Anesthetic Agents and Induction Risks
Barbiturate for Electroconvulsive Therapy (ECT)
- Brevital is a barbiturate frequently used for ECT.
- Mechanism: It works by lowering the seizure threshold, facilitating the therapeutic seizure.
Common Classes of Anesthetic Induction Agents
- Sedative-Hypnotics are primarily used for anesthesia induction.
- Propofol: A widely used agent.
- Etomidate (“eVOMidate”):
- Often causes nausea and vomiting, so prophylactic antiemetics are advisable.
- Beneficial for patients undergoing vascular procedures (e.g., AAA repair, grafts) as it tends to maintain lower blood pressure for up to 24 hours post-induction.
Periods of Highest Myocardial Infarction (MI) Risk
A patient is most vulnerable to a myocardial infarction at two critical junctures:
- During anesthesia induction.
- 2-3 days post-operatively.
Importance of Limiting Peri-Induction Stress
- Rationale: To minimize the risk of MI during induction.
- Strategy: Maintain a calm and secure environment for the patient.
Anesthesia Induction Considerations for Asthmatic Patients
- Pre-Operative Care: Patients should use their inhaler in the pre-operative area.
- Pre-Intubation: Administer a bronchodilator prior to intubation.
- Depth of Anesthesia: The patient will require a deeper plane of anesthesia before attempting intubation.
Patients at Elevated Risk for Aspiration During Induction
Five categories of patients have a higher likelihood of aspirating stomach contents into the lungs:
- Gastroesophageal Reflux Disease (GERD)
- Trauma patients (often not NPO)
- Awake intubation scenarios
- Pregnant patients
- Obese patients
Alternate Term for Cricoid Pressure
- Sellick’s Maneuver is the medical term for applying cricoid pressure to occlude the esophagus during intubation.
Pain Management and Pharmaceutical Agents
Pain Scale Selection
- The choice of pain scale should be guided by the patient’s developmental age.
Examples of Opioid Analgesics
These potent pain medications include:
- Hydromorphone (Dilaudid): A synthetic opioid.
- Meperidine (Demerol): An opioid.
- Fentanyl (Sublimaze): A synthetic opioid.
- Morphine (Duramorph): A natural opioid.
Opioid Causing Nausea/Vomiting (N/V)
- Morphine (Duramorph), a natural opioid, is particularly associated with N/V.
Opioids Causing Chest Wall Rigidity/Respiratory Distress
- Hydromorphone (Dilaudid) and Fentanyl (Sublimaze) can cause chest wall rigidity and respiratory distress, especially in older patients.
- Prevention: Administer these medications very slowly.
Advantages of Hydromorphone/Fentanyl over Morphine
- They do not typically cause N/V.
Sole Approved Use for Meperidine (Demerol)
- The only current approved indication for Meperidine is to treat shivering.
Opioid Reversal Agent and Dosing
- Reversal Agent: Naloxone (Narcan).
- Dose: Administer 0.1 – 0.2 mg at 2-3 minute intervals.
- Strategy: Use repeated small doses to reverse just enough to restore adequate ventilation, rather than full reversal (which can cause acute pain and withdrawal).
- Monitoring: The effect lasts 30-45 minutes, so monitor for the return of respiratory depression.
Benzodiazepines: Uses and Limitations
- Treat: Benzodiazepines primarily alleviate anxiety.
- Do NOT Treat: They do not provide pain relief.
Examples of Benzodiazepines and Reversal Agent
- Examples: Midazolam (Versed), Diazepam (Valium) (also Xanax, Ativan).
- Reversal Agent: Flumazenil (Romazicon).
Midazolam (Versed) vs. Diazepam (Valium) Preference
- Midazolam (Versed) is generally preferred due to its faster metabolism.
- Diazepam (Valium) has a significantly longer half-life, potentially taking days to metabolize. It is also a viscous solution and should be administered slowly.
Flumazenil (Romazicon): Reversal Agent and Contraindications
- Reverses: Benzodiazepines.
- Contraindicated in:
- Seizure patients (can precipitate seizures).
- Patients on tricyclic antidepressants (can reverse their effects).
Key Concern with Benzodiazepines
- They are potent respiratory depressants.
Holistic Therapy Rights
- Patients have the right to have a holistic therapy practitioner (e.g., Reiki practitioner) present during their hospital stay to perform therapeutic interventions.
Muscle Relaxants
Only Depolarizing Paralytic
- Succinylcholine is the sole depolarizing muscle relaxant in common use.
Mechanism of Action: Succinylcholine
- Potassium Release: It causes a temporary expulsion of potassium from muscle cells.
- Depolarization and Paralysis: It depolarizes the muscle end-plate, leading to transient muscle fasciculations (twitches) followed by paralysis.
- Duration: Paralysis lasts 5-10 minutes until it is metabolized by pseudocholinesterase.
Pros and Cons of Succinylcholine
- Advantage: Very short duration of action (5-10 minutes).
- Disadvantages (5):
- Bradycardia.
- Increased Intraocular Pressure (IOP) due to fasciculations (contraindicated in glaucoma patients).
- Oxygen Depletion: Muscles consume oxygen during fasciculations.
- Hyperkalemia: Significant potassium shift out of cells (monitor EKG).
- Absolute Contraindication in Malignant Hyperthermia (MH) Family History.
- Absolute Contraindication in Muscle Disorders: Patients with muscular dystrophies, multiple sclerosis (MS), cerebral palsy, myasthenia gravis, or paraplegia are at risk for severe hyperkalemia because their muscles lack the normal “stop gate” for potassium efflux.
Patients Who Should Never Receive Depolarizing Paralytics
- Individuals with a family history of MH.
- Patients with degenerative muscle disorders or muscle atrophy (e.g., MS, MD, cerebral palsy, myasthenia gravis, paraplegia) due to the risk of severe, uncontrolled hyperkalemia.
Succinylcholine Reversal
- No specific reversal agent exists.
- Major Concern: Patients with pseudocholinesterase deficiency cannot metabolize succinylcholine efficiently, leading to prolonged paralysis and inability to breathe or move upon emergence.
Depolarizing vs. Non-Depolarizing Muscle Relaxants (NDMRs): Mechanism
- NDMRs (e.g., Rocuronium): Act as competitive acetylcholine antagonists. They essentially “block” the motor end-plate, preventing acetylcholine from binding and initiating muscle contraction (like “saran wrap” over the receptor). They take longer to exert their effect.
Speed of Action: Depolarizing vs. NDMRs
- Depolarizing (Succinylcholine) acts faster.
Reversibility of Muscle Relaxants
- NDMRs (e.g., Rocuronium) can be reversed.
- Reversal Agents: Anticholinergics (e.g., Neostigmine + Glycopyrrolate/Robinul, Edrophonium + Atropine) or Sugammadex (for Rocuronium or Vecuronium).
Reasons to Choose an NDMR Over a Depolarizing Relaxant (4)
- Family history of Malignant Hyperthermia (MH).
- Presence of degenerative muscle disorders (MS, MD, Myasthenia Gravis, Cerebral Palsy, paraplegia).
- Known pseudocholinesterase deficiency.
- Need for prolonged paralysis during surgery.
NDMR Reversal Agents and Administration Timing
- Anticholinesterases: These agents (e.g., Neostigmine, Edrophonium) block acetylcholinesterase, increasing acetylcholine concentration to overcome the NDMR blockade.
- Sugammadex: A non-anticholinesterase agent specifically for Rocuronium and Vecuronium.
- Timing for Anticholinesterases: Administer when the patient shows some muscle twitching, indicating a partial recovery and an “edge” for the reversal agent to work effectively.
Side Effects of NDMR Reversal Agents (Anticholinesterases)
- Mechanism: They enhance the parasympathetic nervous system (rest and digest).
- Side Effects (Mnemonic: Brady + Poopy + Slobbery):
- Bradycardia (slow heart rate).
- Bronchospasm.
- Enhanced peristalsis (increased bowel activity).
- Increased oral secretions.
NDMR Reversal Agent Combinations
- Neostigmine is given with Glycopyrrolate/Robinul.
- Edrophonium is given with Atropine (both are fast-acting).
Succinylcholine Reversal (Incorrect Statement)
- You cannot reverse Succinylcholine. The statement “What is given with glycopyrrolate to reverse Succinylcholine? NOTHING, idiot” highlights this crucial point.
Sugammadex: Unique NDMR Reversal Agent
- Specificity: Reverses Rocuronium and Vecuronium ONLY.
- Mechanism: It “engulfs” the paralytic, effectively neutralizing it.
- Timing: Can be given at any time during the block, without needing to wait for a partial recovery or “edge.”
- Class: It is NOT an anticholinesterase.
Inhalation Anesthetics
Reasons Halothane is No Longer Used
- EXAM ALERT: DO NOT ADMINISTER TO MALIGNANT HYPERTHERMIA PATIENTS.
- Cardiac Irritation: Directly irritates the myocardium (heart muscle).
- Arrhythmia Risk: Can induce arrhythmias when combined with epinephrine.
Reasons Isoflurane is Less Commonly Used
- Tourniquet Contraindication: CONTRAINDICATED for use with pneumatic tourniquets.
- CNS Effects: Breaks down the blood-brain barrier (BBB), causing cerebral vasculature to engorge and increasing intracranial pressure (ICP).
- Odor: Has an unpleasant odor, often causing patients to vomit.
Drug of Choice for Inhaled Induction
- Sevoflurane is the preferred inhaled induction agent.
- Advantages: Rapid onset and offset, good for post-operative neurological assessments, has a sweet taste, and is safe for use with pneumatic tourniquets.
List of Inhalation Gas Options (6)
- Volatile (Liquid to Gas): (All typically provide no analgesia)
- Halothane
- Isoflurane
- Sevoflurane
- Ethrane
- Desflurane
- Non-Volatile (Always Gaseous):
- Nitrous Oxide: Provides analgesia.
Inhalation Gas Contraindicated in Seizure Patients
- Ethrane is CONTRAINDICATED in seizure patients as it lowers the seizure threshold in all individuals.
Desflurane: Pros and Cons
- Advantage: FASTEST onset and offset of all inhalation gases. Excellent for ambulatory procedures where rapid discharge is desired.
- Disadvantage: Has a strong, pungent odor and can cause respiratory irritation/spasm, leading to coughing. NOT suitable for neurosurgical patients.
Inhalation Gas to Avoid in Airway Surgery
- Nitrous Oxide should be avoided in airway surgery due to its potential to cause combustion, similar to oxygen.
Post-Operative Considerations with Nitrous Oxide Use
- Patients should receive oxygen in PACU post-operatively, as nitrous oxide displaces oxygen in the lungs.
Waste Anesthetic Gas (WAG) System
- Function: Anesthetic machines use a closed circuit system. Soda lime removes CO2, and the anesthetic gas is recirculated, minimizing waste.
OR Air Exchanges
- The operating room has 20 air exchanges per hour, with 4 of these being with outside air.
Concerns with Patients Exhaling Anesthetic Gas
- PACU Exposure: Patients continue to exhale anesthetic gas in the PACU, which has fewer air exchanges (6 per hour) than the OR. If you can smell the gas, your exposure limits are exceeded.
- Potential Side Effects:
- Headache, irritability, cognitive changes.
- Miscarriage, male and female birth defects, male and female sterility, endometriosis.
- Kidney disease, liver disease, cancer.
- Mitigation: A scavenger system mask can be placed on the patient in recovery.
Malignant Hyperthermia (MH)
Determining MH Risk
- The primary indicator is family history, as MH is an autosomal dominant inherited syndrome.
Individuals Most at Risk for MH
- Family history of MH.
- Scandinavian descent.
- Native American descent.
- Older children/young adults.
- Males (80% of cases).
- Geographic “Hot Spots”: Bay Area California, Wisconsin, North Carolina coast.
Pathophysiology of MH Crisis
- Calcium Release: Calcium is uncontrollably released into the muscle cells (the “door is stuck open”), leading to severe muscle rigidity.
- Mitochondrial Overdrive: Mitochondria are excessively signaled to produce energy, rapidly consuming oxygen and generating massive amounts of heat and CO2 as waste products.
Triggers for MH Episode
Two conditions must be met for an MH episode:
- A genetically susceptible patient.
- Exposure to a triggering agent (Succinylcholine/depolarizing agents, or volatile liquid inhalants).
Earliest Consistent Indicator of MH Crisis
- The rapid and sustained rise in end-tidal CO2 is the earliest and most consistent indicator. (Reflects the intense metabolic activity of mitochondria producing energy, consuming O2, and releasing CO2).
Early vs. Late Indicators of MH Crisis
- Early:
- Rapid rise in CO2 (reflecting metabolic acidosis).
- Jaw tightening (trismus).
- Generalized muscle rigidity (due to calcium release).
- Increased heart rate (tachycardia) (body trying to increase oxygen delivery).
- Increased blood pressure (hypertension) (body trying to increase oxygen delivery).
- Late (Critical Signs):
- Rapid increase in body temperature (a hallmark, but often a late sign).
- Rapid color change in soda lime (due to increased CO2 absorption).
- Decreased SpO2 (hypoxia) (the primary cause of mortality).
- Hyperkalemia (another major cause of mortality from cellular breakdown).
- Myoglobinuria (muscle breakdown, leading to lactic acid production and potential kidney damage).
- Cardiac arrest (resulting from acidosis, hypoxia, and hyperkalemia).
Focus During an MH Episode
- The primary goal is to prevent cardiac arrest by:
- Optimizing oxygenation.
- Correcting acidosis and hyperkalemia (using bicarbonate, calcium, insulin, glucose).
- Managing myoglobinuria (with diuretics and fluids to protect kidneys).
Steps for MH Crisis Management (Comprehensive Protocol)
- Eliminate the Trigger: Immediately stop the triggering agent. Turn off all volatile gases. Flush the anesthesia machine system and change the breathing circuit. Nitrous oxide may be safely used.
- Hyperventilate with Oxygen: Provide 100% oxygen and hyperventilate as rapidly and as much as physiologically possible.
- Call for Expert Consultation: Contact MHAUS (Malignant Hyperthermia Association of the United States) at 1-800-MH-HYPER.
- Administer Dantrolene:
- Dose: 2.5 mg/kg (range 2-3 mg/kg) mixed ONLY with preservative-free sterile water.
- Preparation: Withdraw 60 mL of sterile water, add to the Dantrolene vial, reconstitute, then withdraw and administer.
- Ryanodex: A newer, more concentrated powdered Dantrolene; only requires 1 vial and is more expensive.
- Treat Metabolic Acidosis: Administer intravenous sodium bicarbonate to counteract lactic acidosis and help the liver process it.
- Manage Hyperkalemia: Treat with insulin, glucose/D50 (to prevent hypoglycemia), and calcium (to stabilize cardiac membranes and mitigate cardiac effects of hyperkalemia, such as arrhythmias and QT prolongation).
- Address Myoglobinuria: Administer diuretics and fluids to prevent kidney damage.
- Cool the Patient: Apply ice packs and a cooling blanket. Use iced normal saline IV fluids (avoid LR as it contains potassium and lactate).
- Monitor Labs and ECG: Regularly check electrolytes and perform ECGs for arrhythmias.
- Post-Crisis Care: Transfer the patient to the ICU for prolonged monitoring (longer than 24 hours) as MH can recur.
Dantrolene Dose and Preparation
- Dose: 2.5 mg/kg (2-3 mg/kg).
- Preparation: ONLY mix with preservative-free sterile water. Add 60 mL of sterile water per vial, reconstitute, then draw up and administer.
Average Dantrolene Dose for Adults
- An average adult typically requires 9 vials of Dantrolene, with each vial containing 60 mL.
Hyperkalemia Treatment in MH Crisis
- Insulin.
- Glucose/D50 (to prevent hypoglycemia caused by insulin).
- Calcium (to stabilize the heart and prevent arrhythmias).
Medications to AVOID During MH Crisis
- Calcium Channel Blockers: These are contraindicated because the calcium gates are already “stuck open” and leaking calcium. Calcium channel blockers would only trap more calcium within the cells, worsening the crisis.
Most Effective Ways to Warm a Patient
- Bair Hugger.
- Hot line (fluid warmer).