Arrhythmias final
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cardiac arrhythmias and anaesthesia
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Arrhythmias final
- 6. ECG (EKG) showing wave segments Contraction of atria Contraction of ventricles Repolarization of ventricles
- 39. Empiric Arrhythmia Diagnosis Interventions Clinical Outcomes Pathophysiologic Arrhythmia Diagnosis Known or suspected mechanisms Critical components Vulnerable parameters Targeted subcellular units BLACK BOX Interventions Clinical Outcomes
- 40. Pathophysiologic Arrhythmia Diagnosis Interventions Clinical Outcomes Known or suspected mechanisms Critical components Vulnerable parameters Targeted subcellular units AV node reentrant tachycardia AV node reentry Anatomical fast/slow pathway AV node (slow conduction ) AV nodal action potential L-type Ca ++ channel Ca ++ channel blocker -blocker Sinus rhythm
- 75. Implantable cardioverter defibrillator (ICD) reduces the chances of dying from a second SCA. An ICD is surgically placed under the skin in the chest or abdomen. The device has wires with electrodes on the ends that connect to the heart's chambers. The ICD monitors the heartbeat. If the ICD detects a dangerous heart rhythm, it gives an electric shock to restore the heart's normal rhythm. The electrodes are inserted into the heart through a vein.
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- No signal from the pacemaker site Development of an ectopic pacemaker May arise from conduction cells (most are capable of spontaneous activity) Usually under control of SA node if it slows down too much conduction cells could become dominant Often a result of other injury (ischemia, hypoxia) Development of oscillatory afterdepolariztions Can initiate spontaneous activity in nonpacemaker tissue May be result of drugs (digitalis, norepinephrine) used to treat other cardiopathologies
- Antiarrhythmic therapy has progressed over the past years from a concept of empiric arrhythmia diagnosis; that is, diagnosis solely of the appearance of the electrograms on the surface ECG with interventions aimed at making the ECG and the patient appear more “normal”, to a more scientific approach to current electrophysiology. In current pediatric and adult cardiology practices, an attempt is made at understanding the pathophysiologic diagnosis ( the what and how) of the arrhythmia. This allows the cardiologist to evaluate mechanisms and components of the arrhythmia in order to evaluate vulnerable parameters and target the arrhythmia on a subcellular level. Ultimately this intervention leads to, for the most part, making the ECG and the patient appear more “normal”!
- A simple example of this would be the diagnosis and treatment of AV node reentry tachycardia. The diagnosis of this arrhythmia can be made on a surface electrocardiogram. However, when a Pediatric Cardiologist evaluates this more closely, the AV node reentry circuit that is responsible for this tachycardia is secondary to an anatomic fast and slow pathway within the AV node. The AV node slow conduction pathway provides a retrograde circuit making this much like other types of reentry tachycardia. The vulnerable perimeter in this case would be the AV nodal action potential. On a subcellular level, the L-type calcium channel is prominent within the AV node. Therefore, interventions could be aimed at interfering with this channel either directly with a calcium channel blocker or indirectly with a beta-blocker. In either case, the clinical outcome would be the same and that is returning the patient to sinus rhythm.
- The Vaughn-Williams classification of antiarrhythmic therapy takes into account some of this approach. It is a somewhat confusing mechanism of memorizing antiarrhythmics and we will spend little time discussing the classification system itself. It is based on the cellular properties of the normal his-Purkinje cells. Classification of drugs is dependent upon the ion currents responsible for depolarization and repolarization as well as the beta-adrenergic receptors. Its advantages are that it is a physiologically based system and highlights the beneficial and deleterious effects of the specific drugs. Unfortunately, its disadvantages are that all cells are not normal. Therefore in addition to this, all cells in the heart are not his-purkinje in origin and therefore have different dysrhythmia profiles.
- Therefore, we will focus more on the original approach to antiarrhythmic therapy where you are expected to make an arrhythmia diagnosis based on the surface electrocardiogram and be familiar with some more common antiarrhythmics (including their Vaughn-Williams classification). Your goal would be to identify the dysrhythmia they have in mind certain interventions, which would provide for clinical outcomes.
- The Vaughn-Williams classification as I stated before divides antiarrhythmics based on certain ion channels they affect. Class I antiarrhythmics are sodium channel blockers and have direct membrane action upon the sodium channel. Class II antiarrhythmics are the beta-blockers and affect the heart by sympatholysis (beta blocking). Class III antiarrhythmics prolong repolarization by affecting the potassium channels and Class IV antiarrhythmics are calcium channel blockers. In addition to these classes other antiarrhythmics would include purinergic agonists and the digitalis glycosides, which do not fall in any of the above classifications.
- The sodium channel blockers affect Phase 0 of depolarization-the rapid inflow of sodium through the sodium channels. They are divided into 3 subclasses. 1A includes quinidine, procainamide, and disopyramide. Class 1B includes lidocaine, mexiletine, and phenytoin. Finally, Class IC would include flecainide as well as the others listed on the slide.
- Lidocaine, mexiletine and phenytoin all fall into the Class IB antiarrhythmics. This is a nice group of medications to use as antiarrhythmics. They have little effect on normal tissues but decrease the effective refractory period and the purkinje cells. This decreases automoticity. Resultantly there is an increase in ventricular fibrillation threshold. Phenytoin in particular is useful in suppressing Digoxin-induced dysrhythmias and mexiletine is useful in depressing conduction times especially at higher heart rates. There is actually a slight decrease in the corrected QT interval with both Lidocaine and phenytoin, and mexiletine is quite useful in the treatment of patients with prolonged QT syndrome secondary to sodium channel abnormalities.
- 8 Lidocaine is one of the Class 1B antiarrhythmics that you should feel very comfortable using. As you know, its main use is in the acute treatment of ventricular tachycardia. It acts rapidly and there is no depression of contractility or AV conduction. Its half-life is extremely short-5-10 minutes in its first phase, then 80-110 minutes during its second phase. Therefore, a bolus must be followed relatively closely with a maintenance infusion. You must remember that there is decreased metabolism with congestive heart failure and hepatic failure as well as the certain medications including beta-blockers like propranolol and H2 blockers like cimetidine. There is increased metabolism with medications like Dilantin, Phenobarbital, isuprel.
- 8 The dose is well described in your Harriet Lane manual but basically includes a 1mg/kg bolus followed by a 20-50 microgram/kp/min. infusion.
- 9 Mexiletine, a second 1B antiarrhythmic has good use in postoperative ventricular tachycardia (on the long-term, not acute basis). Its main side affects are gastrointestinal intolerance with a few patients developing some central nervous system complaints.
- 10 Phenytoin or Dilantin is also a useful medicine in postoperative ventricular tachycardia however, its use to remember primarily is that in Digoxin-induced arrhythmias. There are many medications which it affects including coumadin and verapamil. Remember the intravenous form of phenytoin can cause hypotension (secondary to the carrier, fos phenytoin is as effective as an antiarrhythmic without the hypotensive effects).
- 13 These medications are used in a variety of supraventricular as well as ventricular dysrhythmias. All of these medications can interfere with the levels of Digoxin and as well as other antiarrhythmics including amiodarone.
- 13 I have outlined the dose of flecainide, one of the more common antiarrhythmics that you may see, solely for your reference. Again, I would stress hesitancy in using these medications without the guidance of a Pediatric Cardiologist. The Class 1C antiarrhythmics have very little use in adults currently after a particular 1C-encainide was actually shown to have an increased mortality rate in a large adult study of antiarrhythmias. Based on this study, these medications have absolutely no utility in the postoperative patient.
- 14 The Class II agents are commonly referred to as the beta- blockers. The first 5 listed here are the primarily beta-blocker medications you will be exposed to. Sotalol is an interesting beta-blocker designer drug with properties both related to its beta-blocker roots as well as properties of potassium channel blocker like the Class III antiarrhythmics.
- 20 Adenosine’s main treatment use is in the termination of reentry tachycardias. It also can be used in other atrial tachycardias to provide atrio-ventricular block for diagnosis. It is metabolized rapidly by red blood cells and vascular endothelial cells and therefore is a short-acting medication. Its half-life is less than 10 seconds.
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