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Speciality Medicine > Lecture 4: Anesthesiology > Flashcards

Lecture 4: Anesthesiology Flashcards

1
Q

Brief history:

  • Who and when is anesthesia denoted?
  • Who is the father of anesthesia?
  • What was used first on patients? when and by who?
A
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2
Q

Brief history:
* What people did the local and regional?
* What was first used IV?

A
  • 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)
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3
Q

What is anesthesia per holmes?

A

denotes the state that incorporates amnesia, analgesia, and narcosis to make painless surgery possible.

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4
Q
A
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5
Q

How does anesthesia work?

What does inhalational agents interact with? What receptors do they work on?

A

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

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6
Q

What is general anesthesia?

A

an altered physiological state characterized by reversible loss of consciousness, analgesia, amnesia, and some degree of muscle relaxation.

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7
Q

How does anesthesia effect the brain and CNS?

A

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

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8
Q

Measuring Anesthetic Depth
* What are MAC values?
* Mirror what?

A

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

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9
Q

MAC:
* 1.3 MAC=
* 0.4-0.3=
* what is the decrease in MAC per decade of age?

A
  • 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
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10
Q
A
  • 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
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11
Q

What MAC score is needed for hip fx of 85yo? Marijana use in 25yo?

A

Hip: 0.4
Maijuana: 1.3

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12
Q

How does anesthesia work?

  • Inhalational? What is inspiratory concentration and alveloar concentration?
A

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

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13
Q

What are 3 factors that affect how anesthetic agents work?

A
  • 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
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14
Q

What are the different volatile agents?

A
  • 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

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15
Q

Maligenany hyperthermia:
* Common or rare?
* MC where?
* Increased risk in who/?
* Triggered by what?
* Can present more than what?

A

Musculoskeletal diseases: central-core disease, multi-minicore myopathy, King-Denborough syndrome

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16
Q

Malignant Hypertheria:
* What is released? What does it cause?

A

Ryanodine Receptor

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17
Q

Malignany hyperthermia:
* What are the earliest signs? What is a late sign?

A
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18
Q

What are compliactions of malignant hyperthermia?(5)

A
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19
Q

Treatment for MH
* What do you need to stop? What do you turn on?
* GIve what immediately? What is the dosing?

A

  • 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
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20
Q

MH treatment:
* Metabolic acidosis?
* Hyperkalemia?
* Arrthythmias?
* Fever?

A
  • 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)
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21
Q

Anestheia Machine:
* What is CO2 absorber?
* What are vaporizers?
* What scavenfging connector?

A
  • CO absorber: prevents reinhalation of CO2
  • Vaporizes: inhalations meds loaded here
  • Scavenging: Gets rid of inhalation gases
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22
Q
A
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23
Q

how does the flow of gases work?

A
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24
Q

What do you need to continuously monitor?

A
  • 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.
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25
Q

What are the IV anestethics?

A
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26
Q

What are the examples of barbitutes? Benzo?
* What is the reversal agent of benzo?

A

Barb: Thiopental, phenobarbital
Benzo: Midazolam, lorazepam, diazepam
* Reveral agent: :flurmazelil

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27
Q

What are the examples of opiods? What is the antagonist?

A
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28
Q

IV medications:
* What are the neuromuscular blockade agents?

A
  • 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.

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29
Q

fill in for IV medicaitons special considerations?

A
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30
Q
A
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31
Q

What are the indications for RSI?

A
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32
Q

What are the choice of neuromusclar blockade (paralytic)

A

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

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33
Q

Intravenous Medications NM blockade reveral agents:
* Anticholinesterases:
* Non-classic Reveral agents:
* Anticholinergics:

A

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.

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34
Q

What are the adrenergic agonists and antagonists?

A
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35
Q
A

Quick and dirty in the ED (first response drug) will be Norepinephrine (Levophed)

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36
Q
A
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37
Q

What are the anti-hypertensive agents?

A

  • Nitro: CHF patients
  • BB: avoid in Ashtma/COPD
  • Calcium channel blocker: good for A-fib RVR - cardizem, HTN emergency - cardene
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38
Q

Local anesthetics:
* Bind to what? What do they prevent and inhibit?

A

  • 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
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39
Q

Local anesthetics:
* Sensitivity to nerve fibers is determined by what?

A
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40
Q
A
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41
Q

How does local anesthegia work?

A

bind to Na channels

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42
Q

Local anesthetics:
* What affects the onset?

A

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.

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43
Q

LA:
How is durations affected? what about systemic absorption?

A
44
Q
A

  • Esters – metabolized by pseudocholinesterase
  • Procaine – metabolized to PABA (p-aminobenzoic acid) which has been associated with rare anaphylactic reactions
45
Q

Local Anesthetic Systemic Toxicity (LAST)
* What has additive toxic effects?
* Effects seen where?

A
  • Mixing local anesthetics can have additive toxic effects
  • Effects seen in all organ systems
46
Q

Local Anesthetic Systemic Toxicity (LAST)
* What happens neurological?

A

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

47
Q

Cocaine:
* What happens at first? Overdose?
* How can toxicity be treated?
* Cauda equina syndrome use what?
* Neurotoxicity lower when using what?

A
  • 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
48
Q

LAST:
* What happens with cardiovasular?

A

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

49
Q

Local Anesthetic Systemic Toxicity (LAST):
* Major CV toxicity requires what?
* What is with CNS excitation?
* What is most cardiotoxic?
* Cocaine=

A

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

50
Q

What is the txt of LAST?

A

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.

51
Q

Where can all the regional anestheia fo?

A
52
Q

Epidural Blood Patches
* What can happen after?
* When do you see this?
* Don’t repeat spinal/epidural attempt after what? Why?

A
53
Q

What do you do for epidural blood patches?

A

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

54
Q
  • How do you dx CSF leak?
  • Must fail conservative treatments before what?
A
  • Diagnosis: headache improves after laying down
  • Must fail conservative treatments before anesthesia involvement
    * Caffeine, hydration (Gatorade), Ibuprofen
55
Q

Preoperative assessment:
* What is the anesthetic plan?

A
56
Q

fill in for ASA class

A
57
Q

What is the NPO status?

A

(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.

58
Q

What are all the other issues you need to review ofor preoperative assessment?

A
59
Q

What is the postopertive care?

A
60
Q
A
61
Q

Explain where all the CN nerves are down the airway?

A
62
Q
A
63
Q

What are the mallampati classes?

A
64
Q

What position do you need the patient in for MAC blade?

A
65
Q
A
66
Q

What are the two types of airways?

A

  • Nasal Airway – risk of epistaxis with patients taking anticoagulants
  • Oral Airway – multiple sizes
67
Q

What is a suprgolttic airway device? What are the variations?

A

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

68
Q

What is important to remember about the ET tube?

A

KEEP the pilot balloon inflated

69
Q

What are the different laryngoscope blades?

A
70
Q

What are different scopes that are anticipated for difficulat airways?

A
71
Q
A
72
Q
A
73
Q

When can you not ventilate pt?

A

Cannot vent pt with bag mask after sedation

74
Q
A
75
Q

What are the surgical airways?

A
76
Q

IV access:
* What is prefered in OR?
* What is last line due to infections? What can you do with this?

A

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

77
Q
A
78
Q

Contraindications to CVL
* What are the relative

A

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

79
Q

What is there an increased risk when Left sided IJ IV access? Femoral?

A

Left-sided IJ Vein
* Increased risk of pleural effusion and chylothorax

Femoral Vein
* Increased risk of line-related sepsis

80
Q

How do you find the Internal jug vein?

A
81
Q

How do you place a right internal jugluar can?

A
82
Q
A
83
Q

Pulmonary artery cath:
* What catheter is used?
* What can you measure? What does it guide and measure?

A

  • 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
84
Q

What are wedge pressures?

A
85
Q

Pulmonary artery catheterization:
* Still used when?
* What data can be given?
* What about surgeries?

A
86
Q

What are the contraindications to PA catheter?

A
87
Q

In Cardiac OR, what is placed first? What happens next?

A

In Cardiac OR, CVL line placed distal first, then PA catheter proximal

88
Q

Intraarterial access:
* What are the indications?

A
89
Q

How do you monitor the intraarterial access?

A
  • 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.
90
Q

What are the CI for arterial line? What test should you do?

A
  • Arteries with inadequate collateral blood flow
  • Vascular insufficiency
  • Allen’s Test
91
Q

What are the complications of arterial line?

A
  • Hematoma, bleeding
  • Arterial vasospasm
  • Thrombus or Air Embolus
  • Pseudoaneurysm
  • Necrosis
  • Nerve Damage
  • Infection
92
Q

Procedural sedation in ED
* When do you need minimal sedations? Mod? Emergent airway protection?

A
93
Q

Procedural sedation in the ED
* What do you need to know?

A
94
Q

Procedural sedation in the ED:
* What are the consideration?

A
95
Q

sorry it is look

Preparation checklist?

A
96
Q

Procedural sedation in the ED
* What is level A and B?

A
97
Q

Procedural Sedation in the ED
* What is level C?

A
98
Q

Procedural medication
* Ketamine: Safe or not? Maintain what? What type of effects? dose?

A
99
Q

Procedural medications:
* What are the SE of ketamine?

A
100
Q

Propofol:
* Achieve what?
* What is the onset and duration?
* What is the dose?
* What are the SE?

A
101
Q

Procedural Medication: Etomidate
* What type of sedations
* What does it stablize?
* What is the dose?

A
102
Q

What are the SE of etomidate?

A

FOR HfrEF

103
Q

Dexmedetomidine (Precedex)
* Similar to what?
* _ protective
* What type of properties?
* What is the dose?

A
104
Q

Dexmedetomidine
* What are the side effects?

A
  • Hypotension
  • Bradycardia, heart block
105
Q

Using Sedation in the ED
* When to consult for help?

A
  • Patient tolerance to procedure
  • Availability of Anesthesia Staff
106
Q

What are the steps of hypoxic event?

A

Detect Hypoventilation/Apnea -> Stop Sedation -> Change patient position -> Jaw Thrust/Open Airway-> Suction -> Induce Painful Stimuli -> Consider Reversal Agent -> Bask Mask/LMA -> Oral Intubation

Speciality Medicine (12 decks)

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