Shock — Hypovolemic and Hemorrhagic

Compensatory Mechanisms (Early Stage)

• Baroreceptor reflex activation → sympathetic nervous system stimulation produces tachycardia, increased contractility, and vasoconstriction to maintain blood pressure and redistribute blood to vital organs (CNS, heart)
• Renin-angiotensin-aldosterone system (RAAS) activation → angiotensin II causes systemic and renal vasoconstriction while aldosterone promotes sodium and water retention to expand intravascular volume
• Catecholamine release → epinephrine and norepinephrine increase heart rate, contractility, and peripheral vascular resistance through α₁ and β₁ adrenergic effects
• Fluid shifts → decreased capillary hydrostatic pressure allows fluid reabsorption from interstitial space into intravascular compartment via Starling forces

Tissue-Level Hypoperfusion Mechanism

• Reduced cardiac output (CO = HR × SV) results from decreased preload; venous return is insufficient to maintain stroke volume despite compensatory tachycardia
• Microvascular dysfunction → tissue hypoxia activates anaerobic metabolism, producing lactate and hydrogen ions; cellular acidosis impairs mitochondrial function and ATP production
• Endothelial dysfunction → hypoxia induces inflammatory mediators (TNF-α, IL-1, IL-6) and reactive oxygen species, increasing capillary permeability and promoting third-spacing of fluid
• Cellular injury cascade → Na⁺/K⁺-ATPase pump failure from ATP depletion leads to intracellular sodium accumulation, cellular edema, and loss of membrane integrity

Progressive Decompensation

• Loss of autoregulation → as shock becomes severe, cerebral and coronary autoregulation fails; blood flow becomes dependent on systemic blood pressure
• Ischemic organ injury → prolonged hypoperfusion causes myocardial depression, gut mucosal barrier breakdown (bacterial translocation), renal tubular necrosis, and hepatic dysfunction
• Irreversible shock → once microcirculatory and cellular injury becomes extensive (typically >90 min of untreated severe shock), restoration of perfusion cannot prevent multiorgan failure

Hemorrhagic Causes

• Trauma — blunt abdominal/thoracic injury, pelvic fractures, long bone fractures (femur can sequester 1-2 liters of blood internally)
• Gastrointestinal bleeding — peptic ulcer disease, variceal bleeding, Mallory-Weiss tears, diverticulosis, angiodysplasia
• Vascular rupture — abdominal aortic aneurysm (AAA), thoracic aortic dissection, splenic/hepatic artery rupture
• Obstetric hemorrhage — placental abruption, placenta previa, uterine atony, amniotic fluid embolism
• Surgical hemorrhage — intraoperative bleeding, inadequate hemostasis

Non-Hemorrhagic Hypovolemic Causes

• Plasma loss — severe burns, Stevens-Johnson syndrome, toxic epidermal necrolysis
• Fluid losses (GI) — severe vomiting/diarrhea, small bowel obstruction with third-spacing
• Renal losses — diuretic overuse, osmotic diuresis (DKA, HHS), adrenal insufficiency
• Insensible losses — excessive sweating, fever, heat stroke
• Septic hypovolemia — sepsis-induced capillary leak and vasodilation (though typically categorized separately as distributive shock)

Risk Factors

• Anticoagulation (warfarin, DOACs, heparin) or antiplatelet therapy
• Coagulopathies (hemophilia, DIC, vitamin K deficiency, liver disease)
• Thrombocytopenia
• Extremes of age (elderly: reduced compensatory capacity; pediatric: rapid decompensation)
• Comorbid cardiovascular disease (impaired ability to increase HR/contractility)

Cardiovascular Manifestations

• Tachycardia — often the earliest sign; sympathetic compensation to maintain cardiac output with reduced stroke volume
• Hypotension — systolic BP <90 mmHg or MAP <65 mmHg; may be relatively normal early due to compensation ("compensated shock")
• Weak, thready pulse — reduced stroke volume and peripheral vasoconstriction produce diminished pulse amplitude
• Prolonged capillary refill (>2 seconds) — peripheral vasoconstriction delays return of color after blanching

Neurologic Manifestations

• Altered mental status — agitation, confusion, or lethargy from cerebral hypoperfusion; may progress to loss of consciousness in severe shock
• Restlessness and anxiety — catecholamine surge and tissue hypoxia stimulate CNS

Renal Manifestations

• Oliguria/anuria — urine output <0.5 mL/kg/hr indicates inadequate renal perfusion
• Dark, concentrated urine — dehydration from volume depletion

Integumentary Manifestations

• Cool, clammy, mottled skin — intense peripheral vasoconstriction shunts blood centrally; sweating from sympathetic activation
• Pallor — reduced skin blood flow and decreased hemoglobin from blood loss
• Cyanosis — may develop if shock is severe and prolonged

Metabolic Manifestations

• Rapid, shallow breathing — compensatory hyperventilation to address metabolic acidosis
• Nausea and vomiting — gut ischemia and sympathetic stimulation

Source-Specific Signs

• Abdominal trauma: abdominal distension, rigidity, bruising, diminished bowel sounds
• GI bleeding: hematemesis, melena, hematochezia
• AAA: pulsatile abdominal mass, flank pain, hip ecchymosis (Grey Turner's sign)

Clinical Classification of Hemorrhagic Shock (ATLS)

Laboratory Investigations

Complete Blood Count

• Hemoglobin/hematocrit — baseline value; note that Hb may be falsely normal immediately after acute hemorrhage due to hemoconcentration; serial measurements every 2-4 hours better reflect ongoing bleeding
• Platelet count — early indicator of dilutional coagulopathy during massive transfusion

Coagulation and Fibrinolysis

• Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen — assess intrinsic/extrinsic coagulation defects
• D-dimer — elevated in DIC and ongoing fibrinolysis; useful for detecting acute coagulopathy of trauma shock (ACOTS)
• Fibrin degradation products (FDP) — elevated in DIC

Metabolic Assessment

• Serum lactate — most sensitive marker of tissue hypoperfusion and anaerobic metabolism; lactate >4 mmol/L indicates shock; trending lactate (serial measurements) predicts outcomes better than single value
• Base deficit — reflects severity of metabolic acidosis; base deficit >6 correlates with shock severity and transfusion requirements
• Arterial pH — metabolic acidosis (pH <7.35) from lactate and ketone accumulation
• Serum bicarbonate — typically <24 mEq/L in shock

Renal Function

• Creatinine, BUN — elevated creatinine and elevated BUN:creatinine ratio (>20:1) indicate prerenal azotemia from hypoperfusion
• Urine osmolality — typically >500 mOsm/kg in prerenal state (hyperconcentrated urine)

Organ Perfusion Markers

• Liver function tests, transaminases — elevated in severe shock from hepatic ischemia
• Troponin, BNP — elevated if myocardial ischemia or demand ischemia occurs

Imaging Studies

Focused Assessment with Sonography for Trauma (FAST)

• Abdominal ultrasound — rapid assessment for free fluid in trauma setting; positive FAST in unstable patient = indication for emergency laparotomy
• Images four views: perihepatic (Morrison's pouch), perisplenic, pelvic, pericardial

Computed Tomography (CT)

• Performed in stable patients to identify specific bleeding sources (splenic, hepatic, renal lacerations)
• CT angiography of chest/abdomen/pelvis if aortic rupture or vascular injury suspected
• NOT performed in unstable patients due to prolonged scanning time

Plain Radiography

• Chest X-ray — assess for hemothorax, tension pneumothorax, mediastinal widening (aortic injury)
• Pelvic X-ray — identify pelvic fractures requiring stabilization/external fixation to tamponade retroperitoneal bleeding

Point-of-Care Ultrasound

• IVC diameter and collapsibility — guides fluid resuscitation; <2 cm with >50% collapsibility suggests hypovolemia; >2 cm with <50% collapsibility suggests adequate preload or right heart failure

Diagnostic Criteria for Hypovolemic Shock

• Systolic BP <90 mmHg or MAP <65 mmHg (or >30% decrease from baseline in chronic hypertension)
• Signs of tissue hypoperfusion: altered mental status, oliguria, cool extremities, tachycardia
• Elevated lactate (>2 mmol/L) or metabolic acidosis
• Elevated SVRI and decreased CI on hemodynamic monitoring (if available)

Immediate Management (First 5-10 Minutes)

Primary Survey (ATLS)

• Airway + Cervical spine control — intubate if GCS ≤8 to protect airway; maintain in-line immobilization if trauma
• Breathing — supplemental O₂ to maintain SpO₂ >94%; positive pressure ventilation if respiratory failure
• Circulation → Hemorrhage control
• Apply direct manual compression to external bleeding sites
• Elevate bleeding limbs above heart
• Apply tourniquet proximal to bleeding extremity wound (if unable to control by direct pressure)
• Avoid excessive movement (may dislodge clots in pelvic/abdominal bleeding)
• Disability — assess GCS, pupils
• Exposure + Environment — log-roll patient, prevent hypothermia (blankets, warm fluids)

Vascular Access and Initial Fluid Resuscitation

Establish Access

• Two large-bore (14-16 gauge) peripheral IV lines preferred; easier, faster, and allows higher flow rates than central lines
• Intraosseous access if unable to establish IV within 3 attempts or 3 minutes (especially in pediatric patients)
• Central venous catheter (internal jugular, subclavian) only if peripheral access impossible; allows CVP monitoring and vasopressor administration

Permissive Hypotension (Damage Control Resuscitation)

• Target systolic BP 80-90 mmHg in hemorrhagic shock from trauma (until hemorrhage controlled)
• Rationale: lower BP reduces ongoing bleeding; excessive fluid resuscitation → dilutional coagulopathy, hypothermia, acidosis, and rebleeding ("fluid creep")
• Exception: patients with traumatic brain injury require MAP ≥65 mmHg to maintain cerebral perfusion pressure

Fluid Resuscitation Strategy

Hemorrhage Control (Definitive)

Surgical/Interventional Intervention

• Emergency surgery — unstable patient with positive FAST or free peritoneal fluid = immediate OR
• Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) — alternative to resuscitative thoracotomy in select trauma centers
• Angiographic embolization — stable patient with arterial bleeding (splenic, hepatic, pelvic fracture bleeding)
• Endoscopy — GI bleeding source (variceal ligation, epinephrine injection, thermal therapy)

Damage Control Transfusion (DCT) Protocol

Massive Transfusion Protocol

• Goal ratio: 1 unit PRBC : 1 unit FFP : 1 unit Platelets
• Rationale: balanced transfusion reduces dilutional coagulopathy compared to crystalloid-heavy resuscitation

Component Therapy

• Packed RBCs (PRBC)
• Indication: Hb <7 g/dL in shock; higher thresholds (Hb <9) if ongoing hemorrhage or cardiac disease
• Crossmatch: type & cross (5-10 min); type & screen (1 min); O-negative universal donor if emergent
• Rapid infuser/rapid transfusion device increases flow rate

• Fresh Frozen Plasma (FFP)
• Indication: coagulopathy (INR >1.5, aPTT >1.5× normal) or massive transfusion (>4 RBC units)
• Mechanism: replaces depleted coagulation factors (II, V, VII, X)
• Dose: 10-15 mL/kg; check INR/aPTT after each dose

• Platelets
• Indication: thrombocytopenia <50,000 (or <100,000 if ongoing hemorrhage) or platelet dysfunction
• Dose: 1 apheresis unit = 5-6 units from whole blood
• Transfuse early in massive hemorrhage to prevent consumptive coagulopathy

• Cryoprecipitate
• Indication: fibrinogen <100 mg/dL
• Mechanism: replaces fibrinogen, factors VIII and XIII; 10 units provides ~2-3 g fibrinogen
• Preferred over FFP for fibrinogen repletion (smaller volume)

Complications of the shock state

• **Lethal triad of trauma (hypothermia, acidosis, coagulopathy): cold and acidemic blood impairs enzymatic clotting factor function and platelet activity, which worsens bleeding, which worsens hypoperfusion — a self-reinforcing spiral. Signaled by diffuse oozing from IV sites and suture lines with a falling core temperature. Emergency** — mandates damage-control surgery and rewarming rather than definitive repair (ACS Committee on Trauma / ATLS).
• Acute tubular necrosis: outer medullary tubules have the highest O₂ extraction and are the first to infarct. Signaled by oliguria that fails to improve after volume repletion, with muddy brown granular casts.
• **Ischemic hepatitis (shock liver)**: centrilobular (zone 3) necrosis from low hepatic arterial flow; transaminases rise into the thousands within 24–48 hours and fall rapidly once perfusion is restored.
• Gut mucosal barrier failure and bacterial translocation: splanchnic vasoconstriction is the earliest and most prolonged; drives later systemic inflammation, ARDS, and multiorgan dysfunction.
• Demand myocardial ischemia: tachycardia plus anemia raises O₂ demand while diastolic filling time and coronary perfusion pressure fall; troponin rises without plaque rupture (type 2 MI).
• Sheehan syndrome: pituitary infarction after obstetric hemorrhage — failure to lactate is the classic first clue.

Complications of resuscitation

• Abdominal compartment syndrome: large-volume crystalloid causes bowel and retroperitoneal edema. Rising peak airway pressures, oliguria, and a tense abdomen; bladder pressure confirms. Emergency — decompressive laparotomy.
• Citrate-induced hypocalcemia: citrate anticoagulant in stored blood chelates ionized calcium during massive transfusion, producing hypotension, prolonged QT, and worsened coagulopathy. Monitor ionized calcium and replace with IV calcium.
• Hyperkalemia and hypothermia from cold, older stored units; use blood warmers.
• Acute hemolytic transfusion reaction (ABO mismatch): fever, flank pain, hemoglobinuria, DIC. Emergency — stop the transfusion immediately.
• TRALI vs TACO: both cause hypoxemia with bilateral infiltrates; TRALI is non-cardiogenic (normal JVP/BNP, plasma-rich products), TACO is volume overload responsive to diuresis.
• Hyperchloremic metabolic acidosis from large-volume normal saline; balanced crystalloid is preferred.

• Hemodynamic triad that defines the shock type: hypovolemic/hemorrhagic shock = ↓cardiac output, ↓preload (low PCWP/CVP), ↑SVR. Contrast with distributive (↑CO, ↓SVR, warm extremities) and cardiogenic (↓CO, ↑PCWP, ↑SVR). The cool, clammy patient with flat neck veins is the classic stem opening.
• Narrow pulse pressure precedes hypotension: rising diastolic pressure from α₁-mediated vasoconstriction narrows the pulse pressure in Class II hemorrhage while systolic pressure is still "normal." Tachycardia plus narrow pulse pressure is the earliest reliable clue; frank hypotension marks Class III (ATLS classification).
• A normal hemoglobin does not exclude acute hemorrhage: whole blood is lost isotonically, so hematocrit falls only after interstitial fluid shifts or crystalloid dilution. Never use an initial Hb to defer transfusion in a bleeding patient.
• Single best next step in the unstable trauma patient with a positive FAST is the operating room — not CT, not more crystalloid. CT is for the stable patient. This is the most commonly tested decision point in ATLS.
• Tranexamic acid works only early: give within 3 hours of injury in trauma with significant hemorrhage (CRASH-2); benefit is lost and harm possible if started later.
• Give blood, not pressors: vasopressors in uncontrolled hemorrhage raise afterload against an empty ventricle, worsen tissue perfusion, and are the classic distractor. Product ratio is 1:1:1 with definitive hemorrhage control.
• Permissive hypotension has one major exception: traumatic brain injury, where hypotension doubles mortality — maintain cerebral perfusion pressure instead.
• Suspect citrate-induced ionized hypocalcemia in any patient who becomes hypotensive with a prolonged QT during massive transfusion; calcium replacement is part of the protocol.
• Beta blockade or a pacemaker blunts the tachycardic response — an elderly patient may present with a "normal" heart rate in Class III shock. Trust lactate and base deficit over vital signs.