EKG Rhythm Identification
Cardiac anatomy, physiology, and electrophysiology
The heart is a four-chambered hollow muscular organ located in the center of your chest in an area called the mediastinum. The two upper chamber of the heart are the atria; the two lower chambers are the ventricles. The heart has electrical components that dictate the mechanical contractions. Your heart has three tiers of pacemakers. The primary pacemaker is the sinus node (SA node). The SA node generates impulses for the resting adult at a rate of 60 to 100 bpm. If the SA node fails to operate, the heart can be paced from its secondary pacemaker, the AV junction. The AV junction generates impulses for the resting adult at a rate of 40-60 bpm. The heart’s final pacemaker is the ventricular pacemaker. This site is usually only seen when there is no communication from the SA node or the AV junction. It generates impulses at a rate of about 20 to 40 bpm.
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The Wave Form
A standard sinus rhythm will display the following waveforms. The P-wave represents atrial depolarization. The QRS complex represents ventricular depolarization. The ST segment and the T-wave represent ventricular repolarization. It is also important to recognize the PR interval and the QRS duration.
A standard sinus rhythm will display the following waveforms. The P-wave represents atrial depolarization. The QRS complex represents ventricular depolarization. The ST segment and the T-wave represent ventricular repolarization. It is also important to recognize the PR interval and the QRS duration.
A patient's EKG is read by using a systematic analysis approach. You should look for the pacemaker, the rate, the rhythm, the PR interval, and the morphology of the QRS complex. Though far from comprehensive, the following notes may refresh your knowledge of some of the more common ACLS-related dysrhythmias.
The Sinus Family
Sinus rhythms originate from the sinus node (SA node). The key characteristic for recognizing a sinus rhythm is a normal P wave and a causal relationship between P waves and each corresponding QRS complex.
Sinus rhythms originate from the sinus node (SA node). The key characteristic for recognizing a sinus rhythm is a normal P wave and a causal relationship between P waves and each corresponding QRS complex.
Normal Sinus Rhythm
NSR is recognized by its characteristic P wave, rate of 60-100, regular rhythm, normal PR interval, and narrow QRS complex. As a technical aside, if the sinus rhythm has any abnormalities associated with it (i.e., an ectopic beat, a block, a wide QRS, etc.) it is not to be called a normal sinus rhythm. It is a sinus rhythm with an explanation of the abnormality. Sinus rhythm with a PVC is an example.
Don’t assume that the patient is in good shape just because they display a normal sinus rhythm. All this indicates is that the patient has normal electrical impulse flow through the myocardium. Patients with NSR can be having an acute MI, a stroke, or even be pulseless (PEA).
NSR is recognized by its characteristic P wave, rate of 60-100, regular rhythm, normal PR interval, and narrow QRS complex. As a technical aside, if the sinus rhythm has any abnormalities associated with it (i.e., an ectopic beat, a block, a wide QRS, etc.) it is not to be called a normal sinus rhythm. It is a sinus rhythm with an explanation of the abnormality. Sinus rhythm with a PVC is an example.
Don’t assume that the patient is in good shape just because they display a normal sinus rhythm. All this indicates is that the patient has normal electrical impulse flow through the myocardium. Patients with NSR can be having an acute MI, a stroke, or even be pulseless (PEA).
Sinus Tachycardia
Sinus tachycardia shares many of the same characteristics of NSR except that it has a faster rate, generally 100-150 bpm. Sinus tachycardia is often a symptom of some systemic issue like anxiety, pain, hypoxia, or hypovolemia. This rhythm is often perfectly appropriate for the patient’s presentation (like physical exertion). Sinus tachycardia is a signal that we need to identify a potentially treatable underlying cause.
Sinus Bradycardia
Many patients present sinus bradycardia as their normal, everyday rhythm. These people can be divided into two general camps: the healthy and the sick. The healthy group is typically young, athletic and has efficient cardiovascular function due to aerobic conditioning. The other group is older with a significant cardiac pathology and has a cardiologist who has put them on a beta blocker to reduce cardiac workload and oxygen demand.
Sinus bradycardia only requires treatment if it produces signs of cardiogenic hypoperfusion. This is usually not the case until the rate drops below 50. First look for treatable underlying causes such as a vasovagal response, medication reaction, electrolyte imbalance or MI. Be very cautious about raising a patient’s heart rate if there is the possibility of an acute MI.
The
Atrial Family
Atrial rhythms occur from an ectopic atrial site outside the SA node. These rhythms are caused by atrial tissue excitability, re-entry mechanisms, or atrial structure defects such as chronic atrial dilation.
Sinus Rhythm with Premature Atrial Contractions (PAC)
PACs are among the most common and benign of non-sinus dysrhythmias. Everyone has one occasionally and some people have them often. They can be precipitated by minor causative factors such as caffeine, emotion, or exertion. They can also be a sign of more serious problems like hypoxia, metabolic problems, or cardiogenic issues.
PACs are among the most common and benign of non-sinus dysrhythmias. Everyone has one occasionally and some people have them often. They can be precipitated by minor causative factors such as caffeine, emotion, or exertion. They can also be a sign of more serious problems like hypoxia, metabolic problems, or cardiogenic issues.
Atrial Flutter
Atrial flutter is a characterized by a very rapid atrial depolarization cycle that is often running at a rate near 300 bpm. With atrial to ventricular conduction ratios of 3:1 or higher, you can usually see the distinctive saw-toothed baseline. Atrial flutter can have a consistent A-V conduction ratio like the 3:1 conduction ratio seen in the example, but they can also have a variable conduction ratio, causing an irregular ventricular response.
Atrial Fibrillation
Atrial fibrillation is one of the most common cardiac rhythms seen among the geriatric population. The defining criteria for atrial fibrillation are the absence of P waves and a chaotically irregular QRS. Many patients live with atrial fibrillation as their base cardiac rhythm for decades with little outward signs beyond an irregular pulse, but most atrial fibrillation patients will take a combination of medications to control clot formation and heart rate to manage the pathology.
Atrial Fibrillation
Atrial fibrillation is one of the most common cardiac rhythms seen among the geriatric population. The defining criteria for atrial fibrillation are the absence of P waves and a chaotically irregular QRS. Many patients live with atrial fibrillation as their base cardiac rhythm for decades with little outward signs beyond an irregular pulse, but most atrial fibrillation patients will take a combination of medications to control clot formation and heart rate to manage the pathology.
Supraventricular Tachycardia (SVT)
Although listed here as an atrial family rhythm, we are frequently uncertain of an SVT rhythm’s point of origin. The extremely fast ventricular response seen in SVT (generally greater than 150 bpm) crowds the baseline atrial activity into such a small space that we cannot distinguish sinus P waves from atrial or junctional pacemakers. The SVT designation is an admission that you don’t know the exact point of origin, but you do know that the rhythm must be generated from a supraventricular pacemaker because the QRS complexes are narrow and relatively normal. Patients with SVT display a wide range of tolerance for the tachycardia, but even stable presentations require assessment and resolution.
The Junctional Family
Junctional rhythms can be isolated ectopic events or they can indicate failure of the SA node and subsequent movement to back-up pacing function from the AV junction. Junctional complexes are identified by either an inverted P wave tucked up close to the QRS or the complete absence of a P wave if the retrograde atrial depolarization occurred at the same time as ventricular depolarization. The morphology of the QRS complex will not be affected by the change in supraventricular pacemaker location.
Junctional rhythms can be isolated ectopic events or they can indicate failure of the SA node and subsequent movement to back-up pacing function from the AV junction. Junctional complexes are identified by either an inverted P wave tucked up close to the QRS or the complete absence of a P wave if the retrograde atrial depolarization occurred at the same time as ventricular depolarization. The morphology of the QRS complex will not be affected by the change in supraventricular pacemaker location.
Sinus Rhythm with a Premature Junctional Contraction (PJC)
The same statements made regarding PAC’s can be repeated for PJC’s. These are typically considered benign, but can be a signal that something serious is going on. Notice in this example that the ectopic junctional beat does not display a P wave.
Junctional Escape Rhythm
Rhythms stemming from the AV junction are intrinsically slower than a sinus rhythm with rates ranging from 40 to 60 bpm. This rhythm may or may not display the characteristic inverted P wave.Some patients tolerate the lower heart rate well, while other display signs of hypoperfusion due to bradycardia. Regardless of the degree of tolerance, these patients are in sinus node failure and require specialized consultation.
The Ventricular Family
Ventricular ectopic beats and rhythms produce electrical stimulation paths outside normal Purkinje paths and thus change the morphology of the QRS complex. These complexes are wide and strangely shaped.
Premature Ventricular Contraction (PVC)
The PVC is a common ventricular ectopic beat cause by a momentary interruption of the normal cardiac electrical cycle by an extra beat generated from somewhere below the AV junction. A PVC can be a routine and benign event or it can indicate a systemic problem. Evaluate the patient for correctable causes.
The PVC is a common ventricular ectopic beat cause by a momentary interruption of the normal cardiac electrical cycle by an extra beat generated from somewhere below the AV junction. A PVC can be a routine and benign event or it can indicate a systemic problem. Evaluate the patient for correctable causes.
Multifocal PVCs
Certain conditions begin to raise our level of concern with PVCs. The example above has more than one PVC evident, but worse than that, the PVCs are different shapes. The shape of an EKG complex corresponds to its path through the heart. If an EKG shape (morphology) changes, it means that the path of electrical impulse flow has changed as well. These are multifocal PVCs and indicate a greater degree of instability than the presence of unifocal events.
Multifocal PVCs
Certain conditions begin to raise our level of concern with PVCs. The example above has more than one PVC evident, but worse than that, the PVCs are different shapes. The shape of an EKG complex corresponds to its path through the heart. If an EKG shape (morphology) changes, it means that the path of electrical impulse flow has changed as well. These are multifocal PVCs and indicate a greater degree of instability than the presence of unifocal events.
Frequent PVCs
Some patients will produce a great number of PVCs and even produce them in a regular pattern. In the example above, there is a PVC every third complex interposed into what should be a sinus tachycardia. It is perfectly appropriate to call this something very descriptive like “sinus tachycardia with a unifocal PVC every third beat”, but this rhythm is often called sinus tachycardia with ventricular trigeminy. If every second complex was a PVC, it can be called bigeminy. It is important to compare the peripheral pulse rates to the EKG complex rate for this patient. In some cases, the PVC complex does not translate into a palpable pulse so that you have a patient with ventricular bigeminy and an EKG rate of 100 that actually has a bradycardia of 50 at the radial pulse site.
Idioventricular (Ventricular Escape)
In the failure or absence of a faster controlling sinus or junctional pacemaker, the ventricles have the ability to pace themselves intrinsically. Ventricular-paced rhythms are usually much slower (rates of 20-40) than rhythms paced from other sites, but can be accelerated through a variety of mechanisms. The idioventricular EKG above has a rate just above 60 due to some sort of stimulation. It is critical that the patient in an idioventricular rhythm does not receive any medication that can suppress ventricular activity (think lidocaine, procainamide, amiodarone or beta blockers). The resultant ventricular suppression could produce asystole.
Ventricular Tachycardia
Ventricular tachycardia is another rhythm that is produced from the ventricles but it is present due to the rhythm’s overwhelmingly fast rate taking over the pacing function from a normal pacing site. The treatment philosophy for ventricular tachycardia is to suppress the rapid ventricular rhythm with the belief that there is an underlying normal intrinsic pacemaker like the SA node that can restore a rhythm with a physiologically appropriate rate for improved cardiac output. The key to treatment of ventricular tachycardia is to identify and correct the underlying causative pathology, but it is often necessary to treat the rhythm before the cause is identified because of the profound effect this rhythm can have on cardiac output. Some patient can tolerate this rhythm for a period of time but others become quickly unstable even to the point of cardiac arrest.
Ventricular Fibrillation
Ventricular fibrillation is the most common rhythm displayed by the adult patient in the early minutes of cardiac arrest. There are two important facts to understand about ventricular fibrillation in order to respond to this life-threatening emergency appropriately:
- The fibrillating heart is working furiously but futilely. The myocardial tissue is hyperstimulated in early ventricular fibrillation producing copious waste and localized acidosis. Coronary arterial perfusion ceases, leaving no way to evacuate the toxic wastes and acid. The heart begins to poison its local environment with this accumulated byproduct.
- The heart’s electrical system is in a state of extreme chaos. The fibrillating heart is overwhelmed by the chaotic electrical storm of ventricular fibrillation. Coordinated muscular contractions stop and there is no cardiac output. There is no way for the heart to recover from this life-threatening state by itself. This chaos must be terminated by an outside source: the defibrillator.
This fibrillating heart is quivering and contracting in a frenzied but uncoordinated way, using up all available resources (like oxygen, electrolytes, and energy substrates), but without coronary blood flow, these resources are not replenished and the waste products are not eliminated. The only viable treatment to mitigate this terrible situation is immediate, hard, fast, deep, mechanically effective CPR. This generates suboptimal, but necessary coronary blood flow to slow the accumulation of the metabolic waste and replenish needed chemical assets.
Unfortunately, CPR alone will not be enough to save this patient. The chaotic electrical storm of ventricular fibrillation continues despite CPR and must be addressed as well. The most effective treatment available to terminate ventricular fibrillation is with the use of a defibrillator. The defibrillator does not “jump start” the heart back into a normal rhythm. The defibrillator is designed to send a large dose of DC energy through the bulk of the myocardium producing immediate and simultaneous stimulation of every muscle cell at the same time. The result of a successful defibrillation is asystole. Asystole represents the successful termination of the electric instability of ventricular fibrillation and presents a window of opportunity for one of the heart’s intrinsic pacemakers to begin operation and restore a viable rhythm capable of producing a pulse and the resumption of critical perfusion.
Thus, it is the immediate application of continuous, high-quality CPR and early defibrillation that gives the ventricular fibrillation patient the best chance of survival. Other treatments, such as the use of medications, the placement of advanced airway devices, and the application of advanced technologies are doomed to failure if not preceded by these two straightforward actions.
Heart Blocks
Heart blocks include a variety of rhythms characterized by an interruption of normal electrical paths through the heart. Blocks can be episodic or chronic, benign or malignant, nodal or infranodal.
First Degree Heart Block
Any supraventricular rhythm can have a concurrent first degree block. This dysrhythmia is identified by an unusually long conduction delay associated with a recalcitrant AV node. In a sinus rhythm this is seen in a P-R interval greater than 0.2 seconds (5mm).
Any supraventricular rhythm can have a concurrent first degree block. This dysrhythmia is identified by an unusually long conduction delay associated with a recalcitrant AV node. In a sinus rhythm this is seen in a P-R interval greater than 0.2 seconds (5mm).
Second Degree AV Block, Type I (Mobitz I), “Wenckebach”
The Wenckebach rhythm is also caused by a longer than normal delay in conduction through the AV node. Like the first degree block, the Wenckebach has a P-R interval greater than 0.2 seconds (5mm). Unlike the first degree block, the length of the prolonged P-R interval is variable, often with progressive lengthening. Also unlike the first degree block, the Wenckebach displays an occasional atrial P wave without a corresponding QRS complex. This is described as a “long-longer-longest-drop a beat” phenomena. To identify a Wenckebach, look for a rhythm with long P-R intervals and dropped QRS complexes.
Second Degree AV Block, Type II (Mobitz II)
The classic block does not display a long P-R interval because this block is not caused by a refractory AV node. It is instead caused by an intraventricular conduction block that prevents supraventricular stimulus from reaching the ventricles. Each time there is a P wave without a corresponding QRS complex, there is a complete blockage of electrical communication with the ventricles. This is, technically, a complete heart block each time it happens. Many references warn that the danger associated with a classic block is that it can progress to a complete heart block (third degree block). This is very true. As a matter of fact, the patient with this rhythm is in complete heart block for the space of each heartbeat where the QRS is missing.
Third Degree Heart Block, Complete Heart Block, AV Dissociation
When the path of electrical communication from the atria to the ventricles is completely severed, the ventricles have the option of pacing themselves from an ectopic intraventricular site to avoid ventricular asystole. Regular P waves are evident in a complete heart block, but those P waves do not reflect a causative relationship with the QRS complexes. The QRS complexes are generally slow since they are produced by the very slow ventricular escape pacer (20-40 BPM). Since cardiac output is actually ventricular output, the patient is possibly symptomatic of profound bradycardia.
Other Rhythms
Asystole
Asystole (flat line) displays the absence of electrical activity in the heart. The prognosis for the asystolic patient is grim.
Asystole (flat line) displays the absence of electrical activity in the heart. The prognosis for the asystolic patient is grim.
Agonal
An agonal rhythm is similar to asystole and is treated as asystole. The only real difference between agonal and asystole is the presence of very occasional, irregular, wide, nonproductive QRS-like complexes.
Pulseless Electrical Activity (PEA)
PEA is defined as any organized rhythm that does not result in a pulse. There are a number of reasons why a heart whose electrical activity is relatively normal does not produce a pulse from that electrical activity. Common reasons include hypovolemia, hypoxia, electrolyte disturbance, acid-base pathology, hypothermia, trauma, pharmacological interference, pericardial tamponade or thrombosis. The key to survival for the patient in PEA is immediate high quality CPR and an exhaustive search for the underlying pathology.