I. Arrhythmias That Are Of Sinus Origin :
When depolarization originates spontaneously and rhythmically from the sinoatrial node (SA node), then the rhythm is defined as a normal sinus rhythm. In most people, the SA node rhythm is regular and averages between 60 - 100 beats per minute (bpm). If the sinus rhythm is 100 bpm or faster, then it is called a tachycardia or a tachycardic rhythm. If, however, the heart's rhythm is 60 bpm or slower, then it is called bradycardia or a bradycardic rhythm.
A. Respiratory Arrhythmia : When a patient is on continuous monitoring either in the intensive care unit or on a medical-surgical floor, you will frequently see a dysrhythmia that is normal. When a person breathes, their lungs expand and will push into the mediastinal spaces compressing the heart. As the lungs compress the heart, the filling volumes are reduced because the heart is not permitted to expand as much. This will cause the ejected fraction during ventricular systole to be smaller. In order to keep the pressure in the vascular system the same, the heart has to speed up its rate in order to keep the volumes in the vasculature the same. Hence, when the lungs are fully expanded and compressing the heart, the heart rate will be driven higher. When the patient exhales and decompresses the heart, the heart's rate will dramatically slow because it has additional space to expand during ventricular filling time in the cardiac cycle.
In summary, inhalation causes the heart rate to be higher and exhalation results in a reduction in heart rate. We see this most readily as a cyclic compression and retraction of the R wave to R wave intervals - i.e. - the R waves are compressed during inhalation and retract during exhalation.
B. Sinus Arrest : Sinus arrest is also called sinus pause or sinus block. Sinus arrest occurs when the sinoatrial node stops firing. If nothing else were to happen, the patient would die. However, the heart does have other pacemakers that are usually dominated, overdriven or blocked. During sinus arrest, there will be a short time lag before a secondary pacemaker is activated and begins the work of stimulating the heart to rhythmically beat. The appearance of these secondary pacemakers rescue us from death. These rescuing beats produced by these secondary pacemakers are called escape beats or rescue beats.
The rescue beat may occur from a secondary pacemaker high up in the atria near the SA node or the secondary pacemaker may be located much lower in the heart. If the rescuing pacemaker is near the AV node, it is most likely called a junctional pacemaker and if the rescuing pacemaker is located in the ventricles, then it is called a ventricular pacemaker. Secondary pacemakers are also called ectopic pacemakers. Ectopic pacemakers have their own firing rates (discharge rates). Atrial ectopic pacemakers will often have a rate of 60-80 bpm. Ectopic pacemakers located near the AV node will often have a rate of 40 - 60 bpm. The ectopic pacemakers in the ventricles typically have a rate of 30 - 45 bpm.
What can cause the SA node to stop firing or go into sinus arrest ? Causes may be :
Characteristics of Ectopic Pacemakers Creating Rescue Beats :
The most common of the escape phenomenon is the junctional escape beat. With junctional escape beats, the ectopic pacemaker is located near the AV node low in the right atrium. The usual pattern of atrial depolarization is missing and therefore the junctional escape beat will not have a P wave but will have a normal QRS complex and a normal T wave since the AV node is functioning normally. With the junctional escape beat, you have an ectopic pacemaker very close to the AV node that is discharging and stimulating the AV node. The missing P wave is due to the fact that the SA node is silent and the alternate pacemakers around the SA node are also silent.
C. Wandering Pacemaker : In the condition called a Wandering Pacemaker you may have two or more pacemakers competing with each other for control of the heart's rhythm. This condition is usually caused by ischemia due to poor perfusion in the area of the SA node.
The following characteristics are commonly seen in a patient with a wandering pacemaker :
A wandering pacemaker is a sign of cardiac irritability in the atria. This condition can lead to atrial fibrillation. One of the problems associated with atrial fibrillation or any other supraventricular tachycardic dysrhythmia is the formation of blood clots in the atria. Blood clots are formed because the heart's atrial rhythm is so caotic and so fast that blood ceases to flow as smoothly through the atria to the ventricles. Some of the blood is trapped in the auricles of the atria and there is mechanically "beaten up" encouraging the blood to clot. Once the heart falls out of the atrial fibrillation and returns to being a good pump, then all of the blood clots that formed in the atria during the fibrillation period are passed into the lungs from the right side or into the systemic circulation from the left side of the heart. If a patient has had a supraventricular tachycardic dysrhythmia for a prolonged period of time, physicians will frequently place these patients on anticoagulant therapy to break up these clots. Then the patient can be mechanically, electrically or pharmacologically converted out of a supraventricular dysrhythmia back into a normal rhythm without the fear of passing clots downstream and infarcting organ systems.
D. Sick Sinus Syndrome (Brady-Tachy Syndrome) : Some patients with progressive cardiac disease will develop Sick Sinus Syndrome. This is frequently heralded by a history of the patient falling in and out of atrial fibrillation and episodes of severe bradycardia. Sick sinus syndrome is a condition in which the patient experiences :
II. Unsustained Ectopic Supraventricular Dysrhythmias
A. Premature Atrial Contractions or Atrial Premature Beats (PAC's or APB's) : This is a single premature beat meaning that it occurs earlier than expected. The origin of this premature beat is located in the atria but not usually close to the SA node or the AV node. It has the following distinct features :
PAC's may be caused by a number of factors : stress, coffee, tobacco, digitalis toxicity, old myocardial infarctions, low blood potassium levels, and low blood magnesium levels. PAC's can deteriorate into atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia.
B. Premature Junctional Beat (PJB's) : A premature junctional beat occurs from an ectopic focus that is close to the AV node in the right atrium. It is a single beat phenomenon. It is characterized by the following criterion :
III. Sustained Supraventricular Dysrhythmias
A. Paroxysmal Supraventricular Tachycardia (PSVT) : PSVT is also known as paroxysmal atrial tachycardia (PAT). This is a very common dysrhythmia. Its onset is sudden and is often instigated by a premature atrial beat or a premature junctional beat. It will often spontaneously stop. PSVT has a very high rate of between 150 - 250 bpm.
The cause of PSVT is usually a re-entrance phenomenon usually near the AV node. Re-entry is a phenomenon typically seen in an ischemic heart. Ischemic hearts are electrically irritable. Under these conditions, reverberating circuits can be set up and rapid fire discharges can occur from an irritable focus. As the ischemic area fires more rapidly, the heart is driven into a tachycardic state. Some of the characteristics of PSVT are as follows :
Stress, certain drugs and ischemia make this dysrhythmia more likely to occur. Carotid massage can be used to bring a patient out of PSVT. Carotid massage causes baroreceptors to send signals through the vagus nerve to the heart. These signals are responsible for slowing the conduction through the AV node with the net effect of slowing the heart rate. Carotid massage has the effect of interrupting the re-entry circuitry and terminates the tachycardia.
B. Atrial Flutter : Atrial flutter is also known as the Sawtooth Pattern. Atrial flutter can occur in normal hearts as well as in hearts with disease. Atrial flutter has a regular rhythm with P waves appearing at a rate of between 220 - 300/minute. Atrial depolarization occurs at such a rapid rate that the normal P to PR interval that is seen at slower rates simply disappears. The baseline just rises and falls producing a flutter wave. The AV node cannot handle the extraordinary number of atrial impulses bombarding it with the end result that most of the impulses simply are not caught by the AV node. The AV node is insensitive to most of the signals because it has a refractory period. This insensitive period is called AV block. Blocks of 2:1, 3:1, 4:1, and 6:1 are quite common - i.e. - one QRS complex for a specified number of P waves. Carotid massage is often used to increase the block - i.e. - increase it from a 2:1 block to a 4:1 block. Carotid massage has a great deal more effect on the AV node by making it less sensitive to SA nodal bombardment. It does little to slow the SA node's reactivity.
The characteristics of atrial flutter are :
The causes for atrial flutter can be :
Atrial flutter is a serious supraventricular tachydysrhythmia. Before a patient is cardioverted out of atrial flutter into a normal rhythm either using electrical or pharmacological conversion, the physician must seriously think about placing the patient on blood thinning agents. Anytime a patient has been having runs of PSVT, atrial flutter or atrial fibrillation, they may have had the opportunity to form blood clots in the auricles of their atria. Blood clots form their because pooled blood is so mechanically beaten up that it forms clots. Unless the blood clots are dissolved, prior to the patient being successfully converted to a normal rhythm, the clots can be pumped out to downstream sites with the patient auto-embolizing themselves.
C. Atrial Fibrillation : In this supraventricular dysrhythmia, the atrial activity is totally chaotic. The AV node may be bombarded by as many as 500 impulses per minute. Atrial fibrillation has the following characteristics :
Atrial fibrillation is seriuos because individuals who have been in atrial fibrillation may have formed blood clots. This predisposes the patient to embolic events such as myocardial infarctions, infarctions of organ systems - i.e. - strokes. Common causes for this dysrhythmia are : re-entry phenomenon, ischemic disease, or hyperactive accessory pathways.
IV. Ectopic Ventricular Dysrhythmias
A. Premature Ventricular Contractions (PVC's) :
PVC's occur in normal hearts as well as in hearts with disease. Individuals with a normal healthy heart can live normal lives with as many as 50,000 PVCs/day. However, in a person with significant disease, this many PVCs would be alarming.
The salient features of a PVC are as follows :
PVCs may randomly appear or may appear in patterns. As PVC begin to fall into patterns, the clinician should become more concerned. If one normal sinus beat begins to pair up with a PVC in a repeating pattern, this disturbing rhythm is called Bigeminy. If there are two normal sinus beats pairing up with a single PVC in a repeating pattern, then this dysrhythmia is called Trigeminy. If 3 normal sinus beats are paired with a PVC, then this is called Quadrigeminy. Often, the PVC seen in bigeminy, trigeminy and quadrigeminy are from a single irritable focus. However, PVCs may be multifocal - meaning that there may be several irritable foci that are creating these premature ventricular contractions. When this occurs, it is considered a more malignant EKG rhythm.
There are Rules of Malignancy which determine how seriousness of PVC events. They are listed below in an increasing order from least serious to most serious.
B. Ventricular Tachycardia : Ventricular tachycardia is defined as a run of three or more consecutive PVCs. The rate is usually between 100 - 200 bpm. In normal patients, short runs of ventricular tachycardia cause the patient to feel palpatations in the chest and feel faint. If they are sustained for longer periods of time, then unconsciousness will probably result. This is due to poor cardiac output and poor perfusion of the brain and heart. It heralds the onset of a myocardial infarction unless the patient has immediate help. Ventricular tachycardia quickly degenerates into ventricular fibrillation.
Ventricular tachycardia can be caused by : Ischemic heart disease, myocardial infarctions, increased catecholamine release from the adrenal medulla, increased sensitivity of the heart to catecholamines (sniffers), drug toxicity, and re-entry phenomenon.
C. Ventricular Fibrillation : Ventricular fibrillation is seen in dying hearts. There are no true QRS complexes and hence cardiac perfusion as well as whole body perfusion has stopped. The EKG tracing resembles a wandering or undulating baseline. Cardiopulmonary resuscitation (CPR) and electrical defibrillation must be performed to convert the patient out of this life threatening situation.
V. AV Blocks
A. First Degree AV Block : First degree AV block is characterized by a prolonged delay in conduction at the AV node. The wave of depolarization from the SA node proceeds normally over the entire atria. However, when it arrives at the AV node, the conduction potential is held for periods longer than the usual .1 seconds. As a result of this AV nodal conduction delay, the PR interval is prolonged. The characteristics of 1st degree AV block are as follows :
First degree AV block can appear in patients without disease as well as those with heart disease. It appears in patients with drug toxicities, patients with myocarditis and in those that have early ischemic disease of the conduction system.
B. Second Degree AV Block - Mobitz Type I and a Mobitz Type II
Mobitz Type I Second Degree AV Block : The Mobitz Type I second degree AV block is also called a Wenckebach Block. The conduction defect is located below the AV node. It is characterized by the following :
Mobitz Type II Second Degree AV Block : The Mobitz Type II second degree AV block is located high up in the Bundle of His. The characteristics of the Mobitz Type II second degree AV block are :
A Mobitz Type II second degree AV block is a dangerous dysrhythmia. It is dangerous because it will absolutely degenerate into a third degree AV block. A third degree AV block is a medical emergency requiring the implantation of a pacemaker.
C. Third Degree AV Block : In third degree AV block, there is a complete lack of atrial impulses making it through to the AV node and on through the conduction system of the ventricles. For this reason it is called complete heart block. The ventricles respond to this lack of signaling by developing a rescue or escape rhythm from a ventricular focus. The rate of a ventricular pacemaker is quite low - around 30-45 bpm. It is so low, that in most cases, the patient must undergo a pacemaker implant procedure. The atria and the ventricles are functioning completely independent of one another. The P waves that appear on the rhythm strip are not associated with the QRS complexes that appear on the rhythm strip. This dissociation of the atria and the ventricles affects cardiac output and in most cases, the patient will loose consciousness.
VI. Bundle Branch Blocks
Bundle branch blocks are dysrhythmias that occur because of ischemic regions of either the right or the left bundle branch in the heart's conduction system. Since the bundle branchs carry the depolarization wave to their respective ventricular muscle, the changes in the EKG that we look for are in the QRS complexes.
Right Bundle Branch Block : In right bundle branch block, there is a delay of the conduction potential through the right bundle resulting in a delay in right ventricular depolarization. The right ventricle, therefore, does not start to depolarize until nearly all of the left ventricular muscle mass has depolarized. The following characteristics are typical of right bundle branch block :
Left Bundle Branch Block : In left bundle branch block, there is a conduction delay in the conduction potential through the heart's conduction system serving the left ventricle. The characteristics of left bundle branch block are as follows :
VII. U Waves :
U waves are sometimes seen after the T waves. They represent the repolarization of the papillary muscles in the heart. They have the following characteristics :