Regional Anesthesia Flashcards
Regional anesthetic techniques
■ epidural and spinal anesthesia (neuraxial anesthesia)
■ peripheral nerve blocks
■ IV regional anesthesia (e.g. Bier block)
What is regional anesthesia
local anesthetic agent (LA) applied around a peripheral nerve at any point along the length of the nerve (from spinal cord up to, but not including, the nerve endings) for the purpose of reducing or preventing impulse transmission
regional anesthesia monitoring required
monitoring should be as extensive as for general anesthesia
benefits of regional anesthesia
- Reduced perioperative pulmonary complications
- Reduced perioperative analgesia requirements
- Decreased PONV
- Reduced perioperative blood loss
- Ability to monitor CNS status during procedure
- Improved perfusion
- Lower incidence of VTE
- Shorter recovery and improved rehabilitation
- Pain blockade with preserved motor function
epidural and spinal anesthesia indication
most useful for sx performed below level of umbilicus
anatomy of spinal/epidural area
- spinal cord extends to L2, dural sac to S2 in adults
- nerve roots (cauda equina) from L2 to S2
- needle inserted below L2 should not encounter cord, thus L3-L4, L4-L5 interspace commonly used
structures penetrated from outside to inside in epidural and spinal anesthesia
■ skin ■ subcutaneous fat ■ supraspinous ligament ■ interspinous ligament ■ ligamentum flavum (last layer before epidural space) ■ dura + arachnoid for spinal anesthesia
landmarking epidural/spinal anesthesia
• Spinous processes should be maximally flexed • L4 spinous processes found between iliac crests • T7 landmark at the tip of the scapula
classic presentation of dural puncture headache
- Onset 6 h-3 d after dural puncture
- Postural component (worse when sitting)
- Occipital or frontal localization
- ± tinnitus, diplopia
Epidural deposition site
LA injected in epidural space (space between ligamentum flavum and dura) Initial blockade is at the spinal roots followed by some degree of spinal cord anesthesia as LA diffuses into the subarachnoid space through he dura
Spinal deposition site
LA injected into subarachnoid space in the dural sac surrounding the spinal cord and nerve roots
Epidural onset
Significant blockade requires 10-15 min
Slower onset of side effects
Spinal onset
rapid blockade onset in 2-5 minutes
Epidural effectiveness
variable
spinal effectiveness
very effective
epidural difficulty
technically more difficult greater failure rate
spinal difficulty
easier to perform due to visual confirmation of csf flow
epidural patient positioning
Position of patient not as important; specific gravity not an issue
spinal patient positioning
hyperbaric LA solution - position of patient important
specific gravity/spread epidural
Epidural injections spread throughout the potential space; specific gravity of solution does not affect spread
dosage epidural
larger volume/dose of LA (usually > toxic IV dose)
spinal dosage
smaller dose of LA required (usually < toxic IV dose)
epidural continuous infusion
use of catheter allows for continuous infusion or repeat injections
continuous infusion epidural
use of catheter allows for continuous infusion or repeat injections
continuous infusion spinal
none
complications epidural
Failure of technique
Hypotension
Bradycardia if cardiac sympathetics blocked (only if ~T2-4 block), e.g. “high spinal”
Epidural or subarachnoid hematoma
Accidental subarachnoid injection can produce spinal anesthesia (and any of the above complications)
Systemic toxicity of LA (accidental intravenous)
Catheter complications (shearing, kinking, vascular or subarachnoid placement) Infection
Dural puncture
complications spinal
Failure of technique
Hypotension
Bradycardia if cardiac sympathetics blocked (only if ~T2-4 block), eg. “high spinal”
Epidural or subarachnoid hematoma
Post-spinal headache (CSF leak)
Transient paresthesias
Spinal cord trauma, infection
combined spinal - epidural
Combines the benefits of rapid, reliabe, intense blockade of spinal anesthesia together with the flexibility of an epidural catheter
Absolute contraindications to spinal/epidural anesthesia
■ lack of resuscitative drugs/equipment
■ patient refusal
■ allergy to local anesthetic
■ infection at puncture site or underlying tissues
■ coagulopathies/bleeding diathesis
■ raised ICP
■ sepsis/bacteremia
■ severe hypovolemia
■ cardi c lesion with fixed output states (severe mitral/aortic stenosis)
■ lack of IV access
Relative contraindications to spinal/epidural anesthesia
■ pre-existing neurological disease (demyelinating lesions)
■ previous spinal surgery, severe spinal deformity
■ prolonged surgery
■ major blood loss or maneuvers that can compromise reaction
Peripheral nerve block procedure
- deposition of LA around the target nerve or plexus
- ultrasound guidance and peripheral nerve stimulation (needle will stimulate target nerve/plexus) may be used to guide needle to target nerve while avoding neural trauma or intraneural injection most major nerves or nerve plexi can be targeted (brachial plexus block, femoral nerve block, sciatic nerve block, etc.)
- performed with standard monitors
risk of late neurologic injury
approximately 2-4 per 10,000 risk of late neurologic injury
what must be available during peripheral nerve blocks
resuscitation equipment
Absolute contraindications to peripheral nerve blockade
■ allergy to LA
■ patient refusal
Relative contraindications to peripheral nerve blockade
■ certain types of pre-existing neurological dysfunction (e.g ALS, MS, diabetic neuropathy)
■ local infection at block site
■ bleeding disorder
Definition and mode of action of local anesthetics
- LA are drugs that block the generation and propagation of impulses in excitable tissues: nerves, skeletal muscle, cardiac muscle, brain
- LA bind to receptor on the cytosolic side of the Na+ channel, inhibiting Na+ flux and thus blocking impulse conduction
- different types of nerve fibres undergo blockade at differen rates
Absorption, distribution, metabolism of local anesthetics
- LA readily crosses the blood-brain barrier (BBB) once absorbed into the bloodstream
- ester-type LA (procaine, tetracaine) are broken down by plasma and hepatic esterases; metabolites excreted via kidneys
- amide-type LA (lidocaine, bupivicaine) are broken down by hepatic mixed-function oxidases (P450 system); metabolites excreted via kidney
Selection of local anesthetic is based on
■ onset of action: influenced by pKa (the lower the pKa, the higher the concentration of the base form of the LA, and the faster the onset of action)
■ duration of desired effects: influenced by protein binding (longer duration of action when protein binding of LA is strong)
■ potency: influenced by lipid solubility (agents with high lipid solubility penetrate the nerve membrane more easily)
■ unique needs (e.g. sensory blockade with relative preservation of motor function by bupivicaine at low doses)
■ potential for toxicity
Local anesthetic systemic toxicity CNS effects
• CNS effects first appear to be excitatory due to initial block of inhibitory fibres, then subsequent block of excitatory fibres
• effects in order of appearance ■ numbness of tongue, perioral tingling, metallic taste ■ disorientation, drowsiness ■ tinnitus ■ visual disturbances ■ muscle twitching, tremors ■ unconsciousness ■ convulsions, seizures ■ generalized CNS depression, coma, respiratory arrest
CVS effects local anesthetic toxicity
- vasodilaton, hypotension
- decreased myocardial contractility
• dose-dependent delay in cardiac impulse transmission
■ prolonged PR, QRS intervals
■ sinus bradycardia
• CVS collapse
occurs after CNS effects
Treatment of local anesthetic systemic toxicity
- early recognition of signs, get help
- 100% O2, manage ABCs
- diazepam
- manage arrhythmias
- Intralipid® 20% to bind local anesthetic in circulation
Where not to use local anesthetic with epinephrine
ears, fingers, toes, penis nose
local infiltration procedure and use
- injection of tissue with LA, producing a lack of sensation in the infiltrated area due to LA acting on nerves
- suitable for small incisions, suturing, excising small lesions
- can use fairly large volumes of dilute LA to infiltrate a large area
- low concentrations of epinephrine (1:100,000-1:200,000) cause vasoconstriction, thus reducing bleeding and prolonging the effects of LA by reducing systemic absorption
Fracture hematoma block description, procedure
- special type of local infiltration for pain control during manipulation of certain fractures
- hematoma created by fracture is infiltrated with LA to anesthetize surrounding tissues
- sensory blockade may only be partial
- no muscle relaxation
topical anesthetics
- various preparations of local anesthetics available for topical use, may be a mixture of agents (EMLA cream is a combination of 2.5% lidocaine and prilocaine)
- must be able to penetrate the skin or mucous membrane
Common post-op anesthetic complications
Uncontrolled/Poorly Controlled Pain
Nausea and Vomiting
• hypotension and bradycardia must be ruled out
• pain and surgical manipulation also cause nausea
• often treated with dimenhydrinate (Gravol®), metoclopramide (Maxeran®; not with bowel obstruction) prochlorperazine (Stemetil®), ondansetron (Zofran®) granisetron (Kytril®)
Confusion and Agitation
• ABCs first confusion or agitation can be caused by airway obstruction, hypercapnea, hypoxemia
• neurologic status (Glasgow Coma Scale, pupils), residual paralysis from anesthetic
• pain, distended bowel/bladder
• fear/anxiety/separation from caregivers, language barriers
• metabolic disturbance (hypoglycemia, hypercalcemia, hyponatremia – especially post-TURP)
• intracranial cause (stroke, raised intracranial pressure) drug effect (ketamine, anticholinergics, serotonin)
• elderly patients are more susceptible to post-operative delirium
Respiratory Complications
• susceptible to aspiration of gastric contents due to PONV and unreliable airway reflexes
• airway obstruction (secondary to reduced muscle tone from residual anesthetic, soft tissue trauma and edema, or pooled secretions) may lead to inadequate ventilation, hypoxemia, and hypercapnia
• airway obstruction can often be relieved with head tilt, jaw elevation, and anterior displacement of the mandible. If the obstruction is not reversible, a nasal or oral airway may be used
Hypotension
• must be identified and treated quickly to prevent inadequate perfusion and ischemic damage
• reduced cardiac output (hypovolemia, most common cause) and/or peripheral vasodilation (residual anesthetic agent)
• first step in treatment is usually the administration of fluids ± inotropic agents
Hypertension
• pain, hypercapnia, hypoxemia, increased intravascular fluid volume, and sympathomimetic drugs can cause hypertension
• sodium nitroprusside or β-blocking drugs (e.g. esmolol and metoprolol) can be used to treat hypertension
Risk factors for post-operative nausea and vomiting (PONV)
- Young age
- Female
- History of PONV
- Non-smoker
- Type of surgery: ophtho, ENT, abdo/pelvic, plastics
- Type of anesthetic: N2O, opioids, volatile agents
Pain and nociception definitions
- pain: perception of nociception, which occurs in the brain
- nociception: detection, transduction, and transmission of noxious stimuli
Pain classifications
- temporal: acute vs. chronic
* mechanism: nociceptive vs. neuropathic
Acute pain
- pain of short duration (<6 wk) usually associated with surgery, trauma, or acute illness; often associated with inflammation
- usually limited to the area of damage/trauma and resolves with healing
Acute pain mechanism
- tissue damage by thermal, chemical, mechanical forces
- nociceptors detect pain stimulus
- 1st order neuron
- dorsal horn of spinal cord
- 2nd order afferent neuron
- STT
- ventral posterior lateral nucleus of thalamus
- 3rd order afferent neuron
- sensory cortex
Modulatory neurons in the acute pain mechanism release
endorphins, enkephalins, NE, serotonin, GABA
these inhibit release of substance P or make post-synaptic membrane more difficult to polarize
WHO analgesia ladder
non opioid (ex. NSAID) +/- non opioid, +/- adjuvant
opioid for mild to moderate pain (ex. codeine) +- non opioid, +/- adjuvant
opioid for moderate to severe pain (ex. morphine) +- non-opioid, +/- adjuvant
Pharmacological management of acute pain
• ask the patient to rate the pain out of 10, or use visual analog scale, to determine severity • pharmacological treatment guided by WHO analgesia ladde
Patient controlled analgesia (PCA)
■ involves the use of computerized pumps that can deliver a constant infusion and bolus breakthrough doses of parenterally-administered opioid analgesics
■ limited by lockout intervals
■ most commonly used agents: morphine and hydromorphone
Cautionary use of NSAIDs in patients with
asthma
coagulopathy
GI ulcers
renal insufficiency
pregnancy, 3rd trimester
Acetaminophen indications
First-line for mild acute pain
Acetaminophen moa
Unclear, hypothesized cyclooxygenase-2 (COX-2) inhibition Unclear, hypothesized modulation of endogenous cannabinoid system
Acetaminophen dosing/administration
Limited by analgesic ceiling beyond which there is no additional analgesia Opioid-sparing Max dose of 4 g/24 h
Acetaminophen side effects/toxicity
Considered relatively safe Liver toxicity in elevated doses
NSAIDs examples
Aspirin®, ibuprofen, naproxen, ketorolac (IV)
NSAIDs indications
Mild-moderate pai
NSAIDs MOA
Non-selective COX-1 and 2 inhibition reducing proinflammatory prostaglandin synthesis
NSAIDs dosing/administration
Limited by analgesic ceiling beyond which there is no additional analgesia Opioid-sparing Significant inter-individual variation in efficacy
NSAIDs side effects/toxicity
Gastric ulceration/bleeding Decreased renal perfusion Photosensitivity Premature closure of the ductus arteriosus in pregnancy
opioids examples
naproxen, ketorolac (IV)
Oral: codeine, oxycodone, morphine, hydromorphone
Parenteral: morphine, hydromorphone, fentanyl
opioids indications
Oral: moderate acute pain
Parenteral: moderatesevere acute pain
opioids moa
dampens nociceptive transmission between 1st and 2nd order neurons in the dorsal horn 2nd order neurons in the dorsal horn
Activates ascending modulatory pathways resulting in release of inhibitory neurotransmitters
Inhibits peripheral inflammatory response and hyperalgesia
Affects mood and anxiety – alleviates the affective component of perceived pain
opioids dosing/administration
No analgesic ceiling (except for codeine)
Can be administered intrathecally (spinal block) or by continuous infusion
opioids side effects/toxicity
Respiratory depression
Constipaton and abdominal pain
Sedaton
N/V
Pruritus
Confusion (particularly in the elderly)
Dependence
Opioid conversion morphine IV to PO
10 mg IV = 30 mg PO
Opioid conversion hydromorphone IV to PO
2 mg IV = 4 mg PO
Codeine IV to PO dosing
120 mg IV to 200 mg PO
Fentynal IV to PO dosing
100 ug IV to NA PO
Oxycodone IV to PO dosing
N/A IV to 20 mg PO
Common side effects of opioids
- N/V
- Constipation
- Sedation
- Pruritus
- Abdominal pain
- Urinary retention
- Respiratory depression
when prescribing opioids, consider
- Breakthrough dose
- Anti-emetics
- Laxative
PCA parameters
loading dose
bolus dose
lockout interval
continuous infusion (optional)
max 4 hour dose (limit)
advantages of PCA
- Improved patient satisfaction
- Fewer side effects
- Accommodates patient variability
- Accommodates changes in opioid requirements
Codeine relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
200 mg PO
15-30 mg PO
late 30-60 min
moderate 4-6 h
primarily post-op use
not for IV use
Meperidine (Demerol) relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
75 mg IV
2-3 mg/kg IV
moderate 10 min
moderate 2-4 h
anticholinergic, hallucinations, less pupillary constriction than morphine, metabolite build up may cause seizures
morphine relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
10 mg IV, 20 mg PO
- 2-0.3 mg/kg IV
- 4-0.6 mg/kg PO
moderate 5-10 min
moderate 4-5 h
histmaine release leading to decrease in BP
oxycodone controlled release oxyneo relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
15 mg PO
10-20 mg PO (no IV)
late 30-45 min
long 8-12 h
do not split, crush or chew tablet
oxycodone regular tablet (oxy IR) relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
15 mg PO (no IV)
5-15 mg PO
moderate 15 mins
modertate 3-6 h
percocet = oxycodone 5 mg + acetaminophen 325 mg
hydromorphone (Dilaudid) relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
2 mg IV 10 mg PO
40-60 ug/kg IV
2-4 mg PO
moderate 15 mins
moderate 4-5 h
Fentanyl relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
100 ug IV
2-3 ug/kg IV
Rapid <5 min
short 0.5-1h
transient muscle rigidity in very high doses
remifentanil relative dose to 10 mg morphine IV
moderate dose
onset
duration
special consideration
100 ug IV
0.5-1.5 ug/kg IV
rapid (1-3 mins)
ultra short <10 mins
only use during induction and maintenance of anesthesia
PCA vs conventional opioid analgesia for post-op pain
PCA is more effective than standard as-needed administration for reducing post-operative pain. However, patients using PCA consume more opioids overall and have more pruritus
Opioid antagonists
naloxone and naltrexone
opioid antaongists indication
opioid overdose (manifests primarily at CNS, e.g. respiratory depression)
opioid antaongists moa
competitively inhibit opioid receptors, predominantly µ receptors
■ naloxone is short-acting (t1/2 = 1 h); effects of narcotic may return when naloxone wears off; therefore, the patient must be observed closely following its administration
■ naltrexone is longer-acting (t1/2 = 10 h); less likely to see return of opioid effects
opioid antaongists side effects
relative overdose of naloxone may cause nausea, agitation, sweating, tachycardia, hypertension, re-emergence of pain, pulmonary edema, seizures (essentially opioid withdrawal)
epidural vs non epidural or no analgesia in labour
While epidural analgesia appears effective for pain control during labour, it places women at an increased risk of an instrumental delivery, and is not associated with significant differences in C-section risk, maternal pain relief satisfaction long-term back ache or Apgar scores.
chronic pain
• chronic pain: greater than 3 mo, or recurrent pain that occurs at least 3 times throughout three month period
- pain of duration or intensity that persists beyond normal tissue healing and adversely affects functioning
- may have nociceptive and neuropathic components; dysregulation of analgesic pathways implicated
periop management of chronic pain
• in the perioperative period, consider continuing regular long-acting analgesics and augmenting with regional techniques, adjuvants, additional opioid analgesia and non-pharmacological techniques
airway anesthesia considerations in pregnancy
possible difficult airway as tissues becomes edematous and friable especially in labour
resp anesthesia considerations in pregnancy
decreased FRC and increased O2 consumption cause more rapid desaturation during apnea
CVS anesthesia considerations in pregnancy
■ increased blood volume > increased RBC mass results in mild anemia
■ decreased SVR proportionately greater than increased CO results in decreased BP
■ prone to decreased BP due to aortocaval compression – therefore for surgery, a pregnant patient is positioned in left uterine displacement using a wedge under her right flank
CNS anesthesia considerations in pregnancy
■ decreased MAC due to hormonal effects
■ increased block height due to engorged epidural veins
GI anesthesia considerations in pregnancy
■ delayed gastric emptying
■ increased volume and acidity of gastric fluid
■ decreased LES tone
■ increased abdominal pressure
■ combined, these lead to an increased risk of aspiration – therefore for surgery, a pregnant patient is given sodium citrate 30 cc PO immediately before surgery to neutralize gastric acidity
options for analgesia during labour
• psychoprophylaxis – Lamaze method
■ patterns of breathing and focused attention on fixed object
• systemic medication
■ easy to administer, but risk of maternal or neonatal respiratory depression
■ opioids most commonly used if delivery is not expected within 4 h
• inhalational analgesia
■ easy to administer makes uterine contractions more tolerable, but does not relieve pain completely
■ 50% nitrous oxide
• neuraxial anesthesia
■ provides excellent analgesia with minimal depressant effects
■ hypotension is the most common complication
■ maternal BP monitored q2-5min for 15-20 min after initiation and regularly thereafter
■ epidural usually given as it preferentially blocks sensation, leaving motor function intact
options for analgesia during c section
- neuraxial: spinal or epidural
* general: used if contraindications or time precludes regional blockade
nociceptive pathways in labour and delivery
Labour
• Cervical dilation and effacement stimulates visceral nerve fibres entering the spinal cord at T10-L1
Delivery
• Distention of lower vagina and perineum causes somatic nociceptive impulses via the pudendal nerve entering the spinal cord at S2-S4
peds resp system anatomical differences
large head, short trachea/neck, large tongue, adenoids, and tonsils
■ narrow nasal passages (obligate nasal breathers until 5 mo)
■ narrowest part of airway at the level of the cricoid vs. glottis in adults
■ epiglottis is longer, U shaped and angled at 45º; carina is wider and is at the level of T2 (T4 in adults)
resp system physiologic differences in peds
■ faster RR, immature respiratory centres which are depressed by hypoxia/hypercapnea (airway closure occurs in the neonate at the end of expiration)
■ less oxygen reserve during apnea – decreased total lung volume, vital and functional reserve capacity together with higher metabolic needs
■ greater V/Q mismatch – lower lung compliance due to immature alveoli (mature at 8 yr)
■ greater work of breathing – greater chest wall compliance, weaker intercostals/diaphragm, and higher resistance to airflow
CVS system
- blood volume at birth is approximately 80 mL/kg; transfusion should be started if >10% of blood volume lost
- children have a high HR and low BP
- CO is dependent on HR, not stroke volume because of low heart wall compliance; therefore, bradycardia severe compromise in CO
temperature regulation in peds
- vulnerable to hypothermia
- minimize heat loss by use of warming blankets, covering the infant’s head, humidification of inspired gases, and warming of infused solutions
CNS anesthesia differences in peds
- MAC of halothane is increased compared to the adult (0.75% adult, 1.2% infant, 0.87% neonate)
- NMJ is immature for the first 4 wk of life and thus there is an increased sensitivity to non-depolarizing relaxants
- parasympathetics mature at birth, sympathetics mature at 4-6 mo thus autonomic imbalance
- infant brain is 12% of body weight and receives 34% of CO (adult: 2% body weight and 14% CO)
glucose maintenance in infants
- infants <1 yr can become seriously hypoglycemic during pre-operative fasting and post-operatively if feeding is not recommenced as soon as possible
- after 1 yr, children are able to maintain normal glucose homeostasis in excess of 8 h
pharmacology infants
- higher dose requirements because of higher TBW (75% vs. 60% in adults) and greater volume of distribution
- barbiturates/opioids more potent due to greater permeability of BBB
• muscle relaxants
■ non-depolarizing
◆ immature NMJ, variable response
■ depolarizing
◆ must pre-treat with atropine or may experience profound bradycardia and/or sinus node arrest due to PNS > SNS (also dries oral secretions)
◆ more susceptible to arrhythmias, hyperkalemia, rhabdomyolysis, myoglobinemia, masseter spasm and malignant hyperthermia
To increase alveolar minute ventilation in neonates you must
increase resp rate, not tidal volume
neonate resp rate
30-40 breaths/min
age 1-13 resp rate
24 - age/2 breaths/min
ETT sizing in peds
diameter mm of tracheal tube in children after 1 year = age/4+4
length cm of tube = age/2 + 12
Malignant hyperthermia pathophysiology and incidence
hypermetabolic disorder of skeletal muscle
- due to an uncontrolled increase in intracellular Ca2+ (because of an anomaly of the ryanodine receptor which regulates Ca2+ channel in the sarcoplasmic reticulum of skeletal muscle)
- autosomal dominant inheritance
- incidence of 1-5 in 100,000, may be associated with skeletal muscle abnormalities such as dystrophy or myopathy
anesthetic drugs triggering MH include
all inhalational agents except nitrous oxide
depolarizing muscle relaxants: SCh
clinical picture MH
• onset: immediate or hours after contact with trigger agent ■ increased oxygen consumption ■ increased ETCO2 on capnograph ■ tachycardia/dysrhythmia ■ tachypnea/cyanosis ■ diaphoresis ■ hypertension ■ increased temperature (late sign)
• muscular symptoms
■ trismus (masseter spasm) common but not specific for MH (occurs in 1% of children given SCh with halothane anesthesia)
■ tender, swollen muscles due to rhabdomyolysis
■ trunk or total body rigidity
signs of MH unexplained raise in ETCO2 increase in minute ventilation tachycardia rigidity hyperthemia (late sign)
Complications MH
- coma
- DIC
- rhabdomyolysis
- myoglobinuric renal failure/hepatic dysfunction
- electrolyte abnormalities (e.g. hyperkalemia) and secondary arrhythmias
- ARDS
- pulmonary edema
- can be fatal if untreated
MH prevention
- suspect MH in patients with a family history of problems/death with anesthetic
- avoid all trigger medications, use vapour free equipment, use regional anesthesia if possible
- central body temp and ETCO2 monitoring
MH management
- notify surgeon, discontinue volatile agents and succinylcholine, hyperventilate with 100% oxygen at flows of 10 L/min or more, halt the procedure as soon as possible
- dantrolene 2.5 mg/kg IV, through large-bore IV if possible
■ repeat until there is control of signs of MH; up to 30 mg/kg as necessary - bicarbonate 1-2 mEq/kg if blood gas values are not available for metabolic acidosis
- cool patients with core temperature >39ºC
■ lavage open body cavities, stomach, bladder, rectum; apply ice to surface; infuse cold saline IV
■ stop cooling if temperature is <38ºC to prevent drift to <36ºC - dysrhythmias usually respond to treatment of acidosis and hyperkalemia
■ use standard drug therapy except Ca2+ channel blockers as they may cause hyperkalemia and cardiac arrest in presence of dantrolene - hyperkalemia
■ treat with hyperventilation, bicarbonate, glucose/insulin, calcium
■ bicarbonate 1-2 mEq/kg IV, calcium chloride 10 mg/kg or calcium gluconate 10-50 mg/kg for lifethreatening hyperkalemia and check glucose levels hourly - follow ETCO2, electrolytes, blood gases, creatine kinase (CK), core temperature, urine output/colour with Foley catheter, coagulation studies
■ if CK and/or potassium rises persistently or urine output falls to <0.5 mL/kg/h, induce diuresis to >1 mL/kg/h urine to avoid myoglobinuric renal failure - maintain a esthesia with benzodiazepines, opioids, and propofol
- transfer to ICU bed
basic principles of MH management “Some Hot Dude Better Get Iced Fluids Fast” Stop all triggering agents, give 100% O2 Hyperventilate Dantrolene 2.5 mg/kg every 5 min Bicarbonate Glucose and insulin IV fluids; cool patient to 38ºC Fluid output; consider furosemide Tachycardia: be prepared to treat VT
Abnormal pseudocholinesterase
- pseudocholinesterase hydrolyzes SCh and mivacurium
- individuals with abnormal pseudocholinesterase will have prolonged muscular blockade
- SCh and mivacurium are contraindicated in those with abnormal pseudocholinesterase
- if SCh or mivacurium are given accidentally, treat with mechanical ventilation until function returns to normal (do not use cholinesterase inhibitors rebound neuromuscular blockade once drug effect is terminated)
Difficult tracheal intubation in unconscious patient algorithm
A29
difficult tracheal intubtation approach
A 30
ACLS adult cardiac arrest
A31
Adult tachycardia with pulse ACLS
A32
Adult bradycardia with pulse ACLS
A32
