Vasopressor Management by Shock Type
Overview of Vasopressor Selection
Vasopressor choice depends critically on the underlying shock mechanism, with norepinephrine serving as first-line for most shock states except hypovolemic shock where volume restoration takes absolute priority. 1
1. Hypovolemic Shock
Vasopressors are NOT the primary treatment for hypovolemic shock—aggressive fluid resuscitation with balanced crystalloids is the definitive therapy. 1
Management Approach:
- Immediate fluid resuscitation with isotonic crystalloids is the cornerstone of treatment 1
- Vasopressors may be used transiently only in life-threatening hypotension while simultaneously achieving hemorrhage control and volume restoration 1
- Vasopressin has been studied in hemorrhagic shock and may improve blood pressure without increasing blood loss when combined with rapid hemorrhage control 1
- Vasopressors should never substitute for adequate volume replacement 2
Key Caveat:
- The primary goal is restoration of intravascular volume and definitive control of bleeding—vasopressors are a temporizing bridge only 1
2. Cardiogenic Shock
Norepinephrine is the vasopressor of choice for most patients with cardiogenic shock, particularly those with tachycardia, as it causes fewer arrhythmias than alternatives. 1
Primary Vasopressor Strategy:
- Norepinephrine is the preferred agent based on randomized trial data showing improved survival and fewer arrhythmias compared to dopamine 1
- Inotropes (dobutamine or milrinone) are first-line when hypotension occurs with low cardiac output in acute heart failure 1
Specific Clinical Scenarios:
- Persistently hypotensive with tachycardia: Use norepinephrine 1
- Bradycardia present: Consider dopamine 1
- Afterload-dependent states (aortic stenosis, mitral stenosis): Use phenylephrine or vasopressin 1
- Low cardiac output with adequate preload: Add dobutamine (up to 20 μg/kg/min) to norepinephrine 1, 2
Important Considerations:
- Both dobutamine and milrinone improve cardiac output but cause arrhythmias and hypotension; milrinone has a longer half-life and causes more profound hypotension 1
- Drugs with positive chronotropic effects show a trend toward increased mortality (OR 1.16) 1
- Individualized MAP goals are essential, balancing hypoperfusion risk against increased myocardial oxygen consumption 1
3. Obstructive Shock
Obstructive shock requires immediate intervention to remove the mechanical obstruction—vasopressors are only temporizing measures while definitive treatment is arranged. 1, 3
Management Principles:
- Definitive treatment addresses the obstruction (e.g., thrombolysis for massive PE, pericardiocentesis for tamponade, needle decompression for tension pneumothorax) 3
- Norepinephrine can be used as a bridge to maintain perfusion pressure during preparation for definitive intervention 1
- Vasopressors alone will not resolve the underlying pathophysiology and may worsen outcomes if they delay definitive treatment 3
Critical Pitfall:
- Do not rely on vasopressors as primary therapy—the obstruction must be relieved emergently 3
4. Distributive Shock
Norepinephrine is the first-line vasopressor for distributive shock after adequate fluid resuscitation, with vasopressin added as a second agent if hypotension persists. 1, 4, 2
First-Line Management:
- Norepinephrine is recommended as the initial vasopressor after appropriate fluid resuscitation with balanced crystalloids 1, 4, 2
- Target MAP ≥65 mmHg as the standard goal, though this should be individualized based on baseline blood pressure and comorbidities 4, 2
Second-Line Agents:
- Vasopressin (up to 0.03 units/min) should be added if hypotension persists despite norepinephrine, which reduces norepinephrine requirements and possibly reduces need for renal replacement therapy 1, 4, 2
- Vasopressin causes vasoconstriction via V1 receptors and reaches peak effect within 15 minutes 5
Managing Myocardial Depression:
- Myocardial depression occurs in up to one-third of septic shock patients 4
- Add dobutamine to norepinephrine when there is evidence of myocardial dysfunction with elevated filling pressures and low cardiac output 1, 4, 2
- Alternatively, epinephrine as a single agent may be used when myocardial depression is present 2
Monitoring and Titration:
- Serial hemodynamic assessments are required as the physiology is dynamic 1
- Titrate to improvements in mixed venous oxygen saturation, myocardial function indices, and lactate reduction 2
Red Flags:
- Failure to improve with appropriate fluid resuscitation and vasopressors should prompt reassessment for alternative or additional shock types 4
- Do not target supranormal cardiac index levels—this may be harmful 2
General Principles Across All Shock Types
Timing and Monitoring:
- Early vasopressor use reduces organ failure incidence 2
- Vasopressors may be initiated during fluid resuscitation and weaned as tolerated 1
- Arterial catheter placement should occur as soon as practical in all patients requiring vasopressors 2