EKGs Made Easy
Updated: Feb 24, 2023
One of the most important skills that nurses must master is interpretation of cardiac rhythms. This can also be one of the most frustrating skills to learn as a student. The ability to master EKG rhythms takes practice, practice, and more practice. While still learning rhythm interpretation, it is very important to develop a method for identifying dysrhythmias; DO NOT try to rely solely on memorization of what certain rhythms SHOULD look like. Every patient is different and one patient’s atrial fibrillation may look different than the patient’s down the hall. It is also important to seek to understand the CAUSE behind the rhythm. Underlying causes of dysrhythmias can be boiled down to problems with one or more of the following: nerve impulses, myocardial oxygen demand, hormonal fluctuations, and several other factors. In this post, I am going to teach you how to accurately identify some of the most common dysrhythmias, discuss their most common causes, and describe the priority nursing interventions.
1. Sinus rhythm with a first-degree A-V block.
The first step of rhythm interpretation is to apply the 5-step analysis method.
Rate: 70
Rhythm: Regular
P waves: Present for every QRS, upright
PR interval: 0.28
QRS: 0.06
Once you complete these 5 steps, you see that the ONLY abnormality with this strip is the prolonged PR interval (greater than 0.20). This strip is therefore interpreted as Sinus rhythm with first degree A-V block. *Remember, a first-degree is NEVER a rhythm in and of itself. There is no actual BLOCK with a first degree, but rather a DELAY in electrical conduction from the atria to the ventricles. Typically, there is no treatment needed for first degree A-V blocks unless there are additional abnormalities such as a bundle branch block. We will discuss this next.
2. Sinus rhythm with a Bundle Branch Block.
First , the 5-step analysis.
Rate: 70
Rhythm: Regular
P waves: Present for every QRS, upright
PR interval: 0.16
QRS: 0.20
After completing the 5-step analysis, we discover that the ONLY abnormality noted in this strip is a prolonged QRS (greater than 0.12). This rhythm is therefore documented as Sinus Rhythm with a Bundle Branch Block. *Again, bundle branch blocks are NOT rhythms in and of themselves. Since the QRS complex represents ventricular depolarization, a prolonged QRS indicates that there is a delay in conduction through the ventricles. There are several underlying processes that can delay the spread of conduction through the ventricles including cardiomyopathy where there is an increased amount of myocardial tissue through which the impulse has to spread. Other possible causes include valvular insufficiencies such as aortic or mitral stenosis. Anyone with coronary artery disease (CAD) and/or hypertension is also at an increased risk to develop a bundle branch block. Bundle branch blocks (BBB) typically do not cause symptoms or require intervention; it is the underlying cause of the BBB that will require treatment. For example, if a patient develops a BBB due to cardiomyopathy, they may need cardiac resynchronization therapy to alleviate signs and symptoms associated with decreased cardiac output. Let’s discuss more dysrhythmias that cause decreases in cardiac output.
3. Atrial fibrillation.
Rate: 110
Rhythm: Irregular
P waves: Not discernable
PR interval: Not measurable
QRS: 0.08
The 5-step analysis reveals several abnormalities with this strip. The rate is tachycardic, the rhythm is highly irregular, there are no P waves and therefore no PR interval to measure. Given these findings, this rhythm can be interpreted as Atrial Fibrillation. Atrial fibrillation usually results from a cluster of disorganized electric signals causing the atria to quiver. There is a loss of “atrial kick” meaning that there is less blood being pumped from the atria to the ventricles resulting in a decreased cardiac output. Additionally, because the atria are not pumping as they should be, blood is allowed to pool within the atria possibly leading to the formation of a clot that could dislodge and become an emboli (STROKE!). Some of the most common causes of atrial fibrillation include CAD, valve disease, hypertension, and acute myocardial infarction. Another BIG contributor to A-fib is chronic lung disease, like COPD. A-fib and COPD almost go hand in hand; meaning if you see one, you are likely to see the other. Any of these conditions would cause damage to the heart’s structure and place a patient at risk for developing dysrhythmias such as A-fib. The treatment for A-fib includes anti-coagulation to prevent the formation of clots (and prevent stroke) and treatments to control the rate and rhythm. Diltiazem, a calcium channel blocker, is usually the first-line treatment to control the rate in a patient with A-fib. Coumadin is the anti-coagulant of choice to prevent clot formation and stroke. Some patients with recurring or prolonged A-fin unresponsive to treatment may require synchronized cardioversion or ablation therapy. For patients that have been in A-fib for longer than 48 ours, they MUST be anti-coagulated prior to cardioversion.Ablation therapy is performed by the cardiologist in the cardiac cath lab and uses a guided catheter to locate and ablate any cells that are firing erratically within the atria.
4. Supraventricular tachycardia (SVT).
Rate: 210
Rhythm: Regular
P waves: Not discernable
PR Interval: Not measurable
QRS: 0.06
Obviously, there are several things wrong with this strip. The rate is very tachycardic, P waves are not discernable and therefore the PR interval is not measurable. Take note of the major notable difference between this strip and a-fib; the rhythm is REGULAR. A-fib is NEVER regular! Another clue that this is SVT are the extremely narrow QRS complexes. Three major clues that you are looking at SVT: Really fast rate, regular rhythm, and very narrow QRS complexes. Causes for SVT are very similar to causes for other atrial dysrhythmias and include CAD, chronic lung disease, hyperthyroidism, anxiety/stress, and stimulants. It is important to remember that SVT is like an umbrella term for ANY dysrhythmia that originates ABOVE the ventricles and could include sinus tachycardia, A-fib, A-flutter, or Re-entry tachycardia called PSVT (paroxysmal SVT). The nurse’s priority for a patient in SVT is to slow down the rate in order to maintain adequate cardiac output Remember, least invasive methods FIRST. With SVT we want to try and engage the vagus nerve which increases parasympathetic stimulation and slows the heart rate down. We will ask the patient to “bear down”; we may ask them to blow into a syringe, or place a full bag of ice on the bridge of their nose to “shock” them into bearing down and engaging the vagus nerve. If these measures are unsuccessful, the provider may order some adenosine at a dose of 6mg then a second dose at 12mg as needed. Adenosine essentially creates a “heart block” in that it blocks conduction through the A-V node for a short period. Adenosine has a VERY SHORT HALF LIFE and it must be pushed VERY RAPIDLY! Adenosine is especially helpful for re-entry dysrhythmias where an electrical impulse RE-ENTERS the atria through some sort of funky conduction pathway; adenosine will STOP this re-entry from happening. Our hopes when we push adenosine is that the re-entry will be stopped, the rate will slow down, and we will be able to identify the underlying rhythm because remember, SVT is an umbrella term! Our next line of medication for SVT includes IV calcium channel blockers such as diltiazem or beta blockers such as metoprolol, which are used to slow down the heart rate for short term episodes of SVT. Long term management of recurrent SVT will include ablation of the funky conduction pathway, much like in recurrent A-fib.
5. Ventricular Tachycardia (VT).
This is THE deadliest dysrhythmia on the planet so it is a MUST KNOW for every single nurse!
Rate: 180
Rhythm: Regular
P waves: Nope
PR Interval: Nope
QRS: Large and funky
With V-tach, the dysrhythmia is originating within the ventricles so the QRS complex will always be abnormal since the QRS represents ventricular depolarization. There are two types of V-tach that a patient may experience: with a pulse or without a pulse. I have held conversations with patients in a rhythm just like the one pictured above…freaky! Sometimes VT is difficult to distinguish from SVT; that is where something called the Brugada Criteria comes in. The first of these criteria is concordance in leads V1-V6; simply stated, do all the QRS complexes point in the same direction? If the answer is yes, then it is VT. Next, is the R-S interval greater than 100 milliseconds? If the answer is yes, then it is VT. The next question pertains to A-V disassociation. If the P waves aren’t talking to the QRS complexes, then it is VT. Let’s talk about causes. I sort of feel like a broken record because the causes of dysrhythmias tend to overlap, but, again, the most common causes of VT include CAD, cardiomyopathy, old myocardial infarctions that caused structural damage, new MIs causing acute ischemia, and/or heart failure. V-tach happens much more often in patients of advanced age; whereas SVT occurs more frequently in younger patients who have had too many Red Bulls. The treatment for VT depends on the patient’s status; to shock or not to shock is the question. For VT without a pulse, the treatment is CPR and defibrillation. For V-tach with a pulse, the provider will most likely order one of the following anti-dysrhythmics: procainamide, lidocaine, amiodarone, or a beta blocker for rate control. Lidocaine works best for VT related to myocardial ischemia. Amiodarone will be the treatment of choice for most other causes.
That concludes this post covering common dysrhythmias, their causes, and nursing priorities. Drop a comment below if you want to see more EKG posts like this one. I would love to hear which dysrhythmias you are struggling with.
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