Mnemonics for Friday, October 1, 2010

With it being vacation I got confused about what day it was – so Minsoo and I switched days. I’m writing my mnemonics based on what he told me to do.

(1) Antiarrhythmic class IC – block all sodium channels (activated and inactivated)

No affect on AP duration but drastically prolong the refractory period. This can bacially stop the AV nodal conduction and thus cause dangerous arrhythmias. 15% of pts given these drugs die of sudden cardiac death. Therefore, it is considered a last resort.

Drugs: Flecainide, encainide, and propafenone.

Flecainide is the prototype so here is the mnemonic:

Flec the canine died from using the antiarrhythmic class 1 C (fleC)

Encainide = sounds similar, so think And canine died.

Propafenone = Prop up a feline because he needs one. (dogs/cats - helps you remember it)

To remember the 3 drugs in the group: I Can’t Forget that Eerie Pulse. (pulse = deadly arrhythmia)

(2) Digitoxin

Mechanism: By inhibiting the K⁺/Na⁺ exchange pump, less Na⁺ leaves the cell. If there is ↑Na⁺ inside the cell then the Ca⁺²/Na⁺ exchange pump is inhibited (you don’t want to allow more Na⁺ into the cell). End Result (for cardiac muscle) = ↑Ca⁺², which causes more Ca⁺² to be released from the SR, which in term causes more free Ca⁺² inside the cell and therefore STRONG MUSCLE FIBER CONTRACTION.

In other words, no matter how stretched the heart is (due to ↑preload), digoxin makes a strong contraction.

Uses

• Allowing stronger contraction of heart muscle
• Because so much Ca⁺² is inside the cell, the cell becomes more positive = closer to threshold
• Not only true for cardiac muscle but also true for neurons
• Parasympathetic neurons release more ACh
• = slow down HR by ↓AV node conductance J
• Since Parasympathetic is the #1 controller of the SA node, atria and AV node
• Sympathetic neurons release more NE
• = ↑ risk of Ventricular Fibrilation!!!!! L
• Since Sympathetic is the only controller of the ventricles

Why do you give Digoxin along with Quinidine?

• Quinidine is an antiarrhythmic that blocks Na⁺ active channels (Ia), but since it’s a Muscarinic blocker (like Atropine), it causes sympathetic dominance in the SA node = ↑HR
• Digoxin will slow down the AV nodal conductance so that ventricles don’t contract so fast.

Reasons for Digoxin toxicity

• ↓K⁺ because Digoxin competes with K⁺ for the binding site on the K⁺/Na⁺ exchanger, if there is less K⁺ in the blood, then more digoxin can bind to the exchanger
• ↑Quinidine because Quinidine displaces the Digoxin that is attached to plasma proteins (the inactive form of the drug in the body)
• ↓Mg⁺² because the body sometimes confuses Mg⁺² and Ca⁺² in the pump but Mg⁺² can’t bind to Troponin C – basically Mg⁺² is the bodies way of making sure that there isn’t so much Ca⁺² in the cells. If ↓Mg⁺² then the body really does have a lot of Ca⁺² in the cell = making Digoxin toxicity faster and more extreme.

Ways to treat Digoxin toxicity

• Stop administration of Digoxin – duh
• Administer K⁺ to compete with Digoxin for binding site
• Administer Antibodies against Digoxin – to attach to and inactivate the free Digoxin in the blood
• Administer a class 1B antiarrhythmic (which block the inactive Na⁺ channels that only open in depolarized cells). Since with Digoxin the cells have a lot of Ca⁺² (more positive than normal) they are depolarized! Thus, class 1B antiarrhythmics (Lidocaine) will stop the ventricular arrhythmia

Mnemonic

1 = Digi-toxin you can tell by it’s name that it has a low therapeutic range and can easily become toxic

2 = Jocks are strong! So if you take Di–Jock-son your heart will be a stronger pump!