All sinus rhythms have the impulses occurring in the SA node and are regular. Because the impulse occurs in the SA node, there is one P wave for every QRS complex. The only thing that differentiates them is the rate.
Normal sinus rhythm
A normal sinus rhythm is when the impulse originates in the Sinoatrial node (SA node) and follows the normal conduction pathway. The rate for this is 60 to 100 beats per minute.
Sinus bradycardia is a slow regular heartbeat that occurs when the sinoatrial node (SA node) produces impulses at a rate of less than 60 beats per minute. This can be normal in those who are athletes and those who are in good cardiovascular health. Symptomatic bradycardia may be treated with transcutaneous pacing and medications (atropine, epinephrine, ect).
Sinus tachycardia is a regular sinus rhythm where the electrical impulses in the sinoatrial node (SA node) are accelerated and the rate is over 100 beats per minute. A commonly used formula for calculating max heart rate is 220 minus age. Here’s some of the causes of sinus tachycardia: consuming alcohol, caffeine, nicotine, stress, cocaine, meth, fever, anemia, hyperthyroidism, physical exercise, heart failure, low blood pressure, ect. We often treat sinus tachycardia by peeling off the layers and identifying the root cause.
A sinus arrhythmia is a sinus rhythm where the rate fluctuates and becomes irregular. The most common type is respiratory sinus arrhythmia. The other two types are non-respiratory and ventriculophasic (We will not go in-depth on these two right now). Respiratory sinus arrhythmia is a normal alteration of the cardiac cycle based on respirations. This is a common rhythm and the rhythm most likely does not need treatment, only the rate.
Sinoatrial Block (Sinoatrial exit block)
A sinoatrial block occurs when the impulse that leaves the sinoatrial node (SA node) is not conducted in the atria and subsequently not conducted in the ventricles. A sinoatrial block can also mean that the impulse that leaves the SA node is delayed. Like the AV blocks, there can be three degrees of sinoatrial blocks: first degree, second degree (type I and type II), and third degree. You can’t determine if the patient has a first degree or a third degree sinoatrial block on an ECG. This is due to the impulses created by the SA node being to small to be detected on a normal ECG (you need intracardiac electrodes to diagnose them). We’ll cover more in depth on the two second degree sinoatrial blocks in another post. The duration of the pause with a sinoatrial block is the R-R interval measurement within plus or minus 2 small boxes. The pause is the multiple of the R to R intervals. Some causes of sinoatrial block are: sick sinus syndrome, increased vagal stimulation, inferior wall myocardial infarction, myocarditis, and some drugs such as amiodarone, digoxin, betablockers, and calcium channel blockers.
Sinus arrest occurs when there is a temporary cessation of impulses from the sinoatrial node (SA node). Sinus arrest and sinoatrial block are very similar except in a sinoatrial block, the pause is directly correlated to the R-R interval (plus or minus two small boxes). A sinus arrest is not a multiple of R-R intervals. If you map out the sinoatrial block example, you will see the next complex occurs when it should so only one complex was blocked. If the sinus arrest is long enough, the other pace makers (AV node, the atrioventricular bundle branches, and the Purkinje cells) will start to conduct impulses (at a slower rate than the SA node), also called escape beats to prevent the person from experiencing the chronic, yet stable, rhythm of asystole. A sinus arrest that lasts for less than three seconds usually doesn’t need to be treated or investigated; but longer than three seconds does need to be treated and investigated. Some causes of sinus arrest include sinus node dysfunction, hypoxia, myocardial infarction/ischemia, hyperkalemia, and side effects of drugs such as diltiazem, verapamil, and beta blockers. If the sinus arrest is too long, the patient will be fitted with a pacemaker.
Premature Atrial Complex (PAC)
Premature atrial contractions/complexes (PACs) are benign, usually asymptomatic premature beats that originate in the atria outside of the SA node. They are considered premature due to them occurring prior to the next scheduled beat. These ectopic beats can be bigeminal (every other beat is a PAC), trigeminal (every third beat is a PAC), quadrigeminal (every fourth beat is a PAC), couplet (two consecutive PACs) ect. PACs can start to occur due to alcohol use, caffeine use, and even stress. No real treatment is required for these complexes.
Atrial flutter is an abnormal atrial rhythm where the atria are beating faster than the ventricles. Atrial flutter produces waves called F waves or flutter waves. Most flutter is caused by a re-entrant circuit that develops. Typical atrial rate is 250 to 350 beats per minute. The best lead to view atrial activity is V1. Atrial flutter can be described as clockwise or counterclockwise (anticlockwise (most common 90%)) depending on the direction of the circuit. We will go more in depth on this in a future post. Atrial flutter rates can be 1:1, 2:1, 3:1, 4:1, 20:1, variable conduction, ect. In a 2:1 conduction atrial flutter, the atria contract two times per one contraction of the ventricles. In a variable conduction atrial flutter, the ventricular response is irregular and may be alternating between 2:1, 3:1, and 4:1. The example above is a variable conduction atrial flutter. Atrial flutter can be treated using beta blockers, calcium channel blockers, anticoagulants (to prevent clots from forming), electric cardioversions, and ablations.
Note: Because the flutter circuit does not utilize the AV-node, adenosine almost never has an effect on the atrial portion of the arrhythmia; it just temporarily interrupts conduction to the ventricles (EMS 12 Lead, 12 Rhythms of Christmas)
Atrial fibrillation is a common irregulary irregular arrhythmia. In atrial fibrillation, the two atria are beating chaotically and out of sync from the ventricles. In new onset atrial fibrillation, the ECG will show coarse fibrillatory waves; but the longer the person has been in the rhythm, the finer the fibrillatory waves will become. The causes of atrial fibrillation include hypertension, myocardial infarction, coronary artery disease, congenital heart defects, exposure to stimulants, drug toxicity, abnormal heart valves, pulmonary diseases, and viral infections. When the ventricular rate exceeds 100 beats per minute, it can be described as atrial fibrillation with rapid ventricular response (RVR). Secondary to the fibrillatory activity, blood can begin to pool in the atria. This can lead to the formation of clots resulting in pulmonary embolism, coronary embolism, and ischemic stroke. This means the health care provider must take special precautions when treating this rhythm. Similar to atrial flutter, the medications needed to treat this rhythm include: beta blockers, calcium channel blockers, antiarrhythmics, anticoagulants, electric cardioversion, and ablations.
Wandering Atrial Pacemaker
Wandering atrial pacemaker (WAP) is an irregularly irregular atrial rhythm with a rate less than 100 beats per minute. In this rhythm, the impulses occur in the atria by ectopic foci (originating outside of the SA node). There needs to be three or more ectopic foci for it to be WAP. In the example I posted above, you can see the multiple p wave origins. There is one P wave for each QRS complex. The causes of WAP is somewhat unknown but it has been correlated with the use of digoxin, fluctuating vagal tone, COPD, and heart disease. WAP can also be a precursor to multifocal atrial tachycardia (MAT). For the most part, WAP does not need treatment unless digoxin toxicity is thought to be the culprit.
Multifocal Atrial Tachycardia
Multifocal atrial tachycardia (MAT) is very similar to wandering atrial pacemaker (WAP) but it’s rates exceed 100 beats per minute. This is an irregularly irregular tachycardic rhythm with at least three different P wave morphologies. Some causes of MAT include COPD, pneumonia, congestive heart failure, pulmonary embolism, right atrial dilation due to cor pulmonale, beta agonist drugs, electrolyte imbalances, hypoxia, and the drug Theophylline (bronchodilator used to treat emphysema and chronic bronchitis). The main treatment of MAT is detecting and fixing the underlying cause.
Junctional- The junction of the heart originates within the tissue between the atria and the ventricles which is how it obtained its name.
A junctional rhythm occurs when the impulse originates in the AV node or the His bundle. This can cause an inverted P wave prior to the QRS complex, no visible P wave because it’s hiding within the QRS complex, or a retrograde P wave because the atria depolarize after the ventricles. Due to the impulses continuing down the intrinsic conduction system, the QRS complex is generally narrow in nature. This is a regular rhythm that is slower than the normal sinus rate because the AV node takes over as the pacemaker for the heart. There are four types of junctional rhythms; junctional bradycardia (rate below 40 beats per minute), junctional escape rhythm (rate from 40-60 beats per minute), accelerated junctional rhythm (rate from 60-100 beats per minute), and junctional tachycardia (rate is over 100 beats per minute). We’ll only cover junctional escape rhythm in this post due to it being the most common. Causes of a junctional rhythm can be due to digitalis toxicity, hypokalemia, myocardial infarction (often an inferior wall MI), sinus node dysfunction, or the use of amiodarone or verapamil (and a few others).
Junction Escape Rhythm
A junctional escape rhythm occurs usually after a sinus arrest or after PACs. The rate is between 40-60 beats per minute. The impulse comes from the atrioventricular junction which becomes the pacemaker for the heart since the SA node is no longer functioning properly. Some causes of junctional escape rhythm are extreme sinus bradycardia, sinus arrest, sinoatrial block, high degree AV block, hyperkalemia, and as a side effect of certain drugs (digitalis poisoning and beta blocker toxicity). Treatments for symptomatic junctional rhythms should be your basic ACLS treatments for bradycardic rhythms. If the patient is in a high AV block, transcutaneous pacing may be necessary.
Premature Junctional Complex (PJC)
A premature junctional complex (PJC) is a beat that originates in the AV node that occurs prior to the next normal QRS complex. These ectopic beats can be bigeminal (every other beat is a PJC), trigeminal (every third beat is a PJC), quadrigeminal (every fourth beat is a PJC), couplet (two consecutive PJCs), ect. They can occur in patients with drug cardiotoxicity, mitral valve surgery, and electrolyte imbalances. Most of the time, these patients will be asymptomatic so no treatments are necessary.
Supraventricular Tachycardia (SVT)
Supraventricular tachycardia (SVT) is a broad term that’s used to describe any rhythm that is fast in nature that occurs above the ventricles (usually over 150 beats per minute but sometimes less). Lying under the SVT umbrella is atrial fibrillation/flutter, atrial tachycardia, SA nodal reentrant tachycardia (SNRT), multifocal atrial tachycardia (MAT), AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), inappropriate sinus tachycardia, and even junctional tachycardia. AVNRT is the most common form of paroxysmal supraventricular tachycardia (PSVT). We will go more in-depth on the various types in another post due to the complexity of this broad category. Treatments of SVT include vagal maneuvers, electrical cardioversion, adenosine, cardizem, verapamil, other types of calcium channel blockers, and beta blockers. Some patients may need an ablation.
Premature Ventricular Complex (PVC)
A premature ventricular complex (PVC), like all of the other premature ectopic beats, occurs when the ventricles produce an impulse prior to the next scheduled beat/complex. Due to the impulse coming from the ventricles, the normal cardiac cycle is disrupted and leads to the asynchronous depolarization of the two ventricles. This produces a wide complex beat and a pause after it until the normal cardiac cells kick up again. This pause is called a compensatory pause. These ectopic beats can be bigeminal (every other beat is a PVC), trigeminal (every third beat is a PVC), quadrigeminal (every fourth beat is a PVC), couplet (two consecutive PVCs), and NSVT (three consecutive PVCs; NSVT is short for non-sustained ventricular tachycardia). PVCs can also be unifocal (occurring from one site in the ventricles) or multifocal (occurring in two or more sites in the ventricles). Multifocal PVCs will have different morphologies. PVCs may cause the sensation of someone’s heart “skipping a beat”. Some causes of PVCs include stress, anxiety, excessive caffeine intake, myocardial infarction, cardiomyopathies, electrolyte imbalances, and certain medications such as… digoxin which is no surprise because it has been the cause of many arrhythmias in this post. For the most part, PVCs are benign. They become problematic when they cause re-entrant tachycardias to occur (which holds true with PACs as well!!!!). We’ll go more in depth on how and why they can cause these in another post. Another time a PVC may be lethal is in the presence of a patient with a long QT interval. In this instance, an R on T phenomenon can occur and cause the patient to go into a polymorphic ventricular tachycardia called Torsades de Pointes.
Ventricular Escape Rhythm (Idioventricular rhythm) and Accelerated Idioventricular Rhythm
A ventricular escape rhythm (idioventricular rhythm) is a regular, wide complex rhythm that starts in the ventricles (It’s wide due to the slow myocyte to myocyte conduction). The rate for this rhythm is generally less than 50 beats per minute (depending on the source). Accelerated idioventricular rhythm ranges from 50-130 (depending on which source you consult). The pacemaker cells down the conduction pathways of the heart act as a fail safe. When the SA node and AV node are failing to work, the next in-line ventricular pacemaker cells start kicking in to maintain perfusion. Because the impulses occur in the ventricles there are no P waves that correlate to any QRS complexes. Some causes of ventricular escape rhythms include: hyperkalemia, sinus arrest, sinoatrial exit block, high degree heart blocks, beta blocker toxicity, calcium channel blocker toxicity, and of course digoxin.
At times you might see an accelerated idioventricular rhythm in the case of coronary reperfusion (cases of STEMI/OMI). In this case, AIVR is generally a benign rhythm that will spontaneously cease a majority of the time. As the great educator Dr. Amal Mattu says: “when you get this rhythm, you either high five your patient or put your hands in your pockets.” This rhythm will generally convert on its own after a few seconds to a couple of minutes. THIS IS NOT VENTRICULAR TACHYCARDIA. Pay close attention to the rate and remember that v-tach generally produces rates of 120 or 130 (depending on the source you consult). AIVR is usually slower than 120 or 130. It’s essential to monitor the heart rate, watch your patient’s overall level of stability, and gather as much PMH/HPI as possible. Antiarrhythmic drugs can cause haemodynamic deterioration and death. If the rhythm continues after couple minutes, prepare to identify and treat the suspected underlying issue.
Ventricular fibrillation is never a rhythm you wish to see in your patients. It’s a very rapid, chaotic rhythm (rates from 150 to 500 beats per minute), that occurs because the ventricles are fibrillating and not causing a concise contraction. Therefore, there’s no blood being pumped throughout the body. Ventricular fibrillation (VF) can be course as seen above or fine. Course VF occurs first. As time goes on, the wave amplitude decreases and it becomes fine VF. If left untreated, the hundreds of impulses occuring in the ventricles will eventually deteriorate to asystole. There are no clear P waves, QRS complexes, or T waves noted in the rhythm. Ventricular fibrillation has two hypothesized mechanisms that we will dive into on a later date. The first is the multiple wavelet and the second is mother rotor. These aren’t necessarily important in the treatment but fun tidbits to know about the rhythm. Causes of VF are myocardial infarction, aortic stenosis, cardiac tamponade, trauma, long QT, Brugada syndrome, tension pneumothorax, pulmonary embolism (PE), asphyxiation, drug overdoses, sepsis, strokes, and many more. Treatments of VF are early CPR and defibrillation. If the VF is refractory (patient stays in VF after three defibrillations) you might need to change the vector of the electricity by repositioning your pads. Anterior/posterior pad placement is preferred if feasible. Once again, early CPR and defibrillation are key.
Ventricular tachycardia (VT) is a regular, wide complex, tachycardia (in general starts at 120/130 beats per minute (depending on the source you consult) and can reach 300 beats per minute (depending on the source you consult). We personally use 130 as the starting point. VT can cause a reentry circuit in the ventricles. This rhythm can occur in patients with or without a pulse but is considered a deadly rhythm and should be promptly treated in order to prevent deterioration. Even though the rhythm is ventricular, you still might have atrial activity so there can be AV dissociation noted which can cause capture and fusion beats.
VT is an interesting rhythm and you usually only learn about two types in paramedic school; monomorphic (first picture below) and polymorphic (second picture below).
We will mostly cover these two types in this post as these are the most common. There’s actually many more types of V-tach though. There’s right ventricular outflow tract tachycardia (RVOTT), fasicular ventricular tachycardia (first picture below), bidirectional ventricular tachycardia (second picture below), ventricular flutter, catecholaminergic polymorphic ventricular tachycardia (which is genetic), and arrhythmogenic right ventricular dysplasia (which is genetic). Due to the many types, we will go into more detail on the different types in a different post.
Three or more consecutive PVCs is considered V-tach. This is called non-sustained ventricular tachycardia (NSVT). Polymorphic v-tach lacks the symmetrical appearance of monomorphic v-tach. Torsades de Pointes (TdP) is a type of polymorphic v-tach. People often times consider any polymorphic v-tach to be Torsades de Pointes. TdP can only be diagnosed if you note a long QT on the 12-lead (generally you start worrying over 500 milliseconds). A premature beat can then cause the R on T phenomenon and send the patient into TdP. Treatment for this is magnesium. Hypokalemia can exacerbate the risk of TdP and other arrhythmias. Causes of ventricular tachycardia include myocardial infarction, myocarditis, cardiomyopathies, genetics, structural heart defects, heart failure, long QT, electrolyte imbalances, and drug overdoses.
To put things simply, VT is more complex than most people give it credit for. The two main types are monomorphic and polymorphic. Torsades de Pointes is a type of polymorphic v-tach characterized by a long QT. When in doubt, electrically cardiovert the patient if unstable. If stable, you can consider giving an antiarrhythmic drug such as procainamide, lidocaine, or amiodarone. You can even consider beta blockers like metoprolol and propranolol. For polymorphic VT, you should synchronize cardiovert the patient if unstable and if you notice a long QT give magnesium. Electricity is the safest and most effective way of treating tachycardic arrhythmias.
Ventricular flutter is an extremely rapid regular wide complex tachycardia (rates from 250-350 beats per minute). This is a type of ventricular tachycardia and has a typical sinusoidal pattern and is most likely caused by a reentry circuit as the ventricles depolarize in a circular pattern. This rhythm causes the patient’s condition to deteriorate rapidly and is generally a short lived rhythm as patients quickly go into ventricular fibrillation. This rhythm can be seen after the administration of AV nodal blocking agents (amiodarone, diltiazem, adenosine) in the presence of atrial fibrillation with WPW. Patient’s with ventricular flutter are rarely stable due to impending extreme hemodynamic collapse. What is interesting with this rhythm is that it looks identical even if you turn the ECG upside down. This patient needs to be electrically cardioverted quickly.
First Degree Heart Block
A first degree heart block occurs when the impulse is slowed through the AV node which in turn delays action potential from reaching the ventricles, thus causing a prolonged PRI (greater than 0.20 seconds). It’s the only heart block where you describe the rhythm prior to stating the type of block. For example: “normal sinus rhythm with a first degree AV block.” The patient with this block is most likely asymptomatic. In younger patients, a first degree heart block may arise from increased vagal tone. In the elderly, the cause is most likely the fibrotic changes of the cardiac conduction system. Other issues like myocardial infarction, coronary heart disease, and inflammation can also cause a first degree AV block.
Second Degree Heart Block, Type 1 – Mobitz I (Wenckebach)
A second degree AV block type I occurs when there is a varying failure of the impulses making it to the AV node. There is not a 1:1 P to QRS ratio. This rhythm is unique in that there’s a constant delay in the P wave conduction until the P wave does not conduct a QRS complex. The PR-interval progresses in duration until a QRS complex is dropped (longer, longer, longer drop, now you have a Wenckebach). Sometimes when the block is consistent, the QRS complexes are said to demonstrate “group beating.” Various medications that impact the AV node can cause this rhythm. Other causes include: increased vagal tone, hyperkalemia, and Lyme disease. An inferior wall MI can cause this rhythm (as well as other blocks). This is due to the compromised RCA which usually supplies blood to the AV node (along with the SA node). If symptomatic, this can be treated with medications. For extreme bradycardia and hypotension, transcutaneous pacing may be needed for this patient.
Second Degree Heart Block, Type 2 – Mobitz II
A second degree type two AV block occurs due to a conduction failure in the His-Purkinje system. This rhythm is considered a high degree AV block. It’s characterized by intermittent non-conducted P waves without prolongation of the PR interval. In the example above, the P waves occur every 3 boxes and you can easily march them out. There is no variation in the PR interval. These patient’s normally have some structural defects in the heart that can be associated with a LBBB, RBBB or a fascicular block. Some causes of this include myocardial infarction, lyme disease, myocarditis, hyperkalemia, digoxin toxicity, beta blocker toxicity, calcium channel blocker toxicity, amyloidosis, sarcoidosis, and several others. The block occurs below the AV node so transcutaneous pacing is the front line treatment for symptomatic patients presenting with this rhythm. Medications that impact the SA or AV node will not work very well on high degree AV blocks.
Third Degree Heart Block (complete heart block)
A third degree AV block (a high degree AV block) is also called a complete heart block (due to complete AV dissociation). This means the P waves and QRS complexes are not correlated. The atria and ventricles beat independently from each other and are not communicating. The SA node produces atrial activity that gets conducted to the AV node. The AV node then blocks this impulse. The ventricular activity will usually manifest as a ventricular escape, junctional escape, or a fascicular escape rhythm that will normally be bradycardic. Occasionally patients will be asymptomatic but in general they will be extremely hemodynamically unstable and will need immediate transcutaneous pacing.
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