Jordan Goulding on tachydysrhythmias
Join us as we discuss the simplest, most important things you need to know for your next heart racing encounter
There is a wide differential when interpreting EKGs, and an even wider differential when thinking about the causes of these interpretations. A fast rhythm can be SVT, afib with RVR, v-tach, polymorphic v-tach, sinus tach or it can be artifact from a moving ambulance.
We are honored to be joined on this episode of the American Ambulance EMS Podcast by Jordan Goulding, an EMT with American Ambulance. Jason has also had the privilege of working as a field training officer, as well as being a member of the peer support team, which is a system for providers to seek help in the field.
Tachydysrhythmia: Case report
Jordan responded to call from an urgent care office for an elderly gentleman who initially presented with generalized weakness. The provider met him at the door, and explained the gentleman had had several near-syncopal episodes throughout the day without a history of similar symptoms. The provider then handed him an EKG which was wide, regular and fast. Jordan recognized this as monomorphic ventricular tachycardia.
The patient appeared well on initial evaluation. He had a faint pulse, was alert and conversational. When he stood, he became very pale, diaphoretic, and again experienced near syncope. Jordan immediately placed pads on the patient, however was able to auscultate a systolic blood pressure of about 98.
Jordan’s partner did a great job of explaining the next steps to the patient as they wheeled him out to the ambulance and prepared for cardioversion. They gave him 4 mg IV Versed x 2 (this was a larger patient), and attempted synchronized cardioversion. The first attempt did not work. They increased the voltage and tried synchronized cardioversion again. This resulted in an irregular rhythm, which appeared to be a sinus rhythm with frequent PVCs. They initiated 150 mg Amiodarone bolus, and by the time they arrived to the hospital, the patient was in a normal sinus rhythm.
Epidemiology of tachydysrhythmia
We want to keep things simple. Remember the basics with arrhythmias: stable or unstable? Stable means you have time and you have medications. An unstable patient gets electrical cardioversion/defibrillation. Don’t be afraid to use electricity in these patients.
According to studies, there are fewer than 200,000 cases in the U.S. each year of ventricular tachycardia, more common in patients over age 60.
Narrow and regular
Sinus tachycardia is the most common type of tachycardia. This is defined by: a P wave before every QRS, and a QRS after every P. This sounds simple, but can be subtle and difficult to distinguish with fast heart rates. Typically, sinus tachycardia can range from a rate of 100-150. Rates higher than this may still be sinus tachycardia, but we should also be thinking about other things beyond this rate.
Sinus tachycardia can be caused by a number of underlying pathologies. Hypotension or shock, infection, MI, PE, pneumonia, pneumothorax, pain, ingestion, intoxication, just to name a few. Management of this rhythm involves diagnosing and treating the underlying cause.
Supraventricular tachycardia is the next narrow complex, regular rhythm. Technically, any narrow complex tachycardia is “supraventricular”, which means it starts anywhere above the atrium, that’s why it’s narrow. But, when we say “SVT”, we often mean a re-entrant tachycardia that is not following the normal electrical pathway of the heart.
SVT is differentiated on EKG by identifying narrow QRS without obvious P waves preceding. These P waves can be present, however are often retrograde or buried. The rates associated with SVT are often 160 or higher. Rates slower than this should prompt consideration of other rhythms, like a fast sinus tachycardia. Again, there are a number of etiologies for SVT, some common ones include: stress, shock, heart failure, thyroid disease, alcohol use and stimulant use.
Management of SVT is the same as other arrhythmias, differentiating stable versus unstable in the key. For an unstable patient, which is defined by an arrhythmia associated with hypotension, altered mental status, severe chest pain, shortness of breath, loss of consciousness, diaphoresis, you should consider electrical synchronized cardioversion.
For stable patients, there are several options for “breaking” SVT. The Valsalva maneuver is a way to temporarily slow SA nodal activity and AV nodal conduction by stimulating vagus nerve activity. Patients must be cooperative enough to comply, however there are several methods. A carotid massage may be attempted, but this has generally fallen out of favor. Placing ice water on a patient’s face can also stimulate a valsalva response. This is easier done in children. Another technique involves laying supine while exhaling against resistance and lifting the patient’s legs in the air.
When these techniques don’t work, adenosine is a medication that also slows the SA node and AV nodal conduction. This drug needs to be administered very rapidly, in a proximal IV, within 1 to 2 seconds, followed by a normal saline flush. Lift the patient’s arm in the air and inject as fast as possible. The initial dose is 6 mg, followed by 12 mg if not successful. You should prepare your patients for what is about to happen. Often, patients feel as though they are going to die. Medical textbooks write the patient will experience “impending sense of doom.” The most common side effects are facial flushing, shortness of breath, palpitations, chest pain, and lightheadedness. Transient asystole is also possible.
Try to save a rhythm strip for the hospital staff if possible. It’s helpful to show the staff the initial rhythm and how it changed with any intervention you did. Treating SVT in the prehospital setting has been shown to be safe and effective. In a large study performed in Australia including 933 prehospital patients, paramedics correctly identified SVT in 119/123 (97%) of patients. There were 273/882 (31%) patients who spontaneously reverted while in paramedic care. Valsalva maneuver was undertaken by 212/882 (24%) patients and converted the patient successfully in 99/358 (28%) attempts. Verapamil was administered to 38/882 (4%) patients and converted 33 (87%). Synchronised cardioversion (70 J) converted four patients at first attempt. Ultimately, 438 (50%) patients remained in SVT on arrival at hospital. No reported adverse events.
Remember, if the patient is stable, you have time. It may not be necessary to treat these patients, especially if you are not sure. We have tricks we can use in the emergency department to help us see the P waves. Do not feel as though it is your responsibility to treat all of these patients with a cardioversion prior to reaching the hospital.
Narrow and irregular
First, and most common, is atrial fibrillation. On EKG, this is typically seen as a narrow complex, irregularly irregular rhythm with a wave baseline. The rate changes quite frequently and the machines have a difficult time reading the rate, it will constantly be changing. If you have a monitor that beeps, it may sounds “out of time.” Rates can range from 60-180. When rates stay above 120 bpm, this is known as atrial fibrillation with a rapid ventricular rate (Afib with RVR). Causes include: PE, thyroid disease, heart failure and chronic alcohol use.
Management is similar to all other arrhythmias. For an unstable patient, which is defined by an arrhythmia associated with hypotension, altered mental status, severe chest pain, shortness of breath, loss of consciousness or diaphoresis, you should consider electrical synchronized cardioversion.
For a stable patient, get peripheral access and potentially give IV fluids if the patient appears hypovolemic. There are some systems that have incorporated beta blockers or calcium channel blockers into their protocol for controlling atrial fibrillation with a rapid rate. In our local CCEMSA system, we have the ability to give 5 mg Verapamil with a base hospital physician order. We do many different things to control the rate in the emergency department. For the most part, data shows that trying to cardiovert them out of this rhythm causes more harm than good, especially if they have been in this rhythm for a long time. Care must be taken with rate control however, the same medications that lower heart rate usually also lower blood pressure.
An important consideration is anticoagulation. When a heart is in atrial fibrillation, blood can pool in the atria. When blood pools, it has a tendency to clot. That clot can dislodge and enter the bloodstream, causing emboli to scatter anywhere in the body. Many patients are placed on a blood thinning medication to prevent some of the worst complications (stroke). Remember for any patient you bring to the emergency department, if you see, hear, or notice afib in their history, try to pay attention to see if they are on any blood thinning medication. This makes a difference for a number of chief complaints and is always worth noting to the hospital staff.
Another similar pathology is atrial flutter. This is found on EKG as a narrow complex rhythm which can be regular or irregular, but often has a characteristic sawtooth pattern of P waves. This etiology of this is a re-entrant pattern that circles around the right atrium, some beats gets conducted down to the ventricles and some don’t. Rates are often 130-160 bpm. Normally, the atrium will be contracting close to 300 bpm and every other beat gets conducted to the ventricles, so the rate stays around 150 bpm. Causes of atrial flutter can be similar to those of atrial fibrillation, which involve stretching of the atria, such as heart failure, ischemia, longstanding alcohol use or previous myocarditis. Management is also similar to atrial fibrillation, which includes rate control and sometimes rhythm control. It can be difficult to differentiate because atrial flutter can be regular if it stays at a 2:1 block.
Wide and regular
The most concerning rhythm is ventricular tachycardia. This will appear on EKG as a wide complex rhythm that appears regular. This can be scary, because v-tach often means the patient does not have a pulse. Assume any regular wide complex rhythm is v-tach until proven otherwise, put your hand on a pulse and get a blood pressure. The rate will often be over 200. V-tach can rapidly degrade into a pulseless rhythm. There are several potential causes: an acute heart attack, a previous heart attack, history of heart failure, hypoxia or trauma.
Management starts by checking for a pulse. After this, we follow the usual algorithm of assessing unstable vs stable. Typically, we treat all of these patients as unstable or potentially unstable. There is very little time for filling if the ventricles are constantly firing. For unstable patients we consider immediate synchronized cardioversion or defibrillation if they do not have a pulse. First cardioversion uses 100 J, and if this doesn’t work, a second attempt can be used at 200 J. If this does not work, our system allows use of Amiodarone, if the patient has a pulse, you can use 150 mg over 10 minutes followed by another attempt at cardioversion. If the patient does not have a pulse, this is cardiac arrest. Follow your cardiac arrest protocol and defibrillate as soon as possible, every minute sooner that you defibrillate improves mortality by 10%.
A brief aside about cardioversion: when the patient has a pulse, we always want to sync the machine to deliver a shock at the time of maximum depolarization. This is to avoid something called an “R on T phenomenon”. Delivering a shock when the heart is repolarizing can induce an unstable ventricular tachycardia. So, if the patient has a pulse, always use the sync mode.
There is new data coming out from recent studies (ILCOR) regarding optimal placement of pads, so we will provide an update when those recommendations are released. Generally there are two options: antero-lateral and antero-posterior. Follow your local EMS agency’s policies.
Wide and irregular
The scariest rhythm is polymorphic ventricular tachycardia. EKG findings will include a wide complex, irregular rhythm. A specific type of polymorphic ventricular tachycardia is called Torsades de Pointes. This can look like a sine wave that gradually gets bigger and smaller. This generally does not have a pulse, especially if sustained. It can be caused by a prolonged QT interval which is a common side effect of prescription medications, or caused by electrolyte abnormalities, ischemia, trauma, or Brugada syndrome, which is an inherited abnormality in the cardiac conduction system.
Management includes the same pathway we have discussed before. Unstable patients, those who are hypotensive, pulseless, altered mental status, etc., deserve cardioversion. In our local CCEMSA protocol, we include 2 g IV magnesium sulfate over 15 minutes which can help improve some of the underlying causes of the abnormal rhythm.
Another wide complex irregular rhythm is atrial fibrillation with an accessory pathway. This is a patient who has a history of abnormal electrical signaling such as Wolff-Parkinson-White syndrome, which involves an accessory pathway from the atria to the ventricles. When these patients develop atrial fibrillation from any of the reasons we discussed previously, their atrial fibrillation can appear as a wide complex instead of a narrow complex. These patients can degenerate very rapidly if given the typical rate control medications we give for atrial fibrillation. Just know, these patients can be very unstable very quickly. Monitor these patients closely and keep the pads on, ready for cardioversion/defibrillation quickly if necessary.
Takeaways on tachydysrhythmias
- Remain calm, for yourself and your patients.
- Quickly decide if the patient is stable or unstable; this is the main branchpoint for any rhythm.
- Don’t be afraid to use electricity if necessary, this can save the patient’s life.
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