A pacemaker, also known as an artificial cardiac pacemaker, is an implanted medical device that generates electrical pulses delivered by to one or more of the Heart chamber. Each pulse causes the targeted chamber(s) to contract and pump blood, thus regulating the function of the electrical conduction system of the heart.
The primary purpose of a pacemaker is to maintain an even heart rate, either because the heart's natural cardiac pacemaker provides an inadequate or irregular heartbeat, or because there is a heart block in the heart's electrical conduction system. Modern pacemakers are externally programmable and allow a cardiologist to select the optimal pacing modes for individual patients. Most pacemakers are on demand, in which the stimulation of the heart is based on the dynamic demand of the circulatory system. Others send out a fixed rate of impulses.
A specific type of pacemaker, called an implantable cardioverter-defibrillator, combines pacemaker and defibrillator functions in a single implantable device. Others, called biventricular pacemakers, have multiple electrodes stimulating different positions within the ventricles (the lower heart chambers) to improve their synchronization.
Permanent epicardial pacing leads can be implanted surgically and tunneled to the pulse generator pocket. These leads are either passively touching the heart and sewn in place, or have a screw mechanism to actively fix to the heart.
There are three basic types of permanent pacemakers, classified according to the number of Heart chamber involved and their basic operating mechanism:
The pacemaker generator is a hermetically sealed device containing a power source, usually a lithium battery, a sensing amplifier which processes the electrical manifestation of naturally occurring heart beats as sensed by the heart electrodes, the computer logic for the pacemaker and the output circuitry which delivers the pacing impulse to the electrodes.
Most commonly, the generator is placed below the subcutaneous fat of the chest wall, above the muscles and bones of the chest. However, the placement may vary on a case-by-case basis.
The outer casing of pacemakers is so designed that it will rarely be rejected by the body's immune system. It is usually made of titanium, which is inert in the body.
The more complex forms include the ability to sense and/or stimulate both the atrial and ventricular chambers.
+ The revised NASPE/BPEG generic code for antibradycardia pacing ! I | V |
Multisite pacing | |
O = None | |
A = Atrium | |
V = Ventricle | |
D = Dual (A+V) |
From this the basic ventricular "on demand" pacing mode is VVI or with automatic rate adjustment for exercise VVIR – this mode is suitable when no synchronization with the atrial beat is required, as in atrial fibrillation. The equivalent atrial pacing mode is AAI or AAIR which is the mode of choice when atrioventricular conduction is intact but the sinoatrial node of the natural pacemaker is unreliable – sinus node disease (SND) or sick sinus syndrome. Where the problem is atrioventricular block (AVB) the pacemaker is required to detect (sense) the atrial beat and after a normal delay (0.1–0.2 seconds) trigger a ventricular beat, unless it has already happened – this is VDD mode and can be achieved with a single pacing lead with electrodes in the right atrium (to sense) and ventricle (to sense and pace). These modes AAIR and VDD are unusual in the US but widely used in Latin America and Europe. The DDDR mode is most commonly used as it covers all the options though the pacemakers require separate atrial and ventricular leads and are more complex, requiring careful programming of their functions for optimal results.
Automatic pacemakers are designed to be over-ridden by the heart's natural rate at any moment that it gets back to a non-pathologic Sinus rhythm and can reinitiate influencing the electric activity in the heart when the pathologic event happens again. A "ventricular-demand pacemaker" produces a narrow vertical spike on the ECG, just before a wide QRS. The spike of an "atrial-demand pacemaker" appears just before the P wave.
Comparably, a Triggered Pacemaker is activated immediately after an electrical activity is commenced in the heart tissue by itself. A "ventricular triggered pacemaker" produces the impulse just after a pulse is created in the ventricular tissue and it appears as a simultaneous spike with QRS. An "atrial triggered pacemaker" is the mode in which an impulse is produced immediately after an electrical event in the atrium. It appears as a discharge following the p wave but prior to the QRS which is commonly widened.
All electrical circuits require a complete connection between the cathode and the anode. For some pacing leads, both connections to the heart are provided in a single lead ("bipolar") and some only provide a single connection ("unipolar"). In unipolar, the second connection is internally from the heart to the generator through the body (blood, tissue, etc).
Also important is the impedance. The lower the impedance, the more current is needed to achieve the threshold voltage and lowers the battery life. The impedance is affected by the integrity of the pacing lead and the electrode-tissue interface of the lead with the heart.
The minimum voltage to sense an event is called the sensitivity. The higher the sensitivity, the less that is sensed, and vice-versa. Too low of a sensitivity can cause troubles with sensing P waves, T waves, and noise; sensing these things is called "over sensing". A sensitivity too high may result in missed sensing of P waves in the atria and QRS in the ventricles, and is called "under sensing."
CRT devices have at least two leads, one passing through the vena cava and the right atrium into the right ventricle to stimulate the septum, and another passing through the vena cava and the right atrium and inserted through the coronary sinus to pace the epicardial wall of the left ventricle. Often, for patients in normal sinus rhythm, there is also a lead in the right atrium to facilitate synchrony with the atrial contraction. Thus, the timing between the atrial and ventricular contractions, as well as between the septal and lateral walls of the left ventricle can be adjusted to achieve optimal cardiac function.
CRT devices have been shown to reduce mortality and improve quality of life in patients with heart failure symptoms; a LV ejection fraction less than or equal to 35% and QRS duration on EKG of 120 ms or greater.
Biventricular pacing alone is referred to as CRT-P (for pacing). For selected patients at risk of arrhythmias, CRT can be combined with an implantable cardioverter-defibrillator (ICD): such devices, known as CRT-D (for defibrillation), also provide effective protection against life-threatening arrhythmias.
Dynamic pacemaking technology could also be applied to future . Advances in transitional tissue welding would support this and other artificial organ/joint/tissue replacement efforts. Stem cells may be of interest in transitional tissue welding.
Many advancements have been made to improve the control of the pacemaker once implanted. Many of these have been made possible by the transition to microprocessor controlled pacemakers. Pacemakers that control not only the ventricles but the atria as well have become common. Pacemakers that control both the atria and ventricles are called dual-chamber pacemakers. Although these dual-chamber models are usually more expensive, timing the contractions of the atria to precede that of the ventricles improves the pumping efficiency of the heart and can be useful in congestive heart failure.
Rate responsive pacing allows the device to sense the physical activity of the patient and respond appropriately by increasing or decreasing the base pacing rate via rate response algorithms.
The DAVID trials have shown that unnecessary pacing of the right ventricle can exacerbate heart failure and increases the incidence of atrial fibrillation. The newer dual-chamber devices can keep the amount of right ventricle pacing to a minimum and thus prevent worsening of the heart disease.
The batteries within a pacemaker generator typically last 5 to 10 years. When the batteries are nearing the end of life, the generator is replaced in a procedure that is usually simpler than a new implant. Replacement involves making an incision to remove the existing device, disconnecting the leads from the old device and reconnecting them to a new generator, reinserting the new device and closing the skin.
During in-office follow-up, diagnostic tests may include:
The pacemaker patient may find that some types of everyday actions need to be modified. For instance, the shoulder harness of a vehicle seatbelt may be uncomfortable if it falls across the pacemaker insertion site. Women will not be able to wear bras for a while after the operation, and later might have to wear bras with wide shoulder straps.
For some sports and physical activities, special pacemaker protection can be worn to prevent possible injuries, or damage to the pacemaker leads.
Pacemakers may be affected by Magnetic field or electromagnetic fields, and ionising and acoustic radiation. However, a 2013 study found that "The overall risk of clinically significant adverse events related to EMI (electromagnetic interference) in recipients of CIEDs (cardiovascular implantable electronic devices) is very low. Therefore, no special precautions are needed when household appliances are used. Environmental and industrial sources of EMI are relatively safe when the exposure time is limited and distance from the CIEDs is maximized. The risk of EMI-induced events is highest within the hospital environment." The study lists and tabulates many sources of interference, and many different potential effects: damage to circuitry, asynchronous pacing, etc. Some sources of hazard in older devices have been eliminated in newer ones.
Activities involving strong should be avoided. This includes activities such as arc welding with certain types of equipment, and maintaining heavy equipment that may generate strong magnetic fields. Some medical procedures, particularly magnetic resonance imaging (MRI), involve very strong magnetic fields or other conditions that may damage pacemakers.
However, many modern pacemakers are specified to be MR conditional or MRI conditional, safe to use during MRI subject to certain conditions. The first to be so specified was the Medtronic Revo MRI SureScan, approved by the US FDA in February 2011, which was the first to be specified as MR conditional.Husten, Larry. "FDA Approves Second Generation MRI-Friendly Pacemaker System From Medtronic". Forbes, 2013-02-13. There are several conditions to use of MR Conditional pacemakers, including certain patients' qualifications and scan settings. An MRI conditional device has to have MRI settings enabled before a scan, and disabled afterwards.
the five most commonly used cardiac pacing device manufacturers (covering more than 99% of the US market) made FDA-approved MR-conditional pacemakers. The use of MRI may be ruled out by the patient having an older, non-MRI Conditional pacemaker, or by having old pacing wires inside the heart, no longer connected to a pacemaker.
A 2008 US study found that the magnetic field created by some headphones used with portable music players or cellphones may cause interference if placed very close to some pacemakers.
In addition, according to the American Heart Association, some home devices have the potential to occasionally inhibit a single beat. Cellphones do not seem to damage pulse generators or affect how the pacemaker works. It is recommended that objects containing magnets, or generating a significant magnetic field, should not be in close proximity to a pacemaker. Induction cooktops, in particular, can pose a risk.
Before medical procedures, the patient should inform all medical personnel that they have a pacemaker. Having a pacemaker does not imply that a patient requires the use of to be administered before procedures such as dental work.
]] Complications from having surgery to implant a pacemaker are uncommon (each 1–3% approximately), but could include: infection where the pacemaker is implanted or in the bloodstream; allergy to the dye or anesthesia used during the procedure; swelling, bruising or bleeding at the generator site, or around the heart, especially if the patient is taking blood thinners, elderly, of thin frame or otherwise on chronic steroid use.
A possible complication of dual-chamber artificial pacemakers is 'pacemaker-mediated tachycardia' (PMT), a form of reentrant tachycardia. In PMT, the artificial pacemaker forms the anterograde (atrium to ventricle) limb of the circuit and the atrioventricular (AV) node forms the retrograde limb (ventricle to atrium) of the circuit. Treatment of PMT typically involves reprogramming the pacemaker.
Another possible complication is "pacemaker-tracked tachycardia," where a supraventricular tachycardia such as atrial fibrillation or atrial flutter is tracked by the pacemaker and produces beats from a ventricular lead.
It is important to consider leads as a potential nidus for Thrombosis events. The leads are small-diameter wires from the pacemaker to the implantation site in the heart muscle, and are usually placed intravenously through the subclavian vein in order to access the right atrium. Placing a foreign object within the venous system in such a manner may disrupt blood-flow and allow for thrombus formation. Therefore, patients with pacemakers may need to be placed on anti-coagulation therapy to avoid potential life-threatening thrombosis or embolus.
These leads may also damage the Tricuspid valve, either during placement or through wear and tear over time. This can lead to tricuspid regurgitation and right-sided heart failure, which may require tricuspid valve replacement.
Sometimes leads will need to be removed. The most common reason for lead removal is infection; however, over time, leads can degrade due to a number of reasons such as lead flexing. Changes to the programming of the pacemaker may overcome lead degradation to some extent. However, a patient who has several pacemaker replacements over a decade or two in which the leads were reused may require lead replacement surgery.
Lead replacement may be done in one of two ways. Insert a new set of leads without removing the current leads (not recommended as it provides additional obstruction to blood flow and heart valve function) or remove the current leads and then insert replacements. The lead removal technique will vary depending on the surgeon's estimation of the probability that simple traction will suffice to more complex procedures. Leads can normally be disconnected from the pacemaker easily, which is why device replacement usually entails simple surgery to access the device and replace it by simply unhooking the leads from the device to replace and hooking the leads to the new device. The possible complications, such as perforation of the heart wall, come from removing the lead{s} from the patient's body.
The free end of a pacemaker lead is actually implanted into the heart muscle with a miniature screw or anchored with small plastic hooks called tines. The longer the leads have been implanted (starting from a year or two), the more likely that they will have additional attachments to the patient's body at various places in the pathway from device to heart muscle, since the body tends to incorporate foreign devices into tissue. In some cases, for a lead that has been inserted for a short amount of time, removal may involve simple traction to pull the lead from the body. Removal in other cases is typically done with a laser or cutting device which threads like a cannula with a cutting edge over the lead and is moved down the lead to remove any organic attachments with tiny cutting lasers or similar device.
Pacemaker lead malposition in various locations has been described in the literature. Treatment varies, depending on the location of the pacer lead and symptoms.
Another possible complication called twiddler's syndrome occurs when a patient manipulates the pacemaker and causes the leads to be removed from their intended location and causes possible stimulation of other nerves.
Overall life expectancy with pacemakers is excellent, and mostly depends upon underlying diseases, presence of atrial fibrillation, age and sex at the time of first implantation.
+ NASPE / BPEG Defibrillator (NBD) code – 1993 ! I | IV |
Antibradycardia pacing chamber | |
O = None | |
A = Atrium | |
V = Ventricle | |
D = Dual (A+V) |
+ Short form of the NASPE/BPEG Defibrillator (NBD) code | ICD with shock capability only |
ICD with bradycardia pacing as well as shock | |
ICD with tachycardia (and bradycardia) pacing as well as shock |
In 1926, Mark C Lidwill of the Royal Prince Alfred Hospital of Sydney, supported by physicist Edgar H. Booth of the University of Sydney, devised a portable apparatus which "plugged into a lighting point" and in which "One pole was applied to a skin pad soaked in strong salt solution" while the other pole "consisted of a needle insulated except at its point, and was plunged into the appropriate cardiac chamber". "The pacemaker rate was variable from about 80 to 120 pulses per minute, and likewise the voltage variable from 1.5 to 120 volts".
In 1932, American physiologist Albert Hyman, with the help of his brother, described an electro-mechanical instrument of his own, powered by a spring-wound hand-cranked motor. Hyman himself referred to his invention as an "artificial pacemaker", the term continuing in use to this day.
An apparent in the publication of research conducted between the early 1930s and World War II may be attributed to the public perception of interfering with nature by "reviving the dead". For example, "Hyman did not publish data on the use of his pacemaker in humans because of adverse publicity, both among his fellow physicians, and due to newspaper reporting at the time. Lidwell may have been aware of this and did not proceed with his experiments in humans".
A number of innovators, including Paul Zoll, made smaller but still bulky transcutaneous pacing devices from 1952 using a large rechargeable battery as the power supply.
In 1957, William L. Weirich published the results of research performed at the University of Minnesota. These studies demonstrated the restoration of heart rate, cardiac output and mean aortic pressures in animal subjects with complete heart block through the use of a myocardial electrode.
In 1958 Colombian doctor Alberto Vejarano Laverde and Colombian electrical engineer Jorge Reynolds Pombo constructed an external pacemaker, similar to those of Hopps and Zoll, weighing 45 kg and powered by a 12 volt car lead–acid battery, but connected to electrodes attached to the heart. This apparatus was successfully used to sustain a 70-year-old priest, Gerardo Florez.
The development of the silicon transistor and its first commercial availability in 1956 was the pivotal event that led to the rapid development of practical cardiac pacemaking.
In the UK in the 1960s, Lucas Engineering in Birmingham was asked by Mr Abrams of The Queen Elizabeth Hospital to produce a prototype for a transistorised replacement for the electro-mechanical product. The team was headed by Roger Nolan, an engineer with the Lucas Group Research Centre. Nolan designed and created the first blocking oscillator and transistor-powered pacemaker. This pacemaker was worn on a belt and powered by a rechargeable sealed battery, enabling users to live a more-normal life.
One of the earliest patients to receive this Lucas pacemaker device was a woman in her early 30s. The operation was carried out in 1964 by South African cardiac surgeon Alf Gunning, a student of Christiaan Barnard. This pioneering operation took place under the guidance of cardiac consultant Peter Sleight at the Radcliffe Infirmary in Oxford and his cardiac research team at St George's Hospital in London.
In 1959, temporary transvenous pacing was first demonstrated by Seymour Furman and John Schwedel, whereby the catheter electrode was inserted via the patient's basilic vein.
In February 1960, an improved version of the Swedish Elmqvist design was implanted by Doctors Orestes Fiandra and Roberto Rubio in the Casmu 1 Hospital of Montevideo, Uruguay. This pacemaker, the first implanted in the Americas, lasted until the patient died of other ailments, nine months later. The early Swedish-designed devices used batteries recharged by an induction coil from the outside.
Implantable pacemakers constructed by engineer Wilson Greatbatch entered use in humans from April 1960 following extensive animal testing. The Greatbatch innovation varied from the earlier Swedish devices in using primary cells (a mercury battery) as the energy source. The first patient lived for a further 18 months.
The first use of transvenous pacing in conjunction with an implanted pacemaker was by Victor Parsonnet in the United States, Lagergren in Sweden and Jean-Jacques Welti in FranceJean Jacques Welti:Biography, Heart Rhythm Foundation in 1962–63. The transvenous, or pervenous, procedure involved incision of a vein into which was inserted the catheter electrode lead under Fluoroscopy guidance, until it was lodged within the trabeculae of the right ventricle. This became the method of choice by the mid-1960s.
Cardiothoracic surgeon Leon Abrams and medical engineer Ray Lightwood developed and implanted the first patient-controlled variable-rate heart pacemaker in 1960 at the University of Birmingham. The first implant took place in March 1960, with two further implants the following month. These three patients made good recoveries and returned to a high quality of life. By 1966, 56 patients had undergone implantation with one surviving for over years. Blue Plaque Guide
A further impediment to the reliability of the early devices was the diffusion of water vapor from body fluids through the epoxy resin encapsulation, affecting the electronic circuitry. This phenomenon was overcome by encasing the pacemaker generator in a hermetically sealed metal case, initially by Telectronics of Australia in 1969, followed by Cardiac Pacemakers, Inc. of St. Paul, Minnesota in 1972. This technology, using titanium as the encasing metal, became the standard by the mid-1970s.
On July 9, 1974, Manuel A. Villafaña and Anthony Adducci, the founders of Cardiac Pacemakers, Inc. (Guidant), manufactured the world's first pacemaker with a lithium anode and a lithium-iodide electrolyte solid-state battery. Lithium-iodide or lithium anode cells increased the life of pacemakers from one year to as long as eleven years, and has become the standard for pacemaker designs. They began designing and testing their implantable cardiac pacemaker powered by a new longer-life lithium battery in 1971. The first patient to receive a CPI pacemaker emerged from surgery in June 1973.
Liza Morton was fitted with an implantable pacemaker at 11 days old in 1978, at Glasgow’s Yorkhill hospital, Scotland. She was the youngest baby at the time.
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