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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
) Initial clinical signs/symptoms of CNS toxicity are
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
26
2) Higher level of CNS toxicity =
Tonic-clonic convulsion
27
3) Further increase
– cessation of seizure activity>respiratory depression>reparatory arrest
28
Direct action on myocardium | 3
– Produce myocardial depression – Therapeutic advantage – Management of hyper-excitable myocardium
29
– Management of hyper-excitable myocardium (2)
* Premature Ventricular Contraction (PVC) | * Ventricular tachycardia
30
Direct action on peripheral vasculature | 3
– Cocaine and Ropivacaine are vasoconstrictors – All other local anesthetics are vasodilators – Local anesthetics cause hypotension
31
Systemic Action of local Anesthesia others • --- muscle are more sensitive to local irritant properties • --- is generally unaffected unless near overdose
Skeletal | Respiratory
32
Malignant Hyperthermia (2)
``` – 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
Importance of Vasoconstrictors | 5
``` ↓ 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
Natural catecholamines | 3
 Epinephrine  Norepinephrine  Dopamine
35
Synthetic catecholamines | 2
 Isoproterenol |  Levonordefrin
36
Non-catecholamines | 1
 Amphetamine, Ephedrine, Methamphetamine
37
3 modes of action | 3
 Direct acting  Indirect acting  Mixed acting
38
All --- work on adrenergic receptors with | direct acting
Cathecholamines
39
Activation of Alpha  Alpha 1 :  Alpha 2:
Vasoconstriction | Post synaptic inhibitory
40
Activation of Beta  Beta 1:  Beta 2:
located at heart at intestine | Vasodilatation (found in the Bronchi, Vascular beds)
41
Dilution is commonly referred to as
ratio |  Example, 1 to 1000 [1:1000]
42
Concentration of 1:1000 means
 1gram (1000mg) of solute (drug) in 1000ml solution | So 1000mg / 1000ml = 1.0mg/ml of solution
43
--- is the most used vasoconstrictor
Epinephrine
44
--- (antioxidant) is added to delay deterioration
Sodium Bisulfite
45
Shelf life of L.A. with Epi is ~ -- months
18
46
Epi can be synthetic or obtained from ---
adrenal medulla
47
Mode of Action:
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
Potent bronchiole smooth muscle dilator
treat acute asthma
49
Termination:
Reuptake or inactivated by COMT and MAO
50
Epinephrine plasma level does increase after “usual” intra oral injection despite of ---
aspiration
51
Epinephrine plasma level does increase after “usual” intra oral injection despite of aspiration (2)
 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
Intravascular injection of 0.015mg can.. | 2
 Increase heart rate from 25 bpm to 75 bpm |  Systolic blood pressure from 20mmHg to 70mmHg
53
Norepinephrine |  Lack significant -- actions
B2
54
Norepinephrine | Intense
vasoconstriction |  Almost exclusive alpha action
55
Norepinephrine | Dramatic elevation of
blood pressure |  9X higher than epinephrine
56
Levonordefrin
 Most closely resemble norepinephrine
57
Selection of Vasoconstrictor Dependent on the time needed for the procedure  Without epi ~--- mins  With epi ~-- mins
10 | 60
58
Epinephrine produces rebound -- effect
vasodilatory
59
Norepinephrine produces cases of tissue (2)
necrosis and slough  Disadvantage outweigh its advantages
60
 ASA 1:
Normal healthy patient
61
 ASA 2:
Mild systemic disease
62
 ASA 3:
Severe systemic disease that limits activity | Mild diabetes, controlled hypertension, obesity
63
 ASA 4:
incapacitating disease that is a constant threat to life | CHF, Renal Failure
64
 ASA 5:
Moribund patient not expected to survive 24 hours | Ruptured aneurysm
65
 ASA 6:
Brain-dead patient whose organs are being | harvested.
66
Medical Status of the Patient Contraindications to Vasoconstrictor (5)
 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
 3) Severe cardiovascular disease | 5
 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
Patients in categories 1 to 3a through 3d are classified as ASA --risks and NOT normally considered candidates for
4 | elective or emergency dental treatment in the office
69
Whenever possible................. | 3
```  Multiple aspirations  Slow administration  Minimum concentration of both • Vasoconstrictor • Local anesthetic ```

OS & Pain Management (8 decks)

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