Flashcards in Cardiovascular Drugs Deck (26):
List the three most deadly cardiovascular drugs.
List 8 toxicological causes of hypotension and bradycardia:
6. Cholinergic agents
7. Large doses of sedative hypnotics (EtOH, BZD, GHB)
What are the plants from which digitalis can be derived
Lily of the valley
What are the two therapeutic effects of digitalis?
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
- Dig increases vagal tone : sinus bradycardia, impaired AV conduction
- Dig enhances automaticity: ventricular dysrhythmias
List the specific, but not pathognomonic dysrythmias associated with digoxin toxicity.
- 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)
List factors associated with increased risk of digitalis toxicity
- Hypokalemia or hyperkalemia
- Cardiotoxins co-ingestions (BB, CCB, TCA)
- verapamil, diltiazem, nifedipine
What are the most common symptoms of digoxin toxicity?
Is AC indicated in acute digoxin ingestions?
Yes, decreases enterohepatic recirculation
What is the treatment for hyperkalemia in the setting of digoxin toxicity?
- 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
List the indications for administration of Fab fragment in adults and children.
- 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
- 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
- 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
What are the three methods of determining dose of Fab fragments?
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
What is the treatment for bradyarrhythmias in dig toxicity?
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
Which is more likely to cause hyperglycemia, CCB or BB?
CCB b/c it blocks L type Ca channels on pancreas which trigger release of insulin. When this effect is blocked hyperglycemia ensues
List the most toxic β-blockers.
What is the biochemical response to catecholamine action at the β-receptor?
- Activation of adenyl cyclase (G protin mediated) and conversion of AMP to cAMP
- Phosphorylation of Calcium channels and increased intracellular Ca
List 3 actions of β1 receptor stimulation in the heart, and 5 target organs and action of β2 receptor stimulation (and 1 of β3):
o Enhances cardiac contraction (inotrpy)
o Enhances cardiac conduction (dromotropy)
o Accelerates heart rate (chronotropy)
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
o Adipose tissue (lipolysis)
List nonselective and selective β-blockers.
List the 6 β-blockers with significant membrane stabilizing properties.
(Na channel blockers
List 2 BBs with K channel blockade:
Provide a stepwise approach to the treatment of β-blocker poisoning.
4. Ionotropes: glucagon, calcium, HIE, catecholamine pressor, Intralipid, phosphodiesterase inhibitors
What is the antiarrhythmic of choice for recurrent ventricular tachycardia in β-blocker poisoning?
In addition to usual therapy, what can be used in Sotolol overdose?
- Maximize Mg, K
Consider overdrive pacing
Differentiate between the dihydropyridines and nondihydropyridines:
o At therapeutic doses, little effect on cardiac conduction or myocardium
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
What are the effects of CCBS at therapeutic doses?
- 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
List dipiramidole and nondipyamidole CCBs.