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ORTHO > 1st test anasthesia > Flashcards

1st test anasthesia Flashcards

1
Q

Who is in charge of controlling all physiological and physiopathological functions of the organism, administrating drugs to produce desired effects and avoid undesired effects or toxicity, as well as control renal function, hepatic function, temperature etc?

A

anesthesiologist

owner of px controlling all biological and fisiopathological functions during times in OR

therapeutic objective = give and maintain a dose in determined places for a desired effect

analgesia, amnesia

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2
Q

art of anesthesiology

A

must adjust dose and velocity of administration depending on clinical response of px

- (a lot of drugs have to be adminstered slowly)

want desired effect while avoiding undesired side effects/toxicity

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3
Q

what is succinilcoline?

A

it is a depolarizing relaxer

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4
Q

what happens if succilycholine is rapidly administrated?

A

px will present fasciculations or involuntary movements

px se retuerce

increases gastric , intraocular and incracraneal pressure –> broncoaspiration if px ate

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5
Q

3 pillars of anesthesiology

A

physiology, pharmacology, anatomy

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6
Q

ej of how to block a nervous transmission

A

local anesthetic like lidocaine to interrupt transmission of pain sensation

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7
Q

side effects of lidocaine

A

hipotension

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8
Q

role of amnesia in this subject

A

elimination of all memory for a 6-12 hr period is important

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9
Q

The point of general inhaled anesthesia?

A
  • Maintain a central depression or an anesthetic coma for surgeon to operate
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10
Q

What are the 3 aspects/principles of anesthetics?

A

pharmacological
pharmacokinetic
pharmacodynamic

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11
Q

pharmacological principal

A

○ Professional has knowledge of drug (precipirates in sun? pH? Needs to be in cold? Best administration, disolvent)

liposoluble vs hydrosoluble

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12
Q

drug known to irritate a lot veins , painful

A

propofol

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13
Q

pharmacodynamics vs pharmacokinetics

A

Pharmacodynamics is the study of how a drug affects an organism, whereas pharmacokinetics is the study of how the organism affects the drug. …

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14
Q

what are the 4 aspects/parameters of Pharmacokinetics

A

Absorpion
distribution (volume)
metabolization (velocity ,time , etc)
elimination

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15
Q

absorption depends on what 4 aspects?

A

Biodisponibilidad/Bioavailability)
Perfusion grade where it is administered (Plasma concentration of drug is greater when deposited somewhere with a lot of irrigation)
Velocity of administration
Route of administration (determines velocity of absorption)

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16
Q

what does distribution depend on?

A

○ Depends on physical chemical cx of drug, CO, and regional blood flow

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17
Q

Different types of metabolization?

A

oxidation in liver

Reduction

Hydrolysis

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18
Q

types of elimination

A

through kidney or hepatobiliary, pulmonary

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19
Q

info about drug metabolism

A

Drug metabolism is the metabolic breakdown of drugs by living organisms, usually through specialized enzymatic systems.

The study of drug metabolism is called pharmacokinetics.

The metabolism of pharmaceutical drugs is an important aspect of pharmacology and medicine. For example, the rate of metabolism determines the duration and intensity of a drug’s pharmacologic action.

The metabolism of xenobiotics is often divided into three phases:- modification, conjugation, and excretion. These reactions act in concert to detoxify xenobiotics and remove them from cells

Biotransformation occurs only for the agents at physiological pH, having low molecular weight and less complex. Biotransformation is a process specifically to make agents more polar and excretable. If biotransformation does not occur, drugs may have longer duration of action, and undesired effects are observed along with desired ones. Biotransformation, in fact, is the inactivation of pharmacological action of drugs.

Cytochrome P450:
Cytochromes are the heme proteins, present abundantly within the living kingdom. They have about thousand known kinds. Only 50 of these heme proteins are found within the humans, which are divided into 17 families and sub-families. Name is derived because it is a heme protein (abbreviation cyp) and 450 because it reacts with carbon monoxide and during the reaction absorbs light at 450 nm.
NADPH
NADPH is a flavoprotein, less abundant than cyp 450.
For every 10 molecules of cytochrome P450, only one NADPH cytochrome reductase is present

Biochemical Reactions:
Phase I reactions
Phase II reactions
Phase I reactions:
Phase I reactions are non-synthetic catabolic type of chemical reactions occurring mainly within the ER. They are the reactions in which the parent drug is converted into more soluble excretable agents by introduction or unmasking of functional component.
Example includes phenobarbitone, aromatic hydroxylation of which abolishes its hypnotic activity. Similarly, metabolism of azathioprine produces 6-mercaptopurine.
Drug products, which are water soluble are excreted by the kidneys. Sometimes this is not true and phase I compounds do not result in true inactivation and may act as functional components of phase II reactions.
Phase I reactions include:
Oxidation
Reduction
Hydrolysis

ej , reduced, hydrolisized

Reduction
Chloramphenicol, dantrolene, clonazepam

Hydrolysis
Esters: procaine, suxamethonium and aspirin
Amides: procainamide, lidocaine

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20
Q

oxidation vs reduction

A

Oxidation is a reaction in which an atom, molecule or compound loses anelectron. OIL = Oxidation Is Lost; RIG= Reduction Is Gain LEO = Lose Electron in Oxidation; GER = Gain Electron in Reduction (LEO the lion says GER)

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21
Q

oxidation in the liver/ types

A

Types of Biotransformation:
Biotransformation taking place due to different enzymes present in the body/cells is known as enzymatic elimination.

  1. Enzymatic
    a. Microsomal
    Microsomal Biotransformation:
    Enzymes responsible are present within the lipophilic membranes of endoplasmic reticulum. After isolation and putting through homogenization and fractionation, small vesicles are obtained, known as microsomes. They possess all functional, morphological properties of endoplasmic reticulum i.e. smooth and rough. Smooth ER is concerned with biotransformation and contains enzyme components while the rough ER is mainly concerned with protein synthesis.
    Enzymes isolated from ER possess enzymatic activity termed as microsomal mixed function oxidase system.
    Components:
    Cytochrome P450 (ferric, ferrous forms)
    NADPH (flavoprotein)
    Molecular oxygen
    Membrane lipids

b. Non-microsomal
Non-Microsomal Biotransformation:
The type of biotransformation in which the enzymes taking part are soluble and present within the mitochondria.

  1. Non-enzymatic (Hofmann Elimination)

Non Enzymatic Elimination:
Spontaneous, non-catalyzed and non-enzymatic type of biotransformation for highly active, unstable compounds taking place at physiological pH. Very few drugs undergo non-enzymatic elimination. Some of these include:
Mustin HCl converted into Ethyleneimonium
Atracurium converted into Laudanosine and Quartenary acid
Hexamine converted into Formaldehyde
Chlorazepate converted into Desmethyl diazepam

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22
Q

Hydrolysis

A

is a reaction in which a molecule or compound is broken down, by the addition of a water molecule (usually with an acid to catalyze the reaction)

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23
Q

atracurium and Cisatracurium are ?

A

non polarizing relaxers

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24
Q

different routes of administration of drugs

A 
oral = enteral
sublingual
rectal
subcutaneous
intramuscular
Intravenous
Intratecal, BSA, BPD
Pulmonary
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25
Q

cx of enteral administration

A 
most comfortable
economical
commonly used
needs px cooperation
ambulatory
rare in anesthesia tho
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26
Q

80-90% of drugs absorbe where

A

in second part of SI

but some in stomach

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27
Q

cx of sublingual administration

A

○ Allows you to reach greater hematic concentration due to lecho venoso, big irrigations under tongue allows greater absorption than in gastric mucous

used in urgency situatins

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28
Q

cx of rectal administration

A 
○ Fast absoprion
		○ Causes nausea and vomit
		○ Analgesics, antiinflammatories
Common for analgesics in pediatrics
when irritating
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29
Q

cx of subcutaneous administration

A

○ Slow and regular absorption drugs
○ Heparin
○ insulin

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30
Q

cx of IM administration

A

○ Slow absorption for sustancias oleosas
○ Fast for hydric substances (much more irritating)

rare in anesthesia

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31
Q

cx of IV administratin

A

○ Fast start allowing exact dosification
Adequate when administrating large volumes of drug
common in anesthesia - 90%

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32
Q

cx of intratecal, BSA, BPD

A

○ can be subarachnoid or epidural
fast, local
○ Can have effects without affecting CNS/SNS

common in anesthesia - 5-10%

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33
Q

cx of pulmonary administration

A

○ Only used in urgent cases especially when we have px with cardiac arrest that isnt canalized

	○ Drugs can be applied through orotraqueal tube
		§ Atropine Adrenaline - > 90% effectivity
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34
Q

ph with irritation?

A

alkaline irritates a lot –> flebitis(trombo)

use a high flow big vessel

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35
Q

anesthesiologist discharges after what time

A

24hr

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36
Q

theraupetic objective of pharmacodynamics

A

maintain an adequate oncentration of a drug in a specific locations with a determined desired action

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37
Q

pharmacokinetics teacher wants

A

absorption - EV
volume of distribution
metaboliation (velocity, time

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38
Q

bioavailability

A

In pharmacology, bioavailability (BA) is a subcategory of absorption and is the fraction of an administered dose of unchanged drug that reaches the systemic circulation, one of the principal pharmacokineticq properties of drugs. By definition, when a medication is administered intravenously, its bioavailability is 100%.

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39
Q

other route

A

topica, contacto, through dermis

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40
Q

monitorization of px in OR depends on

A

clinical case, severity of px status

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41
Q

minimal monitorization

A

EKG echo continuous thru whole process
non/invasive continuous systemic BP monitoring

saturation - pulse oximetry

monitor temperature

start before putting them to sleep

need pressure oygen source and hemodynamic monitor

continuous suction

laryngoscope , intubation equipment, orotraqual tube

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42
Q

CV evlautation

A

echo, prueba de fuerza, EKG

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43
Q

What is an anesthesia Machine?

A

machine that give px gases

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44
Q

high risk monitorzation

A 
measure depth of coma anesthesico
invasive pressure - arterial pressures
CO
NM relaxation
gasometry
continuous electrolye measurement
balances
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45
Q

hemodynamic monitor vs ventilation monitor

A

HD - BP, HR, CO, etc

Ventilation - ventilator parameters in qx - rate, tidal volume, and oxygen content etc

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46
Q

parts of laryngoscope

A

…

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47
Q

types of laryngoscope

A
  • 2 types: curved and straight (in px with laynx anterior and elevated)
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48
Q

must have equipment by anaesthesiologist

A

need pressure oygen source and hemodynamic monitor

continuous suction

laryngoscope , intubation equipment, orotraqual tube,nasotraqual

have a EV route ready/venous access

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49
Q

what are traqueal tubes?

A

A tracheal tube is a catheter that is inserted into the trachea for the primary purpose of establishing and maintaining a patent (open and unobstructed) airway. … An endotracheal tube is a specific type of tracheal tube that is nearly always inserted through the mouth (orotracheal) or nose (nasotracheal).

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50
Q

cxof difficult intubation

A

prominent maxilar?

macroglosia

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51
Q

naso traqual

canula de mayo

A

at inhalatory or IV with difficult intubation cx and ventilation difficult

An oropharyngeal airway (also known as an oral airway, OPA or Guedel pattern airway) is a medical device called an airway adjunct used to maintain or open a patient’s airway. It does this by preventing the tongue from covering the epiglottis, which could prevent the person from breathing. When a person becomes unconscious, the muscles in their jaw relax and allow the tongue to obstruct the airway.

In respiratory physiology, ventilation is the movement of air between the environment and the lungs via inhalation and exhalation. Thus, for organisms with lungs, it is synonymous with breathing.

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52
Q

what is traqueal intubation

A

placeent of a tube in the traqueal cavity

can be any px

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53
Q

parts of tube

A

balon(cuff?) –> to trap air and keep all gases in alveolos and not eliminated by air

some low pressyre others high pressure

balloons in sondas are to fixate them

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54
Q

first person to intubate`

A

1880 qx sir William macowen

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55
Q

inventor of laringoscope

A

1895 kerstein

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56
Q

formulated scienctific base for intubation

A

1910 Cahavallier

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57
Q

different types of intubation

A

orotraqueal - most frequent,

naso traqueal - Levin in nose

endotraqual - directly in traquea

cricodetomy

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58
Q

indications for intubation

A

To administrate OXYGEN/VENTILATION = #1

  1. Administration of inhalatory gases (nariz o boca)
  2. Px in respiratory arrest
  3. Px that present airway prolems (tumor, burn, FB, secretions)
  4. Px in cerebral coma
  5. Px that cant manage secretions (fibrocystic disease, no strength, need aspirations , fibroscopy)
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59
Q

different calibres for tubes

A

\Adult male = 7.5ml wide - 9ml wide
Woman - 6ml-7.5ml - wide,d

Kids < 5 = age + 16 divded by 4 (plus 4 dived by 5 he said?)
Selecitve intubation tubes = doble lumen

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60
Q

when is nastraqueal canulla CI

A

§ CI in <2yr px due to high incidence of adenoides in this age group

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61
Q

double lumen tubes

A

used in selective pulmonary intubation for example in thoracic qx, can block one lung at a time while working

more expensive

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62
Q

consequences of intubation

A
  • Bleed
    • Perforation of traquea is common and –> emphysema
    • Orotraqueal edema
    • Dentary rupture
    • Gastric colocation is common
    • Vocal cord lesions (wrong tube side)
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63
Q

what does tube size depend on

A

sex and age

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64
Q

Principle function of larynx?

A
  • Protection of low airways against entrance of anything (liquid, solid, bacterial)
    • Contain essential fonation organ = vocal cords (Mobile organ that elevates @ deglution and when making sound)
    • Labor (increases pressure –> increasesa abdominal pressure)
      Defecation
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65
Q

Topographic location of larynx?

A
  • Medial and anterior neck in front of pharnxy and below hyoide bone and above traqueal rings

(pharynx is continuation of esophagus)

- Relation with spine depends on age and sex 
	○lower border More elvated in woman - C4
	○ In man - lower border of larynx - C6

	○ RN C2

can palpate with finger

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66
Q

Dimensions of larynx?

A
  • 7cm long x 4cm wide - adult male

- Woman - 4.6cm long x 2.6 wide

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67
Q

Cartilage of Larynx

A
  • 6:
    ○ Impair epiglottis (search for first in direct larginoscopey), thyroid, cricoid

Pairs arytenoid (also very visible), corniculados (morgani), cuneiforms

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68
Q

classification of larynx muscles

A

extrinsic (depressors and elevators) - movement and fixation of larynx - §one Insertion in larynx and another outside

intrinsic

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69
Q

extrinsic depressor muscles - takes to original position after elvation

A

□ Sternohiodeo
□ Tirohiodeo
□ homoiodeo

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70
Q

extrinsic elevator muscles (in second deglution time and during acute sound)

A 
□ Geniohiodeo
				□ Digastric
				□ Milohiodeo
				□ Stilohiodeo
				□ Medial constricor and inferior of pharynx
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71
Q

intrinsic muscles of larynx -

A

both insertions inside larynx - responsible for vocal cord movement

§ Cricotiroideo... 
		§ Cricoaritenoid posterior muscle - 
			□
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72
Q

irrigation of larynx

A
  • Superior larynx artery
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73
Q

venous drainage of larynx

A
  • Superior laryngeal vein –> internal post. Yugular
    • Infeiror –> superior thyroid vein
    • Posteiror –> inferior thyroid vein
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74
Q

superior innervation of larynx

A

○ 2 branches
○ Internal = sensitive to all internal larynx
○ External = motor to cricoide muscle

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75
Q

inferior innervation of larynx = recurrent

A

○ Purely motor –> 2 branches
○ Internal - motor to internal config of larynx
○ External - extrinisic muscles

tension of vocal cords - must know where it is in qx - irreversible

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76
Q

both innervation of larynx are branches of

A

vagus

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77
Q

other cartilages not really seen

A

sesamoid ant, post - not really seen

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78
Q

cx of cricothyroid muscle

A

originates in lateral side of anterior arc of cricoid cartilage. some fibers go up to post inf border of thyroid lamina an dother go behind and lateral to inferior part of thyroid cartilage. - only muscle of larnx that is innervated by superior laryngeal nerve; lengthens and tenses vocal cords to take them to paramedian line

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79
Q

cx of cricoaritenoid posterior muscle

A

only one that causes apertura of vocal cords (others close)

			□ Originates in posterior part of lamina of cricoids

fibers pass up and out to insert in muscular process of arytenoid cartilage

abducter of vocal cords

innervated y recurrent laryngeal nerve

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80
Q

first anesthetic gases used

A

chloroform (serial killers)

used to be with compressa

now we use tube to administrate all gases

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81
Q

definition of general inhalatory anesthesia

A

absence of all painful stimuli induced by an anasthehtic gas

depression or anesthetic coma for a qx produce induced by inhaled agent

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82
Q

anesthesia a la reina

A

a la reina - no monitrozation of anesthesic points, higher mortalithy

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83
Q

why no balon in kids

A

no ballon in kids because sublglottic is thinnest part (<5yr) - should have some escape of gas

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84
Q

orotraqueal intubation px needs to be

A

asleep (EV resp depression or irregular) and relaxed of orofrangeal muscles (paralysis of muscles) assisted ventilatationo, then intubate and control then mark parameters

which agent depends all on px cx

vs edtraq px can be awake

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85
Q

how many needles

A

4

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86
Q

halothane causes

A

anesthetic gas
bradycardia - give atropine b4
arrhythmias - lidocaine buffer
narcotic for analgesia

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87
Q

how can ventilation be

A

spontaneous

assisted

controlled

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88
Q

Characteristics of an ideal inhalatory agent?

A
  • Shouldn’t be toxic
    ○ El éter, cloroformo, halotano (Hepatotoxicidad), el ciclopropano, el metoxiforano (Nefrotoxicidad y Hepatotoxicidad).
    • should be a good NM relaxer
      ○ Si lo hace la necesidad de utilizar un bloqueador neuromuscular será menor - sevorane best
    • should have a Wide margin of security
      ○ no importa la cantidad de horas o posiciones que el paciente tenga frecuentemente ante un gas no afecte la función de la vida.
    • Induction and recuperation should be fast
      ○ Que necesitamos que el gas duerma rápidamente al paciente pero que también se metabolice rápidamente para que despierte rápido.
    • Few cardiac alterations
      ○ BP, HR, CO MAP variables should be maintained
      ○ Maintain perfusion - not reduce blood flow to organs
      § Halotano
      ○ Al principio provocaban muchos cambios cardiacos, hoy en día los gases de usos diarios como el Isoflurano y Sevoflurano tienen mínima acción sobre la función cardiaca.
    • Should not liberate histamine
      ○ Used to have a lot of anaphylactic reactions which would further complicate hemodynamic situation - high mortality rate
      put blocker beta H1, H2 - antihistamines before
    • Shouldn’t not cause nause and vomit
      ○ Before we used to think px wasn’t recovered until they didn’t vomit cuz they all used to cause it
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89
Q

monitor position in anesthesiologist

A

in front

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90
Q

Inhalatory agents currently used?

A 
nitrous oxide- expensive - y
halothane - not really anymore, cheap
enflurane
isoforane- y
sevorane- expensive
desflurane-y - not in this country
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91
Q

CAM of halotane

A

0.74

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92
Q

Vapor pressure of halotane

A

243

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93
Q

PE of halotane

A

50.2

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94
Q

metabolis of halothane

A

10-20%
inorganic metabolites
took longer to wake up

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95
Q

CAM of enflurane

A

1.68

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96
Q

VP of enflurane

A

175

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97
Q

PE of enflurane

A

56.2

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98
Q

metabolism of Enflurane

A

3-5%

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99
Q

CAM of isoflorane

A

1.40

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100
Q

VP of isoflorane

A

250

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101
Q

PE of isoflorane

A

46.5

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102
Q

metabolism of isoflorane

A

2-3%

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103
Q

CAM of NO2

A

105

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104
Q

VP of NO2

A

1atm

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105
Q

PE of NO2

A

-89.5

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106
Q

CAM of Sevorane

A

1.7-2

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107
Q

VP of Sevorane

A

160

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108
Q

PE of Sevorane

A

55

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109
Q

Metabolism of Sevorane

A

2-3%

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110
Q

CAM of Desfloranes

A

7.2-9

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111
Q

VP of Desfloranes

A

664

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112
Q

PE of Desfloranes

A

23.5

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113
Q

Metabolism of Desfloranes

A

0.02-0.04%wh

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114
Q

what are organic compounds

A

any element that contains a carbon atom inside its molecular structure

99% of pharmacological compounds

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115
Q

potency of any organic element depnds on

A

number of carbon atoms in molecular chain (more carbon, more liposoluble)
also on any halogenated elements in molecular structure

good vapor pressure (the higher the better, start with it high and with increasing breathing rate)

ebullition point < 60 (boiling point)

low blood/gas participation

the more potent the thinner the line between therapeutic and toxic

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116
Q

toxicity dpends on?

A

more carbon means more toxic

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117
Q

how many carbon atoms until toxicity surpases therapeutic effect

A

> 7 C

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118
Q

the only inorganic compound used in medicine today

A

NO2

DONT HAVE CARBON IN molecular structure

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119
Q

the only anesthetic agent that is found in gas form in nature and of organic origen

A

el ciclo propane

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120
Q

why did ciclo propane stop being used

A

super flammable

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121
Q

anesthetic agents used today are made up of what

A

hydrocarbon, carbon and hydrogen

also they are all aliphatic compounds

receive name based on how many carbons are in their structure or depending on form in which Carbon atom is in the structure

1 = methane
2= ethane
3=propane
4=butane
5=pentane

aliphatic = lineal - ALL FARMACOS INALATORIOS
cyclic (ej ciclopropane)

H atom can be substituted for other elements suchs as

iodine (126)
fluor (18)
cloro (35.5)
Bromo (80)

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122
Q

gives potency

A

iodine (126)

cloro (35.5)

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123
Q

gives stability

A

fluor (18/)??

bromo (80) - audio/?

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124
Q

decreases inflammation - halogenated elemends

A

Bromo (80)

A halogenated compound is a combination of one or more chemical elements that includes a halogen; halogens are a group of elements that include fluorine, astatine, chlorine, bromine and iodine

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125
Q

what is the objective of modern anesthesia

A

to maintain a cerebral concentration of anesthetic that is enough to carry out qx and allow rapid recuperation

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126
Q

what do we want out of general anesthesia

A 
amnesia
analgesia
LOC
inhibition of sensorial reflexes and autonomous reflesxes
muscular relaxation
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127
Q

how can we divide general anesthesia based on its goals

A

MONITOR PX
induction to sleep for intubation
maintenance (BIS and hemodynamic observation)
recuperation

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128
Q

first anaesthetics used that were inhaled and were used for a long time

A

NO (only one still used today)
ether
clorform

later came halothane, methoxiflurane, enfflurane, isoflurane, desflurane, sevoflurane

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129
Q

balanced anesthesia

A

when we combine inhalaed and IV anesthetics

or opiods with neuroleptic

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130
Q

stages of general inhaled anesthesia by Guedel (dietileter)

A 
I
analgesia
from administration to sleep
amnesia - w/ benzo
opiod - therefore less need for inhaled agent
II 
excitement and delirium
irregular respiration, arcada
vomit
increased muscle tone, HR, BP, midriasis
finishes when px loses muscle tone
moves around
ends when px chills out

III
qx anesthesia, coma anesthetic qx
respiration controlled, miotic pupuls, decreased ocular reflexes, no ocular movements
40-60%

IV
medular depression
deep coma
depression of vasomotor center
bradycardia, severe hypotension
extreme miosis
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131
Q

what is anesthesic potency

A

the alveolar concentration at 1atm that achieves abolition of motor response to a painful stimulus in 50% of px

need 1.3 cam to abolish this response in 99% of px

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132
Q

why can CAM vary

A

px condition

meds

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133
Q

factors that intervene in potency of inhaled anesthetics (DONT??)

A

type of stimulus
duration of anesthesia
circadian rhythm
sex

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134
Q

factors that increase potency in anesthetics inhaled are

A 
hypoxia
anemia
hypotension
hypothermia
preqx use of an opiod
use of ketamine
previous use of diazepam or other benzos (lowers CAM of inhaled anestetics)
pregnancy (endorphins that act like opiods)
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135
Q

factors that decrease potency of inhaled anesthetic

A

age (mostly decreased/resistance between 1-6 months, little mass)
hyperthermia
chronic ingestion og alcohol, drug addicts on antidepressants

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136
Q

only gas used from past siglos that is seen in gas form in nature

A

NO

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137
Q

current uses of NO

A

analgesic during labor
odontology
given with another agent

doesn’t irritate airway when given through mask inhaled

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138
Q

history of NO

A

used to be used as laughing gas
first time used as anesthetic was in 1844 by Horace wells in Harvard to extract a wisdom tooth, failed b/c didnt know physical properties

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139
Q

physical properties of NO

A

colorless
odorless
dulzon
not irritative

EL MENOS POTENTE

oil/gas coefficient is 1.4 = poorly soluble

blood/gass particion coefficient = 0.46 = induction and recuperation are fast (34x > nitrogen) - passes through alveolo to artery fast - this is why its used with other gasses because since it is faster = FASTEST it also has the ability to drag other anesthetics and accelerate its action

usually inhaled

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140
Q

CAM of NO

A

104% = poor potency

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141
Q

pharmacokinets and dynamics of NO

A

inert gas
not metabolized - full elimination = inert gas
pulmonary elimination > 90%
@ > 60% @ CNS –> amnesia and analgesia

produces general anesthesia through interaction with cell membranes of CNS

@ CV exerts mild sympaticmimetic action causing discerete myocardial depression, mild increase of HR

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142
Q

side effects of NO

A

expan closed air spaces - CI in closed qx

diffusion hypoxia - large V exiting from blood to alveolos dilutes oxygen concentration in alveolo

oxidation of vitamin B12

depression of bone marrow after 4-5d(px with tetanus) - granulocytopenia, TCP

nausea vomiting

teratogenic

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143
Q

why cannot use NO in abdominal qx or long qx like liver transplant , vitrectomy, timpanoplasty, neumotorax or neumoperitoneo, dx laparoscopy

A

due to expansion of closed airspaces in ocluided px could increase risk for distension and perforation

in opthalmological qx can risk increased gas expansion in vitrectomys

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144
Q

mechanism of b12 oxidation by NO

A

NO inactivates metioninsintetase necessary for DNA synthesis and depends on B12

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145
Q

history of halotane

A

introduced in 1956

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146
Q

physical properties of halotane

A

volatile
colorless
good smell - rotten apple
doesn’t irritate - good for mask

decomposes with light and humidity

blood/gas - 2.4 (NO is faster)

oil /gas - 224

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147
Q

CAM of halotaine

A

0.74 = grand potency - THE MOST POTENT

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148
Q

why did we need alternatives to halotane

A

hepatotoxic
mimics viral hepatitis
elevates transaminases, fever, jaundice

massive necrosis causes acute liver failure with high mortality - diff dx - halothane removes blood flow there

necrosis of hepatocytes

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149
Q

factors that increase hepatotoxicity of halotane

A

40-70yrs, feminine, obesity, genetic factors, previous exposure to it

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150
Q

FD of inhaled agents @ CNS

A

all inhaled agents liberate excitatory NT causing central depression and maintain nerve cells depolarized by blocking ion exchange

blocks Ach liberation

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151
Q

FD of inhaled agents @ heart

A

depends on agent

halothane and enflurante reduce CO - reduce systemic vasc resistence –> central bradycardia b/c block depolarization at SA node –> liberating histamine - all this decreases precharge

isoflorane secorane and desflorane don’t really affect CO, lower it minimally - same with MAP, hardy any effect on HR

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152
Q

FD of inhaled agents @ BP

A

mostly reduced by halothane and enflurane (worse if dehydrated)

directly related to alceolar concentration

less decrease by iso, sevo, desflurane

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153
Q

inhaled agent that most modifies HR and depolarization velocity @ SA node

A

halotane

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154
Q

FD of inhaled agents @ kidney

A

decrease renal function
reduce diuresis
reduce GFR and renal BF

secondary to effects on CV system

return to normal after suspension (if persiststs there was previous renal or CV pathology, hydroelectrolitic disorder orincompatible blood administration)

renal condition depends on hemodynamic condition

was px hydrated pre qx?
low BP? - low perfusion?
kidney problems already?
incompatible blood
Methoxyflurane nephrotoxic
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155
Q

isoflurane history

A

made in 1971, commercialization began in 80s

1988 here in DR

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156
Q

halogenated metil-etil-eter and isomer of enflurane

A

isoflurane

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157
Q

FD/FK of isoflurane

A

less biotransformation/metabolism 0.2

least hepatotoxic (maintains flow) - even if lesiones

pulm elimination >80% and as metabolites (trifluoracetico, FL, Cl) thru kidney - 10%

causes a lot of resp depression

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158
Q

FD of isoflurane @ CV system

A

increases HR mild - not risky

VD - coronary (indicated in coronary bypass)

decreases vascular resistence without modifiying CO
maintains hemodynamic stability
direct depressor of myocardial contractibility

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159
Q

FD of isoflurane @ resp systtem

A

irritates. no mask, can cause laringospasms
BD
acts on medullary centers causing resp depression and depression of airway reflexes

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160
Q

FD of isoflurane@ CNS

A

depresses cortical function

decreases excitatory transmion from cerebral cortex

strengthens nondepolarizing muscle relaxers - less need for them

increases ICP slightly

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161
Q

physical cx of sevoflurane

98-2000 here - used alot here

A 
volatile liquid derived from fluorado of metilisopropileter with a halogen (FLUOR) 
7 atoms
no color
good smell
doesn't irritate

can give with simple mask in kids

blood gass - 0.62 - fastested after isoflurane - sleep fast

low blood solublility

oil/gas - 53

not hepato o nephron toxic (doesnt derease flow)

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162
Q

CAM sevoflurane

A

is the one that most varies with age ( less with age and more in kids)

1.7-2%

reduced to half if with NO 60%

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163
Q

boiling point of sevoflurane

A

58.5

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164
Q

vapor pressure of sevoflurane

A

157 so you can give conventional vaporizers

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165
Q

elimination of sevoflurane

A

lungs >90%
kidney - 10%
metabolites 2-3% - in liver using cytochrome P4502E1

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166
Q

hemodynamic and CV effects (FD) of sevoflurane

A

similar to isoflurane

stable

HR same!!!

BP decreases depending on vapor pressure giving, gas flow in the moment - too high, adjust as long as px hydrated and not bleeding

decreases CO

doesn’t modify systemic vascular resistences

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167
Q

resp FD effects of sevoflurane

A

depresses respiration
dosis dependent
no irritaiton

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168
Q

CNS FD of sevoflurane

A

same as iso

potentiates nondepolarizing NMRs

depresses electroencephalograph acvity
dose dependent
no convulsions

changes in cerebral BF
discrete increase in ICP

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169
Q

history of desflurane

A

metil-etil-eter flurado

London 1988

not here in DR yet

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170
Q

physical cx of desflurane

A

volatile liquid
irritative
itchy,spicy
cough laryngeal spasms (cant ventilate - px is rigid)

blood/gass partiicion coefficient - 0.42 = sme as NO
oil/gas coefficient - 18.7 = LOWEST

not nefrotoxic nor hepatotoxic

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171
Q

boiling point of desflurane

A

23.5

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172
Q

vapor pressure of desflurane

A

at 20C is 652
no vaporization possible unless its a Tec type electric evaporizer

high

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173
Q

lowest bloos/gas partition coefficient and oil/gas coefficient of all inhalatory anesthetics

A

desflurane

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174
Q

CAM of desflurane

A

6-9% depending on age

high

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175
Q

metabolization of desflurane

A

0.02%

176
Q

desflurane FD @ CV

A

increases HR mild and MAP

decreases systemic vasc resistence

doesn’t change CO

177
Q

desflurane FD @ resp

A

increases BR

decreases circulating volume which is dose dependent

178
Q

respiratoy complication of general anesthesia

A

obstruction of airways from tongue falling (put Guedel canula, Mayo canula to lift tongue) after qx

tooth/protesis out into a bronquio

gum bleeds

laryngeal edema due to diff intubation (thin laringe, couldnt hiperextend) - closes airway after removing tube

laryngospasm (give a NM relaxer)
(obesity, macroglossia, a lot of time intubates,

hypoventilation from depression of CNS resp centers…decreased costal function due to opiods (excessive stimulation …tx: flumacenil) or due to relaxation of diaphgram from use of NM blockers (tx: anticolinestaricsadministration of neostigmine or sugammadex - increase muscle tone)

neumotorax/hemotorax due to qx or barotrauma from VM, or from guiding sonda perforating traquea , too much vent pressure causing a rupture

atelectasia from accumulated secretions, smoker - if orotraq tube is introduced too deep and only one lung ventilates (tx: bronquial lavage with saline solution)

broncoaspiration of gastric content (SNG in VM) - if px ate before qx - fatal

paralysis of asccesory muscles

relax bronquial SM

179
Q

tx for neumotorax/hemotorax due to qx or barotrauma from VM

A

chest tube

180
Q

CV complications of general anesthesia

A

htn, taki, globo vesical if no sonda - no analsicsdone well - should put 1hr before awake

lower stress bp with sedation, if still high suspend qx- dispara at immediate post qx more dangerous than before qx

hipotension, bled too much and dint put enough liquids

arrythmia

all produce a decrease in sympathetic (dose dependent) causing VD, negative inotropism-cronotropism, blood shunting to splenic organs.
all this is less evident in hypovolemic shock or dehydration

HTA (more common) from pain (give analgesia) or urinary retenhion (globo vesical, less urine, concentrated, low PVC, verify that sonda is well placed), due to hypovolemia (tx: NS0.9% sueros), hemorrhage (concetrates of RBCs) or IC (give dobutamine, efedrine)

arrhythmias that decrease CO and can produce PCR

IAM due to arrhythmias , hypercalcemia or previous cardiopathy

PCR - cardioresp arrest

181
Q

CNS complications of general anesthesia

A

excitation or agitation from pain, hypoxemia or hypercapnia, dehydration or urinary retention

hypothermia - if it wasn’t managed in transqx

delay of waking due to overdose of opiods or anesthetic (antidote) ,

hypoglycemia (glucosalated serum) , hyperventilation

182
Q

other complications of general anethesia

A

nausea and vomiting from opiods and eter (give antiemetics)/GI

anyfilactic reaction (give adrenaline and corticoids)/immunological

endocrines (hypergluciemia, hypercorisolemia) - check beofre during and right after

183
Q

knowledge important for understanding NM relaxers

A

ANS functioning
NTs of ANS
basic anatomy of striated muscle and NM union
physiology of NM union

important for intubation , bronquial relaxation = #1 indication

#2 depends on where qx is - abdominal all thru, 
other area not necessaary

administered with to hlep inhaled anesthetics

NOT anesthesics
dont cross BBB

act at smooth Skeletal muscle

helps ventilation, qx, intubation

help in epilaeptic , asmatic px states

184
Q

second gas effect

A

when a gas has the ability to transport antoher gas

only one with this ability is NO

allowing less consumption with less hemodynamic effects

185
Q

how to tx hypoxia by diffusion caused by NO

A

administer high concentration oxygen for 3-5min after interrupting N2O

186
Q

CAM

A

min # of gas % to cause cerebral coma at 50%

isnt enough, need > 90% so for halotane 2x dose

187
Q

Vapor pressure

A

all these gases come in liquid and are administered vapor (pressure for liquid to evaporate)

in this case, oxygen on liquid surface of an anesthetic is found in a closed recipeint

188
Q

ebulittion point

A
  • Temperature at which a substance as liquid starts evaporating
189
Q

% of organic compounds in pharmacology

A

99%

190
Q

primary - central NT

A

GABA

191
Q

primary - peripheral NT

A

glycine

192
Q

antiarrythmics can use with halotane

A

lidocaine, esmolol

sevorane and isoflurane in cardiac qx (CV stable)

193
Q

which inhaled agent is best for px with emphysema, asthma, chronic bronchitis (restrictive)

A

CANT use enflurane

halothane is best because it BD

sevo , iso wont help but wont hurt

194
Q

agent that most blocks CO2 action on resp center and also causes arrythmias

A

enflurane

195
Q

agent that produces most irribility and when using mask can cause laringospasm

A

enflurane

sevoflurane doesn’t cause this - ideal to use on mask for kids

196
Q

all inhaled agents are metaoblized

A

in liver - oxidation reaction

less in kidney and lung

197
Q

agent that causes most alveolar BD

A

halothane

198
Q

tx status asthamaticus with

A

halotane

199
Q

tx intractable angina with

A

epidural local anesthesics

200
Q

why we put a dose that is 2x the CAM

A

so dose would be around 1.5 for halothane

CAM depends a lot on state of px hemodynamically

unstable dehydrated px doesn’t tolerate minimal CAM, VD, bleedinh

if hypovolemic, in chock I put 1.5 halothane ill deepen his depressed state and px worsens

put blood, use VC

to get a good anesthetic effect should double the CAM

201
Q

least metabolized inhaled gas aka mas noble

A

desflurane

202
Q

least hepatotoxic

A

desflurane

203
Q

least hepatotoxic after desflurane

A

isoflurane

204
Q

lowerst oil/gas coefficient

A

18.7

desflurane

205
Q

gas with least metabolization

A

desflurane

206
Q

desflurane affect on CNS

A
  • CNS decreases peripheral vasc resistence increasing CBF
207
Q

desfluranes affects on non depolarizes NM relaxers

A

strengthens them

208
Q

agent that most relaxes bronquial SM

A

halothane used in asma px

209
Q

enflurane effect on bronquoils

A

BC

210
Q

tx arrhythmic complications

A

selective Beta blocker

lidocaine

211
Q

agent that most decreases hemodynamic parameters

A

Halotane

BP 20-25%

CO 30%

212
Q

most arrythmogenic agen

A

Halotane

213
Q

effect of halogenated agents on mocardium

A

sinsibilize it to sympathetic action

214
Q

agents that produce most NM relaxation

A

sevofluranem isoflurane, enflurane

less NM relaxers needed as a result

215
Q

NM relaxers should never be administered without

A

necessary prep to maintain open airway and ventilation

putting the px to sleep , since doesnt cross BBB px cant move breath so avoid the psychological trauma

216
Q

are NM relaxers anesthetics?

A

no

not hypnotic either

need co-use with hypnotics, sedatives or anesthetics

217
Q

who was savarese Kitz

A

described criteria for ideal relaxer (neither completes all of them)

election depeedns on clinical situation

218
Q 
Kitz criteria
(el hidonio?) - ideal

whixh depends on px and experience

A

non depolarinzing mechanism best
rapid initation of action
adequate duration - 1hr
rapid recuperation
no accumulative effects @ psuedosis ,o rredosis
no CV effects
don’t liverate histamine
easy rapid reversion with neostigmina o sugammadex
no meds interaction
don’t produce active metabolites - elimate in different organs
excretion independent of kidney and liver
without effect on CNS (in ICU) - some metabolites do, none themselves do

without muscular effect in crifical state
pharmacological presenation in stable solutions

219
Q

FK of NM relaxers

A

this references distribution, metabolism, elimination in organisms so plasma concentration is the result of a specific dose administrated

act at NM union NOT plasma

EV (not oral or IM) - ONLY - absorption

union to protein influences distribution, hipoproteinima and rug with hugh union grade to protein (AINES) can increase free fraction of relaxer

the alteration of EC liquid volume
derived as: nephropathy and cardiopathy bodify the distribution volume of relaxers

no obstante , FK of relxers presents individual variations in px with renal failure, liver failure and px taking steroid

220
Q

NMRs act where

A

in the NM union

not in the plasma
meanwhile block starts becoming insaturated, plasma concentration stars decreasing

221
Q

distribution of NMRs

A

are very polarized molecules with escasa diffusion and very hydrofilica

edema, steroids, nefropatiea, too much water - dosis has to be much larger, IC, hepatopathy excess body water

volume distributes EC liquid

don’t pass BBB

and in small quantities placentary barrier without evidence of clinical effect

222
Q

metabolization of NMRs

A

90-95% nondepolarizing at liver- recuronioi vecuronio

other group in plasma

anotther biotrasnform at plasma of sucinilcoline is eliminated in plasma, mivacuruin,(iwth acetilcolinesterasa)

cisatracuruin, and atracuriun
are cleared in plasma through biotransformation (autodestruction)

sucinilcoline and mivacuruin are hydrolyzed by plasma clinerterasic while cisatracuruin and atracuriun are degraded by elimination of Hoffman (autodestruction and temp. and body pH) besides Atracuriun is decomposed by hydrolysis of ester in 20%

steroid relaxers or metabolize mostly in liver

223
Q

elimination of NMRs

A

relaxers that least depend on liver elimination are cistracuruin , atracuriun, mivacuruin, the first two are indicated in px with liver failiure while mivacuruin triples its duration due to decrease of colineterasic

asteroid relaxers that don’t completely degrade are eliminated thru kidney and bile

mivacuruin , atracuriun, cisatracuruin, and sucinilcoline are of election in px with renal failure

224
Q

Depolarizing NMRs

A

these have a chemical structure similar to Ach competes with liberation in synaptic hendidura of the motor plaque por nicotinic post synaptic rec of motor plque

also acting on cholinergic muscarinic receptures they induce bradycardia and increase salivary secretions

225
Q

history of sucinilcoline

A

disvocered in 1951 - Bovet

thought to be ideal relaxer cuz there was no others

most associated with anafilaxis
at 80s othr types were discovered and was used less and less
only used to compare effeects of others and fast intubation

iniciode accion rapida after 60seg 95%

226
Q

only depolarizing relaxer with clinical use

A

sucinilcoline

all are EV

most popular relaxer used and critizzied even today after 50yr

same affect as Ach but longer time - depolarize

limited after the 80s but still in medical arsenal for endotraqual intubation (incierta) and emergency for kids and adults esides some contraindications

227
Q

secondary effects of sucinilcoline

A

fasciculations - more in muscly adults less in kids, muscle contractions

myalgia, post qx pain (worse if muscular px)

increased intragastric pressure

increases intraocular pressure > 10% - CI in glaucoma px

arrythmmia - more common in kids (vagar , transitory) - massive K+ liberation from IC

malignant hyperthermia

bradychardia possible but less common

skin irritation

px with ccolinesterasa atpica - hepatopata - block takes longer

in px with extense burns or neurological disorders (paraplejic, myopathy, reynales? already with kalemia issues CI) can present severe arrhythmia in ventricles mediated by a massive hyperkalemia

alot of anafilactic reaction > 37%
, intolerance to other drugs after this one

increases IC pressure - CI in px with brain pressure increassed

228
Q

why does sucinilcoline cause fasciculations

A

depolarization of presynaptic cholinergic rec

229
Q

how to prevent bradycardia by sucinilcoline

A

with previous use of atropine 3min before

230
Q

structure of sucinicoline, formula

A

formed by 2 Ach molecules united by a metil-acetic group

FORMULA (2 Ach molecules united by metilacetate bridge) very similar to Ach - acts like it but longer, elements(glucometilico, oxygen, nitrogen sufre?? etc)

231
Q

cx of sucinilcoline

A

hydrosoluble
degraded by heat , light and alkaline pH

sould be kept in fridge between 4-10 degrees

232
Q

ultrashort duration of sucinilcoline is due to what

A

metabolism - rapidly hydrolyzed by pseudocolinestearasic plasma enzyme which is made by the liver

much slower than Ach and is in 2 stages

233
Q

half life of eliminiation of SC

A

7-10 min = duration of action destroyed by enzymes, longer in certain types ofpx

initation of action - 60sec

234
Q

2 stages of SC metabolism

A

1 - produces sucinilmonocoline and coline a

2 - produces succinic acid and choline

235
Q

which stage of SC metabolism is faster

A

wst is 6-7x faster than second

236
Q

potency of block of sucinilmonocoline compared to sucinilcoline and coline

A

cuadragesima of sucinicolina

colina only has centesima part

237
Q

are metabolites of SC toxic?

A

no

238
Q

male vs female SC metabolism

A

male - 35% faster than in women

becomes slower with age

239
Q

clinical use of SC

A

RM desp of election for endotraqueal entubation emergency (laryngospasm and full stomach real or virtual)

in PEDS only in urgency

if kid does not have permeable veins can use IM in low dose in electroconvulsive tx

240
Q

clinical dosis of SC/intubation

A

adult of 0.5mgxkg??? - not what he said

pediatrics - 2mg x kg or in px with increased volume, edematized

intubation dose = 1mg/kg

so in qx
bollus every 10min or continous infustion (preffered)

if convulsing also useful

241
Q

initation time of SC

A

30-60 sec (he said 60seg)

242
Q

clinical duration of SC

A

3-10min (he said 7-10)

243
Q

IM routes initation and duration of SC

A

IM - 5mgxkg with

3min initiation

30min duration

244
Q

NM recuperation based on age

A

NM recuperation is faster in kids < yr

245
Q

SC effects on skin

A

rash and gral eritema

246
Q

atypical pseudocolinersterasic

A

SC can cause prolonged block in px ith atypical pseudocolinersterasic -

duration of block varies of 30min - 13hr

247
Q

drugs most associated with anafilactic reaction

A

NM relaxers

Sucinilcoline most commonly

37% of accidents

248
Q

CI of SC

A

K+ > 5

px with family history of malignant hyperthermia

px with severe burns > 7 d

px with IC HTN

px with high IOP

249
Q

what determines FC and FD of NMRs

A

FD = potency, initiation of action, duration, and recovery

physicochemical cx like sterospacial structures

250
Q

how is potency of NMR reresneted, measuresd

A

D051 - OR65 curve

valora effective dose DE50 and DE95!

minimal dose that can cause deprecaccion de impulso electrico a nivel nervioso (DE95)

251
Q

DE50

A

dosis that causes 50% depressio/block of transmissionn of response to unique response

252
Q

DE95

A

dosis which causes depression of 95% of respective to simtulus and is the most vital because en cuanto necessity of ideal qx relaxation

253
Q

DE50 and DE95 of doxacuruin

A

DE50 - 0.012

DE95 - 0.024

MOST POTENT at most minimal dosis causes deprecacion muscular

254
Q

DE50 and DE95 of vecurunio

A

DE50 - 0.027

DE95 - 0.043

255
Q

DE50 and DE95 of cisatracuruin

A

DE50 - 0.029

DE95 - 0.048

256
Q

DE50 and DE95 of mivacuruin

A

DE50 - 0.039

DE95 - 0.075

257
Q

DE50 and DE95 of atracuruin

A

DE50 - 0.120

DE95 - 0.210 (0.5mg to intubate) multiply by 3

258
Q

DE50 and DE95 of sucinilcoline

A

DE95 - 0.260

259
Q

DE50 and DE95 of rocuronio

A

DE50 - 0.147
DE95 - 0.305 (0.295mg/kg????)

LEASST POTENT
to really paralyse have multiply 3x DE95 around 0.6 to intubate

260
Q

Division of NMRs

A

NMRs are composed of cuatenary amonio atendiendo chemical structure is divided into 2 groups

depolariizing and nondepolarinzing

261
Q

Non depolarizing NMRs are divided into 2 groups

A

steroid amino:, pancuronio, vecuronio. pipercuronio, rocuronio - these metabolzied only at liver

benzilisoquinolina group:. D-Tubucuraina, Metocurina, mivacurio (HE SAID NO), doxacuruin, cisatracuruin, atracuruin - undergo autodestruction - dont need liver or kidney for elimination - independent

262
Q

most powerful non depolarizing NMR

A

doxacuruin

263
Q

least potent ND NMR

A

rocuronio

264
Q

potency of vecuronio is similar to

A

vecuronio and cisatracuruin have similar potency

265
Q

atracuruin has similar potency to

A

sucinil coline

266
Q

dosis for NMR for idoneous intubation is

A

3x ED95

for maintence suggeset a dosis that is 1/3 of ED95

267
Q

action initiation of NDNMRs

A

its the precise time to reach a decrease of 100% of contraction force

268
Q

NMR time of initiation of action depends on

A

cx of ED50 relaxer/DE95

of dosis of inductor agent

of hemodynamic situation of px

CO, muscular blood flow

_____________________________________

time that it takes for drug to reach equilibrium between plasma and NM union,

fast eqilibruim decreases initaiotn time

increase in dose has been used to decrease action initiation times of BNM

this leads some to present adverse effects (prolonged muscular block more than desired)

decrease in CO of oldie justifies increase in intitation time

beta blocker px produces same effect

269
Q

time of initiating action of NMRs competitive is propriotal to

A

its potency,

less potency, less initiation action time and vvice verca

270
Q

administration of Rocuronio

A

not potent

2 dosis

ED95 = o.3mg/kg

acts fast, eliminated fast
steroid, need liver and kidney

CI hepatopand renal

271
Q

administration of Doxacuruin

A

lower dosis ED95 = o.o25mg/kg

272
Q

NDNMRs of intermediate action

A

vecuronio 35-45min - metabolized in liver, common here

Atracuruin - 40-50min (40)

Rocuronio - 30-40min - (30-35)50% metaobolized by now, if continuing qx have to continue, common here, metabolized by liver - 2hr to elimate completely

Cisatracuruin - 40-50min (60) $$

after in qx youll give amount thats been eliminated (half? just to maintiin abdominl paralysis?) -

273
Q

NDNMRs of long duration - not really used anymore - hemodynamic problems

A

Doxacuruin - 85-125min

D-tubocararina - 60-100min

Pipecuronio - 80-120min

Pancuronio - 60-80min

274
Q

regarding initiation time/induction to completely block , NMRs are classified into 3 groups - allow you to know when to intubate

A

short intiation action - 1-2min - Succinicoline and rocuronio (90sec)

intermediate - 2-5min - Atracuriun, Vecuronio, Nivacurium

Long - 4-6min - Cisatracuruin and Doxacuruin

275
Q

only clinical situation that needs a brief initiation time of NMRs is in px with

A

full stomach

in other cases its a secondary factor and can use any NMR

276
Q

NMR with shortest initaiton action time and why does that matter

A

sucinilcoline

useful in px with risk for broncoaspiration

277
Q

duration time for succinicoline (short)

A

5-10min

278
Q

duration time for mivacuruin (short)

A

15-20min

279
Q

entubation dosis for atracuruin

A

0.5mgxkg-0.6 with duration of 50min

redosis after 30min is 0.1-0.2mg/kg with clinical duration from 20-35min

these give DE95!

dosis for continuous perfusion is 0.2-0.7mg/kg

280
Q

easily antagonized by anticoineterasics

A

atracuruin

281
Q

side effects of atracuruin?

A

due to histamine liberation can cause skin rash (can be buffered with previous beta blocker)
broncospasm
only seen in high dosis
slow application decreases this liberation

CV can produce arterial hypotension , takicardia

like others can be reverted with anticolinesteases??

282
Q

history of atrcuriun

A

introduced in clinics in 1981
intermediate duration
attractive due to original elimination
which doesn’t produce active metabolites

now comes in 35mg/2ml?

283
Q

FC of atracuriun

A

immiatley after administration plasma levels fall rapidly in a process of multiple metabolization but with one specially through Hoffman, depends on temp of body during qx and control gasometry, physioologicla ph produce 2 metabolites

action duration = 40min - prolonged if temp or desquilibrium

decomposed with heat needs refridge

284
Q

metabolites of atracuriun

A

mono acrylate cuateranrio

laudanosine

285
Q

is laudanocine relaxer?

A

no

high dose can produce CV depression and excitation of CNS postanesthetic

286
Q

mono acrylate cuaternario

A

no farmacological activity - no accumulative effect so give as many redosis as you want

287
Q

plasma clearance of atracuriun

A

5ml/k/min

288
Q

farmacodinamia of atracuriun

A

less potency than cisatracuruin and vecuronio - 60min?

more than rocuronio - 10min more

289
Q

vecuronio history

A

ultilized in clinic first time in 1984

290
Q

FC of vecuronio

A

presents rapid liver capitation in 80%

291
Q

excretion of vecuronio

A

biliar

metabolites- accumulative efffect

es el 3desacetilvecuronio

presents pharmacological activity

292
Q

FD of vecuronio

A

potent relaxer

293
Q

entubation dose of vecuronio

A

0.1mg/kg

294
Q

initiation action of vecuronio

A

2-5min

295
Q

duration of vecuronio

A

35-45min

296
Q

re dosis of vecuronio and duration

A

0.025mgxkg (1/5)

15-20min duration

297
Q

how to reverse vecuronio block and atracuruin

A

neostigmine

298
Q

secondary effects of vecuronio

A

good for CV

doesn’t liberate histamine, secure
nobroncoscpasm

CI in renal hepatopathy px

299
Q

indication of vecuronio

A

in px with CV pathologies

subit to cardiac surgery

300
Q

CI of vecuronio

A

hepatic cirrosis and renal problems

301
Q

history of cisatracuruin

A

introduced in 1996

most recent

302
Q

cx of cisatracuruin

A

potent relaxer with grand security margin safe CV and metabolic
doesnt liberate histamine

ideal for px with unstable hemodynamic risk and px with hepatorenal iinsuff

303
Q

only NMR that doesn’t liberate histaomine

A

FC = similar to atracuruin

cistracuruin

304
Q

cistracuruin elimination

A

Hoffman - 100% biodegradation - depnds on pH and T

305
Q

FD of cistracuruin

A

potency is 4x atracuruin

306
Q

intubation dose for cistracuruin

A

0.1mgxkg

can be sued in continuous infusion at 0.09mgxkg in adult - redosis also

(3x DE95)
0,09
also autodestrcuts like atracuruin

307
Q

initiatin action of cistracuruin

A

5min-6min - a bit too long, ventilate all this time

308
Q

clinical duration of cistracurion

A

45min - prolonged

309
Q

revert cistracuirin block with

A

neotigmina

310
Q

side effects of cistacuruin

A

none
no histamine
no litic vagus effect

311
Q

dose for kids - cistacuruin

A

0.02mgxkg

312
Q

common cx of non opiodes anesthetic

A

LOC
analgesia
amnesia

first line agents in anesthetics

313
Q

why use non opiod anesthetic via EV

A

to facilitate induction of general inhaled anesthesia

314
Q

history of barbiturics

A

beginning of this siglo

first that produced LOC = hexobarbital - problem is that it produced too much involuntary muscular movement

thiopental was first used as anesthesia in 1930 by Walter

since then has been used EV - standard to compare other EV anesthetics - doesn’t make it the ideal

315
Q

how to measure depth of coma

A

BIS - electric apparatus

continues EEG

depening on waves

ideal is between 40-60%

put electrodes in forehead

> 60 - awake - active
40 - sleep

used in long qx

if not use glasgow

316
Q

propofol

A

EV sedative hypnotic non barbituric of short duration

most used these days

slow induction close to physiological sleep (inhaled can excite you before and px gets anxious and barbs)

NOT barb

mechanism unknown but we think its GABAergic - potentializes GABA, blocking excitary

317
Q

FC of propofol

A

EV administration with fast distribution to all tissues

LOC of consciousness iafter 40sec (depends on dosis and velocity of administration) so do side effeects

intiation of action can be affected by pre-medication, dose, velocity of administration and medical condition

crosses placental barrier, -
BBB

high liposolubility so used up by most irrigated tissues - rapid sleep

joins plasma proteins 95-99%

318
Q

duration of action of bolus of 2-2.5mg/kg of propofol

A

3-5min

319
Q

odonotological px use, parto

A

NO - because has analgesic properties - concentrations! others don’t (just amnesia and LOC, muscle relaxer)

can accumulate in fetal blood @ C-section what do we do? do it while shes awake so right when shes out 2-3m to clamp umbilical cord

320
Q

metabolism of propofol

A

rapid liver metabolism
20-25cc/k/min - MR
we think it clears in other places but dont know where yet

extrahepatic (clearing > liver blood flow)
18-20cc/k/min = normal flow

not necessary to adjust dose if px has renal or liver insuff

321
Q

elimination of propofol, half life

A

urine

half life - 3-12hr (accumulates in fat tissue)
tkaes up to 10hr, can accumulate

15-20min up already

322
Q

recuperation of propofol

A

rapid
escasa psychomotor affectation
thats why we dont modify dose in px with liver/renal problems,

inustable, VD px ADJUST DOSE, decrease peripheral vasc resistence, hemodynamic alteration

323
Q

indications of propofol

A

general anesthesia

induction at inhalatory agent and
maintenance - sedation in critical px

superficial sedation for dx procedures or tx

324
Q

presentation of propofol

A

ampollas of 20ml

vials of 50 and 100ml

1ml = 10mg/ml

325
Q

posology , administration, anesthetic induction of propofol

A

adults < 55yr or /and ASA I-II - 2-2.5mg EV

oldies and weak, ASA III or IV
1-1.5mg EV ,

continuous infusion

adults < 55yr or ASA I-II (6-12mg/kg/h)

old wk, ASA III or IV (3-6mg/kg/h)

superficial sedation for dx and tx procudures

dose depends on clinic of px

avoid rapid bolus and high dosis in oldies, weak and those with CV disease

326
Q

CI and precautions with propofol

A

CI in px with hypersensibility to propofol or any of its components

careful with cardiopathy px - higher sideeffects hemodynamic

cerebral vascular disease px or endocraneal HTN can cause decrease in CPP due to hemodynamic effects

oldies and weak might need dose adjustments - avoid bolus in them

ICHTN (even tho it decreases CPP)

REMEMBER it has no analgesic effect - use other drugs

in ppl with soy milk allergies
allergic px
asma px

overdose??

needs to be reridgerated

rich medium for bacteria

327
Q

is propofol an analgesic

A

no

328
Q

side effects of propofol

A 
cardiopulmonary effects 1-3%: 
resp depression, important bradycardia, 
transitory apnea (use opiod or benzo before worse??) - give postive pressure oxygen
hypotension 3-9% depending on dose, velocity of administration and medical state

less: arrhythmias, bigeminism, taki, ECG alterations, involuntary muscle movements,
rare: perioperatory and opistotone myoclonus, urine coloration

takicardia > bradikardia

@ recuperation: nausea and vomit

anafilactic reaction - erythematous rash superiorl thorax and above
(others are much more generalized)
severe broncospasm

NO AMNESIA
NO ANALGESIA
(anesthesia only)

vomit

local pain at infusion zone - very irritative use thick veins - can cause necrosis of tissue if leakes out (so mix it with some lidocaine)

329
Q

most inhaled use

A

sevo, iso, des

330
Q

balanced anesthesia

A

inhaled + EV (opiod)

depress easily - resp - lower dose, mix

331
Q

neuroleptoanalgesic

A

opiod + neuroleptic

332
Q

propofol interactions

A

depressor effects on CNS potentate when used with other drugs with this property

in induction can reduce the dose if px premedicated with opiaceos or sedatives

intoxication , overdose

potentiates inhaled anesthetic

333
Q

why smoking affects potency of inhaled agents, asmas, chronic broncitis

A

thickened alvelo makes transport more difficult into arterial blood

334
Q

history of opiods

A

have been used for 100s of years

to alleviate anxiety and reduce pain in qx

a lot not only used to supplement EV anaglesics but also as principal alone EV analgestics

morphine was isolated from opio thanks to Serturne in 1803

through needle in 1853 by Wood

allowed administration of IM morphine as a premedication

was to compliment anesthesia with Eter or cloform and obtain analgesia in post qx

at the end of siglo administrated large quantities of morphin in factioned EV dosies and IM as a complete anesthetic alone- but due to high morality rate durin 30-40yrs stopped being used during qxas anethetic and ever since co-used with analgesics in immeidate post-qx

introdcuion of barbiduritcs super short ccting as EV anesthetic and popularization of concept of balanced anesthesia revidved enthusaim for their use

335
Q

classification of opiods

A

natural
semisynthetic
synthetic

336
Q

natural opiods

A

morphine (madre de naturaleza)
codein (antitusino)
papaverine (VD)
tebaine (derivatives for chronic pain and to immoblize wild animals)

obtained from plant = papversomniferum

337
Q

semisynthetic opiods

A

heroin - derived from morphine

etorphine derived from tebain - the one used to immobilize animals

338
Q

synthetic opiods

A

morfinano - levofanol

difenilpropilamina - metadona

benzomorphine = pentazocine(sosegon)

fenilpiperidina = 4?
 fentanyl
 - sulfentalnyl. 
Nabulfina (nubain) 
meperidina (demerol) 
tramarol
339
Q

derivatives of tebaina that are used in clinical practice to give analgesic

A

oxymorphine and oxicodone

340
Q

anesthetic coma appropriate for qx

A

glasglow 7-10

reversible

341
Q

when MURR rec are stimulated located at ventricular level and in greay matter will produce vs periacuedcutal vs limbic

A

supraspinal analgesia and resp depression

periacuedcutal produce spinal analgesia

limbic –> abolition of affective response like fear

342
Q

best inhaled hat relaxes

A

sevo

343
Q

stimulation of KAPPA rec produces

A

sedation, miosis, physical dependence

344
Q

where are Kappa rec

A

gel substance , mesencefalo, brainstem

345
Q

@ stimulaltion of cigma ref

A

psycomimetic effect

hallucinateion, disforia, takicardia, midriasis

346
Q

px pueden durar…..

A

VN

hemato, endocrine, metabolic

347
Q

etformin is

A

derived from tebaine

1000x potent that morphine

used to immunize wild animals

348
Q

history of opiod rec

A

1973

murr, kappa, cigma, delta

349
Q

affinity for opiod rec varies with

A 
pH
 T
dose
cronicidad de su uso?
 ,via 
opiod affinity
350
Q

MURR rec localized where

A

periaqueductal, - spinal analgesia

grey matter,
thalamic nuclei,
reticular substance,

limbic structures (..?respuesta afectiva@ px first time taking these)

grey and reticular central , supraspinal analgesia

351
Q

location of cigma rec

A

lamina VI of cortex
solitary nucleo tract
spinal cord gel substsance
trigeminal nucleus

352
Q

stimulation of delta rec

A

produces changes in affective behavior

physical dependence

person changes

353
Q

localization of delta rec

A

lamina II, III, IV of cerebral cortex

acustic nucleo, nucleo olfative tuberculo, pontine nucleo

354
Q

depending on action opiods are classified in

A

pure agonist - when there is direct action on MURR and KAPPA

355
Q

pure opiod agnoists

A

these are for central or peripheral analgesia!

morphine
heroin
codein
methadone
fentanyl
tramadol - useful to tx atypical pain
356
Q

morphine

A

prototype
most used for tx
heals intense pain acute and chronic

357
Q

heroine

A

powerful analgesic

not allowed due to adduction

358
Q

codeine

A

potency and analgesic efficacy are less than morphine

359
Q

metadone

A

tx of px with addictions

360
Q

fentanyl

A

100x more active than morphine, but of fugacism effects

361
Q

ellecion drug for moder anesthetic tecnniques with opiods in CV qqx and UVI

A

fentanyl

362
Q

farmaco de primera linea en anesthesia for (long agrgressive) post qx analgesia

A

opiods

363
Q

morphine at CV

A

at 1mg/kg EV no significant changes regardless of cardiopathy

in px with aortic valvulopathy can have decreased systolic volume and CO probably due to dearease in systemic vascular resistence

@ 5-10mcg/kg can decrease BP through bradikardia , vagal origin, venous VD , shunting of blood in spleen

in some px 1mg/kg liberate plama histamine cause cardiac changes, reduce BP, systemic vasc resistence

px previously tx with H1 H2 blocker, cv response attenuated
decreases venous return to herath, venous dilation - dose dependent

364
Q

equipotency dosis

A

comparing all opiods to morphine to see potency

morphine 10mg = 0.02 levofanol,
 30mg metadona. 
30mg fentasucina,
 10mg fentanyl, 
0.2 sufentalnyl, 
aspirin = 600mg , 
AINES = 7mg
365
Q

agonist-antagonist opiods

A

agonist accion on KAPPA
antagonist on MURR

these can block resp depression affects while maintaining analgestia

nalbuphine
pentazocina

bupenorfine - 25-30x more potent than morphine
analgesia lasts

366
Q

pure antagnost

A

acts on MURR< KAPPA< CIGMA rec

revert desired and undesired affects

naloxone (narcan) more potent than naloxone - simila eficacyis 2altrexone ltrexone , morfinic derived

367
Q

rec of analgesia

A

mu and kappa

368
Q

today 2 opiods VO wich pH of stomach favors absorption

A

codein and morphine

369
Q

endogenous opiods

A

metilencefaline
leuencefaline
B-endorphin
Di-morfine

modulate pain perception - to sorportar wound

high in plasma 24-48hr after trauma , in labor (less analgesia needed post qx trauama)

370
Q

fentalnyl CV effect

A

much more hemodynamically accepted

unstable angina, IAM, low ejection fraction in qx use fentanyl

doesnt modify cardiac variables

371
Q

besides meperidine all opdioss produce

A

decrease in HR (dose dependent)

meperidine INCREASES HR

372
Q

half life of morphine (rapid distribution vs slow)

A

FC
rapid = 0.9 -2-4min to highly irrigated tissues

halflife slow - 10-20min to less irrigated tissues

373
Q

plamsa clearing of morphine

A

10-20mI/kg/min only 10% administrated excreted in urine

374
Q

morphine elimination halflife

A

2-4hr

via urine

375
Q

fentalnyl distribution times

A

halflife rapid 1-3min

slow - 5-20min less irrigated

376
Q

plasma clearance of fental

A

4ml/kg/min

clearance depends on liver metabolism

< 10% of dose is exreted unaltered thru urine

elimination halflife time = 21/2 an d 3.5hr

377
Q

opiord resp efects

A

all that simulate MURR produce resp depression
depending on dose mostly due to direct action on resp center at brainstem

reduce sensibility of resp center to CO2 and increase APNEA threshold

opiaceos reduce hipxic stimulus and break resp stimulus that can be associated with increase in aiway resistsence causing torax lenoso

increases resp pause, delays respiration and produces irregular respiration with slow resp frequenve and reduced volume

after administration as analgesic there is intense depretsion of costal parrilala and relative stability of abdominal diaphragmatic movements

378
Q

physiological factors that influence farmacology of opiods - these ppl are more sensitive to them

A

age - oldies more sensible
hepatopathy px (metabolism), prlong half life of elimination an dclearance
nefropathy
desequilibruim acid base

379
Q

indications for oiods

A

pain
anesthesics in px with poor absorpcion
acute pulmonary edema
suppress cough

diarrhea- not used anymore

digestive hemorrages
t of px with adicciones (especially metadona)

380
Q

CI for opiods

A 
px with brain lesions
pregnancy
px with altered pulm function
px with altered renal function
px with alreaed liver function
px with endocrinal disease
others
381
Q

elevated doses if oiods cause

A

total block of spontaneous respiration - can resond to verbal command and breath when order to

382
Q

resp depression of morphine vs fentanyl

A

slower in morhpne but lasts longer

383
Q

px more susceptible to opiods

A

oldies

384
Q

GI effects of opisd

A

analgesic dose are very emetic due to stimulation of quimorec zone de disparo which is found in posttrema area of medual

also relaed to emesia in increase of trasto GI or decrease of GI activity and prolongation of emptying time

385
Q

used in induction

A

opiods and benzos

lower concentration for maintenance

386
Q

only EV anesthetic whose analgesic factor > anesthitc factorq

A

ketamine

387
Q

why in administering inhaled anesthetics should i increase breathing rate

A

to get more gas exchange from alveolo to arterial blood - saturation

and to CO2 - barrida - ventilatory stimulator and inhibit resp center so you can control breathing

you can lower VP once they are sleep as well

388
Q

hightest CAM - least potnet

A

104
NO
give enough time and in large quantities

389
Q

what are the conditions necessary for halothane to produce hepatotoxicity

A

liver previoiusly detorated (hepatopathy, viral hepatitis)
less hepaticc blood flow (higado graso in obese)
predisposition - genetic
px exposed for long time to halothane

hard to tell if it was hepaittis (fever) or halothane produced (no fever)

390
Q

methoxyflurane … off market why

A

caused nefrotoxicity without predisposing factors

also cloroform and ether as well were very nephrotoxic

391
Q

no clincal evidence of toxicity…

A

isoflurane
sevorane
desflurane

392
Q

inhaled anesthetic with best NM relaxing properties

A

sevorane

393
Q

factors that can cause px to wake up later than normal after cessation of inhaled anesthetic

A

.can be delayed in oldies (slower metabolism, or if have previously used an opiod, hypothermia, acid-base desquilibrium, hypovolemia/acute anemia, hyperglicemia - if not should be awake by 10min after closing vaporizing

394
Q

hemodynamic variables

A

BP, HR, CO MAP

395
Q

best hemodynamic stability of inhaled anesthetic

A

sevorane
isoflurane

dont shunt blood away from organs

396
Q

volatile

A

easily evaporate at normal temperature

all come in liquid form except NO

397
Q

vapor pressure

A

the pressure of a vapour in contact with its liquid or solid form.

pressure gas exerts over liquid surcae in closed system

398
Q

ebullition pooint

A

T in vapor pressure = 1atm

399
Q

most noble gas

A

desflurane because it hardly metabolizes

400
Q

meds in pain management clinic - terminal diseases, CA, dont respond to other analgsics, palliative

A

oxymorphine and oxicodone (10,15,25, 50mg)

if rich - fentanyl patches

401
Q

onyl rec that have to do with analgesia of individual

A

MURR and KAPPA

402
Q

how to get spinal anethesia with opiod

A

@ subdural level

morphine intratecal

403
Q

kappa rec

A

produce central analgesia, miosis, all produce physical dependence,

404
Q

localication of kappa rec

A

gelatinaous substance
mesenfalo
tallo cerebral

405
Q

effect of cigma rec

A

produce psychomimetic symptoms - hallucinations, tachycardia, midriasis, dysphoria

(seen , efects in overdose, excitation of opiod)

406
Q

all opiods.., side effects

A

cause physical dependence

depress respirao=tory centers by making them insensible to the command of CO2 - blocks interaction/sensibility
slow regular respiration

can cause thoracic resistance, paralysingthorax movements (rigid, cant hyperextend)

paralysis of diaphragm

nause and vomitting - reduce gastric empting, increase gastric content, stimulate zone of liparo?? - vomitting, increaseing zone sensbility,
reduce gastrointestinal transit

407
Q

morphine CV effects

A

morphine 1mg/kg - no hemodynamic ateration even with CV problem

any effects are due to histamine liberation (massive) –> VD, less CO

in px with aortic valve problems
less volumen systolico and CO

> 1mg,kg (5-10mg/kg) - morphine itself will cause alterations
decrease BP
, vagal bradycardia,
shut bllood from splenic organs (liver, spleen)
venous VD

can use H1 H2 blocker to buffer

408
Q

unstable angina, IAM, low ejection fraction in qx why not use propofol with this px

A

VD will kill him

409
Q

anesthetic dose vs analgesic dose of fentanyl

A

at analgesic dose of 2-10mg/kg, - mostly used for analgsic purposes in qx

or anesthetic dose of 10-100mg/kg rarelu decreases BP even in px with poor LV function - but if have mad heart problems can use fentanyl as primary inducer

410
Q

how does fentanyl come

A

liquid bllus
100mg/2mL
500mg

411
Q

how to buffer bradicardia caused by all opiods

A

premedication with atropine or flicopirrolate minimizes this

412
Q

who commands our ventilation

A

CO2 stimulates resp centers

413
Q

appeal of atracuriuns elimination

A

biodegrades, autodilutes thru, doesnt need liver or kidney

80% Hoffman hydrolysis

hepatobiliar hydrolysis 20%

414
Q

what does atracuruins elimination depend on

A

depends on body temperature during qx and gasometry

ej at disequilibrium or hypothermia effect is prolonged

415
Q

why atracuruin needs refridgeration

A

decomposes with heat

416
Q

px betablocked, bradicardia dont use

A

halothane lowers HR even more - worst fr heart - central bradi
decrease vasc resistence periferical = VD
secuersro sanguineo de organos splenicos
reduces sytoliv volume and CO
decreases MAP (worse if dehydrated or with hypovolemic shock)
can cause arrythmia - liberates massive K+
oONLY WITH ISOPROTENEROL

need anticholinergic like atropine as long as no isquemia or infart hx

417
Q

GI side effects of halothane

A

nausea

less MAP causes direct reflux?

418
Q

how to measure state of NM relaxation

A

toff meawsures evocated potentials, neursitimulator on peripheral nerve and depending on electirical response we see how relazed they aree

3 de 4?

419
Q

how NM work

A

block depolarization and propagation of electrical impulse @ all nerve cells

block liberation of Na+ channels

420
Q

advantages of succinilcoline

A

initiation action time is fast

can intubate by 60sec

421
Q

4 colinesterasas enzymes

A

pseudocolinesterasa plasmatica - eliminaeted in plasma

422
Q

when can colinesterase enzymes be low/action duration is longer

A

in hepatopathy px, elders, denutruitin, taking anticolesterase medications, polymorfogenetics

423
Q

metabolism of succinilcoline

A

by colinesterase enzymes

424
Q

how do NDNMRs work

A

these no longer work like Ach - instead work the oppsoite

acti in cholinergic rec of muscular membrane
ion channel
liberation of Ach (by stimulus mechanical or nervous) in hendidura sinaptica where acetilcolinesterase enzymes are located, unites to rec colinergic
when occupied , ion channel opens and there is ion exchange NORMALLY

NDNMRs are competitive and compete for this chol rec - ion channel doesnt open and membrane stays despolarizada

425
Q

most resitant muscles of the body

A

those of oropharynx as well as the diaphragm

to paralyse them and well oro aperture you need to multiply x 3 dose (from abdominal muscle)

side effects increase along with this

after intubation and only want abdominal relaxaation just give original DE95 dose

426
Q

first muscle to recuperate

A

diagphragm @ 20% reec, visceras pushed out

427
Q

how many half lives

A

remember there are 4 half lives for any drug to be eliminated - 1st 50%, 2nd 75%, 3rd 87%, 4th 100% - we alsohav edrugs that can revert the rest of this time

428
Q

NMRS he uses

A

vercuroniu, cistracuruin, rovuronio, atracurin

429
Q

inducers of sleep ideal cx

A

EV anesthetics

organic compounds

also can contiain other elements like oxygen, azufre, nitrogen, methy groups

produce LOC, hipnosis - ALL - #1 reason
#2 reason - can be used completely alone now, doesnt need to precede and inhaled, short qx, dx procedures, qx 15-20min, studies, ambulatory procedures, gastro, adontological

most have analgesic properties
some have more anesgelsia than anesthesia (sleep)
most cause amnesia

also are anticonvulsives

barbituric thiopental used to be most used but not anymore

430
Q

metabolite of rocuronio (desmeron)

A

17 acteil rocuronio

431
Q

advantages of rocuronio

A

…glucosa? not accumulative
doesnt liberate histamine,
stable - lung, cardiac

not used much due to effects at liver and kidney

432
Q

4 anticolinesterases

A

ambenonium
neostigmina
Physostigmine
Pyridostigmine

block sction of enzyme acetilcholinesterase and so permits that more Ach reaches union plauqe

potentializes electric impulse

muescarinic effects - bradicardia and salivation

use in px with prolonged block

accelerates autodestruction

check BIS awake but paralysed, myalgia, HTN,

depends on grade of rec occupied (toff 34 - 3 de 4 electrical movemnnt)
if cant measure that measure diaragmatic movement
have to have at least 20% of rec free, not occupied
how do you know? when with electrical impulse you have 1 sole movement (25% occ)
2 movements - 50%
3 - 75%
4 movement - 100% occ ( if you give in this momentmolecules goes into ION CHANNEL - channel block, permanent tkaes 10hr to be able to intubate so need 20% free)

to block diagrphamm last one to be blocked needs 80% at least occupied @ 20% open yyou hav e diaphragmatic movment

433
Q

how to revert muscarinic effects of bradicardia and salivation

A

with anticolinergics like atropine glicopirulato, metoclopramide

434
Q

sugammaden - why beter than neostigmine

A

also reverts affects of NMRs

can use even at 100% rec occupied
DOESNT PRESENT muscarinic effects

hyperpolarized molecule that surrounds molecule of relxer and displaces it, doesnt give it chanve to cause channel block

435
Q

neostigmine dose to use

A

2.5mg - unica dose can revert 80% of NMR effect

436
Q

sugammaden doses

A

dose depends on grade of block that is present in the moment
100% block - dose - 4-6mg/kg
50% - 2mg/kg

437
Q

GB miasthenia gravis px which NMR?

A

much less dose
and prefer non depolarizing
revertible

ORTHO (9 decks)

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