Figure 37-7 ECG for case 2.
From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.
DescriptionHistory
Chief Complaint. Chest tightness for the last 30 minutes.
History of present illness. Patient is a 58-year-old man who was at home resting comfortably when he suddenly began to experience chest tightness radiating to the neck and left arm approximately 30 minutes prior to transport. The chest tightness was graded 5 out of 10 and was associated with rapid, “kind of regular” palpitations, light-headedness, and shortness of breath. On further questioning, the patient stated that the palpitations preceded the chest tightness by a few minutes. The patient stated that he used a total of 3 sublingual nitroglycerin (NTG) tablets approximately 5 minutes apart with no alleviation of the tightness. The sublingual NTG was current and tingled under his tongue while dissolving. The patient appears to be very anxious, states that he “knows he is about to die,” and has a sensation of impending doom. There is no nausea, vomiting, or diaphoresis. The patient called fire rescue for further treatment immediately after administration of the NTG.
Cardiac Risk Factors.
*Note: Family history as a risk factor is different than just plain family history. In order to be a risk factor for CAD, there has to be a premature history of CAD in a first-degree male relative younger than 55 years and/or a first-degree female relative younger than 65 years.
Social History.
Past Medical History. Patient suffered an MI approximately 5 years ago and described the chest tightness as “similar.” Patient did not have palpitations during that event. Patient has had high blood pressure since the age of 25 years that is controlled by medications. Patient has high cholesterol but did not recall his levels.
Family History. Patient’s father died at age 60 and an uncle died at age 65, both of heart attacks. No family history of sudden cardiac death.
Medications. Patient does not have his medication list but knows he takes a baby aspirin daily.
Allergies. Penicillin, caused swelling and itching.
Review of Systems. Patient denies air hunger, orthopnea (shortness of breath on lying supine), paroxysmal nocturnal dyspnea, leg swelling, ascites (fluid in abdominal cavity), cough, sputum production, fever, chills, headache, change in mentation, decreased sensation, muscle weakness, visual difficulties, and imbalance.
Physical Examination
General Appearance. Patient appears to be anxious and is very restless on the stretcher. He is in mild respiratory distress with shallow, rapid respirations but is not using any accessory muscles of respiration. No pallor, cyanosis, or diaphoresis noted.
Blood Pressure. 110/64 mm Hg.
Heart Rate. 136 BPM, irregular, weak bilateral pulses, equal and symmetrical.
Respiratory Rate. 24 breaths per minute, shallow, not using accessory muscles of respiration.
Oxygen Saturation. 94% on room air.
Lungs. Mild inspiratory crackles that cleared on coughing, otherwise within normal limits.
Cardiac. No cyanosis or pallor noted. Slightly elevated jugular venous pressure at 14 cm H2O. + Cannon A waves are seen haphazardly. Arterial pulses are decreased but equal and symmetrical bilaterally. No palpable thrills or heaves are noted. Normal S1 and S2 of variable intensity are noted.
Neurologic. No focality is noted. Exam is within the normal range.
Extremities. No signs of clubbing or cyanosis are noted on the tips of the fingers and toes. Mild pitting edema is noted on both lower legs.
Preliminary Thoughts Based on the History and Physical Exam
Many of you are probably thinking that this case is your typical AMI presentation. However, there are some clinical factors that you need to keep in mind as we work through it. Remember, no two cases are the same and every presentation is different, kind of like fingerprints!
Let’s start off with the obvious: The patient had 30 minutes of substernal chest tightness that radiates to the neck and left arm. Those are classic symptoms of cardiac ischemia/injury/infarct. The patient also stated that the chest tightness was similar to his previous MI, except for the fact that this time, it is associated with rapid, “kind of regular” palpitations and some light-headedness that began a few minutes before the chest pain. Here is where we need a patient–clinician translator or mobile device.
To us, “kind of regular” means regularly irregular. This patient is telling us that he has a tachycardic, regularly irregular rhythm. He is also stating that this rhythm is associated with light-headedness. The lightheadedness is very troubling because it basically means that the brain is not getting enough blood, oxygen, and glucose, and he is, in essence, hypotensive. The hypotension could actually be due to ischemia, medications, increased vagal tone, or the arrhythmia. We need to figure out which one is the culprit and treat it before it gets worse. Finally, the patient is saying that his onset of symptoms did not start with the chest tightness, but with the palpitations. That constellation of symptoms suggests that, rather than a blocked artery, the rhythm may be the culprit. This patient should have a bright red DANGER sign placed on his forehead.
It’s interesting that the patient said, in no uncertain terms, “I know I’m going to die!” and had a sense of impending doom. There are certain things a patient doesn’t want to ever hear—for example, a surgeon in an operating room saying, “Oops!” or a paramedic saying, “Wow! Look, the knife in his chest is actually bobbing with each heartbeat!” Then there are those things a clinician doesn’t want to ever hear. At the top of my list is, “Doctor, I’m going to die!” That statement brings chills to my spine, as there are only two possible outcomes: (1) The patient is not going to die, or (2) the patient is going die, or at least come close. Don’t ever take those words lightly.
CLINICAL PEARL
When patients state that they are going to die, believe them.
Now, let’s get back to the light-headedness for a second. The patient’s blood pressure was 110/64 mm Hg. Not too bad, especially for someone who just took a few hits of sublingual NTG. But, NTG works by causing a decrease in venous return. This patient, therefore, has two things that decrease his venous return: the arrhythmia and the NTG use. If you remember, decreased venous return leads to a decrease in cardiac output and less perfusion to the heart, brain, and rest of the body. As a matter of fact, clinically, NTG could actually make this patient’s blood pressure drop precipitously. So, use it with caution.
The present blood pressure also is concerning for another reason. This patient has had a longstanding history of hypertension since he was 25 years old. Even if he had awesome blood pressure control on his medications, that number is still too low for him, in my opinion. Why? Because patients with longstanding hypertension develop arteries with thickened walls (especially the intimal or muscle layer). The thicker the wall, the greater the resistance and the more pressure it takes to expand compared to normal arteries. So, even though this patient has a decent blood pressure, it is not enough to keep his hardened arteries open. This is a condition known as relative hypotension.
There is another symptom of relative hypotension that the patient is freely expressing. Let me ask you this: How does a patient having an AMI look while on a stretcher? Patients with AMIs are quiet as church mice. They inherently know that any movement will make their pain worse. So, they don’t move; they sit there clutching their chests. Our patient is bouncing off the stretcher and is extremely anxious. In my experience, most of the time these patients are exhibiting a predelirious state that is easily corrected by adequately perfusing the brain. This is also frequently seen in patients with central nervous system bleeds and in postictal states. Beware of any AMI patient who is restless, and think twice before you give this patient thrombolytics!
CLINICAL PEARL
Patients with AMIs are typically quiet and very stationary. If your patient is restless and somewhat manic, consider the possibility that the brain is involved. A heart–brain connection does exist that can even cause micro-infarcts of the heart muscle with regional ST elevation mimicking an AMI. Many of these patients receive thrombolytics and subsequently develop complications with intracranial hemorrhages and death attributed to complications of the medication. This raises the old question: Which came first, the chicken or the egg?
We stated earlier that the relative hypotension was most likely related to his arrhythmia. To strengthen our argument, we turn to the presence of cannon A waves on his physical exam. Cannon A waves are sudden large spikes in the blood column in the jugular veins that occur haphazardly. To see them, we lay the patient partially supine at 45° of head elevation and we look at where the top of the blood column lies in the internal jugular (there are some great YouTube videos on this). Usually, the top of the column moves up and down slightly with each heartbeat. Cannon A waves, as suggested by the word “cannon,” are sudden large spikes of the blood column that occur when the atria contract against closed AV valves. In other words, the atria and the ventricles contract simultaneously. The blood is blocked from entering the ventricles by the closed valves, so it gets ejected backward into the venous system, causing the spikes in the jugular venous pressure.
The most common culprits causing cannon A waves are AV dissociation and third-degree AV block. Can you think of a rhythm that causes a tachycardic, regularly irregular pattern with asynchronous contractions that is associated with AV dissociation? Yep, VTach!
Electrocardiogram
The ECG clearly demonstrates a rapid WCT at a total rate of approximately 136 BPM (Figure 37-7). As we scan the ECG, we see that there are groups of very wide ventricular complexes that are regular with a ventricular rate of 143 BPM. These groups are broken up by obvious capture and fusion beats, providing indirect evidence of AV dissociation. When we take a closer look at the strip, we can clearly see that there are P waves and they are dissociated from the ventricular rhythm. We see them peeking through at a rate of 94 BPM (direct evidence of AV dissociation). The P waves are upright in the inferior leads and probably represent a sinus rhythm. We have labeled the P waves, capture, and fusion beats in Figure 37-8. The ventricular QRS intervals measure approximately 0.17 to 0.18 seconds, and the complexes are positive in lead V1, making this an RBBB-like morphology. Based on these criteria alone, we can make the diagnosis of VTach in this case.
Figure 37-7 ECG for case 2.
From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.
Description
Figure 37-8 ECG answers for case 2.
From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.
DescriptionFor the sake of completeness and to strengthen your clinical eye, let’s go through the checklist (Figure 37-9). The answers on the checklist are pretty self-explanatory and can be easily obtained from the preceding information. In this section, we will concentrate on the aspects we have not already covered.
Figure 37-9 WCT checklist for case 2.
© Jones & Bartlett Learning.
DescriptionUnder morphology, we saw that the patient has an RBBB-like appearance. Looking at V1, we checked the box labeled monomorphic R wave. The reason is that the only true ventricular complex is the last one. Take a look closely at that complex. It does look like there is a small r wave at the start, making this an rSR′ complex. But don’t be fooled; that small r wave is actually a P wave (look at the association of the P wave with the blue line representing the location of a P wave on all four of those leads). The only thing we can state with some certainty then is that the complex looks like a monomorphic R wave. Always try to assess any abnormality by checking out “the company it keeps.”
There is a positive concordance noted throughout the precordial leads, which is another criterion for VTach. Once again, look at the last true ventricular complexes and not the capture or fusion beats to make your determination of concordance.
An electrical axis in the right quadrant with an RBBB-like morphology is significant only for the use of locating the ventricular focus. We will skip this point since it is not really clinically relevant to anyone but an electrophysiologist trying to isolate the main focus in order to ablate it.
The Brugada criteria are positive for the lack of RS complexes and for the presence of AV dissociation. A positive response to just one of those two conditions means that the rhythm is a VTach. The Vereckei aVR criteria are positive for a notch in the descending limb of a completely negative QS complex in aVR and a Vi/Vt ≤ 1, both of which are indicative of a VTach.
Chest X-Ray. No bony deformities are noted. Lung fields are clear. An enlarged cardiac silhouette is present.
After just looking at this ECG for less than a few seconds, you should be able to instantly identify it as an obvious WCT. The patient is hemodynamically unstable because of the persistent chest tightness despite some treatment. The emergent evaluation gives us an idea of the risks of a VTach at approximately 90%. That percentage turned out to be closer to 100% after considering the history, physical exam, ECG, and our checklist due to the overwhelming evidence provided by the large number of indicators that pointed toward the diagnosis of VTach. Note that even though the heart rate is not in the higher end of the VTach spectrum, the patient’s hemodynamic status is compromised. This is partly because of the tachycardia itself, but also because the “wringing” action of the heart is inefficient due to the ventricular origin of the rhythm.
Emergent therapy, according to the advanced cardiac life support and SVT guidelines, should be instituted immediately for rate and rhythm control. The patient may require early cardioversion to avoid any worsening of the clinical status. In addition, treatment and protocols should be started immediately to treat for a possible underlying AMI. However, since the symptoms are most probably related to the VTach, holding off on instituting a percutaneous coronary intervention (PCI) protocol until the rhythm is broken and the patient is reassessed is advisable. If the rhythm cannot be controlled or if the symptoms persist after conversion to normal sinus rhythm, the catheterization (cath) team should be immediately consulted.
The workup and treatment of the relative hypotension causing some neurologic findings depend on whether they are corrected with the reestablishment of a stable rhythm. Correcting the arrhythmia and judicious use of IV fluids should stabilize the situation and return the patient to baseline. If these measures do not, then the patient should be taken for an emergency computed tomography (CT) scan to rule out intracranial bleeding or stroke. Thrombolytics should be avoided if at all possible until the CT proves there is no evidence of bleeding. Consultation with cardiology and neurosurgery should be immediately obtained to plan further treatment options.