TCA and Digoxin toxicity Flashcards

1
Q

3 mechanisms of HCO3 in TCA toxicity

A
  1. Raises serum pH (decreases proportion of unbound active drug available)
  2. increases myocardial contractility
  3. delivers Na ions to cardiac myocytes (overcomes drug induced sodium channel blockade)
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2
Q

TCA Metabolic pathway and T1/2 life

A

Hepatic metabolism via cytochrome P450
T1/2=1-3d

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3
Q

7 TCA receptors

A

Na
K
Serotonin/dopamine (5HT/dopamine)
Histamine
anti-alpha 1
anti-Gaba
muscarinic (cholinergic)

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4
Q

3 electrolyte abnormalities associated with Digoxin toxicity

A
  1. Hypokalemia (chronic toxicity)
    -treat with slow K replacement
  2. Hyperkalemia (acute)
    -treat with antidote Digibind
  3. Hypomagnesemia
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5
Q

4 cardiac arrhythmia’s with

A
  1. Bidirectional VT
  2. slow afib w/ complete HB (any AV block)
  3. New bigeminy
  4. Junctional tachycardia
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6
Q

3 mechanisms of action of digoxin

A
  1. inhibits Na/K+ ATPase pump (increase intracellular Ca–>increases inotropy)
  2. decreases SA depolarizing and AV conduction
  3. increases myocardial automaticity and repolarization
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7
Q

Digoxin toxicity antidote

A
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8
Q

3 cuases of hypotension in TCA toxicity

A
  1. alpha 1 blockade -hypotension
  2. severe acidosis
  3. CV compromise (Na channek blockade)
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9
Q

ECG findings of TCA toxicity

A

1.QRS >100ms
2. terminal 40ms RAD (a. Tall R in aVR, R:S ratio in aVR >0.7)
–>PPV 66-81% TCA poisoning

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10
Q

5 clinical signs of TCA toxicity

A
  1. AMS
  2. Hypotension
  3. Cardiac dysrhythmias
  4. Seizures
  5. Hot and crazy (cholinergic effects)
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11
Q

Toxic dose for most TCAs

A

5 mg/kg
less for some –>nortryptiline, dothepin, doxepin, desipramine
1 pill can kill in peds

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12
Q

Utility of HD in TCA toxicity

A

Large volume of distribution protein binding, large molecules –> therefor not helpful.

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13
Q

5 2nd/3rd line agents for TCA toxicity

A
  1. Hypertonic saline 1-2cc/kg
  2. benzos -seizure control
  3. Magnesium - arrhythmia
  4. Pressors
  5. intralipid 1-1.5 cc/kg IV bolus
  6. lidocaine (class IIb—>arrythmia control)
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14
Q

2 treatment goals in TCA toxicity

A
  1. Narrow QRS <100ms
  2. serum pH 7.45-7.55
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15
Q

When to consider activated charcoal in TCA toxicity

A

acute life threatening ingestions within 1 hr

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16
Q

2 methods for DigiFAB (each for acute and chronic)

A

Acute:
1. unknown amount ingested- empiric 10-20 vials (20 if cardiac arrest, otherwise 10)
2. amount of digoxin ingested/0.5mg/vial

Chronic:
1. empiric-6 vials
2. (serum digoxin level ng/mL)x(wht in kg)/100 = dose in vials

17
Q

5 indications for Digifab

A
  1. serum level >15ng/ml (acute)
  2. tachy dysrhythmias
  3. Brady dysrhythmias
  4. cardiac arrest
  5. Hyperkalemia >5meq/l
  6. Visual impairment- every looks yellow
  7. hypotension
  8. acute ingestion >10 mg (0.3 mg/kg)
  9. Steady state concentration >5ng/mL (chronic)
    5/10/15 rule
  10. co-ingestion with other cardiotoxic drugs
18
Q

5 plants containing cardiac glycosides

A
  1. fox gloves
  2. yellow oleander
  3. white oleander
  4. lilly of valley
  5. Dognbane
  6. Rhododendron
19
Q

3 treatment for tachydysrythmias in digoxin toxicity

A
  1. cardiovert or defibrilate
  2. lidocaine (suppresses ventricular automaticity) ***avoid other anti arrythmics, will make problem worse
  3. magnesium
20
Q

2 treatments for brady dysrythmias

A
  1. Atropine (0.02 mg/kg/dose)
  2. transcutaneous pacing
21
Q

3 other anti-depressants that can cause sodium channel blockade

A
  1. citalopram
  2. fluoxetine
  3. venlafaxine