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Anesthesiologist Assistant > Pharmacology (Orientation) > Flashcards

Pharmacology (Orientation) Flashcards

1
Q

Pharmacokinetics

A

a quantitative study of the absorption, distribution, metabolism, and excretion of injected and inhaled drugs and their metabolites “What the body does to the drug”

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2
Q

Pharmacodynamics

A

study of the intrinsic sensitivity or responsiveness of receptors to a drug and the mechanics by which these occur “What does the drug do to the body”

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3
Q

Tolerance

A

hyporeactive owing to chronic exposure to a drug
Cross-tolerance is common b/w drugs that produce similar pharmacologic effects (alcohol & inhaled anesthetics)

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4
Q

Tachyphylaxis

A

tolerance that develops acutely; reflects cellular tolerance

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5
Q

Additive

A

two drugs (inhaled anesthetics) interact to produce an effect (MAC) equal to algebraic summation

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6
Q

Synergetic

A

two drugs interact to produce an effect greater than algebraic summation

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7
Q

Agonist

A

a drug that activates a receptor by binding the receptor

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8
Q

Partial agonist

A

a drug that binds weakly to the receptor and produces minimal pharmacological effect

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9
Q

Antagonist

A

a drug that bind to a receptor w/out activating the receptor, and at the same time, prevents an agonist from stimulating the receptor

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10
Q

Competitive

A
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11
Q

Non-Competitive

A
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12
Q

2-Compartment Model

A

A drug is injected intravenously into the central compartment and subsequently distributes to the peripheral compartment, only to return eventually to the central compartment where clearance from the body occurs
Any residual drug present in the peripheral compartment at the time of repeat intravenous injection will result in a cumulative effect

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12
Q

Elimination Half-Time-

A

the time necessary for the plasma concentration to decrease by 50% during the elimination phase (Only reflects elimination in the central compartment)

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13
Q

Context-Sensitive Half-Time-

A

time necessary for the plasma concentration to decrease 50% after terminating an infusion of a particular duration (Describes multicompartment pharmacokinetics )

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14
Q

Oral Drug Administration

A

Undergoes liver first-pass , which decreases the amount of the drug being systemically circulated. Small intestine is the principal sight of injection
Oral Transmucosal Administration (Sublingual, Buccal, nasal mucosal )- No Hepatic first-pass

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15
Q

Transdermal administration

A

(Sub-Q, IM, IV)- Rapid and precise drug delivery best achieved w/ IV administration, Hepatic first-pass does not occur (Vs. Enteral- Thru alimentary tract)

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16
Q

Vd (Volume of Distribution)-

A

a mathematical expression (dose of IV drug administered/resulting plasma concentration) that depicts the distribution characteristics of a drug in the body
* Binding to plasma proteins and poor lipid solubility limit passage of a drug to tissues, thus maintaining a nigh concentration in the plasma and a small calculate Vd
* A lipid-soluble drug that is highly concentrated in tissues w/ a resulting low plasma concentration will have a high calculated Vd

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17
Q

Clearance

A

the volume of plasma cleared of drug by renal excretion and/or metabolism in the liver or other organs

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18
Q

Systemic Clearance

A

Permanent removal of a drug

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19
Q

Intercompartmental Clearance

A

movement of drug from one compartment to another (Main cause of termination of effect for drugs)

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20
Q

Cytochrome p450

A

Responsible for the biotransformation of endogenous compounds, pharmacological agents, and environmental xenobiotics
* Propofol, Fentanyl, midazolam, morphine, lidocaine

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21
Q

Drug Concentration

A

Given as a weight (Mass)/ volume. Defines how much you have (Propofol conc.= 10mg/mL)

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22
Q

Drug Dose

A

Given as a mass of drug per unit mass of the patient (Defines how much you give (Adult induction of propofol is 2 mg/kg

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23
Q

Red Man Syndrome

A

an infusion-related reaction peculiar to vancomycin. It typically consists of pruritus, an erythematous rash that involves the face, neck, and upper torso. Less frequently, hypotension and angioedema can occur

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24
Q

Hyperalgesia

A

More sensitive to a pain stimulus
* Work in a longer-acting opioid when stopping a remifentanil infusion

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25
Q

Suboxone

A

mix of Buprenorphine and Naloxone used to treat heroin and methadone addiction

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26
Q

Scopolamine Patch

A

Motion sickness patch, helps with PONV and works up to 3 days
Works Quickly
Will dilate eyes if you touch the patch and then touch your eyes
Can cause dry mouth and dry eyes
Anticholinergic

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27
Q

Type and Screen

A

Screen patient’s blood to make sure we have that product available. (Screening takes a long time) (About an hour)

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28
Q

Type and Cross

A

Crossmatched with the units available and ready (About 20 mins after we have a type and screen)
Anticipate blood loss, just start with a type and screen, it can be over 2 hours during busy times.
Sometimes pre-op nurse doesn’t have time to send type and screen, use 2 pink vials.
One will print, the other put a patient label on there.

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29
Q

Dilute Phenylephrine

A

2.5cc+7.5 NS Phenylephrine

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30
Q

Dilute Ephedrine

A

1+9 ephedrine

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31
Q

Dilute Dilaudid

A

(1+9)=10 =200 mcg/mL

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32
Q

Norepinephrine Dilution

A

2cc concentrate +8cc NS

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33
Q

SYstemic Drug Redistribution

A

As the plasma concentration of a drug decreases below than in highly perfused tissues (liver, heart, brain, lungs), the drug leaves these tissues to be redistributed to less well-perfused sites, such as skeletal muscles and fat

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34
Q

Biotransformation

A

substance changing from one chemical to another

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35
Q

Tissue Metabolism

A

Cleared in tissues or plasma via ester hydrolysis (Sux, Esmolol, Remifentanil) (Succinylcholine, Esmolol, Remifentanil)

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36
Q

Renal Clearance

A

Kidneys eliminate drugs through filtration by the glomerulus
Steroidal musle relaxants (Vecuronium/Rocuronium)

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37
Q

Distribution Clearance

A

Removal of drug from one compartment to another (blood to tissue)

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38
Q

Protein Binding

A

Protein-bound drugs are not “bioavailable” to exert their effect

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39
Q

The Half-Life of a drug is increased with

A

a large Vd and decreased with a small Vd. Can’t be metabolized or cleared if it’s not in plasma or reaching the liver

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40
Q

Plasma concentration of a drug with a long half-life can still fall rapidly as

A

It redistributes from a vessel-rich compartment (Muscle/fat/synovial fluid)

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41
Q

Half Life is not a predictor of

A

Drug effect

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42
Q

Narcotic Bag at UC Anschutz includes

A
  • 2 Propofol 20 vials
    • Ephedrine 10 cc (5mcg/mL)
    • 2mL vials of Fentanyl (x2)
      1 vial of Dilaudid (2mg/mL)*Diluted)
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43
Q

Quick reversal of Benzodiazepines can result in

A

Propofol can help with this!

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44
Q

1% Lidocaine concentration

A

10mg/mL

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45
Q

2% Lidocaine Concentration

A

2mg/mL

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46
Q

.5% Lidocaine Concentration

A

5mg/mL

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47
Q

.25% Lidocaine COncentration

A

2.5mg/mL

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48
Q

1:1000 Epi concentration

A

1g Epi in 1000mL of solution
or 1mg/mL

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49
Q

Morphine Opioid index

A

Morpine =1
Dilaudid =10
Fentanyl =100
Remi= 100-300
Sufentanil 500-1000
Alfentanil= 10-20x
Meperidine= 1/10

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50
Q

What are the active Metabolites of Morphine

A

M6G, M3G

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51
Q

What drug is dosed on total body weight instead of ideal body weight

A

Succinylcholine

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52
Q

Properties of drugs with a high volume of distribution (Vd)

A

-Higher tissue concentration than in plasma
-Relatively lipid soluble
-Distributed intracellularly
-Not efficiently removed by hemodialysis

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53
Q

Role of metabolism

A

convert a pharmacologically active, lipid-soluble drug into water soluble, pharmacologically inactive metabolites

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54
Q

Types of IV Access

A

Peripheral
Central Line
Picc Line
Tunneled Central Line (Hickman/ Broviac cath (No Reservoir)
Mediport/Portacath (reservoir)

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55
Q

Gauge of an IV

A

DIameter of the lumen
inversely proportional (Bigger number, smaller the diameter)

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56
Q

Supplies needed to start an IV

A

IV Bag
Tourniquet
Gloves
Alcohol wipes/Chloraprep
IV Catheter
Tegaderm
Tape
4x4 Gauze
Local**

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57
Q

Peripheral IV complications

A

Infection
- Phlebitis
-Sepsis
-Infiltration

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58
Q

Phlebitis

A

Inflammation of a vein that the body tries to naturally repair by clotting (Thrombosis)
This is bad if it travels to the heart

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59
Q

Sepsis

A

Systemic bloodstream infection

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60
Q

Infiltration

A

Blown Vein
Cannula situated outside the vein (extravasation), leaking fluids/meds in the tissue , causing necrosis, cellulitis, and pain

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61
Q

Central Line

A

Subclavian
Femoral
Internal Jugular
infuses large volumes quickly , remains for longer periods than an PIV
better for long-term pressor infusions

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62
Q

Central Line Complications

A

Pneumothorax (Punctured Lung)
Hematoma, arrhythmia (tip of cath touches the heart wall , causing electrical conduction to change)

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63
Q

Tunneled Central Line (Hickman or Broviac)

A

Plastic cath with cuff (balloon) near exit site. Does not have reservoir
Large diameter (13fr)
Multiple lumens for simultaneous drug administration

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64
Q

Mediport

A

Has a small reservoir subcutaneous (Under Skin)
Increased pt. comfort, accessed when needed, no tubing exiting skin
Decreased infection rates

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65
Q

Total Body Water

A

Avg

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66
Q

Two major fluid compartments

A

ICF-Intracellular Fluid
ECF- Extracellular Fluid

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67
Q

ECF (Extracellular Fluid)

A

Intravascular- in the bloodstream (mostly plasma)
PLUS
Interstitial- all fluid outside cells and outside vascular system

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68
Q

Rule of Approximate Thirds

A
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69
Q

Normal Sodium (Na+ ) values

A

140

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70
Q

Normal Potassium(K+) Values

A

4.5

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71
Q

Normal Magnesium(Mg) Value

A

1.2

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72
Q

Normal Calcium(Ca2+) Value

A

2.4

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73
Q

Normal Chloride (Cl-) Value

A

100

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74
Q

Normal Bicarb (HCO3) Values

A

25

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75
Q

Normal Phosphorus (P) Values

A

1.2

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76
Q

Capillary Hydrostatic Pressure

A

Pressure drives fluid out of capillary (filtration) and occurs highest at arteriolar end of capillary and lowest at venular end (think feeding tissues)

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77
Q

Edema

A

Occurs when fluid moves into insterstitial space faster than it can be drained by the lymphatic system

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78
Q

Why is edema harmful

A

it increases the distance between capillary and tissue cells and that reduces the effectiveness of meeting metabolic needs

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79
Q

Causes of edema

A

hypervolemia
Decreased renal fxn
cardiac failure

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80
Q

INterstitial fluid pressure

A

Pressure determined by interstitial fluid volume and by the compliance of the tissue

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81
Q

Plasma colloid osmotic Pressure

A

Because the capillary barrier is permeable to ions, the osmotic pressure within the capillary is principally determined by plasma proteins (oncotic) that are relatively impermeable

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82
Q

Fxn of plasma colloid osmotic pressure

A

Draws from interstitial space back to capillaries

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83
Q

Molarity

A

Moles per liter

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84
Q

Molality

A

Moles per Kg

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85
Q

Normal Osmolarity

A

285-290 mOsm/L around 273 mOsm/L

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86
Q

NS (Normal Saline)

A

Slightly hyperosmolar
at 308 mOsm/L

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87
Q

LR (Lactated Ringers)

A

Slightly hypoosmolar at 283 mOsm/L

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88
Q

Plasmalyte

A

Isoosmolar (Seen mostly in cardiac trauma, and large blood loss cases)

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89
Q

Crystalloids

A

Used to replace maintenance of fluid requirement, deficits, evaporate losses, and third space losses

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90
Q

Fluid that is cheap, readily leave intravascular system and go to the interstitial space

A

Crystalloids

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91
Q

Normal Saline

A

Has same NaCL balance as the body

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92
Q

Large volumes of NaCl can cause

A

Dilutional hyperchloremic acidosis b/c of its high Cl- concentration

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93
Q

Normal saline uses

A

Renal disease patients (No K+)
Giving PRBCs (No Calcium)

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94
Q

Lactated Ringers (LR)

A

Most physiological solution when large volumes are needed

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95
Q

LR Osmolarity

A

SLightly hypotonic, 100mL free water/L

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96
Q

The liver metabolizes lactate into

A

Bicarbonate

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97
Q

5% Dextrose in Water (D5W)

A

Dextrose in metabolized leaving a large volume of free water
Used for pts on Sodium (Na+) Restriction

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98
Q

Percentages in IV Fluids and medications represent

A

Number of grams per mL of dilutent %g/mL

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99
Q

IV half-life of crystalloids

A

20-30 min

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100
Q

IV Half-Life of COlloids

A

3-6 hours

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101
Q

Colloids replace blood loss at what ratio

A

1:1

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102
Q

Colloids

A

Used to replace blood loss or restore intravascular volume
It’s a solution of proteins & sugars with high molecular weight….large enough to exert oncotic pressure

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103
Q

Types of Colloids

A

Albumin
Hetastarch & Pentastarch

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104
Q

Hetastarch and Pentastarch

A

derived from plasma proteins or synthetic glucose polymers

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105
Q

Albumin

A

derived from human blood (5% or 25%)

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106
Q

Which type of fluid replacement type is a plasma volume expander?

A

Colloids

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107
Q

Which is more expensive? Colloids or crystalloids?

A

Colloids

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108
Q

Hetastarch

A

Derived from the starch amylopectin, given as 6% solution in 0.9%NS or LR
Effect: is plasma volume expansion
Elimination: by kidney, degraded by circulating enzyme amylase
Half life IV: Hetastarch 25 hours

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109
Q

Hetastarch/ Pentastarch contraindications

A

pts with known sensitivity to hydroxyethyl starch, with a coagulopathy, with Congestive heart failure (CHF) where vol overload is a problem or with pts with oliguria or anuria (little urine or no urine)

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110
Q

Use for Albumin

A

Used to increase intravascular volume for decreased blood pressure

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111
Q

Complications of fluid therapy

A

Peripheral Edema
Pulmonary Edema
Increased Intracranial Pressure (ICP)
Coagulopathies
Colloid allergy

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112
Q

Fluid losses are greater when

A
  • vomiting, diarrhea, bowel prep
    • fever
    • hyperventilation
    • loss of skin integrity (burns)
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113
Q

Insensible fluid loss

A

No electrolytes involved like in sweat.
Evaporative water loss from the respiratory tract.
-Insensible daily loss is 400 mL in adult
Evaporation of H2O that crosses skin via diffusion.
-Insensible loss from respiration is 400 mL/day

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114
Q

Redistribution (3rd Spacing)

A

Shifting of fluid from vasculature to interstitial space
Traumatized tissue becomes edematous
3rd space loss is isotonic- replaces with LR

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115
Q

3rd Spacing is caused by

A

caused by tissue edema (ie: surgical trauma pulls fluid from interstitial space)

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116
Q

Blood Loss calculation

A

Volume in suction minus irrigation used
Volume on drapes
Volume on the floor
Volume in surgical sponges

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117
Q

If there is substantial bloood loss intraoperatively, what should occur?

A

Serial monitoring of the patient’s hematocrit is warranted

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118
Q

4x4 sponge holds how much blood?

A

10mL

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119
Q

Raytec sponge will hold how much blood?

A

10-20mL

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120
Q

Laps

A

will hold 100mL of blood fully soaked

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121
Q

Normal urine output in the OR

A

1-2mL/kg/hr

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122
Q

Oligouria

A

Reduced urine production
<.5mL/kg/hr
May be a sign of dehydration, urinary obstruction, renal failure

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123
Q

Anuria

A

No urine output

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124
Q

H&H consists of

A

Hemoglobin and Hematocrit

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125
Q

Normal Hemoglobin levels

A

10-13

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126
Q

Normal Hematocrit Values

A

Men: 42-52
Women: 37-47

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127
Q

How do Hemoglobin and Hematocrit relate?

A

Hematocrit = 3 x Hgb

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128
Q

EBV Equation

A

kg x BV (mL/kg)

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129
Q

Blood volume for neonates

A

Premature 95 mL/kg
Full-term 85mL/kg

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130
Q

Blood Volume for Infants

A

80mL/kg

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131
Q

Blood volume for adults

A

Male 75mL/kg
Female 65mL/kg

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132
Q

ABL

A

Allowable Blood Loss

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133
Q

ABL Equation

A

ABL = EBV x (Hct i – Hct f)/
Hct i
Wt = Weight in kg
EBV = Estimated blood volume (mL)
Hct i = Hematocrit initial (use in decimal value) Ie: Hct = 45%, use 0.45
Hct f = Hematocrit final

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134
Q

Loss of skin causes

A

hypothermia, increased water loss, increases risk for infection and sepsis

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135
Q

Minimal tissue trauma additional fluid replacement

A

2-4mL/kg

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136
Q

Moderate tissue trauma additional fluid replacement

A

4-6 mL/kg

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137
Q

Severe tissue trauma addional fluid replacement

A

6-8mL/kg

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138
Q

Midazolam/Versed Drug class

A

Benzodiazepine

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139
Q

Midazolam uses

A

Anxiolysis (anterograde) amnesia, sedation, andiconvulsant

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140
Q

Midazolam concentration

A

1mg/mL

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141
Q

Midazolam MOA

A

GABA Agonist- activates inhibitory neurotransmitter in the brain

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142
Q

Midazolam usual adult bolus

A

1-2mg

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143
Q

Caution for Midazolam

A

Synergy w/ Opioids
Liver Biotransformation into end products that are renally secreted (renal failure leads to prolonged effect)
Elderly require less or none at all because of risk of delirium

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144
Q

Benzodiazepine Reversal Drug

A

Flumazenil

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145
Q

Flumazenil use

A

reversing the sedative and respiratory depression of a benzodiazepine overdose

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146
Q

Cautions on Flumazenil

A

Can cause siezures in patients with rapid benziodiazepine reversal

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147
Q

Adult dose for flumazenil (reversal)

A

.2mg over 5 seconds
Repeat .1mg q 1min to a total of 1mg

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148
Q

Fentanyl Concentration

A

50mcg/mL

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149
Q

Fentanyl Dose

A

1-2mcg/kg

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150
Q

Fentanyl Infusion Dose

A

1-2 mcg/kg/hr

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151
Q

Routes of administration for Fentanyl

A

PO, IV, Transdermal patch

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152
Q

Duration of Action for Fentanyl

A

30-60 minutes

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153
Q

How is fentanyl metabolized?

A

75% is metabolized by pulmonary uptake, which helps it last longer

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154
Q

How strong is fentanyl compared to morphine?

A

100x stronger than morphine

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155
Q

Which opioid is preferred over Morphine because it causes less histamine release?

A

Dilaudid

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156
Q

Dilaudid Concentration

A

1-2mg/mL

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157
Q

Dilaudid dose

A

01-.05mg/kg

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158
Q

Bolus dose for Dilaudid

A

0.2mg/dose titrated to respiratory rate

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159
Q

Routes of administration for Dilaudid

A

IV, PO

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160
Q

Peak effect of Dilaudid

A

10-20min

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161
Q

Duration of Dilaudid

A

3-4 Hours

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162
Q

How strong is Dilaudid in comparison to Morphine?

A

10x stronger

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163
Q

Dilaudid Metabolism and Clearance

A

H3G Liver biotransformation, can be neurotoxic (active metabolite)
Renal Clearance

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164
Q

Meperidine Trade Name

A

Demerol

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165
Q

Use for Meperidine/Demerol

A

Post-Op Shivering

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166
Q

Dose for Meperidine

A

12.5mg
May be repeated once
Post-Op Shivering 25mg IV

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167
Q

Time to peak effect of Meperidine

A

15min

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168
Q

Duration of Action for Meperidine

A

2-3 hours

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169
Q

Meperidine strength compared to Morphine?

A

1/10x

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170
Q

Meperidine Metabolism/ Clearance

A

Liver biotransformation into norMeperidine, an active metabolite
Renal Excretion of metabolite can lead to CNS Excitability

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171
Q

Remifentanil Trade Name

A

Ultiva

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172
Q

Remifentanil MOA

A

Potent Mu agonist mainly used as an infusion due to its rapid onset and metabolism

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173
Q

Remifentanil Dose

A

Titrated infusion .5-1mcg/kg/min

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174
Q

Bolus Dose for Remifentanil

A

1-2mcg/Kg (not as common)

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175
Q

Duration of Action for Remifentanil

A

3-4 Minutes (stays consistent regardless of duration of infusion)

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176
Q

Remifentanil metabolism

A

Broken down by non-specific tissue esterases into remifentanil acid
Renal Excretion

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177
Q

What drug is used to reverse Opioids

A

Naloxone/ Narcan

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178
Q

Narcan/ Naloxone use

A

Reversing sedative and respiratory depression of a relative opiod overdose

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179
Q

Considerations when administering Narcan/ Naloxone

A

It may wear off before the opioid effects do and may require re-dosing
May cause flash pulmonary edema

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180
Q

Onset of Naloxone/Narcan

A

2 min

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181
Q

Duration of Action of Narcan

A

30 Min

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182
Q

Typical adult dose of Narcan

A

0.04mg IV (40 mcg)
Needs to be dilutedS

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183
Q

Stock concentration of Naloxone/Narcan

A

.4mg/mL *Needs to be diluted

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184
Q

Mechanism of Action for Local Anesthetics

A

Block nerve transmission by blocking Na+ Channels inside the cell, inhibiting Na+ influx and propagation of an action potential (Nerve impulse)

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185
Q

Ionic movement in Local anesthetic Mechanism of action

A

LAs must be uncharged to pass thru the cell membrane, but then need to be charged to bind to Na+ channel inside the cell

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186
Q

Onset of Local Anesthetics can be affected by

A

Decreasing pKa Speeds onset

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187
Q

How does chloroprocaine work so fast?

A

Results from high concentration used despite its high pKa

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188
Q

What is the fastest acting Local Anesthetic

A

Chloroprocaine, used in emergency C-sections

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189
Q

How does Lipid solubility relate to potency in Local Anesthetics?

A

Lipid Solubility increases potency

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190
Q

Local Anesthetics in order of potency

A

Tetracaine-> Bupivicaine-> Lidocaine-> MepivicaineA

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191
Q

Amide Local Anesthetics

A

Have an I in them
LIdocaine
MepIvicaine
BupIvicaine
RopIvicaine

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192
Q

Ester Local Anesthetics

A

Procaine
Chloroprocaine
Tetracaine
Cocaine
Benzocaine

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193
Q

How are amide local anesthetics metabolized

A

Liver biotransformation

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194
Q

How are Ester local anesthetics metabolized?

A

Pseudocholinesterases

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195
Q

Lidocaine infiltration dose

A

5mg/kg without Epi
7mg/kg with epi

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196
Q

Lidocaine use in intubation

A

Used to blunt airway reflexes during induction at 1mg/kg given IV

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197
Q

What local anesthetic can be given IV?

A

Lidocaine

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198
Q

Can Bupivicaine be delivered Intravenously

A

NO,
can lead to Local Anesthetic Toxxicity (LAST) and cardiac arrest

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199
Q

Routes of administration for Bupivicaine

A

Skin infiltration, neuraxial

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200
Q

Neuraxial anesthesia

A

Spinal
Epidurals

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201
Q

Max dose of Bupivicaine

A

2.5mg/Kg
3 mg/Kg w epi

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202
Q

Propofol MOA

A

GABA Mediated

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203
Q

Propofol Dose

A

1.5-2.5mg/kg

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204
Q

Propofol Concentration

A

10mg/mL

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205
Q

Propofol Infusion Dose

A

25-200 mg/kg/min

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206
Q

Considerations for Propofol

A

Can cause bacterial growth due to lipid emulsion. Change tubing after 6 hours

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207
Q

Propofol effects

A

Decrease BP, Cardiac Contractility
Respiratory depressant causing apnea
Cerebral Protectant (Lower oxygen demand in the brain)
Causes burning on IV Push (Give Lidocaine first)

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208
Q

Propofol metabolism and clearance

A

Liver metabolism
Renal Clearance

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209
Q

Etomidate Cardiac Effects

A

Cardiostable
Can be used for induction for patients with cardiomyopathy

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210
Q

Etomidate MOA

A

Reticular activating system depression

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211
Q

Concentration of Etomidate

A

2mg/mL

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212
Q

Dose of Etomidate

A

.1-.4mg/kg (Adult)

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213
Q

Effects of Etomidate

A

Burns when injected
PONV
Myoclonus
Causes Adrenal Suppression

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214
Q

Etomidate Metabolism/Clearance

A

Liver Enzymes and plasma Esterases (Not as rapid as propofol)

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215
Q

Ketamine Drug Class

A

Phencyclidine (PCP)

216
Q

Ketamine MOA

A

NMDA Antagonist (Dissociation of Thalmic and Limbic systems)

217
Q

Ketamine Concentration

A

10, 50, 100mg/mL

218
Q

Induction dose for Ketamine (IV)

A

1-2.5mg/kg

219
Q

IM induction dose for Ketamine

A

4-8mg/kg

220
Q

Uses for ketamine

A

Induction, Analgesia, Amnesia

221
Q

Ketamine effect on the heart

A

Doesn’t depress HR and BP, good for Cardiomyopathy

222
Q

Benefit of using Ketamine as an analgesic vs. Opioids

A

Doens’t depress respiratory rate
Great for analgesia and avoiding opioid induced side effects/Respiratory depression

223
Q

What medication can be given IM for induction?

A

Ketamine (4-8mg/kg)

224
Q

Side effects of Ketamine

A

Increase RR, HR, BP
Increase in Salivation
Causes Delirium/hallucinations

225
Q

What adjunct drugs can we use for Ketamine’s side effects (Delirium/hallucinations + excess salivation)?

A

Midazolam for delirium
Glycopyrrolate for excess secretions

226
Q

Absorption time for Ketamine when given IM

A

10-15mins

227
Q

Ketamine Metabolism/ Clearance

A

Biotransformed into active metabolite Norketamine
Renal Excretion- with large doses can be prolonged in ESRD

228
Q

Volatile Anesthetics currently used

A

Nitrous Oxide
Sevoflurane
Desflurane
Isoflurane

229
Q

Which volatile anesthetic can be used for induction

A

Sevoflurane

230
Q

Why can’t desflurane be used for gas induction?

A

It is an airway irritant

231
Q

Why can’t Isoflurane be used for gas induction?

A

It takes too long to take effectWh

232
Q

Why can’t Nitrous oxide be used for gas induction?

A

It is impossible to achieve 1 MAC with nitrous oxide

233
Q

How do volatile anesthetics work?

A

Causes general anesthesia (Amnesia, Anesthesia, Akinesia) at varying concentrations in the blood/lungs

234
Q

How is volatile anesthetic effectiveness measured

A

MAC- Minimum alveolar concentration

235
Q

Define MAC-1

A

The concentration of gas that suppresses movement in 50% of surgical patients

236
Q

How does MAC change with age?

A

Decreases by 6% every decade after 40 years

237
Q

What factors can increase MAC

A

Acute Amphetamine use
Cocaine Use
Ephedrine
Ethanol (Chronic use)
hypernatremia
Hyperthermia

238
Q

MAC is highest at what age?

A

6 months

239
Q

Factors that decrease MAC

A

barbituates
Benzodiazepines
Ketamine
Ethanol (Acute use)
Local Anesthetics
Opioids
Lithium
Verapimil
Elderly age
Anemia
Pregnancy

240
Q

How are volatile anesthetics metabolized?

A

Absorbed via the lungs and eliminated via the lungs

241
Q

Anesthetic effect of volatile anesthetics is determined by

A

The partial pressure of the brain (Pbr)
Hard to measure clinically, so we use the lungs as a surrogate

242
Q

With volatile anesthetics, when does induction occur?

A

When FA=Fi

243
Q

Blood Gas Partition Coefficient

A

The ratio of gas dissolved in the blood versus what does not dissolve is a unique property of each gas and determines onset/uptake of the gas
Agents with low solubility in the blood saturate the blood quicker. Any additional molecules of gas after saturation are then transferred to the brain

244
Q

Blood Gas Partition Coefficient for Nitrous Oxide

A

0.47

245
Q

MAC % for Nitrous Oxide

A

104%

246
Q

Blood Gas Partition Coefficient for Desflurane

A

0.45

247
Q

Desflurane MAC%

A

6

248
Q

Sevoflurane Blood Gas Partition Coefficient

A

.65

249
Q

Sevoflurane MAC%

A

2

250
Q

Isoflurane MAC%

A

1.4

251
Q

Isoflurane Blood Gas Patition Coefficient

A

1.4

252
Q

Volatile anesthetic effects on BP

A

Decreases with increasing concentration of volatiles

253
Q

Volatile Anesthetic effects on HR

A

HR incrases with increasing concentrations of volatiles (Desflurane above 1 MAC is most clinically relevant)

254
Q

Volatile Anesthetic effects on Respiratory rate

A

Increase RR and lower tidal volumes in varying concentrations

255
Q

What type of drug is a bronchodilator?

A

Volatile Anesthetics

256
Q

What drugs can be used during bronchospasms or asthma attacks

A

Volatile Anesthetics, specifically Sevoflurane

257
Q

Volatile Anesthetic effects on Cerebral Bloodflow (CBF)

A

Increased Cerebral Bloodflow and can decrease Cerebral metabolic rate

258
Q

Volatile Anesthetic effects on Neuromonitoring

A

Can cause Decreased SSEP and MEP firings

259
Q

Sevoflurane Induction

A

Slower than Desflurane, faster than Isoflurane
Intermediate emergence time

260
Q

Sevoflurane concerns

A

Can be metabolized and broken down into a neprotoxic byproduct called compound A at low fresh gas flows

261
Q

Desflurane onset time

A

Fastest of the volatile anesthetics
Also has fast emergence

262
Q

Desflurane Concerns

A

Cost
Airway Irritant
Pungent smell
Caution in patients with Asthma/ COPD
Can lead to Carbon Monoxide poisoning in older CO2 Absorbers

263
Q

Isoflurane characteristics

A

Slow onset time, cannot be used for inhalation induction
Pungent and can be an airway irritant
Cheap

264
Q

Nitrous Oxide Onset speed

A

Fast

265
Q

Nitrous Oxide Concerns

A

PONV
Can fill enclosed airspaces
Avoid in COPD/ Lap procedures/inner ear/ LMA/ Intracranial procedures/ Pneumothorax

266
Q

How does Nitrous Oxide affect Vitamin Metabolism?

A

Can affect Vitamin B12 Metabolism

267
Q

Four Stages of Anesthesia

A

Analgesia
Excitation
Surgical Anesthesia
Coma

268
Q

Stage 1 of Anesthesia

A

Analgesia
The patient becomes sedated

269
Q

Stage 2 of Anesthesia

A

Excitation
There is an increase in heart rate and blood pressure

270
Q

Stage 3 of Anesthesia

A

HR and BP begin to return to normal
Patient is deep enough for surgery to begin

271
Q

Stage 4 of Anesthesia

A

Coma
The patient’s vital signs collapse

272
Q

Uses for Neuromuscular blockers

A

Chemically paralyze skeletal muscle at the NMJ

273
Q

NdMB MOA

A

Blocking nicotinic acetylcholine receptors

274
Q

D-NMBA MOA

A

Causing a prolonged depolarization

275
Q

WHich neuromuscular blocking agent is short acting

A

Succinylcholine

276
Q

What is a long-acting non-depolarizing Neuromuscular Blocking agent

A

Pancuronium

277
Q

Succinylcholine MOA

A

prolonged depolarization of NMJ (inactivating Na+ channels)

278
Q

Succinylcholine dose

A

1-2mg/kg, can also be given IM

279
Q

DOA for Succinylcholine

A

Rapid onset 30-60 seconds, hydrolyzed in 5-10 minutes

280
Q

Metabolism of Succinylcholine

A

Hydrolyzed by pseudocholinesterases in plasma prior to reaching the NMJ

281
Q

Situations where SUccinylcholine is preferred

A

RSI
Full stomach
Difficult Airway

282
Q

Side effects of Succinylcholine

A

Cardiac Dysrhythmias
Bradycardia, junctional rhythm, Sinus arrest
Hyperkalemia
Myalgia
Sore Muscles
Myoblobinemia
Increased intragastric/intracranial/
intraocular pressure

283
Q

Contraindications of Succinylcholine

A

Muscular Dystrophy
Burn Patients
Muscle Atrophy patients

284
Q

Pseudocholinesterase defficiency

A
285
Q

Pseudocholinesterase

A

a glycoprotein enzyme produced by the livr

286
Q

Dibucaine

A

An Amide Local Anesthetic used to test for Pseudocholinesterase deficiency
When administered IV, capable of inhibting the plasma cholinesterase enzyme

287
Q

In normal patients, dibucaine will inhibit

A

80% of enzyme activity which corresponds to dibucaine number of 80

288
Q

Homozygous typical pseudocholinesterase

A

Normal Dibucaine 70-80

289
Q

Heterozygous atypical Pseudocholinesterase

A

1/480 incidence
Lengthended response 50-100%
Dibucaine number 50-60

290
Q

Homozygous atypical pseudocholinesterase

A

1/3200
Dibucaine Number 20-30
Prolonged 4-8 hours

291
Q

Which genotype for pseudocholinesterase will have a prolonged effect for 4-8 hours and require a transfer to the ICU?

A

Homozygous Atypical
Dibucaine number 20-30

292
Q

Rocuronium COncentration

A

10mg/mL

293
Q

Intubation dose of ROcuronium

A

.6-1.2 mg/kg

294
Q

Onset of Rocuronium

A

1-3 minutes

295
Q

DOA of ROcuronium

A

30-80 mins

296
Q

Clearance of Rocuronium

A

Hepatic Metabolism and Renal excretion

297
Q

Cautions when using ROcuronium

A

ESRD patients
Reduce in chronic kidney disease liver

298
Q

Doses of 1.2mg/kg of Rocuronium can achieve what

A

Muscle paralysis in <1min, making it useful for RSI when Sux is contraindicated

299
Q

Vecuronium concentration

A

1mg/mL
from a 10mg Powder

300
Q

intubation dose of Vecuronium

A

.08-.12 mg/kg

301
Q

Vecuronium onset

A

3-5 mins

302
Q

Vecuronium DOA

A

20-35

303
Q

Vecuronium Clearance

A

Hepatic Metabolism and renal excretion

304
Q

Cisatracurium COncentration

A

2mg/mL

305
Q

Cisatracurium intubation dose

A

.1-.2 mg/kg

306
Q

ONset of Cisatracurium

A

3-5min

307
Q

DOA of Cisatracurium

A

20-35 min

308
Q

Clearance of Cisatracurium

A

Organ dependent form of elimination by being broken down by Hoffman Elimination in plasma

309
Q

What patient population is especially good for Cisatracurium use? WHy?

A

Due to its unique clearance, cisatracurium is generally used in severe renal or liver failure patients

310
Q

What neuromuscular blockers cannot be reversed with Sugammadex?

A

Succinylcholine
Cisatracurium

311
Q

Train of 4 Monitoring

A

Peripheral stimulation of 4 successive electrical impulses from a nerve stimulator
Each twitch causes a release of ACh at the NMJ

312
Q

If there is no paralysis, how will the TOF monitor reflect?

A

4/4 (4 twitches) with no fade

313
Q

If the patient is fully paralyzed, how will the TOF Monitor reflect?

A

0/4 (No Twitches)

314
Q

The degree of twitches indicates the degree of

A

Paralysis
this will guide the dose of the reversal agent

315
Q

How do neuromuscular blocking reversals work?

A

Unbinding the NMB from the Ach Receptor (Sugammadex) or indirectly by outcompeting the NMB from the Ach receptor by flooding the NMJ w/ Ach (Neostigmine)

316
Q

Common TO4 MOnitoring Sites

A

Ulnar Nerve
Facial Nerve
Posterior Tibial nerve

317
Q

TOF Ratio

A

> =0.9 as measured by the Adductor POlicis Muscle

318
Q

Neostigmine MOA

A

Anticholinesterase
Inhibits breakdown of Ach in the NmJ, allowing a higher amount of Ach to compete with NMBA at the NMJ

319
Q

Dose of Neostigmine

A

.04-.08mg/kg with a max dose of 5mg (Lower doses preferred w/ lower TOF ratios)

320
Q

DOA of Neostigmine

A

10-30 min for full effect since it is an inhibiting enzyme and indirectly increasing Ach levels

321
Q

Side effects of Neostigmine

A

SLUDGE
It increases ACh unspecifically by inhibiting AChE, it causes parasympathetic activation as well

322
Q

Since Neostigmine produces a parasympathetic activation as a side effect, what must we do?

A

Give an antimuscarinic (Glycopyrrolate) as an adjunct

323
Q

SLUDGE

A

Salivation
Lacrimation
Urination
Defecation
GI Upset
Emesis
Bradycardia/Bronchospasm

324
Q

Sugammadex

A

Directly antagonizes steroid NMB (Roc/Vec) by encapsulating the drug

325
Q

How fast does sugammadex work?

A

2-3 minutes with very few side effects

326
Q
A
327
Q

Concerns with Sugammadex

A

THe bound drug is renally cleared and may not be removed with dialysis, so use with caution in ESRD Patients

328
Q

Sugammadex dose in 4/4 TOF

A

1 mg/kg

329
Q

Sugammadex dose in 3/4

A

2 mg/kg

330
Q

Sugammadex dose in 2/4

A

2 mg/kg

331
Q

Sugammadex dose in 1/4

A

4mg/kg

332
Q

Sugammadex dose in 0 TO4 w/ 4/4 PTC

A

4mg/kg

333
Q

Sugammadex dose in 0 TO4 with NO PTC

A

16 mg/kg

334
Q

PONV

A

`POst-Operative Nausea and Vomiting

335
Q

Risks for PONv

A

Female
Nonsmoker
History of PONV
History of MOtion sickness
<50yo

336
Q

What do we use/do that can cause PONV

A

VOlatile Anesthetics
Use of N2O
Duration of Anesthesia
Type of Surgery
Use of Opioids intraoperatively
post-op opioids

337
Q

Dexamethasone typical adult dose

A

4mg

338
Q

Dexamethasone contraindications

A

Diabetic Patients

339
Q

Side effects of dexamethasone

A

Can have an intense burning in apocrine glands after IV Push (armpits and genitals burn like crazy)

340
Q

Ondansetron MOA

A

5-HT3 receptor

341
Q

What is Zofran best for

A

Preventing vomiting better than preventing nausea

342
Q

ZOfran Dose

A

4mg IV or 8mg PO as ODT

343
Q

Zofran concerns

A

Can Cause QT Prologations

344
Q

Nausea is beleived to be regulated by

A

The CTZ (Chemoreceptor Trigger zone) in the brainstem through several different receptors

345
Q

Benadryl Drug class

A

H1, H2, M1 Antagonist

346
Q

DOse of Benadryl

A

1mg/kg (Generally 12.5 mg for anti-emetic)

347
Q

Cautions with Benadryl

A

Can cause sedation

348
Q

ONset of Benadryl

A

<30 mins

349
Q

Uses for benadryl

A

Anti-emetic
Anaphylaxis
Puritis

350
Q

Reglan MOA/Drug class

A

D1 Antagonist, cholinergic Agonist

351
Q

Dose for Reglan

A

5-10mg

352
Q

Properites of Reglan

A

Anti-Emetic
Promotes GI MOtility via cholinergic agonism

353
Q

Onset of Reglan

A

<30 Min

354
Q

Contraindications of Reglan

A

Avoid in Parkinson’s
GI Obstruction

355
Q

Droperidol MOA

A

Dopamine Antagonist

356
Q

Dose of Droperidol

A

.625 mcg for anti-emetic

357
Q

Concerns with Droperidol

A

avoid in people with Prolonged QT syndrome , Parkinson’s

358
Q

Onset time of Droperidol

A

3-10mins (Given Prior to wakeup)

359
Q

Phenergan(Promethazine) MOA/

A

H1, M1, D1 Antagonist

360
Q

Dose for Phenergan

A

6.25mg for anti-emetic

361
Q

Phenergan COncerns

A

May cause sedation
Avoid in Parkinsons

362
Q

ONset of Phenergan

A

3-5 mins

363
Q

Use of Phenergan

A

Used as a rescue anti-Emetic in PACU due to fast onset

364
Q

Main goal of anesthesia

A

TO augment and control the autonomic nervous system during surgery

365
Q

Sympathetic Nervous system

A

Fight or Flight

366
Q

Parasympathetic Nervous system

A

Rest and digest

367
Q

Sympathetic nervous system characteristics

A

SHort pre-ganglionic fibers and long post-ganglionic fibers

368
Q

Parasympathetic Nervous system characteristics

A

Long Preganglionic fibers with short post-ganglionic fibers

369
Q

Alpha 1 Agonists (Adrenergic)

A

Vasoconstrictors
INcreases BP
Increased SVR

370
Q

B1 Agonists (Adrenergic)

A

Increases HR
Contractility
(Chronotropy/inotropy)

371
Q

B2 Agonist (Adrenergic)

A

Bronchodilators

372
Q

The CHolinergic (PNS) Response

A

Decrease HR
Decrease BP
Bronchoconstriction

373
Q

4 Factors that affect BP

A

HR
PReload
Contractility
Afterload

374
Q

COx SVR

A

=BP

375
Q

(HRx SV) x SVR

A

=BP

376
Q

(HR x (LVEDV-LESV)))x SVR

A

=BP

377
Q

LVEDV

A

Preload

378
Q

LVESV

A

Contractility of the heart

379
Q

HRx (Preload-Contractility)) x Afterload

A

=BP

380
Q

Vasoactive Medications typically

A

Increase or Decrease HR, BP, and SVR

381
Q

What is the goal for Anesthesia when maintaining BP/HR

A

Maintaining values and output within 20% of pre-operative values

382
Q

Epinephrine Drug class

A

Catechloamine/ Sympathiomimetic

383
Q

Epinephrine Use

A

Increase HR/ BP
Treat Anaphylaxis
Treat Bronchospasm
Used in Cardiac Arrest
Can be aerosolized to treat airway edema and croup

384
Q

Croup

A

disease that causes swelling in the airways and problems breathing. Children with croup often have a high-pitched “creaking” or whistling sound when breathing in. This is called stridor

385
Q

EPinephrine MOA

A

Alpha 1
Alpha 2
Beta 1
Beta 2
AGONIST

386
Q

Concentration of Epinephrine

A

1mg/mL

387
Q

Dose of Epinephrine

A

.01-.05 mcg/kg/min (Titrate to effect)

388
Q

Small Dose of Epi Receptor Effects

A

1-2mcg/min
Beta 2 Agonist

389
Q

Medium Dose of Epi

A

4mcg/min
Beta 1 Agonist

390
Q

Large Dose of Epi

A

10-20 mcg/min
Alpha and Beta Agonist

391
Q

Epinephrine as an Alpha 1 Receptor Agonist

A

Increased Vasoconstriction
Increased Peripheral Vascular Resistance
Decreased Mucosal Edema

392
Q

Epinephrine as an Alpha 2 Receptor Agonist

A

Decrease Insulin Release
Decreased Norepinephrine Release

393
Q

Epinephrine as a Beta 1 Agonist

A

Increased Inotropy
Increased Chronotropy

394
Q

Epinephrine as a Beta 2 Agonist

A

Increased Bronchodilation
Increased Vasodilation
Increased Glycogenesis
Decreased Mediator Release

395
Q

Norepinephrine Drug Class

A

Catechloamine/ Sympathiomimetics

396
Q

MOA of Levophed/ Norepinephrine

A

Potent Alpha 1 Agonist with enough Beta 1 to prevent reflex bradycardia/ Maintain HR and Cardiac Output

397
Q

MOA of Levophed/ Norepinephrine

A

Considered an Alpha 1 agonist with some B1 effects

398
Q

Concentration of Levophed/ Norepinephrine

A

1 mg/mL

399
Q

Dose of Norepinephrine

A

.01-.5mcg/kg/min (Titrate to effect)

400
Q

What is the general use of Levophed/ Norepinephrine?

A

Generally given centrally in septic/ Vasoplegic shock patients

401
Q

Concerns with Levophed

A

High doses peripherally can cause distal tissue necrosis/ ischemia from the vasoconstriction

402
Q

Ephedrine Drug glass

A

Synthetic Non-Catechloamine/ Sympathiomimetics

403
Q

Uses for Ephedrine

A

Increases HR
Increases Contractility
Increases BP

404
Q

Concentration of Ephedrine

A

5-10mg/mL

405
Q

Dose of Ephedrine

A

5-20mg

406
Q

MOA of Ephedrine

A

Stimulates release of catechloamines in pre-junctional nerve terminals and binds to alpha and beta receptors on the post-junctional membrane

407
Q

Onset of Ephedrine

A

Onset is relatively short
but longer compared to catechloamines due to its indirect mechanism of action

408
Q

Tachyphylaxis

A

Tolerance where subsequent doses are not effective, as catechloamine stores are depleted pre-junctionally

409
Q

Ephedrine indirectly releases what catechloamine

A

Norepinephrine

410
Q

Concerns with Ephedrine

A

Tachyphylaxis
Persistent blockade of adrenergic receptors
Depletion of Norepi storage

411
Q

Phenylephrine class

A

Synthetic non-catechloamine/Sympathiomimetics

412
Q

Phenylephrine MOA

A

Stimulates the Alpha 1 receptor (Increase BP/Afterload)

413
Q

Use for Phenylephrine

A

Vasoconstrictor
(increase BP, can be used as a nasal decongestant )

414
Q

Bolus DOse of Phenylephrine

A

500-100mcg or more depending on BP response

415
Q

Infusion Dose of Phenylephrine

A

.1-1 mcg/kg/min

416
Q

Cautions with Phenylephrine

A

Increases afterload, making it undesirable with certain cardiomyopathies/ Valvular Problems

Also causes Reflex Bradycardia

417
Q

What is our first choice agent when BP is low and Cardiac output is thought to be adequate

A

Phenylephrine

418
Q

Albuterol Drug Class

A

Beta 2 Agonist

419
Q

Albuterol Drug type

A

Bronchodilator
Causes smooth muscle relaxation in the bronchioles - adminstered via an inhaler or nebulizer

420
Q

Albuterol Uses

A

Treat restrictive airway disease (COPD), asthma, emphysema, bronchitis (Bronchospasm)

421
Q

What is an alternate use for Albuterol

A

Can also be used to slow premature labor

422
Q

Vasopressin

A

An endogenous form of ADH released from the posterior pituitary gland and works on V1 and V2 Receptors

423
Q

Vasopressin works on which receptors?

A

V1
V2

424
Q

Vasopressin V1 MOA

A

Increases BP via increased SVR without theoretically reducing cardiac output

425
Q

Vasopressin V2 MOA

A

Increased blood Volume by increasing water reabsorption from the kidney (ADH Action)

426
Q

Vasopressin Metabolism

A

Hepatic/Renal

427
Q

Vasopressin Half-Life

A

10-20 Mins

428
Q

Bolus Dose of Vasopressin

A

.5-1.0 unit bolus for refractory Hypotension

429
Q

Septic Shock Dose for Vasopressin

A

.02-.1 Units/min for septic shock infusion

430
Q

Cautions for Vasopressin

A

Gastric hypoperfusion from potent vasoconstriction: Bowel Ischemia/ Raised Liver enzymes/ reduced platelet count

431
Q

Higher doses of Vasopressin may cause

A

Myocardial Ischemia
Hyponatremia
Cutaneous Necrosis from extravasation

432
Q

Hyponatremia

A

Low Sodium Values

433
Q

Effect of Hyponatremia

A

Seizures, delirium

434
Q

Indications for Vasopressin

A

Vasoplegic/ Septic Shock
Refractory Hypotension
+ Lisinopril administration

435
Q

What patient population would benefit from Vasopressin over other pressors?

A

Pulmonary Hypertension patients could benefit from Vasopressin since there is alpha receptors in the pulmonary artery , but not V1 receptors

436
Q

How can vasopressin be substituted for epineprine in a code/ Cardiac Arrest?

A

Single dose of 40 units IV may replace a round of 1mg of epi in a code

437
Q

Anti-Hypertensives

A

Metoprolol
Labetalol
Esmolol
Hydralazine (Vasodilator)
Calcium Channel Blocker ( Nicardipine)

438
Q

Beta Blockers MOA

A

Work by blocking B1 receptors (Decrease HR, Inotropy, and BP)

439
Q

Overdosing a beta blocker can result in

A

Bradycardia
CHF in cardiomyopathy

440
Q

Which Beta Blocker has a higher affect on BP than HR?

A

Labetalol

441
Q

Labetalol affects what receptors?

A

Alpha 1
Beta 1
Beta 2

442
Q

Labetalol Use

A

Lowe HR and BP (Better at lowering BP)

443
Q

Concetration of Labetalol

A

5mg/mL

444
Q

Bolus dose of Labetalol

A

5mg boluses titrated to effect

445
Q

Esmolol Drug class

A

Cardioselective B1 Blocker

446
Q

Esmolol Use

A

Short-Term Decrease in HR

447
Q

Esmolol Concentration

A

10mg/mL in 10mL

448
Q

Dose of Esmolol

A

Titrated boluses usually

449
Q

Esmolol Duration of Action

A

Short DOA
1-3 minutes due to elimination by plasma esterases

450
Q

Metoprolol Drug Class

A

Cardioselective B1 Blocker

451
Q

Uses for Metoprolol

A

Decrease HR/BP

452
Q

Concentration of Metoprolol

A

1mg/mL

453
Q

Dose of Metoprolol

A

1-2mg

454
Q

Metoprolol DOA

A

Longer DOA and often used for chronic HTN

455
Q

Hydralazine Class

A

Vasodilator

456
Q

Hydralazine use

A

HTN-Great for hypertensive patient who may have some underlying cardiomyopathy where decreasing inotropy/ HR may be contraindicated

457
Q

Concentration of Hydralazine

A

20mg in 1 mL

458
Q

Dose of Hydralazine

A

5mg 10mg titrated to effect

459
Q

Onset of Hydralazine

A

15-20mins

460
Q

Duration of Hydralazine

A

6-8 hours

461
Q

Cautions of Hydralazine

A

Prinicpal arterial dilator and long onset time, so easy to overdose and cause hypotension

462
Q

Two types of calcium channel blockers

A

Dihdydropyridines
Non-dihydropiridines

463
Q

Dihydropyridines

A

Ca2+ channel blockers
Primary vasodilators (Don’t decrease HR)

464
Q

Non-Dihydropyridines

A

Ca2+ Channel blockers
More cardioselective and decrease HR and causes vasodilation

465
Q

Nicardipine Uses

A

Lowers BP without causing an increase in ICP

466
Q

Non-dihydropyridine drugs

A

Diltiazem, verapamil

467
Q

What cases would probaby benefit from Nicardipine?

A

Neuro cases or those that require tight BP control

468
Q

Dihydropyridine drugs

A

Nicardipine, Clevidopine, nifedipine, amlodipine

469
Q

Nicardipine infusion dose

A

5-15mg/hr

470
Q

Nicardipine blous dose

A

100-200mcg

471
Q

Nicardipine Onset

A

1-5 mins

472
Q

Nicardipine Concentration

A

.2mg/mL

473
Q

Anticholinergic Drugs

A

Glycopyrrolate, Atropine, Scopolamine

474
Q

MOA of Anticholinergics

A

Antagonizes the sympathetic NS via blockade of muscarinic Ach receptors

475
Q

Uses for Anticholinergics

A

Bradycardia Treatment
Used in conjunction with acylcholinesterase inhibitors to block parasympathetic activation (Neostigmine)
Bronchodilation
PONV prevention

476
Q

Atropine Uses

A

Bradycardia response
Vagal Response
NMB Reversal

477
Q

Concentration of Atropine

A

.4mg/mL

478
Q

Atropine bradycardia dose

A

.4-.6 mg (up to 3mg)

479
Q

Which drug works faster? Glycopyrrolate or Atropine

A

Atropine

480
Q

Which Anticholinergic drug crosses the bloodbrain barrier?

A

Atropine

481
Q

Glycopyrrolate uses

A

Antisialagogue
NMB Reversal
Bradycardia

482
Q

Concentration of Glycopyrrolate

A

.2mg/mL

483
Q

Premed antisialagogue dose of Glycopyrrolate

A

.2mg IM

484
Q

Glycopyrrolate reversal dose

A

.2mg per 1mg Neostigmine

485
Q

Glycopyrrolate Bradycardia dose

A

.2mg or more

486
Q

Scopolamine Uses

A

Antiemetic
delivered via transdermal patch behind the ear

487
Q

Precedex trade name

A

Dexmedetomidine

488
Q

Side effects from Scopolamine crossing the BBB

A

Blurred vision
Dry mouth and throat
Slight sedative/ delirium in elderly patients

489
Q

Precedex MOA

A

Alpha 2 agonist (Binds presynaptic ganglion inhibiting Norepi release)

490
Q

Use for Precedex

A

Sedation/ anxiolysis without respiratory depression and able to respond to commands, analgesia, sedation for fiberoptic intubations, smooth emergence

491
Q

Concentration of Precedex

A

Diluted typically to 4mcg/kg over 5-15 minutes followed by infusion dose of .2-1mcg/kg/hr

492
Q

Precedex Metabolism

A

Liver

493
Q

Side effects of Precedex

A

Large boluses can cause HTN, but more frequently we see sympthiolysis (Bradycardia/ hypotension) with infusion

494
Q

Precedex is great for

A

Sedation with minimal respiratory depression and the patient will respond to commands . Also a great analgesic and is used frequently for multimodal pain modalities

495
Q

Describe the negative Feedback Loop of Precedex

A

Precedex blocks presynaptic Alpha 2 receptors in a negative feedback loop, resulting in the suppression of Norepinephrine release

496
Q

5 A’s of Anesthesia

A

Amnesia
Anesthesia
Analgesia
Anxiolysis
Akinesa

497
Q

Amnesic

A

Causes Memory loss for an event/time period

498
Q

ASA 1

A

Normal Healthy Patient

499
Q

ASA 2

A

Patient with mild systemic disease

500
Q

ASA 3

A

Patient with severe systemic disease that is not a constant threat to life

501
Q

ASA 4

A

Patient with severe systemic disease that is a constant threat to life

502
Q

ASA 5

A

Moribund patient not expected to survive with or without surgery

503
Q

ASA 6

A

Organ donor, Brain Death, DCD

504
Q

STOP BANG Questions

A

Snoring
Tirdedness
Observed Apnea
Pressure
BMI >35kgm^-2
Age over 50
Neck Circumference >40
Gender (Male)

505
Q

High risk for OSAS (STOP-BANG)

A

> =3 positive responses

506
Q

Low risk for OSAS (Stop-Bang)

A

<3 positive Responses

507
Q

Contraindications for Nasopharyngeal Airway

A

Skull Fractures
Anticoagulants
Actively bleeding nose (Epitaxis)

508
Q

Contraindications for Oropharyngeal Airway

A

Gag Reflex intact
Foreign body obstructing the airway
Mouth Surgery

509
Q

What is the concern when a patient is under sedation without a protected airway?

A

Aspiration

510
Q

LMA/SGA Absolute Contraindications

A

Trauma
Non-Fasted Patients (RSI-GETA)
Bowel Obstruction
Emergency Surgery
Delayed Gastric Emptying

511
Q

LMA/SGA Relative Contraindications

A

Major Abdominal surgery
Pregnancy >14 weeks
Prone Positioning
Airway Surgery
Laparoscopic Surgery
Obesity (BMI>30)
Decreased Lung Compliance (W PIP>20cm H2O)
Altered Mental Status

512
Q

Why shouldn’t we let the vent pressure (w/ LMA) or bag mask pressure exceed 20cm H2O

A

Because the esophageal sphincter is opened at pressures higher than 20 cmH20

513
Q

How long do we wait after pushing Rocuronium for ET tube placement

A

3 Minutes
Start the NIBP, bag mask if not RSI

514
Q

What do we set the vent to after we have placed the ETT?

A

PCV-VG

515
Q

Most common blade sizes for direct laryngoscopy

A

Miller 2
MAC 3

516
Q

Where does the MAC Blade sit inside the patient’s mouth/airway?

A

Inside the Vallecula

517
Q

Where does the miller blade sit in the patient’s airway/mouth?

A

Elevates the epiglottis

518
Q

What can we do to improve our view during direct laryngoscopy?

A

Cricoid pressure
Video Scope
try a different blade
Try getting in a better sniff position
elevate the head of the bed for better visualization

519
Q

What classification system is used for views obtained by direct laryngoscopy?

A

Cormack-Lehane

520
Q

Predictors of difficult bag mask Ventilation

A

BOOTS
Moans
Beard, Old , Obese, toothless, snores

Mask seal
obstruction
Age
No teeth
Stiff lungs

521
Q

In theory, how long can we bag mask a patient?

A

Forever

522
Q

DAMMITS

A

Drugs
Airway
Machine
Monitors
IVs
Tube
Suction

523
Q

Drugs used for a typical GETA case

A

Versed
Fentanyl
Lidocaine
Propofol

Sux
Roc
Ephedrine/Phenylephrine

524
Q

What airway supplies will we need for each ETT Placement?

A

Stylet
Eye Tape
TUbe Tape
Laryngoscopes+ blades
Bite Block
Oral/Nasal Airway

525
Q

What’s included in Standard ASA Monitors

A

Temp
EKG (3 or more leads)
Pulse Oximeter
NIBP
EtCO2

526
Q

Malampatti I

A

Complete visualization of the soft palate

527
Q

Malampatti II

A

Complete visualization of the uvula

528
Q

Malampatti Class III

A

Visualization of only the base of the vulva

529
Q

Malampatti Class IV

A

Soft palate is not visible at all

530
Q

Planned procedure during which the patient undergoes local + sedation and analgesia. Patient is typically able to breathe on their own and respond to commands

A

MAC- Monitored Anesthesia Care

531
Q

Unlike IV drugs ___ are absorbed via the lungs and eliminated via the lungs

A

Volatile Anesthetics

532
Q

When is anesthesia achieved with volatile anesthetics

A

When inaled= ExhaledT

533
Q

TIVA-

A

Total IV Anesthesia

534
Q

Increased Risk of PONV

A

Female
Type of Surgery
Dehydration
Smoking Decreases PONV Risk
Pre-Op Anxiety

535
Q

In Volatile Anesthetics, how does Cardiac Output affect induction

A

Slow cardiac output increases speed of induction

536
Q

Induction is achieved when

A

Fa=Fi (Inspired)

537
Q
A
538
Q
A

Anesthesiologist Assistant (12 decks)

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