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Toxicology > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

List the three most deadly cardiovascular drugs.

A
  • Digitalis
  • Propranolol
    Verapamil
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2
Q

List 8 toxicological causes of hypotension and bradycardia:

A
  1. BB
  2. CCB
  3. digoxin
  4. Clonidine
  5. Opiates
  6. Cholinergic agents
  7. Large doses of sedative hypnotics (EtOH, BZD, GHB)
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3
Q

What are the plants from which digitalis can be derived

A 
Foxglove
Digitalis
Lily of the valley
Bufo toad
Milk weed
Oleander
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4
Q

What are the two therapeutic effects of digitalis?

A
  1. Increase force of myocardial contraction by direct inhibition of Na+ - K+ ATPase: improved ionotropy for CHF
  2. Indirectly increases vagal tone therefore decrease AV conduction: rate control Afib

IE
- Dig increases vagal tone : sinus bradycardia, impaired AV conduction
- Dig enhances automaticity: ventricular dysrhythmias

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5
Q

List the specific, but not pathognomonic dysrythmias associated with digoxin toxicity.

A
  • Atrial fibrillation with slow, regular ventricular rate (AV dissociation)
  • Nonparoxysmal junctional tachycardia (70-130/min)
  • Atrial tachycardia with block (atrial rate usually 150-200/min)
  • Bidirectional ventricular tachycardia (++rare)
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6
Q

List factors associated with increased risk of digitalis toxicity

A 
Renal failure

Heart disease
- Congenital
- Ischemia
- CHF
- Myocarditis

Metabolic abnormalities:
- Hypokalemia or hyperkalemia
- Hypomagnesemia
- Hypercalcemia
- Alkalosis
Hypothyroidism

Medications:
- Sympathomimetics
- Cardiotoxins co-ingestions (BB, CCB, TCA)

Drug interactions:
- Quinidine
- Amiodarone
- Erythromycin
- verapamil, diltiazem, nifedipine
- Captopril
- 
Elderly woman
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7
Q

What are the most common symptoms of digoxin toxicity?

A
  • Nausea
  • Anorexia
  • Fatigue
    Visual disturbance
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8
Q

Is AC indicated in acute digoxin ingestions?

A

Yes, decreases enterohepatic recirculation

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9
Q

What is the treatment for hyperkalemia in the setting of digoxin toxicity?

A
  • Digibind is definitive treatment! Can temporize with the following if waiting on digibind:
    o Insulin and glucose
    o Sodium bicarbonate if acidotic
    o CAUTION with b-agonists because of their pro-arrhythmic effects
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10
Q

List the indications for administration of Fab fragment in adults and children.

A

Adults:
Clinical:
- Co-ingestion of cardiotoxic drugs (BB, CCB, TCA
- Severe ventricular dysrhythmias
- Progressive and hemodynamically significant bradydysrhythmias not responsive to atropine
- Rapidly progressive rhythm disturbance or rapidly rising K

Biochemical:
- K GT 5.0 mmol/L in acute ingestion
- Acute ingestion GT 10mg PLUS any 1 other indication
- Steady state level >7.8 nmol/L (6ng/mL) PLUS any 1 other indication

Children:
- Ingestion of >0.1-0.3mg/kg or steady state level >6.5nmol/L (5ng/mL) PLUS rapidly progressive Sx/Sings or serious dysrhythmias or K>6.0mmol/L
- Co-ingestion of other cardiac drugs with additive or synergistic activity
Ingestion of a plant known to contain cardiac glycosides PLUS severe dysrhythmias

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11
Q

What are the three methods of determining dose of Fab fragments?

A
  1. Empiric: In sick, unstable patient
    a. Arrest: 20 vials
    b. Acute: 10 vials (adult or pediatric)
    c. Chronic: adults 5 vials; Peds 2 vials
  2. By ingested dose: In patient who meets criteria but have time to think
    a. KNOW: One vial = 40 mg of digiFab, binds 0.5mg of digoxin and bioavailability of digoxin is 80% (0.80)
    b. First calculate body dig load = mg ingested x 0.8
    c. Second calculate # vials = body load / 0.5mg
  3. By steady state serum concentration at 6-8 hours
    a. Convert nmol/mL to ng/mL by dividing level by factor 1.3 (can do this before or after you make the calculation
    b. Dose = ([dig ng/mL] x wt) / 100
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12
Q

What is the treatment for bradyarrhythmias in dig toxicity?

A 
Try atropine (likely wont work)
Avoid pacing b.c greater automaticity but if have to try transcutaneous
Avoid Mg b/c can impair impulse formation and AV conduction
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13
Q

Which is more likely to cause hyperglycemia, CCB or BB?

A

CCB b/c it blocks L type Ca channels on pancreas which trigger release of insulin. When this effect is blocked hyperglycemia ensues

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14
Q

List the most toxic β-blockers.

A
  • Propranolol
  • Acebutolol
  • Oxeprenolol
    Alprenolol
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15
Q

What is the biochemical response to catecholamine action at the β-receptor?

A
  • Activation of adenyl cyclase (G protin mediated) and conversion of AMP to cAMP
  • Phosphorylation of Calcium channels and increased intracellular Ca
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16
Q

List 3 actions of β1 receptor stimulation in the heart, and 5 target organs and action of β2 receptor stimulation (and 1 of β3):

A
  • Β1:
    o Enhances cardiac contraction (inotrpy)
    o Enhances cardiac conduction (dromotropy)
    o Accelerates heart rate (chronotropy)
  • Β2:
    o Vascular smooth muscle relaxation and vasodilation
    o Liver glycogenolysis and gluconeogenesis – thus may result in hypoglycemia if blocked
    o Increased insulin secretion, glucagin release
    o Lung bronchodilation
    o Adipose tissue lipolysis, release of free fatty acids
    o Uterus smooth muscle relaxation
  • B3
    o Adipose tissue (lipolysis)
17
Q

List nonselective and selective β-blockers.

A 
Non selective
Propranolol
Nadolol
Labetalol
Carvedilol
Sotalol
Timolol
Pindolol
Oxprenolol
Selective
Atenolol
Bisoprolol
Metoprolol
Esmolol
Celiprolol
Acebutolol
Bebivolol
Betaxolol
18
Q

List the 6 β-blockers with significant membrane stabilizing properties.
(Na channel blockers

A
  • Propranolol
  • Nadolol
  • Acebutalol
  • Pindolol
  • Labetolol
    Oxeprenol
19
Q

List 2 BBs with K channel blockade:

Qt prolongation

A
  • Sotalol

Acebutolol

20
Q

Provide a stepwise approach to the treatment of β-blocker poisoning.

A
  1. ABs
  2. Decontamination
  3. Atropine
  4. Ionotropes: glucagon, calcium, HIE, catecholamine pressor, Intralipid, phosphodiesterase inhibitors
  5. Pacing
  6. ECMO
  7. Dialysis
21
Q

What is the antiarrhythmic of choice for recurrent ventricular tachycardia in β-blocker poisoning?

A
  • Lidociane
22
Q

In addition to usual therapy, what can be used in Sotolol overdose?

A
  • Maximize Mg, K

Consider overdrive pacing

23
Q

Differentiate between the dihydropyridines and nondihydropyridines:

A
  • Dihydropyridines:
    o At therapeutic doses, little effect on cardiac conduction or myocardium
  • Nondihydropyridines:
    o At therapeutic doses have profound effect on SA, AV nodal tissue, and myocardial L-type Ca channels
    o Predominantly peripheral smooth muscle L-Ca channel blockade : vasodilation
24
Q

What are the effects of CCBS at therapeutic doses?

A
  • Block slow calcium channels: α-subunit, L-type channel
    o Myocardium – coronary vasodilation
    o Vascular smooth muscle – peripheral vasodilation
  • Reduce contractility, Depress SA node activity, Slow AV conduction
25
Q

List dipiramidole and nondipyamidole CCBs.

A

Nondihydropyradine

Verapamil
Diltiazem
Benzothiazepine
Phenylalkylamine

Dihydropyridine

Nifedipine
Nicardipine
Nimodipine
Amlodipine
Felodipine
Isradipine
Nisoldipine
26
Q

What is the order of ionotropes in CCB poisoning?

A

a. Order in CCB = Calcium > catecholamine pressor > HIE > Glucagon > IFE / Phosphodiseterase inhibitirs

Toxicology (16 decks)

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