Part 2: Agitation and Sedation Assessment and Management
Comprehensive sedation assessment (RASS, SAS complete scoring tables), light sedation targets, sedative agent pharmacology and dosing (propofol, dexmedetomidine, midazolam, ketamine), propofol infusion syndrome, daily sedation interruption protocols, and nurse-driven sedation algorithms.
Sedation Assessment
Routine, validated sedation assessment is the foundation of optimal sedation management. Sedation depth should be assessed at least every 2–4 hours and more frequently during titration (every 15–30 minutes). The two recommended scales are the Richmond Agitation-Sedation Scale (RASS) and the Sedation-Agitation Scale (SAS).1 2
Richmond Agitation-Sedation Scale (RASS) — Complete Scoring Table
The RASS is a 10-point scale ranging from −5 (unarousable) to +4 (combative). It is the most widely used and validated sedation assessment tool in the ICU, with excellent interrater reliability (weighted kappa 0.91–0.94) across physicians, nurses, and other providers.1 3
| Score | Term | Description | Assessment Method |
|---|---|---|---|
| +4 | Combative | Overtly combative or violent; immediate danger to staff | Observation (no stimulation needed) |
| +3 | Very agitated | Pulls on or removes tube(s) or catheter(s); aggressive toward staff | Observation (no stimulation needed) |
| +2 | Agitated | Frequent non-purposeful movement; fights ventilator | Observation (no stimulation needed) |
| +1 | Restless | Anxious or apprehensive but movements not aggressive or vigorous | Observation (no stimulation needed) |
| 0 | Alert and calm | Spontaneously pays attention to caregiver | Observation (no stimulation needed) |
| −1 | Drowsy | Not fully alert, but has sustained (> 10 seconds) awakening, with eye contact, to voice | Verbal stimulation: call patient’s name, ask to open eyes and look at speaker |
| −2 | Light sedation | Briefly (< 10 seconds) awakens with eye contact to voice | Verbal stimulation |
| −3 | Moderate sedation | Any movement (but no eye contact) to voice | Verbal stimulation |
| −4 | Deep sedation | No response to voice, but any movement to physical stimulation | Physical stimulation: sternal rub or trapezius squeeze |
| −5 | Unarousable | No response to voice or physical stimulation | Physical stimulation |
RASS Assessment Protocol (Step-by-Step):
Observe the patient for 30 seconds without stimulation
- If the patient is alert, restless, agitated, or combative → score +1 to +4
- If the patient is calm and alert → score 0
If not alert, use verbal stimulation — say the patient’s name and ask them to open their eyes and look at you
- Eye contact sustained > 10 seconds → score −1
- Eye contact sustained < 10 seconds → score −2
- Movement but no eye contact → score −3
If no response to verbal stimulation, use physical stimulation — apply sternal rub or trapezius squeeze
- Any movement to physical stimulation → score −4
- No response to physical stimulation → score −5
Sedation-Agitation Scale (SAS) — Complete Scoring Table
The SAS is a 7-point scale ranging from 1 (unarousable) to 7 (dangerous agitation). It has good interrater reliability (weighted kappa 0.92) and correlates well with RASS.1 4
| Score | Term | Description |
|---|---|---|
| 7 | Dangerous agitation | Pulling at endotracheal tube, trying to remove catheters, climbing over bedrail, striking at staff, thrashing side-to-side |
| 6 | Very agitated | Requiring restraint and frequent verbal reminding of limits; biting endotracheal tube |
| 5 | Agitated | Anxious or physically agitated; calms to verbal instructions |
| 4 | Calm and cooperative | Calm; awakens easily; follows commands |
| 3 | Sedated | Difficult to arouse; awakens to verbal stimuli or gentle shaking but drifts off again; follows simple commands |
| 2 | Very sedated | Arouses to physical stimuli but does not communicate or follow commands; may move spontaneously |
| 1 | Unarousable | Minimal or no response to noxious stimuli; does not communicate or follow commands |
RASS-to-SAS Correlation
| RASS | SAS | Clinical State |
|---|---|---|
| +4 | 7 | Dangerous agitation |
| +3 | 6 | Very agitated |
| +2 | 5 | Agitated |
| +1 | 5 | Restless |
| 0 | 4 | Alert and calm / Calm and cooperative |
| −1 | 3 | Drowsy / Sedated |
| −2 | 3 | Light sedation |
| −3 | 2 | Moderate sedation |
| −4 to −5 | 1–2 | Deep sedation to unarousable |
Choosing a Sedation Target
The 2018 guidelines strongly recommend targeting light sedation (RASS 0 to −2, SAS 3–4) for most mechanically ventilated ICU patients, unless there is a specific clinical indication for deeper sedation.1 2
Evidence for Light Sedation
| Outcome | Light vs. Deep Sedation | Reference |
|---|---|---|
| Duration of mechanical ventilation | Reduced by 2.0–3.5 days | Multiple RCTs5 6 |
| ICU length of stay | Reduced by 2.0–4.0 days | Multiple RCTs5 6 |
| Tracheostomy rate | Reduced | Observational data |
| Delirium incidence | Reduced by 30–50% | Meta-analyses |
| Self-extubation rate | No significant increase with protocolized approach | Multiple RCTs |
| 90-day mortality | Reduced (HR 0.60, 95% CI 0.36–0.99 in one landmark trial) | Strøm et al.5 |
| Long-term cognitive function | Improved | Observational data |
| Post-traumatic stress disorder | Mixed evidence; may be increased with recall of frightening experiences | Observational data |
Indications for Deeper Sedation (RASS −3 to −5)
| Clinical Indication | Target RASS | Rationale |
|---|---|---|
| Severe ARDS with prone positioning | −3 to −4 | Prevent self-extubation; reduce oxygen consumption; facilitate prone compliance |
| Therapeutic hypothermia / targeted temperature management | −4 to −5 | Prevent shivering; reduce metabolic demand |
| Refractory intracranial hypertension | −4 to −5 | Reduce cerebral metabolic rate; reduce ICP |
| Status epilepticus (burst suppression) | −5 | Achieve seizure cessation |
| Neuromuscular blockade in use | −4 to −5 | Ensure awareness is prevented during paralysis |
| Open abdomen | −3 to −4 | Prevent increases in intra-abdominal pressure |
| Severe agitation refractory to other measures | −3 | Short-term deeper sedation for safety, with plan for reassessment and lightening |
Recommendation: Reassess the need for deep sedation at least daily and lighten sedation as soon as clinically feasible.1
Sedative and Analgesic Agents for Sedation
Agent Selection Principles
The 2018 guidelines recommend:1 2
- Analgesia-first approach — treat pain before adding sedation
- Prefer non-benzodiazepine agents (propofol or dexmedetomidine) over benzodiazepines for sedation in mechanically ventilated adults (conditional recommendation)
- Avoid benzodiazepines as first-line sedation — associated with increased delirium, prolonged ventilation, and longer ICU stay
- Use the minimum effective dose for the shortest duration
Propofol
| Parameter | Details |
|---|---|
| Mechanism | GABA-A receptor agonist; enhances inhibitory neurotransmission |
| Onset | 1–2 minutes |
| Offset | 5–10 minutes (after short infusions); prolonged offset after prolonged use due to redistribution from fatty tissues |
| Bolus dose | 5–20 mcg/kg/min (0.3–1.2 mg/kg/h) boluses rarely used for sedation in ICU; if needed for emergent control: 0.25–0.5 mg/kg IV push |
| Infusion range | 5–80 mcg/kg/min (0.3–4.8 mg/kg/h); typical starting dose 5–10 mcg/kg/min |
| Target | Titrate to RASS 0 to −2 |
| Maximum recommended dose | 80 mcg/kg/min; doses > 70 mcg/kg/min for > 48 hours increase propofol infusion syndrome (PRIS) risk |
| Advantages | Rapid onset/offset; easily titratable; no active metabolites; reduces ICP; antiemetic properties; anticonvulsant at high doses |
| Disadvantages | Hypotension (dose-dependent vasodilation and myocardial depression); respiratory depression; hypertriglyceridemia (lipid emulsion delivers 1.1 kcal/mL); PRIS risk; no analgesic properties; requires dedicated IV line |
| Monitoring | Triglycerides q 24–48 h (hold if > 400–500 mg/dL); CK, lactate, electrolytes if PRIS suspected; hemodynamics |
| Caloric content | 1.1 kcal/mL from lipid emulsion — must be counted in nutrition calculations |
Propofol Infusion Syndrome (PRIS)
PRIS is a rare but potentially fatal complication of propofol infusion. Incidence is estimated at 1–4% when doses exceed 70 mcg/kg/min for more than 48 hours.7
Risk factors:
- High infusion rates (> 70 mcg/kg/min or > 4.2 mg/kg/h)
- Duration > 48 hours
- Concomitant catecholamine or corticosteroid use
- Critical illness with high catecholamine state
- Traumatic brain injury
- Pediatric patients (higher susceptibility)
- Low carbohydrate intake
Clinical features of PRIS (diagnosis requires ≥ 2 of the following):
| Feature | Details |
|---|---|
| Metabolic acidosis | Unexplained lactic acidosis (base deficit > 10 mEq/L) |
| Rhabdomyolysis | Elevated CK (often > 10,000 U/L); myoglobinuria |
| Hypertriglyceridemia | Lipemic serum; triglycerides > 500 mg/dL |
| Cardiac dysfunction | Brugada-like ECG pattern; bradycardia; conduction abnormalities; cardiac failure; asystole |
| Renal failure | Acute kidney injury secondary to myoglobinuria |
| Hepatomegaly / liver failure | Elevated transaminases; fatty liver |
| Hyperkalemia | From rhabdomyolysis and impaired mitochondrial fatty acid oxidation |
PRIS prevention:
- Limit propofol to ≤ 70 mcg/kg/min (4.2 mg/kg/h)
- Limit duration when possible; consider alternatives for prolonged sedation (> 48–72 h)
- Ensure adequate carbohydrate intake (≥ 6–8 mg/kg/min glucose)
- Monitor triglycerides, CK, and lactate every 24–48 hours
- Monitor for unexplained metabolic acidosis
PRIS management:
- Immediately discontinue propofol
- Aggressive IV fluid resuscitation
- Hemodynamic support (vasopressors, inotropes)
- Correct hyperkalemia, acidosis, and electrolyte abnormalities
- Consider renal replacement therapy for refractory acidosis, hyperkalemia, or rhabdomyolysis-related AKI
- Switch to alternative sedation (dexmedetomidine, midazolam, ketamine)
- Mortality: 18–33% even with early recognition and treatment
Dexmedetomidine
| Parameter | Details |
|---|---|
| Mechanism | Selective alpha-2 adrenergic agonist (alpha-2:alpha-1 selectivity ratio 1,620:1); activates receptors in the locus coeruleus producing sedation that mimics natural sleep; analgesic properties via spinal cord alpha-2 receptors |
| Onset | 5–10 minutes (without loading dose); peak effect at 15–30 minutes |
| Offset | 30–60 minutes after discontinuation |
| Loading dose | 0.5–1.0 mcg/kg IV over 10–20 minutes (often omitted in hemodynamically unstable patients due to bradycardia/hypotension risk) |
| Infusion range | 0.2–1.5 mcg/kg/h; starting dose 0.2–0.4 mcg/kg/h |
| Maximum dose | 1.5 mcg/kg/h (higher doses used off-label for alcohol withdrawal, up to 2.5 mcg/kg/h) |
| Advantages | Arousable sedation (cooperative sedation — patient can follow commands while sedated); no respiratory depression at typical doses; reduces delirium incidence compared to benzodiazepines and propofol; analgesic-sparing (reduces opioid requirements by 30–50%); anti-shivering properties; anxiolytic; reduces sympathetic response |
| Disadvantages | Bradycardia (incidence 5–20%); hypotension (incidence 15–30%); limited depth of sedation achievable (max ~RASS −3); slow onset; more expensive than propofol or midazolam; rebound hypertension and tachycardia with abrupt discontinuation after prolonged use; dry mouth |
| Contraindications | Advanced heart block (2nd or 3rd degree) without pacemaker; heart rate < 50 bpm; use with caution if SBP < 90 mmHg or on high-dose vasopressors |
| Monitoring | Heart rate (watch for bradycardia < 50); blood pressure; sedation level (RASS) |
Key trial evidence:
| Trial | Finding |
|---|---|
| MENDS (2007) | Dexmedetomidine vs. lorazepam: more delirium-free and coma-free days; reduced 28-day mortality in sepsis subgroup8 |
| SEDCOM (2009) | Dexmedetomidine vs. midazolam: shorter time to extubation (3.7 vs. 5.6 days); lower delirium prevalence (54% vs. 76.6%)9 |
| DahLIA (2016) | Dexmedetomidine for delirium resolution in ventilated patients: faster delirium resolution; more ventilator-free hours10 |
| SPICE III (2019) | Dexmedetomidine as sole or primary sedation vs. usual care: no difference in 90-day mortality; more hypotension and bradycardia11 |
Midazolam
| Parameter | Details |
|---|---|
| Mechanism | Benzodiazepine; potentiates GABA-A receptor activity |
| Onset | 2–5 minutes |
| Offset | Variable; 1–2 hours after short use; highly unpredictable after prolonged use (days to weeks) due to active metabolite accumulation and lipophilic redistribution |
| Bolus dose | 0.01–0.05 mg/kg IV (0.5–4 mg) q 15 min–1 h PRN |
| Infusion range | 0.02–0.1 mg/kg/h (1–7 mg/h); starting dose 1–2 mg/h |
| Active metabolite | Alpha-hydroxymidazolam — 50% activity of parent compound; renally cleared; accumulates in renal impairment |
| Advantages | Rapid onset; amnestic; anticonvulsant; anxiolytic; reversible with flumazenil; inexpensive |
| Disadvantages | Increases delirium (strongest evidence among all sedatives); prolongs mechanical ventilation; unpredictable offset with prolonged use; tolerance and dependence develop rapidly; paradoxical agitation (especially elderly); respiratory depression; accumulation in obesity, hepatic failure, and renal failure |
| When to use | Active seizures (first-line); acute severe agitation refractory to non-benzodiazepine agents (rescue); alcohol withdrawal (often better managed with alternative agents in ICU); procedural sedation (single dose) |
| When to avoid | First-line ICU sedation; prolonged infusion (> 48 h); elderly patients; patients at high delirium risk; hepatic or renal failure |
Ketamine for Sedation
| Parameter | Details |
|---|---|
| Mechanism | NMDA receptor antagonist; also acts at opioid, monoaminergic, cholinergic, and sigma receptors |
| Onset | 30 seconds–1 minute IV |
| Offset | 10–20 minutes (emergence from dissociation) |
| Sub-dissociative/analgesic dose | 0.1–0.5 mg/kg/h (see Part 1) |
| Sedation dose | 0.5–2 mg/kg/h; bolus for induction: 1–2 mg/kg IV |
| Advantages | Maintains airway reflexes and respiratory drive; bronchodilator; sympathomimetic (supports hemodynamics); analgesic; no histamine release; useful in refractory status asthmaticus; may reduce delirium compared to benzodiazepines |
| Disadvantages | Emergence reactions (vivid dreams, hallucinations, dysphoria — 10–30%, reduced by concurrent benzodiazepine or dexmedetomidine); increased secretions (co-administer glycopyrrolate 0.2 mg IV if needed); increases heart rate and blood pressure (disadvantage in myocardial ischemia); historically cautioned in raised ICP but evidence does not support this concern in ventilated patients |
| Emerging role | Increasingly used as adjunct sedation to reduce propofol/opioid requirements (“ketafol” approach); sedation in burn patients; refractory status epilepticus; hemodynamically unstable patients needing sedation for intubation or procedures |
Sedative Agent Comparison Summary
| Feature | Propofol | Dexmedetomidine | Midazolam | Ketamine |
|---|---|---|---|---|
| Onset | 1–2 min | 5–10 min | 2–5 min | < 1 min |
| Offset | 5–10 min | 30–60 min | Variable (hours–days) | 10–20 min |
| Depth achievable | RASS −5 | RASS −3 (max) | RASS −5 | RASS −5 (dissociation) |
| Respiratory depression | Yes | No (at typical doses) | Yes | No (preserves drive) |
| Hemodynamic effects | Hypotension | Bradycardia, hypotension | Minimal at low doses | Sympathomimetic (increases HR/BP) |
| Delirium risk | Moderate | Lowest | Highest | Low-Moderate |
| Analgesic properties | None | Mild-Moderate | None | Strong |
| Cost (relative) | Low | High | Low | Moderate |
| Preferred first-line | Yes (< 72 h) | Yes (light sedation, extubation facilitation) | No | Adjunct role |
Sedative Selection Algorithm
Is the patient intubated and expected to require sedation > 72 hours?
├── YES → Dexmedetomidine (if light sedation target achievable)
│ OR Propofol (monitor for PRIS, TG q 24–48 h)
│ Consider ketamine as adjunct to reduce doses of either
│ AVOID midazolam as routine infusion
│
└── NO (< 72 hours expected)
├── Light sedation needed (RASS 0 to −2)?
│ → Dexmedetomidine or propofol (either first-line)
│
├── Deep sedation needed (RASS −3 to −5)?
│ → Propofol first-line (achieves deeper sedation)
│ → Add ketamine if hemodynamically unstable
│ → Midazolam ONLY if propofol contraindicated AND dexmedetomidine inadequate
│
└── Hemodynamically unstable?
→ Ketamine (sympathomimetic)
→ Midazolam (less hemodynamic depression than propofol)
→ Dexmedetomidine with caution (avoid loading dose)
→ Propofol at low dose with vasopressor support
Daily Sedation Interruption — Spontaneous Awakening Trials (SAT)
Rationale
Daily sedation interruption (also known as spontaneous awakening trial, or SAT) involves temporarily stopping all sedative and analgesic infusions each day to reassess the patient’s neurologic status, pain, agitation, and need for continued sedation. When paired with a spontaneous breathing trial (SBT), the “wake up and breathe” protocol significantly improves outcomes.5 12
SAT Safety Screen
Before initiating an SAT, a safety screen must be passed. The SAT is contraindicated if any of the following are present:
| Safety Screen Criterion | Rationale |
|---|---|
| Active seizures | Sedation required for seizure suppression |
| Alcohol or substance withdrawal requiring escalating sedation | Risk of withdrawal crisis |
| Receiving neuromuscular blocking agents | Must not awaken during paralysis |
| Myocardial ischemia within prior 24 hours | Sympathetic surge may worsen ischemia |
| Intracranial pressure elevation (ICP > 20 mmHg) | Agitation increases ICP |
| Actively requiring deep sedation for clinical indication | See deep sedation indications above |
SAT Protocol
- Pass the safety screen (see above)
- Stop all continuous sedative and analgesic infusions at a designated time each morning (typically 06:00–08:00)
- Observe for up to 4 hours (or until patient meets failure criteria)
- Assess for wakefulness: patient is considered awake if they open eyes to voice, follow simple commands, or have RASS ≥ −1
- If patient tolerates the SAT: proceed immediately to an SBT (spontaneous breathing trial)
- If the SAT fails (see criteria below): restart sedation at half the previous rate and titrate to the targeted RASS
SAT Failure Criteria
Restart sedation at 50% of the prior rate if any of the following occur:
| Failure Criterion | Definition |
|---|---|
| Sustained anxiety or agitation | RASS ≥ +2 for > 5 minutes |
| Respiratory distress | RR > 35/min for > 5 min, SpO2 < 88% for > 5 min, acute respiratory distress |
| Self-extubation or device removal | Unplanned removal of ETT, central line, chest tube, or other critical device |
| New cardiac arrhythmia | New atrial fibrillation, ventricular tachycardia, or other hemodynamically significant arrhythmia |
Paired SAT-SBT Protocol (“Wake Up and Breathe”)
The landmark ABC Trial demonstrated that pairing daily SAT with SBT, compared to SBT alone, resulted in:12
- 3.1 more ventilator-free days (14.7 vs. 11.6 days; p = 0.02)
- 4 fewer ICU days
- Reduced 1-year mortality (HR 0.68, 95% CI 0.50–0.92; p = 0.01)
- No increase in self-extubation
Coordinated SAT + SBT Protocol:
Step 1: SAT Safety Screen → PASS
Step 2: Stop all sedative/analgesic infusions
Step 3: Wait for patient to awaken (RASS ≥ −1)
→ If SAT fails → Restart at 50% dose, reassess next day
→ If SAT passes → Proceed to Step 4
Step 4: SBT Safety Screen → PASS
Step 5: SBT (T-piece, CPAP 5, or PSV 5–8 / PEEP 5 for 30–120 min)
→ If SBT fails → Return to prior ventilator settings; sedation PRN
→ If SBT passes → Assess for extubation readiness
Step 6: Evaluate for extubation
→ Positive cuff leak (if applicable)
→ Ability to protect airway
→ Manageable secretions
→ Extubate
Nurse-Driven Sedation Protocol
Nurse-driven sedation protocols empower bedside nurses to titrate sedation to achieve and maintain a physician-ordered RASS target. Implementation of nurse-driven sedation protocols has been associated with reduced duration of mechanical ventilation, shorter ICU stays, and decreased sedative use.1 13
Example Nurse-Driven Sedation Protocol
Prerequisites:
- Physician order specifying: target RASS, preferred sedative agent, initial infusion rate, and titration parameters
- Pain assessed and treated first (BPS < 5 or CPOT < 3)
Assessment schedule:
- RASS every 2 hours (minimum)
- RASS every 15–30 minutes during active titration
- BPS/CPOT/NRS at each RASS assessment
Titration rules (propofol example):
| Patient RASS vs. Target | Action |
|---|---|
| ≥ 2 points above target (more agitated) | Administer bolus (10–20 mcg/kg/min for 5 min); increase infusion by 10 mcg/kg/min; reassess in 15 min |
| 1 point above target | Increase infusion by 5–10 mcg/kg/min; reassess in 30 min |
| At target | No change; reassess in 2 h |
| 1 point below target | Decrease infusion by 5–10 mcg/kg/min; reassess in 30 min |
| ≥ 2 points below target (more sedated) | Hold infusion for 15–30 min; restart at 50% of previous rate; reassess in 15 min; notify provider if RASS remains ≥ 2 below target after 1 h |
Titration rules (dexmedetomidine example):
| Patient RASS vs. Target | Action |
|---|---|
| ≥ 2 points above target | Increase by 0.2 mcg/kg/h; consider rescue bolus of alternative agent (propofol 10–20 mg or fentanyl 25–50 mcg); reassess in 15 min |
| 1 point above target | Increase by 0.1–0.2 mcg/kg/h; reassess in 30 min |
| At target | No change; reassess in 2 h |
| 1 point below target | Decrease by 0.1–0.2 mcg/kg/h; reassess in 30 min |
| ≥ 2 points below target | Hold infusion; reassess in 15–30 min; restart at 50% dose; notify provider if HR < 50 or SBP < 80 |
Sedation-Related Adverse Events and Management
| Adverse Event | Signs | Immediate Action |
|---|---|---|
| Over-sedation (RASS < target) | Unresponsive to voice; RR < 8; hypotension | Hold sedation; reassess pain; restart at reduced rate when RASS returns to target |
| Under-sedation / agitation (RASS > target) | Self-removal of devices; patient-ventilator asynchrony; tachycardia | Rule out pain, delirium, hypoxia, full bladder, and other reversible causes BEFORE escalating sedation |
| Propofol-related hypotension | SBP < 90; MAP < 65; new vasopressor requirement | Reduce rate by 50%; consider fluid bolus; switch to alternative if persistent |
| Dexmedetomidine bradycardia | HR < 50 | Hold or reduce infusion; atropine 0.5 mg IV if symptomatic; consider alternative agent |
| Benzodiazepine over-sedation | Prolonged unresponsiveness; respiratory depression | Flumazenil 0.2 mg IV q 1 min (max 1 mg); caution in benzodiazepine-dependent patients (seizure risk) |
| Emergence delirium (ketamine) | Agitation, hallucinations, dysphoria on emergence | Low-dose midazolam (1–2 mg IV) or dexmedetomidine; reassurance; dim lights; reduce stimulation |
Neuromuscular Blocking Agents (NMBA) — Considerations
NMBAs are occasionally required in the ICU for specific indications. When NMBAs are used, adequate sedation and analgesia must be assured because the patient cannot communicate distress. The following principles apply:1 14
| Principle | Details |
|---|---|
| Sedation depth | Target RASS −4 to −5 before initiating NMBA; continue monitoring with processed EEG (BIS) if available |
| Pain management | Ensure adequate analgesia — pain assessment tools (BPS, CPOT) are unreliable during paralysis |
| Indications | Severe ARDS (early, for 48 h, when P/F < 150 with optimal ventilator settings); to facilitate prone positioning; to manage refractory ICP; during therapeutic hypothermia (prevent shivering); to reduce oxygen consumption in shock |
| Train-of-four (TOF) monitoring | Target 1–2 twitches out of 4 to avoid over-paralysis; assess q 4–6 h |
| Duration | Use for the shortest duration possible; reassess need at least q 12 h |
| Drug holiday | Consider daily interruption of NMBA to reassess underlying sedation and need for continued paralysis |
| ICUAW risk | Prolonged NMBA use (especially with concurrent corticosteroids) increases risk of ICU-acquired weakness; minimize duration |
Common NMBA Dosing in the ICU
| Agent | Bolus | Infusion | Metabolism | Considerations |
|---|---|---|---|---|
| Cisatracurium | 0.1–0.2 mg/kg | 1–3 mcg/kg/min | Hofmann elimination (organ-independent) | Preferred in hepatic/renal failure; does not cause histamine release |
| Rocuronium | 0.6–1.2 mg/kg | 4–16 mcg/kg/min | Hepatic | Reversible with sugammadex; onset faster than cisatracurium; may accumulate in liver failure |
| Vecuronium | 0.08–0.1 mg/kg | 0.8–1.2 mcg/kg/min | Hepatic (active metabolite) | Active metabolite (3-desacetylvecuronium) accumulates in renal failure; less preferred |
References
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