Figure 37-2 ECG for case 1.
From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.
DescriptionHistory
Chief Complaint. Cough with yellowish sputum for 3 to 4 days.
History of Present Illness. The patient is a 38-year-old woman who presented to her physician’s office stating that approximately 2 weeks prior to this visit she had developed a cold with “flulike” symptoms that included body aches, dry cough, low-grade fevers, and muscle and joint pain. The patient’s 10-year-old son had the same symptomatology at the time. The patient self-medicated with fluids and acetaminophen, and the symptoms lasted approximately 5 days, then resolved completely.
Three or 4 days prior to this visit, she began to develop a resurgence of the symptoms, which progressed into a cough with copious yellowish sputum, some mild shortness of breath, pain (grade 3 out of 10) on deep inspiration in the lower right front area of the chest wall, fevers associated with severe chills (rigors), and global headaches during the febrile periods.
Cardiac Risk Factors.
Social History.
Past Medical History. Patient had some mild childhood asthma. She denies any other pertinent past medical illnesses, conditions, or surgical procedures. No prior ECGs or rhythm strips were available.
Family History. No family history of CAD or sudden death.
Medications. Oral contraceptives.
Allergies. None.
Review of Systems.
Patient denied significant shortness of breath or air hunger, dyspnea on exertion, palpitations, nausea, vomiting, diaphoresis, radiation of the chest pain, rashes, neck stiffness, lack of sensation or weakness, dysarthria, change in the color of her stool or urine, and easy bruisability.
Physical Examination
General Appearance. Patient appears to be in mild respiratory distress but is not using accessory muscles of respiration. Tachypnea is noted with shallow respirations. No pallor, cyanosis, or diaphoresis noted.
Blood Pressure. 118/68 mm Hg.
Heart Rate. 150 BPM, regular rate and rhythm with a rapid tachycardia, normal bilateral pulses, equal and symmetrical.
Respiratory Rate. 24 breaths per minute, shallow breaths with some noticeable splinting on the right side on deep inspiration, not using accessory muscles of respiration.
Oxygen Saturation. 92% on room air.
Lungs. Patient does have a productive cough with yellow-green sputum. Patient’s thorax is symmetrical, but splinting is visible over the lower right anterior and flank areas of the chest wall. No point tenderness or crepitations noted in this area, but the patient appears to be splinting to pain in that area during deep inspiration. Breath sounds are increased over the affected area, consistent with an underlying consolidation.
Cardiac. No cyanosis or pallor was noted on the extremities. Patient had no clubbing on the fingers or toes. Jugular venous distention was normal. Arterial pulses are of normal intensity and equal and symmetrical bilaterally. No palpable thrills or heaves are noted. Normal S1 and S2 are noted, but murmurs and gallops could not be appreciated due to the tachycardia.
Preliminary Thoughts Based on the History and Physical Exam
The chief complaint of the patient is focused primarily on the resurgence of the more serious infectious pulmonary signs and symptoms she has developed over the past 2 weeks or so. The main culprit behind our patient’s visit is a classic worsening of a right middle lobe pneumonia due to a bacterial superinfection.
Even though the patient did not give a classic history of cardiac complications or arrhythmias complicating the right middle lobe pneumonia, cardiac involvement should always be suspected in any sick patient with a heart rate of 150 BPM. Generally speaking, young, healthy patients, especially children, tend to compensate for high heart rates and moderate hemodynamic compromise easily until they cross a particular threshold. After crossing that individual threshold, however, any further worsening will cause some serious problems to develop exponentially. Think of it like someone walking off a cliff. They walk along easily on the flat ground until they reach the edge of the cliff. Then, one more step and . . .splat!
Putting the infectious and pulmonary problems aside for now, our main emergent problem is that heart rate of 150 BPM. The ECG, which would definitely shed some light on this issue, should be obtained as soon as possible. But, even without the ECG, we have enough to work with at this point and can actually make a preliminary list of possible diagnoses based on the information we have and the heart rate.
We’ve mentioned multiple times that a heart rate of exactly 150 BPM should make you think of a particular rhythm. Does that number ring a bell? That number is associated most commonly with an atrial flutter. Why? Well, the flutter, or F, waves typically occur most commonly at rates of 300 BPM (0.2 seconds, or one big block). Note that this is the exact time needed to complete a run through the entire macro-reentrant circuit. Since the atrioventricular (AV) node does not like to transmit impulses at a rate of 300 BPM, it blocks the second impulse from getting through for self-preservation. The net result is that the F waves depolarize the ventricles using a 2:1 conduction rate, making the ventricular rate exactly 150 BPM.
Putting it all together (so far), we have a young woman who originally developed an upper respiratory infection with a subsequent bacterial superinfection of the right middle lobe leading to a lobar pneumonia. The patient presents with a heart rate of 150 BPM, the classic figure associated with an atrial flutter with 2:1 conduction. Can we make a connection here that incorporates all the information? Yep, we sure can. On the Differential Diagnosis box in Chapter 20, Atrial Fibrillation, page 286, we covered a mnemonic for the differential diagnosis of new-onset atrial fibrillation/flutter. That mnemonic was MAD RAT PPP. Going through it, we see the following:
M = Myocardial infarction
A = Atherosclerotic heart disease
D = Drugs (especially digoxin)
R = Rheumatic heart disease
A = Alcoholic holiday heart syndrome
T = Thyrotoxicosis
P = Pulmonary embolus
P = Pericarditis
P = Pneumonia (especially right middle lobe pneumonia)
So, going over our list, we see three possibilities: (1) alcoholic holiday heart syndrome, (2) pericarditis, and (3) right middle lobe pneumonia. Alcoholic holiday heart syndrome is a possibility because the patient does binge on alcohol during the weekends, which could suggest an aspiration pneumonia. This possibility is something to keep in mind but is not at the top of our hit parade for now.
Pericarditis by itself does not match our clinical picture. However, pericarditis as a complication of the pneumonia is possible since the pneumonia can irritate the pericardium. Good thought. We should keep this possibility in mind and place it in the number 3 spot for now.
Right middle lobe pneumonia definitely matches our presentation and is the most likely cause of our atrial flutter. There are a couple of ways the pneumonia could cause an atrial flutter in our patient. The first way, which we covered earlier, is a direct irritation of the pericardium or right atrium by the infection that almost completely surrounds this area. The second way would be through sepsis, hormonal imbalances, fevers, or hypoxemia that could irritate the myocardium directly. Either way, we have a good idea of the forces at work here from just analyzing the history and physical and using some simple deductive reasoning.
Electrocardiogram
On first glance, this ECG shows an obvious WCT with a ventricular rate of 150 BPM and wide QRS complexes at 0.14 seconds (Figure 37-2). The patient appears to be hemodynamically stable, but the heart rate is still very fast and potentially dangerous. These findings place her in the emergent/urgent stages of her evaluation. According to our initial assessment of the ECG, we know there is an 80% chance that this rhythm is a VTach. At this point, if the patient were hemodynamically unstable, we would initiate emergent WCT treatment protocol until the rate and rhythm were stabilized, assuming this is a VTach.
Figure 37-2 ECG for case 1.
From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.
DescriptionHowever, since the patient is hemodynamically stable and we have some borrowed time, we can take a closer look at the issues at play. First of all, are we dealing with a VTach? Well, since the patient has a right middle lobe pneumonia and the heart rate is exactly 150 BPM, the chances that we are dealing with an SVT-A have increased. Specifically, our chances that this is an atrial flutter with 2:1 conduction have increased for the reasons we stated earlier.
Armed with an increased chance that this is an SVT-A, we can make a strong argument for giving her supportive care (oxygen by mask or nasal cannula, intravenous [IV] fluids, acetaminophen, and so forth) and keeping a close eye on her while we spend a few more minutes trying to quickly assess the ECG further. Isolating the rhythm into either a VTach or an SVT-A can provide us with more options and a more definitive treatment strategy, thereby increasing our chances of success while decreasing our chances of complications and adverse reactions.
Let’s take our calipers out and get to work. The ECG shows a WCT at 150 BPM with the width of the QRS complexes at 0.14 seconds. Any QRS complex wider than 0.12 seconds should immediately make you ask: Is this a bundle branch block (BBB) or a BBB-like pattern, and if so, are we dealing with a right bundle branch block (RBBB), a left bundle branch block (LBBB), or an intraventricular conduction delay or a BBB-like pattern?
The decision tree for determining between these patterns begins by examining lead V1 and applying our turn signal analogy (Figure 37-3). Specifically, do the QRS complexes point up (positive) or down (negative) in lead V1? In our example, they point up, or positive. Moving our turn signal up means we go right. So, since this is a WCT, is this a true RBBB pattern (found in SVTs-A) or an RBBB-like pattern (found in VTachs)?
Figure 37-3 Complexes wider than 0.12 seconds need to be assigned to one of three possibilities: RBBB, LBBB, or intraventricular conduction delay (BBB-like). Using our “turn signal” analogy, we can easily assign them based on the established criteria.
© Jones & Bartlett Learning.
DescriptionA true RBBB pattern is positive in lead V1 and has slurred S waves in leads I and V6. An RBBB-like pattern is positive in lead V1, but the QRS complexes in lead V6 are typically more negative than positive (R:S ratio < 1). Our ECG shows a classic RBBB pattern with positive QRS complexes in lead V1, slurred S waves in leads I and V6, and QRS complexes that are very positive in lead V6 (R:S ratio > 1). Such a classic RBBB pattern points us in the direction of an SVT-A.
Now that we have that out of the way, we want you to sit down and dissect this ECG further by using the criteria and algorithms that we went through in Chapter 36, Wide-Complex Tachycardia: Criteria. Do you remember them all? If you can, you’re a medical machine! If you can’t, you are not alone; most of us are right there with you. This is where our checklist comes in. The checklist is a tool that will help to reinforce your memory and make life simpler during the learning process. As you use it, keep in mind that the ultimate goal should be to incorporate the material into your daily practice and to be functional without it. Let’s get started by putting it to use on our ECG and see what we come up with (Figure 37-4).
Figure 37-4 WCT checklist for case 1.
© Jones & Bartlett Learning.
DescriptionWhen we fill out the history section on the checklist, we see that only one criterion is checked that would point us in the direction of a VTach, the patient’s age being greater than 35 years. That pertinent positive by itself is really not enough to make the diagnosis of VTach. In contrast, the pertinent negatives actually point us in the opposite direction, toward the possibility that the strip is an SVT-A.
Both SVTs-A and VTachs can be either stable or unstable hemodynamically. The most we can say is that the presence of hemodynamic instability points us in the direction of VTach. Once again, since our patient is hemodynamically stable, this factor favors an SVT-A. So far, the score is SVT-A = 2, VTach = 0.
The ventricular rate is 150 BPM. There appears to be a clear P (or F) wave before each of the QRS complexes (Figure 37-5). However, as we have discussed, an exact rate of 150 BPM should immediately make you think of an atrial flutter. So, take out your calipers and start measuring! Place each pin of the calipers on the tallest or lowest points of the visible P waves. We see that the pins fall exactly two big blocks apart. Now, since the most common conduction rate is 2:1, divide the distance between the caliper tips in half to one big block by moving the right pin closer to the left pin. If you can spot any visible deflection at the one big block mark, you have a buried F wave at that spot (see red arrows in Figure 37-5).
Figure 37-5 Finding the hidden P or F waves.
© Jones & Bartlett Learning.
Getting back to the heart rate of 150 BPM, look back at the patient’s ECG (Figure 37-2). Place a blue arrow on every obvious P or F wave that you can spot. Now, using your newfound knowledge of isolating buried P or F waves, are there any deflections halfway between the obvious waves? Yes, we can see a deflection at the end of the QRS complex. Place a red arrow on those. Walk your calipers across the strip at a distance of one big block. Do all the arrows map (i.e., are they equidistant from each other?)? Yes, they do. This is your solid proof that we are dealing with an atrial flutter with 2:1 conduction. (We’ve taken the liberty of marking those for you in Figure 37-6.) One last thing: Other SVTs-A can present at heart rates of 150 BPM. How can we tell we are dealing with atrial flutter? Look for a constantly undulating baseline, which we do have on this ECG. Now you’ve made the diagnosis of atrial flutter. The score just went to SVT-A = 3, VTach = 0.
Figure 37-6 Establishing the rhythm in case 1.
From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.
DescriptionNote that we can stop there since we know it is an atrial flutter with 2:1 conduction, but just for fun and practice, let’s keep going.
CLINICAL PEARL
How to Train Your Eyes!
To start training your eye to spot hidden F waves faster, mentally take a step back and look at the baseline. If you look for it, the second F wave becomes easier to spot. This is what occurs in lead II of our ECG: We see the second F wave right at the end of the QRS complex; it is superimposed on the slurred S wave of the RBBB pattern, but the morphologic similarities between the F waves are too much to just be a chance occurrence.
In regard to our regularity section, both our atrial and ventricular rhythms are very regular. The only thing that breaks up the ventricular rhythm is a premature junctional complex (PJC), which is labeled in Figure 37-6. Note that the PJC does not alter the F-wave pattern in the least.
The morphology section is a very important section in this particular ECG. We saw earlier that this is a classic RBBB pattern that is typically seen when there is a conduction block somewhere along the right bundle that causes aberrant conduction throughout the rest of the ventricle. As additional support for our argument is the presence of the rSR′ pattern of the complexes we see in lead V1. This points us in the direction of an SVT-A, most probably due to either a preexisting BBB or a rate-related aberrancy.
In order to get an RBBB-like pattern, the origin of the ventricular complex must be an ectopic ventricular pacer. This would lead to a conduction of the ventricular depolarization wave that would occur by direct cell-to-cell conduction and, therefore, the atypical pattern.
Our ECG also shows no direct or indirect evidence of AV dissociation or concordance of the QRS complexes in the precordials. The absences point us in the direction of an SVT-A. Finally, the electrical axis of the heart is in the left quadrant since the QRS complexes are positive in lead I and negative in lead aVF.
Turning to the algorithms, none of the criteria for VTach are checked off in either the Brugada or the Vereckei aVR algorithms. This points us toward the rhythm being an SVT-A with a high degree of certainty.
That’s it, we’re done looking at this ECG. We’d like to point out that reading about our answers on the checklist took about 10 to 20 times longer than actually filling out the form. As you begin to master these concepts, it will literally take you less than a minute to make your final electrocardiographic determination.
Chest X-Ray. Right middle lobe infiltrate is noted, consistent with pneumonia. Some blunting of the right costophrenic angle is noted.
To wrap it all up, we have a 38-year-old woman who complained of upper respiratory infection symptoms approximately 2 weeks prior to this presentation. The symptoms spontaneously resolved within a few days without any treatment. Subsequently, however, she developed a bacterial superinfection of the right middle lobe leading to a pneumonia. The pneumonia led to her seeking medical treatment, where she presented with an asymptomatic WCT at a rate of 150 BPM. Subsequent workup revealed the presence of an atrial flutter with 2:1 conduction on the ECG. Treatment should focus primarily on emergently treating the arrhythmia and returning the patient to a sinus rhythm as quickly as possible, with the focus then shifting to treating the underlying pneumonia and prevention of a recurrence of the arrhythmia.