Electrocardiography (Proceedings)


Electrocardiography is an integral part of the cardiological exam. It is the only way to determine heart rhythm accurately and to determine if there are any conduction abnormalities. This is also the most useful part of an ECG. ECGs can do other things however, these are not nearly as important.

Electrocardiography is an integral part of the cardiological exam. It is the only way to determine heart rhythm accurately and to determine if there are any conduction abnormalities. This is also the most useful part of an ECG. ECGs can do other things however, these are not nearly as important.

An ECG is a recording of the electrical activity of the heart recorded on the surface of the body (or from the esophagus). Standard lead systems have been developed, these help determine the orientation of the depolarizing forces, an indirect indicator of the position of the heart in the chest cavity. These lead systems are however not needed to determine rhythm, you could in theory record the ECG from the fingertips if you have to.

I. ECG basics

      1. How can an ECG be recorded: A standard lead system can be used an electrodes attached to the limbs. This does require that the patient be in right lateral recumbency. This must be done if amplitude measurements are to be made (only in lead II). Alternatively a direct chest lead system can be used for rhythm diagnosis. Telemetry, holter monitors (24 hour ambulatory ECG) and cardiac event recorders (push a button and it records ECG immediately before and after the button is pushed) are other specialized ECG forms.

      2. What can an ECG do extremely well: Only the ECG can determine rhythm or conduction abnormalities.

      3. What can an ECG do well: The ECG can be helpful in evaluating for heart enlargement. These changes are however not specific nor sensitive. It is more sensitive in cats because there are less confounding breed differences. The ECG is also more helpful with certain congenital heart diseases. It can be helpful for diagnosing pericardial effusion and hyperkalemia.

      4. What can an ECG not do: It cannot give a definitive answer regarding heart size, imaging studies are needed. ECGs also do not reflect the mechanical strength of the heart, an ECG can be normal and no pulse may be present.

      5. What are the indications for an ECG: arrhythmia on auscultation, syncope, heart murmur, pre-, intra- and postop monitoring, dyspnea, cyanosis, drug monitoring (digoxin, beta blocker, tricyclic antidepressants), emergency cases (trauma, GDV, urethral obstruction, hyperkalemia suspect), periocardiocentesis (VPCs indicate the needle is tickling the heart), certain breeds (doberman, boxer), unexplained brady- or tachycardia.

II. Interpreting ECGs

      1. Waveforms and how they are generated: in the heart, as with many things the fastest wins, usually this is the sinus node, however any cell in the heart can develop pacemaker role. The electrical impulse depolarizes the heart muscle leading to contraction.

           a. P-wave: generated by the sinus node as the pacemaker, it is a sign of the depolarization of the right and then left atrium, usually positive in Lead II. Sometimes it is necessary to check the other leads recorded as the P-wave may be more obvious on other leads. A negative Lead I P-wave is an indication of faulty electrode placement.

           b. P-R interval: reflects the time it takes for a sinus beat to begin, depolarize the atria and get conducted through the AV node to begin initiating ventricular depolarization.

           c. QRS complex: The QRS complex represents ventricular depolarization. The Q wave is the first negative deflection before the R-wave. The R-wave is the first positive deflection after the P. The S-wave is the first negative deflection after an R. Remember, not all parts of a QRS have to be present.

      2. Determine heart rate

      3. Determine rhythm: This is something that requires practice.

      4. Measure complexes: measurement is overrated, it is mainly needed for enlargement patterns which are at times not very useful. Two things are measured, amplitudes and durations. Amplitudes can only be measured when a standard, by-the-book Lead II is recorded. You need to know the calibration of the machine, usually 1 cm (10 small boxes) is 1 mV. The other leads are helpful to determine MEA.

           a. Amplitudes: P-wave, QRS complex, ST segment depression or elevation.

Tall P= right atrial enlargement (P-pulmonale, no more than 4 small boxes tall in a dog)

Tall QRS=ventricular enlargement (no more than 25 to 30 boxes tall in a dog, 9 in a cat)

ST segment changes= hypoxia, epicarditis, electrolyte problems, etc.

           b. Durations: P-wave, PR, QRS duration

Increased P=left atrial enlargement (dog no more than 2 small boxes)

Increased QRS=ventricular enlargement or conduction abnormality (normal no more than 2 boxes, with bundle branch block then QRS duration >8msec, 4 boxes at 50 mm/sec)

PR=prolongation is 1st degree heart block (more than 6.5 small boxes in a dog), shortening is consistent with ventricular preexcitation.

Before embarking on antiarrhythmic drug therapy it is important to consider the goals present. My personal feeling is that 2 goals are potentially present

      1. Treat clinical signs resulting from an arrhythmia

      2. Prevent sudden death in a patient from an arrhythmia

Unfortunately, many of the drugs we use cannot accomplish the latter goal and those medications that could are difficult to use in an emergent situation because of the side effects present.

Clinical signs from an arrhythmia can result because of rapid or slow heart rates. With rapid heart rates ventricular filling is inadequate and therefore also cardiac output. This also often eliminates the atrial "kick" from contraction of the atria, this is obviously the case if it is a ventricular arrhythmia. With slow heart rates cardiac output will also suffer since cardiac output is related to stroke volume times heart rate.

Types of antiarrhythmic agents:

           A. Class I agents: Sodium channel blockers (sometimes called membrane stabilizers), responsible for phase 0 of the action potential.

           a. Class Ia, Prolongs AP duration by prolonging repolarization and also increases the refractory period, examples include procainamide and quinidine

           b. Class Ib, shortens AP duration by shortening repolarization and also increases the refractory period, examples include lidocaine, mexilitine and tocainide. Preferential effect on diseased cells.

           B. Class II agents: beta blockers. Can be selective (beta 1) or non-selective (Beta 1 and 2), commonly used include propranolol (NS), atenolol (S), metoprolol (S), sotalol (low dosages NS, at higher dosages it also has Class III effects) and carvedilol (NS with vasodilator and antioxidant effects). These agents suppress automaticity and can block triggered events since high sympathetic tone predisposes to afterdepolarization.

           C. Class III agents: Block the outward potassium channel delaying repolarization. No pure Class IIIs are used, sotalol does have this effect. Amiodarone is getting much attention lately. However because these agents markedly prolong AP they can predispose to afterpotentials. Amiodarone also has Class I, II, and IV effects.

           D. Class IV: calcium channel (reentry) blockers. Nondihydropyridine are active in the heart, the others more in the vasculature. Diltiazem most commonly used.

What drug for what arrhythmia?

Supraventricular tachycardias (atrial fibrillation, atrial tachycardia), often the goal is heart rate control, not return to normal rhythm.

      1. Vagal maneuver: in atrial tachycardia, increasing vagal tone (carotid massage, pressure on eyes) can break the tachycardia for therapeutic and diagnostic purposes.

      2. Digoxin: Will help to increase AV nodal function. Good for use in CHF since it improves cardiac function mildly. Check digoxin levels 1 week after starting. Goal used to be to have a trough level (6 to 8 hours post pill) of 1-2 ng/ml, it probably is sufficient to have 1 ng/ml. Hypokalemia predisposes to toxicity, combination with spironolactone can be especially useful in this situation. Have the owner be vigilant, better to DC once too often than one time not. Will predispose to ventricular arrhythmias.

      3. Diltiazem 0.5-1.5 mg/kg regular TID, in cats also consider sustained release products (SID dosing). Calcium channel blocker that will increase AV nodal function, more powerful effect than digitalis in regard to rate control. Tends to not decrease cardiac output significantly

      4. Beta Blockers (atenolol 0.2 to 1 mg/kg dog SID to BID, 6.25 mg SID to BID in cats; propranolol 0.2 to 1.0 mg/kg TID dog, 2.5 to 5 mg BID to TID in cats) effectively decrease heart rate and also block ventricular arrhythmias. They do however decrease cardiac output so that they can severely compromise a patient with CHF. Wean off slowly or there can be a rebound effect where arrhythmias get much worse. More commonly used in cats since they often have HCM where the effects of beta blockers do not tend to cause problems. Can prolong life so in theory a very attractive group of drugs.

Ventricular tachycardias need to be treated if symptomatic or if thought that arrhythmia is malignant (possible degeneration to ventricular fib/flutter). Overtreated in veterinary medicine

      1. Class 1 agents (lidocaine like) These agents are useful, though they do not prolong lifespan (possibly they do in veterinary medicine) though they do control the overall number of irregular beats which can make the patient less symptomatic (improves perceived quality of life, less like to euthanize). Lidocaine (2-4 mg/kg bolus, 40-80 mcg/kg/min CRI if needed in dogs, cats 0.25 to 0.75 mg/kg side effects common) is commonly used. Good for emergency management, does not drop cardiac output significantly. Toxicity can occur (excitation, vomiting, seizures) is however rare except in cats. For long term therapy mexilitine (4-8 mg/kg TID) can be given, though it is expensive. Procainamide can be used in place of lidocaine or in combination with it (cumulative toxicity) since it can be given by injection. It is also available as an oral medication (10-20 possibly 30 mg/kg TID of sustained release product, CRI of 20-50 mcg/kg/min, i.v.bolus of 2 mg/kg over 5 minutes, up to total dose of 20 mg/kg, not in cats). Efficacy is uncertain.

      2. Beta Blockers; can prevent sudden death. Decrease cardiac output. Good choice in cats with HCM (Atenolol 6.25 mg SID to BID). In dogs with CHF, titrate upward slowly over weeks to months to avoid adverse side effects. Atenolol/mexilitine combination may work in Boxers with v-tach, though sotalol is better. Best combo is mexilitine with sotalol.

      3. Sotalol: beta blocker and other effects. Very effective and with minimal adverse side effects (1-2 mg/kg BID)

Bradycardias (if not symptomatic ask yourself if you need to treat)

      1. Sick sinus syndrome: can be a combination of tachycardia/bradycardia. These are tough to treat since treating one component can make the other worse. Sometimes require pacemaker to prevent the bradycardia and then aggressive treatment of the tachycardia. Bradycardia can be treated with theophyllin (10-20 mg/kg of sustained release product BID) though excitation and GI signs can develop. If atropine responsive use of probantheline (1-2 mg/kg BID to TID) can be considered, causes atropine side effects (constipation, dry mouth, etc.).

      2. AV blocks: Try to see if atropine responsive. Without response can try theophylline. Third degree is generally non-responsive to medical therapy. For short term stabilization, isoproterenol can be used (0.04 to 0.09 mcg/kg/min).

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