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Eduovisual

Emergency & Toxicology

Hemorrhagic shock: classification and resuscitation

Clinical Overview and When to Suspect Hemorrhagic Shock

— Loss of intravascular volume → decreased preload → decreased stroke volume → compensatory tachycardia and vasoconstriction

— Sympathetic surge maintains BP until ~30% volume loss is reached; normotension does not exclude significant hemorrhage, especially in young patients

— Progressive shock → anaerobic metabolism, lactic acidosis, endothelial injury, and the "lethal triad": hypothermia, acidosis, coagulopathy

— Trauma: blunt or penetrating with tachycardia, narrow pulse pressure, or altered mentation

— GI bleed: hematemesis, melena, hematochezia with orthostasis or syncope

— Obstetric: postpartum hemorrhage, ruptured ectopic, placental abruption

— Vascular: ruptured AAA in older male with back/flank pain and hypotension

— Occult: retroperitoneal bleed (anticoagulated patient, post-cath), splenic rupture (mono, blunt trauma), femur or pelvic fracture

— SBP <90, HR >120, lactate >4, base deficit ≥−6

— Shock index (HR/SBP) >1.0 suggests significant hemorrhage; >1.4 predicts massive transfusion need

— Cool, mottled extremities with delayed capillary refill despite "normal" vitals

Definition: Hemorrhagic shock = inadequate tissue perfusion due to acute blood loss, a subset of hypovolemic shock with distinct coagulopathy and transfusion implications.
Core physiology:
When to suspect on Step 3:
Red flags demanding immediate action:
Step 3 management: The first move in suspected hemorrhagic shock is simultaneous resuscitation and source identification—do not delay transfusion or hemorrhage control to "complete the workup." Activate massive transfusion protocol (MTP) early when criteria are met rather than chasing crystalloid boluses.
Board pearl: A young trauma patient with HR 110 and BP 118/96 (narrow pulse pressure) is in compensated Class II shock, not stable—act before decompensation. Pulse pressure narrowing precedes hypotension because diastolic rises from catecholamine-driven vasoconstriction while systolic is maintained by tachycardia.
Solid White Background
Presentation Patterns and Key History

— Blunt: MVC, falls, assaults → suspect chest, abdomen, pelvis, long bones, retroperitoneum as the "five places blood hides"

— Penetrating: GSW/stab → trajectory dictates likely vascular injury; thoracoabdominal wounds may involve both cavities

— Upper GI: hematemesis, coffee-ground emesis, melena; ask about NSAIDs, alcohol, cirrhosis, prior ulcer, anticoagulants

— Lower GI: hematochezia, often diverticular or angiodysplasia in elderly; brisk upper bleeds can also present with hematochezia

— First trimester: ectopic pregnancy (unilateral pain, amenorrhea, hCG positive)

— Third trimester/peripartum: abruption (painful bleeding, rigid uterus), previa (painless), uterine atony (boggy uterus postpartum), retained products, accreta spectrum

— AAA rupture: older smoker/HTN male, sudden tearing back/abdominal pain, pulsatile mass, syncope

— Aortoenteric fistula: prior aortic graft + GI bleed = until proven otherwise

— Post-procedure: cardiac cath (retroperitoneal hematoma → flank/back pain), liver biopsy, thoracentesis

— Anticoagulation: warfarin, DOACs, heparin—always ask last dose and indication

— Mechanism, time of onset, estimated blood loss, prior episodes

— Medications: anticoagulants, antiplatelets, beta-blockers (mask tachycardia), NSAIDs

— Comorbidities: cirrhosis, CKD, cardiac disease, bleeding disorders

— Last meal (for surgical planning), tetanus status, allergies

Trauma presentations:
GI bleeding patterns:
Obstetric/gynecologic:
Vascular catastrophes:
Iatrogenic and occult sources:
Key history elements:
Key distinction: Beta-blocker use blunts the tachycardic response—a patient on metoprolol with HR 85 and SBP 100 may already be in significant shock. Similarly, elderly patients have diminished compensatory reserve and pregnant patients have 30–50% expanded plasma volume, so signs of shock appear late but decompensation is precipitous.
Board pearl: A patient with prior AAA repair presenting with even one episode of GI bleeding warrants emergent CT angiography to rule out aortoenteric fistula—missing this diagnosis is uniformly fatal.
Solid White Background
Physical Exam Findings and Hemodynamic Assessment

Class I: <15% (<750 mL) — normal vitals, mild anxiety, urine >30 mL/hr

Class II: 15–30% (750–1500 mL) — HR >100, narrowed pulse pressure, RR 20–30, mild anxiety, urine 20–30 mL/hr; BP still normal

Class III: 30–40% (1500–2000 mL) — HR >120, hypotension, RR 30–40, confusion, urine 5–15 mL/hr

Class IV: >40% (>2000 mL) — HR >140 or bradycardia, severe hypotension, lethargic, negligible urine output, immediately life-threatening

— Pallor, diaphoresis, cool/clammy extremities, mottling (knees, elbows)

— Mental status: anxiety → confusion → obtundation as perfusion falls

— Tachycardia (early, sensitive but nonspecific)

— Narrow pulse pressure (early); hypotension (late)

— Weak/thready peripheral pulses; prolonged capillary refill (>3 sec)

— Abdominal distension, peritonitis, Cullen/Grey-Turner signs (retroperitoneal)

— Pelvic instability on gentle compression (don't rock repeatedly—dislodges clot)

— Long-bone deformity; femur fracture can sequester 1–1.5 L

— Rectal exam: gross blood, melena, high-riding prostate (urethral injury)

Shock index = HR/SBP; normal 0.5–0.7; >1.0 concerning; >1.4 predicts MTP

FAST exam for free fluid in trauma; eFAST adds pneumothorax/hemothorax

— Lactate and base deficit reflect tissue hypoperfusion

ATLS hemorrhagic shock classification (70-kg adult, ~5 L blood volume):
General appearance:
Cardiovascular:
Respiratory: Tachypnea from metabolic acidosis compensation and sympathetic drive
Source-specific findings:
Bedside hemodynamic tools:
CCS pearl: Order vital signs q15 minutes during active resuscitation, place two large-bore (16-gauge or larger) peripheral IVs, and trend lactate every 2–4 hours until clearance. Persistent lactate >2 after resuscitation predicts mortality and demands source reassessment.
Solid White Background
Diagnostic Workup — Initial Labs, Imaging, and Bedside Studies

— Point-of-care glucose, lactate, hemoglobin (iSTAT/VBG)

Type and crossmatch (send before transfusion; use uncrossmatched type O while waiting)

— ECG if age >50, chest pain, or cardiac history—rule out demand ischemia

— CBC: initial hemoglobin can be normal in acute hemorrhage (hemoconcentration); trend serially

— Coagulation: PT/INR, aPTT, fibrinogen (target >150–200 mg/dL in trauma), platelets

— Chemistry: BUN/Cr (elevated BUN/Cr ratio in upper GI bleed), electrolytes, calcium (ionized—drops with citrated blood)

— Lactate, ABG/VBG with base deficit

— Type and screen; β-hCG in any reproductive-age female

— Troponin if hemodynamic instability or chest pain

TEG or ROTEM guides component therapy in trauma and massive hemorrhage—identifies hyperfibrinolysis, factor deficiency, platelet dysfunction faster than conventional coags

— Trauma: eFAST first (free fluid, pneumothorax, pericardial); chest and pelvic X-ray; CT if hemodynamically stable

— GI bleed: upright CXR for free air; CT angiography if brisk and source unclear; endoscopy is diagnostic and therapeutic

— Suspected AAA: bedside ultrasound (sensitive for aneurysm, not rupture); CT angiography if stable

— Obstetric: transvaginal US for ectopic; bedside US for abruption/previa

Immediate bedside (within minutes):
Critical labs:
Viscoelastic testing:
Imaging by source:
Board pearl: In acute hemorrhage, the initial hemoglobin reflects pre-bleed status, not current losses, because plasma and RBCs are lost proportionally. Equilibration with extravascular fluid over hours drops the Hgb. Do not wait for a low Hgb to transfuse a patient in clinical shock.
Step 3 management: In an unstable trauma patient with positive FAST, the next step is immediate OR for laparotomy, not CT. CT is for the stable or transient responder—pushing an unstable patient to the scanner is a tested error.
Solid White Background
Diagnostic Workup — Advanced and Confirmatory Studies

— Gold standard for stable patients to localize bleeding source

Active extravasation ("contrast blush") identifies vessels amenable to embolization

— Used in trauma (chest, abdomen, pelvis), GI bleed (when endoscopy non-diagnostic or bleeding too brisk), AAA, post-procedural bleeding

Upper endoscopy (EGD) within 12–24 hours of presentation for upper GI bleeding (within 12 hours for variceal/severe)

— Colonoscopy within 24 hours for stable lower GI bleed after rapid bowel prep

— Push enteroscopy or video capsule for obscure small-bowel bleeding

— Diagnostic and therapeutic (embolization)

— Detects bleeding rates ≥0.5 mL/min

— Useful for pelvic fracture bleeding, hepatic/splenic injury, post-procedure hemorrhage, refractory GI bleed

— Detects slower bleeding (≥0.1 mL/min), localizes to a region, less precise than angio

— Useful for intermittent lower GI bleeding

— Exploratory laparotomy for unstable abdominal trauma with positive FAST

— Damage control surgery: abbreviated procedure to control hemorrhage and contamination, then ICU resuscitation, then definitive repair

— Bronchoscopy for massive hemoptysis

— Cystoscopy and retrograde urethrogram for GU bleeding/injury

— DPL (diagnostic peritoneal lavage) — largely replaced by FAST/CT

CT angiography (CTA):
Endoscopy:
Angiography:
Tagged RBC scan:
Operative exploration:
Specialty studies:
Key distinction: CT angiography vs. conventional angiography—CTA is faster, less invasive, and excellent for diagnosis; conventional angiography is therapeutic via embolization. Order CTA first in stable patients to localize, then proceed to IR for embolization. Skip CTA in unstable patients—go directly to OR or hybrid suite.
Board pearl: A "transient responder" (initial improvement with fluid/blood but recurrent hypotension) has ongoing hemorrhage and needs definitive source control—imaging or OR—not more fluid boluses.
Solid White Background
Risk Stratification and First-Line Resuscitation Logic

ABC score ≥2 (penetrating mechanism, SBP ≤90, HR ≥120, positive FAST)

— Shock index >1.4

— Anticipated need for >10 units PRBC in 24 hours or >4 units in 1 hour

Permissive hypotension in penetrating trauma without TBI: target SBP 80–90 mmHg until hemorrhage controlled

Avoid SBP <110 if traumatic brain injury (need cerebral perfusion)

Minimize crystalloid—excess causes dilutional coagulopathy, acidosis, hypothermia, abdominal compartment syndrome, ARDS

Balanced resuscitation: PRBC : FFP : platelets in 1:1:1 ratio (one apheresis platelet = 6 units)

— Brief crystalloid bolus (1 L balanced crystalloid like LR or Plasma-Lyte) while blood arrives—not 2 L as in older ATLS

— Transition rapidly to blood products

Avoid normal saline in massive resuscitation (hyperchloremic acidosis, AKI)

Tranexamic acid (TXA) 1 g IV over 10 min, then 1 g over 8 hr within 3 hours of trauma (CRASH-2); also in PPH (WOMAN trial)

— Reverse anticoagulation: 4-factor PCC for warfarin/DOAC-associated bleeding; idarucizumab for dabigatran; andexanet alfa for apixaban/rivaroxaban

— Direct pressure, tourniquets, pelvic binders, wound packing, REBOA in select centers

— MAP ≥65, urine output ≥0.5 mL/kg/hr, lactate clearance, base deficit normalization, mentation improvement

Massive transfusion protocol (MTP) activation criteria:
Damage control resuscitation principles:
Initial fluid strategy:
Hemorrhage control adjuncts:
Endpoints of resuscitation:
CCS pearl: Order in this sequence: (1) two large-bore IVs, (2) type and cross + send labs, (3) activate MTP, (4) TXA if trauma <3 hr, (5) call surgery/IR for source control, (6) Foley to monitor UOP, (7) warming measures. Document reassessment after each intervention.
Board pearl: Permissive hypotension does not apply to TBI, elderly, or known cerebrovascular disease—maintain MAP ≥80 and SBP ≥110 in TBI.
Solid White Background
Pharmacotherapy and Blood Component Therapy

— Each unit raises Hgb ~1 g/dL in a 70-kg adult

Restrictive threshold (Hgb <7) for stable patients including most ICU and GI bleed (non-variceal); <8 for ACS, postop cardiac

— In active hemorrhagic shock, transfuse based on clinical status, not numbers

— Type O negative for females of reproductive age; O positive for males/post-menopausal until type-specific available

— Replaces all coag factors; dose 10–15 mL/kg

— Goal INR <1.5–1.8 in active bleeding

— 1:1 ratio with PRBC in MTP

— One apheresis unit ≈ 6 pooled units, raises count by ~30K

— Target >50K in active bleeding; >100K in TBI or neurosurgical bleeding

— Concentrated fibrinogen, vWF, factor VIII, XIII

— Give if fibrinogen <150–200 mg/dL; typical dose 10 units

— Citrate in stored blood chelates calcium → hypocalcemia → worsens coagulopathy and cardiac function

— Give 1 g calcium gluconate (or 1 g CaCl via central line) per 4 units PRBC; monitor ionized calcium

— Warfarin (INR ≥2 with bleeding): 4-factor PCC 25–50 units/kg + vitamin K 10 mg IV

— Dabigatran: idarucizumab 5 g IV

— Apixaban/rivaroxaban: andexanet alfa or 4-factor PCC if unavailable

— Heparin: protamine sulfate

— Antiplatelet agents: platelet transfusion only if neurosurgical bleeding or CNS hemorrhage

Packed red blood cells (PRBC):
Fresh frozen plasma (FFP):
Platelets:
Cryoprecipitate:
Tranexamic acid: 1 g IV over 10 min then 1 g over 8 hr; trauma within 3 hr, PPH, GI bleed (controversial—HALT-IT showed no mortality benefit)
Calcium replacement:
Anticoagulation reversal:
Step 3 management: Hypocalcemia, hypothermia, and acidosis are the "diamond of death" in massive transfusion—actively monitor ionized calcium, use a fluid warmer/Bair Hugger, and correct acidosis with source control (not bicarbonate as a primary fix).
Solid White Background
Procedures and Definitive Hemorrhage Control

Exploratory laparotomy for unstable abdominal trauma with positive FAST or peritonitis

Damage control laparotomy: rapid hemorrhage and contamination control, temporary abdominal closure, ICU resuscitation, return for definitive repair in 24–48 hr

— Thoracotomy: emergency department resuscitative thoracotomy for penetrating chest trauma with witnessed loss of vitals (<15 min)

Angioembolization for splenic, hepatic, pelvic, renal injuries with contrast blush in stable patients; also for GI bleed when endoscopy fails

REBOA (resuscitative endovascular balloon occlusion of aorta): zone 1 for abdominal/pelvic hemorrhage, zone 3 for pelvic; bridge to definitive control

TIPS for refractory variceal bleeding

— Variceal: band ligation (first-line) or sclerotherapy; octreotide infusion 50 mcg bolus then 50 mcg/hr; ceftriaxone prophylaxis

— Non-variceal ulcer: epinephrine injection + thermal or mechanical (clip) combination therapy; high-dose PPI (pantoprazole 80 mg bolus then 8 mg/hr or intermittent dosing)

— Balloon tamponade (Blakemore/Minnesota tube) as temporizing bridge for massive variceal bleed

— Uterine atony: oxytocin, methylergonovine (avoid in HTN), carboprost (avoid in asthma), misoprostol; bimanual massage; intrauterine balloon (Bakri)

— Refractory: uterine artery embolization, B-Lynch suture, hysterectomy

— Ruptured AAA: endovascular aortic repair (EVAR) preferred when anatomy permits; open if EVAR not feasible

Surgical hemorrhage control:
Endovascular and interventional:
Endoscopic hemostasis (GI bleed):
Obstetric hemorrhage control:
Vascular:
CCS pearl: For variceal bleeding, the CCS order set is: IV access × 2, type and cross, octreotide drip, ceftriaxone 1 g IV, IV PPI, urgent GI consult for EGD within 12 hours, ICU admission. Do not forget antibiotic prophylaxis—reduces mortality and rebleeding in cirrhotics.
Solid White Background
Special Populations — Elderly and Renal/Hepatic Impairment

Diminished physiologic reserve: baseline lower cardiac output, decreased β-receptor responsiveness, stiff vasculature

— Often on beta-blockers, calcium channel blockers that blunt tachycardia—HR may stay normal despite significant blood loss

— Baseline hypertension means a "normal" SBP of 120 may represent relative hypotension; trend from patient's baseline

— Higher risk of silent occult bleeding (retroperitoneal, intracranial after falls)

— Lower threshold for head CT after any fall, especially if anticoagulated

— Reverse promptly with PCC, vitamin K, or specific reversal agents

— Even minor trauma can cause major bleeding (subdural hematoma, retroperitoneal hematoma)

Uremic platelet dysfunction—consider desmopressin (DDAVP) 0.3 mcg/kg IV for active bleeding

— Adjust drug doses (TXA dose-reduced in CrCl <30)

— Avoid LR caution in hyperkalemia, though balanced crystalloids generally preferred

— Contrast nephropathy risk with CTA—hydrate, but do not withhold imaging when needed for hemorrhage diagnosis

— Baseline coagulopathy (elevated INR), thrombocytopenia, decreased fibrinogen

— Variceal bleeding very high mortality—prophylactic ceftriaxone reduces SBP and rebleeding

— Avoid over-transfusion of PRBC (target Hgb 7–8, not higher) in variceal bleeding—raises portal pressure and worsens rebleeding

— Lactate may be elevated at baseline; trend from individual baseline

Elderly patients:
Anticoagulated elderly:
Renal impairment (CKD/ESRD):
Hepatic impairment (cirrhosis):
Board pearl: A normotensive elderly trauma patient on beta-blockade with mottled knees and confusion is in shock until proven otherwise—do not be reassured by vital signs alone. Order lactate and base deficit immediately.
Step 3 management: In cirrhotic variceal bleeding, the bundle is: octreotide + ceftriaxone + early EGD + restrictive transfusion (Hgb >7). Over-transfusion is a tested wrong answer.
Solid White Background
Special Populations — Pregnancy, Pediatrics, and Obstetric Hemorrhage

Plasma volume increases 40–50% by third trimester—signs of shock appear late but decompensation is rapid

— Resting tachycardia and lower BP normal in pregnancy; HR >120 or SBP <100 concerning

Left lateral tilt (15–30°) to displace gravid uterus off IVC and improve venous return in any pregnant trauma patient >20 weeks

— Resuscitate the mother to resuscitate the fetus—maternal hemodynamics drive uteroplacental perfusion

Antepartum: placental abruption (painful bleeding, rigid uterus, often with trauma or HTN), placenta previa (painless bleeding), uterine rupture, ruptured ectopic

Postpartum (the 4 T's): Tone (atony, most common), Trauma (lacerations), Tissue (retained products), Thrombin (coagulopathy, DIC, accreta)

— Bimanual massage + oxytocin 20–40 units in 1 L IV

— Methylergonovine 0.2 mg IM (contraindicated in HTN, preeclampsia)

— Carboprost 250 mcg IM (contraindicated in asthma)

— Misoprostol 800–1000 mcg rectal/sublingual

— Tranexamic acid 1 g IV within 3 hours of birth

— Bakri balloon, uterine artery embolization, B-Lynch suture, hysterectomy

— Children compensate via tachycardia longer; hypotension is a late and ominous sign

— Estimated blood volume: 80 mL/kg (infants 90 mL/kg)

— Initial crystalloid bolus 20 mL/kg, then 10 mL/kg PRBC if no response after 2 boluses

— IO access if IV unattainable within 90 seconds

— Non-accidental trauma: investigate inconsistent histories, patterned bruising, retinal hemorrhages

Pregnancy physiologic changes:
Causes of obstetric hemorrhage:
PPH management ladder:
Pediatric considerations:
Key distinction: Placental abruption vs. previa—abruption is painful with concealed hemorrhage possible (uterine rigidity, fetal distress) often after trauma; previa is painless bright red bleeding. Never perform digital vaginal exam in suspected previa—use ultrasound.
Board pearl: Rh-negative pregnant trauma patients need Rh immune globulin (RhoGAM) within 72 hours; consider Kleihauer-Betke to dose appropriately for large fetomaternal hemorrhage.
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Complications and Adverse Outcomes

Hypothermia (<35°C): impairs coagulation enzymes, platelet function

Acidosis (pH <7.2): impairs clotting factor activity, vasopressor response

Coagulopathy: dilutional, consumptive, and trauma-induced (TIC)

Hypocalcemia (from citrate): worsens cardiac function and clotting

TRALI (transfusion-related acute lung injury): non-cardiogenic pulmonary edema within 6 hr; supportive care

TACO (transfusion-associated circulatory overload): volume overload, especially elderly/cardiac patients; diurese, slow rate

— Acute hemolytic reaction (ABO mismatch): fever, flank pain, hemoglobinuria; stop immediately

— Febrile non-hemolytic, allergic/anaphylactic reactions

— Hyperkalemia from cell lysis in stored blood; hypocalcemia from citrate

Abdominal compartment syndrome: intra-abdominal pressure >20 mmHg with organ dysfunction; from massive crystalloid, retroperitoneal hematoma, packing; treat with decompressive laparotomy

— ARDS from massive transfusion and crystalloid

— Dilutional thrombocytopenia and coagulopathy

— Acute kidney injury (ischemic ATN)

— Hepatic shock liver (centrilobular necrosis, transaminases in thousands)

— Bowel ischemia, stress ulceration

— Anoxic brain injury

— Sheehan syndrome (pituitary necrosis after PPH) → secondary hypothyroidism, adrenal insufficiency, agalactorrhea

— Multi-organ dysfunction syndrome (MODS)

— Sepsis from translocation or wound infection

— Critical illness myopathy, ICU-acquired weakness

— Post-traumatic stress disorder

Lethal triad / diamond of death:
Transfusion-related complications:
Resuscitation-related complications:
End-organ injury:
Late complications:
Board pearl: A postpartum hemorrhage patient with failure to lactate, fatigue, and amenorrhea months later has Sheehan syndrome—check anterior pituitary hormones and replace; cortisol replacement before thyroid hormone to avoid adrenal crisis.
Step 3 management: Monitor bladder pressure in any patient with massive resuscitation, severe abdominal trauma, or tense abdomen—bladder pressure >20 mmHg with new organ dysfunction mandates surgical decompression.
Solid White Background
When to Escalate Care — ICU, Consults, and Transfer

— Any trauma patient with shock, positive FAST, peritonitis, or penetrating torso injury

— Ruptured AAA, mesenteric ischemia, ruptured ectopic

— Refractory GI bleed despite endoscopy

— Stable patient with active extravasation on CTA (splenic, hepatic, pelvic, renal)

— Post-procedural hemorrhage (retroperitoneal hematoma from cardiac cath)

— Refractory GI bleed when endoscopy fails or source not identified

— Ongoing hemodynamic instability or vasopressor requirement

— Massive transfusion (>4 units in 1 hour or >10 in 24 hours)

— Post-damage-control surgery

— Mechanical ventilation

— Persistent lactate elevation, acidosis, coagulopathy requiring ongoing correction

— Trauma center designation: Level I or II for major trauma; transfer if local facility lacks surgical/IR capability

EMTALA requires stabilization before transfer and accepting facility agreement

— Air vs. ground transport based on distance and stability; ensure blood products travel with patient

Immediate surgical consultation:
Interventional radiology:
Gastroenterology: All upper and lower GI bleeds for endoscopic evaluation within 24 hours (12 hours for variceal/severe)
OB/Gyn: All obstetric hemorrhage, ruptured ectopic, gynecologic bleeding
ICU admission criteria:
Transfer considerations:
CCS pearl: When ordering ICU admission in CCS, also order: continuous cardiac monitoring, arterial line, central venous access if vasopressors needed, Foley catheter, NG tube if obtunded or post-op, DVT prophylaxis (mechanical until bleeding controlled, then pharmacologic), stress ulcer prophylaxis, glycemic control, and family communication.
Step 3 management: In a community ED with a hemodynamically unstable trauma patient needing a higher level of care, stabilize what you can (airway, IV access, hemorrhage control, blood products) and transfer immediately—do not delay for imaging that won't change the next step. Call the trauma center directly; transfer must be physician-to-physician.
Board pearl: Cirrhotic patients with variceal bleeding belong in ICU regardless of initial stability—rebleeding rate is high in the first 48 hours.
Solid White Background
Key Differentials — Other Causes of Shock

Hypovolemic (hemorrhagic or non-hemorrhagic): low CO, low PCWP, high SVR

Cardiogenic: low CO, high PCWP, high SVR

Obstructive: low CO, variable PCWP, high SVR (tamponade, tension PTX, massive PE)

Distributive (septic, anaphylactic, neurogenic): high CO, low PCWP, low SVR

— Severe vomiting/diarrhea, burns, DKA, third-spacing (pancreatitis, bowel obstruction)

— Same initial resuscitation (crystalloid) but no transfusion needed

— Acute MI, decompensated HF, severe valvular disease, myocarditis

— Clues: JVD, pulmonary edema, S3, cool extremities, elevated troponin

Avoid aggressive fluid—will worsen pulmonary edema

Cardiac tamponade: Beck's triad (hypotension, JVD, muffled heart sounds), pulsus paradoxus; bedside echo, pericardiocentesis

Tension pneumothorax: tracheal deviation, absent breath sounds, hyperresonance; needle decompression, chest tube

Massive PE: sudden dyspnea, RV strain on echo/ECG (S1Q3T3); systemic thrombolysis or thrombectomy

Septic: fever, infection source, warm/flushed early then cool; lactate elevated, broad-spectrum antibiotics, fluids, vasopressors

Anaphylactic: hives, wheezing, exposure history; epinephrine IM

Neurogenic (spinal cord injury above T6): hypotension with bradycardia (loss of sympathetic tone), warm dry skin

The four shock categories (all can mimic hemorrhagic shock):
Non-hemorrhagic hypovolemic shock:
Cardiogenic shock:
Obstructive shock:
Distributive shock:
Key distinction: Bradycardia with hypotension in a trauma patient suggests neurogenic shock from spinal cord injury (not hemorrhagic, which causes tachycardia). Look for sensory level, flaccid paralysis, priapism. However, rule out hemorrhage first—the two can coexist.
Board pearl: A trauma patient with persistent hypotension despite adequate transfusion who has distended neck veins has obstructive shock until proven otherwise—think tension pneumothorax, tamponade, or air embolism—not more blood.
Solid White Background
Key Differentials — Mimickers and Concurrent Pathology

— Patient on chronic steroids without stress-dose coverage, autoimmune disease, recent steroid taper

— Hypotension refractory to fluids, hyperkalemia, hyponatremia, hypoglycemia

— Treat empirically with hydrocortisone 100 mg IV if suspected

— Storm: tachycardia, fever, agitation, AF, hypotension late

— Myxedema: hypothermia, bradycardia, hypotension, altered mentation

— Heat stroke, prolonged GI losses, DKA, HHS—respond to crystalloid alone

— Antihypertensive overdose (especially CCB, β-blocker, ACEi)

— Sedative/opioid overdose

— Anaphylaxis from contrast, drugs, food

— Vasovagal episode with self-limited hypotension; not true shock

— Reassess after recovery

— Trauma patient may have MI, PE, sepsis, or dissection as the precipitating event before injury (e.g., elderly driver had syncope/MI causing crash)

— Always check ECG, troponin, and consider non-traumatic causes when shock persists despite hemorrhage control

— Iron, salicylates, sympatholytics

— Carbon monoxide (lactic acidosis, headache, exposure history)

Adrenal crisis / Addisonian shock:
Thyroid storm or myxedema coma:
Severe dehydration mimicking hemorrhage:
Drug-induced hypotension:
Vagal/syncope mimics:
Concurrent pathology in trauma:
DKA in trauma: May contribute to acidosis and hypovolemia; check glucose and ketones
Toxic ingestions:
Key distinction: Pulse pressure helps differentiate shock types—narrow pulse pressure suggests hypovolemic/cardiogenic (low SV, high SVR); wide pulse pressure suggests distributive (low SVR) or aortic regurgitation. Use in conjunction with bedside echo and clinical picture.
Step 3 management: When a "trauma" patient has disproportionate shock for visible injuries, broaden differential: occult retroperitoneal bleed, MI causing the crash, PE, dissection, septic source. Order ECG, troponin, lactate, CTA chest/abdomen/pelvis, and consider bedside echo.
Board pearl: Aortic dissection can present with shock and hemothorax; suspect in older HTN patient with chest/back pain, unequal pulses, mediastinal widening.
Solid White Background
Secondary Prevention and Discharge Planning

— Address the underlying cause to prevent recurrence

— Comprehensive medication reconciliation, especially anticoagulants/antiplatelets

— Coordinate outpatient specialty follow-up before discharge

PPI for 8 weeks (peptic ulcer) or indefinite (Barrett's, severe esophagitis)

H. pylori test and treat if ulcer disease

— Stop NSAIDs; if essential, add PPI and use lowest dose

— Resume aspirin within 1–7 days post-bleed if cardiovascular indication (mortality benefit outweighs rebleed risk)

— Variceal bleed: non-selective beta-blocker (propranolol/nadolol) + serial band ligation until obliterated; consider TIPS if recurrent

— Avoid alcohol; hepatology follow-up for cirrhosis management

— Wound care instructions, signs of infection, tetanus booster if indicated

— DVT prophylaxis for prolonged immobility

— Mental health screening for PTSD; brief intervention for alcohol/substance use if contributory

— Driver safety, helmet use, fall prevention (older adults)

— Reassess indication after major bleed

— For warfarin-associated GI bleed: resume warfarin in most patients within 7–14 days (mortality benefit if indication strong)

— DOACs preferred over warfarin for most indications (lower ICH risk)

— Consider LAA closure (Watchman) for AF patients with bleeding contraindication to anticoagulation

— Iron supplementation for postpartum anemia

— Screen for Sheehan syndrome (failure to lactate, fatigue, amenorrhea)

— Contraception counseling; future pregnancy planning with high-risk OB

— CT surveillance at 1, 6, 12 months then annually for EVAR endoleak

— Smoking cessation, BP and lipid management

Post-resuscitation discharge planning:
GI bleed discharge:
Trauma discharge:
Anticoagulation considerations:
Obstetric hemorrhage follow-up:
AAA repair follow-up:
Step 3 management: After a major GI bleed in a patient with AFib, the question of "when to resume anticoagulation" is high-yield—resume within 7–14 days in most cases unless rebleeding risk extreme. Multidisciplinary discussion documented in chart.
Board pearl: Aspirin held >7 days after ACS-related GI bleed doubles cardiovascular mortality—reintroduce promptly with PPI cover.
Solid White Background
Follow-Up, Monitoring, and Rehabilitation

— Primary care within 1–2 weeks for medication reconciliation, anemia recheck

— Specialty (GI, surgery, OB, vascular) within 2–4 weeks depending on cause

— Repeat CBC at 1–2 weeks to confirm hemoglobin recovery; iron studies if persistent anemia

— Oral iron (ferrous sulfate 325 mg every other day—better absorbed than daily dosing)

— IV iron (iron sucrose, ferric carboxymaltose) for malabsorption, intolerance, or large deficit

— Reticulocyte response within 1 week; Hgb normalization in 6–8 weeks

— Physical therapy for deconditioning, fracture recovery

— Occupational therapy for ADL support

— Speech therapy if dysphagia post-intubation or TBI

— Cognitive rehabilitation for TBI

— Psychological support: PTSD screening at follow-up, referral to mental health

— Return-to-work and driving evaluation

— Pain management plan; minimize opioids, multimodal approach

— Substance use counseling if relevant

— Trends in Hgb, iron studies, renal function

— Anticoagulation INR if on warfarin, periodic CBC/Cr on DOACs

— Endoscopic surveillance for varices (q1–3 years), Barrett's esophagus

— Smoking cessation (huge mortality impact, especially AAA, PUD)

— Alcohol moderation/abstinence

— NSAID avoidance with PPI co-prescription if necessary

— Fall prevention in elderly (home assessment, vision, vitamin D, balance training)

Post-discharge follow-up cadence:
Iron deficiency management:
Trauma rehabilitation:
Functional outcomes assessment:
Monitoring parameters:
Counseling and lifestyle:
CCS pearl: Schedule follow-up before discharge with specific date and provider, not "follow up as needed." Order CBC and basic metabolic panel at 1–2 week follow-up to confirm stability. For postpartum hemorrhage patients, schedule visits at 1 week and 6 weeks with attention to lactation, mood, and pituitary function.
Board pearl: Persistent fatigue and exercise intolerance after a major bleed warrants iron studies even if Hgb has recovered—ferritin can be low with normal Hgb, and iron repletion improves symptoms.
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Ethical, Legal, and Patient Safety Considerations

— Life-threatening hemorrhage allows implied consent for blood products and emergent surgery when patient cannot consent and no surrogate is available

— Document the emergency and inability to obtain consent

— Competent adult patients may refuse blood products even when life-threatening—must be honored

— Explore acceptable alternatives: cell saver, erythropoietin, IV iron, tranexamic acid, factor concentrates, fibrinogen concentrate

— Document detailed informed refusal; involve ethics consultation if conflict

— Minors: courts can override parental refusal for life-saving transfusion; obtain emergency court order

— Gunshot wounds, stabbings, assaults — report to law enforcement (state-specific)

— Suspected child abuse, elder abuse, intimate partner violence with signs of coercion (varies by state)

— Motor vehicle crashes with injury (often reported via EMS already)

— Hierarchy when patient incapacitated: legal guardian → spouse → adult children → parents → siblings

— Honor advance directives and POLST forms; check before initiating aggressive resuscitation

— DNR does not equal "do not treat"—still resuscitate with blood products, IV fluids, treatment of reversible causes unless explicitly declined

— Clarify scope of care with patient/family early; reassess goals if shock refractory

Handoff communication (SBAR or IPASS) critical when transferring from ED → OR → ICU → floor

— Medication reconciliation at every transition prevents anticoagulant re-initiation errors that cause rebleed

Closed-loop communication with blood bank during MTP to track products and verify identity

Informed consent in emergencies:
Jehovah's Witnesses and blood refusal:
Mandatory reporting:
Surrogate decision-making:
DNR/DNI in the bleeding patient:
Patient safety in transitions:
Step 3 management: When a Jehovah's Witness presents with hemorrhagic shock, document the conversation in detail, offer all non-blood alternatives, involve ethics and palliative care if mortality is high, and explore whether the patient accepts fractionated products (some accept albumin, factor concentrates) on an individual basis—this is patient-specific.
Board pearl: Never delay a life-saving transfusion in an unconscious trauma patient awaiting consent—emergency exception applies. Document the rationale.
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High-Yield Associations and Rapid-Fire Facts
Shock index >1.0 = significant hemorrhage; >1.4 = MTP likely needed
Pulse pressure narrows before SBP drops — early warning of shock
Class II shock (15–30% loss): tachycardia + narrow pulse pressure + normal SBP
Class III shock (30–40%): tachycardia + hypotension + confusion + oliguria
TXA within 3 hours of trauma reduces mortality (CRASH-2); also in PPH (WOMAN)
1:1:1 ratio PRBC:FFP:platelets in massive transfusion (PROPPR trial)
Permissive hypotension SBP 80–90 in penetrating trauma without TBI
Avoid permissive hypotension in TBI (need MAP ≥80)
Citrate toxicity = hypocalcemia → give Ca gluconate 1 g per 4 units PRBC
Lethal triad: hypothermia, acidosis, coagulopathy
Five places blood hides: chest, abdomen, retroperitoneum, pelvis/thigh, "on the floor" (external)
Femur fracture: 1–1.5 L blood loss; pelvic fracture: up to 4 L
FAST exam views: pericardial, RUQ (Morison's pouch), LUQ (splenorenal), pelvis (rectovesical/pouch of Douglas)
eFAST adds anterior chest for pneumothorax
Variceal bleed bundle: octreotide + ceftriaxone + EGD <12 hr
Restrictive transfusion Hgb <7 for most stable patients (TRICC, TRISS)
Hgb <8 target for ACS, postop cardiac surgery
BUN/Cr >30 suggests upper GI bleed (digested blood is protein meal)
Sheehan syndrome: failure to lactate after PPH = pituitary necrosis
Aortoenteric fistula: AAA graft + GI bleed = until proven otherwise
REBOA zones: zone 1 (supraceliac) for abdominal hemorrhage; zone 3 (infrarenal) for pelvic
Damage control: abbreviated surgery → ICU resuscitation → return for definitive repair
TRALI = lung injury within 6 hr of transfusion; TACO = volume overload
Methylergonovine contraindicated in HTN; carboprost contraindicated in asthma
Idarucizumab reverses dabigatran; andexanet alfa reverses Xa inhibitors
DDAVP for uremic platelet dysfunction
Board pearl: The single most predictive bedside number for massive transfusion need is the shock index (HR/SBP) >1.4—memorize and use it.
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Board Question Stem Patterns

— 22-year-old MVC, HR 118, BP 122/98, anxious, cool extremities → Class II shock; answer: transfuse / activate MTP, not "observe"

— 78-year-old fall on warfarin, HR 82, BP 110/70, confused, lactate 4 → suspect occult hemorrhage; answer: CT head + reverse anticoagulation with 4-factor PCC + vitamin K

— Hypotensive after MVC, FAST positive for free fluid in Morison's pouch → answer: emergent laparotomy, not CT

— Cirrhotic with hematemesis, HR 120, BP 90/60 → answer: IV access, type and cross, octreotide, ceftriaxone, urgent EGD; not "wait for stability"

— Trauma patient initial fluid response then BP drops again → answer: ongoing hemorrhage, OR or IR, not more crystalloid

— Hemorrhagic shock, refuses blood, competent adult → answer: honor refusal, offer alternatives, document, ethics consult

— Boggy uterus, vaginal bleeding after delivery → answer: bimanual massage + oxytocin first, then methylergonovine (not in HTN), carboprost (not in asthma)

— 10th unit PRBC, perioral numbness, QT prolonged → answer: calcium gluconate IV

— PPH 6 months ago, fatigue, amenorrhea, failure to lactate → answer: anterior pituitary hormone panel, replace cortisol before thyroid hormone

— Prior AAA repair + GI bleed → answer: CT angiography urgently

— Hypotensive after head injury → answer: target MAP ≥80, not permissive hypotension

Pattern 1 — Young trauma with "normal" vitals:
Pattern 2 — Beta-blocked elderly with subtle shock:
Pattern 3 — Unstable trauma with positive FAST:
Pattern 4 — Variceal bleed:
Pattern 5 — Transient responder:
Pattern 6 — Jehovah's Witness:
Pattern 7 — Postpartum hemorrhage ladder:
Pattern 8 — Hypocalcemia after massive transfusion:
Pattern 9 — Sheehan syndrome:
Pattern 10 — Aortoenteric fistula:
Pattern 11 — TBI + shock:
Step 3 management: In CCS, when given an unstable bleeding patient, the highest-yield orders are: two large-bore IVs, type and crossmatch, activate MTP, TXA if trauma <3 hr, source-specific consult, blood products before crystalloid bolus #2.
Board pearl: When stems describe a "stable" patient with concerning lactate or base deficit, trust the labs over the vitals—occult shock is the answer.
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One-Line Recap

Hemorrhagic shock requires simultaneous resuscitation and rapid hemorrhage source control, using balanced 1:1:1 blood product ratios, permissive hypotension (except in TBI), and TXA within 3 hours—because tachycardia and narrow pulse pressure precede hypotension, and waiting for a low blood pressure or low hemoglobin to act is the most common tested error.

Recognize early: Shock index >1.0, narrow pulse pressure, mottling, and rising lactate identify shock before SBP falls; beta-blocked and elderly patients hide their tachycardia—trust the labs and the exam.
Resuscitate smart: Brief crystalloid bridge → blood products in 1:1:1 ratio, TXA within 3 hours for trauma/PPH, permissive hypotension SBP 80–90 in penetrating trauma without TBI, and calcium gluconate every 4 units PRBC to prevent citrate-induced hypocalcemia. Avoid crystalloid overload to prevent dilutional coagulopathy and ARDS.
Source control wins: No volume of blood replaces stopping the bleeding—unstable + positive FAST → OR; stable + contrast blush → IR embolization; variceal bleed → EGD with banding plus octreotide and ceftriaxone; PPH → uterotonics ladder; AAA rupture → EVAR.
Avoid the killers: Prevent the lethal triad (hypothermia, acidosis, coagulopathy) with warming, balanced resuscitation, and definitive source control. Reverse anticoagulants promptly (4-factor PCC, idarucizumab, andexanet alfa). Don't push unstable patients to CT, don't over-transfuse variceal bleeders (target Hgb >7), and don't withhold blood awaiting consent in an unconscious patient.
CCS pearl: Memorize the order set—2 large-bore IVs, type and cross, activate MTP, TXA, source consult (surgery/IR/GI/OB), Foley, warming, ICU—and reassess vitals, lactate, and Hgb after every intervention. The exam rewards continuous reassessment over reflexive bolusing.
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