Vasopressor Selection in Hypotensive Patients
Norepinephrine is the mandatory first-line vasopressor for hypotension in patients with septic shock, regardless of cardiac history, and should be initiated early to achieve a mean arterial pressure (MAP) ≥65 mmHg. 1, 2
Initial Vasopressor Strategy
Start norepinephrine at 0.02 mcg/kg/min and titrate upward to maintain MAP ≥65 mmHg after administering a minimum of 30 mL/kg crystalloid fluid bolus, though in life-threatening hypotension, vasopressors may be started simultaneously with fluid resuscitation rather than waiting for complete volume repletion. 2, 3
Norepinephrine should be used as monotherapy initially and titrated up alone before adding any second agent—there is no evidence supporting simultaneous initiation of multiple vasopressors. 2
Early administration of norepinephrine is particularly critical when diastolic blood pressure is ≤40 mmHg or when the diastolic shock index (heart rate/diastolic blood pressure) is ≥3, as profound and prolonged hypotension independently increases mortality. 4, 3
Sequential Escalation Protocol
When norepinephrine alone fails to achieve target MAP despite adequate fluid resuscitation:
Add vasopressin at 0.03 units/min as the second vasopressor when norepinephrine reaches 0.1-0.2 mcg/kg/min without achieving target MAP—vasopressin should never be used as initial monotherapy. 1, 2
Add epinephrine (0.05-2 mcg/kg/min) as the third vasopressor if hypotension persists despite norepinephrine plus vasopressin, particularly when myocardial dysfunction is present due to its inotropic effects. 2, 5
Special Considerations for Cardiac History
In cardiogenic shock with tachycardia, norepinephrine remains the recommended vasopressor, but individualized MAP goals are required as hypoperfusion risk must be balanced against potential negative impacts on cardiac output, myocardial oxygen consumption, and dysrhythmias. 1
In cardiogenic shock with bradycardia, dopamine may be considered, though it carries higher arrhythmia risk compared to norepinephrine. 1
If myocardial dysfunction is evident with low cardiac output despite adequate MAP and filling pressures, add dobutamine (2.5-10 mcg/kg/min) rather than escalating vasopressors further. 1, 2
Critical Pitfalls to Avoid
Never use dopamine as first-line therapy—it is associated with higher mortality and more arrhythmias compared to norepinephrine and should only be considered in highly selected patients with absolute or relative bradycardia and low risk of tachyarrhythmias. 1, 2
Do not use dopamine for "renal protection"—this provides no benefit and is strongly discouraged. 1, 2
Do not delay norepinephrine initiation while attempting to achieve complete fluid resuscitation in profoundly hypotensive patients, as duration and depth of hypotension strongly worsen outcomes. 4, 3
Phenylephrine should be reserved for salvage therapy only, such as when norepinephrine causes severe arrhythmias or when cardiac output is high but blood pressure remains low. 1, 2
Monitoring Requirements
Place an arterial catheter as soon as practical for continuous blood pressure monitoring in all patients requiring vasopressors. 2
Monitor beyond MAP targets alone—assess tissue perfusion using lactate clearance, urine output, mental status, skin perfusion, and capillary refill to ensure adequate end-organ perfusion. 1, 2
Target MAP ≥65 mmHg for most patients, but consider higher targets (70-75 mmHg) in patients with chronic hypertension due to impaired autoregulation from atherosclerosis. 1, 2
Hemodynamic Benefits of Early Norepinephrine
Early norepinephrine administration increases cardiac output through increased cardiac preload and contractility, even in patients with poor baseline left ventricular ejection fraction (≤45%), by transforming unstressed blood volume into stressed blood volume and increasing mean systemic filling pressure. 6
This beneficial effect occurs in patients with preserved and reduced ejection fraction, except when MAP values ≥75 mmHg are achieved in patients with baseline LVEF ≤45%. 6