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OS & Pain Management > Local Anesthesia pt. 2 > Flashcards

Local Anesthesia pt. 2 Flashcards

1
Q

Most meds to Circulatory system =

A

Clinical

effect

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2
Q

Local Anesthesia to Circulatory system =

A

will

cease to provide desired effect

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3
Q

Most local anesthetics have — effect

A

vasodilatation

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4
Q

Procaine:

A

most potent vasodilator

• Treat accidental intra-arterial injection of thiopental

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5
Q

Vasodilatation

– Clinical undesirable effect

A

• ↑ rate of absorption into blood, potential systemic

overdose

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6
Q

Cocaine:

A

the only local anesthetic with constrictor

effect

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7
Q

Cocaine

Inhibition of

A

catecholamine re-uptake

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8
Q

• Oral Route

A

– Poorly absorbed except cocaine

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9
Q

• Topical Route

3

A

– Rapid absorption to mucous membrane
• (tracheal>pharyngeal>esophageal)
– Non Intact skin (Sunburn remedy)
– EMLA cream for intact skin

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10
Q

• Injection

A

– For management of ventricular dysrhythmias (PVC)

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11
Q

•— , initially, have higher blood level of anesthetics

A

Highly perfused organ

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12
Q

• — muscle has greatest % of anesthetics

A

Skeletal

– b/c largest tissue mass in the body

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13
Q

Elimination of drug through

2

A

– Metabolic pathways

– Excretory pathways

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14
Q

Elimination half-life (t ½)

A 
– Time needed for 50% reduction in blood level
• 1st t ½ 50%
• 2nd t ½ 75%
• 3rd t ½ 87.5%
• 4th t ½ 94 %
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15
Q

ALL local anesthetics cross (2)

A

blood-brain barrier, and placenta

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16
Q

• Ester local anesthesia

3

A

– Hydrolyzed in plasma by pseudocholinesterase
into paraaminobenzoic acid (PABA)
– Allergic reaction is related to PABA
– Atypical pseudocholinesterase (1/2800 persons)
• May lead to potential for toxicity

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17
Q

• Amide local anesthetics

4

A

– Primary biotransformation site is Liver
– Liver function/ hepatic perfusion influence
biotransformation
• Cirrhosis / CHF or Hypotension
– Relative contraindication for
• ASA IV to V patient with liver dysfunction, heart failure
– Sedative effect of Lidocaine active metabolite

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18
Q

• Methemoglobinemia:

2

A

– Blue Baby Syndrome
– Primary metabolite of Prilocaine can be
the cause

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19
Q

– Blue Baby Syndrome

3

A

• Inherited blood disorder
• Atypical hemoglobin
– Unable to deliver oxygen efficiently

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20
Q

Methemoglobinemia
S/S of patient:
(2)

A
  • Easily tired

* Bluish tint on lip or skin

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21
Q

Pharmacology of Local Anesthesia
Excretion
(2)

A
  • Kidneys are primary excretory organ

* In urine

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22
Q 
Pharmacology of Local Anesthesia
Excretion
• Kidneys are primary excretory organ
• In urine
(3)
A

– Procaine appears as PABA (90%)
– 10% cocaine found
– Amides with parent compound > esters

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23
Q

Local anesthesia readily cross

A

blood-brain barrier

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24
Q

Pharmacological action is

A

CNS depression

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25
Q

) Initial clinical signs/symptoms of CNS toxicity are

A

Excitatory!!
– Numbness of tongue and circumoral region (symptoms)
– Slurred speech, shivering, A/V disturbances, Disorientation, tremor.. (signs)
– Luckily, lidocaine don’t have these s/s but mild sedation or drowsiness

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26
Q

2) Higher level of CNS toxicity =

A

Tonic-clonic convulsion

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27
Q

3) Further increase

A

– cessation of seizure activity>respiratory depression>reparatory arrest

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28
Q

Direct action on myocardium

3

A

– Produce myocardial depression
– Therapeutic advantage
– Management of hyper-excitable myocardium

29
Q

– Management of hyper-excitable myocardium (2)

A
  • Premature Ventricular Contraction (PVC)

* Ventricular tachycardia

30
Q

Direct action on peripheral vasculature

3

A

– Cocaine and Ropivacaine are vasoconstrictors
– All other local anesthetics are vasodilators
– Local anesthetics cause hypotension

31
Q

Systemic Action of local Anesthesia
others
• — muscle are more sensitive to local irritant properties
• — is generally unaffected unless near overdose

A

Skeletal

Respiratory

32
Q

Malignant
Hyperthermia
(2)

A 
– No documented cases in 
medical or dental literature  
(past 25 years) supporting 
the concept of amide 
anesthetics triggering 
malignant hyperthermia

The Malignant Hyperthermia
Association of the United
States

33
Q

Importance of Vasoconstrictors

5

A 
↓ Perfusion to site of administration
Slow the absorption of L.A. into Cardiovascular system
Minimize the risk of systemic toxicity
↑Duration of action for L.A.
↓Hemorrhage
34
Q

Natural catecholamines

3

A

 Epinephrine
 Norepinephrine
 Dopamine

35
Q

Synthetic catecholamines

2

A

 Isoproterenol

 Levonordefrin

36
Q

Non-catecholamines

1

A

 Amphetamine, Ephedrine, Methamphetamine

37
Q

3 modes of action

3

A

 Direct acting
 Indirect acting
 Mixed acting

38
Q

All — work on adrenergic receptors with

direct acting

A

Cathecholamines

39
Q

Activation of Alpha
 Alpha 1 :
 Alpha 2:

A

Vasoconstriction

Post synaptic inhibitory

40
Q

Activation of Beta
 Beta 1:
 Beta 2:

A

located at heart at intestine

Vasodilatation (found in the Bronchi, Vascular beds)

41
Q

Dilution is commonly referred to as

A

ratio

 Example, 1 to 1000 [1:1000]

42
Q

Concentration of 1:1000 means

A

 1gram (1000mg) of solute (drug) in 1000ml solution

So 1000mg / 1000ml = 1.0mg/ml of solution

43
Q

— is the most used vasoconstrictor

A

Epinephrine

44
Q

— (antioxidant) is added to delay deterioration

A

Sodium Bisulfite

45
Q

Shelf life of L.A. with Epi is ~ – months

A

18

46
Q

Epi can be synthetic or obtained from —

A

adrenal medulla

47
Q

Mode of Action:

A

both alpha and Beta
 Beta 2 is more sensitive to epinephrine
 Epi injection, first with alpha action… later, dilatation b/c beta action (usually 6hrs later)

48
Q

Potent bronchiole smooth muscle dilator

A

treat acute asthma

49
Q

Termination:

A

Reuptake or inactivated by COMT and MAO

50
Q

Epinephrine plasma level does increase after “usual” intra oral injection despite of —

A

aspiration

51
Q

Epinephrine plasma level does increase after “usual” intra oral injection despite of aspiration
(2)

A

 Increased in cardiac output and stroke volume
 Minimum change in blood pressure and heart rate
-This would explain why patient felt palpitation after injection

52
Q

Intravascular injection of 0.015mg can..

2

A

 Increase heart rate from 25 bpm to 75 bpm

 Systolic blood pressure from 20mmHg to 70mmHg

53
Q

Norepinephrine

 Lack significant – actions

A

B2

54
Q

Norepinephrine

Intense

A

vasoconstriction

 Almost exclusive alpha action

55
Q

Norepinephrine

Dramatic elevation of

A

blood pressure

 9X higher than epinephrine

56
Q

Levonordefrin

A

 Most closely resemble norepinephrine

57
Q

Selection of Vasoconstrictor
Dependent on the time needed for the procedure
 Without epi ~— mins
 With epi ~– mins

A

10

60

58
Q

Epinephrine produces rebound – effect

A

vasodilatory

59
Q

Norepinephrine produces cases of tissue (2)

A

necrosis and
slough
 Disadvantage outweigh its advantages

60
Q

 ASA 1:

A

Normal healthy patient

61
Q

 ASA 2:

A

Mild systemic disease

62
Q

 ASA 3:

A

Severe systemic disease that limits activity

Mild diabetes, controlled hypertension, obesity

63
Q

 ASA 4:

A

incapacitating disease that is a constant threat to life

CHF, Renal Failure

64
Q

 ASA 5:

A

Moribund patient not expected to survive 24 hours

Ruptured aneurysm

65
Q

 ASA 6:

A

Brain-dead patient whose organs are being

harvested.

66
Q

Medical Status of the Patient
Contraindications to Vasoconstrictor
(5)

A

 1) Blood pressure in excess of 200 mmHg systolic or 115 mmHg
 2) Uncontrolled hyperthyroidism
 3) Severe cardiovascular disease
 4) Undergoing general anesthesia with halogenated agents
 5) Patient receiving nonspecific B-blocker, MAOi, Tricyclic antidepressants

67
Q

 3) Severe cardiovascular disease

5

A

 a) Less than 6 months after myocardial infarction
 b) Less than 6 months after cerebrovascular accident
 c) Daily episodes of angina pectoris or unstable angina
 d) Cardiac dysrhythmias despite appropriate therapy
 e) Postcoronary artery bypass surgery (CABG), less than 6 months

68
Q

Patients in categories 1 to 3a through 3d are classified as ASA –risks and NOT normally considered candidates for

A

4

elective or emergency dental treatment in the office

69
Q

Whenever possible……………..

3

A 
 Multiple aspirations
 Slow administration 
 Minimum concentration of both 
• Vasoconstrictor
• Local anesthetic

OS & Pain Management (8 decks)

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