Lecture 4: Anesthesiology Flashcards
Brief history:
- Who and when is anesthesia denoted?
- Who is the father of anesthesia?
- What was used first on patients? when and by who?
Brief history:
* What people did the local and regional?
* What was first used IV?
- Local and Regional: Gaedicke (1855), Niemann (1860), Koller & Halsted (1884), Bier (1898), Pages (1921) & Dogliotti (1931)
- Intravenous: Barbiturates were first followed by benzodiazepines, ketamine, etomidate, then propofol (1986)
What is anesthesia per holmes?
denotes the state that incorporates amnesia, analgesia, and narcosis to make painless surgery possible.
How does anesthesia work?
What does inhalational agents interact with? What receptors do they work on?
Inhalational agents: interaction with ion channels in CNS and PNS
* Excitatory receptors of the brain (NMDA)
* GABA receptors
* Protein receptors that block excitatory channels or promote inhibitory channels
* Non-specific membrane effects
Bottled/gas state
What is general anesthesia?
an altered physiological state characterized by reversible loss of consciousness, analgesia, amnesia, and some degree of muscle relaxation.
How does anesthesia effect the brain and CNS?
Effects on brain areas & throughout CNS
* RAS, cerebral cortex, cuneate nucleus, olfactory cortex, hippocampus
* Spinal cord: dorsal horn excitatory transmission depression
* Suppression of purposeful withdrawal: spinal cord and brain stem
Measuring Anesthetic Depth
* What are MAC values?
* Mirror what?
Mininum Alveolar Concentration (MAC) Values
* The alveolar concentration that prevents movement in 50% of patients in response to a standardized stimulus (i.e. surgical incision)
* ”mirrors” brain partial pressures
MAC:
* 1.3 MAC=
* 0.4-0.3=
* what is the decrease in MAC per decade of age?
- 1.3 MAC = prevents movement in 95% of patients (ED95)
- 0.3-0.4 MAC = awakening from anesthesia (MAC awake)
- 6% decrese in MAC per decade in age
- RASS score: -5 is appropriated to general anesthesia
- RASS will be utilized when sedating an intubated patient. Genereally target sedation will be a RASS of -3 to -5
What MAC score is needed for hip fx of 85yo? Marijana use in 25yo?
Hip: 0.4
Maijuana: 1.3
How does anesthesia work?
- Inhalational? What is inspiratory concentration and alveloar concentration?
Inhalational: achieving therapeutic tissue concentrations in the CNS
* Inspiratory concentration (Fi)
* Gas concentration: rate of gas flow, breathing circuit volume, circuit absorption
Alveolar concentration (FA)
* Partial pressures of anesthetic in blood stream -> to the brain
What are 3 factors that affect how anesthetic agents work?
- Solubility in the blood: The more soluble the anesthetic agent, the less it is taken up by the blood->i.e. Nitrous Oxide (soluble) –> alveolar concentration of nitrous oxide rises faster than that of halothane so induction of anesthesia is faster
- Alveolar blood flow
- Difference of partial pressure between alveolar gas and venous blood
What are the different volatile agents?
- Nitrous oxide
- Halothane
- Isoflurane
- Desflurance- Fastest
- Sevoflurane: MC used and MC in peds because of rapid onset and the desflurane causes airway irritation
Coefficient: lower the number= faster
Maligenany hyperthermia:
* Common or rare?
* MC where?
* Increased risk in who/?
* Triggered by what?
* Can present more than what?
Musculoskeletal diseases: central-core disease, multi-minicore myopathy, King-Denborough syndrome
Malignant Hypertheria:
* What is released? What does it cause?
Ryanodine Receptor
Malignany hyperthermia:
* What are the earliest signs? What is a late sign?
What are compliactions of malignant hyperthermia?(5)
Treatment for MH
* What do you need to stop? What do you turn on?
* GIve what immediately? What is the dosing?
- Dantrolene must be mixed with ONLY sterile water
- Fairly safe drug, used to also treat thyroid storm and neuroleptic malignant syndrome (NMS)
- Give through central line if possible due to risk of phlebitis in peripheral IV’s
MH treatment:
* Metabolic acidosis?
* Hyperkalemia?
* Arrthythmias?
* Fever?
- Metabolic acidosis: Sodium Bicarbonate 1-2 mEq/kg
- Hyperkalemia : Dextrose 25-50g IV, Regular Insulin 10-20 units IV, Calcium Chloride (10 mg/kg) or Calcium Gluconate (30 mg/kg)
- Arrhythmias: avoid calcium channel blockers.
- Fever: Cooling measures (lavage, cooling blanket, cold IV solution)
Anestheia Machine:
* What is CO2 absorber?
* What are vaporizers?
* What scavenfging connector?
- CO absorber: prevents reinhalation of CO2
- Vaporizes: inhalations meds loaded here
- Scavenging: Gets rid of inhalation gases
how does the flow of gases work?
What do you need to continuously monitor?
- Electrocardiogram
- Pulse Oximetry
- Non-invasive Blood Pressure
- Temperature
- End-tidal CO2 Wave Capnography
- Urinary Output
- Blood Loss
- Peripheral Nerve Stimulation
- OR vs ER… considerations are the same. Any sedated patient should have continuous EKG monitor, pulse ox, BP, and co2 monitoring….This is a standard or care.
- This would apply for procedural sedation such as joint reduction, laceration repair, or any aggigitated patient.
What are the IV anestethics?
What are the examples of barbitutes? Benzo?
* What is the reversal agent of benzo?
Barb: Thiopental, phenobarbital
Benzo: Midazolam, lorazepam, diazepam
* Reveral agent: :flurmazelil
What are the examples of opiods? What is the antagonist?
IV medications:
* What are the neuromuscular blockade agents?
- Depolarizing: succinylcholine
- Non-Depolarizing: Rocuromiun (Pop dt reversal agent) and Cisatracurium (Good for renal disease)
Works on the Ach receptors
* Normal neuromuscular transmission depends on ACh (Acetylcholine) binding to nicotinic cholinergic receptors on motor-end plate.
fill in for IV medicaitons special considerations?
What are the indications for RSI?
What are the choice of neuromusclar blockade (paralytic)
Succinylcholine – avoid in hyperkalemia, renal failure
* difficult airways, difficult ventilation
Rocuronium – longer acting, longer onset
* helpful for patients who are easy to bag mask and ventilate in case of a “can’t intubate” scenario
Intravenous Medications NM blockade reveral agents:
* Anticholinesterases:
* Non-classic Reveral agents:
* Anticholinergics:
Cholinergic side effects = SLUDGE – Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress, Emesis
-cholinesterase inhibitors (Anticholinesterases) indirectly increase the amount of acetylcholine available to compete with nondepolarizing agent – thereby reestablishing neuromuscular transmission
Glycopyrrolate (quarternary amine) is used bc it cannot cross blood brain barrier and does not affect CNS or ophthalmic activity
-also has a longer duration of action than atropine (2-4hrs vs 30 mins)
Atropine and Scopolamine (Tertiary amine) cross the blood brain barrier.
What are the adrenergic agonists and antagonists?
Quick and dirty in the ED (first response drug) will be Norepinephrine (Levophed)
What are the anti-hypertensive agents?
- Nitro: CHF patients
- BB: avoid in Ashtma/COPD
- Calcium channel blocker: good for A-fib RVR - cardizem, HTN emergency - cardene
Local anesthetics:
* Bind to what? What do they prevent and inhibit?
- With high enough local anesthetic concentrations, and enough bound to Na channels, an action potential cannot be generated and impulse propogation is abolished.
- Local anesthetics have a greater affinity for the Na channel in the open or inactive state than in a resting state
Local anesthetics:
* Sensitivity to nerve fibers is determined by what?
How does local anesthegia work?
bind to Na channels
Local anesthetics:
* What affects the onset?
Onset: lipid solubilty and its pKa
* Less potent, less lipid-soluble agents generally have a faster onset than the more potent, more lipid soluble agents
* Adding epinephrine/sodium bicarb speeds the onset and improves quality of block
LA’s with a pKa closest to physiological pH (~7.4) will have a more rapid onset of action.
LA:
How is durations affected? what about systemic absorption?
- Esters – metabolized by pseudocholinesterase
- Procaine – metabolized to PABA (p-aminobenzoic acid) which has been associated with rare anaphylactic reactions
Local Anesthetic Systemic Toxicity (LAST)
* What has additive toxic effects?
* Effects seen where?
- Mixing local anesthetics can have additive toxic effects
- Effects seen in all organ systems
Local Anesthetic Systemic Toxicity (LAST)
* What happens neurological?
Neurological: pre-monitory signs of increased blood concentrations in awake patients
* Circumoral numbness, tongue paresthesia, dizziness, tinnitus, blurred vision
* Restlessness, agitation, nervousness, feeling of “impending doom”
* Muscle twitching -> tonic-clonic seizures
* Coma, respiratory depression and/or arrest
Cocaine:
* What happens at first? Overdose?
* How can toxicity be treated?
* Cauda equina syndrome use what?
* Neurotoxicity lower when using what?
- Cocaine – euphoria with initial CNS stimulation overdose: restlessness, emesis, tremors, convulsions, arrhythmias, respiratory failure, cardiac arrest
- Cocaine toxicity can treated with intralipid
- Cauda equina syndrome – use of 5% lidocaine for spinal anesthesia
- Neurotoxicity lower when using ropivacaine or bupivacaine for intrathecal injection
LAST:
* What happens with cardiovasular?
Cardiovascular: all local anesthetics depress myocardial automaticity
* High concentrations – smooth muscle relaxation; arteriolar vasodilation
* Low concentrations – vasoconstriction; inhibition of nitric oxide
Accidental intravenous injection of bupivacaine can cause severe CV toxicity: LV depression, AV blocks, V-tach, V-fib
Local Anesthetic Systemic Toxicity (LAST):
* Major CV toxicity requires what?
* What is with CNS excitation?
* What is most cardiotoxic?
* Cocaine=
Major CV toxicity requires about 3x the amount required to produce seizures
* Tachycardia and hypertension with CNS excitation
* Bupivacaine = most “cardiotoxic”
* Cocaine = arrhythmias treat with adrenergic and Ca2+ channel antagonists
What is the txt of LAST?
Rapidly give 1.5 mL/kg bolus of 20% Intralipid IV
* Start an infusion at 0.25 mL/kg/min
* May repeat loading dose (max 3 total doses). May increase infusion rate (max 0.5 mL/kg/min).
Propofol CANNOT be used in place of Intralipid. Benzodiazepines like midazolam can be used to treat seizures.
Where can all the regional anestheia fo?
Epidural Blood Patches
* What can happen after?
* When do you see this?
* Don’t repeat spinal/epidural attempt after what? Why?
What do you do for epidural blood patches?
Injecting patient’s own blood into epidural space (20-30 mL)
* Inject close to initial puncture site if possible
* Slow injection, pressure and discomfort is normal
- How do you dx CSF leak?
- Must fail conservative treatments before what?
- Diagnosis: headache improves after laying down
- Must fail conservative treatments before anesthesia involvement
* Caffeine, hydration (Gatorade), Ibuprofen
Preoperative assessment:
* What is the anesthetic plan?
fill in for ASA class
What is the NPO status?
(8 hours full meal, 6 hours light meal, 4 hours full liquids, 2 hours clear liquids)
Some ”stable appendix” for example can wait 8 hours to achieve appropriate NPO status vs. “emergent perforated viscous”, NPO status matters less.
What are all the other issues you need to review ofor preoperative assessment?
What is the postopertive care?
Explain where all the CN nerves are down the airway?
What are the mallampati classes?
What position do you need the patient in for MAC blade?
What are the two types of airways?
- Nasal Airway – risk of epistaxis with patients taking anticoagulants
- Oral Airway – multiple sizes
What is a suprgolttic airway device? What are the variations?
Supraglottic Airway Device – Laryngeal Mask Airway (LMA)
Variations in LMA design:
* ProSeal LMA – permits passage of a gastric tube to decompress the stomach
* I-Gel – gel occluder rather than an inflatable cuff
* Fastrach intubation LMA – facilitates endotracheal intubation through the LMA device
* LMA CTrach – incorporates a camera to help facilitate passage of an endotracheal tube
What is important to remember about the ET tube?
KEEP the pilot balloon inflated
What are the different laryngoscope blades?
What are different scopes that are anticipated for difficulat airways?
When can you not ventilate pt?
Cannot vent pt with bag mask after sedation
What are the surgical airways?
IV access:
* What is prefered in OR?
* What is last line due to infections? What can you do with this?
Risks with CVL – line infection, blood stream infection, air of thrombus embolism, arrhythmias, hematoma, pneumothorax, hemothorax, hydrothorax, chylothorax, cardiac perforation, cardiac tamponade, trauma to nearby nerves and arteries, thrombosis
Contraindications to CVL
* What are the relative
Tumors, Clots, Tricuspid Valve Vegetations
* Related to Cannulation Site:
* Subclavian Vein – patients receiving anticoagulants, greater risk of pneumothorax
* Site of previous Carotid Endarterectomy
* Presence of other central catheters or pacemaker leads
What is there an increased risk when Left sided IJ IV access? Femoral?
Left-sided IJ Vein
* Increased risk of pleural effusion and chylothorax
Femoral Vein
* Increased risk of line-related sepsis
How do you find the Internal jug vein?
How do you place a right internal jugluar can?
Pulmonary artery cath:
* What catheter is used?
* What can you measure? What does it guide and measure?
- SV high, SVR low = vasodilatory shock (sepsis) – vasoconstrictor drug
- SV low, low PCOP/LVEDP = hypovolemia – volume administration
- SV low, high PCOP/LVEDP = “full” heart – positive inotropic drug
What are wedge pressures?
Pulmonary artery catheterization:
* Still used when?
* What data can be given?
* What about surgeries?
What are the contraindications to PA catheter?
In Cardiac OR, what is placed first? What happens next?
In Cardiac OR, CVL line placed distal first, then PA catheter proximal
Intraarterial access:
* What are the indications?
How do you monitor the intraarterial access?
- Radial artery – superficial and substantial collateral flow
- Ulnar artery – more difficult than radial, deeper and more tortuous: increased risk of compromising blood flow to hand
- Brachial artery – less waveform distortion, prone to kinking near the elbow
- Femoral artery – prone to atheroma and pseudoaneurysm, increased infection risk: aseptic necrosis of femur head in children
- Dorsalis pedis & posterior tibial – distorded waveforms
- Axillary artery – surrounded by axillary plexus and increased nerve damage, air or thrombi quick to flow to cerebral circulation.
What are the CI for arterial line? What test should you do?
- Arteries with inadequate collateral blood flow
- Vascular insufficiency
- Allen’s Test
What are the complications of arterial line?
- Hematoma, bleeding
- Arterial vasospasm
- Thrombus or Air Embolus
- Pseudoaneurysm
- Necrosis
- Nerve Damage
- Infection
Procedural sedation in ED
* When do you need minimal sedations? Mod? Emergent airway protection?
Procedural sedation in the ED
* What do you need to know?
Procedural sedation in the ED:
* What are the consideration?
sorry it is look
Preparation checklist?
Procedural sedation in the ED
* What is level A and B?
Procedural Sedation in the ED
* What is level C?
Procedural medication
* Ketamine: Safe or not? Maintain what? What type of effects? dose?
Procedural medications:
* What are the SE of ketamine?
Propofol:
* Achieve what?
* What is the onset and duration?
* What is the dose?
* What are the SE?
Procedural Medication: Etomidate
* What type of sedations
* What does it stablize?
* What is the dose?
What are the SE of etomidate?
FOR HfrEF
Dexmedetomidine (Precedex)
* Similar to what?
* _ protective
* What type of properties?
* What is the dose?
Dexmedetomidine
* What are the side effects?
- Hypotension
- Bradycardia, heart block
Using Sedation in the ED
* When to consult for help?
- Patient tolerance to procedure
- Availability of Anesthesia Staff
What are the steps of hypoxic event?
Detect Hypoventilation/Apnea -> Stop Sedation -> Change patient position -> Jaw Thrust/Open Airway-> Suction -> Induce Painful Stimuli -> Consider Reversal Agent -> Bask Mask/LMA -> Oral Intubation
