What is the recommended pharmacologic and fluid management for the different types of circulatory shock (hypovolemic, septic, cardiogenic, obstructive, and anaphylactic)?

Pharmacotherapy of Circulatory Shock

Crystalloids are the first-line fluid for all shock types, with norepinephrine as the first-choice vasopressor when hypotension persists despite adequate volume resuscitation, targeting a mean arterial pressure of at least 65 mmHg. 1

Initial Fluid Resuscitation Strategy

Crystalloid Administration

• Administer at least 30 mL/kg of crystalloid within the first 3 hours for hypovolemic, septic, and distributive shock; this is a minimum target, not a ceiling—most patients require substantially more. 1, 2
• Use balanced crystalloids (lactated Ringer's or Plasma-Lyte) over normal saline when available to reduce the risk of hyperchloremic metabolic acidosis and acute kidney injury progression. 2
• Continue fluid challenges as long as hemodynamic parameters improve, guided by dynamic measures (pulse-pressure variation, stroke-volume variation, passive leg raise) or static variables (arterial pressure, heart rate, mental status, urine output, peripheral perfusion). 1, 2

When to Add Albumin

• Add albumin when several liters of crystalloids have been administered and the patient still requires volume support, particularly in states of oncotic deficit or prolonged shock. 1, 2

Fluids to Avoid

• Never use hydroxyethyl starch solutions—they increase mortality and acute kidney injury risk in septic and critically ill patients. 1
• Avoid gelatin solutions when crystalloids are available. 1

Vasopressor and Inotropic Therapy

First-Line Vasopressor

• Start norepinephrine immediately when mean arterial pressure remains below 65 mmHg despite adequate fluid resuscitation. 1, 2
• Place an arterial catheter as soon as practical in any patient requiring vasopressors to allow accurate blood pressure monitoring. 1, 2

Escalation Algorithm

1. Norepinephrine alone targeting MAP ≥ 65 mmHg. 1
2. Add vasopressin (0.03 U/min) if additional MAP support is needed or to reduce norepinephrine dose. 1, 2
3. Add epinephrine if MAP remains inadequate despite norepinephrine plus vasopressin. 1, 2
4. Avoid dopamine except in highly selected patients with bradycardia and low risk of tachyarrhythmias—it increases cardiac adverse events. 1, 2
5. Never use phenylephrine except in rare circumstances: norepinephrine-associated serious arrhythmias, high cardiac output with persistently low blood pressure, or as salvage therapy. 1

Inotropic Support

• Administer dobutamine (up to 20 µg/kg/min) when myocardial dysfunction with low cardiac output persists despite adequate volume status and MAP, particularly in patients with reduced ejection-fraction heart failure. 1, 3
• Titrate dobutamine to end points reflecting tissue perfusion and reduce or discontinue if worsening hypotension or arrhythmias develop. 1

Shock Type-Specific Considerations

Hypovolemic Shock

• Restore intravascular volume with rapid crystalloid boluses (20 mL/kg over 5–10 minutes), titrated to reverse hypotension, increase urine output, and normalize capillary refill and mental status. 1, 4
• Vasopressors may be transiently required to sustain life during ongoing resuscitation if life-threatening hypotension persists, but fluid replacement remains the definitive treatment. 1

Septic Shock

• Administer broad-spectrum antibiotics within the first hour of septic shock recognition. 2, 5
• Identify and control the infection source within 12 hours when feasible, using the least invasive effective intervention (e.g., percutaneous drainage over open surgery). 1, 2
• Remove intravascular access devices promptly if they are a possible infection source, after establishing alternative vascular access. 1, 2, 5

Cardiogenic Shock

• Avoid aggressive fluid boluses if hepatomegaly or pulmonary rales are present—these indicate volume overload rather than hypovolemia. 1
• Initiate inotropic support (dobutamine) early when cardiac output is low despite adequate preload. 1, 3
• Use vasopressors cautiously to maintain MAP without excessively increasing cardiac afterload. 1

Obstructive Shock

• Perform immediate life-saving intervention to relieve the obstruction (e.g., pericardiocentesis for tamponade, thrombolysis or embolectomy for massive pulmonary embolism). 4
• Fluid resuscitation and vasopressors are temporizing measures only—definitive treatment requires removing the mechanical obstruction. 4

Anaphylactic Shock (Distributive)

• Administer intramuscular epinephrine immediately as the primary treatment. 4
• Follow with aggressive crystalloid resuscitation to address the relative hypovolemia from pathological vasodilation. 4
• Use norepinephrine infusion if hypotension persists despite epinephrine and fluids. 1, 4

Hemodynamic Monitoring Principles

Dynamic Assessment Preferred

• Use dynamic variables (pulse-pressure variation, stroke-volume variation, passive leg raise-induced stroke-volume change) to predict fluid responsiveness whenever available. 1, 2
• Central venous pressure (CVP) alone is unreliable for predicting fluid responsiveness, particularly in the 8–12 mmHg range. 2
• Static pressure measurements (CVP, pulmonary-artery occlusion pressure) lack predictive value for fluid responsiveness and should not guide fluid therapy in isolation. 2

When Dynamic Tools Are Unavailable

• Rely on static clinical signs: mean arterial pressure, heart rate, mental status, urine output, skin perfusion, and lactate clearance. 1, 2

Critical Pitfalls to Avoid

• Do not adopt a "maintenance-fluid" mindset—shock management requires active, repeated resuscitation guided by hemodynamic response, not fixed infusion rates. 2
• Do not delay resuscitation due to concerns about fluid overload—delayed resuscitation increases mortality more than judicious fluid administration. 2
• Do not use low-dose dopamine for renal protection—it is ineffective and contraindicated. 1, 2, 3
• Do not withhold the initial 30 mL/kg crystalloid bolus in patients with chronic systolic heart failure—evidence does not support this practice. 3
• Do not use vasopressors as a substitute for adequate volume resuscitation—restore intravascular volume first, then add vasopressors if hypotension persists. 1, 2