What is the initial management of a patient presenting with shock?

Initial Management of Shock

Begin immediate fluid resuscitation with at least 30 mL/kg of intravenous crystalloid within the first 3 hours while simultaneously identifying the shock type and initiating type-specific interventions. 1

Immediate Assessment and Stabilization (First 5–10 Minutes)

• Rapidly assess vital signs including heart rate, blood pressure, respiratory rate, temperature, oxygen saturation, and mental status to confirm shock and gauge severity. 1, 2

• Establish vascular access immediately (large-bore peripheral IV or intraosseous if IV access fails) to enable rapid fluid administration. 1

• Begin high-flow oxygen therapy via face mask or high-flow nasal cannula to achieve SpO₂ > 90–95%, improving tissue oxygenation while the underlying cause is addressed. 1, 3

• Measure serum lactate immediately at presentation; lactate ≥ 4 mmol/L or ≥ 2 mmol/L with hypotension indicates severe tissue hypoperfusion requiring aggressive resuscitation. 1, 2

• Assess clinical perfusion markers including mental status (confusion or lethargy), capillary refill time (target ≤ 2 seconds), skin temperature and mottling, peripheral pulse quality, and urine output. 1, 3, 2

Fluid Resuscitation (First 3 Hours)

• Administer 30 mL/kg of isotonic crystalloid (approximately 2 liters for a 70-kg adult) within the first 3 hours as rapid boluses of 500–1000 mL over 15–30 minutes. 4, 1, 3, 2

• Use balanced crystalloids (lactated Ringer's or Plasmalyte) or normal saline as first-line fluids; balanced solutions may reduce hyperchloremic acidosis but either is acceptable. 4, 2

• Reassess hemodynamic response after each bolus by checking blood pressure, heart rate, capillary refill, mental status, and urine output to guide further fluid administration. 1, 2

• Continue fluid boluses as long as hemodynamic improvement is observed, using dynamic indices (pulse-pressure variation, stroke-volume variation) or static variables (arterial pressure, heart rate, urine output) to guide therapy. 4

• Monitor vigilantly for fluid overload by assessing jugular venous pressure, respiratory rate, oxygen saturation, and lung auscultation; stop or reduce fluids if signs of pulmonary edema develop. 3

• Avoid hydroxyethyl starches under all circumstances as they increase mortality and acute kidney injury risk. 4, 2

Hemodynamic Targets (First 6 Hours)

• Target mean arterial pressure (MAP) ≥ 65 mmHg in most adults; for patients with chronic hypertension, aim for MAP 70–85 mmHg because their autoregulatory curve is shifted rightward. 4, 1, 3, 2

• Maintain urine output ≥ 0.5 mL/kg/hour (approximately 35 mL/hour for a 70-kg adult) as a bedside marker of adequate renal perfusion. 1, 3, 2

• Achieve capillary refill ≤ 2 seconds, warm extremities, normal pulses, and normal mental status as clinical endpoints of adequate tissue perfusion. 1, 3

• Repeat lactate measurement within 6 hours if initially elevated; guide resuscitation toward lactate normalization as a marker of resolving tissue hypoperfusion. 1, 3, 2

Vasopressor Therapy (When Fluids Insufficient)

• Initiate norepinephrine as the first-choice vasopressor when MAP remains < 65 mmHg after the initial 30 mL/kg fluid bolus, starting at 0.05–0.1 µg/kg/min (approximately 5–10 µg/min for a 70-kg adult) and titrating upward. 4, 1, 3, 2

• Norepinephrine can be started via peripheral IV to avoid delays while central venous access is obtained, but transition to central access as soon as feasible. 3

• Add vasopressin 0.03 U/min to norepinephrine when additional MAP support is needed or to reduce norepinephrine dose; vasopressin should never be used as the sole initial vasopressor. 4, 3

• Introduce epinephrine as a third-line agent if MAP targets remain unmet despite norepinephrine plus vasopressin. 4, 3

• Avoid dopamine except in highly selected patients with low risk of tachyarrhythmias and absolute or relative bradycardia, as it causes more arrhythmias than norepinephrine. 4

• Consider dobutamine 2.5–5 µg/kg/min when myocardial dysfunction or persistent tissue hypoperfusion ("cold shock" with cold extremities, confusion) is evident despite adequate MAP and volume status. 3, 2

Type-Specific Interventions

Distributive Shock (Septic Shock)

• Administer IV broad-spectrum antimicrobials within 1 hour of recognizing sepsis or septic shock; each hour of delay increases mortality by approximately 7.6%. 3, 2

• Obtain at least two sets of blood cultures (aerobic and anaerobic) before starting antibiotics, but never delay antimicrobials beyond 45 minutes to obtain cultures. 3, 2

• Identify or exclude a specific anatomic infection source requiring emergent control (abscess, infected device, bowel perforation) within 12 hours of shock onset. 3, 2

• Perform definitive source-control procedures (drainage, debridement, removal of infected devices) as soon as medically and logistically feasible. 3, 2

Hemorrhagic Shock

• Control the source of bleeding as the highest priority through direct pressure, tourniquet application, or emergent surgical/interventional control. 4, 5

• Initiate crystalloid resuscitation while arranging for blood product transfusion and definitive hemorrhage control. 4

• For patients with pelvic ring disruption in hemorrhagic shock, perform immediate pelvic ring closure and stabilization (pelvic binder or external fixation). 4

• Employ damage control surgery in severely injured patients presenting with deep hemorrhagic shock, ongoing bleeding, coagulopathy, hypothermia, or acidosis. 4

• Maintain hemoglobin at a minimum of 10 g/dL during active hemorrhagic shock resuscitation to ensure adequate oxygen-carrying capacity. 4

Cardiogenic Shock

• Perform urgent echocardiography to identify the cause (myocardial infarction, valvular dysfunction, tamponade) and characterize the shock phenotype. 6

• Arrange emergent coronary angiography when acute myocardial ischemia is suspected, followed by culprit-vessel revascularization if indicated. 6

• Titrate norepinephrine to restore MAP and dobutamine to restore cardiac output and organ perfusion in cardiogenic shock. 6

Obstructive Shock

• Perform immediate life-saving intervention to relieve the obstruction (needle decompression for tension pneumothorax, pericardiocentesis for tamponade, thrombolysis or embolectomy for massive pulmonary embolism). 7

Respiratory Support

• Prepare for endotracheal intubation when mental status deteriorates, airway protection is compromised, or hypoxemia is refractory to oxygen therapy. 3

• Administer fluid boluses and initiate vasopressors before intubation to reduce the risk of hemodynamic collapse during the procedure. 3

• Use ketamine with atropine premedication for sedation and intubation in shock, as it maintains cardiovascular stability through intact adrenal axis function. 4

• Avoid etomidate for intubation in septic shock, as even a single dose is independently associated with increased mortality, possibly due to adrenal suppression. 4

• If mechanical ventilation is required, employ lung-protective strategies: tidal volume 6 mL/kg predicted body weight, plateau pressure ≤ 30 cm H₂O, and head-of-bed elevation 30–45°. 3

Ongoing Monitoring

• Continuously monitor vital signs including temperature, pulse oximetry, blood pressure, ECG, and urine output. 1

• Reassess frequently (every 15–30 minutes initially) to evaluate response to treatment and need for escalation of care. 3, 2

• Establish central venous access and arterial pressure monitoring in patients with fluid-refractory shock to guide advanced hemodynamic management. 4

• Use dynamic measures of fluid responsiveness (passive leg raise, pulse-pressure variation) rather than static measures like CVP alone, as CVP poorly predicts fluid responsiveness. 2

Critical Pitfalls to Avoid

• Do not delay fluid resuscitation while waiting for laboratory results or imaging studies; begin the 30 mL/kg crystalloid bolus immediately upon recognizing shock. 1, 2

• Do not delay antimicrobials in suspected septic shock while waiting for cultures or imaging; administer broad-spectrum antibiotics within 1 hour. 3, 2

• Do not rely solely on MAP to assess adequacy of resuscitation; normal MAP can coexist with severe tissue hypoperfusion ("cold shock"). 3

• Do not overlook the need for source control in infectious causes of shock; inadequate source control is independently associated with increased mortality. 3, 2

• Do not continue aggressive fluid administration when vasopressor support is clearly required; excessive fluid delays definitive therapy and risks fluid overload. 3