BeatMap

This is the normal rhythm of a healthy heart. The sinus node fires between 60 and 100 times per minute at rest, each signal follows the normal wiring, and the atria and ventricles squeeze in the proper order. Your heart rate rises with exercise, stress, fever, pain, or dehydration, and it slows during sleep or in people who are very fit. A fast sinus rhythm is called sinus tachycardia and a slow one is called sinus bradycardia. Both are usually the heart responding correctly to what the body needs rather than an electrical problem in the heart itself.

On the EKG

Every beat shows a P wave, then a narrow QRS complex, then a T wave, all evenly spaced.

What is happening

The sinus node is still in charge, but it is firing too slowly or pausing. A slow sinus rhythm is normal in athletes and during sleep. When the sinus node has worn out with age or been damaged, it can become unreliable, firing slowly, stopping for several seconds at a time, or alternating between too slow and too fast. This is called sick sinus syndrome.

What you might feel

Tiredness, poor exercise tolerance, lightheadedness, or brief spells of near-fainting or fainting when the heart pauses. Some people notice nothing and it is found on a monitor.

Risk factors and causes

Age is the most common factor. Others include coronary artery disease, previous heart surgery, an underactive thyroid, sleep apnea, and medicines that slow the heart, such as beta blockers, diltiazem, verapamil, and digoxin. Sick sinus syndrome often occurs together with atrial fibrillation.

How it is treated

The first step is to stop or adjust any medicine that is slowing the heart and to treat reversible causes. When the slow rate or the pauses cause symptoms, the treatment is a permanent pacemaker, usually one with a lead in the atrium so that the device can take over the job of the sinus node. See the pacemaker section below.

A bundle branch block is not an arrhythmia. The sinus node is still in charge and the heart rate is normal. The problem is in the wiring below the AV node. One of the two bundle branches is blocked or slowed, so the signal reaches one ventricle late by spreading through the muscle from the other side. Both ventricles still squeeze, but not quite together.

What is happening

The right bundle branch is blocked. The signal travels normally down the left bundle branch, activates the left ventricle on time, and then spreads slowly across the septum through muscle to activate the right ventricle late.

What it means

Right bundle branch block is common and is often found in people with completely normal hearts, especially as they get older. It can also be seen with lung disease, a blood clot in the lungs, some congenital heart conditions, or after heart surgery. In the absence of other problems it does not cause symptoms, does not affect how well the heart pumps, and does not need treatment. Your doctor may order an echocardiogram (an ultrasound of the heart) once to make sure the heart itself is normal.

On the EKG

The rhythm and rate are normal, but each QRS complex is wide. The animation switches to lead V1, the chest lead that sits over the right ventricle, where RBBB shows its classic shape with a second upward bump at the end of the QRS.

What is happening

The left bundle branch is blocked. The signal travels down the right bundle branch, activates the right ventricle first, and then spreads slowly across the septum through muscle to activate the left ventricle late. Because the left ventricle is the main pumping chamber, this delay can make its squeeze less efficient.

What it means

Left bundle branch block is more likely than right bundle branch block to be a sign of an underlying heart condition, such as long-standing high blood pressure, coronary artery disease, a weakened heart muscle, or aortic valve disease. It can also appear after procedures on the aortic valve. Many people with LBBB feel entirely well. Your doctor will usually order an echocardiogram and sometimes a stress test to look for a cause. A new LBBB in someone with chest pain is treated as a possible heart attack until proven otherwise.

How it is treated

There is no treatment for the block itself, and it does not need one if the heart is otherwise healthy. If LBBB occurs together with heart failure and a weak heart muscle, a special pacemaker that resynchronizes the two ventricles (called CRT, or cardiac resynchronization therapy) can improve symptoms and heart function. Compare the LBBB animation with the CRT animation in the pacemaker section. Very rarely, bundle branch block progresses to a complete block of the AV node, which would require a regular pacemaker.

On the EKG

The rhythm and rate are normal, but each QRS complex is wide and often notched, and the T wave points the opposite way from the QRS.

What is happening

Every signal gets through, but the AV node holds each one for longer than normal. The atria and ventricles still beat in sequence at a normal rate.

What it means

First-degree block is common, often causes no symptoms, and by itself is usually harmless. It is more common with age, in athletes, and in people taking beta blockers, diltiazem, verapamil, or digoxin. It can also follow a heart attack or occur with Lyme disease. It rarely needs treatment, although your doctor may review your medicines and keep an eye on it over time.

On the EKG

The gap between the P wave and the QRS (the PR interval) is longer than normal, but every P wave is followed by a QRS.

What is happening

The AV node gets progressively more tired with each beat. It holds the signal a little longer, then longer still, until one signal does not get through at all and a beat is dropped. The AV node then recovers and the pattern starts again.

What it means

Wenckebach block is usually benign. It is common during sleep, in athletes, and in people on heart-slowing medicines. It is caused by the AV node itself, which is a reliable structure, so it rarely progresses to complete block. Most people need no treatment. A pacemaker is considered only if the dropped beats cause symptoms such as dizziness or fainting.

On the EKG

The PR interval gets longer with each beat until a P wave appears with no QRS after it. The pattern repeats in groups.

What is happening

Signals get through normally and then, without warning, one is dropped. The problem here is usually below the AV node, in the bundle of His or the bundle branches, which is the fast wiring that carries the signal to the ventricles. That wiring is less reliable than the AV node and can fail suddenly.

What it means

Mobitz II is more serious than type 1 because it can progress without warning to complete heart block, which can cause fainting or cardiac arrest. It is usually caused by disease of the conduction system from aging, a previous heart attack, or a cardiomyopathy. A permanent pacemaker is recommended for most people with Mobitz II even if they feel well.

On the EKG

The PR interval stays the same from beat to beat, and then a P wave suddenly appears with no QRS after it.

What is happening

No signals get through from the atria to the ventricles. The atria keep beating under the control of the sinus node, but the ventricles are cut off. Fortunately the heart has backup pacemaker cells below the block, in the bundle of His or in the ventricles themselves, and these take over. The backup is slow, often 30 to 45 beats per minute, and it is not reliable. On the animation you can see the atria and ventricles beating completely independently of each other.

What you might feel

Severe tiredness, shortness of breath, lightheadedness, fainting, or in some cases cardiac arrest. Some people with a stable backup rhythm feel surprisingly little.

Risk factors and causes

Aging of the conduction system is the most common cause. Others include a heart attack, heart surgery or valve procedures, cardiomyopathies, infections such as Lyme disease, some inherited conditions, and medicine toxicity. Complete heart block can be present from birth.

How it is treated

Complete heart block is treated with a pacemaker. In the emergency department a temporary pacemaker or medicines may be used until a permanent device can be placed. Because the sinus node usually still works, a dual chamber pacemaker is typical: it senses each atrial beat and then paces the ventricles a fraction of a second later, restoring the normal sequence. See the pacemaker section below.

On the EKG

P waves march along at one rate and QRS complexes at a slower rate, with no fixed relationship between them.

What is happening

A spot in the atria fires one beat early, before the sinus node was due. The early beat travels through the AV node normally, so the ventricles squeeze early too. The sinus node then resets, which leaves a short pause before the next normal beat.

What you might feel

Most PACs are not felt at all. When they are, people usually notice the pause rather than the early beat, and describe it as a skipped beat, a flutter, or a thump. The beat after the pause can feel stronger because the heart had extra time to fill.

Risk factors and causes

Almost everyone has PACs. They are more frequent with caffeine, alcohol, nicotine, stress, poor sleep, dehydration, and stimulant medicines. Very frequent PACs can be a sign that atrial fibrillation may develop later.

How it is treated

Usually no treatment is needed beyond reassurance and avoiding triggers. If they are frequent and bothersome, a beta blocker can reduce them.

What is happening

A spot in the ventricles fires one beat early. Because the signal starts in the muscle rather than the wiring, the ventricles squeeze in an uncoordinated way and the beat pumps less blood than normal. The next sinus signal usually arrives while the ventricles are still recovering and does not get through, so there is a longer pause before the next normal beat.

What you might feel

A skipped beat, a pause, or a hard thump. The thump is the strong beat after the pause. Many people feel PVCs most at rest, in bed, or after a meal.

Risk factors and causes

PVCs occur in healthy hearts and are more frequent with caffeine, alcohol, stress, lack of sleep, low potassium or magnesium, and an overactive thyroid. They are also more common in people with previous heart attacks, cardiomyopathy, or heart failure. When PVCs make up more than about 10 to 15 percent of all beats over a day, they can gradually weaken the heart.

How it is treated

In a normal heart, occasional PVCs need no treatment. If they are frequent or bothersome, a beta blocker or calcium channel blocker can help, and catheter ablation can eliminate the rogue spot. Your doctor may order an echocardiogram and a 24-hour monitor to count them and to check the heart muscle.

What is happening

In atrial fibrillation, many different spots in the atria fire off electrical signals at the same time in a chaotic way. Most of these rogue signals come from the area where the pulmonary veins enter the left atrium. With hundreds of signals per minute coming from everywhere, the atria cannot squeeze properly. Instead they quiver. The AV node is bombarded with signals and lets some of them through at random, so the ventricles beat irregularly and often too fast.

What you might feel

Some people feel a fluttering, pounding, or irregular heartbeat. Others feel tired, short of breath, lightheaded, or notice that they cannot exercise like they used to. Many people feel nothing at all, and AFib is found on a routine EKG or a smartwatch.

Risk factors and causes

AFib becomes more common with age. Other risk factors include high blood pressure, heart failure, heart valve disease, coronary artery disease, obesity, diabetes, sleep apnea, an overactive thyroid, lung disease, and heavy alcohol use, including binge drinking. It can also be triggered temporarily by surgery, infection, or a serious illness. AFib sometimes runs in families.

How it is treated

Treatment has three main goals: preventing stroke, keeping the heart rate comfortable in the short term, and getting the heart back into normal rhythm and keeping it there.

1. Preventing stroke. This is the most important goal. Because the atria quiver instead of squeezing, blood can pool and form clots, especially in a small pouch of the left atrium called the left atrial appendage. If a clot breaks loose it can travel to the brain and cause a stroke. Your doctor estimates your stroke risk using a score based on your age, sex, and medical conditions. Most people with AFib and other risk factors are advised to take a blood thinner (an anticoagulant) such as apixaban, rivaroxaban, dabigatran, or warfarin. People who cannot take blood thinners may be candidates for a procedure that seals off the left atrial appendage.

2. Rate control. Medicines such as beta blockers (metoprolol, carvedilol), calcium channel blockers (diltiazem, verapamil), or digoxin slow the AV node so that fewer signals get through to the ventricles. The AFib is still there, but the heart beats at a comfortable rate. This is the first step in the emergency department and in the days that follow, because a fast, irregular heartbeat is what makes most people feel unwell, and slowing it down stabilizes the heart and brings relief quickly. Rate control is a bridge, and for many people it is not the end of the story.

3. Rhythm control. This means restoring normal sinus rhythm and keeping the heart there. Doctors used to think that controlling the rate was all that was needed, but we now know that AFib begets more AFib. The longer the atria spend fibrillating, the more they stretch and scar, the harder it becomes to restore normal rhythm later, and over years the fast, irregular rate can weaken the heart muscle. For these reasons rhythm control is now considered a primary strategy, and most people deserve a real attempt at being kept in normal rhythm for as long as it can be maintained, especially when the AFib is recent. The options include an electrical cardioversion (a brief, controlled shock delivered under sedation, often called a DCCV), antiarrhythmic medicines such as flecainide, propafenone, sotalol, dofetilide, or amiodarone, and catheter ablation, a procedure in which a cardiologist uses a thin tube to isolate the pulmonary veins so the rogue signals cannot reach the rest of the atrium. Ablation is increasingly offered early rather than as a last resort. Some people with long-standing AFib, or with other conditions that make normal rhythm hard to hold, do well with rate control alone, and that decision is made together with your cardiologist. Press the Shock button above to see a cardioversion.

Treating the causes matters too. Controlling blood pressure, treating sleep apnea, losing weight, limiting alcohol, and staying active all reduce how often AFib comes back.

When to seek care right away

Go to the emergency department or call 911 for chest pain, fainting, severe shortness of breath, or any sign of stroke such as sudden weakness, facial droop, or trouble speaking.

On the EKG

There are no P waves. The baseline looks wavy or scribbly, and the QRS complexes are irregularly spaced with no pattern.

What is happening

Atrial flutter is a close cousin of atrial fibrillation, but it is more organized. Instead of chaos, a single electrical signal gets caught in a loop that circles around the right atrium, usually around the tricuspid valve, about 300 times per minute. The AV node cannot pass signals that quickly, so it usually lets through every second one, giving a ventricular rate of about 150 beats per minute. Sometimes it lets through every third or fourth signal instead.

What you might feel

People often notice a fast, steady pounding heartbeat, tiredness, shortness of breath, or lightheadedness. Because the rate is often stuck at exactly 150, it can feel constant rather than fluttering.

Risk factors and causes

The risk factors are the same as for atrial fibrillation: age, high blood pressure, heart failure, valve disease, lung disease, sleep apnea, thyroid problems, alcohol, and recent heart surgery. Many people with flutter also have episodes of AFib, and the two often occur together.

How it is treated

Flutter carries the same risk of stroke as AFib, so the same blood thinner rules apply, including the rules around cardioversion. Rate control medicines can be used but often work less well than in AFib because the loop is so regular. Electrical cardioversion usually stops flutter easily. The best long-term treatment for typical flutter is catheter ablation, in which a small line of tissue in the right atrium is cauterized to break the loop. This cures typical flutter in more than 90 percent of people, which is why ablation is often recommended early.

On the EKG

Instead of P waves there is a continuous sawtooth pattern, with a QRS complex after every second or third tooth.

What is happening

In ectopic atrial tachycardia, a single small cluster of cells somewhere in the atria, outside the sinus node, starts firing faster than the sinus node. Because it is faster, it takes over. Each of its signals spreads across the atria, passes through the AV node normally, and reaches the ventricles, so the heart beats fast but in an organized way, usually between 100 and 250 beats per minute. It can come in short bursts or run continuously for hours or days.

What you might feel

A racing or pounding heartbeat, sometimes with shortness of breath, lightheadedness, or chest discomfort. When it runs continuously for weeks or months without being noticed, the fast rate can weaken the heart muscle. This weakness usually recovers once the rhythm is controlled.

Risk factors and causes

Often no cause is found. It can be associated with underlying heart or lung disease, an overactive thyroid, low potassium or magnesium, too much caffeine, alcohol, or stimulants, and certain medicines. It is one of the rhythms that can be caused by too much digoxin.

How it is treated

Correcting triggers such as electrolytes, thyroid problems, and stimulants comes first. Beta blockers or calcium channel blockers can slow the rhythm or reduce how often it happens. Antiarrhythmic medicines are an option. Catheter ablation, in which the cardiologist finds the rogue cluster of cells and cauterizes it, can be a cure. This rhythm does not carry the same clot and stroke risk as atrial fibrillation because the atria still squeeze.

On the EKG

The rhythm is fast and regular. There is a P wave before every QRS, but it has a different shape from a normal sinus P wave because the signal starts in a different place.

What is happening

AVNRT stands for atrioventricular nodal reentrant tachycardia. It is the most common cause of sudden fast heartbeat in adults with otherwise healthy hearts. In some people the AV node has two lanes rather than one: a fast lane and a slow lane. Usually this causes no problem. Occasionally, often after an early extra beat, a signal goes down the slow lane and comes back up the fast lane, and then repeats. The signal is now circling inside the AV node itself. With every lap it sends a signal down to the ventricles and up to the atria at the same time, driving the heart at 150 to 220 beats per minute.

What you might feel

A sudden racing heartbeat that starts and stops abruptly. Because the atria and ventricles squeeze at the same moment, many people feel a pounding or fluttering in the neck. Lightheadedness, shortness of breath, chest tightness, and a strong urge to urinate afterward are common. Fainting is rare.

Risk factors and causes

The two lanes are something you are born with. AVNRT is more common in women and often first appears in the teens through the forties. Episodes can be brought on by caffeine, alcohol, stress, exhaustion, stimulant medicines, or nothing in particular. In a structurally normal heart it is uncomfortable but not dangerous.

How it is treated

Vagal maneuvers, such as bearing down hard or the modified maneuver of bearing down and then lying back with the legs lifted, stop many episodes at home. In the emergency department, adenosine ends the rhythm within seconds in most cases, and diltiazem or a beta blocker are alternatives. Press the Adenosine button above to see this. For people with frequent episodes, daily beta blockers or calcium channel blockers reduce recurrences, and some people carry a single dose to take when an episode starts. Catheter ablation of the slow lane cures AVNRT in more than 95 percent of people, with a small risk of about 1 percent of damaging the AV node enough to need a pacemaker.

On the EKG

A fast, very regular, narrow rhythm. P waves are usually invisible because they are buried inside the QRS complexes.

What is happening

AVRT stands for atrioventricular reentrant tachycardia. Some people are born with an extra strand of muscle that connects an atrium directly to a ventricle, bypassing the AV node. This is called an accessory pathway. Normally the insulating layer between the upper and lower chambers has only one doorway, the AV node. With an accessory pathway there are two. A signal can travel down through the AV node to the ventricles and then race back up the accessory pathway into the atria, where it starts the whole loop again. The loop spins round and round, driving the heart at 150 to 250 beats per minute.

What you might feel

Episodes typically start and stop suddenly, like a switch. People describe a racing heart, pounding in the neck, lightheadedness, shortness of breath, or anxiety. Fainting is uncommon but can occur.

Risk factors and causes

The accessory pathway is present from birth, so this rhythm is often first noticed in children, teenagers, or young adults. It can run in families. Episodes may be triggered by exercise, stress, caffeine, alcohol, or lack of sleep, but often there is no trigger at all. When the pathway is visible on a resting EKG, the condition is called Wolff-Parkinson-White syndrome, described in the next card.

How it is treated

During an episode, vagal maneuvers such as bearing down hard, or bearing down and then lying flat with the legs raised, can break the loop. In the emergency department a medicine called adenosine briefly stops the AV node and interrupts the loop within seconds. Press the Adenosine button above to see this. Longer term, catheter ablation of the accessory pathway is the preferred treatment. It cures the problem in about 95 percent of people and is usually recommended for anyone who has had symptoms. Beta blockers or calcium channel blockers can be used while waiting for ablation.

On the EKG

During an episode the rhythm is fast, regular, and narrow, with a small inverted P wave hiding just after each QRS.

What is happening

WPW is what an accessory pathway looks like on a resting EKG, between episodes of fast heartbeat. The sinus node is in charge and the rate is normal, but every signal reaches the ventricles by two routes at once: the normal route through the AV node, and a shortcut through the accessory pathway. The shortcut has no built-in delay, so a small part of the ventricle is activated a fraction of a second early. This early activation is called pre-excitation.

What it means

Many people with the WPW pattern never have a problem. Others develop episodes of AVRT, the loop rhythm described above. The main concern is what happens if a person with WPW develops atrial fibrillation. The AV node normally protects the ventricles by filtering the hundreds of chaotic signals in AFib, but the accessory pathway does no filtering, so the ventricles can be driven at 250 beats per minute or more. This is rare, but it can cause collapse or cardiac arrest, and it is the reason WPW is taken seriously.

How it is treated

People with WPW and symptoms are usually offered catheter ablation of the pathway, which is curative in about 95 percent of cases. People with the pattern but no symptoms may be offered testing in the electrophysiology lab to see whether the pathway is capable of conducting dangerously fast; if it is, ablation is recommended. Some common heart medicines, including digoxin, verapamil, and diltiazem, are avoided in people with WPW because they can make conduction over the pathway faster.

On the EKG

The PR interval is short and the start of the QRS is slurred, which is called a delta wave. Watch for the small early activation of the left ventricle near the extra pathway in the animation.

Try the demonstration

With the WPW pattern showing, press "Trigger atrial fibrillation" under the tracing to see what happens when AFib starts in a heart with an extra pathway. Then press "Give adenosine (the wrong drug)" to see why the usual medicines for a fast heart rhythm are dangerous here: blocking the AV node removes the only filter, the extra pathway conducts every signal, and the ventricles collapse into fibrillation. The Shock button then shows the correct emergency treatment.

What is happening

This is the most dangerous situation an extra pathway can create. Atrial fibrillation sends hundreds of signals a minute toward the ventricles. In a normal heart the AV node acts as a filter and lets only a fraction through. The extra pathway has no such filter, so signals race down it as fast as the atria produce them. The ventricles are driven at 200 to 300 beats per minute in a fast, wide, irregular rhythm, and this can deteriorate into ventricular fibrillation.

Why the usual medicines are dangerous

The medicines normally used to slow a fast heart rhythm, including adenosine, digoxin, verapamil, and diltiazem, and to a lesser degree beta blockers, all work by slowing the AV node. In pre-excited atrial fibrillation that removes the only filter and pushes every signal down the extra pathway, which can make the heart rate faster and trigger ventricular fibrillation. This is why people with WPW should tell every doctor and every emergency team about it.

How it is treated

If the person is unstable, the treatment is an immediate electrical cardioversion. If the person is stable, medicines that slow the extra pathway itself, such as procainamide or ibutilide, are used instead of AV node blockers. After the emergency, catheter ablation of the pathway is strongly recommended, and it removes the risk.

On the EKG

A fast, irregular rhythm with wide, bizarre QRS complexes that vary in shape from beat to beat, sometimes with an occasional narrow beat that came through the AV node.

What is happening

In ventricular tachycardia, the rogue signals come from the ventricles themselves rather than from the atria or the AV node. A patch of ventricular muscle, very often an area of scar from an old heart attack, begins firing on its own or traps a signal in a loop. Because the signal starts in the muscle and spreads slowly from cell to cell instead of using the fast wiring, the ventricles squeeze in an uncoordinated way at 120 to 250 beats per minute. The atria are no longer in charge and often keep beating on their own schedule in the background. At these speeds the ventricles do not have time to fill, so much less blood is pumped with each beat.

What you might feel

Palpitations, lightheadedness, chest pain, shortness of breath, or fainting. Sustained VT is a medical emergency because it can cause the blood pressure to collapse and can deteriorate into ventricular fibrillation, which is cardiac arrest. Short bursts of a few beats may cause no symptoms at all.

Risk factors and causes

The most common cause is scar tissue from a previous heart attack. Other causes include heart failure and a weakened heart muscle from any cause, inherited heart conditions such as hypertrophic cardiomyopathy, long QT syndrome, Brugada syndrome, and arrhythmogenic cardiomyopathy, very low or high potassium or magnesium, certain medicines, and stimulant drugs such as cocaine. Some forms of VT occur in completely normal hearts and are much less dangerous.

How it is treated

If the blood pressure is low or the person is unwell, VT is treated immediately with an electrical shock (cardioversion). Press the Shock button above to see this. If the person is stable, medicines such as amiodarone, procainamide, or lidocaine may be tried. Fixing the cause matters: opening blocked arteries, correcting potassium and magnesium, and stopping offending drugs. To protect against sudden death, many people with VT and a weakened heart are offered an implantable cardioverter-defibrillator (ICD), a small device under the skin that watches the rhythm and delivers a shock if VT or ventricular fibrillation occurs. Beta blockers and antiarrhythmic medicines reduce how often VT happens, and catheter ablation can target the scar tissue where the loop lives.

On the EKG

The rhythm is fast and the QRS complexes are wide and bizarre looking, because the signal is spreading slowly through muscle instead of along the fast wiring.

What is happening

Ventricular fibrillation is the ventricular version of atrial fibrillation, and it is fatal within minutes if it is not treated. Countless spots in the ventricles fire chaotically, the ventricles quiver instead of squeezing, and no blood is pumped at all. The person collapses, stops breathing normally, and has no pulse. This is cardiac arrest.

Risk factors and causes

VF is most often triggered by a heart attack in progress, by ventricular tachycardia that deteriorates, or by a severely weakened heart. Inherited conditions such as Brugada syndrome and long QT syndrome, severe electrolyte disturbances, drug overdoses, electrocution, and a blow to the chest at exactly the wrong moment can also cause it.

How it is treated

The only effective treatment is a defibrillation shock, delivered as quickly as possible, together with CPR to keep blood moving until the shock can be given. Every minute of delay reduces the chance of survival by about 10 percent. This is why automated external defibrillators (AEDs) are placed in public buildings and why bystander CPR matters so much. Press the Shock button above to see a defibrillation. People who survive VF, or who are at high risk of it, are usually offered an implantable cardioverter-defibrillator (ICD), which detects VF and delivers the shock automatically within seconds.

On the EKG

A completely disorganized, wavy line with no recognizable P waves, QRS complexes, or T waves.

What is happening

The QT interval on the EKG measures how long the ventricles take to reset after each beat. In long QT syndrome the reset takes too long, because of a fault in the tiny channels that move potassium and sodium in and out of heart cells. Most of the time the heart beats normally. The danger is that an early beat can land while the ventricles are still resetting and set off a fast, twisting form of ventricular tachycardia called torsades de pointes. Torsades often stops on its own after a few seconds, causing a faint, but it can also deteriorate into ventricular fibrillation. The animation shows normal beats with a long QT. Press "Trigger an early beat" under the tracing to see the early beat land on the T wave and set off torsades, then use the Shock button to end it.

Risk factors and causes

Long QT can be inherited, in which case it often first shows itself as fainting during exercise, swimming, emotional stress, or a sudden loud noise, and there may be a family history of fainting or unexplained sudden death at a young age. Far more often it is acquired: caused by medicines, low potassium or magnesium, or a slow heart rate. Many common medicines can prolong the QT, including some antibiotics, antifungals, antinausea medicines, antipsychotics, antidepressants, and methadone. Combining several of these, or taking them with diarrhea or vomiting, raises the risk.

How it is treated

Torsades in progress is treated with intravenous magnesium, correction of potassium, stopping the offending medicine, and sometimes temporary pacing to speed the heart up. A shock is used if the person loses their pulse. For inherited long QT, beta blockers are the main long-term treatment and are very effective. People at highest risk may be offered an ICD. Everyone with long QT should keep a list of medicines to avoid, and a reference list is maintained at crediblemeds.org.

On the EKG

The T wave arrives late, so the distance from the start of the QRS to the end of the T wave is long. Torsades appears as a fast rhythm whose peaks seem to twist around the baseline, growing and shrinking.

What is happening

Torsades de pointes is a special form of ventricular tachycardia that occurs when the ventricles take too long to reset after each beat, which is what a long QT interval means. An early beat lands while parts of the ventricle are still resetting and the signal begins to spiral through the muscle. The name is French for "twisting of the points," because on the EKG the peaks of the beats seem to twist around the baseline, growing taller and then shorter. The heart rate is usually 200 to 250 beats per minute, and very little blood is pumped.

What you might feel

Short runs cause a sudden faint, a seizure-like spell, or a few seconds of pounding and dizziness, and then the rhythm often stops on its own. Longer runs can turn into ventricular fibrillation and cardiac arrest.

Risk factors and causes

Anything that lengthens the QT interval sets the stage: inherited long QT syndrome, low potassium or magnesium, a slow heart rate, and especially medicines. Many common drugs prolong the QT, including certain antibiotics, antifungals, antinausea medicines, antipsychotics, antidepressants, and methadone. The risk climbs when several are combined, when the kidneys or liver are not clearing them, or when vomiting or diarrhea drains potassium and magnesium. Women and older adults are more susceptible.

How it is treated

Intravenous magnesium is the first treatment and often stops the rhythm even when the magnesium level is normal. Potassium is corrected, every QT-prolonging medicine is stopped, and if the heart rate is slow it is sped up with a temporary pacemaker or a medicine such as isoproterenol, because a faster rate shortens the QT. If the person has no pulse, a shock is given at once. Torsades is different from ordinary ventricular tachycardia in one important way: some of the standard VT medicines, such as amiodarone and procainamide, lengthen the QT themselves and can make torsades worse, so they are avoided.

On the EKG

A fast, wide rhythm whose peaks grow and shrink in a twisting pattern around the baseline, usually starting after an early beat that lands on the previous T wave.

What is happening

Brugada syndrome is an inherited condition of the sodium channels in heart cells. Most of the time the heart beats in perfectly normal sinus rhythm and the person feels well. The problem is that a small region of the right ventricle, near its outflow tract, recovers unevenly after each beat, which creates the conditions for ventricular fibrillation to start without warning. This most often happens during sleep or rest, with fever, or after heavy meals or alcohol.

What it means

Brugada syndrome is a cause of sudden cardiac death in young, otherwise healthy people, more often men, and it often runs in families. Many people are found because a relative had an event, or because the pattern is spotted on an EKG done for another reason. Having the EKG pattern does not mean an event will happen; risk is highest in people who have already fainted or been resuscitated.

How it is treated

The most important measures are simple: treat fevers promptly with acetaminophen, avoid heavy alcohol, and avoid a specific list of medicines that block sodium channels, which includes some antiarrhythmics, some antidepressants, and some anesthetics. A current list is kept at brugadadrugs.org. People who have had a cardiac arrest or unexplained fainting are offered an implantable cardioverter-defibrillator (ICD). A medicine called quinidine and, in some centers, ablation of the affected area of the right ventricle can reduce episodes. First-degree relatives are usually offered screening.

On the EKG

The rhythm itself is normal. The clue is in leads V1 and V2, the chest leads that sit over the right ventricle, where the segment after the QRS is elevated in a coved, downsloping shape with an inverted T wave. The animation switches the tracing to lead V1 so you can see this pattern.

What is happening

The sinus node has become unreliable (sick sinus syndrome), so a lead in the right atrium takes over its job. Each pacing pulse starts the beat in the atrium, and from there the signal spreads across the atria and travels through the AV node and the normal wiring to the ventricles, exactly as a sinus beat would. Because the rest of the heart's wiring is used, the ventricles squeeze in a fully coordinated way.

When it is used

Atrial pacing is used when the sinus node is slow or pausing but the AV node and the wiring below it are healthy. Most modern devices for this situation also have a ventricular lead as a backup, in case the AV node develops problems later, but they are programmed to let the heart's own conduction do the work whenever possible.

On the EKG

A thin spike, then a P wave, then a normal narrow QRS.

What is happening

In this example the person has complete heart block: the sinus node works and the atria beat normally, but nothing gets through to the ventricles. A single lead in the right ventricle paces the ventricles at a steady rate. The pacing pulse starts near the tip of the right ventricle and spreads from cell to cell through the muscle, first through the right ventricle and then across to the left, so the QRS on the EKG is wide. The atria continue to beat on their own timetable, unconnected to the ventricles.

When it is used

A single ventricular lead is the simplest solution and is often chosen when the atria are in permanent atrial fibrillation, so there is no organized atrial beat to keep in step with, or when a simple backup is all that is needed. When the atria beat normally, as in this example, a dual chamber pacemaker is usually preferred because it keeps the atria and ventricles working in sequence.

On the EKG

P waves march along on their own. Each spike is followed by a wide QRS.

What is happening

Two leads are used, one in the right atrium and one in the right ventricle. The device paces the atrium, waits a fraction of a second for the atria to squeeze and push blood into the ventricles, and then paces the ventricle. This copies the normal sequence of the heart and keeps the upper and lower chambers working together, which improves how much blood is pumped and how the person feels. In this example both chambers are being paced because the sinus node is unreliable and the AV node is blocked.

How it adapts

A dual chamber pacemaker is constantly listening. If the sinus node produces its own beat on time, the device does not pace the atrium; it simply waits and, if the beat does not get through the AV node, paces the ventricle in step with it. If the heart conducts normally, the device does nothing at all. Most modern pacemakers also have a sensor that raises the paced rate when the person is active.

On the EKG

Two spikes per beat: one before the P wave and one before the wide QRS.

What is happening

CRT, also called a biventricular pacemaker, is a treatment for heart failure rather than for a slow heart rate. In this example the person has a weak heart and a left bundle branch block, so the left ventricle is activated late and the two ventricles squeeze out of step, which wastes energy. A CRT device has a lead in the right atrium, a lead in the right ventricle, and a third lead threaded through a vein that runs along the outside of the left ventricle. After each atrial beat the device paces both ventricles at the same moment, so they squeeze together again. Compare this animation with the LBBB animation above.

When it is used

CRT is offered to people with heart failure who still have symptoms despite good medicines, whose heart pumps weakly (a low ejection fraction), and whose EKG shows a wide QRS, especially a left bundle branch block. In the right people it improves symptoms, reduces hospital admissions, and helps the heart recover some of its strength. It is often combined with an ICD in one device. Newer approaches pace the heart's own wiring directly (conduction system pacing) to achieve the same goal.

On the EKG

A spike before each QRS, and the QRS is narrower than it was with the bundle branch block.