Figure 37-14 Presenting rhythm for the patient in case 4.
From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.
History
Chief Complaint. Patient is complaining of palpitations and light-headedness.
History of Present Illness. You are called to the side of a 52-year-old man complaining of palpitations and light-headedness. The patient states that he had been feeling some slight indigestion after eating pizza about 2 hours earlier. The indigestion was partially relieved by antacids and didn’t really worry him. However, about 15 minutes ago he began feeling light-headed and felt some palpitations in his chest. The palpitations and lightheadedness progressed to the point that he felt he was going to pass out. This scared him and he called fire rescue.
The patient states that the palpitations have been ongoing and seem to last forever and that he started feeling light-headed about 15 or 20 seconds after they started. The patient describes the palpitations as a very fast, regular fluttering sensation in his chest. The episodes are associated with a subjective sensation of shortness of breath. There has been no associated diaphoresis, nausea, vomiting, or chest pain. The patient has a history of smoking (1 pack per day for 30 years) and hypertension that is controlled with some unknown medication.
Cardiac Risk Factors.
Social History
Past Medical History. Patient denies any pertinent past medical illnesses, conditions, or surgical procedures. No prior ECGs or rhythm strips were available.
Family History. None available.
Medications. No list available.
Allergies. None.
Review of Systems. Negative.
Physical Examination
General Appearance. Patient appears to be in no acute distress.
Blood Pressure. 110/60 mm Hg.
Heart Rate. 60 to 70 BPM, regularly irregular rhythm, weak and thready, bilateral pulses, equal and symmetrical.
Respiratory Rate. 24 breaths per minute, regular.
Oxygen Saturation. 92% on room air.
Lungs. Mild crackles at the bases. No wheezes or rubs are noted.
Cardiac. Jugular venous pressure was normal, but some pulsations were stronger than others. Arterial pulses are weak and thready, equal and symmetrical bilaterally. No palpable thrills or heaves are noted. Cardiac auscultation revealed a heart rate of approximately 125 BPM. Normal S1 and S2 are noted without any murmurs. No evidence of an S3 and S4 is noted on auscultation. Note that some cardiac pulsations did not cause palpable mechanical contractions.
Extremities. No signs of clubbing or cyanosis are noted on the tips of the fingers and toes. Skin was cold and clammy. Decreased capillary refill was noted throughout, with blanching of the nail beds when pressure was applied and a full return of color within 2 to 3 seconds of release.
Preliminary Thoughts Based on the History and Physical Exam
The patient was mainly complaining of palpitations and near syncope. In general, palpitations and light-headedness are very nonspecific symptoms that can be present without any observable rhythm disturbances. However, by asking some key questions, we can help make these symptoms a bit more relevant. Were the palpitations fast or slow? If so, how fast or how slow? Did the palpitations feel regular or irregular? In addition to just asking about the palpitations, you can ask the patient to tap out the pattern of the palpitations so that you can get a feel for any possible rhythm abnormality.
The history of indigestion after ingesting pizza could be a red herring, but in light of the palpitations it could also be a symptom of cardiac ischemia or infarction. According to statistics, indigestion can be the presenting symptom for an infarct in about 20% of cases. This is especially true in women, the elderly, or anyone with any neurologic problem that could alter pain perception—for example, a previous stroke.
Does the history that he received some symptomatic relief with antacids make you feel more comfortable? It shouldn’t. Symptomatic relief with antacids is a relatively nonspecific finding that is frequently seen in many infarct patients. The cause for this relief is unclear, but a perceived decrease in the cardiac pain is real. The ruling thought is that the visceral pain of indigestion and AMI both use the same nerves that merged during the embryologic stage of development. Do not make the mistake of believing that relief of the pain with antacids means the patient is having indigestion! Antacids will relieve both gastric and cardiac pain in some cases. The misconception that pain relieved with antacids or a “GI cocktail” is noncardiac can lead to the misdiagnosis of a potentially life-threatening condition.
The clinical history of the hypertension and the 30 years of smoking should elevate your suspicion about the presence of atypical cardiac ischemia or infarction. Remember, there are five main risk factors for CAD: hypertension, cigarette smoking, diabetes, high cholesterol level, and a family history of CAD before the age of 55 in male and 65 in female relatives.
By the way, which hypertension medications is the patient taking? The interviewer could not supply this vital piece of information. We need to keep this potential problem in mind as we go on because many drugs can actually trigger malignant arrhythmias (proarrhythmogenic effects). The possibility of electrolyte imbalances caused by medications will also need to be kept in mind, especially if the drugs include a diuretic or an ACE inhibitor.
With this history, your suspicion of ischemia or infarct should be high. The description of the palpitations that the patient gave as being fast and regular helps you to narrow it down to a tachycardia, but it really doesn’t help much otherwise. Keep in mind, however, that any arrhythmia in a patient with ischemia or infarction can be very dangerous because it can cause an increase in the oxygen consumption of the heart or a decrease in oxygen delivery to these tissues by decreasing cardiac output.
Let’s start by looking at the vital signs. The patient’s blood pressure is 110/60 mm Hg. This is a normal blood pressure, right? It can be, as long as we keep in mind a few other factors. This patient is normally hypertensive. He is controlled on medications, but this level of control is a little too good. Hypertensive patients usually need normal or slightly elevated levels of blood pressure in order to perfuse their organs. The elevated pressures in these patients is needed to overcome the anatomic consequences of hypertension. These consequences include a thickening of the blood vessel walls and an increase in the vascular tone. Remember this clinical pearl: A low or low-normal blood pressure in a patient with a history of hypertension could represent relative hypotension due to the potentially life-threatening effects of ischemia or infarction. Be suspicious and be careful! This patient can be having relative hypotension.
The heart rate is 60 to 70 BPM and irregular. The irregularity is helpful in our list of possible diagnoses, but the heart rate we palpate can lead to disaster. The palpable heart rate can easily mislead us into thinking that we are not dealing with a tachycardia. Luckily for us, both auscultation and, later on, the rhythm strip will let us see that we are actually dealing with a much faster rate.
Why do we get such a low palpable pulse rate? Well, sometimes the tachyarrhythmias are electrically conducted but the heart cannot mechanically contract at the same fast rate. In other words, the heart’s electrical conduction system transmits the impulse that quickly, but the heart muscle itself does not contract that fast. If the heart muscle does not contract, then it also does not pump blood. It is, in essence, a missed mechanical contraction. These missed mechanical contractions can add up and lead to hypotension or relative hypotension in many cases. Sound familiar?
The oxygen saturation is decreased at 92%. This could be due to the smoking history, but, with the findings of cool, clammy skin and slightly prolonged capillary refill, you have to wonder about decreased perfusion to the extremities. Once again, the concept of relative hypotension rears its ugly head.
It is unclear what the examiner meant by “occasional jugular venous distention seen in the neck.” AV dissociation causes some very large venous pulsations that occur irregularly. These are the cannon A waves we talked about earlier. Cannon A waves are a physical exam finding of the presence of some sort of AV dissociation.
At this point in your clinical reasoning, you have some strong suspicions. Sure, this could represent a vagal response causing light-headedness in an anxious patient with indigestion after eating pizza. But, this subtle clinical scenario could be due to a more ominous problem: cardiac ischemia or an infarct. The patient appears to be having atypical chest pain and is near syncopal. He is a smoker and is on antihypertensive medications. What about the palpitations? Are they benign or can they be representative of a life-threatening arrhythmia? You need a rhythm strip to solve this issue.
At this point, you are handed the ECG strip.
Electrocardiogram
We are dealing with a WCT. As we proceed, we need to keep in mind that any structural abnormality, presence of cardiomyopathy, or presence of ischemia would favor the diagnosis of VTach over SVT-A. The patient’s history and physical exam are both consistent with ischemia. In addition, statistically, you would be correct in quickly assuming that is VTach since over 80% of WCTs are VTach.1-5 But, let’s look closely at the strip and make a definitive diagnosis before we move on, since the patient is at least moderately clinically stable and the clinical situation, in our judgment, allows us the luxury of a few seconds before initiating treatment.
The ECG strip shows a WCT at a rate of about 125 BPM (Figure 37-14). The rhythm is regular and there appears to be some variation in the morphology of the QRS complexes throughout the strip, especially the next-to-last complex. There is a persistent hump in the ST segment of the complexes, which could represent a P wave. However, the hump is upright. Normally, retrograde P waves are inverted, so this doesn’t appear to be a P wave, but just a part of the repolarization process.
Figure 37-14 Presenting rhythm for the patient in case 4.
From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.
What do we do now? Well, let’s start by looking at the one thing that can give us the most additional information as quickly as possible. How about getting multiple leads? The rhythm strip in Figure 37-15 was taken at the same time as the original strip. As a matter of fact, the shaded area represents the strip that we showed you at the beginning. Is the rhythm a little easier to analyze now that we have multiple leads? Yes!
Figure 37-15 Multiple leads taken at the time of presentation that includes the patient’s strip (Figure 37-14, shown with a blue background). Use all the leads to isolate the specific findings.
From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.
DescriptionObtaining multiple leads when you are stuck is a critical decision point to remember. We know that many of you are saying that we should have given you lead II because it would have been easier. You would be absolutely right in making that statement. But you have to realize that you would be right only in this one case. For another patient, maybe lead V1 would have been the best lead to identify the arrhythmia. In a third patient, it could have been lead III. The point is you never know which is the best lead, and you never know which lead or which part of the rhythm strip you will be handed. Always obtain multiple leads or a full 12-lead ECG when you are dealing with a complex arrhythmia. Do not assume that lead II will always be the best lead to look at arrhythmias.
As we mentioned before, a corollary to that pearl is that you should obtain long rhythm strips, if possible. This is because arrhythmias, and cardiac events in general, evolve. They are not stagnant events. The causative factors and presentation are constantly changing, moving, and evolving. Just because something is not there in this section of the strip, does not mean it will not be there in the following 10 seconds. Remember, a strip is only a static picture of the cardiac events for a few seconds (or however long your strip is). An ECG is, likewise, only 10 seconds long. Long strips help to pick up minute details that can be critical in arrhythmia interpretation. For example, a long strip can be very helpful in picking up the presence of capture and fusion beats, which may occur intermittently.
In this discussion, we will provide you with a longer three-lead strip (Figure 37-16). In addition, we have labeled the complexes from 1 through 10 to facilitate the discussion. We will be using the longer strip and the multiple leads to help facilitate our discussion. We could have arrived at the same diagnostic conclusion from our little strip on lead I, but it would have been a lot tougher.
Figure 37-16 Multiple leads of a patient with ventricular tachycardia. The important features are labeled and/or numbered, and they will be discussed within the text.
From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.
DescriptionThe complex labeled 1 in Figure 37-16 is the patient’s normal complex. Note the P wave, normal QRS complex, and inverted T wave in lead II. The PR interval is prolonged and consistent with a first-degree heart block, as seen in Chapter 28, Atrioventricular Blocks.
Complex 2, however, is a bit different. This QRS complex is still positive, but it is wider than the normal one. It also has a different ST-segment and T-wave morphology. In addition, in lead V1 we see the start of a normally occurring P wave (see the blue arrow), which is interrupted by a premature complex. This premature QRS complex could be a PVC or a PJC with aberrancy. An argument can be made either way, and it really doesn’t matter which one it is. The important thing is that the premature complex triggers a new rhythm starting with complex 3. This new rhythm can easily be seen in all three leads.
Now let’s examine this new rhythm. The morphology of the complexes is wide. They are at least 0.14 seconds wide (3½ small boxes, not shown). We see a small notch in the downsloping S wave that looks like a Josephson’s sign (see red arrow). These two findings are both predictive of VTach. We’re getting warmer, but we’re not there yet.
An axis in the extreme right quadrant would be helpful. However, we can’t figure out the exact electrical axis because lead aVF is not available. We can state that the axis is not in the extreme right quadrant because the complexes would have to be negative in lead I if that were the case, and they are positive on our strip. There is one thing we can tell, though, and that is that the axis of the new rhythm must point in a different direction than the normal electrical axis. We can say this because the polarity in the complexes of the new arrhythmia is pointing in the opposite direction from those of complex 1 in leads II and V1. This is nice to know, but it doesn’t help us distinguish between VTach and SVT very clearly.
There is some minimal irregularity in the rhythm and some small morphologic differences in complex 3 and those labeled collectively as complex 4. But, we know that at the onset of VTach, the rhythm can be a little irregular and the morphology can change a little bit. These changes will stabilize as the rhythm matures over time. Still could be VTach.
Complexes 5, 7, 9, and 10 provide the best diagnostic evidence for VTach on this rhythm strip. Notice that their morphologies are completely different from the others in the group. Complex 5 is a bit like complexes 3 and 4, but it is just not as deep or as wide. In addition, the T wave associated with it is different. Complex 7 is narrower and the axis is different in leads II and V1. As a matter of fact, it is similar to the normal complex 1, isn’t it? Complex 9 is somewhere between complexes 5 and 7.
Can you figure out why these complexes have these differing morphologies? The answer is that they are fusion complexes. None of them are capture beats, even though complex 7 is close, because none of them are morphologically identical to complex 1. They all have a little bit of fusion with the ventricular complexes. These morphologic differences are even obvious in our lead I rhythm strip.
We were able to isolate the presence of a VTach based on just this rhythm strip. We really don’t need to use the checklist, but as we said before, it never hurts to try. Let’s turn to our checklist in Figure 37-17 and see what we get.
Figure 37-17 WCT checklist for case 4.
© Jones & Bartlett Learning.
DescriptionThe history section is positive only for an age greater than 35 years. The patient is hemodynamically stable with a ventricular rate of 125 BPM. The morphologic pattern in V1 is consistent with an RBBB-like presentation. We can use the width of the complexes in leads I and II to isolate the QRS interval and the location of the starting and ending points. We can then use a straightedge or our calipers to transfer those measurements to lead V1. By doing so, we see that the pattern in V1 is an rsR′.
As we stated previously, the presence of AV dissociation was evident on the strip with the peek-a-boo P waves occurring every so often and the presence of fusion complexes. This is the strongest evidence we have in favor of a VTach on this strip. Remember, the presence of AV dissociation provides an almost 100% certainty that you are dealing with a VTach.
Due to the absence of many leads, the algorithms cannot be properly completed. However, the presence of AV dissociation in the Brugada algorithm is almost definitive for a VTach. The lack of aVR does not allow us to make any assumptions based on the Vereckei aVR algorithm.
Is there any other evidence of AV dissociation? The only hard evidence is the presence of fusion complexes. Some soft evidence is found in the fact that the T-wave morphology of the complexes immediately before the fusion complexes is slightly different from the typical T waves seen prior to the ventricular beats. This happens because the P waves of the fusion complexes are buried somewhere inside those of the preceding T waves. The superimposed P and T waves alter the morphology of the resultant T wave.
Many of you are still thinking that the notches identified by the green arrow represent P waves. There are some arguments against that possibility, the main one being that the notches still occur after the QRS complexes in the fusion complexes. If they were P waves, they should occur before the QRS in the fusion complexes because there has to be some normal capture of the ventricle by definition. In other words, in order to create a fusion complex, you have to have even a minimal amount of normal capture by the P wave. A P wave occurring after the QRS complex just doesn’t fit. As mentioned earlier, that notch represents a repolarization sequence found in the ventricular complexes.
In this discussion, we did most of our traditional “putting it all together” while we were analyzing the patient’s rhythm. This was done purposely to facilitate discussion. We want to point out, however, that there really are no fine lines as to what should be under the answer to any of the questions. The important thing is to get to the final conclusion. The information that we have gathered from this rhythm strip does not leave much room for doubt. This rhythm is VTach.
We hope that you have found this review of VTach and the analysis of this very complex rhythm strip helpful. We could have made it easier, but, unfortunately, you won’t always get classic examples of arrhythmias in real life. This real-life strip is just one example of what you could get. Don’t panic. Approach the situation with a clear head, using everything you have at your disposal to get an accurate diagnosis. We feel that if you can interpret the difficult strips, the easy ones will be a cakewalk.