- Differentiate sinus tachycardia from other atrial rhythms.
- Relate the ECG tracing to the physiological function of the heart.
- Describe the causes and treatments of abnormal atrial rhythms.
Atrial kick: Increased ventricular filling produced by atrial contraction.
Depolarization: Reduction of the heart cell membrane potential to a less negative value.
Embolism: An obstruction in a blood vessel caused by a blood clot or foreign body.
Ectopic beat: Abnormal cardiac beat resulting from a non-pacemaker heart cell that depolarizes.
Mitral valve: The two-cusp valve between the left atrium and left ventricle of the heart.
Paroxysmal supraventricular tachycardia: An ectopic atrial rhythm that begins abruptly, is perfectly clock regular, and is 150 bpm or greater.
Sinus node: Specialized heart tissue that generates the cardiac electrical impulse in a normal heart rhythm.
Sympathetic nervous system: System that enables the body to respond to fear (fight or flight) by increasing heart rate, blood pressure and cardiac output.
Tachycardia: Heart rate faster than 100 bpm in an adult.
Thyrotoxicosis: Condition in which the thyroid gland produces an excess of thyroid hormone.
I was working in an emergency department (ED) in western Georgia one evening when a call came over the radio: ˙Medical Center, this is Medic 27, inbound to your facility with a 60-year-old woman with palpitations. Monitor shows a pulse rate of 158. Request an order for adenosine, over.Ó
This case gave me pause for reflection. The patient was a 60-year-old female having what the medic suspected wasparoxysmal supraventricular tachycardia (PSVT). Typically, PSVT turns on abruptly, like flipping on a light switch, so it would be unusual in a 60-year-old patient unless associated with ischemia, structural heart disease or a chronic condition. If the arrhythmia had occurred over many years, it could be simple chronic PSVT of a benign cause.
On the other hand, if you use the formula ˙220 minus ageÓ as the maximum possible sinustachycardia, then 220 Ï 60 = 160. With a pulse rate of 158, it was possible that this rhythm was sinus tachycardia, meaning that this patient was really, really sick. It could have been anything from sepsis to a pulmonaryembolism.
Because adenosine works by shutting down the heart's conduction system for a few secondsƒand can be a dangerous drug if misused in a critically ill patientƒI asked the medic how long the patient had been feeling sick. After a moment, he replied, ˙She's been feeling bad for about three days. We've got a line, so can we go ahead and push the adenosine?Ó It seemed to me that he had taken little history on the patient, and I was concerned with his diagnostic abilities, including his interpretation of the rhythm strip.
In emergency medicine we have a few ˙best bang for the buckÓ questions for patient histories, and luckily, there's one for PSVT. So I asked, ˙Medic 27, has this lady had these palpitations before?Ó Another moment passed until the medic replied, ˙No, she has no history of any heart condition. Now can weplease go ahead and just push the adenosine?Ó
It was highly unlikely that the total cause of a 60-year-old's problem was new-onset PSVT. Many problems could be cranking her up to a near-maximum output heart rate. I considered the case essentials: An IV had been established if we needed a fluid bolus, PSVT is a fairly benign rhythm that can resolve spontaneously, and if we were going to use adenosine diagnostically, I wanted to be with the patient.
The medic reported a six-minute transport time, so it wouldn't be long before they arrived. I could bolus sinus tach with fluids, and PSVT shouldn't deteriorate by then. So I ordered a volume bolus of 250 cc normal saline, and asked the medic to re-evaluate vitals and provide an update in three minutes.
The patient arrived seven minutes later. Her pressure was 90 systolic. She had been sick for three days with a cough and malaise and had gotten progressively worse. She had crackles in the base of her right lung. The monitor showed a regular, narrow complex tachycardia at a rate of 158 with visible P waves.
Still a little unsure of the rhythm, we administered a volume bolus of 500 cc of normal saline, and her pulse slowed to 148. Itwas sinus tachycardia. Subsequent workup showed that the woman had pneumonia of the right lower lobe and was very dehydrated and septic.
The Science of Evaluating Heart Rhythm
Patient assessment is an art form learned through intense training, practiced during thousands of patient encounters and tempered in the fires of experience. All three of these elementsƒtraining, practice and experienceƒare necessary. Without any one of these, the art can fail.
Electrocardiography and the window into a patient it offers have been present for more than a century. Augustus Waller published the first human electrocardiogram (ECG) in 1887, using a ˙capillary electrometer.Ó(1) Willem Einthoven witnessed a demonstration of this technique in 1889 on Waller's pet dog, Jimmy. Einthoven intensified the research on this technique and coined the term ˙electrocardiogramÓ in 1893.
Two years later, Einthoven described the P, Q, R, S and T waves.(2,3)Figure 1 shows one of the earliest ECG recordings on record, presented in Einthoven's address when accepting the 1924 Nobel Prize for Physiology and Medicine.(4)
In 1905, Einthoven began the transmission of human ECG recordings by telephone line to his laboratory a mile away, a task that we still struggle with from EMS units in many parts of the world. In 1906, he first described normal and abnormal ECGs, including ventricular hypertrophy, the U wave, and other disturbances of rhythm and conduction.(5)
In 1912, Einthoven published his famous ˙triangleÓ for the standardization of lead placement.(6) Promoting studies using three leads, he wrote that ˙by means of these multiple leads it's possible to measure the direction and manifest magnitude of the potential variations in the heart itself.Ó He had discovered that the heart's anatomy could be visualized by placing three leads measuring electrical voltage at angles to each other, visualizing the functioning heart as no other person in history had ever done.
The ECG records the electrical activity of the heart. This activity reveals the actual electrical components of what's physically occurring in the heart. Understanding the anatomy of the heart and its conduction system is the only way to truly interpret ECGs. Reading ECG strips without understanding the anatomy of the heart is mere ˙strip memorization,Ó which can be fraught with error and is inconsistent with the role of the critical-care EMS provider.
Thesinus node is invisible on the ECG. After the sinus node fires, the atrial internodal branches spread the impulse through the atria (including Bachman's bundle into the left atrium), producing the P wave. The impulse is nearly instantaneously transmitted to the AV node, where nerve-cell synapses occur, slowing down the impulse for a period of 0.12 to 0.21 seconds, a length of three to five small blocks on standard ECG paper moving at the customary 25 mm/second. This is the PR interval. The effect of this slowing is atrial contraction occurring about one-tenth of a second before ventricular contraction, allowing the ventricles to fill more completely and contract harder.
The AV node then releases the impulse, sending it quickly down the bundle of His through the bundle branches, firing the Purkinje fibers and stimulating both ventricles simultaneously, producing the QRS complex. Ventricles being stimulated simultaneously will produce a QRS complex measuring less than 0.12 seconds, which is three small blocks on the ECG strip moving at normal speed.
To review this important electrical anatomy, the P wave is thedepolarization of the atria, the PR interval is produced by the delay at the AV node, and the QRS complex is produced by the depolarization of the ventricles. Disturbances of the atria affect P waves, disturbances of the AV node affect the PR interval, and disturbances of conduction through the ventricles affect the QRS complex.
Importantly, any rhythm originating above the branching point of the bundle branches is termed a ˙supraventricular rhythm.Ó Any rhythm originating below that point is considered a ˙ventricular rhythm.Ó
Thus, the beat seen on an ECG strip is an actual electrical video recording of the physiology of the heart at work.Sinus Tachycardia vs. Arrhythmia
Our approach to emergency patients must be to quickly determine the severity of their illnesses by rapidly performing an accurate initial assessment. It's often difficult to tell if a patient is experiencing sinus tachycardia or an arrhythmia, but the development of sinus tachycardia is one of the most telling signs of asympathetic nervous system response to a physiological crisis, unless it's being produced by drugs, such as albuterol or cocaine.
The sympathetic nervous system responds during distress to produce many signs and symptoms, from thirst and anxiety to pallor, diaphoresis and dilated pupils. Thus, we place patients on ECG monitors early on to get a ˙visual viewÓ of the patient's cardiac activity. But it's essential to conduct a careful and ongoing assessment of how a patient's physiology is produced or affected by the displayed ECG rhythm so that the proper treatment can be initiated.
A useful measure to determine if a patient's rapid rhythm is a sinus tachycardia is to quickly perform the usual assessment of the rhythm as seen inTable 1.
If the ventricular rate is rapid (above 100 in adults, i.e., tachycardia), the rhythm is regular, P waves are seen with each ventricular beat, the PR interval is unchanging, and the QRS complex is narrow, then this rhythm originates in the atria somewhere. How then do we decide if this tachycardia is produced by accelerating the sinus node or by some other mechanism?
As alluded to in the opening case, the sinus node can be accelerated by the sympathetic nervous system generally to the rate of 220 minus the patient's age in years. The ˙220 minus ageÓ formula doesn't give an ˙absoluteÓ figure for every patient. Patients in excellent physical condition, for example, may be able to accelerate their heart rate slightly more, but this formula has been tested and found to be reliable for most purposes.(7)
So a newborn baby could have a sinus tachycardia as high as 220. A 20-year-old female with severe lower abdominal pain from a rupturing ectopic pregnancy could present with a sinus tachycardia as high as 200. At 54 years of age, sinus tachycardia could reach as high as 166. Patients at 90 years of age generally can't get their sinus tachycardia much over 130.
Many patients with sinus tachycardia caused by a sympathetic nervous system response are very ill, possibly having a life-threatening condition, such as shock, pulmonary embolism, sepsis, myocardial infarction (MI) or diabetic ketoacidosis. Younger patients may have a very rapid sinus tachycardia. A pale, diaphoretic 30-year-old woman with a history of PSVT could present with a sinus tachycardia as high as 190. Without a careful history and physical examƒwhich could reveal, for example, aspirin use and black, tarry stools consistent with hemorrhagic shock from a perforated ulcerƒyou could be deceived into thinking that her rapid rhythm was due to PSVT.
The take-home message is that when you approach a patient with tachycardia, if the monitor shows what appears to be a rhythm originating in the atria (as opposed to a wide complex tachycardia with no P waves, suspicious for ventricular tachycardia), quickly do the ˙220 minus ageÓ calculation. If the speed of the ECG rhythm is within that range (less than or equal to 220 minus age), attempt to rule out sinus tachycardia as a cause before you administer any medications to the patient. Adenosine, diltiazem and verapamil can be potentially detrimental to a patient in shock.
Figure 2 shows the conduction system of the heart. All emergency medicine providers must commit this illustration to memory in order to accurately assess arrhythmias. As a refresher, the impulse begins in the SA node, traverses the internodal pathways through the atria to the AV node, descends through the bundle of His to the bundle branches, and on to the Purkinje fibers and the ventricular muscle.
An abnormal impulse can originate in virtually any part of the heart, disturbing normal conduction. A common example is for an abnormal beat to originate from somewhere in the atria other than the SA node. An atrial beat not originating in the SA node is called anectopic beat.
Ectopic atrial beats: A beat that originates in the atria that's not part of normal conduction is called an ˙ectopic atrial beatÓ (EAB). If the beat comes before the expected next beat of a normal rhythm, it's considered a ˙premature atrial beatÓ (PAB). If the impulse is transmitted down the conduction system and makes the ventricles contract, it's a ˙premature atrial contractionÓ (PAC). Most ectopic atrial beats produce PACs.
If the sinus node slows down for some reason, an atrial ectopic focus may take over and become the primary rhythm generator until the sinus node picks up again. This focus would typically have a P wave with a different shape than the beats originating in the sinus node.
Treatment: EABs may have no significance, or they may have a great deal of importance. A nervous college student drinking pots of coffee to stay awake may have many PACs, and treatment for that individual is a good night's sleep and reduced caffeine. A patient withthyrotoxicosis might be having many PACs, and treatment for this patient would include the management of the thyroid condition. If the patient was having chest pain, oxygen would be the first treatment, because PACs may be a sign of ischemia or infarction. A medical chest pain protocol would then be followed if an acute coronary syndrome was suspected.
Atrial fibrillation (A Fib): The normal conduction system of the heart provides a smooth pathway for the spread of the electrical impulses generated by the SA node. If this smooth pathway is lost, hundreds of individual sites in the heart muscle depolarize each minute in a chaotic, random manner. If this chaos occurs in the atria alone, it's called ˙atrial fibrillation.Ó Many of these atrial impulses are conducted through the AV node to the ventricles. With atrial fibrillation, the ventricles demonstrate organized, although irregular, depolarization.
The risk of developing A Fib increases with age, from about one in 200 patients ages 50Ï59 to up to 9% of patients 80 years of age or older. Ischemic heart disease (coronary artery disease), congestive heart failure (CHF), hypertension, alcohol use and other medical conditions increase the risk of developing A Fib.
In A Fib, organized depolarization of the atria is lost. Thus, the additional filling by the atria to the ventricles to gain extra kick is lost as well. In people with marginal heart function who have been in sinus rhythm and suddenly go into A Fib, the loss of theatrial kick to the ventricles may be enough to cause acute congestive heart failure.
A Fib may come and go, or it may be chronic. The normal depolarization of the atria allows for blood to be swept out during atrial contraction. When A Fib occurs, the atria don't have that smooth emptying, and blood can actually form clots inside of the atria. If the normal rhythm is restored (or even in the absence of the return of a normal rhythm), clots can be swept into the pulmonary or peripheral circulation with devastating effects, such as strokes or clots to other organs and the extremities.(8)
Treatment: A Fib generally causes either increased heart rate or clots breaking loose into the body, as described above. The elevated heart rate associated with A Fib can cause symptoms ranging from palpitations all the way to CHF. In the latter setting, rate control may be very important.
After the application of oxygen to the patient, the initial approach to rate control is the administration of a medication that will block the number of impulses that can get through the AV node per minute. A healthy AV node may allow as many as 200 or more atrial impulses to get through per minute. Diltiazem, a calcium channel blocker (CCB), can provide a inhibiting effect to the AV node, as can beta blockers. Esmolol as a drip is one such beta blocker, with the benefit that it may be turned off and quickly metabolized. Digoxin has been a mainstay of treatment for rate control for years, and with new onset A Fib, digoxin provides conversion to sinus rhythm in about 60% of cases within 24 hours. Amiodarone may offer a slight additional benefit.(9)
One important treatment for A Fib includes either elective or, if the patient is unstable, emergent cardioversion. A patient who has developed A Fib due to an acute MI and then develops hypotension may require sedation and cardioversion in the back of the ambulance.
A Fib is sometimes similar to sinus tachycardia in that it may be more a symptom of an underlying problem than a primary disease. For example, the CHF patient who lives in chronic, rate-controlled A Fib that presents with a rapid ventricular response may have CHF exacerbation as the root cause, not the A Fib itself. If you focus only on rate control using diltiazem, for example, rather than using nitroglycerin for the congestive heart failure, you may be doing the patient a disservice. Likewise, if an adult patient, previously well, presents with new onset A Fib, you should suspect an underlying medical condition, such as hyperthyroidism, pulmonary embolism or alcoholism.
PSVT: Some people have abnormal wiring in their hearts. It's normal to have conduction from the SA node and the atria down to the AV node. It's not normal, though, to have a pathway that sends the current from the AV node back up to the atria. When this pathway occurs (more commonly in females than in males), a PAC can set off a process in which the impulse goes down to the AV node and on to the ventricles. But the abnormal pathway also sends the impulse right back up to the atria, where it's then sent right back down to the AV node and on to the ventricles. This circular pathway (sometimes called a ˙circus pathwayÓ) happens very quickly.
The result is the abrupt onset of a tachycardia that ˙turns on like a light switch.Ó The ventricular rates are typically 150 on the low end and up to 250 on the upper end, although 200 is usually the maximum a paramedic would see.(10) The patient usually experiences palpitations and possibly some shortness of breath. Rarely PSVT is caused by ischemia, so you must always be careful to look for a history of chest pain or coronary artery disease.
PSVT usually begins in young people between the ages of 12 and 30, especially anxious people who are exhausted, drink caffeine, drink alcohol or smoke cigarettes. As mentioned previously, PSVT can rarely be seen with myocardial ischemia. People who are hypoxic and prone to arrhythmia may develop PSVT.Mitral valve disease may be a cause of PSVT as well.
Another important fact to remember is that several other abnormal pathways exist, one of which is the ˙KentÓ bundle going from the atria directly to the ventricles, bypassing the AV node. This condition is called the Wolff-Parkinson-White syndrome (WPW). It's often dormant and perhaps even undiagnosed. The significance for prehospital providers is that PSVT can occur in WPW, and because one ventricle may be stimulated before the other, the complex can be wide, giving the appearance of ventricular tachycardia.(11)
Finally, it's vital for paramedics to understand that PSVT is almost always a fairly benign rhythm. It's usually a disease of young people beginning fairly early in life. New-onset PSVT later in life, such as in middle age, is a sign of some sort of problem ranging from valvular heart disease to thyroid disease to myocardial ischemia. You should always take a careful history of patients and especially be sure to ask, ˙How old were you when this started happening to you?Ó
Above all, it's critical to ensure the patient isn't having sinus tachycardia. Sinus tachycardia and PSVT can look a lot alike, and if the patient's tachycardia falls into the range of 220 minus age, then youmust make sure the condition isn't sinus tachycardia. We don't want to give adenosine to a 20-year-old woman with a history of PSVT who has a narrow complex tachycardia with a rate of 180, but who is late with her period, is having severe lower abdominal pain, is pale and diaphoretic, and has a systolic blood pressure of 90. She has a ruptured ectopic pregnancy until proven otherwise. Adenosine is not a benign drug. It works by shutting down the heart's conduction system for a few seconds, and a moment of asystole is something you want to avoid in a patient in shock.
Treatment: As with A Fib, the goal (once you're positive you're dealing with PSVT) is to block the AV node to stop the ˙circusÓ rhythm from going back up to the atria. Adenosine is a naturally occurring chemical in the body that, when given via IV, slows AV nodal conduction and produces a transient AV nodal block. Adenosine is quickly cleared from the circulation with a half-life of less than five seconds.(12)
A typical adult dosage would be 6 mg, followed by a 12 mg dose if needed. For pediatrics, the dose range is 50Ï250 ug/kg. In patients with a history of prolonged QT syndrome, polymorphic ventricular tachycardia has been reported with adenosine use for PSVT.
Calcium channel blockers that block the AV node may be used to treat PSVT. Verapamil (5 mg IV over two minutes, which may be repeated in five to 10 minutes) or diltiazem (20 mg over two minutes) may also be used. The PSVT should respond within five minutes in 90% of patients. These drugs have about equal efficacy to adenosine. If hypotension is present, these drugs should be avoided and adenosine used instead.
Wide complex tachycardias (WCT) may worsen after IV adenosine or CCBs. The problem is telling the difference between what you think may be PSVT with a wide complex rather than ventricular tachycardia (VT). Wellens and his colleagues noticed that 69% of VT cases had QRS durations greater than 140 milliseconds, but they found that no PSVT patients had QRS duration in this range.(13) Amiodarone (a class III agent) can terminate PSVT and VT. It is the agent of choice for stable WCT, particularly if you're unsure if the rhythm is VT or PSVT.
Lidocaine can be administered, and it may convert the rhythm to sinus if it's VT. Procainamide can be used, but it has to be given slowly to prevent hypotension during administration. Finally, if the patient has become hypotensive or is having PSVT with an MI, cardioversion may be indicated.
Atrial flutter (A Flutter): Sometimes, an ectopic focus in the atria begins to fire over and over again in a rapid, rhythmic manner. In this setting the atria depolarize very quickly in an organized manner. The rate of depolarization can be 250Ï350 times per minute, and the impulses are conducted to the AV node. Depending on the ability of the patient's AV node to conduct, the ratio of atrial beats to ventricular beats can be 1:1, 2:1, 3:1 or more, especially if the patient is already on medication that blocks the AV node. As many as 10% of people presenting with supraventricular arrhythmias may have atrial flutters.
The ECG features show the characteristic ˙saw toothÓ baseline, with very fast, identical P waves. The saw tooth baseline may be hard to see, and a 12-lead ECG may be required to make the diagnosis. Importantly, though, this isn't a ˙circusÓ or re-entrant rhythm but rather a continuous rapid firing of an atrial ectopic focus.
Treatment: The management of A Flutter involves, once again, blocking the AV node. Diltiazem (20 mg IV over two minutes) is useful, as are beta-blocking agents, such as metoprolol or esmolol. Amiodarone and digoxin can be used as well. Cardioversion remains a mainstay of therapy, and if the patient becomes hypotensive, consider synchronized cardioversion based on protocol or after obtaining on-line medical direction.
Multifocal atrial tachycardia (MAT): This rhythm is exactly as the name implies. It's fast, it originates in the atria, and it has at least two different types of P waves. It usually occurs in patients who have lung disease and develop pulmonary hypertension. Ultimately, the right atrium becomes distended from the pulmonary hypertension and becomes irritable due to hypoxia. In addition, CHF, sepsis, acute MI or theophylline toxicity may induce MAT.
Treatment: Normally, MAT is treated by gaining control of the underlying condition. COPD exacerbation may be treated with oxygen, beta-agonists (carefully in the setting of tachycardia) and steroids. Theophylline toxicity can be identified and controlled. Cardioversion is rarely successful. Specific antiarrhythmic therapy is not indicated.
Ectopic atrial tachycardia: This is a rare atrial tachycardia in which a single ectopic focus in the atria fires continuously and rapidly, with the impulses being conducted down the AV node.
It's not PSVT because no re-entrant pathway is present. It isn't sinus tachycardia because it doesn't come from the sinus node. It isn't A Fib because it's a single atrial focus. And it isn't A Flutter because the atrial rate is much slower. It's most commonly seen in children, although it may occur in adults. It may be associated with a tachycardia-induced cardiomyopathy.
An ECG rhythm that's regular like PSVT but has a rate slightly slower than 150, appears more like sinus tachycardia but doesn't respond to a fluid bolus, will be the key to diagnosis.
Treatment: These patients may present in circulatory collapse due to impaired heart function. Amiodarone may be effective in rate control in children.Summary
Never before have EMS professionals had as many tools available to look as deeply into patients for answers to clinical crisesƒtools ranging from ECG monitors to 12-leads to waveform capnography, even ultrasound. The interpretation of ECG rhythms long ago became a standard in the industry but remains an area requiring great study and steady use during a career to achieve and maintain mastery.
The anatomical approach to understanding ECG rhythms is an essential element for success. Learn and keep in your memory the layout of the heart's conduction system for as long as you practice EMS. Also, remember the ˙220 minus ageÓ formula, and always determine if the patient's tachycardia is a sinus tachycardia before pushing drugs.
With these thoughtful approaches to skill and practice, the management of your patients will be far more accurate and safe for the patient and much more rewarding for you as a professional.
1. Waller AD: ˙A demonstration on man of electromotive changes accompanying the heart's beatÓ. Journal of Physiology 1887;8:229-234.
2. Einthoven W: ˙Ueber die Form des menschlichen ElectrocardiogrammsÓ. Arch f d Ges Physiol 1895;60:101-123.
3. ECG Library.www.ecglibrary.com.
4. Einthoven W: ˙Nobel Lecture.Ó.http://nobelprize.org/nobel_prizes/medicine/laureates/1924/einthoven-lecture.pdf.
5. Einthoven W: ˙Le telecardiogrammeÓ. Archives Internationales de Physiologie 1906;4:132-164. (Translated into English: American Heart Journal. 53:602Ï615, 1957.)
6. Einthoven W: ˙The different forms of the human electrocardiogram and their significationÓ. Lancet 1912;1:853-861.
7. Mesquita A, Trabulo M, Mendes M: ˙The maximum heart rate in the exercise test: The 220Ïage formula or Sheffield's table?Ó. Revista Portuguesa de Cardiologia (Portuguese Journ