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CCP 213 Critical Care Anesthesia 💉 Flashcards

1
Q

PACE plan steps

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. primary
  2. alternate
  3. contingency
  4. emergency
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2
Q

4 A’s of anesthesia

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. amnesia
  2. analgesia
  3. areflexia
  4. autonomic stability
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3
Q

Big syringe (“three syringes principle”)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. induction agent. “amnesia”.

2. typically a “big syringe” because push dose propofol is done in a 20cc syringe

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4
Q

Little syringe (“three syringes principle”)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. analgesic agent and/or paralytic agent. “analgesia” + “areflexia”.
  2. usually a 10cc syringe “little” because it’s smaller than the 20cc propofol syringe
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5
Q

Chaser syringe (“three syringes principle”)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

4 is actually super important. like lets say you’re gonna be inducing someone who is super hemodynamically tenuous. Like, if you’re gonna be giving them ketamine, even though its a relatively “stable” agent, it would probably behoove you to preload them with hemodynamic support BEFORE you give them the sedative that way you’re not behind the curve playing catch up

  1. hemodynamic support agent.
  2. examples include push dose epinephrine, phenylephrine, atropine
  3. “chases” your induction to maintain autonomic stability.
  4. depending on how unstable the patient is, you may lead with your chaser syringe
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6
Q

life threatening adverse reaction to rocuronium

A

anaphylaxis

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7
Q

depolarizing NMBA and mechanism

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. succinylcholine

2. binds to and activates the ACh receptor, at first causing muscle contraction, then paralysis

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8
Q

non-depolarizing NMBA and mechanism

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. rocuronium

2. competitively blocks the binding of ACh to its receptors

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9
Q

dosing for succinylcholine in RSI

A

1.5 mg/kg

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10
Q

dosing for rocuronium in RSI

A

0.6-1.2 mg/kg

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11
Q

The three stages of anesthesia

A
  1. Induction
  2. Maintenance
  3. Emergence
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12
Q

Novel reversal agent for non-depolarizing neuromuscular blocking agents

A

Sugammadex

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13
Q

CCP Indications for intubation

Hint, there’s more than you learned in ALS…

A
  1. Failure to oxygenate
  2. Failure to ventilate
  3. Failure to protect airway
  4. Predicted clinical course
  5. Refractory shock (offload systemic demand)
  6. Profound metabolic acidosis (offload systemic demand)
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14
Q

potential causes of hypotension following induction

A
  1. SNS ablation from sedatives (sympathetic tone)
  2. PPV compression of vasculature (preload)
  3. Myocardial depressant and vasodilatory action of drugs (preload, contractility)
  4. Patient could be catecholamine deplete (sympathetic tone)
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15
Q

Anaesthetics MOA

A

Propofol (GABA-A receptor agonist, direct activation of the GABA receptor)
Etomidate (GABA-A)
Midazolam (GABA-A)
Ketamine (noncompetitive NMDA receptor antagonist)
Opiates (Mu receptor agonist)

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16
Q

Propofol MOA

A

GABA-A receptor agonist

  1. Activates post-synaptic GABA-A receptor causing influx of chloride leading to hyperpolarization and reduction in nerve impulse transmission
  2. direct activation of the GABA receptor
17
Q

Benzodiazepines MOA

A

GABA-A receptor agonist

  1. Activates post-synaptic GABA-A receptor causing influx of chloride leading to hyperpolarization and reduction in nerve impulse transmission
18
Q

Ketamine MOA

A

NMDA receptor antagonist

  1. Antagonizes post-synaptic NMDA receptors
  2. This stops influx of sodium and calcium and prevents efflux of potassium

NMDA receptors are responsible for pain and awareness

19
Q

predicted difficult BMV mnemonic

A 
Bearded
Obese
Old
Toothless
Snoring
20
Q

predicted difficult laryngoscopy mnemonic

A 
Look
Evaluate 3-3-2
Mouth opening (mallampati)
Obese/obstruction
Neck mobility
21
Q

What might indicate that propofol infusion syndrome is developing?

A

Increasing lactate without other cause of shock.

(consider propofol infusion as one of your differentials for a suspiciously elevated lactate level with no other known source)

22
Q

Risk factors for propofol infusion syndrome include:

A

1) > 80mg/kg/hr
2) Young age
3) Prolonged infusion (ie. > 12 hr)

23
Q

Dexmedetomidine for ICU sedation

A
  1. centrally acting α2-agonist with sedative/analgesic properties
  2. has minimal impact on respiratory drive
  3. studies comparing dexmedetomidine to benzodiazepines have demonstrated a shorter duration of mechanical ventilation and lesser delirium
  4. Not suitable for deep sedation regardless of dosage (only provides light/moderate sedation)
  5. start 1 μg/kg IV loading dose, then 0.2-1.4 μg/kg/h
  6. watch out for bradycardia
24
Q

Benzodiazepines for ICU sedation

A
  1. Can be given as a bolus or infusion.
  2. In critically ill patients, the pharmacokinetics can be altered, leading to accumulation and prolonged sedation.
  3. Associated with increased delirium.
  4. Not a first-line drug for sedation.
25
Q

Propofol for ICU sedation

A
  1. lipophilic agent that can rapidly penetrate the blood-brain barrier with minimal change in clearance in critical illness
  2. propofol is shown to decrease the duration of mechanical ventilation compared with benzodiazepines
  3. Can be rapidly turned off, allowing for serial neurologic exams
  4. Can cause hypotension and bradycardia, use caution when initiating in hypovolemic patients or patients simultaneously receiving the initiation of positive pressure ventilation
26
Q

Fentanyl for ICU analgesia

A
  1. Fentanyl may be the preferred opioid in patients with renal insufficiency
  2. Loading dose: 25 to 100 μg (or 1-2 μg/kg)
  3. Continuous infusion: weight based 0.7 to 10 μg/kg/h, (usual dosing for adults 50 to 200 μg/h)
27
Q

Remifentanil for ICU analgesia

A
  1. shorter-acting opiate that is degraded by plasma esterases, has more predictable metabolism, and a shorter half-life
28
Q

describe the main GABA receptors in the CNS

A
  1. GABA-A receptors (Cl− channels)
  2. GABA-B receptors (G-protein-linked)
  3. majority of commonly used sedative/hypnotics, such as barbiturates, benzodiazepines, ethanol, propofol, etomidate, and chloral hydrate, are GABA-A agonists
29
Q

define procedural sedation

A
  1. medications given to attenuate anxiety or pain and to improve compliance with and tolerance of a specific procedure
30
Q

key items to have available during procedural sedation

A
  1. oxygen
  2. suction
  3. physiologic monitoring equipment
  4. resuscitation medications
  5. age-appropriate equipment for airway and ventilatory rescue.
31
Q

8 P’s of intubation (indications for intubation)

A
  1. Protect (airway protection)
  2. Pulmonary toilet
  3. PPV (correct hemodynamics and/or acid-base)
  4. Patency
  5. Procedures (eg surgery)
  6. Pain management (eg requires deep sedation and analgesia for burns)
  7. Pacify (patient is a pain in the ass)
  8. Public health (ebola/sars/MERS/COVID)
32
Q

Labetalol MOA

A
  1. think of labetalol as an “adrenergic block” or a “sympatholytic”
  2. it is a selective a1 blocker (reduces vascular smooth muscle resistance), and non-selective beta blocker (will reduce B1 and B2 leading to decreased cardiac inotropy, chronotropy, dromotropy)
  3. beta effects are more pronounced over alpha effects
  4. will not cause reflex tachycardia from the drop in pressure, means it is cardio-protective
33
Q

Hydralazine MOA

A
  1. think of Hydralazine as a “direct acting arterial dilator”
  2. promotes NO release and relaxation of vascular smooth muscle
  3. Inhibition of calcium release from the sarcoplasmic reticulum promotes endothelial relaxation
  4. will cause a reflex tachycardia from the drop in pressure
  5. the fall in BP can stimulate the adrenergic system to cause tachycardia, RAAS activation
34
Q

labetalol vs hydralazine for BP reduction

A
  1. labetalol is more of an “adrenergic blocker” or “sympatholytic” than hydralazine, which is a direct acting arterial vasodilator.
  2. labetalol is going to give you a1 and b1+2 blockade, but has 7x more effect on beta than alpha!
  3. typically for pure BP reduction hydralazine is a better agent. if you need to control the sympathetic response like in aortic dissection labetalol would be your first line agent augmented with hydralazine if you need to target higher alpha reduction to hit your SBP target
  4. if you are just targeting BP reduction with hydralazine beware of the reflex tachycardia you can get d/t RAAS/sympathetic activation. you don’t get this in labetalol because of the co-existing beta blockade. Therefore, in patients who you are worried about inducing tachycardia in (HF or people with otherwise shitty hearts) make sure they have some sort of beta blocker on board, whether that be their pre-existing PO metoprolol or whatever. or just use labetalol

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