14: Anesthesia - Stefani Flashcards Preview

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Flashcards in 14: Anesthesia - Stefani Deck (34)

ABC in operating room



watch NEJM video




oropharyngeal airway

- measure to correct size at angle of mandible
- contraindicated: intact gag reflex


nasopharngeal airway

- measure to tip of earlobe
- can be used with intact gag reflex or pt who will not open mouth
- insert bevel down parallel to soft palate and NOT toward the abse of skull


ventilation options

1. Mouth to mouth (Microshield or Barrier Mask)
2. Bag-mask Ventilation (with or without airway adjuncts) – usually a prelude to intubation
3. Supraglottic airways
4. Endotracheal intubation (oral or nasal)
5. Surgical airway (tracheostomy or crichothyroidotomy)


position of laryngeal mask airway

supraglottic when inflated


five basic intubation steps

1*Optimal positioning of the patient
2 Adequate opening of the mouth
3 Correct insertion of the blade in the mouth
4 Advancement of the blade with exposure and identification of the larynx
5 Placement of the endotracheal tube through the glottis into the trachea


WHEN to intubate

- Failure of airway protection
- Failure of oxygenation
- Failure of ventilation
- Is there a need for extended mechanical ventilation?


the seven Ps

proper prior preparation prevents piss poor performance



airway exam

- Mallampati Score (1-4 based on visibility in open mouth, 4 is bad)
- Thyromental distance
- Mouth opening
- Neck Mobility –Normal extension is 45 to 70 degrees
- Ability to protrude lower jaw
- Foreign material in the airway


blade you should use for intubation

miller 2 blade
- very narrow, can get in the mouth, straight


When intubating in an emergency situation ALWAYS use a ...

styleted endotracheal tube


cormack-lehane classification

what you see when doing an endotracheal tue
Grade 1-4, 4 bad


Sellick's maneuver

- cricoid pressure
- push trachea posteriorly and compress esophagus


what helps blind nasotracheal intubation?

High airway velocity will help channel tip of ET tube thru the vocal cords


contraindications to blind nasal intubation

- Should be avoided in severe nasal or midface trauma
- In basal skull fracture, ET tube placed nasally could enter the brain thru the fracture site
- Patients being considered for thrombolytic therapy or patients on anticoagulants or who have a coagulapathy should not be nasally intubated


general MOA general anesthesia

- General anesthesia molecules cause disruption of the loops that bind receptor sites and cause interference with ion flow
- a decrease in the flow of the electron transport chain decreased energy levels and enhances the effects of anesthetics


______ MAC will prevent movement in 95% of patients



factors with decreased anesthetic requriement

- acute ETOH
- elderly
- hyponatremia
- hypothermia
- anemia
- hypercarbia
- hypoxia
- pregnancy *


mask induction

– Mask is placed on the patient’s face and the inhalation agent concentration is gradually increased until patient is unconscious
-- Usually used in infants and small children who do not tolerate an IV start


IV induction

-- In adults and cooperative children, an IV is started and an IV induction agent is used so induce loss of consciousness.
-- These agents have a rapid distribution and are eventually excreted. Blood levels fall quickly causing their apparent duration of action to be short ( known as context-sensitive t1/2
-- Immediately followed by simultaneous administration of other agents to deepen anesthetic level


effects of inhalation anesthetic agents

- They cause loss of consciousness, immobility, amnesia and muscle relaxation ( except Nitrous Oxide which increases skeletal muscle tone )
- They do not necessarily provide analgesia
- Because they administered by a calibrated vaporizer, their effects can be easily titrated
- They affect multiple organ systems
- They lower BP by decreasing SVR and to a lesser extent through myocardial depression
- They decrease alveolar ventilation but not total ventilation except at higher doses resulting in gradual rise of PCO2
- Cerebral vasodilators and can inhibit cerebral autoregulation and cause ICP to increase
- Interferes with hypoxic pulmonary vasoconstriction (HPV) which causes increased shunting of blood in the lungs to poorly ventilated areas - ↓ PO2


induction agents

Barbiturates – Sodium thiopentol the “gold standard” but now of less importance

Propofol – most commonly used induction agent

Benzodiazepenes– primarily Midazolam. It enhances the effect of GABA at the receptor

Ketamine – causes dissociation and can be used as sole anesthetic for certain procedures


Induction dose for Propofol is ..

2.5 -2 mg/kg

The assumption is that the concentration in the blood will equal the effect site
[effect site]=[brain]

The dose of the drug is determined by it’s therapeutic window


what do you give after induction?

- After induction of anesthesia, other drugs will be administered to provide the best outcome for the surgical procedure being performed
- Neuromuscular blocking drugs may be given to facilitate airway management and provide surgical relaxation
- Opioids will be given to provide analgesia during the procedure and to provide analgesia after emergence
- An anticholinergic may be given to dry the airway and to maintain the heartrate
- Benzodiazepines may be given to decrease risk of recall
- Antinausea medications are usually given to reduce the risk of nausea and vomiting in the postoperative period
- Nonopioid IV analgesics can also be given to reduce the postoperative analgesic requirements
( ie – IV ketorolac , acetominophen )
- The surgeon may inject local anesthetics into or near the operative site to provide additional longer term pain relief


"balanced anesthesia"

To minimize the undesirable side effects of any one class of drug, they are given as a combination of inhalation anesthetic drugs and intravenous agents – a concept known as “balanced anesthesia”

Ideally this will provide a smoother anesthetic and more rapid emergence with fewer intraoperative and postoperative complications


clinically used neuromuscular blocking agents

Depolarizing muscle relaxants. Only one used clinically is succinylcholine

Nondepolarizing muscle relaxants. Curare-like actions. Contain an aminosteroid nucleus


MOA succinylcholine

Binds to ACH receptor and prevents repolarization

Hydrolyzed by pseudocholinesterase

After the drug is metabolized, the NMJ can repolarize

Initial response is muscle contraction followed by relaxation

Fasciculations are seen and repolarization is inhibited


succinylcholine pharmacology

Hydrolyzed by plasma pseudocholinesterase
Plasma half-life


side effects succinylcholine

Sinus Bradycardia and possibly cardiac arrest with a second dose
Anaphalaxis (rare)
Hyperkalemia- do not use on burns cases, cases with major tissue damage or in patients with neuromuscular diseases ( ie: muscular dystrophy )


MOA nondepolarizing muscle relaxants

Work both presynaptically and postsynaptically
Presynaptically – bind to alpha3 beta2 receptors to inhibit mobilization of Ach and inhibit it’s release
Postsynaptically- competes with Ach for binding sites on the alpha subunit of the nicotinic receptor and prevents depolarization of the neuromuscular end plate…no muscle contraction
Agent only has to block one of the alpha subunits to be effective
Cisatracurium and Atracurium are nondepolarizing muscle relaxants with no steroid nucleus
They are tetrohydroisoquinilone derivatives
Cisatracurium is one of twelve isomers of atracurium and associated with less histamine release than the parent drug
Does not rely on hepatic or renal metabolism
Metabolism by ester hydrolysis and Hofmann elimination


dosing of neuromuscular blocking drugs ***

These are polar molecules so the Vd of these molecules is only to the extracellular fluid compartment
They do not distribute to lipid compartment
**********Dosing of these drugs is not based on total body weight but lean body weight*********
Dosing on total body weight leads to drug overdose and difficult reversal


reversal of neuromuscular blockers?

- Administration of pseudocholinesterase inhibitors slow breakdown of Ach to allow it to compete for alpha unit binding sites
- Most commonly used drugs are Neostigmine and Edrophonium. Neostigmine 12 times more potent than Edrophonium
- In addition to the nicotinic receptors in muscle cells, Ach also binds at muscarinic receptors
- When NM blockers are reversed, the increased Ach acting at these muscarinic receptors cause undersirable side effect
- These would include bradycardia, bronchospasm, increased intestinal motility and increased salivation
- For this reason an anticholinergic drug is given at the same time neostigmine or edrophonium is given ( atropine or glycopyrralate )
- These drugs act at the muscarinic receptors to prevent these side effects


Newest drug to being reverse neuromuscular blockade by primarily Rocuronium is ...


Directly binds Rocuronium and to a lesser extent Vecuronium and Pancuronium
Binds drugs with an aminosteroid nucleus only

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