Note: arrhythmia and dysrhythmia are the same thing. I'll use arrhythmia.
Cardiac Rhythm
Our hearts are like metronomes, and we don't want to mess up the beat. All heart cells can contract on their own when electricity runs through them (automaticity), but that causes an arrhythmia. Instead, we want the nodes to electrocute things in order. Specifically, we want the SA node to electrocute the atria first. This turns on the AV node and His-Purkinje System, which electrocutes the ventricles.
When heart cells get electrocuted and contract, it's called depolarization.
What causes arrhythmia? Either impulses stop happening or the cells stop responding to ("conducting") them. Also, electric impulses might happen too frequently or a single impulse might electrocute more than once in a heart beat, a phenomena called reentry, or circus movement.
classes. There are supraventricular (atrial) tachy-arrhythmias and ventricular dysrythmias. You treat the first one by blocking the AV node. You treat the second one by restoring rhythm.
arrythmias. The most common is atrial fibrillation where impulses override the SA node. Atrial flutters are the smallest waves and can easily become fibs. Supraventricular tachycardias begin above the purkinje fibers. Ventricular tachycardias can be monomorphic (look like mountain peaks) or polymorphic (look like earthquake readings). V-tacs have wide QRS complexes, greater than or equal to .12 seconds.
H&Ts [effects of arrhythmia]. H: hypovolemia, hydrogen ion increase (acidosis), hypoxia, hypoglycemia, hypothermia, hypo- (or hyPER-!) kalemia. T: toxins, tamponade (heart squeezed by fluid around the heart in the pericardium), tension pneumothorax (air between lung and chest wall that makes it harder to breathe), thrombosis (coronary or pulmonary), trauma
treatment. Empirical (trial and error). Recent drug trials including CAST show that antiarrhythmic drugs significantly raise mortality rates. Vigilance in dosing, blood level monitoring, and follow-up are necessary to stop the #1 problem with arrythmias: other (possibly more fatal) arrythmias! Sinus rhythm is important to maintain. Therapy is tougher if a patient has coronary artery disease, heart failure, or hypertension. Keep in mind the following: renal and hepatic function, electrolyte balance, and anticoagulation. Basically, start the therapy at a low dose and titrate up. Keep going if it works, and abandon treatment if you see adverse or no effects.
EKG waves. One EKG wave is made up of PQRSTU. It is also broken down into PR (really PQ) and QT intervals, an ST segment, and a QRS complex. A systole (ventricle contraction) spans the length of QRST. The diastole spans the rest of the wave. The atrial contraction spans the PR interval.
Action Potential
Action potentials seem difficult but are easy once you understand them. Here's what you need to know: the action potential is 5 phases or steps (0, 1, 2, 3, and 4) including a refractory period (phases 1-3). We talked about this, but when a cell gets electrocuted and contracts, it's called depolarization. Depolarization means the cells get more positive. Basically, heart cells are normally at a negative charge (-70mV). When sodium pours in, they become positive, depolarizing to about +30mV (which is phase 0). The heart cells flex and everyone's happy. At +30mV, the sodium hatch closes and the cells pull out hoses to spray out potassium. Getting rid of all those positive K+ ions makes the cells negative, partially repolarizing (phase 1). Phase 2 is a charge plateau where the calcium hatch slowly opens, letting Ca+ in to balance out the K+ being lost. In phase 3, the calcium hatch closes and potassium hose continues to spray, greatly losing charge and repolarizing to less than -70mV. In phase 4, the autorhythmic or pacemaker potential phase, the potassium hose is kinked and the sodium hatch begins to open, slowly bring the cell more positive, back up to -70mV.
Antiarrythmic classes
A guy named Vaughan Williams classified antiarrythmia drugs into 4 categories:
1) sodium channel blockers
2) beta blockers
3) potassium channel blockers
4) calcium channel blockers
Each of these classes affects the action potential at a different phase or step. Class 1 sodium channel blockers stop phase 0 depolarization. Class 2 beta blockers disrupt phase 4 autorhythmicity (=automaticity). Class 3 potassium channel blockers prolong the refractory period (and therefore the whole action potential) by making the potassium hoses spray slower and repolarize slower. Class 4 calcium channel blockers disrupt phases 1 and 2 (the only ones that deal with calcium) and let potassium spray out of the hose without balancing it, causing repolarization to happen more quickly.
Class 1 sodium channel blockers
There are three kinds of sodium channel blockers: IA, IB, and IC. IC drugs simply slow conduction and include flecainide, propofenone, and moricizine. IC is the only one that isn't out of favor due to side effects, but the slides only want to discuss IA and IB, so here we go! IA includes the centuries-old quinidine, although we will focus on procainamide. IB includes lidocaine (and its oral analog mexiletine) and treats V-arrythmias.
PROCAINAMIDE
Indications: broad-spectrum antidysrhythmic, V-tac (pulseless & not) during CPR*, refractory V-fib during CPR, paroxysmal supraV-tac prophylaxis, conversion to sinus rhythm for A-fib/paroxysmal A-tac/A-flutter
* Note: this drug is now the "last choice" for advanced CPR support because of its toxicity
MOA: prolongs refractory period and suppresses arrythmia by blocking sodium ion channel
ARs: NVH, ab pain, fever w/ anorexia, weakness, psychosis (high dose), severe hypotension (rapid IV infusion), Lupus-like syndrome (30-50% of patients who take it over a year with increasing titer of antinuclear antibodies)
for Nurses: hold < 60 HR, IV=run continuous EKG strip, PO with full glass of water, weigh weekly & report 2lb weight gain or swelling, patient should report chest pain, shortness of breath, excess bleeding, fainting, dizziness, and hallucinations
LIDOCAINE
Note: this drug was removed from AHA Simplified Pulseless Arrest Diagram to emphasize high quality CPR and early defibrillation rather than drugs (lidocaine is used for IV V-arrythmias in CPR)
Indications: stable monomorphic VT (normal ventricle function), stable polymorphic VT (normal left ventricle function, QT interval), and correction of electrolyte imbalances. Lidocaine is NOT used for regular AMI prophylaxis
ARs: hypotension, bradycardia, arrhythmia, cardiac arrest. Some are due to hypoxemia s/t respiratory depression
Class 2 beta blockers
These slow the heart (negative chronotropes) and decrease conduction velocity of the heart cells by blocking calcium channels in the SA and AV nodes (they also block sodium channels throughout the heart and reduce automatic contraction, smooth muscle contraction, and relaxation rate). Specifically, beta blockers act on the SA node to reduce automaticity and the AV node to slow conduction velocity. Main benefit: they treat atrial dysrhythmias for heart failure. How? Reducing automaticity stabilizes arrhythmias. Beta blockers have dangerous side effects, so the only ones approved for arrhythmia are propanolol, acebutolol, esmolol, and sotalol.
Beta blockers can cause bronchospasms.
PROPRANOLOL
Type: nonselective
Indications: exercise-induced tachycardia, A-dys, V-dys, premature V contractions, digoxin-induced tachydys
ARs: few at therapeutic doses, high doses can = bradycardia, hypotension, heart failure, and bronchospasm
for Nurses: creatinine clearance prior, monitor for 3 days after, be careful with betapace, Class 2, and Class 3
Class 3 potassium channel blockers
AMIODARONE (CORDARONE)
