- effective for pt with both sustained ventricular tachycardia and fibrillation
- includes an arrhythmia detection circuit, a power source, and capacitors to store and release electrical current
what AICD does
- cardioversion - heart arrhythmias to sinus rhythm
- defibrillation
- rate sensing
- ventricular pacing
leads implanted by a sternotomy, thoracotomy or subxiphoid approach
AICD implantation at
- drug refractory ventricular tachycardia
- globally depressed left ventricular function without aneurysm
- arrhthmia noninducible at EP study
- frequent ventricular tachycardia in a pt who cannot undergo direct resection
complications
- programming errors
- component failures
- infection
- generator migration
- skin erosion
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Angina pectoris is chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Greek ankhon ("strangling") and the Latin pectus ("chest"), and can therefore be translated as "a strangling feeling in the chest".
Worsening ("crescendo") angina attacks, sudden-onset angina at rest, and angina lasting more than 15 minutes are symptoms of unstable angina (usually grouped with similar conditions as the acute coronary syndrome). As these may herald myocardial infarction (a heart attack), they require urgent medical attention and are generally treated as a presumed heart attack.
Symptoms
Most patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen), back, neck, jaw, or shoulders. Typical locations for radiation of pain are arms, shoulders, and neck. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating and nausea in some cases. It usually lasts for about 1 to 5 minutes, and is relieved by rest or specific anti-angina medication. Chest pain lasting only a few seconds is normally not angina.
Myocardial ischemia comes about when the myocardium, which is more commonly called as the heart’s muscles, fails to take in the much needed blood and oxygen in order to function correctly. The inability to acquire blood and oxygen, on the other hand, is due to blocked or narrowed blood vessels.
Some experience "autonomic symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting and pallor.
Major risk factors for angina include family history of premature heart disease, cigarette smoking, diabetes, high cholesterol, and high blood pressure.
A variant form of angina (Prinzmetal's angina) occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women.
DiagnosisIn patients with the occasional angina who are not having chest pain, an electrocardiogram (ECG) is typically normal, unless there have been other cardiac problems in the past. During pain, depression or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test ("treadmill test") may be performed, during which the patient exercises to their maximum ability before fatigue, breathless or, importantly, pain supervenes; if characteristic ECG changes are documented (typically more than 1mm of flat or downsloping ST depression), the test is considered diagnostic for angina. The exercise test is also useful in looking for other markers of myocardial ischaemia: blood pressure response (or lack thereof, particularly a drop in systolic pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram (in patients that cannot exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest) or Stress Echocardiography.
In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG), treatment only with medication, or other treatments. In patients who are in hospital with unstable angina (or the newer term of "high risk acute coronary syndromes"), those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly.
[edit] Pathophysiology
Increases in heart rate result in increased oxygen demand by the heart. The heart has a limited ability to increase its oxygen intake during episodes of increased demand. Therefore, an increase in oxygen demand by the heart (eg, during exercise) has to be met by a proportional increase in blood flow to the heart.
Myocardial ischemia can result from:
- a reduction of blood flow to the heart caused by the stenosis or spasm of the heart's arteries
- resistance of the blood vessels
- reduced oxygen-carrying capacity of the blood.
Atherosclerosis is the most common cause of stenosis (narrowing of the blood vessels) of the heart's arteries and, hence, angina pectoris. Some people with chest pain have normal or minimal narrowing of heart arteries; in these patients, vasospasm is a more likely cause for the pain, sometimes in the context of Prinzmetal angina and syndrome X.
Myocardial ischemia also can be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as seen with severe anemia (low number of red blood cells), or long-term smoking.
Treatment
The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and of course death. An aspirin (75 mg to 100 mg) per day has been shown to be beneficial for all patients with stable angina that have no problems with its use. Beta-blockers have a large body of evidence in morbidity and mortality benefits (fewer symptoms and disability and live longer) and short-acting nitroglycerin medications are used for symptomatic relief of angina. Calcium channel blockers (such as nifedipine and amlodipine), Isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and lastly, statins are the most frequently used lipid/cholesterol modifiers which probably also stabilise existing atheromatous plaque.
Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension (high blood pressure), encouraging stopping smoking and weight optimisation.
--------------------------------------------------------------------------implantable cardioverter-defibrillator (ICD) is a device that is implanted under the skin of patients that are at risk of sudden cardiac death due to ventricular fibrillation. The rudiments of cardiac arrhythmia detection and treatment are incorporated into the implantable device. The device was designed primarily to deal with ventricular fibrillation. Its current use has however extended to include atrial and ventricular arrhythmias as well as the ability to perform biventricular pacing in patients with congestive heart failure and to pace should there be any marked bradycardia.
The process of implantation of an ICD is similar to implantation of a pacemaker. Similar to pacemakers, these devices typically include a wire that runs through the right chambers of the heart, usually ending in the apex of the right ventricle.
ICDs constantly monitor the rate and rhythm of the heart and can deliver therapies when the heart rate goes over a set number. All ICDs are programmed to deliver an electrical shock when the ventricles of the heart go faster than the set rate. More modern devices can distinguish between ventricular fibrillation and ventricular tachycardia (VT), and may try to pace the heart faster than its intrinsic rate in the case of VT, to try to break the tachycardia before it progresses to ventricular fibrillation. This is known as fast-pacing, overdrive pacing, or anti-tachycardia pacing (ATP). ATP is only effective if the underlying rhythm is ventricular tachycardia, and is never effective if the rhythm is ventricular fibrillation.
Many modern ICDs use a combination of various methods to determine if a fast rhythm is normal, ventricular tachycardia, or ventricular fibrillation.
Rate discrimination evaluates the rate of the lower chambers of the heart (the ventricles) and compares it to the rate in the upper chambers of the heart (the atria). If the rate in the atria is faster than or equal to the rate in the ventricles, then the rhythm is most likely not ventricular in origin, and is usually more benign. If this is the case, the ICD does not provide any therapy.
Rhythm discrimination will see how regular a ventricular tachycardia is. Generally, ventricular tachycardia is regular. If the rhythm is irregular, it is usually due to conduction of an irregular rhythm that originates in the atria, such as atrial fibrillation.
Morphology discrimination checks the morphology of every ventricular beat and compares it to what the ICD believes is a normally conducted ventricular impulse for the patient. This normal ventricular impulse is often an average of a multiple of beats of the patient taken in the recent past.
Initially ICDs were implanted via thoracotomy with defibrillator patches applied to the epicardium or pericardium. The device was attached via subcutaneous and transvenous leads to the device contained in a subcutaneous abdominal wall pocket. The device itself acts as an electrode. Most ICDs nowadays are implanted transvenously with the devices placed in the pectoral region similar to pacemakers. Intravascular spring or coil electrodes are used to defibrillate. The devices have gotten smaller and less invasive as the technology advances. Current ICDs weigh only 70 grams and are about 12.9 mm thick.
--------------------------------------------------------------------------Ventricular fibrillation (V-fib or VF) is a cardiac condition that consists of a lack of coordination of the contraction of the muscle tissue of the large chambers of the heart that eventually leads to the heart stopping altogether.
Ventricular fibrillation is a medical emergency. If the arrhythmia continues for more than a few seconds, blood circulation will cease, as evidenced by lack of pulse, blood pressure and respiration, and death will occur.
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly, rather than contracting in unison, and so the ventricles fail to pump blood into the arteries and into systemic circulation. Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, mostly brought on by ischaemic heart disease. Despite much work, the underlying nature of fibrillation is not completely understood. Most episodes of fibrillation occur in diseased hearts, but others occur in so-called normal hearts. Much work still has to be done to elucidate the mechanisms of ventricular fibrillation.
Mechanisms of ventricular fibrillation
Zipes divides the mechanisms of arrhythmia genesis into disorders of impulse formation and disorders of impulse conduction or both [Zipes DP 1994]. Zipes reminds us of the caveat that the present diagnostic tools do not permit unequivocal determination of the electrophysiological mechanisms responsible for most clinically occurring arrhythmias or their ionic basis. This he states is especially true for ventricular arrhythmias. In general terms, it is almost impossible to separate re-entry and automaticity. In most circumstances, we are able only to suggest that such an arrhythmia is consistent with a particular underlying mechanism.
[edit] Detailed description
Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" [Moe et al. 1964]. A more complete definition is that ventricular fibrillation is a "turbulent, disorganised electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction" [Robles de Medina 1978].
Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority, it is a manifestation of underlying ischaemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis and other heart pathologies. It is also seen with electrolyte disturbances and overdoses of cardiotoxic drugs. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.
Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40 [Viskin S et al 1990]. It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently-described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with evidence of right bundle-branch block (RBBB) and ST elevation in the chest leads V1-V3, with an underlying propensity to sudden cardiac death [Brugada P et al. 1992].
Treatment
The condition can often be reversed by the electric discharge of direct current from a defibrillator. If no defibrillator is available, a precordial thump can be delivered at the onset of VF to regain cardiac function. Antiarrhythmic agents like amiodarone or lidocaine can help, but, unlike atrial fibrillation, VF rarely reverses spontaneously in large adult mammals. Although a defibrillator is designed to correct the problem, and its effects can be dramatic, it is not always successful.
In patients at high risk of ventricular fibrillation the use of an implantable cardioverter defibrillator has been shown to be beneficial.
[edit] Re-entry
The role of re-entry or circus motion was demonstrated separately by Mines and Garrey [Mines GR 1913, Garrey WE 1914]. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue were stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue.
It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance - the propagation velocity - will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront.
In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.
[edit] Abnormal automaticity
Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. This may well lead to the generation of a circus-entry arrhythmia. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may be the trigger to generate re-entry arrhythmias.
It is interesting to note that most cardiac pathologies with an associated increased propensity to arrhythmia development have an associated loss of membrane potential. That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Cellular depolarisation can be due to a raised external concentration of K+, a decreased intracellular concentration of Na+, increased permeability to Na+, or a decreased permeability to K+. The ionic basis of automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV. Myocardial cells are exposed to different environments. Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia. In conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation include the resulting decreased internal K+ concentration, the increased external K+ concentration, norepinephrine release and acidosis [Ho K 1993].
[edit] Triggered activity
Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). All afterdepolarisations may not reach threshold potential, but, if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.
--------------------------------------------------------------------------Atrial fibrillation (AF or afib) is an abnormal heart rhythm (cardiac arrhythmia) which involves the two small, upper heart chambers (the atria). Heart beats in a normal heart begin after electricity generated in the atria by the sinoatrial node spreads through the heart and causes contraction of the heart muscle and pumping of blood. In AF, the regular electrical impulses of the sinoatrial node are replaced by disorganized, rapid electrical impulses which result in irregular heart beats.
Atrial fibrillation is the most common cardiac arrhythmia. The risk of developing atrial fibrillation increases with age — AF affects four percent of individuals in their 80s. An individual may spontaneously alternate between AF and a normal rhythm (paroxysmal atrial fibrillation) or may continue with AF as the dominant cardiac rhythm without reversion to the normal rhythm (chronic atrial fibrillation). Atrial fibrillation is often asymptomatic, but may result in symptoms of palpitations, fainting, chest pain, or even heart failure. These symptoms are especially common when atrial fibrillation results in a heart rate which is either too fast or too slow. In addition, the erratic motion of the atria leads to blood stagnation (stasis) which increases the risk of blood clots that may travel from the heart to the brain and other areas. Thus, AF is an important risk factor for stroke, the most feared complication of atrial fibrillation.
The symptoms of atrial fibrillation may be treated with medications which slow the heart rate. Several medications as well as electrical cardioversion may be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent atrial fibrillation in certain individuals. People with AF are often given blood thinners such as warfarin to protect them from strokes.
Diagnosis
[edit] Electrocardiogram
Atrial fibrillation is diagnosed on an electrocardiogram, an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are (a "rhythm strip" of lead II is shown):
- absence of P waves
- unorganized electrical activity in their place
- irregularity of R-R interval due to irregular conduction of impulses to the ventricles
If paroxysmal AF is suspected, episodes may be documented with the use of Holter monitoring (continuous ECG recording for 24 hours or longer).
[edit] Other investigations
While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count. A chest X-ray is generally performed. In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced. A transesophageal echocardiogram may be indicated to identify any intracardiac thrombus. [1]
[edit] Pathophysiology
| Conduction | ||
Sinus rhythm  | Atrial fibrillation  | |
The normal electrical conduction system of the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to and stimulate the myocardium (muscle of the heart). When the myocardium is stimulated, it contracts. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped to the body.
In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated discharges produced by larger areas of atrial tissue. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw toothed waves on the electrocardiogram.
Often, the rhythm produced is more rapid than normal, but the difficulty is in obtaining control of the heart rate both at rest and with exercise. Good rate control will usually require two drugs, and can only be checked by observing heart rate response to exercise.
An organized electrical impulse in the atrium produces atrial contraction; the lack of such an impulse, as in atrial fibrillation, produces stagnant blood flow, especially in the atrial appendage and predisposes to clotting. The dislodgement of a clot from the atrium results in an embolus, and the damage produced is related to where the circulation takes it. An embolus to the brain produces the most feared complication of atrial fibrillation, stroke, while an embolus may also lodge in the mesenteric circulation (the circulation supplying the abdominal organs) or digit, producing organ-specific damage.
[edit] Treatment
The main goals of treatment of atrial fibrillation are to prevent temporary circulatory instability and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter.[5]
AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. There are two ways to approach these symptoms: rate control and rhythm control. Rate control treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase. Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial (Wyse et al., 2002).
AF with a persistent rapid rate can cause a form of heart failure called tachycardia induced cardiomyopathy. This can significantly increase mortality and morbidity. The early treatment of AF through either rate-control or rhythm-control can prevent this condition and thereby improve mortality and morbidity.
[edit] Rate control
Rate control methods include:
- Beta blockers (e.g. metoprolol)
- Cardiac glycosides (e.g. digoxin)
- Calcium channel blockers (e.g. verapamil)
These medications work by slowing the generation of impulses from the atria and the conduction of those impulse from the atria to the ventricles.
In refractory cases where none of the above drugs are sufficient, a variety of other antiarrhythmic drugs, most commonly including quinidine, flecainide, propafenone, disopyramide, sotalol, or amiodarone may be used. Of these, only propafenone, sotalol, and amiodarone (which possess some beta blocking activity) control the ventricular rate; the others may maintain sinus rhythm, but may actually increase the ventricular rate. Many of these drugs are less frequently used today than in the past. All (with the possible exception of amiodarone) increase the risk of ventricular tachycardia, which can be fatal. In symptomatic patients with normal heart function, however, the small increase in risk is usually felt to be acceptable. In the presence of heart failure, the only antiarrhythmic drugs thought to be safe are amiodarone and dofetilide. In the United States, it should be noted that many of these agents are not approved by the FDA for this use.
In emergencies, when circulatory collapse is imminent due to uncontrolled tachycardia, immediate cardioversion may be indicated. [2]
[edit] AV nodal ablation
In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker instead. A more complex technique involves ablating groups of cells near the pulmonary veins where atrial fibrillation is thought to originate, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself.[3]
[edit] Rhythm control
Rhythm control methods include electrical and chemical cardioversion:
- Electrical cardioversion involves the restoration of normal heart rhythm either through the application of a DC electrical shock (electrical cardioversion)
- Chemical cardioversion is performed with drugs, such as amiodarone, propafenone or flecainide.
The anti-arrhythmic medications often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion. However, the AFFIRM study showed no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment, compared to those who have only rate control.[6]
The main risk of cardioversion is systemic embolization by a bloodclot from the previously fibrillating left atrium. It should not be performed without adequate anticoagulation in patients who have been in atrial fibrillation for more than 48 hours.
Whichever method of cardioversion is used, approximately 50% of patient relapse within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and increasing age.
[edit] Radiofrequency ablation
Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. It is used in recurrent AF. The energy emitting probe (electrode) is placed into the heart through a catheter. The practitioner first "maps" an area of the heart to locate the abnormal electrical activity before the responsible tissue is eliminated. Ablation is a newer technique and has shown some promise for cases unresponsive to conventional treatments. New techniques include the use of cryoablation (tissue freezing using a coolant which flows through the catheter), and microwave ablation, where tissue is ablated by the microwave energy "cooking" the adjacent tissue. The abnormal electrophysiology can also be modified in a similar way surgically, and this procedure referred to as the Cox maze procedure, is commonly performed concomitantly with cardiac surgery. More recently, minimally invasive surgical variations on the Cox Maze procedure ("minimaze" procedures) have also been developed.
This is an area of active research, especially with respect to the RF ablation technique and emphasis on isolating the pulmonary veins that enter into the left atrium.
[edit] Cox maze Procedure
James Cox, MD, and associates developed the Cox maze procedure, an open-heart surgical procedure intended to eliminate atrial fibrillation, and performed the first one in 1987. "Maze" refers to the series of incisions made in the atria (upper chambers of the heart), which are arranged in a maze-like pattern. The intention was to eliminate AF by using incisional scars to block abnormal electrical circuits (atrial macroreentry) that AF requires. This procedure required an extensive series of endocardial (from the inside of the heart) incisions through both atria, a median sternotomy (vertical incision through the breastbone) and cardiopulmonary bypass (heart-lung machine). A series of improvements were made, culminating in 1992 in the Cox maze III procedure, which is now considered to be the "gold standard” for effective surgical cure of AF. The Cox maze III is sometimes referred to as the “traditional maze”, the “cut and sew maze”, or simply the "maze".
[edit] Minimaze surgical procedures
Minimaze surgery is minimally invasive cardiac surgery intended to cure atrial fibrillation. Minimaze refers to "mini" versions of the original maze procedure. These procedures are less invasive than the Cox maze procedure and do not require a median sternotomy (vertical incision in the breastbone) or cardiopulmonary bypass (heart-lung machine). These procedures use microwave, radiofrequency, or acoustic energy to ablate atrial tissue near the pulmonary veins.
[edit] Anticoagulation
In confirmed AF, anticoagulant treatment is a crucial way to prevent stroke. Treatment of AF patients over age 60, who also have one or more of: previous strokes (or warning strokes), hypertension (high blood pressure), diabetes, or congestive heart failure, with warfarin (also known as Coumadin® or Marevan®) results in a 60 to 70 percent reduction in the subsequent risk of stroke. Patients under age 65 who have any structural heart disease (i.e. valvular heart disease, ejection fraction <= 35%, history of heart attack) may also benefit from warfarin.
It is worth noting that patient with AF who are being rhythm controlled are not treated any differently from patients with permanent AF when it comes to determining anticoagulation.
Signs and symptoms
Atrial fibrillation is usually accompanied by symptoms related to either the rapid heart rate or embolization. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally produce angina and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified with the onset of a stroke or a transient ischemic attack (TIA). It is not uncommon to identify atrial fibrillation on a routine physical examination or electrocardiogram (ECG/EKG), as it may be asymptomatic in some cases.
Paroxysmal atrial fibrillation is the episodic occurrence of the arrhythmia and may be difficult to diagnose. Episodes may occur with sleep or with exercise, and their episodic nature may require prolonged ECG monitoring (e.g. a Holter monitor) for diagnosis.
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Atrial flutter is a rhythmic, fast rhythm that occurs in the atria of the heart. This rhythm occurs most often in individuals with organic heart disease (ie: pericarditis, coronary artery disease, and cardiomyopathy).Atrial flutter is typically not a stable rhythm, and frequently degenerates to atrial fibrillation. However, it may persist for months to years.
Overview
Atrial flutter is a regular, rhythmic tachycardia originating in the atria. The rate in the atria is over 220 beats/minute, and typically about 300 beats/minute. The morphology on the surface EKG is typically a sawtooth pattern.
The ventricles typically do not beat as fast as the atria in atrial flutter. The AV node acts as a safety valve in the event of any fast rhythm of the heart, including atrial fibrillation and atrial flutter. The AV node slows down conduction of the electrical activity, and if it receives the next action potential before it is ready, the impulse will be blocked at the AV node level, and never reach the ventricles.
[edit] Ratios
In the case of atrial flutter, there is a very particular block pattern at the AV node level. In atrial flutter, the AV node typically will block every other electrical impulse, or three out of four impulses. If every other impulse is blocked, known as 2:1 block, while the atrial rate is 300 beats/minute, the ventricular rate will be 150 beats/minute. If three out of four beats are blocked, known as 4:1 block, while the atrial rate is 300 beats/minute, the ventricular rate will be 75 beats/minute.
In many people, the degree of block is variable - sometimes every other beat is transmitted, sometimes two beats are dropped before the third is transmitted, etc. This is known as varying block. For reasons that are not well understood, a stable 3:1 block is not commonly seen in individuals with atrial flutter. A single individual can have varying degrees of block at different times. The varying degree of block is due to a multitude of factors, including catecholamine release and the use of any drugs that inhibit conduction through the AV node, such as beta blockers, digitalis, and calcium channel blockers.
The term 2:1 block comes from the fact that for every two electrical impulses that reach the AV node, only one is transmitted to the ventricle. Similarly, 4:1 block comes from the fact that for every four impulses that reach the AV node, only one is transmitted to the ventricle.
[edit] Symptoms
While atrial flutter can sometimes go unnoticed by sufferers, its onset is often marked by characteristic sensations of rapid thumping and palpitations in the chest; such sensations usually last for the entire duration of the episode. Atrial flutter may also be accompanied by shortness of breath, lightheadedness or dizziness, nausea and, in some patients, by nervousness and feelings of impending doom.
[edit] Mechanism of action
Atrial flutter is caused by a reentrant rhythm in either the right or left atrium. Typically initiated by a premature electrical impulse arising in the atria, atrial flutter is initiated due to differences in refractory periods of atrial tissue. This creates a loop of reentry moving along the atrium. Recent studies have shown that patients with typical atrial flutter demonstrate longer refractory periods in the lower right atrial tissue.
Types of atrial flutter
There are two types of atrial flutter, known as type I and type II.1 Most individuals with atrial flutter will manifest only one of these types of atrial flutter. Rarely someone may manifest both types of flutter; however, they can only manifest one type at a time.
[edit] Type I flutter
Type I atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 350 beats/minute. However, this rate may be slowed by antiarrhythmic agents.
Type I flutter can be entrained by rapid atrial pacing. This means that the re-entrant rhythm of the flutter can be broken if a stimulus enters the re-entrant cycle at just the right point, breaking the cycle and thereby terminating the atrial flutter. While this can be performed with a pacemaker, it is performed almost exclusively in the electrophysiology lab by pacing the atrium at a rate just above the rate of the atrial flutter. While entrainment may break atrial flutter and cause the individual to revert to a normal sinus rhythm, the rapid atrial pacing may cause the individual to go into atrial fibrillation. Type I atrial flutter is increasingly easy to cure in the electrophysiology lab due to its dependence on a fixed anatomic structure known as the isthmus. The isthmus is a body of fibrous tissue that makes up a portion of the reentrant loop. Catheter ablation of the isthmus prevents reentry, and terminates atrial flutter if successful.
Type I flutter has two subtypes, known as counterclockwise atrial flutter and clockwise atrial flutter.
[edit] Counterclockwise atrial flutter
Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen than clockwise atrial flutter. The flutter waves in this rhythm are inverted in II, III, and aVF.
[edit] Clockwise atrial flutter
Clockwise atrial flutter is less common than counterclockwise atrial flutter. The flutter waves are upright in II, III, and aVF in this rhythm.
[edit] Type II flutter
Type II flutter is faster than type I flutter, and usually is 340-430 beats/minute.
Unlike type I flutter, the rhythm of type II flutter cannot be entrained by rapid atrial pacing.
[edit] Complications
[edit] Clot formation
In atrial flutter, as in atrial fibrillation, there is no effective contraction of the atria. In individuals with structural heart disease, this causes stasis of blood in the atria. The stasis of blood leads to formation of thrombus material (clots) within the heart. In the left side of the heart, thrombus is most likely for form in the left atrial appendage. This is important because, since the left side of the heart supplies blood to the entire body, any thrombus material that dislodges from the left side of the heart can potentially embolize to the brain, causing a stroke. Of course, the thrombus material can also embolize to any other portion of the body.
[edit] Sudden death
Sudden death is not directly associated with atrial flutter. However, in individuals with a pre-existing accessory conduction pathway, such as the bundle of Kent in Wolff-Parkinson-White syndrome, the accessory pathway may conduct activity from the atria to the ventricles much faster than the AV node. In this case, the atrial rate of 300 beats/minute will lead to a ventricular rate of 300 beats/minute. The ventricles, unable to sustain a ventricular tachycardia at such a high rate, will go into ventricular fibrillation, which will quickly lead to hemodynamic collapse and death.
[edit] Treatment
In general, atrial flutter should be treated the same as atrial fibrillation. Both rhythms do not provide effective contraction of the atria. Because of this, there is stasis of blood in the atria. This stasis of blood leads to the potential formation of thrombus material in the atria. Therefore, individuals with atrial flutter require some form of anticoagulation or anti-platelet agent.
[edit] Ablation
Because of the reentrant nature of atrial flutter, it is possible to ablate the circuit that causes atrial flutter. This is done in the electrophysiology lab by causing a ridge of scar tissue that crosses the path of the circuit that causes atrial flutter. Ablation of the isthmus, as disscussed above, is a common treatment for typical atrial flutter.
[edit] Rate control
Control of the ventricular rate in atrial flutter may be more difficult than if the individual was in atrial fibrillation. This is because of properties of the AV node. In atrial fibrillation, the AV node is typically bombarded with signals from the atria at rates in excess of 400 beats/minute. This causes a high degree of block within the AV node, with many signals partially penetrating the node and blocking at the lower levels of the AV node. This phenomenon is known as concealed conduction. In atrial flutter, on the other hand, the AV node receives signals very rhythmically at a rate of about 300/minute. Since the atrial flutter is an organized rhythm of the atria, the block at the AV node will be consistently at the same level, and paradoxically a higher number of impulses will get through per minute.
Because of this, it may be easier to control the rate of some individuals if they are converted from atrial flutter to atrial fibrillation. While there are no guidelines for this procedure at this time, this may be attempted in the electrophysiology lab by pacing the atria at rates well over 300 beats/minute.
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Tachycardic arrhythmias
An electrocardiogram tracing can distinguish several different forms of rapid abnormal heartbeat:
If the heart's electrical system is functioning normally, except that the rate is in excess of 100 beats per minute, it is called sinus tachycardia. This is caused by any of the factors mentioned above, rather than a malfunction of the heart itself.
Supraventricular tachycardia (SVT) occurs when an abnormal electrical impulse originates above the ventricles, but instead of causing a single beat and a pause, it causes rapid local impulse cycling and initiates many rapid beats.
[edit] Ventricular tachycardia
Ventricular tachycardia (VT or V-tach) is a similar phenomenon occurring within the tissue of the ventricles, causing an extremely rapid rate with poor pumping action.
Abnormal accelerated ventricular rhythm with a usual rate of 150-200 beats/minute. Because ventricular tachycardia originates in the ventricle, the QRS complexes on the electrocardiogram are widened (>0.12 seconds). A potentially unstable rhythm that may result in fainting, low blood pressure, shock, or sudden death. Ventricular tachycardia has the potential of degrading to the more serious ventricular fibrillation. Ventricular tachycardia is a common, and often lethal, complication of acute myocardial infarction (heart attack).[1]
[edit] Exercise-induced ventricular tachycardia
Exercise-induced ventricular tachycardia is a phenomenon related to sudden deaths, especially in patients with severe heart disease (ischaemia, acquired valvular heart and congenital heart disease) accompanied with left ventricular dysfunction.[2] A case of a death from exercise-induced VT was the death on a basketball court of Hank Gathers, the Loyola Marymount basketball star, in March 1990.[3]
Both of these rhythms normally last for only a few seconds to minutes (paroxysmal tachycardia), but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.
The vagus reflex may help as a first-aid measure.
[edit] Treatments
Arrhythmias can be treated using drugs, ablation, intervention, or implantable devices.
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Torsades de pointes is a medical condition, the name of which means in French "twisting of the points". The name is derived from a manoeuvre in ballet, similarly named. It is a potentially deadly form of ventricular tachycardia. On the electrocardiogram (ECG/EKG), it will present like ventricular tachycardia, but the QRS complexes will swing up and down around the baseline in a chaotic fashion, which prompted the name. The etiology of TdP (Torsades de pointes) is prolongation of the QT interval.
Causes
The primary cause for torsades de pointes is hypomagnesemia (low blood levels of magnesium). It is commonly seen in malnourished individuals like alcoholics, as chronic abuse of alcohol will lead to low levels of magnesium, calcium, thiamine, and other nutrients.
[edit] Treatment
Acute treatment is with withdrawal of the offending agent (if related to medication - such as Class 1A anti-arrhythmic drugs), infusion of magnesium sulfate, defibrillation/cardioversion (however, it is frequently refractory to cardioversion) and antiarrhythmic drugs.
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Through electricity or drug therapy, cardioversion converts heart arrhythmias to normal rhythms.
Similar to defibrillation, electrical cardioversion differs in that it uses much lower electricity levels, and is only performed on patients that are not currently in cardiac arrest. Pharmacologic cardioversion uses medication instead of an electrical shock.
Electrical cardioversion
In the case of electrical shock, the patient lies on his or her back with one electrical conducting pad placed on the back and another on the upper chest. These pads are connected to an ECG machine which is also capable of delivering current. When the patient is sedated, a shock is delivered and the patient's ECG is checked for sinus rhythm. The shocks can be performed until sinus rhythm is attained or until further electrical shocks could cause burning of the epidermis. The patient is monitored for half an hour to ensure stability of the sinus rhythm. The risks are minimal and the patient feels very little during the procedure.
Electrical cardioversion is used to treat heart problems such as atrial fibrillation and atrial flutter. In the case of ventricular arrhythmias (such as ventricular fibrillation), a defibrillator is used; in most emergency settings the same appliance can be used for both cardioversion and defibrillation. The pace of the procedure for defibrillation is always fast owing to the life-threatening circumstances that it is used to treat. However, the speed used to initiate a cardioversion procedure may be nearly as quick as a defibrillation (as in the case of an unstable patient with atrial fibrillation), or slower, if the patient is stable but has a potentially life-threatening dysrhythmia.
[edit] Pharmacologic cardioversion
Various antiarrhythmic agents can be used to return the heart to sinus rhythm. Although this method is slower than electrical cardioversion, it is often attempted first for non-urgent atrial fibrillation.
--------------------------------------------------------------------------Defibrillation is a medical technique used to counter the onset of ventricular fibrillation, (VF) a common cause of cardiac arrest, and pulseless ventricular tachycardia, which sometimes precedes ventricular fibrillation but can be just as dangerous on its own. In simple terms, the process uses an electric shock to stop the heart, in the hope that the heart will restart with rhythmic contractions.
Uses
Defibrillation is a technique used in emergency medicine to terminate ventricular fibrillation or pulseless ventricular tachycardia. It uses an electrical shock to reset the electrical state of the heart so that it may beat to a rhythm controlled by its own natural pacemaker cells. It is not effective for asystole (complete cessation of cardiac activity, more commonly known as "flatline") and pulseless electrical activity (PEA). Ventricular tachycardia with a pulse is treated with medication (if hemodynamically stable), or syncronized cardioversion (if hemodynamically unstable).
The purpose of defibrillation of ventricular arrhythmias is to apply a controlled electrical shock to the heart, which leads to depolarization of the entire electrical conduction system of the heart. When the heart repolarizes, the normal electrical conduction may assert itself, in which case the ventricular arrhythmia is terminated. However, if not enough energy is used for defibrillation, the heart may not be completely depolarized, in which case the ventricular tachycardia or fibrillation may not be terminated. Also, if the heart itself is not getting enough oxygen or if there is an instability of the electrolytes in the cardiac cells, the ventricular arrhythmia may recur.
The shock is generally conducted through the heart by two electrodes, in the form of two hand-held paddles or adhesive patches depending on the variety of the defibrillator. One electrode is placed on the right side of the front of the chest just below the clavicle, and the other electrode is placed on the left side of the chest just below the pectoral muscle or breast. Open-chest defibrillators also exist, which have electrodes in the form of two cup-shaped paddles that surround the sides of the heart and shock it directly. Open-chest defibrillators generally require less energy to operate due to direct contact with the heart.
Electrodes
[edit] Design
The most well-known type of electrode is the traditional metal paddle with an insulated handle. This type must be held in place on the patient's skin while a shock or a series of shocks is delivered. Before the paddle is used, a gel must be applied to the patient's skin, in order to ensure a good connection and to minimize electrical resistance, also called chest impedence (despite the DC discharge).
Another type of resuscitation electrode is designed as an adhesive pad. When a patient has been admitted due to heart problems, and the physician or nurse has determined that he or she is at risk of arrhythmia, they may apply adhesive electrodes to the patient in anticipation of any problems that may arise. These electrodes are left connected to a defibrillator. If defibrillation is required, the machine is charged, and the shock is delivered, without any need to apply any gel or to retrieve and place any paddles.
Both solid- and wet-gel adhesive electrodes are available. Solid-gel electrodes are more convenient, because there is no need to clean the patient's skin after removing the electrodes. However, the use of solid-gel electrodes presents a higher risk of burns during defibrillation, since wet-gel electrodes more evenly conduct electricity into the body.
Adhesive electrodes are designed to be used not only for defibrillation, but also for non-invasive pacing and electrical cardioversion.
While the paddles on a Monitor/Defibrillator may be quicker than using the patches, adhesive patches are superior due to their ability to provide appropriate EKG tracing without the artifact visible from human interference with the paddles. Many monitor defibrilators provide three, five or 12-lead EKG monitoring to compensate for this downfall of the paddles. Adhesive electrodes are also inherently safer than the paddles for the operator of the defibrillator to use, as they minimize the risk of the operator coming into physical (and thus electrical) contact with the patient as the shock is delivered, by allowing the operator to stand several feet away. Another inconvenience of the paddles is the requirement of around 25lbs of pressure to be applied while defibrillating.
[edit] Placement
Resuscitation electrodes are placed according to one of two schemes. The anterior-posterior scheme (conf. image) is the preferred scheme for long-term electrode placement. One electrode is placed over the left precordium (the lower part of the chest, in front of the heart). The other electrode is placed on the back, behind the heart in the region between the scapula. This placement is preferred because it is best for non-invasive pacing.
The anterior-apex scheme can be used when the anterior-posterior scheme is inconvenient or unnecessary. In this scheme, the anterior electrode is placed on the right, below the clavicle. The apex electrode is applied to the left side of the patient, just below and to the left of the pectoral muscle. This scheme works well for defibrillation and cardioversion, as well as for monitoring an ECG.
--------------------------------------------------------------------------Cardiopulmonary resuscitation (CPR) is an emergency first aid protocol for a victim of cardiac arrest. It can be performed by trained lay persons or by healthcare or emergency response professionals. It is normally begun on an unbreathing unconscious person and continued until action can be taken to restart the heart or otherwise diagnose the problem. CPR essentially consists of a pattern of chest compressions and rescue breaths (i.e. artificial blood circulation and lung ventilation) and is intended to maintain a trickle of oxygenated blood to the brain and the heart and thereby extend the otherwise brief window of opportunity for successfully restarting the heart without permanent brain damage. CPR itself is not intended to restart the heart but must be performed continuously until medical responders can attempt to restart the heart by other means.
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Cardiac arrhythmia is a group of conditions in which the muscle contraction of the heart is irregular or is faster or slower than normal. Cardiac dysrhythmia is technically more correct, as arrhythmia would imply that there is "no rhythm," but this term is not used frequently.
Some arrhythmias are life-threatening medical emergencies that can cause cardiac arrest and sudden death. Others cause aggravating symptoms, such as an awareness of a different heart beat, or palpitation, which can be annoying. Some are quite benign and normal. Sinus arrhythmia is the mild acceleration followed by slowing of the normal rhythm that occurs with breathing. In adults the normal heart rate ranges from 60 beats per minute to 100 beats per minute. The normal heart beat is controlled by a small area in the upper chamber of the heart called the sinoatrial node or sinus node. The sinus node contains specialized cells that have spontaneous electrical activity that starts each normal heart beat.
Fibrillation
A serious variety of arrhythmia is known as fibrillation. The muscle cells of the heart normally function together, creating a single contraction when stimulated. Fibrillation occurs when the heart muscle begins a quivering motion due to a disunity in contractile cell function. Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation); ventricular fibrillation is imminently life-threatening.
Atrial fibrillation is the quivering, chaotic motion in the upper chambers of the heart, known as the atria. Atrial fibrillation is often due to serious underlying medical conditions, and should be evaluated by a physician. It is not typically a medical emergency.
Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest, and an individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.
CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the intervention which is most likely to restore a more healthy heart rhythm. It does this by applying an electric shock to the heart, after which sometimes the heart will revert to a rhythm that can once again pump blood.
Almost every person goes into ventricular fibrillation in the last few minutes of life as the heart muscle reacts to diminished oxygen or general blood flow, trauma, irritants, or depression of electrical impulses themselves from the brain.
[edit] Origin of impulse
When an electrical impulse begins in any part of the heart, it will spread throughout the myocardium and cause a contraction; see Electrical conduction system of the heart. Abnormal impulses can begin by one of two mechanisms: automaticity or reentry.
[edit] Automaticity
Automaticity refers to a cardiac muscle cell firing off an impulse on its own. Every cardiac cell has this potential: if it does not receive any impulses from elsewhere, its internal "pacemaker" will fire off an impulse after a certain amount of time. A single specialized location in the atrium, the sinoatrial node, has a higher automaticity (a faster pacemaker) than the rest of the heart, and therefore is usually the one to start the heartbeat.
Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus, and is by definition a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart's pumping efficiency, because the signal reaches the various parts of the heart muscle with slightly different timing than usual and causes a poorly coordinated contraction.
Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm depends on where the first signal begins: if it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus, many types of dysrhythmia can result.
[edit] Reentry
Reentrant dysrhythmias occur when an electrical impulse travels in a circle within the heart, rather than moving outward and then stopping. Every cardiac cell is able to transmit impulses in every direction, but will only do so once within a short period of time. Normally the impulse spreads through the heart quickly enough that each cell will only respond once, but if conduction is abnormally slow in some areas, part of the impulse will arrive late and will be treated as a new impulse, which can then spread backward. Depending on the timing, this can produce a sustained abnormal rhythm, such as atrial flutter, a self-limiting burst of supraventricular tachycardia, or the dangerous ventricular tachycardia.
