Anesthesia: Analgesia, Sedation, and Neuromuscular Blockade



Anesthesia: Analgesia, Sedation, and Neuromuscular Blockade














TABLE 2.1. Commonly Used Agents for Intravenous Sedation/Anesthesia

































































Drug Initial IV Dosagea Maintenance Infusiona Comments
Barbiturates
Pentobarbital 5–20 mg/kg Onset: <1 min Duration: 15 min 1–4 mg/kg/h Infuse loading dose over 2 h
Rapid administration produces hypotension and hemodynamic instability
Thiopental 3–4 mg/kg Onset: 10–20 s Duration: 5–15 min Not applicable Alkaline solution; decreases cardiac index
Benzodiazepines
Diazepam 0.1–0.2 mg/kg Onset: 1–3 min Duration: 1–2 h Not applicable Active metabolite with long half-life (desmethyldiazepam) contributes to activity
Lorazepam 0.04 mg/kg Onset: 5–15 min Duration: 1–6 h 0.02–0.1 mg/kg/h No active metabolites
Approximately 5 times more potent than diazepam
Midazolam 0.025–0.035 mg/kg Onset: 1–3 min Duration: 30 min–3 h 0.05–5 μg/kg/min Elderly patients may develop apnea when midazolam is administered with narcotics
Approximately 3–4 times more potent than diazepam
Active metabolites accumulate in renal failure
Unpredictable elimination in critically ill patients (e.g., shock, liver failure)
Initial dose: 0.5–1 mg and titrate to effect in 0.5–2 mg increments
Other
Propofol 1–2 mg/kg Onset: <1 min Duration: 5–10 min 5–75 μg/kg/min Generally a rapid recovery
Pain on injection is common with peripheral administration
Hypotension may occur especially with rapid bolus in hypovolemic or elderly patients
Propofol may increase serum triglyceride levels when used at high infusion rates; take caution when using in patients with pancreatitis
Doses of propofol of 5 mg/kg/h have been associated with cardiac failure and death
Safety of propofol has not been established for ICU sedation of children
Propofol contains 1.4 mmol of PO4=/100 ml
Dexmedeto- midine 1 μg/kg IV over 10 min 0.2–0.7 μg/kg/h for up to 24 h Alpha-2 adrenergic agonist with analgesic and sedative properties
Numerous cardiovascular effects including brady- and tachyarrhythmias, hyper- and hypotension, and atrioventricular block
Does not produce respiratory depression
Ketamine 1–2 mg/kg (or 5–10 mg/kg IM) Onset: <1 min Duration: 5–10 min 9–45 μg/kg/min Usually preserves airway reflexes
Central sympathetic stimulation; hypertension; tachycardia; advantageous in hypovolemic patients
Tachyphylaxis is rare
Etomidate 0.3–0.4 mg/kg Onset: <1 min Duration: 3–5 min Not recommended
Produces adrenal suppression in continuous infusion		 Minimal cardiovascular effects
Myoclonic muscle movements
Pain on IV injection
Remifentanil 0.05 μg/kg Onset: <1 min Duration: <4 min 0.05–0.2 μg/kg/min Ultrashort acting narcotic analgesic; used primarily as an intraoperative analgesic; elimination not dependent on liver or kidney function
CNS, central nervous system; ICU, intensive care unit; IM, intramuscular; IV, intravenous
aBolus doses and rates of infusion should be individualized to provide the desired level of sedation with consideration of potential hemodynamic compromise. Doses should generally be reduced for elderly and hypovolemic patients. It may be beneficial to wake patients daily and assess their CNS function during maintenance infusions to determine the minimal dose required for sedation.











TABLE 2.2. Tracheal Intubation Techniques
































































Technique Clinical Setting Procedural Features Cautions
All listed below Indications: Upper airway obstruction
Airway protection
Tracheal toilet		 Minimum required monitoring ECG, BP, pulse oximetry
Prepare patient for 100% O2
Establish IV access for rapid administration of resuscitative drugs and fluids if necessary
Equipment and drugs: Oxygen bag-mask ventilation equipment, monitors, suction laryngoscopes, ETT, stylettes, cuff, syringes, “Code Blue” cart
Anesthetics: Neuromuscular blocking agents, Sedative/hypnotic agents		 Aspiration
Loss of airway
Dental damage
Trauma to airway
Hemodynamic compromise
Awake Anticipated difficult laryngoscopy
Full stomach
Minimize risk of airway loss as a result of sedation or neuromuscular blockade
Assessment and protection of neurologic function in cervical spine instability
Can be performed without depression of airway reflexes
Requires patient cooperation		 Patient maintains airway and ventilation Vomiting from pharyngeal stimulation
Hypertension and tachycardic response to intubation is undesirable in certain clinical settings (e.g., myocardial ischemia, cerebral or aortic aneurysm)
Topical anesthesia of larynx or nerve blocks of larynx obtunds protective airway reflexes
Conscious: Oral Allows largest diameter ETT Topical anesthesia of pharynx or pharyngeal nerve blocks
Intubation with direct vision		  
Conscious: Blind nasal   Apply vasoconstrictor and topical anesthetic to nasal mucosa
Gently dilate nasal passage with soft nasal airways
Gently advance ETT from nose to trachea during inhalation		 Nasal bleeding, avoid in coagulopathic patients
Sinusitis
Avoid in craniofacial trauma
Fiberoptic (oral or nasal)   Consider administering an antisialagogue (glycopyrrolate 0.2 mg IV)
Topical anesthetic and vasoconstrictor (for nasal)
Insert bronchoscope through ETT and directly into trachea
Advance ETT over bronchoscope and remove bronchoscope		  
Not Awake Uncooperative patients
Preexisting loss of consciousness (e.g., cardiac arrest, heavy sedation)
Blunts tachycardic and hypertensive response
Minimizes unpleasantness of procedure		   Risk of apnea, aspiration, airway loss
Unsedated unconscious Cardiac arrest Bag-mask ventilation until intubation equipment available
Immediate oral laryngoscopy and intubation		  
Rapid-sequence: oral (see Table 2.3) Full stomach or risk of aspiration in a patient without an anatomically difficult airway for laryngoscopy Administration of sedative and neuromuscular blocking agents
Cricoid pressure
Rapid intubation after onset of neuromuscular blockade
Check ETT placement
Remove cricoid pressure		 Risk of airway loss
Hemodynamic compromise may result from sedation or positive pressure ventilation
Reintubation Nonfunctioning ETT (e.g., cuff leak)
Placement of an ETT with different features (e.g., larger diameter)		 Sedate and administer neuromuscular blockade Chronically intubated patients may have swelling or traumatic changes of larynx making reintubation difficult
Patients who are dependent on high oxygen concentrations or PEEP may become hypoxemic
Direct vision extubation and reintubation Laryngoscopy possible Perform laryngoscopy with existing ETT in place
If glottis is visualized, remove existing ETT and replace with new one		 Loss of airway
Styletted reintubationa Difficult laryngoscopy anticipated Insert stylette into existing ETT
Remove ETT without removing stylette
Insert new ETT over stylette		  
BP, blood pressure; ETT, endotracheal tube; ECG, electrocardiogram; IV, intravenous; PEEP, positive end-expiratory pressure
aaRefers to specific intubating stylettes and not to those routinely used to stiffen ETT during routine intubation.









TABLE 2.3. Suggested Drugs for Rapid Sequence Intubation












































Drug Dosage Comment
Sedatives/Anesthetics
Thiopental 3–4 mg/kg IV Reduce dose in elderly and hemodynamically unstable patients (0.25–1 mg/kg)
May produce hypotension and hemodynamic instability
Blunts intracranial hypertensive response to intubation and is useful in hemodynamically stable patients with elevated ICP
Ketamine 1–2 mg/kg IV
4–10 mg/kg IM		 Useful in hypovolemic patients as this drug tends to support the circulation; may rarely produce myocardial depression
Produces hypertension, tachycardia, and elevates ICP; therefore, avoid in patients with myocardial ischemia, severe hypertension, or intracranial mass lesions
Etomidate 0.3–0.4 mg/kg IV Hemodynamic stability
Patients often have benign nonpurposeful muscle movements during induction which may be blunted by low doses of fentanyl (50–100 μg)
Propofol 1–2.5 mg/kg IV Reduce dose in elderly and hemodynamically unstable patients (0.25–0.5 mg/kg)
May produce hypotension and hemodynamic instability
Muscle Relaxantsa
Cisatracurium 0.15–0.2 mg/kg IV Slower in onset than succinylcholine
Less histamine release than atracurium
Hemodynamic stability
Duration of action is dose-dependent (30 min–1 h)
Rocuronium 0.6–1.2 mg/kg IV Reported as most rapid onset of nondepolarizing neuromuscular blocking drugs (60–90 s)
Not recommended in Caesarean section patients
Hemodynamic stability
Duration of action is dose dependent (30 min–1 h)
Succinylcholine 1 mg/kg IV Depolarizing agent
Because of rapidity of onset, drug of choice unless specifically contraindicated (see Table 2.4)
Duration of action ≅10 min for patients with normal pseudocholinesterase activity
Vecuronium 0.1–0.28 mg/kg Slower onset than succinylcholine
Hemodynamic stability
Duration of action is dose dependent (30 min–1 h)
ICP, intracranial pressure; IM, intramuscular; IV, intravenous
aFor most clinical situations, cost may be the overriding consideration when choosing among the available nondepolarizing muscle relaxants.










TABLE 2.4. Neuromuscular Blockade—Bolus Dosing



































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Jun 16, 2016 | Posted by in CRITICAL CARE | Comments Off on Anesthesia: Analgesia, Sedation, and Neuromuscular Blockade

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Agent Dosage Onset/Duration Comments
Depolarizing Relaxant
Succinylcholinea Bolus: 1–2 mg/kg Onset: 1 min
Duration: 10 min		 Prolonged effect in pseudocholinesterase deficiencies
Contraindications: family history of malignant hyperthermia, neuromuscular disease, hyperkalemia, open eye injury, major tissue injury (burns, trauma, crush); increased intracranial pressure; not indicated for routine use in children or adolescents
Side effects: bradycardia (especially in children), tachycardia, increased serum potassium
Nondepolarizing Relaxants
Atracurium Bolus: 0.5 mg/kg Onset: 2 min
Duration: 30–40 min		 Rapid injection of atracurium bolus doses >0.6 mg/kg releases histamine and may precipitate asthma or hypotension
Metabolized in the plasma by Hofmann elimination and ester hydrolysis
Duration not prolonged by renal or liver failure; otherwise, see comments with vecuronium
Cisatracurium Bolus: 0.15 mg/kg Onset: 2 min
Duration: 30–40 min		 Less histamine release than racemic atracurium (see above)
Metabolism and duration of action similar to atracurium
Mivacurium Bolus: 0.15 mg/kg followed in 30 s by 0.10 mg/kg Onset: 1.5 min
Duration: 25 min		 Inject over 30 s
May cause histamine release
Metabolized by pseudocholinesterase
Rocuronium Bolus: 0.6 mg/kg Onset: 1 min
Duration: 30–40 min