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Chest Pain and Transient ST-Segment Elevation

EMS was called to an office building for a 61-year-old male complaining of chest pain.

Just prior to EMS arrival the patient became nauseated and lightheaded. When they found him he was lying supine on the floor and appeared ashen.

Onset: 45 minutes ago following a meeting with an important client
Provoke: Nothing makes the pain better or worse
Quality: “Squeezing”
Radiate: The pain does not radiate to the arms, back, neck, or jaw
Severity: 10/10
Time: No previous episodes

He was alert and oriented to person, place, time, and event with a relatively calm demeanor.

Vital signs were assessed.

RR: 24 (mildly labored)
HR: 60 (weak radial pulses)
NIBP: 87/40
Temp: 98.4°F
SpO2: 95% on room air

Breath sounds were clear bilaterally.

His medical history was remarkable only for hypertension and high cholesterol. He was unable to recall the names of his medications.

A 12-lead ECG was acquired.

ST-segment elevation is present in leads V2-V5 and the T-waves are hyperacute. It is unclear why the computer is not giving the *** MEETS ST ELEVATION MI CRITERIA *** message. This does not look like early repolarization or hyperkalemia.

Then about two and a half minutes later…

We now have R-on-T PVCs, almost in bigeminy. The ST-segment elevation has resolved but the T-waves are still disproportionately large compared to the QRS complexes.

The treating paramedic correctly suspected that the patient was suffering an acute coronary syndrome, but there was uncertainty about whether or not it was a STEMI.

The patient was treated with aspirin and IV fluids for hypotension. The closest hospital was bypassed and the patient was transported to a PCI-hospital about 25 minutes away.

About 7 minutes later the patient’s blood pressure had improved to 102/69 but he was still complaining of 10/10 chest pain.

The ST-segment elevation has returned and the T-waves are unambiguously hyperacute. The computerized interpretive statement now reads *** MEETS ST ELEVATION MI CRITERIA ***

The ECG was transmitted to the hospital, IV fluids were continued, and 0.4 mg sublingual nitroglycerin was administered q 5min PRN, with moderate alleviation of the patient’s chest pain.

Vital signs were re-assessed.

RR: 20
HR: 64
NIBP: 114/76
SpO2: 98% on room air

About fifteen minutes later this 12-lead ECG was acquired.

Once again the ST-segment elevation has resolved but there are still some troubling findings. R-wave progression has been obliterated and the T-waves are still disproportionately large when compared to the QRS complexes.

The ECG continued to show dynamic ST-segment and T-wave changes but they were mostly resolved by arrival at the hospital. The attending physician was waiting and there was some hesitation about sending the patient straight to the cardiac cath lab.

Before the patient could be moved from the paramedic’s stretcher the cardiac monitor automatically printed another 12-lead ECG.

The ST-segments and T-waves are back “on the way up” and once again the computer is giving the *** MEETS ST ELEVATION MI CRITERIA *** statement.

The cardiac cath lab was activated. Angiography revealed a 99% occlusion of the proximal left anterior descending artery (LAD), which was stented.

Discussion Points

1.) Obtain a 12-lead ECG with the first set of vital signs!

Myocardial infarction is a dynamic disease process. Coronary arteries can become totally occluded, partially reperfused, and totally occluded again!

There are case reports demonstrating resolution of ST-segment elevation after administration of nitroglycerin.¹ Stephen Smith, M.D. (@SmithECGBlog) writes about it here. Tom Bouthillet (@tbouthillet) writes about it here. Brooks Walsh, M.D (@BrooksWalsh) writes about it here and questions whether it’s really due to nitroglycerin here.

2.) Should transient STEMI be sent directly to the cardiac cath lab?

The short answer is probably.

This hasn’t been widely studied but there is literature to support early activation of the cardiac cath lab when dealing with transient STEMI. One study published in Annals of Emergency Medicine concluded that positive serial ECGs were more sensitive and more specific for identifying ACS patients who require anti-ischemic therapy, evaluation for reperfusion, and/or admission to an ICU.²

Articles in Prehospital Emergency Care and American Heart Journal show that while patients with transient STEMI were likely to have less myocardial damage, higher rates of thrombolysis, and better cardiac function, they still benefit from early invasive therapy.^3,4

Check out this post from Stephen Smith, M.D. for an example of what can go wrong if you don’t send them for PCI!

3.) What is the significance of hyperacute T-waves?

T-waves corresponding with myocardial injury become taller, wider, and more symmetrical in morphology — a phenomenon referred to as “hyperacute T-waves”.

Hyperacute T-waves are the most reliable indicator of salvageable myocardium at risk!

Hyperacute T-waves are considered to be a STEMI equivalent even when the conventional mm criteria are not met. Look for these changes both as the ST segments are “on the way up” and “on the way down.”

4.) What’s the significance of those PVCs?

Patients suffering an acute myocardial infarction are at increased risk of developing lethal arrhythmias. Ischemic myocardium is “irritable” and the presence of PVCs may be a helpful prognostic indicator.

Proximity of PVCs to the preceding T-waves (“R-on-T” PVCs) present a greater risk that the patient will develop VT or VF as premature depolarization occurs during the relative-refractory period of the previous cardiac cycle.

5.) What is the significance of bradycardia in LAD/LCX occlusion?

This patient was unable to provide the names for his antihypertensive medication so it’s likely that he was prescribed a beta blocker or calcium channel blocker.

A less likely possibility is that there was ischemia of the SA node brought about by repeated occlusion/reperfusion of the circumflex artery.

This has been found in case reports and animal studies to cause transient episodes of sinus bradycardia, even though sinus bradycardia is more typical of acute inferior STEMI (RCA occlusion). ^5,6

References
1) Mahoney BD, Hildebrandt DA, Allegra P. Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. Prehospital Emergency Care 2008;15:105, Abstract 24
2) Fesmire FM. Usefulness of Automated Serial 12-Lead ECG Monitoring During the Initial Emergency Department Evaluation of Patients With Chest Pain. Ann Emerg Med 1998;31(1):3-11
3) Ownbey M. et al. Prevalence and interventional outcomes of patients with resolution of ST-segment elevation between prehospital and in-hospital ECG. Prehosp Emerg Care 18(2);174-9. Apr-Jun 2014
4) Meisel SR, et al. Transient ST-elevation myocardial infarction: clinical course with intense medical therapy and early invasive approach, and comparison with persistent ST-elevation myocardial infarction. Am Heart J 155(5):848
5) Lin, C.-F., & Cheng, S.-M. (2006). Symptomatic Bradycardia due to Total Occlusion of Left Circumflex Artery without Electrocardiographic Evidence of Myocardial Infarction at Initial Presentation. Texas Heart Institute Journal,33(3), 396–398.
6) William A. Alter, III, PH.D., Robert N. Hawkins, PH.D., and Delbert E. Evans. Etiology of the Negative Chronotropic Responses to Transient Coronary Artery Occlusion in the Anesthetized Rhesus Monkey. Circulation. 1978;57:756-762

Syncope with Acute Inferior STEMI and 3 Different AV Blocks

This is a case from the “old days” when prehospital 12-lead ECGs were still a bit of a novelty. Many of the details have been lost to time but patient’s heart rhythms will be the focus of this review.

The patient was a young woman in her late 40s who presented with syncope while playing tennis. Syncope during exercise is troubling and suggests a possible cardiac cause, which is potentially life threatening.

EMS arrived on scene and obtained a detailed history. The woman admitted to some chest discomfort. Vital signs were assessed and the cardiac monitor was attached.

The initial ECG showed second degree AV block with 2:1 conduction.

This is often called second degree AV block type 2 with 2:1 conduction but second degree AV block with 2:1 conduction is untypeable.

There appears to be an acute injury pattern even though the rhythm strip is recorded in ‘monitor’ mode with the low frequency / high pass filter set to 1.0 Hz.

A few minutes later a rhythm change was noted on the monitor.

Now the rhythm is third degree AV block with junctional escape rhythm. The atrial rate is about 60 and the ventricular rate is 41.

(The initial 12-lead ECG showed poor data quality but paramedics understood that the patient was suffering acute STEMI.)

Aspirin was given and an IV was started. Nitroglycerin was also given and the patient became hypotensive.

Remember, this case is over 10 years old. At that time there was a lot less emphasis on things like right ventricular infarction and the cardiac cath lab was not activated based on the prehospital 12-lead ECG.

0.5 mg atropine was given rapid IVP and another 12-lead ECG was obtained.

The atrial rate has doubled to about 125. The ventricular rate has increased modestly to about 47. The ECG is diagnostic for acute inferior-posterior STEMI.

On arrival in the Emergency Department the staff obtained their own 12-lead ECG.

Now the heart rhythm is second degree AV block type 1 (Wenckebach).

How can you tell? In the first place we see clustering of QRS complexes (huge tip-off) and we already know that AV conduction is precarious. The initial cardiac cycle of each cluster shows a constant PR-interval.

When we take a closer look at the rhythm strip we see progressive prolongation of the PR-interval until a P-wave is “dropped” proving that the heart rhythm is second degree AV block type 1 (Wenckebach).

The ECG shows worsening of the ST-segment elevation. The patient was sent to the cardiac cath lab. As far as I know she made a full recovery.

Discussion

Heart blocks in the setting of acute STEMI can result either from ischemia of the AV node or increased parasympathetic tone, which is a manifestation of the Bezold-Jarisch reflex.

Consider these excerpts from Braunwald’s Heart Disease (Fifth Edition). It’s an old book but it contains some interesting information.

“The AV conduction system has a dual blood supply, the AV branch of the RCA and the septal perforating branch from the LAD. Therefore, complete heart block can occur in patients with either anterior or inferior infarction. Complete heart block develops in 5 to 15% of all patients with AMI; the incidence may be even higher in patients with RV infarction. As with other forms of AV block, the prognosis depends on the anatomical location of the block in the conduction system and the size of the infarction.”

“Complete heart block in inferior infarction usually results from an intranodal or supranodal lesion and develops gradually, often progressing from first degree or type I second degree block. The escape rhythm is usually stable without asystole and often junctional, with a rate exceeding 40 beats/min and a narrow QRS complex in 70% of cases and a slower rate and wide QRS in the others […] The mortality may approach 15% unless RV infarction is present, in which case the mortality associated with complete AV block may be more than doubled.”

“[P]atients with inferior MI and AV block have larger infarcts and more depressed right ventricular and left ventricular function than do inferior infarcts with no AV block. As already noted, junctional escape rhythms with narrow QRS complexes occur commonly in this setting…”

“Only when complete heart block develops in less than 6 hours after the onset of symptoms is atropine likely to abolish the AV block or cause acceleration of the escape rhythm. In such cases the AV block is likely to be transient and related to increases in vagal tone rather than the more persistent block seen later in the course of MI, which generally requires cardiac pacing.”

Wide Complex Tachycardia Treated With Amiodarone and Synchronized Cardioversion

A 55 year old male presents to EMS with complaint of intermittent shortness of breath.

Symptom onset occurred while he was taking his daily walk about 15 minutes prior to EMS arrival.

The patient has a Glasgow Coma Score of 15, with a patent airway, clear lung sounds, and mild respiratory distress. Strong and regular bilateral radial pulses are noted, with no obvious signs of hypoperfusion.

The following medical history is reported:

Hypertension
Coronary artery disease
2 coronary stents of unknown location
Occasional smoking and alcohol consumption

Medications include metoprolol, nitroglycerin tablets, and daily supplements.

Vital signs are assessed.

RR: 25
HR: 62
NIBP: 141/91
SpO2: 99% on room air
BGL: 97 mg/dL

The patient is placed on the cardiac monitor.

Normal sinus rhythm with flattened T waves. Otherwise, nothing alarming.

A few seconds later the patient complains of acute shortness of breath, while the initial 12 lead ECG is obtained.

The following questions come to mind:

What is the rhythm?
Could this be the cause of the sudden onset of shortness of breath?
Is the patient stable or unstable?
What will your treatment consist of?

We should note that there is a regular Wide Complex Tachycardia (WCT) which should be presumed to be Ventricular Tachycardia (VT) until proven otherwise. You may or may not have time to fully scrutinize the ECG depending on the patient status.

A regular WCT should be presumed as VT until proven otherwise!

One important reason this should be our train of thought is that VT is less likely to be tolerated by a patient with a cardiac history or structural heart disease compared to a younger individual without these mitigating factors.

Three main possible causes of WCT should be considered:

VT
SVT with aberrancy (i.e. reentry tachycardia with a Bundle Branch Block)
Antidromic AVRT (requires an accessory pathway)

There are multiple criteria to differentiate VT from SVT with aberrancy. The two conditions can be difficult to distinguish and in some cases, impossible.

Findings considered supportive of VT:

Structural heart disease or previous myocardial infarction
An extremely wide QRS complex > 160 ms (0.16s)
The presence of AV dissociation
The presence of fusion and captured beats
QRS concordance in the precordial leads (i.e., all negative or all positive)
Extreme Right Axis Deviation (ERAD)
However, the absence of ERAD does not rule out VT
Wellens, Brugada, or Verekei’s Criteria (outside the scope of this case study)

Let’s take a look at the same ECG again with some highlighted points.

There is a very broad QRS of at least 180 ms (0.18s)
Extreme right axis deviation is noted at -176 degrees
Ventricular complexes outnumber atrial complexes by a 2:1 ratio (marked with red circles)
There is a monophasic R wave in lead V1

All of these findings support the diagnosis of ventricular tachycardia, but again, VT should be your default diagnosis!

Oxygen was given via nasal cannula @ 3 LPM, IV access was established, defibrillation pads were placed, and 150 mg amiodarone drip was started.

A few seconds after starting the amiodarone drip the patient reported relief of shortness of breath and the following 12-lead ECG was recorded.

Normal sinus rhythm with left anterior fascicular block and right atrial enlargement.

Approximately 4 minutes later the shortness of breath returned along with substernal chest pressure.

The patient is back in ventricular tachycardia but with a slower rate due to the amiodarone.

The presence of one or more of the following qualifies a patient as unstable.

Hypotension
Ischemic chest pain
Dyspnea
Pulmonary edema
Altered mental status

The patient was given 2 mg of midazolam and synchronized cardioversion was performed @ 100 J which converted the patient back to sinus rhythm. The amiodarone drip was completed and the patient’s symptoms were completely resolved by arrival in the emergency department.

Discussion

Consider this recommendation from the 2010 AHA ECC Guidelines (unchanged in 2015):

“For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy. If IV antiarrhythmics are administered, procainamide (Class IIa, LOE B), amiodarone (Class IIb, LOE B), or sotalol (Class IIb, LOE B) can be considered. Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation (Class III, LOE B). If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered (Class IIa, LOE C).”

Although procainamide, lidocaine and sotalol are proven to be effective and even preferred by some clinicians, amiodarone (Class III antiarrhythmic with potassium, calcium, and sodium channel blocking properties) remains the primary antiarrhythmic agent in the prehospital setting for wide complex tachycardia.

Adenosine can be used initially for stable regular wide complex tachycardia. This is because a WCT caused by SVT with aberrancy (and right ventricular outflow tract ventricular tachycardia) are responsive to adenosine.

Synchronized Cardioversion is the preferred treatment for unstable WCT.

Conclusion

Wide complex tachycardia should be treated as ventricular tachycardia until proven otherwise
Stable WCT can be addressed with antiarrhythmic agents or synchronized cardioversion
Administration of multiple antiarrhythmic agents should be avoided without expert consultation
Treatment of unstable WCT should be synchronized cardioversion
Synchronized cardioversion is acceptable and avoids some of the pitfalls of antiarrhythmic infusion

Reference
Neumar R, Otto C, Link M et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18_suppl_3):S729-S767. doi:10.1161/circulationaha.110.970988.

How to Master Tracheal Intubation

According to the 2000 AHA ACLS Guidelines, tracheal intubation should only be attempted “by healthcare providers experienced in performing this skill”, and expand further by stating that “ALS providers unable to obtain regular field experience… should use alternative, noninvasive techniques for airway management”. This year ILCOR examined evidence to determine if one airway is superior to another in terms of survival and neurologic outcome in cardiac arrest. According to the evidence summary “there is inadequate evidence to show a difference in survival or favorable neurologic outcome”, and recommend that the “choice of bag-mask device versus advanced airway insertion, then, will be determined by the skill and experience of the provider”. The clinician must have sufficient initial and continuing education for whatever airway they choose, and must effectively do so while limiting interruptions in quality CPR.

Some EMS services have demonstrated a 99% success rate for endotracheal intubation, but they probably make up a very small percentage of EMS providers that achieve such proficiency. So why do so many people struggle? The cause of difficulty with skill acquisition is multifactorial, but anecdotally, what I have found from interviewing many students is that their initial education was full of dogma that inevitably left them unprepared to manage difficult airways.

I started my personal airway endeavor with mixed results. When I did successfully place the tube in the trachea, it was usually after several attempts, sweaty palms, and multiple prayers. I thought I knew what I was doing, but had no clue. Once I placed the blade in the mouth, I found structures yet to be defined. So, I took advice from everyone, and was always given different pointers, but nothing worked. Eventually I came to terms with my meager ability to intubate. I accepted the fact that I sucked at laryngoscopy, and the patient would benefit from a supraglottic airway instead of my repeatedly damaging attempts.

Then, at some point I started browsing different blogs, videos, and articles. What I found was that almost all of the airway experts recommend the same basic approach and technique, and nearly all of what others suggested was wrong! I don’t claim to be an expert, but now I approach the airway with confidence knowing what I’m doing is right. I no longer blindly insert the blade only to find unrecognizable tissue, but can actually identify crucial landmarks.

What is the best blade size?

What not to do: Use a Mac 4 on everyone. If the blade is too long, simply back out.

What you should do: While sometimes appropriate, a Mac 4 is not always the best choice for every patient. Novices tend to advance too far, bypassing critical landmarks in the process. A Mac 3 blade is typically long enough for a large majority of adults. A Mac 3 also allows you to lift the tongue and mandible with LESS force than a Mac 4. This video demonstrates the “mechanical disadvantage” of a longer blade.

How do I position the patient?

What not to do: Hyperextend the neck

What some people consider this sniffing position is neck and head extension. I’ve witnessed some people pulling the patient up to the head of the stretcher and letting the head to drop off the edge. This makes the airway more anterior, and intubation more difficult. Dr. Scott Weingart calls this the “bad sniffing position”.

What you should do: Place the patient in the Ear-to-Sternal-Notch position with the face plane parallel to the ceiling.

In this position there is flexion of the neck, and extension of the head (figure 1). The laryngeal axis, pharyngeal axis, and mouth are appropriately in line with the operator’s vision (figure 2). To obtain this position, simply elevate or “ramp” the shoulders and head until the ear-hole is in line with the sternal notch (ramping is particularly useful in obese patients). Position the face on a horizontal plane. This is easily achieved with blankets, pillows, or a combination of both and raising the head of the stretcher.

Figure 1: Copyrighted by Airway Cam Technologies, Inc. (Source: http://www.airwaycam.com/airway-images-drawings)

Figure 2. Source: http://www.ojhas.org/issue38/2011-2-16.htm

How do I shape the stylet?

What not to do: Use an arcuate (curved) shape to follow the contour of the tongue.

An arcuate shaped stylet frequently obstructs the line of sight, and can make it difficult to manipulate to tip of the tube towards the pharynx.

What you should do: Instead, shape the stylet and ETT straight to the cuff, and then bend the remaining length at 30-35 degrees—much like a hockey stick (figure 3). This allows you to enter from the right side of the mouth, and easily manipulate the tip of the ETT toward the glottic opening. Dr. Richard Levitan demonstrates why straight-to-cuff shaping is superior.

Figure 3

How do I control the tongue?

What not to do: Insert the blade to the right, and sweep the tongue to the left.

What you should do: As stated before, a common error of most novice clinicians is they miss the landmarks. The most important landmark by far is the epiglottis. Dr. Richard Levitan, known by many as an airway pioneer, said:

“Novice laryngoscopists commonly advance the blade too aggressively, succumb to epiglottis camouflage, and become lost in the pink mucosa of the esophagus with no idea of what they are looking for or how to fix the problem.”

Instead, he recommends inserting the tip of the blade midline, and in very short, methodical movements, slowly advance the blade in a progressive fashion until the edge of the epiglottis is visualized, then gently slide the tip into the vallecular fossa. Dr. Levitan refers to this as epiglottoscopy.

With the tip of tip of the blade properly positioned, the epiglottis can then be lifted via the hyoepiglottic ligament.

If the epiglottis has been identified, enough force must be applied to successfully lift the epiglottis off the pharynx. Often we’re taught to look for the “vocal cords,” but in reality they may be hidden in darkness and not easily identifiable. The only landmark one has to identify is the interarytenoid notch (Figure 4). Once it’s identified, the ETT can be placed anteriorly into the trachea.

Figure 4: Sourced from Wikimedia Commons

I still don’t have a good view. Now what?

What not to do: Use cricoid pressure to improve your view.

Cricoid pressure does not always compress the esophagus, and can actually displace the larynx making intubation even more difficult. There are more novel methods to improve laryngeal exposure.

What you should do: External Laryngeal Manipulation (ELM) – Also known as bimanual laryngoscopy, ELM involves using the operator’s free hand to manually manipulate the thyroid cartilage. Holding the laryngoscope in the left hand, the operator then reaches around and manipulates the thyroid cartilage with his or her right hand, and moves it back, up, or sided to side to improve the view. Once the structures are visualized, an assistant can take over ELM, and the laryngoscopist can verbally express which way the assistant should manipulate the larynx (Figure3). This is NOT BURP (Backward, upward, rightward pressure) or cricoid pressure.

Head Elevated Laryngoscopy Positioning (HELP) – Maybe counterintuitive to some who “hyper-extend” the neck, elevating the head can result in an improved laryngeal view when compared to the “normal” sniffing position. Hochman et. al. concluded that:

“Increasing head elevation and laryngoscopy angle (neck flexion) significantly improves POGO scores during laryngoscopy on fresh human cadavers.”

Held elevation can be performed by an assistant who elevates the head beyond the ear to sternal notch position and decreases the angle between the patients chin and their chest.

How do I confirm tube placement?

The answer to this question is and should be unequivocally continuous waveform capnography. With a sensitivity and specificity of 100% reported by some studies, initial confirmation as well as continuous monitoring should be performed using waveform capnography. This sensitivity could be less in circumstances such as massive pulmonary embolism, or prolonged cardiac arrest, but these are most certainly rare exceptions. Clinical assessment is still key and should be relied on to ensure placement is not in the right main stem.

In summary:

Preparation
a. Select the right blade size.
b. Shape the stylet and ETT straight to the cuff, then bend at a 30-35 degree angle.
c. Properly position the patient Ear-to-Sternal-Notch with face plane parallel to ceiling.
Epiglottoscopy
a. Progressively and methodically advance the tip of the blade midline and gently seat in the vallecula.
Laryngeal Exposure
a. If the view is still not optimal, consider trying ELM, or HELP to improve visualization.
Tube Delivery
a. Using straight-to-cuff shaping, insert near the right corner of the mouth and advance upward.
b. Pass the tip anterior to the interarytenoid notch.
c. Ensure the cuff of the tracheal tube is below the level of the cords.
Tube Confirmation and Maintenance
a. Direct visualization
b. Absent sounds over the epigastrium
c. Equal bilateral breath sounds
d. Good compliance with the BVM
e. Tube fogging (never primary)
f. Continuous waveform capnography (for confirmation and maintenance)
g. Rising SpO2 (for patients with a pulse)

References
http://www.ncbi.nlm.nih.gov/pubmed/12605198
King County 2013 Annual Report. Weblog post. Kingcounty.gov. N.p., n.d. Web. 7 Nov. 2015.
Levitan, Richard M. The Airway Cam Guide to Intubation & Practical Emergency Airway Management. Wayne, PA: Airway Cam Technologies, 2004. Print.
Levitan, Richard. “Head Elevated Laryngoscopy Position.” H Ead-Elevated Laryngoscopy Position: Improving Laryngeal Exposure During Laryngoscopy by Increasing Head Elevation (n.d.): n. pag. Web. 8 Nov. 2015.
Nickson, Chris. “ETT Stylet | LITFL: Life in the Fast Lane Medical Blog.” LITFL Life in the Fast Lane Medical Blog. N.p., n.d. Web. 08 Nov. 2015.
Nickson, Chris. “Cricoid Pressure.” LITFL Life in the Fast Lane Medical Blog. N.p., n.d. Web. 08 Nov. 2015.
Rogers, Joe. “NOVEL TIPS FOR AIRWAY MANAGEMENT – Emdocs.” Emdocs. N.p., 30 Dec. 2014. Web. 08 Nov. 2015.

Treating Supraventricular Tachycardia with Adenosine

EMS is called to a local medical clinic for a 53 year old female complaining of weakness and palpitations.

Symptoms started earlier in the day at tennis camp. The patient experienced one other episode about 2 years prior that proved to be self-limiting.

She takes no medications and has no known drug allergies.

The patient appears anxious but is oriented to person, place, time, and event.

Vital signs are assessed:

HR: 200
NIBP: 134/102
RR: 18
Temp: 98.4 F
SpO2: 95% on RA
BGL: 88

A 12-lead ECG is obtained by paramedics.

A rhythm strip is also recorded.

Paramedics note a regular narrow complex tachycardia at a rate of about 200/min.

Could this be sinus tachycardia?

It is doubtful. There are no visible P-waves. In addition, the maximum theoretical sinus rate is 220 minus age (plus or minus 10%). For this patient that works out to somewhere between 167 and 184.

Vagal maneuvers are attempted but are unsuccessful.

As a side note, the REVERT Trial which was published this year introduced a postural modification (leg elevation and supine positioning) to the standard Valsalva maneuver for the treatment of SVT which returned 40% of patients to sinus rhythm compared with 17% for the standard Valsalva maneuver.

You can watch a video of the technique here: https://www.youtube.com/watch?v=8DIRiOA_OsA

In this case, an IV is started and 12 mg of adenosine is given rapid IV push followed by a 20 ml syringe bolus of 0.9% normal saline.

The rhythm is successfully converted and another 12-lead ECG is obtained.

It should be noted that modest nonspecific ST/T wave abnormalities are not uncommon immediately following the conversion of SVT to sinus rhythm. The main determinant of myocardial oxygen demand is heart rate!

Take-away points

The maximum theoretical sinus rate is 220 minus age (plus or minus 10%).

Adenosine should be used for regular tachycardias only! It can be dangerous in the setting of atrial fibrillation and Wolff-Parkinson-White Syndrome.

Record a 12-lead ECG whenever possible prior to treating a narrow complex tachycardia with adenosine. It can be helpful later on when the patient is referred to a cardiologist or electrophysiologist.

Consider a postural modification (leg elevation and supine positioning) to the Valsalva maneuver to improve the conversion rate.

Consider applying defibrillation pads prior to the administration of adenosine.

The drugs Dipyridamole (Persantine) and Carbamazepine (Tegretol) can potentiate adenosine.

Accepted or your money back.