Cardiac Electrophysiology An Treatment Of Arrhythmias Flashcards
Explain what ECG changes occur with hyperkalemia.
Tented T waves
Decreased r wave amplified
Prolonged QRS and PR intervals
ST segment depression
Prolonged QT interval
P wave disappearance with atrial standstill and resultant sinoventricular rhythm
Final stage = ventricular flutter, Vfib or ventricular asystole
What happens on an ECG with hypokalema?
Inverted T waves QT prolongation Mild ST depression Tornadoes de pointes Ventricular fibrillation
What happens on an ECG with severe hypermagnesemia?
PR prolongation AV block Sinus arrest Atrial standstill Widened QRS Prolonged QT
What happens on an ECG with severe hypomagnesemia?
This results in increased concentration of cytosolic calcium and prevents accumulation of intracellular potassium
Changes are clinically similar to hypokalmeia -
Prolonged PR, QT and QRS duration
Depressed ST segment
Catch and fibrillation
Torsades de pointes
Hypomagnesemia can lead to refractory hypokalemia, and it can also inhibit PTH secretion, resulting in hypocalcemia
Name examples of cardiac glycosides and what they do.
Examples: Digitalis, Foxglove, Oleander, Lily of the Valley, Azaleas (Rhododendron), Yew
Result in PR prolongation and can cause any degree of AV block
Toxicity can result in sinus bradycardia or arrest, atrial tachycardia, junctional ectopic beats/ junctional tachycardia, VPCs and ventricular tachycardia
What is the mechanism of action of class I antiarrhythmics? What are examples of these drugs?
Class I - sodium channel blockers - have the ability to interfere with sodium conductance during phase 0 of the cardiac action potential, and therefore interfere with impulse propagation in sodium dependent tissues.
Also called membrane stabilizing agents
Class 1a - block the fast sodium channel, which depresses phase 0 depolarization, which decreases conduction velocity. They decrease Vmax with intermediate strength while prolonging the durian ion of the action potential and the effective refractory period — EXAMPLES - quinidine, procainamide, disopyramide
Class 1b - decrease Vmax weakly and shorten both the action potential duration and the duration of refractories. They have a fast onset and offset, meaning that they have little effect at slower heart rates. More specific for voltage gated Na channels than 1a. — EXAMPLES - lidocaine, mexiletine
Class 1c = produce the greatest decrease in Vmax (decrease in conductivity) and minimally alter the duration of the action potential and effective refractory period. These have the most potent sodium channel blocking effects. They are more effective at faster heart rates — EXAMPLES - encainide, flecainide, propanfanone
What is the mechanism of action of class II antiarrhythmic agents and examples of these drugs?
Aka beta blockers
Have 4 levels of antiarrhythmic action: 1 )direct competitive blockade at the peripheral receptor level
2) central reduction of adrenergic outflow
3) anti ischemic
4) membrane stabilizing effect at high concentrations
Results in a decrease in spontaneous and triggered premature contractions
Diminished sinus rates and slowing of AV node conduction
An increase in ventricular fibrillation thresholds
These medications may help to suppress a variety of supraventricular or ventricular arrhythmias, and are also negative
Inotropes
Examples: Esmolol, propranolol, timolol, atenolol, etc
What is the mechanism of action of class III antiarrhythmic drugs and what are some examples?
Prolong the cardiac action potential (phase 3)/ potassium channel blockers. This prolongs the repolarization and duration of refractories in a variety of cardiac tissues
They maintain the normal conduction velocity
They exhibit reverse use dependence (refractoriness of ventricular myocytes increases at lower HR/ drug works better at lower HR — exception = amiodarone)
Examples = amiodarone, sotalol
What are class IV antiarrhythmic drugs and what are some examples?
Class IV = calcium channel blockers - act to depress the slow inward calcium current occurring during the cardiac action potential
Sinus and AV nodes are calcium dependent and are most affected. In these tissues, calcium channel blockade results in a decreased in max voltage and phase 4 automaticity
these properties allow calcium channel blockers to be effective for the treatment of supraventricular tachycardia , particularly those involving the AV node
These have minor effect on action potential of sodium dependent tissues
They are more effective at faster HR
EXAMPLES: Verapamil, diltiazem, nifedipine