Procedural Sedation in the ICU — Capnography, Agents & the Safety Bundle

Overview & definition

The procedural sedation is a drug-induced depression of the consciousness for a painful or an unpleasant procedure, with the maintained spontaneous ventilation and the airway reflexes. It is distinct from the general anaesthesia, where the patient is unrousable, the airway is unprotected, and the ventilation is supported. The goal of the procedural sedation is the analgesia plus the anxiolysis plus the amnesia plus the immobility, with the cardiorespiratory stability and the rapid recovery.[1]

The ICU indications: the central venous catheterization, the arterial lines, the cardioversion, the chest tubes, the bronchoscopy, the endoscopy, the fracture and the joint reduction, the dressing changes, and the lumbar puncture.[1]

The continuum of the sedation

The sedation depth lies on a continuum (the ASA definition):[1]

As the depth increases, the airway, the reflexes, the respiration, and the cardiovascular function are progressively compromised — the operator must be prepared to rescue at the next deeper level.[1]

The safety bundle

The pre-procedure assessment

• The history — the allergies, the medications, the OSA, the obesity, the difficult-airway predictors (the Mallampati, the neck mobility, the beard, the receding chin).[1]
• The fasting — the 2 hours for the clear fluids, the 6 hours for the light meal (the ASA guidance). In the ICU, the patient is often not fasted and is treated as the full stomach (the aspiration risk) — balance the urgency against the risk, and prefer the airway-protective techniques (the RSI) for the higher-risk sedation.[1]
• The ASA physical status — the stratification of the risk (the ASA 3 to 4 at the higher risk of the complications).[1]
• The informed consent, the IV access, the emergency equipment.[1]

The monitoring during the procedure

• The continuous ECG, the pulse oximetry, and the BP (every 3 to 5 minutes).[1]
• The capnography (the end-tidal CO2) — the standard of care. It detects the apnoea and the respiratory depression EARLIER than the pulse oximetry (the oximetry lags, especially on the supplemental oxygen).[1]
• The supplemental oxygen.[1]
• The level of the consciousness (the responsiveness) and the respiratory rate.[1]

The personnel

• The dedicated observer (the trained nurse) — NOT the operator. The observer monitors the patient and the airway; the operator performs the procedure.[1]
• The rescue equipment — the bag-valve-mask, the suction, the advanced airway, the resuscitation drugs.[1]
• The reversal agents at the bedside (the naloxone, the flumazenil).[1]

The agents

Propofol

The induction agent. The rapid onset and offset; the deep sedation; the titrated 0.5 to 1 mg/kg boluses. The hypotension and the respiratory depression (the apnoea) are the dose-dependent effects. The propofol infusion syndrome (PRIS) with the prolonged high-dose. The preferred agent for the rapid, the brief, the deep sedation.[1]

Ketamine

The dissociative anaesthesia. The maintained airway reflexes and the cardiovascular stability (the sympathetic stimulation); the analgesia and the anaesthesia; the bronchodilation (useful for the asthma). The emergence reactions (the hallucinations, the agitation) — reduced by the midazolam. The increased secretions (give the antisialogogue). The dose 0.5 to 1 mg/kg. The good agent for the haemodynamically unstable or the asthmatic patient.[1]

Midazolam and fentanyl

The classic combination. The midazolam (the benzodiazepine) gives the anxiolysis and the amnesia; the fentanyl (the opioid) gives the analgesia. The titrated, the incremental doses. The slower onset and offset than propofol; the respiratory depression; the paradoxical agitation in the elderly. The reliable, the moderate-sedation combination.[1]

Etomidate

The induction agent. The haemodynamically stable — the preferred for the RSI in the unstable or the shocked patient. The adrenal suppression (the single dose is controversial). The myoclonus and the nausea. For the intubation (the RSI), not the routine procedural sedation.[1]

Dexmedetomidine

The alpha-2 agonist. The sedation without the respiratory depression (the patient is arousable); the analgesia-sparing; the weaning and the procedural sedation. The bradycardia and the hypotension. The slower onset.[1]

Nitrous oxide (the entonox)

The inhaled 50 % nitrous oxide with the 50 % oxygen (the entonox), the self-administered via the demand-valve mask. The rapid onset and offset (1 to 2 minutes); the minimal cardiovascular and respiratory depression; the analgesia and the anxiolysis for the brief, the mildly painful procedures (the dressing changes, the wound care, the labour). The contraindications: the pneumothorax, the bowel obstruction, the middle-ear disease, the raised ICP (the expansion in the closed gas-filled spaces). The occupational hazard (the scavenging).[1]

The reversal agents

• The naloxone (the opioid reversal) — 40 to 100 µg titrated (avoid the full reversal that precipitates the pain and the pulmonary oedema). The shorter half-life than the opioid — the re-sedation risk (re-dose, the observation).[1]
• The flumazenil (the benzodiazepine reversal) — 0.2 mg titrated. The shorter half-life than the benzodiazepine — the re-sedation risk. The seizure risk in the chronic benzodiazepine users. The reserve for the over-sedation with the respiratory depression.[1]

The complications and the rescue

• The respiratory depression and the apnoea, the airway obstruction, the hypoxia, the hypotension, the aspiration. The management: the airway opening (the chin lift, the jaw thrust), the bag-valve-mask ventilation, the supplemental oxygen, the vasopressors, and the reversal if indicated. The early detection by the capnography prevents the deterioration.[1]
• The post-procedure recovery monitoring until the patient returns to the baseline (the RASS, the protective reflexes).[1]

[1]

Red flags

The agent pharmacology — the detailed comparison

The agent choice is matched to the patient, the procedure, and the desired depth. No single agent is "best"; the principle is the titration to the effect, the anticipation of the adverse effect, and the readiness to rescue.[1][2]

[1]

The propofol — the rapid and the deep

The propofol is the workhorse of the brief, the deep procedural sedation. The onset in the 30 to 60 seconds; the offset in the 5 to 10 minutes (the rapid redistribution). The titrated boluses (the 0.5 to 1 mg/kg, the repeat every 1 to 2 minutes) — never the single large bolus, which precipitates the apnoea and the hypotension. The dose-dependent cardiovascular and respiratory depression; the pain on the injection (the lidocaine, the larger vein).[3][4]

The propofol infusion syndrome (PRIS) — the rare but the lethal complication of the prolonged high-dose infusion (the > 4 mg/kg/h for the > 48 h, the high cumulative dose). The features: the metabolic acidosis, the rhabdomyolysis, the cardiac failure, the hepatomegaly, the hyperkalaemia, the renal failure. The risk factors: the high dose, the prolonged duration, the steroids, the catecholamines, the child, the neurologic injury. The management: the stop the propofol, the supportive care, the alternative agent (the dexmedetomidine, the benzodiazepine).[1]

The ketamine — the dissociative

The ketamine produces the dissociative anaesthesia — the cataleptic state with the preserved airway reflexes, the spontaneous ventilation, and the cardiovascular stability (the sympathetic surge raises the HR and the BP). The profound analgesia; the bronchodilation (the asthma); the maintained tone in the skeletal muscle. The dose 0.5 to 1.5 mg/kg IV (the 4 to 5 mg/kg IM for the IV access impossible).[6]

The adverse effects: the emergence reactions (the vivid hallucinations, the agitation on the recovery — reduced by the benzodiazepine, the quiet environment, the adult dose-adjustment; the more common in the adults than the children); the increased secretions (the antisialogogue — the glycopyrrolate); the emesis (the commonest in the children); the sympathetic surge (the relative contraindication in the ischaemic heart disease and the raised ICP, though the recent evidence questions the ICP significance).[6][7]

The Green meta-analyses (the 8,282 children): the high-dose age — the airway adverse events cluster in the very young (the < 2 years) and the high IM dose; the recovery agitation is predicted by the age (the older child) and the adjunctive medication.[6][7]

The midazolam and the fentanyl — the classic combination

The midazolam (the benzodiazepine) provides the anxiolysis, the amnesia, and the modest sedation; the fentanyl (the opioid) provides the analgesia. The titrated, the incremental doses (the 0.02 to 0.05 mg/kg of the midazolam; the 0.5 to 1 µg/kg of the fentanyl, the repeat every 2 to 3 minutes). The slower onset and offset than the propofol; the longer recovery (the 30 to 60 minutes); the cumulative effect (the re-dosing stacks the depression).[1]

The pitfalls: the synergy with the opioid (the profound respiratory depression — give the opioid first, the benzodiazepine second, the titrate slowly); the paradoxical agitation in the elderly and the hepatic impairment; the hypotension in the volume-depleted. The reversible (the flumazenil, the naloxone), but with the re-sedation risk.[1]

The fentanyl and the chest-wall rigidity

The fentanyl, in the high bolus dose or the rapid push, can precipitate the glottic and the chest-wall rigidity (the "wooden chest") — the sudden inability to ventilate from the skeletal-muscle and the vocal-cord tone. The management: the naloxone (the reversal), the neuromuscular blockade (the suxamethonium) if the naloxone alone fails, and the airway support (the bag-valve-mask, the intubation). The preventive principle: the titration (the slow, the small increments), never the rapid bolus.[1]

The dexmedetomidine — the cooperative sedation

The alpha-2 agonist produces the unique "cooperative" sedation — the patient is calm and the easily arousable, the interaction preserved, the respiratory drive maintained. The analgesia-sparing (the opioid-sparing up to the 50 %); the weaning-friendly (no the respiratory depression, the reduced delirium). The dose 0.2 to 1 µg/kg/h infusion, with or without the loading dose (the 0.5 to 1 µg/kg over the 10 minutes — the loading causes the bradycardia and the transient hypertension).[2]

The adverse effects: the bradycardia (the careful in the heart block, the beta-blocker); the hypotension (the volume-depleted); the slower onset (the 5 to 10 minutes — not for the immediate, the brief procedure); the dry mouth. The good agent for the longer, the awake, the weaning-context sedation (the bronchoscopy, the awake intubation, the weaning).[2]

The etomidate — the haemodynamically stable, the adrenal caveat

The etomidate is the haemodynamically neutral induction agent — the preferred for the RSI in the shocked, the head-injured, or the cardiac patient. The rapid onset (the 30 to 60 seconds); the brief duration (the 5 to 15 minutes). The adrenal suppression (the blockade of the 11-β-hydroxylase) — the single dose is the clinically relevant in the septic shock (the debate ongoing; the STAR trial suggests the harm in the septic shock); the prophylactic steroid is the practice in some units. The myoclonus; the nausea; the pain on the injection. The role: the intubation (the RSI), not the routine procedural sedation — the adrenal suppression makes it the second-line for the prolonged PSA.[1]

The ASA physical status classification

The ASA physical status stratifies the patient for the sedation risk — the higher the class, the higher the risk of the cardiorespiratory complication.[2]

[1]

The ICU patient is rarely the ASA I or II — most are the ASA III to IV (the multi-organ disease, the shock, the full stomach). The capnography, the dedicated observer, and the rescue equipment are the standard for the ASA III and above. The ASA IV and above — consider the airway-protection (the RSI) rather than the procedural sedation, as the margin for the deeper-level rescue is the narrow.[2]

The sedation-depth assessment — the Ramsey and the RASS

The depth of the sedation must be the measured, not the assumed. The dedicated observer applies the scoring system continuously and the operator titrates to the target.[1]

The Ramsey sedation scale (the classic, the PSA)

The Richmond Agitation-Sedation Scale (the RASS, the ICU standard)

The target for the procedural sedation recovery is the return to the baseline RASS (the typically the 0, or the pre-sedation score) and the protective reflexes. The discharge from the recovery requires the sustained RASS of the 0 or the baseline.[1]

The Observer's Assessment of Alertness/Sedation (the OAA/S)

The OAA/S is the composite (the responsiveness, the speech, the facial expression, the eyes), scored 5 (the alert) to 1 (the deep sedation). The moderate sedation is the OAA/S of the 3 (the responds to the commands spoken loudly and the repeatedly); the deep sedation is the OAA/S of the 2 or the less. The OAA/S is the validated for the procedural sedation and the favored by the anaesthesia societies.[2]

The monitoring — the capnography and the waveforms

The capnography is the standard of care for the procedural sedation — the ASA, the ACEP, and the ED guidelines converge. The Deitch RCT and the Burton observational study show the capnography detects the apnoea and the airway obstruction MINUTES before the oximetry, especially in the patient on the supplemental oxygen.[4][5]

The capnography — what the waveform tells

The normal waveform: the baseline (the CO2-free inspired gas), the ascending limb (the expiration), the alveolar plateau (the end-tidal CO2), the descending limb (the inspiration). The end-tidal CO2 (the EtCO2) is the peak — the 35 to 45 mmHg in the normal.[4]

[1]

The principle: the capnography is the EARLIEST indicator of the respiratory compromise. The oximetry lags — on the supplemental oxygen, the SpO2 may remain in the 90s for the minutes after the apnoea. The Deitch trial: the supplemental oxygen DELAYED the detection of the hypoxia by the oximetry, but the capnography detected the apnoea at the onset. The conclusion: the capnography is the non-negotiable, and the routine supplemental oxygen does NOT substitute for the capnography (it may mask the deterioration).[3][4]

The monitoring — the full bundle

[1]

The rescue airway equipment

The rescue equipment is at the bedside BEFORE the first dose. The operator must be able to manage the airway at one level deeper than the intended.[1][2]

[1]

The discharge criteria — the Aldrete and the PDRE

The discharge from the recovery area requires the objective, the scored recovery — the patient returns to the baseline across the five domains. The Aldrete score (the modified post-anaesthesia recovery score) is the validated and the widely used.[10]

[1]

The discharge threshold: the score of the 9 to 10 (out of the 10), the sustained for the 20 to 30 minutes, and the return to the baseline. The ACEP adds the Post-Sedation Discharge Readiness criteria — the stable vitals, the normal mental status, the protective reflexes, the ambulation, the toleration of the oral intake, the no nausea, the responsible adult to accompany.[1][10]

[1]

The procedural sedation in the special populations

The obese and the OSA patient

The obese patient (the BMI > 30) and the OSA patient are the high-risk for the procedural sedation. The issues: the difficult airway (the Mallampati, the neck circumference, the OSA predicts the difficult mask and the difficult laryngoscopy); the rapid desaturation (the reduced functional residual capacity, the increased oxygen consumption, the atelectasis); the hypoventilation (the opioid and the benzodiazepine sensitivity); the dose adjustment (the lean body weight for the lipophilic agents — the propofol, the benzodiazepines — to avoid the overdose; the dosing on the total body weight over-sedates).[2]

The strategy: the dose on the lean body weight (the propofol 0.5 mg/kg of the LBW); the titrate the small increments; the capnography mandatory (the early apnoea detection); the prefer the agents with the rapid offset (the propofol, the dexmedetomidine) over the long-acting (the midazolam); the avoid the opioids where possible (the dexmedetomidine); the ramped position for the bag-mask and the intubation; the rescue airway and the difficult-airway equipment at the bedside; the consider the awake fiberoptic intubation for the predicted difficult airway.[2]

The elderly patient

The elderly (the > 65) are the increased sensitivity to the sedatives (the reduced clearance, the increased receptor sensitivity, the reduced volume) and the increased comorbidity. The pitfalls: the paradoxical agitation with the midazolam; the prolonged sedation with the midazolam and the benzodiazepine (the reduced hepatic clearance); the hypotension with the propofol (the reduced vascular tone, the diuretics, the beta-blocker); the delirium (the benzodiazepine is the strongest risk factor for the ICU delirium).[1]

The strategy: the reduce the dose by the 30 to 50 %; the titrate the small increments; the prefer the propofol (the rapid offset) and the dexmedetomidine (the delirium-sparing) over the midazolam; the avoid the benzodiazepine where possible (the delirium risk); the capnography (the hypoventilation); the consider the geriatric-friendly protocol (the ketamine for the analgesia, the propofol for the sedation).[1]

The pregnant patient

The procedural sedation in the pregnancy is the high-stakes — the two patients (the mother and the foetus), the aspiration risk (the reduced lower-oesophageal-sphincter tone, the increased intra-abdominal pressure, the delayed gastric emptying — the "full stomach" from the second trimester), the aortocaval compression (the supine — the left lateral tilt), the altered pharmacology (the increased volume, the reduced protein binding, the placental transfer).[1]

The agent selection: the propofol (the category B; the rapid offset; the preferred for the deep sedation); the ketamine (the category B; the bronchodilation; the preserved BP — good for the shocked obstetric patient; the increased uterine tone in the high dose); the fentanyl (the category B; the analgesia; the neonatal respiratory depression near the term — the close to the delivery, the avoid); the dexmedetomidine (the category C; the limited data). The avoid: the midazolam (the category D in the first trimester — the teratogenicity; the neonatal floppy-baby syndrome near the term); the nitrous oxide (the teratogen — the avoid in the first trimester; the megaloblastosis); the etomidate (the limited obstetric data).[1]

The strategy: the left lateral tilt (the aortocaval); the RSI for the deep sedation (the full stomach — the aspiration); the obstetric and the anaesthetic consult for the deep or the prolonged procedure; the foetal monitoring for the viable gestation; the senior operator and the airway-trained assistant.[1]

Exam practice

[1] [1]

The clinical pearls

The trials and the evidence

[1] [2] [3] [4] [6] [7]

The workflow — the procedural sedation from the decision to the discharge

[1] [1]

The additional red flags

The exam high-yield — the one-line answers

• The capnography is the standard of care — the earliest detector of the apnoea, the earlier than the oximetry (the lags on the supplemental oxygen).[4][5]
• The dedicated observer, not the operator — the monitoring is the separate role.[1]
• The rescue at the one deeper level — the operator must be able to rescue the airway at the next deeper level than the intended.[2]
• The propofol — the rapid, the deep, the titrated 0.5 to 1 mg/kg; the hypotension, the apnoea; the PRIS in the prolonged high-dose.[1]
• The ketamine — the preserved airway and the BP, the bronchodilation, the emergence reactions, the secretions; the avoid the IHD and the raised ICP (the sympathetic surge).[6]
• The fentanyl — the analgesia, the chest-wall rigidity in the high bolus.[1]
• The dexmedetomidine — the cooperative sedation, the no respiratory depression, the bradycardia.[2]
• The etomidate — the haemodynamically stable, the adrenal suppression; the RSI, the not the routine PSA.[1]
• The nitrous oxide — the self-administered entonox; the contraindicated in the pneumothorax, the bowel obstruction, the raised ICP.[1]
• The naloxone (the opioid) and the flumazenil (the benzodiazepine) — the shorter half-life than the agonist; the re-sedation risk; the observe.[1]
• The obese — the dose on the lean body weight; the capnography mandatory; the dexmedetomidine preferred.[2]
• The elderly — the half the dose; the avoid the benzodiazepine (the delirium, the prolonged sedation); the propofol and the dexmedetomidine.[1]
• The pregnancy — the full stomach; the propofol and the ketamine (the category B); the avoid the midazolam (the category D) and the nitrous oxide (the teratogen).[1]
• The discharge — the Aldrete 9 to 10, the stable vitals, the protective reflexes, the responsible adult.[10]
• The ICU patient is the full stomach — the aspiration risk; the prefer the RSI for the deeper sedation.[1]

References

1. [1]Godwin SA, Burton JH, Gerardo CJ, Haines RW, Smally CM. Clinical policy: procedural sedation and analgesia in the emergency department Ann Emerg Med, 2014.PMID 24438649
2. [2]American Society of Anesthesiologists Task Force on Moderate Procedural Sedation and Analgesia. Practice Guidelines for Moderate Procedural Sedation and Analgesia 2018: A Report by the American Society of Anesthesiologists Task Force on Moderate Procedural Sedation and Analgesia, the American Association of Oral and Maxillofacial Surgeons, American College of Radiology, American Dental Association, American Society of Dentist Anesthesiologists, and Society of Interventional Radiology Anesthesiology, 2018.PMID 29334501
3. [3]Deitch K, Chudnofsky CR, Dominici P, Latta B, Salamanca Y. The utility of supplemental oxygen during emergency department procedural sedation with propofol: a randomized, controlled trial Ann Emerg Med, 2008.PMID 18294729
4. [4]Deitch K, Miner J, Chudnofsky CR, Dominici P, Latta B. Does end tidal CO2 monitoring during emergency department procedural sedation and analgesia with propofol decrease the incidence of hypoxic events? A randomized, controlled trial Ann Emerg Med, 2010.PMID 19783324
5. [5]Burton JH, Harrah JD, Germann CA, Dillon DC. Does end-tidal carbon dioxide monitoring detect respiratory events prior to current sedation monitoring practices? Acad Emerg Med, 2006.PMID 16569750
6. [6]Green SM, Roback MG, Krauss B, et al. Predictors of airway and respiratory adverse events with ketamine sedation in the emergency department: an individual-patient data meta-analysis of 8,282 children Ann Emerg Med, 2009.PMID 19201064
7. [7]Green SM, Roback MG, Krauss B, et al. Predictors of emesis and recovery agitation with emergency department ketamine sedation: an individual-patient data meta-analysis of 8,282 children Ann Emerg Med, 2009.PMID 19501426
8. [8]Vargo JJ. Safety in numbers: the case for endoscopist-directed propofol sedation Endosc Int Open, 2015.PMID 26528491
9. [9]Miner JR, Gray RO, Buhumaid R, Patel R, McGill JW. Alfentanil for procedural sedation in the emergency department Ann Emerg Med, 2011.PMID 20947206
10. [10]Aldrete JA. A postanesthetic recovery score Anesth Analg, 1970.PMID 5534693