Neuraxial Flashcards
What is the relationship between cardiac arrest and LA?
Patients may be refractory to treatment because local anesthetic-induced sympathetic nervous system blockade, which decreases circulating blood volume, may also cause a defective neuroendocrine response to stress
What is true about SNS blockade with LA?
Sympathetic nervous system blockade results in arteriolar dilatation but systemic BP does not decrease proportionally because of compensatory vasoconstriction in areas with intact sympathetic nervous system innervation
What is the most important CV response produced by spinal anesthesia?
Most important CV response produced by spinal anesthesia are those that result from changes in the venous circulation
What is the characteristics o the CV response from spinal anesthesia?
Unlike arterioles denervated by sympathetic nervous system blockade, venules do not maintain intrinsic tone and dilate maximally during spinal anesthesia
What is the result of increased vascular capacitance?
decreases venous return to the heart, leading to decreases in cardiac output and systemic BP
What are hypovolemic patients at risk for?
Risk of extreme systemic hypotension in patients who are hypovolemic
What is true regarding blockade of preganglionic cardiac accelerator fibers (T1 to T4) results in?
HR slowing, especially if decreased venous return and central venous pressure decrease stimulation of intrinsic stretch receptors in the right atrium (Bezold Jarisch reflex)
What is true regarding positioning and HR from blockade of T1 and T4?
The HR will increase with a head-down position that increases venous return and central venous pressure so as to stimulate these receptors
What is true about myocardial oxygen consumption?
requirements are decreased as a result of decreased HR, venous return, and systemic BP
What can occur with an excessive level of spinal anesthesia?
Apnea
What does apnea with spinal reflect?
Reflects ischemic paralysis of the medullary ventilatory centers due to profound hypotension and associated decreases in cerebral blood flow
What can produce analgesia when injected intravenously?
Lidocaine and procaine
Why is injection of Lidocaine and procaine limited in?
Use is limited by small margin of safety between IV analgesic doses and those that produce systemic toxicity
What is low dose of lidocaine infusion produce?
(to produce a plasma concentration of 1-2 ug/ml) decreases the severity of postoperative pain and decreases the requirements for opioids without producing systemic toxicity
Lidocaine IV also reduces anesthetic requirements for ________
volatile anesthetics
What is tumescent liposuction?
SQ infiltration of large volumes (5 or more liters) of solution containing highly diluted lidocaine (0.05 to 0.1%)
What is the dose of lidocaine with tumescent liposuction?
When highly diluted lidocaine solutions are administered, the dose of lidocaine may range from 35-55 mg/kg (mega-dose lidocaine)
Large volumes of lidocaine will peak in how many hours?
Slow and sustained release of lidocaine peak 12-14 hours after injection and declines gradually over the next 6-14 hours
What is true about epinephrine with lidocaine for tumescent liposuction?
Epinephrine peaks at 3 hours following injection and returns to normal after about 12 hours
What is high dose of lidocaine used for?
Commonly used in liposuction and reconstructive plastic surgery
What are related to increased mortality associated with tumescent liposuction?
- Lidocaine toxicity
- Local anesthetic-induced depression of cardiac conduction and contractility
What classifies local anesthetics as a ester or amide?
Local anesthetics are classified as ester or amide type based on the linkage between the lipophilic phenyl ring and the hydrophilic tertiary amine
What is the difference between ester or amide LA reflected by?
This difference is reflected in their physiochemical and pharmacokinetic properties
What do local anesthetics bind to?
Local anesthetics bind to voltage gated Na+ channels and block depolarizing Na+ current through these channels
What effects LA speed of onset, potency and duration of action?
Properties such as lipid solubility, protein binding, and pKa of individual local anesthetics affect their speed of onset, potency, and duration of action
What is the characteristics of raising the pH of local anesthetic solutions?
favors the membrane-permeable neutral form and accelerates onset of action
What is true of voltage gated NA+ channels with LA?
Voltage gated Na+ channels transition between resting, activated (open), and inactivated states via coordinated conformational changes
What do LA have a higher affinity for?
the activated and inactivated states than the resting state
The same dose of local anesthetic can result in ____________________
higher plasma concentration and potential for systemic toxicity depending upon the type/location of block
What is the metabolism of ester local anesthetics?
What can increase risk of systemic toxicity with ester LA?
Decreased activity or absence of plasma cholinesterase can increase the risk for systemic toxicity with ester type local anesthetics
What is the metabolism of amide LA?
undergo biotransformation mainly in the liver
What can increase risk of systemic toxicity with amide LA?
Patients with decreased hepatic or renal function have longer elimination times and are at an increased risk for systemic toxicity
What limits the clinical use of la?
systemic and local toxicity of local anesthetics
What is the manifestation of la?
Systemic toxicity manifests primarily in CNS and and cardiovascular effects and local toxicity by nerve degeneration (neurotoxicity)
What is the key components of treatment of LAST?
Lipid emulsion infusion and avoidance of hypoxia and acidosis are recognized as crucial in the treatment of local anesthetic toxicity
What is true about lipid emulsion?
should be available whenever local anesthetics are administered in large doses such as during placement of PNBs and neuraxial blocks
What is neuraxial opioids?
Placement of opioids in the epidural or subarachnoid space to manage acute or chronic pain occurs by diffusion of opioid to mu receptors in substantia gelatinosa of spinal cord
What is neuraxial opioids not associated with?
Analgesia produced by neuraxial opioids not asso. w/sympathectomy, sensory block, or motor block
What is true about opioid epidurals?
undergo uptake into epidural fat, systemic absorption, & diffusion into CSF; produces CSF concentration of drug; penetration into dura influenced by lipid solubility of opioid drug
What is the CSF concentration peak of fentanyl?
20 minutes
What is the CSF concentration peak of sufentanil?
6 minutes
What is the CSF concentration peak of morphine?
1-4 hours
What is the characteristics of the epidural space?
Extensive venous plexus; extensive vascular absorption of opioids
What is the examples of extensive vascular absorption of opioids from the epidural space?
- Blood concentration of fentanyl peak in 5-10 minutes
- Even less time with sufentanil
- Blood concentration of morphine peaks after 10-15 minutes
What decreases systemic absorption of neuraxial opioids?
Epinephrine added to solution w/ LA & opioid placed epidural space decreases systemic absorption
What are the side effects of neuraxial opioids?
Pruritis, urinary retention, sedation
What is the characteristics of pruritis?
caused by cephalad migration of opioid in CSF; interaction w/opioid receptors in trigeminal nucleus
What is the treatment of pruritis?
Tx w/opioid antagonist naloxone
What is a safety issue with neuraxial opioids?
Obstructive sleep apnea
What is OSA?
OSA characterized by recurrent episodes of apnea/hypopnea due to upper airway collapse during sleep
What impact do OSA and opioids have?
Opioids pose risk to OSA patients d/t effects on ventilation
What is true about patients with OSA?
OSA patients have increased sensitivity to respiratory depressant effects of opioids
What is the recommendations for patients with OSA?
minimize amount of opioid; highest risk for postop opioid-induced respiratory depression on 1st postop day; may peak on 3rd postop night & persist up to 7 days
What is the types of depression of ventilation?
Early depression of ventilation and Delayed depression of ventilation
What are the components of early depression of ventilation?
- occurs within 2 hours of neuraxial injection
- d/t systemic absorption of lipid-soluble drug and/or cephalad migration of opioid in CSF
- early depression of vent unlikely w/morphine
What is the medications most commonly associated with early depression of ventilation?
epidural admin of fentanyl or sufentanil
What are the components of delayed depression of ventilation?
occurs more than 2 hours of neuraxial injection; d/t cephalad spread of opioid in the CSF & interaction w/opioid receptors in medulla
What is the medications most commonly associated with delayed depression of ventilation?
Typically involves morphine which occurs 6-12 hours after epidural or intrathecal injection; coughing may affect movement of CSF & increase likelihood of depression of ventilation
________ reliably detects opioid-induced arterial hypoxemia
Pulse oximetry
What is the treatment of hypoxemia of neuraxial opioids?
Supplemental O2 an effective tx for hypoxemia but may mask hypercarbia & significant hypoventilation
What is the most reliable clinical sign of depression of ventilation?
depressed level of consciousness
What is the late sign of hypoventilation, in patients receiving supplemental O2?
hypoxemia
Pulse oximetry of limited value in detection of _______________
opioid-induced respiratory depression
What may need to be done in some situations for neuraxial opioids?
Continuous respiratory rate or carbon dioxide monitoring may be indicated in some settings
