#5799 - 06/22/05 11:06 PM
esophageal spasm
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Corey Ricketson
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I had a woman today who attempted to swallow two very large pills at once. To no suprise it didn't work. She was in a lot of pain and drooling . I called St. David's for an order for Nitro to relax the esophagus and was denied. Reason per Dr. Jackson "I just don't like to give orders". I explained that the side effects of nitro are minimal and short lived and that we don't carry glucagon (don't get me started on that one). He agreed that the nitro treatment would have been perfectly appropriate but he just doesn't like to give orders . If you call st. David's for an order and you hear Dr. Jackson on the other end, you might as well hang up and ask the wall you are next to for the order. 
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#5800 - 06/22/05 11:11 PM
Re: esophageal spasm
[Re: Corey Ricketson]
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Patrick Murphy
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Heavy, heavy sigh..... 
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#5802 - 06/24/05 06:06 PM
Re: esophageal spasm
[Re: Laurie Emmer]
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Corey Ricketson
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I have always had pretty good luck with it Laurie. The goal is to decrease HR in order to improve cardiac output. Unless they are hypotensive or have a wide QRS I',m really not that worried about giving it. I will sometimes call if the HR is under 150 but I still want to give it.
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#5806 - 06/28/05 04:56 PM
Re: esophageal spasm
[Re: Marc Peek]
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Patrick Murphy
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Good call putting the pads on. Cardioversion or NA channel blockade is the treatment of choice for WPW with A-fib. (NA blockade works on the accessory pathways, Kent bundle in this case) Anything that increases the refractory period of the AV node is bad news in these patients due to unopposed conduction in the accessory pathway.
Cardiazem or adenosine can be used in PSVT with WPW, as long as the QRS remains WNL. As always, contact a physician for orders if needed... Hang up if you get Dr. Jackson 
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#5807 - 06/28/05 05:26 PM
Re: esophageal spasm
[Re: Patrick Murphy]
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Patrick Murphy
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FYI... from Emedicine.com
We can use Amiodarone here in place of procainamide...still requires an order tho.... 
Authored by Mel Herbert, MD, MBBS, Assistant Professor of Medicine and Nursing, Department of Emergency Medicine, Olive View-University of California at Los Angeles Medical Center
Coauthored by Griffith Tully, MD, Staff Physician, Department of Emergency Medicine, University of California at Los Angeles Medical Center
Mel Herbert, MD, MBBS, is a member of the following medical societies: American College of Emergency Physicians
Edited by Theodore Gaeta, DO, Program Director, Department of Emergency Medicine, Adjunct Assistant Professor, New York College of Osteopathic Medicine, Program Director, Department of Emergency Medicine, Cornell University Medical College, New York College of Osteopathic Med; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Gary Setnik, MD, Chair, Assistant Professor, Emergency Medicine, Harvard Medical School, Department of Emergency Medicine, Mount Auburn Hospital, Cambridge, Massachusetts; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Scott H Plantz, MD, Research Director, Assistant Professor, Department of Emergency Medicine, Mount Sinai Medical Center
Background: Preexcitation was defined by Durrer et al in 1970 when he wrote, "Preexcitation exists, if in relation to atrial events, the whole or some part of the ventricular muscle is activated earlier by the impulse originating from the atrium than would be expected if the impulse reached the ventricles by way of the normal specific conduction system only." Of the various preexcitation syndromes, the most common is Wolff-Parkinson-White (WPW) syndrome. Emergency physicians should be familiar with this syndrome and the proper treatment of its associated arrhythmias to avoid unnecessary morbidity and mortality.
Pathophysiology: Accessory connections between the atrium and ventricle are the result of anomalous embryonic development of myocardial tissue bridging the fibrous tissues that separate the two chambers. Although dozens of locations for bypass tracts can exist in preexcitation, including atriofascicular, fasciculoventricular, intranodal, or nodoventricular, the most common bypass tract is an accessory atrioventricular pathway otherwise known as a Kent bundle. This is the anomaly seen in WPW syndrome. Conduction through a Kent Bundle can be anterograde, retrograde, or both.
Frequency:
Internationally: WPW affects approximately 0.15-0.2% of the general population. Of these, 60-70% have no other evidence of heart disease.
Mortality/Morbidity: Death from WPW occurs secondary to the associated arrhythmias, or from mistreatment of these arrhythmias with inappropriate medications. Little data is available regarding the mortality rate of such arrhythmias, but most studies report the incidence of sudden death in the 0-4% range.
Sex: Men are affected to a greater degree (60-70%) than women. Typically, those affected are young, otherwise healthy individuals.
Age: Although this disease affects people of all ages, it is most commonly recognized in children and young adults presenting to the ED with an arrhythmia. Conduction speed in the accessory pathway appears to attenuate with age. CLINICAL Section 3 of 10
History:
Patients may present with anything from mild chest discomfort or palpitations to severe cardiopulmonary distress or arrest. Occasionally, the disease is picked up on routine electrocardiography performed for a reason other than acute cardiac symptomatology.
Patients commonly present with heart rates in the 250 beat/minute range, often with associated hypotension.
Patient usually is aware of his or her cardiac condition, but may be diagnosed in the ED.
Physical: There are no specific examination features of WPW, only those that may accompany the arrhythmias.
On physical examination, the patient may be cool, diaphoretic, and hypotensive.
Crackles in the lungs are common, as the high heart rate causes diastolic heart failure.
DIFFERENTIALS Section 4 of 10
Atrial Fibrillation
Atrial Flutter
Ventricular Tachycardia
Other Problems to be Considered:
Supraventricular tachycardia
Ventricular tachycardia
WORKUP Section 5 of 10
Other Tests:
Electrocardiogram (ECG)
Classically, the ECG morphology of WPW is described as a shortened PR interval, a widened QRS complex, and a delta wave. In reality, however, morphology varies greatly.
Depending upon the location of the accessory pathway in relation to the sinus node and the relative transmission characteristics of the accessory pathway and the atrioventricular (AV) node, the morphology of the ECG may vary from a classic presentation to near normal.
In some cases, the electrical impulse's arrival into the ventricle occurs slightly earlier through the accessory pathway, creating preexcitation.
QRS is widened because the ventricles are initially activated via the accessory pathway outside the normal conducting system in the muscle tissues, producing slow initial forces and a delta wave. This is known as a revealed accessory pathway because it is easily identifiable on ECG.
In other cases, however, arrival of the electrical impulse to the ventricle occurs nearly simultaneously through both the accessory pathway and the AV node.
When this occurs, preexcitation is absent and ECG appears normal.
Thus, morphology of the ECG depends directly upon the degree of preexcitation.
An accessory pathway that does not reveal itself on ECG is revealed when the rate exceeds the refractory period of the AV node. This has been described as latent.
A latent accessory pathway can conduct both anterograde and retrograde.
An accessory pathway in which only retrograde transmission of impulses can occur is called concealed and is utilized only during circus movement tachycardias (CMTs).
Although any type of arrhythmia can occur in a patient with WPW, the two most common are CMTs and atrial fibrillation. CMT is the more common arrhythmia of the two.
CMT typically is initiated by a critically timed, premature, atrial beat that occurs during the refractory period of the accessory pathway. The impulse, therefore, travels solely down the AV node but returns through the accessory pathway, resulting in CMT.
This CMT, termed orthodromic, shows a narrow complex rate limited by the refractory period of the AV node. Complex is narrow, as the impulses travel only antegrade through the AV node, and regular, as circus movement occurs at a regular rate.
Differential diagnosis of this arrhythmia includes paroxysmal supraventricular tachycardia (PSVT), but differentiating the two in an emergent presentation is unnecessary because treatment for both is the same. Adenosine (6 mg rapid IV push; if unsuccessful, follow by 12 mg rapid IV push) blocks the AV node temporarily and interrupts CMT, usually converting the patient to sinus rhythm. Note that an orthodromic CMT is the only common WPW arrhythmia in a patient with a concealed accessory pathway.
Orthodromic CMTs are 10-15 times more likely than antidromic CMTs.
Antidromic CMTs are wide and may potentially be faster because of the relatively short refractory period of most accessory pathways. They are wide because anterograde transmission occurs down the accessory pathway, creating preexcitation of the ventricle adjacent to it, yet they are still regular because of the regular nature of the circus movement.
Differential diagnosis includes ventricular tachycardia (v-tach), which also is regular (unless it is torsades de pointes) or PSVT with aberrancy. Any regular, wide, complex tachycardia should be considered v-tach until proven otherwise, but as in regular, narrow complex tachycardias a stable patient may initially be treated with adenosine.
Most cases of wide complex CMT associated with WPW that are treated with adenosine consequently are converted to sinus rhythm.
Atrial fibrillation in patients with WPW is very common with an incidence of 11-38%. It also is the deadliest arrhythmia for these patients as a result of the possibility of deterioration into ventricular fibrillation (v-fib).
In normal hearts, one is protected from exceptionally high rates by the relatively long refractory period of the AV node. In patients with WPW, however, the accessory pathway often has a much shorter anterograde refractory period, allowing for much more rapid transmission of impulses and correspondingly higher rates.
In addition, sympathetic discharge secondary to hypotension may lead to further shortening of the refractory period and subsequent increase in ventricular rate. If the rate becomes too high, v-fib may result.
Note that atrial fibrillation through an accessory pathway appears as a bizarre, wide-complex, irregular tachycardia on ECG, with rates often in the 250-bpm range or higher.
TREATMENT Section 6 of 10
Prehospital Care: Therapy in the prehospital setting depends upon the patient's degree of stability and the specific arrhythmia.
Emergency Department Care: Upon presentation, immediately place an IV line in the patient and connect him or her to cardiac, blood pressure, and pulse oximetry monitors. Administer oxygen if the patient is hypoxic. A patient who is grossly unstable should be cardioverted immediately. If a patient is in cardiac arrest, treat according to advanced cardiac life support (ACLS) guidelines. Arrhythmias associated with WPW should be treated with caution.
Treatment of atrial fibrillation (a-fib) associated with WPW is necessarily different than for a patient with a normal heart. This is an irregular rhythm as opposed to the regular rhythm seen in CMTs.
Basic treatment principle in WPW a-fib is to prolong the anterograde refractory period of the accessory pathway, relative to the AV node. This slows the rate of impulse transmission through the accessory pathway, and thus the ventricular rate.
If a-fib were to be treated in the conventional manner by drugs that prolong the refractory period of the AV node (eg, calcium channel blockers, beta-blockers, digoxin), the rate of transmission through the accessory pathway would likely increase, with a corresponding increase in ventricular rate. This could have disastrous consequences, possibly causing the arrhythmia to deteriorate into v-fib.
Procainamide (17 mg/kg IV infusion, not to exceed 50 mg/min; hold for hypotension or 50% QRS widening) blocks the accessory pathway, but it will have the added effect of increasing transmission through the AV node. Thus, although it may control the a-fib rate through the accessory pathway, it may create a potentially dangerous conventional a-fib that may require treatment with other medications. Prompt cardioversion of patients with WPW and a-fib is recommended.
Medical management may be a viable option in some patients, but it may have unpredictable results. Note that cardioversion is always the treatment of choice in unstable patients.
Treatment of CMTs associated with WPW is similar to treating PSVT. Focus is on breaking the cyclical transmission of impulses. This is best done by temporarily prolonging the refractory period of the AV node with drugs such as adenosine.
In a stable patient, adenosine (6 mg rapid IV push; if unsuccessful, 12 mg rapid IV push) should be the first line treatment in any regular tachycardia, regardless of whether the complex is wide or narrow.
Once the circus movement is broken, patient usually converts to sinus rhythm. Note that whether the QRS complex is regular or irregular distinguishes between CMTs and atrial fibrillation on ECG.
If the QRS complex is regular, the arrhythmia can be treated safely with adenosine as if it were CMT or PSVT.
If the QRS complex is irregular, the arrhythmia is likely a-fib. In this case adenosine theoretically could increase the rate.
Cardioversion, or in some cases, procainamide, are the treatment choices in these situations (irregular QRS complex), providing the necessary rate control.
If in doubt about the regularity of the rhythm, it is safer to err on the side of treating for a-fib.
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#5808 - 06/28/05 06:18 PM
Re: esophageal spasm
[Re: Patrick Murphy]
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Patrick Murphy
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In response to a message I recieved re: Lidocaine in the above patients. Again, from Emedicine.com:
Atrial flutter/fibrillation or wide-complex tachycardia
Atrial flutter/fibrillation can be recognized by the presence of abnormal QRS complexes and irregular R-R intervals. In this setting, drugs that prolong the refractory period of the bypass tract should be used, especially those that also block the AV node (by prolonging refractoriness). Examples of such drugs include procainamide (class IA agent) and propranolol (class II beta-blocker).
If wide-complex tachycardia is present and the diagnosis of ventricular tachycardia cannot be excluded, the drugs of choice are intravenous procainamide or amiodarone (in lieu of cardioversion if the patient is stable hemodynamically). Ibutilide may also be useful in this setting, although data are lacking.
Importantly, avoid lidocaine in this setting. It does not prolong refractoriness in the accessory pathway. Lidocaine may increase the ventricular response if atrial fibrillation is present.
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. He told me that he didn't see it that day even in a NSR (he found out later) and there was no way I would have seen it with her rate as high as it was. Anyway, a learning experience.
