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.”
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.
Artifact on the electrocardiogram can result from a variety of internal and external causes from Parkinsonian muscle tremors to dry electrode gel.
Most of the time it will be obvious that you are dealing with artifact and troubleshooting the problem will be straight forward. However, there are occasions when artifact mimics ECG abnormalities that can cause problems for patient care.
Once when I was a cardiac monitoring technician the alarm sounded and it appeared as though ventricular tachycardia was on the monitor. When we rushed to the patient’s room it turned out she was brushing her teeth!
With a trained eye you can often learn to spot the underlying rhythm “marching” through this type of artifact. Other times it’s not that easy (PDF).
Here are some types of artifact you may encounter along with some tips to help you achieve excellent data quality on your ECG tracings.
Loose lead artifact
You will frequently encounter loose lead artifact when dealing with patients who are diaphoretic because the electrodes simply will not stick to the patient’s body. You may also see this type of artifact when placing the electrode over hair.
To troubleshoot this problem make sure you prep the skin carefully!
Consider tincture of benzoin. It works great for diaphoretic patients. However, tincture of benzoin is flammable! You don’t want to use it for defibrillation pads.
In this example loose lead artifact can be seen in leads I and II.
What electrode do leads I and II have in common?
Lead I is a dipole with the negative electrode on the right arm and the positive electrode on the left arm.
Lead II is a dipole with the negative lead on the right arm and the positive electrode on the left leg.
Lead I and lead II share the right arm electrode! That is the electrode that is causing this problem.
Wandering baseline artifact
Wandering baseline artifact presents as a slow, undulating baseline on the electrocardiogram. It can be caused by patient movement, including breathing.
I have also noticed that stopping or accelerating the ambulance can cause wandering baseline. Some references suggest that wandering baseline can be caused by loose or dry electrodes.
Some paramedics ask patients to hold their breath while they capture a 12-lead ECG. I don’t do this because it can alter the patient’s heart rate.
There are times when your patient is acutely short of breath and it’s simply impossible to capture a 12-lead ECG with excellent data quality.
Muscle tremor artifact
Muscle tremor (or tension) artifact is a type of motion artifact. Usually it’s happening because your patient is cold and shivering. However, it can also happen when patients prop themselves up by their arms.
The example below was obtained from a young, healthy firefighter during routine training. It was cold in the fire station and he was shivering.
The next example was taken after a large towel was placed over the firefighter. It made quite a difference didn’t it?
Electromagnetic interference (EMI)
Electromagnetic interference (EMI) artifact usually results from electrical power lines, electrical equipment, and mobile telephones. In the United States this is sometimes referred to as 60 cycle interference (or 60 Hz pickup).
Creative Commons: ECGGuru.com
To help minimize 60 cycle interference you can set the diagnostic mode of your 12-lead ECG monitor to 0.05 – 40 Hz. As long as the low frequency / high pass filter (the lower number) is set to 0.05 Hz you should get accurate ST-segments.
My department has been doing this for so long that I don’t have any good examples of 60 cycle interference!
CPR compression artifact
This ECG was automatically recorded during a cardiac arrest.
The wavy line after the shock is CPR artifact. Using the small block method (1500/13=115) we can determine that the compression rate was about 115/min. which is perfect!
There may be times when CPR artifact makes it difficult to determine the underlying rhythm. However, if you’re performing CPR at a 30:2 compression to ventilation ratio you can see the underlying rhythm during ventilations!
Neuromodulation artifact
Here’s a type of artifact we’re starting to see more frequently as implantable neurostimulators become more prevalent.
These devices are used to treat a variety of symptoms including tremors, seizures, chronic pain, nausea and vomiting related to gastroparesis, problems with bladder or bowel control, visual impairment, and hypertension.
If you see artifact that looks like this you should ask your patient if he or she has any implantable medical devices. Some devices can be temporarily turned off with a magnet but you should consult with the prescribing physician.
Echo distortion artifact
This type of artifact is associated with transcutaneous pacing (TCP). Echo distortion causes a pseudo-QRS complex after the pacing spike which is sometimes referred to as “false capture.”
The pacing spike is a graphical representation that electrical current is about to pass between the pacing pads. It is followed by a short “blanking period” of about 40 ms (one small block) where the monitor essentially “closes its eyes”. If it did not, the signal would go right off the ECG paper!
After the blanking period the monitor “opens its eyes” to see the QRS complex that is created by the pacing stimulus. However, sometimes the monitor catches the pacing current as it returns to baseline causing a pseudo-QRS complex on the ECG.
You can read more about the problem of false capture here.
Arterial pulse tapping artifact
This unusual artifact causes large, bizarre T-waves on the ECG. The phenomenon was first reported in 2005 by Özhan et al. as a “bizzare electrocardiogram” thought to be associated with abnormal left ventricular motion.
Subsequent work by Aslanger solved the issue in favor of arterial pulse tapping (which explains why the artifact occurs synchronously with the cardiac cycle on the ECG.)
Consider these two ECGs which were recorded from the same patient less than 1 minute apart. The first ECG shows simple motion artifact in leads I, III, and aVL.
Courtesy of Frank Intessimoni (@njmedic3228)
The second ECG shows large, bizarre T-waves that were concerning to the paramedics on the call.
Courtesy of Frank Intessimoni (@njmedic3228)
You will note that the artifact is most pronounced in leads I, II, and aVR. Lead III appears perfectly normal. This suggests that the right arm electrode was placed over the radial artery.
But if that’s true why is there also artifact in other leads?
Aslanger explains:
“[O]ne may expect that the leads not connected to the electrode affected by the source of disturbance would be free of distortion; but this is not the case. When one of the limb electrodes is affected by a source of disturbance, it distorts not only the corresponding derivation but also [the others] which are all calculated by mathematical equations…”
“…precordial leads [are also affected] because the Wilson central terminal, which constitutes the negative pole of the unipolar leads, is produced by connecting 3 limb electrodes via a simple, resistive network to give an average potential across the body.”
References Aslanger E, Yalin K. Electromechanical association: a subtle electrocardiogram artifact. Journal of Electrocardiology. 2012;45(1):15-17. doi:10.1016/j.jelectrocard.2010.12.162.
Aslanger E, Bjerregaard P. Mystery of “bizarre electrocardiogram” solved. Journal of Electrocardiology. 2011;44(6):810-811. doi:10.1016/j.jelectrocard.2011.04.001.
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)
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.
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.
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%).
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.
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