How to Give Inotropes in the ICU
Indications for Inotropic Therapy
Inotropes should be initiated when a patient demonstrates clinical hypoperfusion with elevated cardiac filling pressures despite adequate fluid resuscitation, specifically when systolic blood pressure is <90–100 mmHg or cardiac index <2.2 L/min/m² accompanied by end-organ dysfunction. 1
Clinical Signs Requiring Inotropic Support
Before starting inotropes, confirm the presence of:
- Cold, clammy skin with peripheral vasoconstriction 2
- Oliguria (urine output declining) 2
- Rising serum lactate or metabolic acidosis 1, 3
- Altered mental status or confusion 1
- Renal impairment (rising creatinine) 2, 1
- Hepatic dysfunction (increasing liver enzymes) 2, 1
- Elevated jugular venous pressure or pulmonary artery wedge pressure >18 mmHg 2, 1
Critical Pre-Inotrope Requirements
- Complete volume optimization FIRST – patients must receive adequate fluid resuscitation before any inotrope is considered 1, 4
- Administer intravenous loop diuretics if fluid overload is present 2
- Verify elevated cardiac filling pressures clinically or via invasive monitoring 2, 1
Selection of First-Line Inotrope Based on Hemodynamic Profile
Profile 1: Low Cardiac Output with Preserved Blood Pressure (SBP >100 mmHg)
Start dobutamine at 2–3 µg/kg/min 2, 1, 5
- This profile indicates dilated, hypokinetic ventricles with adequate systemic pressure but insufficient cardiac output 2
- Dobutamine is the first-choice inotrope when mean arterial pressure is adequate and left ventricular filling pressure is elevated 4, 6
Profile 2: Low Cardiac Output with Hypotension (SBP <90–100 mmHg)
Begin norepinephrine to restore mean arterial pressure ≥65 mmHg, then add dobutamine once pressure stabilizes 1, 3, 6
- Norepinephrine is the first-line vasopressor for hypotension in shock states 3, 6, 7
- Once blood pressure is adequate, add dobutamine (2–3 µg/kg/min) to increase cardiac output 4, 3
- The combination of norepinephrine and dobutamine is recommended as first-line treatment for septic shock with low cardiac output 4
Dobutamine Dosing and Titration
Initial Dosing
- Start at 0.5–1.0 µg/kg/min or 2–3 µg/kg/min without a loading dose 2, 1, 5
- Titrate every 3–5 minutes based on clinical response 5
Target Dosing Range
- Usual effective range: 2–20 µg/kg/min 2, 5
- Maximum dose: up to 40 µg/kg/min in rare cases 5
- In patients on beta-blockers, doses up to 20 µg/kg/min may be required to overcome receptor blockade 2
Preparation
- Dilute to at least 50 mL using 5% Dextrose, 0.9% Sodium Chloride, or Lactated Ringer's 5
- Standard concentrations: 500 µg/mL, 1,000 µg/mL, or 2,000 µg/mL 5
- Use within 24 hours of preparation 5
- Do NOT mix with sodium bicarbonate or strongly alkaline solutions 5
Timing of Initiation
Administer inotropes as early as possible when hypoperfusion is identified – delay in initiation is associated with increased mortality risk 2, 1
- Begin in the emergency department without delay if criteria are met, as early intervention improves outcomes 2, 1
- Rapid intervention is critical for patients with decompensation and shock 2
Monitoring During Inotrope Therapy
Continuous Monitoring Requirements
- Continuous ECG telemetry to detect arrhythmias (atrial and ventricular) 2, 1
- Blood pressure monitoring – invasive arterial line preferred for precise titration 2, 1
- Hourly urine output with target >100 mL/h 1
- Oxygen saturation maintained >94% 3
Daily Laboratory Monitoring
- Serum electrolytes, BUN, and creatinine daily during active titration 2, 1
- Arterial blood gases and serum lactate as markers of tissue perfusion 3
- Central venous oxygen saturation (ScvO₂) target ≥70% if available 4
Clinical Perfusion Assessment
- Skin temperature and capillary refill 1
- Mental status 1
- Fluid intake and output 2
- Body weight measured at the same time daily 2
Invasive Hemodynamic Monitoring
Consider pulmonary artery catheter placement when filling pressures and perfusion adequacy cannot be reliably determined by clinical assessment alone 2, 1
Special Considerations and Pitfalls
Beta-Blocker Interaction
- Continue beta-blockers in most patients unless hemodynamic instability is severe 1
- Higher dobutamine doses (up to 20 µg/kg/min) may be needed to overcome beta-blockade 2, 1
- Alternative agents (milrinone, levosimendan) work independently of β-receptors and may be preferred 2, 3
Arrhythmia Risk
- Dobutamine and dopamine facilitate AV nodal conduction and can cause tachycardia in atrial fibrillation 2
- All inotropes increase risk of atrial and ventricular arrhythmias 2
Hypotension Risk
- Avoid inotropes in patients with systolic blood pressure <90 mmHg until vasopressor support establishes adequate perfusion pressure 2
- Dobutamine can worsen hypotension in patients with low systemic vascular resistance 6
Extravasation
- Norepinephrine causes tissue necrosis if extravasated – central line administration is strongly preferred 3
Withdrawal Strategy
Withdraw inotropes as soon as adequate organ perfusion is restored and congestion is reduced 2, 1
- Gradual tapering is essential – decrease dobutamine by 2 µg/kg/min increments 2
- Simultaneously optimize oral heart failure therapy during weaning 2
Limitations and Mortality Considerations
Inotropes do NOT improve mortality and are associated with increased adverse events including arrhythmias and myocardial injury 2, 1, 8, 9
- Use as bridge therapy only – to mechanical circulatory support, transplantation, or recovery 2, 1, 10
- Patients requiring frequent inotrope infusions represent advanced heart failure and should be evaluated promptly for mechanical circulatory support or cardiac transplantation 1
Alternative Inotropic Agents
Milrinone (Phosphodiesterase III Inhibitor)
- Causes less tachycardia than dobutamine and works independently of β-receptors 2, 3
- Useful in patients on beta-blockers or with low cardiac output and elevated systemic vascular resistance 2
Levosimendan (Calcium Sensitizer)
- Overcomes receptor desensitization and provides inotropic support without increasing myocardial oxygen demand 2, 8
- May be useful in post-myocardial infarction cardiac dysfunction and septic shock 8