Very simply put, an "arrhythmia" is an "irregular heartbeat." It is a general description of a group of heart conditions which present with abnormal heartbeats, not a specific diagnosis. Unfortunately, many patients, after extensive cardiology evaluations, have been told that they they have an "arrhythmia." This is like saying someone has a "heart condition." It is vague and irrelevant.
A specific arrhythmia diagnosis must be made in order to help prognosticate a patient and guide treatment. Not all arrhythmias are created equal. Some are completely innocuous while others are associated with sudden cardiac arrest and instant fatality. It is simply not enough to make a diagnosis of "arrhythmia."
To understand any arrhythmia, one needs to have a basic understanding of the anatomy and physiology of the heart. The heart is divided into four chambers. The top two chambers are the atria and the lower two are the ventricles.
The right atrium (RA) collects blood from the veins and sends it to the right ventricle (RV), which then pumps the blood to the lungs to get it oxygenated. The fresh blood then returns to the left atrium (LA) which sends it to the left ventricle (LV) and then the left ventricle pumps the blood out to the body for general circulation. The atria and the ventricles must work in close synchrony for their optimal performance and the person's well being.
Because the heart must work in a well coordinated, synchronized fashion, any disturbances of the normal relationship between the chambers can cause various symptoms such as shortness of breath, lightheadedness, fainting spell, and even sudden death.
To understand why this occurs, let's examine the physiology of a normal heartbeat. The impulse of a heartbeat comes from its own intrinsic pacemaker, the "sino-atrial node" (SAN, a.k.a. "sinus node"), which resides in the top right portion of the right atrium (RA). This first activity of a heartbeat then causes the atria to activate, generating what is known as the "P wave" on an EKG (see diagram below).
This impulse than propagates to the relay station, the AV node (AVN), which resides near the center of the heart between the atrium and the ventricle. The AV node sends the signal down to the ventricles through a series of intricate network of conduction fibers called the His-Purkinje system. Two major cables of this system are the right bundle branch (RBB) and the left bundle branch (LBB). Via these cables the ventricles are activated, resulting in what we see as "QRS" on an EKG. The QRS portion of the EKG represents the activation of the ventricles, each of the three letters representing different portion of this event demarcated by a sudden change in the direction of the electrical forces (up and down). The final event is what we call "repolarization" and this shows up as the "T wave" on an EKG. Every normal heartbeat, thus, consists of this series of electrical events, designated in alphabetical order as "P-Q-R-S-T."
In order for the heart to work properly, this coordinated series of electrical activities must occur in this exact order for every single heartbeat. Any disturbance to this relationship is, by definition, an "arrhythmia" and can cause various symptoms, the degree of which depends on how badly this normal relationship has been altered by the arrhythmia. Thus, an arrhythmia such as a premature atrial contraction (PAC) causes relatively minor disturbances to the normal electrical activities and, for most patients, minimal to no symptoms. On the other hand, an arrhythmia such as ventricular fibrillation (VF) causes major alteration and the results are dramatic and fatal.
|What is Premature Atrial Contraction (PACs)?
This is one of the most common forms of arrhythmias. It is due to the premature discharge of an electrical impulse in the atrium, causing a premature contraction. Therefore, it is named "premature atrial contraction," or PAC. A PAC is premature because the it occurs earlier than the next regular beat should have occurred.
What are symptoms of PACs?
Most often, patients with PACs complain of palpitation. However, rather than reporting sustained racing heartbeat, they usually describe "missing" or "skipping" of the heartbeat. Some patients even feel that the heart has "stopped" while others describe a sensation of "flip-flop." This is due to the fact that the PAC comes too early (prematurely) in the cardiac cycle to have resulted in an effective pulse or heartbeat. Therefore, no heartbeat is felt until the next regularly-timed heartbeat occurs after a pause (so-called compensatory pause). Incidentally, the beat after the PAC usually occurs with stronger contraction than usual and can be associated with an urge to cough. Symptoms of PACs are virtually indistinguishable from those ofPVCs as the physiological effects are identical.
What causes PACs?
In the majority of cases, PACs occur in normal healthy individuals without any evidence of heart disease. Stress or stimulants such as tea, coffee, or alcohol can increase the frequency of PACs. In the minority of cases, PACs can be a sign of underlying heart condition in the atrium associated with hypertension or valvular condition.
Consequences of PACs.
The great majority of PACs are completely benign and require little if any treatment at all. As mentioned above, in rare cases, PACs may be the only sign of underlying heart conditions and these should be ruled out with appropriate evaluations.
As most PACs are benign, treatment is optional and is usually geared toward alleviation of symptoms. Medications such as beta blocker or calcium blockers are often used but with mixed result. Most important treatment, after ruling out severe underlying heart conditions, is patient reassurance and teaching of various coping mechanisms.
|What is Atrial Fibrillation?
Atrial fibrillation (commonly referred to as "AF" or "AFib") is a chaotic, irregular rhythm originating in the upper chambers of the heart, or the atria. It leads to a rapid and irregular heartbeat or pulse. This is one of the most common irregular heartbeats of patients over age 65 and one of the most preventable causes of stroke in America.
The sources of these discharges often come from the pulmonary veins (PVs) in the back side of the left atrium. As such, these areas are the target for curative ablation of atrial fibrillation.
Atrial fibrillation can be divided into three major categories: paroxysmal atrial fibrillation, persistent atrial fibrillation, and permanent atrial fibrillation.
What are symptoms of AF?
Surprisingly, many patients with AF are completely asymptomatic, or minimally symptomatic. Many patients are discovered to have AF during routine annual physicals. Some patients may feel only the hemodynamic consequences of AF and complain of nonspecific symptoms like fatigue, dizziness, or shortness of breath. Yet other patients may feel the irregularity and rapidity of the heartbeat, reporting symptoms of "pounding" or "palpitating" heart.
What causes AF?
Age is the most important factor for AF. Up to 10% of those over age 80 may have AF. Other common causes include high blood pressure, heart failure, heart valve disease, thyroid problem, lung problem, and open heart surgery. Increasingly common are patients with "lone AF," or AF without an identifiable cause. These patients are generally young and without evidence of concomitant heart condition. This type of AF can be cured byradiofrequency ablation.
Consequences of AF.
The most devastating consequence of AF is stroke. It does so by forming a blood clot in the left atrium, which can dislodge and embolize (carried by blood to distant site) to the brain. Along with hypertension, AF is one of the top preventable causes of stroke in America. Other serious consequences of AF include congestive heart failure and fainting, which are due to the uncontrolled rapid rates of AF and abnormal slowing of the heart, respectively.
There are many different treatment options for AF, the most important of which is stroke prevention with anticoagulation (thinning of blood with medication like Coumadin or warfarin). Without anticoagulation, patients with AF run the risk of stroke at about 5-10% per year. This figure is significantly higher if the patient also has heart failure, diabetes, hypertension, or severe heart valve problems. Frequently, patients also may need medications to help regulate or slow down AF. Cardioversion (electrical shock treatment) can also be performed to restore normal rhythm. Apacemaker can be useful in the case of slowing of heartbeat. An emerging therapeutic option that is gaining increasing acceptance isradiofrequency ablation.
Case Study 1.
A 52 year-old man came to the office with increasing shortness of breath for several months. He has been diagnosed with chronic AF for many years and heart rate had been very difficult to control, despite multiple medications. His heart rate was 140 bpm and he was in heart failure, with anejection fraction of 15%. He underwent a biventricular defibrillator implantation in conjunction with AV junction ablation. His heart rate was finally controlled and his heart failure symptoms improved. Six months later, his ejection fraction improved to 40% and he remained asymptomatic.
Case Study 2.
A 40 year-old man has many year history of paroxysmal (on and off) AF which is difficult to control despite several antiarrhythmic medications andcardioversion attempts. In addition, he developed several side effects from the medications that he had tried. Eventually, he was referred forablation of AF whereby the areas near the opening of the veins in the left atrium were target for ablation. Three months later, he was asymptomatic except for rare skipping of the heartbeat. His AF was cured and there was no need for further medications.
|What is atrial flutter?
Atrial flutter is a common arrhythmia with properties very similar to atrial fibrillation. It frequently coexists with AF in the same patient. An important difference, however, is that atrial flutter is a REGULAR rhythm whereas AF is always IRREGULAR. A fairly classic pattern of "saw-tooth" appearance can be seen on EKG (see below, arrows), but only in certain electrodes (typically inferior leads). It is important to make this distinction because almost all forms of flutter can be easily cured with radiofrequency ablation. All too frequently, atrial flutter is mis-classified as atrial fibrillation, therefore patient not offered the option of ablation.
What are symptoms of atrial flutter?
Symptoms of atrial flutter are indistinguishable from those of atrial fibrillation. Furthermore, as in patients with AF, many patients with atrial flutter can be completely unaware of fast heartbeat until it is too late (i.e., when heart failure develops).
What causes atrial flutter?
Everything that causes atrial fibrillation can also lead to atrial flutter. However, unlike atrial fibrillation, electrical impulses in atrial flutter follow a large and predictable circuit (see diagram), making it possible to interrupt this circuit with curative radiofrequency ablation. While atrial flutter frequently occur in otherwise healthy patients without structural heart disease, it is also very common among patients with prior cardiac surgery (especially those with corrected congenital heart diseases), where the electrical circuits form around the area of previous surgical scars in the atrium.
Consequences of atrial flutter.
All the sequelae of atrial fibrillation can occur with atrial flutter, including stroke. Furthermore, prolonged and uncontrolled rapid heartbeat can lead to heart failure via the mechanism of "tachycardia-mediated cardiomyopathy." Basically, a heart that pumps too rapidly over prolonged periods of time will dilate and weaken, resulting in failure to pump blood effectively. Rarely, in young patients whose heart rate can conduct very rapidly (i.e., 1:1 AV conduction with hear rate over 250 bpm), fainting and sudden death can occur.
Treatment options are nearly identical to those in atrial fibrillation with the following important exception. Essentially all forms of flutter can be CURED with radiofrequency ablation. In the typical form of atrial flutter, cure rate can be as high as 98% and for the atypical forms, between 80% and 90%. Success rate is significantly enhanced by the ability to perform so-called 3-D mapping (electro-anatomic mapping) study.
A 60 year-old woman came to the hospital emergency room because of rapid heart beat. She had an ASD (hole in the heart) repaired 30 years ago. "Atrial fibrillation" has been diagnosed by her physician for many years and she has been told that she will always be in "atrial fibrillation" for the rest of her life. EKG on admission showed that she was in fact in atrial flutter. 3-D mapping study was performed which showed the electrical circuits to be around the area of surgical scars created during her previous heart surgery. Ablation performed during the same session terminated the flutter and restore normal rhythm for the first time in many years. She remained in normal rhythm a year later.
|What is sick sinus syndrome?
Also known as "tachy-brady syndrome," sick sinus syndrome is a common condition that affects the elderly, accounting for the majority of patients undergoing pacemaker implantation in the U.S. It is frequently associated with atrial fibrillation or atrial flutter.
In brief, it is due to the inability of the heart to maintain and regulate a steady and normal heartbeat. It either goes too fast (during atrial fibrillation or flutter) or too slow (after conversion to normal rhythm), and rarely just right. The heart can sudden stop for up to 6 seconds, as in the case below.
What are symptoms of sick sinus syndrome?
Symptoms of SSS are caused by the frequent alternation of rapid and slow heart beat, resulting in palpitation (pounding heart beat), fainting, fatigue, and shortness of breath.
What causes sick sinus syndrome?
Everything that causes atrial fibrillation and atrial flutter can cause sick sinus syndrome. Age is the number one risk factor for developing SSS. It is frequently exacerbated by the use of medications (i.e., digoxin, beta blocker, calcium channel blocker). The main purpose of these medications is slow down the fast heartbeat in this syndrome, but the often inevitable trade-off is excessive slowing of the heart rate to the point of needingpacemaker.
Consequences of sick sinus syndrome.
The main feature of this syndrome is inability to maintain normal stable heart rate. The resultant symptoms can include palpitation, shortness of breath, easy fatigue, and fainting spells.
In patients with predominantly a slow heart rate problem, pacemaker is the treatment option of choice. There are no reasonable medical alternatives as no medications can speed up the heartbeat effectively and safely on a long term basis. For those with both fast and slow heart rate problem, medications used to control the rapid heartbeat in this syndrome often slow the heart rate to the point of requiring a pacemaker. This is the classic "rock and hard place" scenario where if left untreated, the rapid heart rate can potentially lead to other serious consequences. Very frequently, patients end up with a combination of medications plus pacemaker.
An 80 year-old lady came to the emergency room having fallen and broken her hip, requiring urgent hip surgery. She was not sure if she had passed out or simply "tripped" over a phone cord. At the time of admission, she was found to be in rapid atrial fibrillation, which later converted back to regular rhythm. However, in doing so, the heart slowed down after the conversion and stopped for 5 seconds, causing her to pass out again. A pacemaker was later implanted for the management of the slow heart beat and medications added to control the rapid heartbeat. She had her hip fixed and did fine thereafter.
What is supraventricular tachycardia? Simply stated, an SVT is an arrhythmia that originates from above ("supra") the ventricle. This term encompasses a large number of arrhythmias and therefore the term "SVT" is only a general description, not a specific diagnosis. Most commonly, however, it refers to one of 3 commons types of arrhythmias, AV Nodal Reentrant Tachycardia, Atrial Tachycardia, and Wolff-Parkinson-White syndrome.
What are symptoms of SVT? Palpitation, or racing heartbeat, is the predominant symptom in SVT. Occasionally, some patients have no awareness of rapid heartbeat, whose only symptoms may be fatigue and fainting. Other patients describe chest paint, shortness of breath, and a sense of fullness in the neck. Children with SVT often report to their parents that their "heart hurts" since they do not have the full vocabulary that adults do.
What causes SVT? An "extra nerve" exists in the heart of nearly all patients with SVT, which over time becomes active and causes fast heartbeat. Most cases of SVT are genetic. In other words, patients are born with this "extra nerve" in the heart but it may remain dormant for many years, often surfacing when patients reach their 20s and 30s. Rarely, some patients may be diagnosed for the first time in their 60s and 70s.
Importantly, one must distinguish between the cause and the trigger for SVT. This is often a source of confusion for patients. While the "extra nerve" causes SVT, an attack of SVT may require certain triggers, which include caffeine, alcohol, some herbal medications, and some over-the-counter cold medications containing stimulants. Just because a large ice tea triggered an SVT attack, it does not mean that it caused the SVT. For, without the ice tea, the "extra nerve" is still present, just waiting for another trigger to cause another attack later.
Consequences of SVT. Most patients with SVTs usually have a benign clinical course. In other words, SVTs as a rule do not usually cause fatality. However, in some patients when heart rate reach very high level (above 250 bpm) serious consequences can occur, including fainting spells and sudden death. In some cases, heart failure can result from chronic uncontrolled rapid SVT.
Treatment options. Most SVTs can be treated with medications but medications represent a temporizing measure, not a cure for the condition. For children or young adults, life-long therapy with medication(s) may not be reasonable. Radiofrequency ablation is the only curative treatment options for SVT. It works by selectively destroying the "extra nerve" via a minimally invasive procedure.
|What is AVNRT?
AVNRT is the most common type of SVT. It originate from the AV node, located near the center of the heart. It is due to "reentry," or circular movement of electricity (see red arrows), between the normal nerve in the AV node ("fast pathway") and the extra nerved called the "slow pathway."
This arrhythmia can occur in the form of typical AVNRT (slow-fast reentry) or atypical AVNRT (fast-slow or slow-slow reentry). AVNRT accounts for about 80-90% of all SVTs.
What are symptoms of AVNRT?
Symptoms of AVNRT are similar to all other types of SVT, mainly that of palpitation, or racing heartbeat. Often patients may report a sense of fullness in the neck and urinary urgency. The latter is due to the stretch of the atrium that releases a diuretic hormone. Occasionally, fainting can occur as the result of extremely rapid heart beat.
A typical feature of this arrhythmia is that patients can often break the attack by bearing down and holding their breath at the same time (Valsalva maneuver). Putting cold water on the face can trigger similar neurological reaction (vagal) which can stop the arrhythmia. The following EKG shows a classic pattern of AVNRT with a sudden stop and return to normal rhythm.
What causes AVNRT?
Most patients with AVNRT are born with an extra nerve called "slow pathway" which resides in the lower portion of the AV node, situated at the junction between the upper (atrium) and the lower (ventricle) chamber of the heart. Over time, this nerve matures and becomes active, causing the rapid heartbeat, usually when patients reach their 30s to 50s. Even though there may be many triggers of an AVNRT attack (see SVT section), the underlying cause is the extra nerve. In other words, taking away the triggers may temporize the issue, but does not solve the problem. Similarly, taking medications to suppress the triggers does not cure the underlying problem.
Consequences of AVNRT.
Patients with AVNRT usually have a benign clinical course. In other words, fatality is unusual. However, in some patients when heart rate reaches very high level (above 250 bpm) serious consequences can occur, including fainting spells and sudden death. In some cases, heart failure can result from chronic uncontrolled rapid SVT.
In the emergency room, physicians frequently administer an intravenous medication called "Adenosine" or "Adenocard." This medication's effect lasts only a few seconds, but it has the ability to get into the electrical circuit of AVNRT and break it temporarily. Because the effects are short lasting, it has no clinical application other than in the emergency room.
Outside of an ER, AVNRT can be treated with chronic suppressive medications. While medications may work well for some patients with AVNRT, many patients can have frequent breakthrough attacks. Furthermore, there are several draw backs of medications, such as costs and long-term side effects. Most importantly, medications do not cure the condition, only temporarily putting a "band-aid" on the situation. In other words, when one stops medications, the episodes will recur.
For younger patients, especially, radiofrequency ablation may be the preferred treatment option over life-long drug therapy. This minimally invasive procedure works by selectively destroying the culprit "slow pathway." It is successful in about 98% of cases. Patients can expect a permanent cure of this condition with rare recurrence rates (1-4%). The procedure is easily done on an outpatient basis with minimal risks. In 1% of the cases of ablation for AVNRT, one may experience AV block (excessive slowing of the heart rate) so as to require a pacemaker.
Case Study 1.
Mary is a 30-year old house wife with a busy life, caring for three growing children and a husband that is busy building his career. For the last several years, she has been experiencing intermittent racing heart beat and a severe sense of anxiety, lasting 10 to 30 minutes each. She has not passed out but occasionally felt that she was about to. She has gone to the emergency room several times but by the time she reaches the ER, the fast heartbeat has stopped. The EKG and extensive evaluation in the ER showed no abnormality and she was sent home with a diagnosis of "palpitation." Her family physician prescribed outpatient monitoring (24-hour Holter) but the episodes did not occur during the recording period and therefore the monitor was read as "normal." She was diagnosed with "anxiety and panic attack" and prescribed anti-anxiety medications, to no avail.
After 2 years of recurrent attacks, she had an episodes long enough that when the paramedics arrived, she was still in the tachycardia and it was recorded on an EKG. She was referred to an electrophysiologist and the diagnosis was confirmed, followed by an outpatient radiofrequency ablation. She had no further attacks since then and is considered cured, without need for medications.
Case Study 2.
John is a 50 year-old executive with a long history of palpitation, previously diagnosed with SVT. Cardizem and verapamil did not prevent recurrences of the attack, and he was switched to Toprol. Although it helped, episodes still occurred once to twice a year. Furthermore, he travels frequently out of the country for business and he is an avid skier. Some episodes had occurred while he was on the airplane or on the ski slope. After several such attacks, he was referred to an electrophysiologist followed by a curative radiofrequency ablation. AVNRT was confirmed at the time of the study and the "slow pathway" ablated successfully He was taken off all medications and had no further symptoms.
What is atrial tachycardia?
|What is Atrial Tachycardia?
This is a type of SVT that originates from either the right or the left atrium (top chamber of the heart). It is usually due to an irritable focus in the atrium (automatic AT) or due to a small (micro-reentry) or large area (macro-reentry) of electrical circuit in the atrium. This tachycardia occurs independent of the rest of the heart. In other words, the focus or the circuit is confined to the atrium, without involvement of the AV Node (as in AVNRT) or the ventricle (as inWPW).
What are symptoms of AT?
Clinical presentation of AT is indistinguishable from other forms of SVTs. Symptom mainly consists of palpitation, or racing heartbeat. Occasionally, fainting can occur as the result of extremely rapid heart beat. Sometimes even an experienced cardiologist can not distinguish an EKG of an AT from that of AVNRT. The diagnosis is often made at the time electrophysiology study.
What causes AT?
Most atrial tachycardias occur without any identifiable causes. However, they may also be the results of prior open heart surgical with resultant scars on the atrium itself. Drugs, thyroid, and lung conditions may be additional causes.
Consequences of AT.
They are similar to all other SVTs. Patients with AT usually have a benign clinical course. In other words, fatality is unusual. However, in some patients when heart rate reaches very high level (above 250 bpm) serious consequences can occur, including fainting spells and sudden death. In some cases, heart failure can result from chronic uncontrolled rapid SVT.
In the emergency room, adenosine can be given but because the reentrant circuit does not involve the AV node, adenosine will NOT break the tachycardia, but only slowing it down by blocking the AV node. Finding of continuation of AT with AV block confirms the diagnosis of AT. Cardizem may be given to slow the AV node conduction.
Chronic medications usually do not suppress the attacks in patients with AT. Medications to slow the heart rate, such as cardizem, verapamil, atenolol, and Toprol, are the first line of therapy, followed by an antiarrhythmic medication (amiodarone, sotalol, flecainide, propafenone) to prevent the atrial focus from firing. Radiofrequency ablation can be performed with success rates in the 80% to 90% range. With the advent of 3-D mapping, the success rate had been greatly enhanced because of the ability to pinpoint the small focus of these arrhythmias.
Mr. W. is a 50 year-old man with recent onset of rapid heartbeat. He showed up in the emergency room with HR up to 200 beats per minute, complaining of symptoms of racing heartbeat, dizziness, and near-fainting. EKG in the ER confirmed the diagnosis of SVT. Several medications were added on but tachycardia continued to recur several times a day. An electrophysiologist saw him in consultation and noted that cardizem slowed down the heart rate but the tachycardia continued in the atrium at 200 bpm. A diagnosis of AT is suspected and he was transferred to a facility with 3-D mapping capability, and Radiofrequency ablation easily eliminated the small focus located in the right atrium. He has no further symptoms after that and enjoyed excellent health thereafter without needs for medications.
|What is WPW syndrome?
This is a syndrome consisting of various types of arrhythmias all of which are the result of an extra nerve connecting atrium and the ventricle, called "accessory pathway" or a "bypass tract." In individuals without WPW, there is only one electrical connection between the atrium and the ventricle, the AV node. In patients with WPW syndrome, the extra connection, the "accessory pathway" or "bypass tract," allows electrical impulses to travel back and forth between the atria and the ventricles, resulting in rapid heartbeats (commonly referred to as orthodromic AV Reentry Tachycardia or antidromic AV Reentry Tachycardia). Atrial fibrillation and atrial flutter can also occur as the result of WPW syndrome.
What are symptoms of WPW syndrome?
Most commonly, palpitation is the major symptom, although fainting and rarely sudden cardiac death may occur if heart rate is fast enough. Children, unable to verbalize because of limited vocabulary, often can have atypical symptoms such as "chest pain." Most patients will be symptomatic before the teenage years, but some patients are not diagnosed until much later in life because of relatively mild or limited symptoms.
Patients with WPW syndrome can have extremely rapid heart rate during an attack, especially when it is due to atrial fibrillation. Heart rate as fast as 300 beats per minute has been recorded and this can be a serious cause of sudden cardiac arrest.
A diagnosis is easily made with an EKG, even when patients are not having an active attack of tachycardia. That is because the present of the extra nerve causes the EKG to be very abnormal, due to the presence of "pre-excitation" of the ventricle. The extra-nerve allows the electrical impulse to reach the ventricle from the atrium before the normal impulses from the AV node arrives. In other words, it "beats" the AV node to the ventricle and thus "pre-excites" the ventricle, resulting in the classic appearance of a "delta wave" (arrows).
In some patients, the extra nerve conducts on in the retrograde (backward) direction. Because this nerve does not "re-excite" the ventricle, the typical "delta wave" is not seen, and the condition is called "concealed accessory pathway." Thus, EKG in these patients can be completely normal in appearance and the diagnosis of the extra pathway can be made only at the time of an electrophysiology study.
What causes WPW syndrome?
WPW syndrome is due to the presence an extra nerve that connects the atrium and the ventricle. This nerve is often present at birth but can remain dormant for many years until it becomes active and starts causing rapid heartbeat.
As in all SVTs, one must distinguish between the cause and the trigger for WPW. While the "extra nerve" causes the syndrome, an attack of rapid heartbeat may require certain triggers, which include caffeine, alcohol, some herbal medications, and some over-the-counter cold medications containing stimulants. Just because a large ice tea triggered an episode of attack, it does not mean that it caused WPW syndrome. For, without the ice tea, the "extra nerve" is still present, just waiting for another trigger to cause another attack later.
Conversely, taking away the triggers or taking suppressive medications does not cure the condition, only temporizing it. The "extra nerve" is still present whether the triggers are there or whether patients are on medications.
Consequences of WPW syndrome.
Most patients with WPW syndrome have a benign clinical course, interrupted by bouts of rapid heartbeat and its associated symptoms. Very rarely,sudden death can occur in those patients whose extra nerve conducts electrical impulses extremely rapidly so as to result in a cardiac arrest.
As discussed above, taking medications or avoiding triggers only temporarily prevents or reduces the occurrences of the attack, but does not cure the condition. Medications useful in this condition includes beta blockers, calcium blocker, and anti-arrhythmic medications that either predominantly blocks the sodium channels of the heart (flecainide, propafenone, procainamide) or the potassium channels (sotalol, amiodarone).
In the emergency room, medications such as adenosine and cardizem may be useful in terminating a "reentrant" arrhythmia involving the AV node. However, when patients present with atrial fibrillation and WPW, these medications are contraindicated. For, blocking the AV node with these medications can result in extremely rapid and unopposed conduction down the accessory pathway, leading to cardiac arrest. In the case of WPW with atrial fibrillation, direct current cardioversion (electrical shock to the heart) is the preferred treatment option in the acute setting.
In the chronic setting, medications may be useful for the suppression of attacks but does not cure the condition. Because this condition occurs mainly in young patients, one must also consider the long-term consequences of life-long medications. Therefore, the overwhelmingly preferred treatment option is radiofrequency ablation. This minimally invasive, catheter-based procedure can achieve a cure rate of 98% in most forms of WPW syndrome.
Jerry is a 16 year-old high school student in excellent health, without any prior known health problem. On a Sunday afternoon while watching TV, he suddenly collapsed without any identifiable trigger or prodromal symptoms. When the paramedics arrived, he was in ventricular fibrillation and was successfully defibrillated and resuscitated. After he was transferred to the emergency room, he was in a coma because of the cardiac arrest. EKG at that time showed classic "delta waves" and the diagnosis of WPW was made. In the hospital, he had several episodes of rapid heartbeat documented on EKG monitors. Two weeks later, he began to recover from the deep coma which resulted from the brain injury sustained during the cardiac arrest. He was referred to radiofrequency ablation at another hospital and a right sided "accessory pathway" was confirmed at the time of the study. Subsequent radiofrequency ablation was successful in eliminating this extra pathway.
|What is Premature Ventricular Contraction (PVCs)?
This is one of the most common forms of arrhythmias. It is due to the premature discharge of an electrical impulse in the ventricle, causing a premature contraction. Therefore, it is named "premature ventricular contraction," or PVC. A PVC is premature because the it occurs earlier than the next regular beat should have occurred.
What are symptoms of PVCs?
Most often, patients with PVCs complain of palpitation. However, rather than reporting sustained racing heartbeat, they usually describe "missing" or "skipping" of the heartbeat. Some patients even feel that the heart has "stopped" while others describe a sensation of "flip-flop." This is due to the fact that the PVC comes too early (prematurely) in the cardiac cycle to have resulted in an effective pulse or heartbeat. Therefore, no heartbeat is felt until the next regularly-timed heartbeat occurs after a pause (so-called compensatory pause). Incidentally, the beat after the PVC usually occurs with stronger contraction than usual and can be associated with an urge to cough. Symptoms of PVCs are virtually indistinguishable from those ofPACs as the physiological effects are identical.
What causes PVCs?
In the majority of cases, PVCs occur in normal healthy individuals without any evidence of heart disease. Stress or stimulants such as tea, coffee, or alcohol can increase the frequency of PVCs. In the minority of cases, PVCs can be a sign of underlying heart condition such as heart failure or previous heart attack, but these are the exceptions rather than the rules.
Consequences of PVCs.
The great majority of PVCs are completely benign and require little if any treatment at all. As mentioned above, in rare cases, PVCs may be the only sign of underlying heart conditions and these should be ruled out with appropriate evaluations.
As most PVCs are benign, treatment is optional and is usually geared toward alleviation of symptoms. Medications such as beta blocker or calcium blockers are often used but with mixed result. Most important treatment, after ruling out severe underlying heart conditions, is patient reassurance and teaching of various coping mechanisms.
|What is ventricular tachycardia associated with Genetic Syndromes?
This is an inheritable, potentially life-threatening condition, resulting in rapid irregular heartbeats in the ventricle. The basis of most of these conditions is the abnormal formation of "ion channels" in cardiac tissue (usually potassium or sodium channels) which result in abnormal electrical conduction. Common examples are the Brugada syndrome, Arrhythmogenic Right Ventricular Dysplasia (ARVD), Hypertrophic Cardiomyopathy (HCM), and long QT syndrome (LQTS). VT associated with these syndromes are serious and can lead to cardiac arrest.
What are symptoms of ventricular tachycardia associated with Genetic Syndromes? ?
Syncope, or fainting spell, is a common presentation for patients with these syndrome. In some patients, sudden cardiac arrest may be the first and only symptoms of these conditions. In yet other patients, there may be no symptoms at all and the diagnosis was made only when one of their close relatives was diagnosed with these syndromes.
This is an example of a patient with Long QT and rapid ventricular tachycardia called Torsades de Pointes. The QT interval is markedly prolonged (arrow), resulting in premature beats, which then became a sustained life-threatening tachycardia.
What causes ventricular tachycardia associated with Genetic Syndromes? ?
As mentioned above, this is a genetic disorder resulting in abnormal ion channel formation and arrhythmia. One can not "acquire" these conditions, but rather patients were born with the them. However, certain medications or physiological conditions may precipitate the attacks of VT in susceptible individuals.
Consequences of ventricular tachycardia associated with Genetic Syndromes.
The majority of cases of these types of VT are associated with serious consequences, ranging from fainting spells to sudden cardiac arrest.
The implantable defibrillator is the most commonly prescribed treatment options for patients with these conditions who fall in the category of "high risk" based on a number of clinical and laboratory criteria. In patients who have experienced episodes of ventricular tachycardia or who had suffered cardiac arrest, an implantable defibrillator is mandatory.
What is idiopathic Ventricular Tachycardia?
By definition, "idiopathic" means "without a cause." In other words, an identifiable cause for VT can not be found with standard cardiac testing. There is no evidence of coronary disease, cardiomyopathy, or genetic syndromes. The heart is structurally normal and the condition is due to abnormal electrical conduction of the heart.
It is important to make this diagnosis as the treatment is very different from that for most other forms of VT discussed so far. There are two important varieties of idiopathic VT: Right Ventricular Outflow Tract (RVOT) or Left Ventricular Outflow Tract VT (LVOT) and Left Ventricular Fascicular Tachycardia. Most of these tachycardias occur in patients' 4th and 5th decade of life. These two major forms of VT have very characteristic appearance on EKG.
RVOT tachycardia arises from the right ventricular outflow tract area, commonly just under the pulmonic valve, but occasionally above the valve in the pulmonary artery. The typical EKG appearance shows marked inferior axis deviation (large positive R waves in leads II, III, AVF), and left bundle branch block appearance, with R wave late peaking in the precordial electrodes.
LVOT tachycardia originates on the left ventricular outflow tract. The EKG can be very similar to that from RVOT tachycardia, with the exception of an "early precordial transition." The R wave becomes "positive" earlier the the precordial leads.
Left Ventricular Fascicular Tachycardia originates in the left ventricular apical inferior septum and results from "reentry" within the Purkinje fibers (normal electrical cables within the ventricle). The typical appearance is that of right bundle branch block appearance with "superior axis" deviation (negative in leads II, III, AVF). Because the origin is in the septum near the normal conduction cables, the tachycardia can have a fairly narrow QRS appearance, mimicking SVT. This tachycardia can respond to IV verapamil, causing more confusion with SVT.
What are symptoms of idiopathic VT?
Most common symptoms are palpitation and fainting. Sudden cardiac death is rare in these conditions. Symptoms from ventricular tachycardia can be virtually indistinguishable from those of SVT, thus the critical importance of having an EKG diagnosis.
What causes idiopathic VT?
As discussed above, there is no identifiable cause and hence the term "idiopathic." These conditions are due to abnormal electrical impulses in the ventricles and are not the results of hardening of the artery (coronary artery disease) or disease process in the muscle of the heart (myopathy). These conditions must be ruled out by appropriate tests before making the diagnosis of idiopathic VT.
Consequences of idiopathic VT.
Generally, this form of VT has a benign clinical course and sudden cardiac arrest is rare. Symptoms, however, can be incessant, recurrent, and disabling, with frequent fainting spells.
Medications such as beta blocker or calcium channel blockers can be effective for these arrhythmias. In the ER, the outflow tract tachycardia can be stopped with intravenous adenosine. Fascicular VT can often be terminated with verapamil. Stopping a ventricular tachycardia in the ER with adenosine or verapamil should alert the clinician to the possibility of a curable form of ventricular tachycardia.
Nearly all forms of idiopathic ventricular tachycardia can be readily cured with radiofrequency ablation in the right or the left ventricle. Because the success rates for curing these arrhythmias are in excess of 95%, ablation has become the standard of care for most patients afflicted with idiopathic ventricular tachycardia.
|What is ventricular fibrillation?
This is a lethal arrhythmia that leads to instant death within minutes. Most patients do not survive an episode of VF unless they are immediately resuscitated by medical personnel using a defibrillator. This is the mechanism by which patients with heart disease die suddenly (so-called "sudden cardiac death").
This is an extremely rapid and chaotic rhythm that occurs in the ventricle, leading to loss of a coordinated contraction of the ventricles with instant hemodynamic collapse and subsequent sudden cardiac arrest.
What are symptoms of ventricular fibrillation?
There are usually no symptoms to speak of as this arrhythmia usually occurs as sudden cardiac death (see below) with little or no prodromal symptoms (warning sign). Patients will die within minutes of the onset of this arrhythmia unless resuscitated immediately.
What causes ventricular fibrillation?
With rare exceptions, most patients who suffer VF arrest have severe underlying heart disease, such as a prior large heart attack and/or severe heart failure and cardiomyopathy. In other cases, certain medications and some genetic diseases (such as Long QT Syndrome and Brugada syndrome) can also cause VF. In patients with heart failure, the worse the heart function is (as measured by Ejection Fraction), the higher the chance of patients developing this deadly arrhythmia.
Consequences of ventricular fibrillation.
Almost without exception, VF will lead to sudden death unless patients are resuscitated in a timely manner (usually within minutes).
All patients with ventricular fibrillation must be treated with an implantable defibrillator, unless the VF episode was due to a "reversible cause" (a cause that can be identified, corrected, and guaranteed not to recur -- a rare entity). It is no longer an acceptable medical practice to treat patients with this deadly disease with medications alone without a defibrillator.
What is sudden cardiac death?
This is a deadly condition that is a consequence of a disease rather than a disease itself. Sudden cardiac death occurs when a patient goes into an extremely rapid and dangerous rhythm such as ventricular fibrillation, ventricular tachycardia, and rarely some forms of supraventricular tachycardia. The rapidity of the heart beat (often above 250 beats per minute, sometimes over 300) results in ineffective heart pumping function and hemodynamic collapse. The heart, in layman's term, basically "stops" (but in actuality, it goes too fast), resulting in sudden loss of consciousness, and frequently, if not resuscitated immediately, loss of life.
What are symptoms of sudden cardiac death?
As in ventricular fibrillation, there are often no waning signs since death can strike within minutes of the onset of this arrhythmia. Some patients, however, prior to the onset of sudden cardiac death, may suffer from periodic lapse of consciousness, or fainting spells (syncope), due to less severe or self-limiting forms of this arrhythmia.
What causes sudden cardiac death?
Risk factors for sudden cardiac death are the same as those for ischemic ventricular tachycardia and ventricular fibrillation. It usually occurs in patients with severely damaged and enlarged heart associated with congestive heart failure.
Consequences of sudden cardiac death.
Self-evident. Death can be imminent, thus the term sudden cardiac death.
As with ventricular fibrillation, there are no reasonable treatment alternatives other than implantable defibrillators. With rare exceptions, all patients who have survived sudden cardiac death should undergo implantation of a defibrillator.
|What is bradycardia and heart block?
Bradycardia means, simply, "slow heartbeat." This can be due to many reasons, one of which is heart block. Heart block refers to a condition where the electrical impulses in the normal activation sequence are blocked at certain level and fail to reach the ventricle (see section on basic cardiac anatomy and physiology). The result is the loss of heartbeat and subsequent loss of blood pressure leading to fainting or near-fainting.
What are symptoms of bradycardia and heart block?
Because a heart with slow heartbeat can not generate enough blood flow to the brain, most patients experience fainting spells with bradycardia or heart block. In other patients, symptoms can be very subtle, such as dizziness, fatigue, lack of stamina, heart failure, or simply exercise intolerance (e.g. can play only 9-hole rather than the usual 18-hole golf).
What causes bradycardia and heart block?
Medications are common causes for slow heart beat and heart block. Today, many elderly patients are taking multiple medications for blood pressure and other heart conditions, many of which can interfere with the normal heartbeat. Rarely, low thyroid state and acute heart attack can cause slow heartbeat. In the absence of these identifiable causes, slow heartbeat or heart block are due to natural ageing of the cardiac electrical system.
The condition of "heart block" should be distinguished from "blockage of artery." Blockage of artery occurs as a result of cholesterol buildup in the coronary arteries (arteries supplying blood to the heart muscle) leading to heart attack. Heart block, on the other hand, is a electrical problem of conduction disorder and does not imply blockage or hardening of the arteries.
Consequences of bradycardia and heart block.
Fainting, or transient lapse of consciousness, is a common consequence of this condition. The most serious consequence of bradycardia and heart block are the results of the trauma associated with fainting and falling. Head injury and hip fracture are common, often requiring intensive inpatient treatment and surgery. Occasionally, sudden death can occur if the heart rate drops very suddenly and irreversibly.
Unless an identifiable cause for slow heartbeat is found (such as medications that can be safely stopped), most patients with slow heartbeat with symptoms need to have a permanent pacemaker implanted.
What is bundle branch block?
There are two main electrical cables in the heart that conduct electrical impulses, designated the right and left bundle branch (see section on basic cardiac anatomy and physiology). When electrical impulses in one of these two cables are delayed or blocked, the EKG shows a pattern of "bundle branch block."
When the right bundle does not conduct normally, it is called "right bundle branch block." When the left bundle is affected it is called "left bundle branch block."
Like "heart block," this type of "block" should be distinguished from "blockage of artery."
What are symptoms of bundle branch block?
For the most part, there are no symptoms, except in cases of advanced block (see below).
What causes bundle branch block?
Most commonly there are no specific causes. In 5% of healthy individual, one can observe "right bundle branch block pattern." In some cases, bundle branch block occurs as a result of heart attack. In others, it can be the manifestation of underlying severe heart disease. And yet in others, they can be normal variation.
Consequences of bundle branch block.
Usually there are no specific consequences of an isolated finding of bundle branch block. Two notable exceptions are bundle branch block associated with a new heart attack, and alternating bundle branch block. In these cases, a pacemaker may be necessary.
Unless symptoms of slow heartbeat are noted, most patients with bundle branch block do not require treatment.
What is AV block?
AV block occurs when there is a delay or interruption of electrical impulse from the atrium into the ventricle (see basic cardiac anatomy and physiology). The terms 1st, 2nd, and 3rd degree AV block denote the relative severity of such heart block.
The level of the block can be at the AV node, the His Bundle, or below the His Bundle. The lower the level of block, the more ominous the prognosis.
This is an example of 3rd degree AV block, a.k.a. complete heart block, where the P waves from the atrium continues but no conduction occurs into the ventricle, thus no R wave and complete "flat line."
What are symptoms of AV block?
1st degree AV block usually does not cause symptoms. As the severity of heart block increases, symptoms can consist of fatigue, dizziness, fainting, black out, and sudden death.
What causes AV block?
Medications are most common causes for AV block. Sometimes, AV block occurs as a result of aging related deterioration in the conduction tissue. Uncommonly, they can be the results of certain type of arthritis, muscular dystrophy, and infection (Lymes disease).
Consequences of AV block.
In higher degree blocks, symptoms of dizziness and even fainting spells can occur, accompanied by the injuries associated with the fall. Occasionally, sudden death can occur if the heart rate drops very suddenly and irreversibly.
Any patients with AV block associated with symptoms should have a permanent pacemaker implanted. If symptoms are equivocal or degree of block is not certain, additional evaluation such as electrophysiology study or long term EKG monitoring may be necessary.
What is syncope?
Syncope in English means "transient lapse of consciousness." It differs from sudden death only in terms of degree (reversible versus irreversible loss of consciousness) and not absolute terms. Therefore, the condition of syncope shares many common causes with sudden death. The challenge in the evaluation and treatment of this condition is that syncope is not a disease, but a condition which can be caused by many different diseases.
Furthermore, many people confuse the condition of syncope with seizure, stroke, or transient ischemic attack (TIA). Failure to make the correct diagnosis can lead to delay in appropriate treatment.
What are symptoms of syncope?
Fainting, or transient loss of consciousness (fainting, black out, etc)" are the presenting symptoms of this condition..
What causes syncope?
As mentioned above, syncope and sudden death often differ only in degree, not in absolute terms. Therefore, any condition that leads to sudden death can often manifest as fainting. In fact, fainting can often be a harbinger of sudden death in patients with certain heart diseases. Furthermore, those with dizziness may have a mild form of syncope (pre-syncope or near syncope).
Common causes of syncope include irregular heartbeat (both fast and slow), unstable blood pressure, medication, vasovagal reaction, and a long list of other causes.
Consequences of syncope.
For obvious reasons, injuries, often serious, can occur in patients who faint. In susceptible patients, usually those with serious heart conditions such as heart attack and heart failure, fainting can often be a harbinger of subsequent sudden death.
There is no single treatment for fainting and syncope because there are many different causes for this condition. Slow heartbeat causing fainting must be treated with a pacemaker, whereas rapid heartbeat causing syncope should be treated with an implantable defibrillator or ablation. Establishing a diagnosis (finding out what causes fainting), therefore, is of utmost importance. Evaluation and treatment for fainting remains one of the biggest diagnostic challenges in today's medicine. The next section on Evaluation and Diagnostic Tests will go into details on how some difficult diagnoses can be made.