Introduction to CV Pharmacology - Orlando Health

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CV Pharmacology AP Phase Response ECG Waveform Phase 0 Rapid Depolarization Phase 1 Peak Phase Phase 2 Plateau Phase Phase 3 Beginning Repolarization Phase Phase 4 Resting Phase The initial upswing indicates rapid depolarization by the influx of sodium into the myocardial cell. Potassium begins exiting cells. This peak reflects the brief period that sodium channels close. Calcium channels open for a slow influx of calcium ions to prolong depolarization. Calcium plays a key role in myocardial contraction. This rapid downswing marks the closure of sodium and calcium channels to prevent any further entry of sodium or calcium into the cell. Potassium begins to move back into the cell. The cell is now ready for another depolarization stimulus. QRS Absolute Refractory Period QRS Absolute Refractory Period QRS Absolute Refractory Period QRS and first half of T wave Absolute refractory period until midpoint of T wave, then becomes relative refractory period, the last half of T-wave. Absolute Refractory Period Relative Refractory Period Last half of T wave as it returns to isoelectric line Relative Refractory Period Keep in mind the ECG only represents electrical heart activity, not the actual contraction of the heart. Based on these previously mentioned principles, antidysrhythmic drugs are designed to modify the movement of ions in the various AP phases by altering the electrophysiology of the cardiac cell. Based on this principle, antidysrhythmics are classified based on their mechanisms of action and effects on the action potential. Currently there are four main classes of antidysrhythmics. The classification system (Vaughan- Williams) can assist you in recalling the actions and adverse effects. Class I - - Block sodium ion channel o o o Class Ia Class Ib Class Ic Class II (beta-blockers) - Block beta receptors Class III - Block potassium ion channels Class IV (calcium channel blockers) - Block calcium ion channels In general, drugs within the same class are similar in action and adverse effects and some drugs may have properties of more than one class category. (Example: amiodarone, sotalol). It is also important to note that all antidysrhythmics have the potential (some worse than others) to 2010 Orlando Health Education & Development 11
CV Pharmacology produce proarrhythmic effects on the patient. This means they can either worsen the dysrhythmia or trigger new ones. Antidysrhythmics can also prolong the QT interval (QTI) resulting in lethal dysrhythmias. Consequently, it is critical to closely monitor patients during initiation and usage of antidysrhythmics. This includes closely monitoring the ECG measurement of the QTI or QT interval corrected (QTc). Note: It is essential to identify drugs that prolong the QTI. For further information, read below for “ECG Measurement: The QTI and QTc,” or use a current drug reference, and internet resources such as: http://www.long-qt-syndrome.com/ekg_readout.html http://www.qtdrugs.org ECG Measurement: The QTI and QTc Introduction The interpretation of changes in the QT interval is an important aspect in the evaluation of an ECG tracing. The QT interval, (QTI) represents depolarization and repolarization of the ventricles. The QTI includes the “relative refractory period,” during which the heart is vulnerable to any ectopic foci that can initiate a stimulus. Accurate measurement is significant, as a prolonged QTI has been linked to monomorphic ventricular tachycardia, polymorphic ventricular tachycardia (torsades de pointes), and sudden cardiac death. The use of the QT interval in clinical practice is not without controversy. The literature clearly indicates that prolongation of the QTI in certain situations is associated with dysrhythmias or sudden cardiac death within 6-48 hours of lengthening. Far from perfect, yet deemed important, evaluation of the QTI/QTc remains a hot topic as researchers strive to discover methods that will provide better sensitivity and specificity for detecting the electrophysiologic changes that increase the risk of arrhythmias and sudden death. Lack of standardization: An identified problem is lack of a uniform approach to measurement. Some institutions do not measure the QTI unless physician ordered, while others measure only the QTI and not the QT C . Underlying problems such as a bundle branch block will affect the rate, and yet a standard for evaluation has not been agreed upon. Data collection and interpretation: First, it is not clear precisely how the measurement can be used to predict and prevent sudden cardiac death. Second, specific values of parameters vary depending on the population and circumstances. Data collection for the purpose of investigating different formulas is difficult, as it requires a very large population with high quality ECG data. QTI variation though 24 hours: Another problem is that the QTI changes depending on wake and sleep states, lead selection, heart rate, sympathetic and parasympathetic tone. QTI and a wide QRS: A widened QRS due to a ventricular conduction block causes the QT interval to be longer without prolonged depolarization. Two methods are available for measuring the QTI in the presence of a wide QRS due to a conduction block: it can be measured from the end of the QRS (at the J point) to the end of the T wave, or the QRS interval can be subtracted from the QTI. It is important to note that many different pharmaceutical agents other than CV agents have the potential to prolong the QTI. Please refer to current drug references and the links listed below. © 2010 Orlando Health, Education & Development 12
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CV Pharmacology References AEHLERT,
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