Syok — LevelUp. Archive

Risk Factors

Trauma, burns, severe infection, acute MI, massive PE, anaphylaxis, spinal cord injury, severe dehydration, adrenal insufficiency

Etiology

Inadequate cellular oxygen delivery resulting from decreased cardiac output, reduced systemic vascular resistance, or both

Presentation

Hypotension (systolic BP <90 mmHg or MAP <65 mmHg), tachycardia, altered mental status, oliguria, cool or mottled extremities

Classic Exam

Tachycardia, weak or thready pulse, delayed capillary refill (>3 seconds), skin mottling, diaphoresis; warm and flushed skin in early distributive shock; distended neck veins in obstructive and cardiogenic shock; flat neck veins in hypovolemic shock

Diagnostics

Elevated serum lactate (>2 mmol/L), metabolic acidosis on ABG, decreased mixed venous oxygen saturation ( $S v O_{2}$ <65%), elevated base deficit; hemodynamic profiles on pulmonary artery catheter or bedside echocardiography distinguish the type

Management

IV crystalloid resuscitation (30 mL/kg for septic shock), vasopressors (norepinephrine first-line for most types), identify and treat the underlying cause, blood products for hemorrhage, inotropes for pump failure

KEYWORDS

"Lactic acidosis," "end-organ hypoperfusion," "cold and clammy," "warm shock," "JVD," "flat neck veins," "MAP <65," "narrow pulse pressure," "wide pulse pressure"

01Pathophysiology

Shock is defined as a state of circulatory failure that results in inadequate oxygen delivery to meet the metabolic demands of tissues. The fundamental equation that governs oxygen delivery is:

$DO_2 = CO \times CaO_2$

where $D O_{2}$ is oxygen delivery, $C O$ is cardiac output, and $C a O_{2}$ is arterial oxygen content. Cardiac output itself is the product of heart rate and stroke volume, and stroke volume depends on three determinants: preload (ventricular filling), contractility (myocardial pump strength), and afterload (resistance the ventricle must overcome). Mean arterial pressure, the driving pressure for organ perfusion, is governed by:

$MAP = CO \times SVR$

Every type of shock disrupts one or more of these variables. Hypovolemic shock reduces preload. Cardiogenic shock impairs contractility. Distributive shock collapses SVR. Obstructive shock mechanically impedes cardiac filling or outflow. Regardless of the initial insult, the downstream consequence is the same: cellular hypoxia forces a switch from aerobic to anaerobic metabolism, generating lactate and hydrogen ions. This is why elevated serum lactate is the universal laboratory marker of tissue hypoperfusion across all shock types.
The body initially compensates through the sympathetic nervous system and the renin-angiotensin-aldosterone system. Catecholamine release drives tachycardia and peripheral vasoconstriction, which is why the earliest clinical sign of shock is often tachycardia rather than frank hypotension. Blood is shunted away from the skin, kidneys, and gut toward the heart and brain. This compensatory phase can mask the severity of shock, and a patient can lose up to 15 to 30 percent of circulating blood volume before blood pressure drops. This is the concept of "compensated shock", a classic exam scenario where the blood pressure is still normal, but the heart rate is elevated and the patient has cool, clammy skin and oliguria.
When compensatory mechanisms are overwhelmed, the patient enters decompensated shock: hypotension becomes overt, organ dysfunction accelerates, and a vicious cycle of worsening acidosis, myocardial depression, and microvascular thrombosis develops. Without intervention, this progresses to irreversible shock, where cellular injury becomes so widespread that even restoring perfusion cannot prevent death.

02Classification and Clinical Manifestation

Hypovolemic (hemorrhagic)

MECHANISM: Loss of circulating blood volume
COMMON CAUSES: Trauma, GI bleeding, ruptured ectopic pregnancy, ruptured AAA
PRELOAD (CVP/PCWP): Low
CARDIAC OUTPUT: Low
SVR: High
CLASSIC EXAM FINDINGS: Flat neck veins, cool and clammy skin, tachycardia, narrow pulse pressure

Hypovolemic (non-hemorrhagic)

MECHANISM: Loss of plasma or fluid volume
COMMON CAUSES: Burns, diarrhea, vomiting, third-spacing (pancreatitis), DKA
PRELOAD (CVP/PCWP): Low
CARDIAC OUTPUT: Low
SVR: High
CLASSIC EXAM FINDINGS: Dry mucous membranes, poor skin turgor, flat neck veins

Cardiogenic

MECHANISM: Pump failure
COMMON CAUSES: Acute MI, acute valvular rupture, myocarditis, end-stage heart failure, arrhythmia
PRELOAD (CVP/PCWP): High (elevated PCWP)
CARDIAC OUTPUT: Low
SVR: High
CLASSIC EXAM FINDINGS: JVD, pulmonary crackles (rales), S3 gallop, peripheral edema, cool extremities

Distributive (septic)

MECHANISM: Pathologic vasodilation from systemic inflammation
COMMON CAUSES: Bacterial infection (gram-negative most common), fungal, viral
PRELOAD (CVP/PCWP): Low to normal
CARDIAC OUTPUT: High (early), Low (late)
SVR: Low
CLASSIC EXAM FINDINGS: Warm shock early (warm, flushed, bounding pulses, wide pulse pressure); cold shock late (cool, mottled, thready pulses)

Distributive (anaphylactic)

MECHANISM: IgE-mediated systemic vasodilation and capillary leak
COMMON CAUSES: Drug allergy, food allergy (peanuts, shellfish), insect stings, latex
PRELOAD (CVP/PCWP): Low
CARDIAC OUTPUT: High initially, then low
SVR: Low
CLASSIC EXAM FINDINGS: Urticaria, angioedema, wheezing, stridor, hypotension within minutes of exposure

Distributive (neurogenic)

MECHANISM: Loss of sympathetic tone
COMMON CAUSES: Spinal cord injury above T6, spinal anesthesia
PRELOAD (CVP/PCWP): Low
CARDIAC OUTPUT: Low
SVR: Low
CLASSIC EXAM FINDINGS: Bradycardia with hypotension (distinguishes from other shock types, which cause tachycardia), warm and dry skin below the level of injury

Obstructive (cardiac tamponade)

MECHANISM: Impaired diastolic filling from pericardial fluid
COMMON CAUSES: Penetrating chest trauma, malignancy, uremia, post-cardiac surgery, aortic dissection
PRELOAD (CVP/PCWP): High (equalized pressures)
CARDIAC OUTPUT: Low
SVR: High
CLASSIC EXAM FINDINGS: Beck triad: muffled heart sounds, JVD, hypotension; pulsus paradoxus (>10 mmHg drop in SBP during inspiration); electrical alternans on ECG

Obstructive (tension pneumothorax)

MECHANISM: Mediastinal shift compresses heart and great vessels
COMMON CAUSES: Chest trauma, mechanical ventilation (barotrauma), central line placement
PRELOAD (CVP/PCWP): High
CARDIAC OUTPUT: Low
SVR: High
CLASSIC EXAM FINDINGS: Absent breath sounds and hyperresonance on the affected side, tracheal deviation away from affected side, JVD

Obstructive (pulmonary embolism)

MECHANISM: Acute RV outflow obstruction
COMMON CAUSES: DVT, immobilization, surgery, hypercoagulable state, OCP use
PRELOAD (CVP/PCWP): High CVP, Low PCWP
CARDIAC OUTPUT: Low
SVR: High
CLASSIC EXAM FINDINGS: JVD, RV heave, acute right heart strain on ECG (S1Q3T3, right axis deviation, new RBBB), acute hypoxia with clear lung fields

TYPE	MECHANISM	COMMON CAUSES	PRELOAD (CVP/PCWP)	CARDIAC OUTPUT	SVR	CLASSIC EXAM FINDINGS
Hypovolemic (hemorrhagic)	Loss of circulating blood volume	Trauma, GI bleeding, ruptured ectopic pregnancy, ruptured AAA	Low	Low	High	Flat neck veins, cool and clammy skin, tachycardia, narrow pulse pressure
Hypovolemic (non-hemorrhagic)	Loss of plasma or fluid volume	Burns, diarrhea, vomiting, third-spacing (pancreatitis), DKA	Low	Low	High	Dry mucous membranes, poor skin turgor, flat neck veins
Cardiogenic	Pump failure	Acute MI, acute valvular rupture, myocarditis, end-stage heart failure, arrhythmia	High (elevated PCWP)	Low	High	JVD, pulmonary crackles (rales), S3 gallop, peripheral edema, cool extremities
Distributive (septic)	Pathologic vasodilation from systemic inflammation	Bacterial infection (gram-negative most common), fungal, viral	Low to normal	High (early), Low (late)	Low	Warm shock early (warm, flushed, bounding pulses, wide pulse pressure); cold shock late (cool, mottled, thready pulses)
Distributive (anaphylactic)	IgE-mediated systemic vasodilation and capillary leak	Drug allergy, food allergy (peanuts, shellfish), insect stings, latex	Low	High initially, then low	Low	Urticaria, angioedema, wheezing, stridor, hypotension within minutes of exposure
Distributive (neurogenic)	Loss of sympathetic tone	Spinal cord injury above T6, spinal anesthesia	Low	Low	Low	Bradycardia with hypotension (distinguishes from other shock types, which cause tachycardia), warm and dry skin below the level of injury
Obstructive (cardiac tamponade)	Impaired diastolic filling from pericardial fluid	Penetrating chest trauma, malignancy, uremia, post-cardiac surgery, aortic dissection	High (equalized pressures)	Low	High	Beck triad: muffled heart sounds, JVD, hypotension; pulsus paradoxus (>10 mmHg drop in SBP during inspiration); electrical alternans on ECG
Obstructive (tension pneumothorax)	Mediastinal shift compresses heart and great vessels	Chest trauma, mechanical ventilation (barotrauma), central line placement	High	Low	High	Absent breath sounds and hyperresonance on the affected side, tracheal deviation away from affected side, JVD
Obstructive (pulmonary embolism)	Acute RV outflow obstruction	DVT, immobilization, surgery, hypercoagulable state, OCP use	High CVP, Low PCWP	Low	High	JVD, RV heave, acute right heart strain on ECG (S1Q3T3, right axis deviation, new RBBB), acute hypoxia with clear lung fields

Hemorrhagic Shock Classification (ATLS)

BLOOD LOSS (mL): <750
BLOOD LOSS (%): <15%
HEART RATE: <100
BLOOD PRESSURE: Normal
RESPIRATORY RATE: 14-20
MENTAL STATUS: Slightly anxious
FLUID REPLACEMENT: Crystalloid

BLOOD LOSS (mL): 750-1500
BLOOD LOSS (%): 15-30%
HEART RATE: 100-120
BLOOD PRESSURE: Normal
RESPIRATORY RATE: 20-30
MENTAL STATUS: Mildly anxious
FLUID REPLACEMENT: Crystalloid

III

BLOOD LOSS (mL): 1500-2000
BLOOD LOSS (%): 30-40%
HEART RATE: 120-140
BLOOD PRESSURE: Decreased
RESPIRATORY RATE: 30-40
MENTAL STATUS: Anxious, confused
FLUID REPLACEMENT: Crystalloid + blood

BLOOD LOSS (mL): >2000
BLOOD LOSS (%): >40%
HEART RATE: >140
BLOOD PRESSURE: Decreased
RESPIRATORY RATE: >35
MENTAL STATUS: Confused, lethargic
FLUID REPLACEMENT: Crystalloid + blood + massive transfusion protocol

CLASS	BLOOD LOSS (mL)	BLOOD LOSS (%)	HEART RATE	BLOOD PRESSURE	RESPIRATORY RATE	MENTAL STATUS	FLUID REPLACEMENT
I	<750	<15%	<100	Normal	14-20	Slightly anxious	Crystalloid
II	750-1500	15-30%	100-120	Normal	20-30	Mildly anxious	Crystalloid
III	1500-2000	30-40%	120-140	Decreased	30-40	Anxious, confused	Crystalloid + blood
IV	>2000	>40%	>140	Decreased	>35	Confused, lethargic	Crystalloid + blood + massive transfusion protocol

Note that blood pressure does not fall until Class III. A question presenting a trauma patient who is tachycardic but normotensive is testing your ability to recognize Class II hemorrhage and begin resuscitation before decompensation occurs.

03Diagnostic Workup

Serum lactate

PURPOSE: Best initial marker of tissue hypoperfusion
KEY FINDINGS: >2 mmol/L suggests inadequate oxygen delivery; >4 mmol/L associated with high mortality

Arterial blood gas (ABG)

PURPOSE: Assess acid-base status
KEY FINDINGS: Metabolic acidosis (low pH, low bicarbonate, elevated base deficit)

CBC

PURPOSE: Evaluate for hemorrhage and infection
KEY FINDINGS: Low hemoglobin in hemorrhagic shock; leukocytosis or leukopenia in septic shock

Basic metabolic panel (BMP)

PURPOSE: Organ function and electrolytes
KEY FINDINGS: Elevated creatinine (renal hypoperfusion), elevated BUN, hyperkalemia in late shock

Blood cultures (x2 sets)

PURPOSE: Identify infectious source in suspected sepsis
KEY FINDINGS: Draw before antibiotics; positive cultures guide targeted therapy

Procalcitonin

PURPOSE: Distinguish bacterial infection from other causes
KEY FINDINGS: Elevated in bacterial sepsis; helps differentiate from non-infectious SIRS

Troponin

PURPOSE: Evaluate myocardial injury
KEY FINDINGS: Elevated in cardiogenic shock from MI; may also rise from demand ischemia in any shock type

Coagulation studies (PT/INR, PTT, fibrinogen)

PURPOSE: Assess for DIC
KEY FINDINGS: Prolonged PT/PTT, low fibrinogen, elevated D-dimer in DIC

Type and crossmatch

PURPOSE: Prepare for transfusion
KEY FINDINGS: Essential in hemorrhagic shock

Chest X-ray

PURPOSE: Assess for pneumothorax, pulmonary edema, widened mediastinum
KEY FINDINGS: Tension pneumothorax is a clinical diagnosis treated before imaging; CXR shows pulmonary edema in cardiogenic shock

Bedside echocardiography (POCUS/TTE)

PURPOSE: Evaluate cardiac function, pericardial effusion, RV strain
KEY FINDINGS: Best initial test to differentiate shock type at the bedside; shows reduced EF in cardiogenic, pericardial effusion in tamponade, RV dilation in PE

Pulmonary artery (Swan-Ganz) catheter

PURPOSE: Gold standard hemodynamic profiling
KEY FINDINGS: Directly measures CVP, PCWP, CO, and SVR; rarely used clinically now but heavily tested for interpretation

CT pulmonary angiography

PURPOSE: Confirm pulmonary embolism
KEY FINDINGS: Filling defect in pulmonary arteries

FAST exam (Focused Assessment with Sonography for Trauma)

PURPOSE: Detect free fluid in trauma
KEY FINDINGS: Positive FAST in unstable trauma patient directs to operating room

TEST	PURPOSE	KEY FINDINGS
Serum lactate	Best initial marker of tissue hypoperfusion	>2 mmol/L suggests inadequate oxygen delivery; >4 mmol/L associated with high mortality
Arterial blood gas (ABG)	Assess acid-base status	Metabolic acidosis (low pH, low bicarbonate, elevated base deficit)
CBC	Evaluate for hemorrhage and infection	Low hemoglobin in hemorrhagic shock; leukocytosis or leukopenia in septic shock
Basic metabolic panel (BMP)	Organ function and electrolytes	Elevated creatinine (renal hypoperfusion), elevated BUN, hyperkalemia in late shock
Blood cultures (x2 sets)	Identify infectious source in suspected sepsis	Draw before antibiotics; positive cultures guide targeted therapy
Procalcitonin	Distinguish bacterial infection from other causes	Elevated in bacterial sepsis; helps differentiate from non-infectious SIRS
Troponin	Evaluate myocardial injury	Elevated in cardiogenic shock from MI; may also rise from demand ischemia in any shock type
Coagulation studies (PT/INR, PTT, fibrinogen)	Assess for DIC	Prolonged PT/PTT, low fibrinogen, elevated D-dimer in DIC
Type and crossmatch	Prepare for transfusion	Essential in hemorrhagic shock
Chest X-ray	Assess for pneumothorax, pulmonary edema, widened mediastinum	Tension pneumothorax is a clinical diagnosis treated before imaging; CXR shows pulmonary edema in cardiogenic shock
Bedside echocardiography (POCUS/TTE)	Evaluate cardiac function, pericardial effusion, RV strain	Best initial test to differentiate shock type at the bedside; shows reduced EF in cardiogenic, pericardial effusion in tamponade, RV dilation in PE
Pulmonary artery (Swan-Ganz) catheter	Gold standard hemodynamic profiling	Directly measures CVP, PCWP, CO, and SVR; rarely used clinically now but heavily tested for interpretation
CT pulmonary angiography	Confirm pulmonary embolism	Filling defect in pulmonary arteries
FAST exam (Focused Assessment with Sonography for Trauma)	Detect free fluid in trauma	Positive FAST in unstable trauma patient directs to operating room

The best initial test in undifferentiated shock is a combination of clinical assessment, serum lactate, and bedside echocardiography (point-of-care ultrasound). The echo rapidly distinguishes between the four shock categories: a hyperdynamic, underfilled left ventricle points to hypovolemic or distributive shock; a dilated, hypokinetic ventricle points to cardiogenic shock; a pericardial effusion with diastolic collapse suggests tamponade; and isolated RV dilation with a D-shaped septum suggests PE.
The most accurate test for hemodynamic profiling is the pulmonary artery catheter, which directly measures filling pressures ( $C V P$ , $P C W P$ ), cardiac output, and allows calculation of $S V R$ . While clinical practice has moved toward noninvasive monitoring, exam questions still test your ability to interpret Swan-Ganz numbers. The classic hemodynamic profiles you must know cold are summarized in the classification table above.
Serum lactate is the single most important laboratory value in shock. A lactate level above 2 mmol/L indicates tissue hypoperfusion, and serial lactate measurements are used to gauge the adequacy of resuscitation. Lactate clearance (a decrease of at least 10 to 20 percent over 2 to 6 hours) is a validated marker of improving perfusion and is a frequently tested concept.
For tension pneumothorax, the diagnosis is entirely clinical. Do not order imaging. The correct next step is immediate needle decompression followed by tube thoracostomy. A question that provides classic findings (absent breath sounds, tracheal deviation, hypotension, JVD) and offers "chest X-ray" as an answer choice is a trap.

04Management and Treatment

Hypovolemic (hemorrhagic)

FIRST-LINE TREATMENT: Crystalloid bolus (1-2 L), then packed RBCs; activate massive transfusion protocol if Class III-IV
VASOPRESSOR / INOTROPE: Vasopressors only as bridge while restoring volume
ADJUNCTS: Tranexamic acid (TXA) within 3 hours of injury; 1:1:1 ratio of pRBC:FFP:platelets in massive transfusion
CONTRAINDICATIONS / CAUTIONS: Avoid excessive crystalloid (dilutional coagulopathy); target permissive hypotension (SBP 80-90 mmHg) until surgical control

Hypovolemic (non-hemorrhagic)

FIRST-LINE TREATMENT: Isotonic crystalloid (normal saline or lactated Ringer's)
VASOPRESSOR / INOTROPE: Rarely needed if volume restored
ADJUNCTS: Correct underlying cause (insulin for DKA, antiemetics for vomiting)
CONTRAINDICATIONS / CAUTIONS: Avoid normal saline in large volumes (hyperchloremic metabolic acidosis); prefer lactated Ringer's

Cardiogenic

FIRST-LINE TREATMENT: Avoid large fluid boluses; small aliquots (250 mL) with reassessment
VASOPRESSOR / INOTROPE: Dobutamine 2-20 mcg/kg/min (first-line inotrope); add norepinephrine if MAP still low
ADJUNCTS: Emergent reperfusion (PCI) for acute MI; mechanical circulatory support (IABP, Impella, ECMO) for refractory cases; diuresis if pulmonary edema
CONTRAINDICATIONS / CAUTIONS: Do NOT give aggressive fluids (worsens pulmonary edema); avoid pure vasoconstrictors (increase afterload on a failing heart)

Septic

FIRST-LINE TREATMENT: 30 mL/kg IV crystalloid within 3 hours
VASOPRESSOR / INOTROPE: Norepinephrine first-line; add vasopressin (up to 0.03 U/min) as second agent; add epinephrine if still refractory
ADJUNCTS: Broad-spectrum antibiotics within 1 hour; source control (drainage, debridement); hydrocortisone 200 mg/day IV if vasopressor-refractory (>2 agents)
CONTRAINDICATIONS / CAUTIONS: Avoid dopamine (higher arrhythmia risk); stress-dose steroids only if refractory to vasopressors

Anaphylactic

FIRST-LINE TREATMENT: Epinephrine 0.3-0.5 mg IM (1:1000 concentration) into anterolateral thigh; repeat every 5-15 min as needed
VASOPRESSOR / INOTROPE: IV epinephrine drip if refractory to IM dosing
ADJUNCTS: IV crystalloid 1-2 L bolus; diphenhydramine 25-50 mg IV (H1 blocker); famotidine 20 mg IV (H2 blocker); methylprednisolone 125 mg IV (prevents biphasic reaction)
CONTRAINDICATIONS / CAUTIONS: Never give epinephrine IV push in anaphylaxis (risk of fatal arrhythmia); IM is the correct route; do NOT substitute antihistamines for epinephrine

Neurogenic

FIRST-LINE TREATMENT: IV crystalloid bolus
VASOPRESSOR / INOTROPE: Phenylephrine (pure alpha-1 agonist) or norepinephrine if bradycardia is present; atropine for symptomatic bradycardia
ADJUNCTS: Spinal stabilization; avoid hypothermia
CONTRAINDICATIONS / CAUTIONS: Avoid pure beta-agonists (will not address the loss of vascular tone)

Cardiac tamponade

FIRST-LINE TREATMENT: Pericardiocentesis (emergent drainage)
VASOPRESSOR / INOTROPE: Vasopressors as temporizing bridge
ADJUNCTS: IV fluid bolus to augment preload while preparing for drainage; surgical pericardial window if recurrent
CONTRAINDICATIONS / CAUTIONS: Avoid diuretics and nitrates (reduce preload, worsen tamponade physiology)

Tension pneumothorax

FIRST-LINE TREATMENT: Needle decompression (2nd intercostal space, midclavicular line) followed by tube thoracostomy
VASOPRESSOR / INOTROPE: Vasopressors as bridge
ADJUNCTS: Positive-pressure ventilation after decompression
CONTRAINDICATIONS / CAUTIONS: Do not delay for imaging; this is a clinical diagnosis requiring immediate intervention

Pulmonary embolism (with shock)

FIRST-LINE TREATMENT: Systemic thrombolytics (alteplase 100 mg IV over 2 hours)
VASOPRESSOR / INOTROPE: Norepinephrine for hemodynamic support
ADJUNCTS: IV fluids (cautious, 500 mL bolus); consider surgical embolectomy or catheter-directed therapy if thrombolytics contraindicated
CONTRAINDICATIONS / CAUTIONS: Avoid large-volume fluid resuscitation (RV is already volume-overloaded; excess fluid worsens RV failure by shifting the septum)

SHOCK TYPE	FIRST-LINE TREATMENT	VASOPRESSOR / INOTROPE	ADJUNCTS	CONTRAINDICATIONS / CAUTIONS
Hypovolemic (hemorrhagic)	Crystalloid bolus (1-2 L), then packed RBCs; activate massive transfusion protocol if Class III-IV	Vasopressors only as bridge while restoring volume	Tranexamic acid (TXA) within 3 hours of injury; 1:1:1 ratio of pRBC:FFP:platelets in massive transfusion	Avoid excessive crystalloid (dilutional coagulopathy); target permissive hypotension (SBP 80-90 mmHg) until surgical control
Hypovolemic (non-hemorrhagic)	Isotonic crystalloid (normal saline or lactated Ringer's)	Rarely needed if volume restored	Correct underlying cause (insulin for DKA, antiemetics for vomiting)	Avoid normal saline in large volumes (hyperchloremic metabolic acidosis); prefer lactated Ringer's
Cardiogenic	Avoid large fluid boluses; small aliquots (250 mL) with reassessment	Dobutamine 2-20 mcg/kg/min (first-line inotrope); add norepinephrine if MAP still low	Emergent reperfusion (PCI) for acute MI; mechanical circulatory support (IABP, Impella, ECMO) for refractory cases; diuresis if pulmonary edema	Do NOT give aggressive fluids (worsens pulmonary edema); avoid pure vasoconstrictors (increase afterload on a failing heart)
Septic	30 mL/kg IV crystalloid within 3 hours	Norepinephrine first-line; add vasopressin (up to 0.03 U/min) as second agent; add epinephrine if still refractory	Broad-spectrum antibiotics within 1 hour; source control (drainage, debridement); hydrocortisone 200 mg/day IV if vasopressor-refractory (>2 agents)	Avoid dopamine (higher arrhythmia risk); stress-dose steroids only if refractory to vasopressors
Anaphylactic	Epinephrine 0.3-0.5 mg IM (1:1000 concentration) into anterolateral thigh; repeat every 5-15 min as needed	IV epinephrine drip if refractory to IM dosing	IV crystalloid 1-2 L bolus; diphenhydramine 25-50 mg IV (H1 blocker); famotidine 20 mg IV (H2 blocker); methylprednisolone 125 mg IV (prevents biphasic reaction)	Never give epinephrine IV push in anaphylaxis (risk of fatal arrhythmia); IM is the correct route; do NOT substitute antihistamines for epinephrine
Neurogenic	IV crystalloid bolus	Phenylephrine (pure alpha-1 agonist) or norepinephrine if bradycardia is present; atropine for symptomatic bradycardia	Spinal stabilization; avoid hypothermia	Avoid pure beta-agonists (will not address the loss of vascular tone)
Cardiac tamponade	Pericardiocentesis (emergent drainage)	Vasopressors as temporizing bridge	IV fluid bolus to augment preload while preparing for drainage; surgical pericardial window if recurrent	Avoid diuretics and nitrates (reduce preload, worsen tamponade physiology)
Tension pneumothorax	Needle decompression (2nd intercostal space, midclavicular line) followed by tube thoracostomy	Vasopressors as bridge	Positive-pressure ventilation after decompression	Do not delay for imaging; this is a clinical diagnosis requiring immediate intervention
Pulmonary embolism (with shock)	Systemic thrombolytics (alteplase 100 mg IV over 2 hours)	Norepinephrine for hemodynamic support	IV fluids (cautious, 500 mL bolus); consider surgical embolectomy or catheter-directed therapy if thrombolytics contraindicated	Avoid large-volume fluid resuscitation (RV is already volume-overloaded; excess fluid worsens RV failure by shifting the septum)

Septic shock management deserves additional emphasis because it is the most frequently tested shock subtype. The current resuscitation bundle includes the following steps, ideally completed within the first hour:
Measure serum lactate. Obtain blood cultures before starting antibiotics. Administer broad-spectrum antibiotics within one hour of recognition. Begin 30 mL/kg of IV crystalloid for hypotension or lactate above 4 mmol/L. Apply vasopressors (norepinephrine) if the patient remains hypotensive during or after fluid resuscitation, targeting a MAP of at least 65 mmHg.
If the patient requires two or more vasopressors to maintain adequate MAP, this defines vasopressor-refractory shock, and the next step is to add stress-dose hydrocortisone at 200 mg per day (given as 50 mg IV every 6 hours or as a continuous infusion). Do not give corticosteroids to every septic patient; they are reserved for refractory cases.
For cardiogenic shock, the key management principle is to support forward flow without worsening pulmonary congestion. Dobutamine is the first-line inotrope because it increases contractility and mildly reduces afterload through beta-2 stimulation. If the patient remains hypotensive despite dobutamine, add norepinephrine. For cardiogenic shock caused by acute STEMI, the most important intervention is emergent percutaneous coronary intervention (PCI), not pharmacologic management alone.
For anaphylactic shock, intramuscular epinephrine is the first and most important step. A common exam trap is offering IV antihistamines (diphenhydramine) as the first-line treatment. Antihistamines are adjuncts; they do not reverse airway edema or cardiovascular collapse. Only epinephrine does.

05Differential Diagnosis and Distractors

Cardiogenic vs. hypovolemic shock

WHY IT IS SIMILAR: Both present with tachycardia, hypotension, and cool extremities
KEY DISCRIMINATOR: JVD and pulmonary crackles present in cardiogenic; flat neck veins and clear lungs in hypovolemic; echo shows poor contractility in cardiogenic vs. hyperdynamic underfilled ventricle in hypovolemic

Septic shock vs. anaphylactic shock

WHY IT IS SIMILAR: Both are distributive with warm skin, low SVR, and hypotension
KEY DISCRIMINATOR: Urticaria, angioedema, and wheezing within minutes of an exposure point to anaphylaxis; fever, identified infectious source, and gradual onset point to sepsis

Cardiac tamponade vs. tension pneumothorax

WHY IT IS SIMILAR: Both cause obstructive shock with JVD and hypotension
KEY DISCRIMINATOR: Muffled heart sounds and pulsus paradoxus in tamponade; absent breath sounds and tracheal deviation in tension pneumothorax; CXR (if obtained) shows a large cardiac silhouette in tamponade vs. collapsed lung and mediastinal shift in pneumothorax

Cardiogenic shock vs. cardiac tamponade

WHY IT IS SIMILAR: Both show elevated CVP, JVD, and low cardiac output
KEY DISCRIMINATOR: Pulmonary edema (crackles, CXR infiltrates) in cardiogenic shock; clear lung fields in tamponade (because the problem is impaired filling, not pump failure); echo shows pericardial effusion with diastolic collapse in tamponade

Neurogenic shock vs. hypovolemic shock in trauma

WHY IT IS SIMILAR: Both present with hypotension after trauma
KEY DISCRIMINATOR: Bradycardia in neurogenic shock (loss of sympathetic tone) vs. tachycardia in hypovolemic shock (sympathetic compensation); warm, dry skin in neurogenic vs. cool, clammy skin in hypovolemic

Septic shock vs. adrenal crisis

WHY IT IS SIMILAR: Both cause distributive shock with hypotension refractory to fluids
KEY DISCRIMINATOR: Hyperkalemia, hyponatremia, and hypoglycemia in adrenal crisis; history of chronic steroid use with abrupt discontinuation; septic shock shows leukocytosis and elevated procalcitonin

PE with shock vs. acute RV MI

WHY IT IS SIMILAR: Both show RV failure, JVD, elevated CVP, and clear lungs
KEY DISCRIMINATOR: Acute onset dyspnea, pleuritic chest pain, and risk factors for DVT in PE (with RV dilation and D-shaped septum on echo); inferior ST elevation on ECG extending to right-sided leads (V4R) in RV MI

DIFFERENTIAL	WHY IT IS SIMILAR	KEY DISCRIMINATOR
Cardiogenic vs. hypovolemic shock	Both present with tachycardia, hypotension, and cool extremities	JVD and pulmonary crackles present in cardiogenic; flat neck veins and clear lungs in hypovolemic; echo shows poor contractility in cardiogenic vs. hyperdynamic underfilled ventricle in hypovolemic
Septic shock vs. anaphylactic shock	Both are distributive with warm skin, low SVR, and hypotension	Urticaria, angioedema, and wheezing within minutes of an exposure point to anaphylaxis; fever, identified infectious source, and gradual onset point to sepsis
Cardiac tamponade vs. tension pneumothorax	Both cause obstructive shock with JVD and hypotension	Muffled heart sounds and pulsus paradoxus in tamponade; absent breath sounds and tracheal deviation in tension pneumothorax; CXR (if obtained) shows a large cardiac silhouette in tamponade vs. collapsed lung and mediastinal shift in pneumothorax
Cardiogenic shock vs. cardiac tamponade	Both show elevated CVP, JVD, and low cardiac output	Pulmonary edema (crackles, CXR infiltrates) in cardiogenic shock; clear lung fields in tamponade (because the problem is impaired filling, not pump failure); echo shows pericardial effusion with diastolic collapse in tamponade
Neurogenic shock vs. hypovolemic shock in trauma	Both present with hypotension after trauma	Bradycardia in neurogenic shock (loss of sympathetic tone) vs. tachycardia in hypovolemic shock (sympathetic compensation); warm, dry skin in neurogenic vs. cool, clammy skin in hypovolemic
Septic shock vs. adrenal crisis	Both cause distributive shock with hypotension refractory to fluids	Hyperkalemia, hyponatremia, and hypoglycemia in adrenal crisis; history of chronic steroid use with abrupt discontinuation; septic shock shows leukocytosis and elevated procalcitonin
PE with shock vs. acute RV MI	Both show RV failure, JVD, elevated CVP, and clear lungs	Acute onset dyspnea, pleuritic chest pain, and risk factors for DVT in PE (with RV dilation and D-shaped septum on echo); inferior ST elevation on ECG extending to right-sided leads (V4R) in RV MI

06Traps and High-Yield Pearls

The single most common way students get shock questions wrong is by failing to match the hemodynamic profile to the shock type. When a question presents Swan-Ganz catheter data (CVP, PCWP, CO, SVR), the student must categorize the shock type before selecting a treatment. A high PCWP with low CO and high SVR is cardiogenic shock, and the answer is dobutamine, not IV fluids. A low PCWP with low CO and high SVR is hypovolemic shock, and the answer is volume resuscitation, not vasopressors. Confusing these two results in selecting a treatment that worsens the patient.
Another frequent trap involves the timing of interventions in septic shock. The exam tests whether you know that antibiotics must be given within one hour and that lactate must be measured early. Offering "obtain blood cultures, then start antibiotics" is correct only if both happen rapidly. An answer choice that delays antibiotics to wait for culture results is always wrong.
In trauma, the classic trap is the normotensive trauma patient who is tachycardic. Students dismiss this as a normal stress response, but the question is testing recognition of Class II hemorrhagic shock, where compensatory vasoconstriction maintains blood pressure while the patient is actively bleeding. The correct next step is aggressive volume resuscitation, not watchful waiting.
For obstructive shock, remember that tension pneumothorax is a clinical diagnosis treated at the bedside. The wrong answer is always "order a chest X-ray." If the stem gives you absent breath sounds, hyperresonance, JVD, and hypotension, the answer is needle decompression followed by chest tube.
In anaphylaxis, the trap is selecting diphenhydramine or corticosteroids as the first-line treatment. Epinephrine IM is always the answer. Furthermore, the route matters: the answer is intramuscular, not intravenous push, and the concentration is 1:1000 (1 mg/mL) for IM dosing.
Finally, for cardiogenic shock from acute MI, do not get lured into choosing "start dobutamine" when the stem describes an acute STEMI. The best answer is emergent PCI to restore perfusion to the ischemic myocardium. Inotropes are supportive, not definitive.
The core competency being tested across all shock questions is your ability to (1) recognize shock in a patient who may not yet be frankly hypotensive, (2) classify the type using physical exam and hemodynamic data, and (3) select the correct initial intervention without worsening the underlying physiology.