↑ early (warm phase) and ↓ late (cold phase).

Priority interventions:

• Lactate and blood cultures drawn before antibiotics.
• Broad-spectrum antibiotics within 1 hour of recognition.
• 30 mL/kg crystalloid for hypotension or lactate 4 mmol/L or higher.
• Norepinephrine (first-line vasopressor) for MAP under 65 during or after fluids.
• Source control: drain the abscess, remove the infected line, as ordered.

Monitor: MAP, HR, temperature, repeat lactate, urine output, mentation, WBC, lung sounds during fluid resuscitation, signs of organ dysfunction (creatinine, bilirubin, platelets).

NCLEX trap: warm, pink skin does not mean the patient is fine. In early septic shock, warm and flushed is the shock.

What is failing: the pipes and possibly the airway. A severe allergic reaction triggers mass release of histamine and other mediators, causing sudden vasodilation, leaky capillaries, airway swelling, and bronchospasm.

Common causes: medications (antibiotics such as penicillins, NSAIDs, contrast dye), foods (peanuts, tree nuts, shellfish), insect stings, latex, blood products.

Key clues: rapid onset after exposure, HR up, hives, flushing, itching, swelling of lips, tongue, or face, stridor, hoarseness, wheezing, GI cramping or vomiting, flat neck veins, sense of doom.

Hemodynamics: CVP ↓, CO ↓, SVR ↓, PCWP ↓.

Priority interventions:

• Stop the trigger (stop the infusion or transfusion).
• Epinephrine IM first, in the anterolateral thigh: 0.01 mg/kg of 1 mg/mL (1:1,000), maximum 0.5 mg in adults. Repeat every 5 to 15 minutes if symptoms continue, as ordered.
• Airway: high-flow oxygen; be ready for intubation if swelling progresses.
• Position: lay flat with legs raised if hypotensive, or sitting up if breathing is the main problem. Do not let the patient suddenly stand or sit up.
• IV fluids for hypotension. Antihistamines, bronchodilators, and corticosteroids are add-ons, never a replacement for epinephrine.

Monitor: airway and voice, breath sounds, SpO2, BP and HR, skin, and watch for a biphasic (second) reaction hours later.

NCLEX trap: diphenhydramine is not first. If the question describes anaphylaxis, the answer is IM epinephrine.

What is failing: the pipes and the heart rate. Injury to the spinal cord (usually at T6 or above) cuts off sympathetic nerve signals. Without sympathetic tone, the vessels dilate and the heart rate is left to the unopposed vagus nerve.

Common causes: cervical or high thoracic spinal cord injury, spinal anesthesia that spreads too high.

Key clues: bradycardia with hypotension (the only shock type with a slow heart rate as the classic sign), warm, dry skin below the injury, flat neck veins, poor temperature control (takes on the room temperature), loss of motor and sensory function below the injury.

Hemodynamics: CVP ↓, CO ↓, SVR ↓, PCWP ↓.

Priority interventions:

• Airway first, with spinal precautions. High cervical injuries can stop the diaphragm.
• Keep the spine aligned; log roll.
• IV fluids, then vasopressors (norepinephrine is common) to reach the MAP target. Spinal cord injury often has a higher MAP goal than 65 for several days, per provider orders.
• Atropine for symptomatic bradycardia, as ordered; be ready for pacing.
• Keep the patient warm or cool as needed to maintain normal temperature.

Monitor: HR and rhythm (especially during suctioning or turning, which can trigger severe bradycardia), MAP, respiratory effort, temperature, neuro checks, urine output.

NCLEX trap: do not confuse neurogenic shock with spinal shock. Spinal shock is the temporary loss of reflexes and movement below the injury. Neurogenic shock is the hemodynamic problem: low BP and low HR.

What is failing: the heart and volume may be fine, but something physically blocks blood from filling the heart or leaving it. Blood backs up into the veins (JVD) and output drops.

Common causes:

• Tension pneumothorax: air trapped in the chest compresses the heart and great vessels. Clues: absent breath sounds on one side, tracheal deviation away from the affected side (a late sign), severe dyspnea, JVD.
• Cardiac tamponade: fluid or blood in the pericardial sac squeezes the heart. Clues: Beck's triad (hypotension, JVD, muffled heart sounds) and pulsus paradoxus (SBP drops more than 10 mmHg on inspiration). Watch after cardiac surgery, chest trauma, and central line placement.
• Massive pulmonary embolism: a large clot blocks blood leaving the right ventricle. Clues: sudden dyspnea, pleuritic chest pain, hypoxemia, tachycardia, JVD, and risk factors (immobility, recent surgery, DVT, cancer, pregnancy, estrogen).

Key clues overall: HR up, skin cool and pale, JVD, lung sounds depend on the cause, normal temperature.

Hemodynamics: CVP ↑, CO ↓, SVR ↑. PCWP ↓ or ↔ in PE and tension pneumothorax, ↑ in tamponade.

Priority interventions: fix the blockage.

• Tension pneumothorax: needle decompression, then chest tube.
• Tamponade: pericardiocentesis or surgical drainage.
• Massive PE: anticoagulation, thrombolytics, or clot removal (catheter or surgical), as ordered.
• Oxygen and fluids support the patient while the blockage is being fixed, but they do not cure it.

Monitor: breath sounds, tracheal position, heart sounds, JVD, SpO2, BP, HR, chest tube function, bleeding if thrombolytics are given.

NCLEX trap: do not wait for a chest X-ray to treat a tension pneumothorax in a crashing patient. It is a clinical diagnosis; the priority is decompression.

• Bradycardia + hypotension + warm, dry skin after a spinal injury = neurogenic.
• Crackles + JVD + low BP = cardiogenic. Fluids can hurt.
• Fever + warm, flushed skin + low SVR = early septic.
• Stridor or wheeze + hives after an exposure = anaphylactic. IM epinephrine first.
• Flat neck veins + bleeding or fluid losses = hypovolemic.
• JVD + muffled heart sounds, tracheal deviation, or absent breath sounds = obstructive. Fix the blockage.

Start these within 1 hour of recognizing sepsis or septic shock:

1. Measure lactate. Remeasure if the first result is over 2 mmol/L.
2. Draw blood cultures before antibiotics.
3. Give broad-spectrum antibiotics.
4. Give 30 mL/kg crystalloid for hypotension or lactate 4 mmol/L or higher.
5. Start vasopressors if the MAP stays under 65 during or after fluids.

1. WHAT IS INSTANTLY LIFE-THREATENING? (ABC Hierarchy)

Shock is a circulation problem, but airway and breathing still come first. Shock example: a patient in anaphylaxis has stridor and a BP of 82/50. The airway is the priority, and IM epinephrine treats both the airway swelling and the vasodilation.

2. WHERE IS THE ACTUAL BREAKDOWN HAPPENING? (Pathophysiological Site)

Name which part of the system failed: volume, pump, pipes, or blockage. That choice decides the treatment. Shock example: two patients have BP 84/52. One has flat neck veins and melena (volume: give blood). The other has crackles and JVD after an MI (pump: support the heart, careful with fluid). Same BP, opposite treatment.

3. IS IT A REAL PROBLEM OR JUST A SYMPTOM/COMPENSATION?

Tachycardia, tachypnea, cool skin, and low urine output are usually the body compensating. Do not "fix" the compensation; fix the cause. Shock example: a post-op patient has HR 124 and BP 108/92. The tachycardia is compensation and the narrow pulse pressure is the warning. Giving a drug to slow the heart would remove the patient's last defense. The breakdown is volume, likely bleeding.