ECG: Anesthetist's guide to common abnormalities and treatment options (Proceedings)

The electrocardiogram is a useful monitoring tool, but its proper use requires training. It provides a heart rate and a picture of the electrical activity of the heart muscle. The anesthetist should be trained to recognize many commonly encountered intraoperative arrhythmias (e.g., multifocal and unifocal ventricular premature complexes, atrioventricular blockade, ventricular tachycardia, etc.) and the veterinarian should be prepared to treat arrhythmias when they occur (if necessary).

Rhythms seen on the ECG reflect the summation of electrical events within the heart during the cardiac cycle. The first step to identification of rhythms is understanding the normal origins and pathways which participate in depolarization and repolarization. General locations of the origins of ectopic beats or blocks can then be identified and decisions made by the anesthetist about the probable impact these dysrhythmias will have on cardiovascular function.

Normal sinus rhythm

Normal depolarization and repolarization of the heart produces a characteristic ECG rhythm. Interpretation of this ECG includes determination of rate, presence of normal wave amplitudes, and correct intervals between the portions of the ECG. Normally, the first step in heart depolarization is the depolarization of the SA node. This is followed by the spread of the wave across the atrial muscle (P-wave). The wave of depolarization enters the AV node and starts the relatively long process of AV node depolarization, bundle of His depolarization, and right and left bundle branch depolarization (appears as the delay between P-wave and beginning of QRS complex). Next the ventricular muscle depolarizes and creates the characteristic shape of the QRS complex. The different parts reflect depolarization of the different surfaces of the ventricle (e.g., intraventricular septum, free walls, etc.). The final ECG step of the cardiac cycle is appearance of the T-wave which represents repolarization of the ventricular muscle. This can take on many normal appearances. However, changes in T-wave morphology with time can represent serious conditions including myocardial hypoxia and hyperkalemia, which require immediate attention.

A potentially life-threatening dysrhythmia that is occasionally seen during anesthesia, especially in breeds such as miniature schnauzer or West Highland white terriers is sinus bradycardia or arrest. This is associated with disease of the sinus node termed Sick Sinus Syndrome. Some animals will have bradycardia or sinus pauses noticed during the preanesthetic physical, however some animals will be asymptomatic until after administration of anesthetic drugs. The danger of this disease is sinus arrest and subsequent ventricular asystole the occurs during anesthesia, exacerbated by anesthetic drug associated electrical depression and opioid-associated increased vagal tone. If sick sinus syndrome has been diagnosed or suspected, special care and monitoring must be available and potentially pacemaker placement needed.

Atrial abnormalities

Atrial conduction abnormalities are not generally as likely to cause severe morbidity or mortality during anesthesia. However there are some atrial abnormalities which can lead to adverse outcomes. Probably the most commonly encountered problems are sinus tachy- and brady- dysrhythmias. These are usually caused by changes in the balance of sympathetic and parasympathetic nervous system efferent activity. Atrial fibrillation is another disturbance that may be seen. It most commonly occurs in larger breed dogs, or dogs with enlarged atria secondary to diseases such as mitral valve insufficiency. Atrial fibrillation by itself is not necessarily going to cause severe adverse events during anesthesia. However, if high ventricular rates cause low cardiac output; blood pressure and tissue perfusion may suffer. A concurrent complication is the loss of "atrial kick" reducing ventricular loading.

AV-node abnormalities

The most commonly identified AV-node abnormality during anesthesia is some form of AV-block. There are three main types - 1st, 2nd, and 3rd degree blocks. First degree block is rarely diagnosed (although likely occurs relatively frequently), and rarely is a problem because the manifestation is simply a longer delay between the normal coupling of atrial and ventricular activities.

Second degree AV block is relatively common when anesthetic and preanesthetic drugs that enhance vagal tone are used (e.g., opioids, alpha 2 adrenergic agonists, low doses of anticholinergics). Two subclasses of second degree AV block are described, the first is Mobitz type I (more commonly called Wenckenbach arrhythmia). The second is Mobitz type II. This is not associated with a progressive increase of P-R interval, but a sudden and complete failure of the AV node. Type II is often associated with organic disease in or near the AV node and may be more serious than Type I which reflects a progressive fatigue of the AV node. Regardless of the type of second degree AV block, treatment with an antimuscarinc such as atropine or glycopyrrolate is usually warranted. Untreated second degree AV block may progress to third degree AV block or cardiac standstill with the administration of anesthetic drugs.

Third degree AV block is relatively uncommon, but can be associated with high mortality if unrecognized prior to anesthesia. The characteristics of third degree AV block are complete dissociation between atrial activity and ventricular activity. This is because the AV node inhibits all transmission, resulting in ventricular escape beats assuming the pacemaking for the ventricle. Ventricular escape beats MUST BE DIFFERENTIATED from ventricular premature contractions since escape beats MUST NOT BE SUPPRESSED. Immediate cardiac arrest would result. Additionally, anesthetic drugs often tend to suppress escape rhythms and cardiac arrest could occur with induction. Pacemaker implantation is usually the treatment of choice for longstanding third degree AV block.

Ventricular ectopic activity

Ventricular ectopic beats are relatively common and often garner much attention. However, some ventricular arrhythmias do not need to be aggressively treated while others will result in rapid deterioration and death. The first step is to identify a ventricular site of origin of the electrical activity and the potential for progression to a severe problem.

The hallmark of a ventricular premature contraction (VPC) is the early (premature) depolarization of the ventricle from a site distal to the atria, AV-node, and conduction pathways. Typically the QRS complex will occur before the next expected P-wave, be wider and longer in duration than a normal QRS, and have a different amplitude (either positive or negative) than normal QRS complexes. An additional tool to identify a VPC is a compensatory pause following depolarization.

When to treat VPCs

Treating VPCs is a subject of debate, although there are times when it clearly may be beneficial. Ventricular tachycardia (Vtach) is characterized by a continuous run of ventricular beats. Vtach does not always need to be treated, but is often because of a concern for worsening of the rhythm to ventricular fibrillation. Additionally, if the ventricular rate is rapid enough it may cause significant drop in cardiac output and blood pressure. Slow Vtach not associated with hypotension or degredation is sometimes not treated.

Another scenario where treatment for VPCs would be warranted is when there is danger of "R-on-T." This is when a VPC occurs during repolarization of the ventricle from the previous beat. R-on-T can result in Vtach, ventricular flutter, or ventricular fibrillation.