Lecture

• Dromotropic: affects conductivity or conduction velocity at the AV node
• Phase 0: Na+ rapidly influxes into the cell which causes a large jump in membrane potential

  
• Phase 1: Na+ channels close and K+ channels open which makes them leak out and causes a small deflection.

  
• Phase 2: Ca+ channels open and it flows in which helps prolong the membrane potential and counteract the effects of K+ flowing out

  
• Phase 3: Ca+ channels close and K+ flows out rapidly which causes a sharp drop in membrane potential

  
• Phase 4: K+ channel closes which maintains resting potential. Pacemaker cells will have a slow leak of Na+ to back in to trigger another action potential.

  
• Phase 4 is more of a gradual incline for pacemakers cells due to the flow of Na+ but its flat for any other cell
• Absolute refractory period(ARP): the cell is completely unexcitable to a new stimulus
• Effective refractory period (ERP): ARP + shortsegment of phase 3, stimulus may cause the cell to depolarize but not propagate another action potential.

  
• Relative refractory period (RRP): a greater than normal stimulus will depolarize the cell and cause an action potential

  
• The RRP is extremely important as R on T phenomenon may occur here as it overlaps with the T wave; could cause V tac/ V fib if this occurs
• Supranormal period: a hyperexcitable period during which a weaker than normal stimulus will depolarize the cells and cause an action potential.

  
• Arrhythmias are caused by disturbances in properties of the heart and ions
• Antiarrhythmic drugs affect the electrophysiological properties of the cardiac membrane restore the proper movement of ions
• Antiarrhythmic drugs aren't cures and they could possibly make it worse or cause new arrhythmias; these are called proarrhythmic
• Dude that classified the antiarrhythmics is called Vaughn Williams
• Class 1A drugs are moderate Na+ channel blockers, Class 1B are mild and Class 1C are marked
• Class 1A drugs interferes with Na+ channels and has a moderate negative effect on phase 0. Has negative chronotropic and dromotropic effects. It specifically prolongs the QRS and QT segments
• Class 1B drugs interfere with Na+ channels and have a mild negative effect in Phase 0. They decrease ventricular automaticity and have no effect on the QRS
• Class 1C have a marked negative effect in phase 0. It causes QRS prolongation
• Quinidine is a class 1A drug used to treat A flutter, A fib and ventricular arrhythmias. It causes depression of cardiac conduction system thru decreased excitability, slowed conduction and decreased force of contraction.
• Adverse effects of Quinidine: Produces anticholinergic and alpha blocking effects such as irritation of GI tract, smooth muscle weakness, widened QT/PR interval(Can lead to PACs/PVCs or cardiac arrest). Rarely used for these reasons
• Lidocaine(Xylocaine) is a class 1B drug that is used for local anesthesia primarily but also for ventricular arrhythmias(Post MI). It's not useful for atrial arrhythmias. It causes depressed automaticity and must be given IM/IV
• Lidocaine (Xylocaine) is rapidly metabolized by the liver which can impair it. High doses can cause unwanted anesthetic effects and seizures
• Class 2 drugs are beta blockers. They have a negative chronotropic and dromotropic effect. They decrease heart rate, AV conduction, ventricular automaticity and increase the PR interval
• Class 2 drugs are used for supraventricular arrythmias and reoccurring MIs
• Esmolol(Brevibloc) is a class 2 drug that has negative chronotropic and ionotropic effects; its only given IV cuz of its rapid metabolism and its only given in emergency situations
• Propanol(Inderal) causes bronchoconstriction and affects the CNS while Esmolol(Brevibloc) has delayed AV conduction as an adverse effect(Not including their shared effects of hypotension and bradycardia)
• Class 3 drugs increase he ERP by interfering with K+ channels. It slows the efflux of K+ during repolarization and has negative chronotropic effects. It prolongs ventricular repolarization and the QT segment

  
• Amiodarone(Cordarone) is a class 3 drug that primarily blocks K+ channels but also affects Na+ and Ca+ while have some alpha/beta blocking effects. It's used for supraventricular and ventricular arrhythmias
• Amiodarone(Cordarone) prolongs the refractory period, decreases HR and AV conduction(Negative chronotropic and dromotropic).
• Adverse effects of amiodarone(Cordarone): long half life(about 60 days), interferes with thyroid fxn(contains Iodine within it), can cause bradycardia/heart failure/proarrhythmic, CNS effects(ataxia and tremors) and rarely cause skin discolouration. Hypotension is the most common adverse affect of IV admin
• Amidarone(Cordarone) prolongs the PR and QRS interval and is a drug thats commonly used by ACPs
• ALIVE trial is an experiment in 2001 in which amiodarone and lidocaine were compared in how they help VF patients. The ALPS(Amiodarone, Lidocaine, Placebo study) was conducted in 2016 and added saline as a placebo and was a double blind study.
• Class 4 drugs are Ca+ channel blockers and they decrease entry of Ca+ into excitable cells. In phase 2, Ca+ is important for sustained depolarization so it cuts down the PR interval and has negative chronotropic, ionotropic and dromotropic effects. Its negative ionotropic effects are not desirable in cardiac tissue but are useful in vascular smooth muscle(cause vasodilation)

  
• Verapamil(Isoptin) and diltiazem(Cardizem/Tiazac) are class 4 drugs that are indicated for arrhythmias originating in the AV node and supraventricular tachycardias. They primarily decrease and slow conduction thru AV node and then slow firing of SA node.
• Adverse effects of Verapamil(Isoptin), diltiazem(Cardizem/Tiazac): high doses lead to heart blocks, decrease myocardial contractility, hypotension and constipation
• Diltiazem(Cardizem/Tiazac) is more potent but has more adverse effects than Verpamil(Isoptin)
• Adenosine(Adenocard) is in its own category of antiarrhythmics(Used to be 5). It has the opposite effect of class 3 drugs as it increases K+ efflux and causes hyperpolarization. It slows conduction thru AV node, ventricular rate and a small effect of decreasing SA node rate. It's primarily used to terminate SVT and it acts within 15-30 seconds
• Adverse effects of adenosine(Adenocard): transient asystole, transient bronchospasm and literally causes a feeling of impending doom