How is systemic vascular resistance managed in sepsis?

Management of Systemic Vascular Resistance in Sepsis

Norepinephrine should be used as the first-line vasopressor for managing systemic vascular resistance in septic shock, targeting a mean arterial pressure (MAP) of 65 mmHg. 1

Understanding Vascular Resistance in Sepsis

Sepsis causes profound alterations in systemic vascular resistance (SVR) that require targeted management:

• Pathophysiology: Sepsis typically causes vasodilation and decreased SVR due to inflammatory mediators, leading to hypotension despite adequate cardiac output
• Hemodynamic patterns: Patients may present with:
  • Low SVR with normal/high cardiac output (most common)
  • Low SVR with low cardiac output
  • High SVR with low cardiac output (less common)

Initial Fluid Resuscitation

Before initiating vasopressors to manage SVR:

• Administer crystalloids as first-line fluid therapy (30 mL/kg initially) 1
• Use balanced/buffered crystalloids rather than 0.9% saline 1, 2
• Avoid hydroxyethyl starches (strong recommendation) 1
• Avoid gelatins (weak recommendation) 1
• Consider albumin when patients require substantial amounts of crystalloids 1
• Continue fluid administration as long as hemodynamic parameters improve 1
• Monitor for signs of fluid overload (pulmonary edema, hepatomegaly) 1, 2

Vasopressor Therapy for Low SVR

First-line agents:

• Norepinephrine is the first-choice vasopressor 1
  • Increases SVR through α-adrenergic effects
  • Preserves cardiac output better than pure vasoconstrictors
  • Target MAP of 65 mmHg 1

Second-line options:

• Vasopressin (0.03 units/minute) can be added to:

  • Raise MAP to target
  • Decrease norepinephrine dosage
  • Should not be used as the initial vasopressor 1, 3

• Epinephrine can be added or substituted for norepinephrine when an additional agent is needed 1

• Dopamine should be limited to highly selected patients with:

  • Low risk of tachyarrhythmias
  • Absolute or relative bradycardia 1

Managing Different Hemodynamic Patterns

Low SVR with normal/high cardiac output:

• Norepinephrine as first-line therapy 1
• Add vasopressin if high-dose norepinephrine is required 1

Low SVR with low cardiac output:

• Norepinephrine as first-line therapy 1
• Consider adding dobutamine for myocardial dysfunction 1
  • Indicated when cardiac filling pressures are elevated with low cardiac output
  • Or when signs of hypoperfusion persist despite adequate MAP and volume

High SVR with low cardiac output (less common in sepsis):

• Vasodilator therapy in addition to inotropes 1
• Options include:
  • Type III phosphodiesterase inhibitors (milrinone)
  • Nitrosovasodilators
  • Calcium sensitizers (levosimendan)

Monitoring Response to Therapy

• Use advanced hemodynamic monitoring when available 1

  • Cardiac output/cardiac index
  • SVR measurements
  • Central venous oxygen saturation (ScvO2)

• Track trends in blood lactate levels 1

  • Persistent elevation indicates incomplete resuscitation

• Do not rely solely on bedside clinical signs to categorize shock as "warm" or "cold" 1

Pitfalls and Caveats

• Avoid excessive fluid administration which can worsen outcomes 4, 5

  • Fluid overload increases mortality
  • Consider early vasopressors rather than excessive fluid loading

• Do not delay vasopressor initiation when hypotension persists despite initial fluid resuscitation 5

  • Can be started peripherally if central access is delayed

• Beware of vasopressor extravasation when administered peripherally

  • Monitor IV site frequently
  • Obtain central access as soon as feasible

• Recognize adrenal insufficiency in refractory shock

  • Consider hydrocortisone therapy in patients with fluid-refractory, catecholamine-resistant shock 1

• Avoid targeting higher MAP (>65 mmHg) unless specific indications exist

  • Higher targets increase vasopressor exposure without improving outcomes