CARDIOVERSION AND DEFIBRILATOR

Cardioversion is a medical procedure by which an cardiac arrhythmia is converted to a normal rhythm, using electricity or drugs.

2types of cardioversion-

1. Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart, at a specific moment in the cardiac cycle.

2. Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock

Synchronized electrical cardioversion

To perform synchronized electrical cardioversion two electrode hand-held paddles are used each comprising a metallic plate which is faced with a saline based conductive gel.

The pads are placed on the chest of the patient, or one is placed on the chest and one on the back.

These are connected by cables to a machine which has the combined functions of an ECG display screen and the electrical function of a defibrillator.

A synchronizing function (either manually operated or automatic) allows the cardioverter to deliver a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R wave of the QRS complex on the ECG.

Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation.

If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable. However, if the patient is hemodynamically unstable or unconscious, the shock is given immediately upon confirmation of the arrhythmia.

When synchronized electrical cardioversion is performed as an elective procedure, the shocks can be performed in conjunction with drug therapy until sinus rhythm is attained.

After the procedure, the patient is monitored to ensure stability of the sinus rhythm.

INDICATION-

Synchronized electrical cardioversion is used to treat hemodynamically significant supraventricular (or narrow complex) tachycardias, including atrial fibrillation and atrial flutter.

It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present.

Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation.

Pharmacologic cardioversion- Drugs that are effective at maintaining normal rhythm after electric cardioversion, can also be used for pharmacological cardioversion. Drugs like amiodarone, diltiazem, verapamil and metoprolol are frequently given before cardioversion to decrease the heart rate, stabilize the patient and increase the chance that cardioversion is successful.

INDICATIONS-

To return the heart to normal sinus rhythm.

Especially good option in patients with fibrillation of recent onset.

There are various classes of agents that are most effective for pharmacological cardioversion.

Class I agents - sodium (Na) channel blockers (which slow conduction by blocking the Na+ channel) and are divided into 3 subclasses a, b and c.

Class Ia slows phase 0 depolarization in the ventricles and increases the absolute refractory period. Procainamide, quinidine and disopyramide are Class Ia agents.

Class 1b drugs shorten phase 3 repolarization. They include Lidocaine, Mexiletine and Phenytoin.

Class Ic greatly slow phase 0 depolarization in the ventricles Flecainide, moricizine and propafenone are Class Ic agents.

Class II agents are beta blockers which inhibit SA and AV node depolarization and slow heart rate. They also decrease cardiac oxygen demand and can prevent cardiac remodeling. Not all beta blockers are the same, some are cardio selective (affecting only beta 1 receptors) while others are non-selective (affecting beta 1 and 2 receptors). Beta blockers that target the beta-1 receptor are called cardio selective because beta-1 is responsible for increasing heart rate; hence a beta blocker will slow the heart rate.

Class III agents (prolong repolarization by blocking outward K+ current): Amiodarone and sotalol are effective Class III agents.

Ibutilideis another Class III agent but has a different mechanism of action (acts to promote influx of sodium through slow-sodium channels). It has been shown to be effective in acute cardioversion of recent-onset atrial fibrillation and atrial flutter.

Class IV drugs are calcium (Ca) channel blockers. They work by inhibiting the action potential of the SA and AV nodes.

If the patient is stable, adenosine may be administered first, as the medicine performs a sort of "chemical cardioversion" and may stabilize the heart and let it resume normal function on its own without using electricity.

DEFIBRILATORNEED FOR A DEFIBRILLATOR Ventricular fibrillation is a serious cardiac emergency resulting from asynchronous contraction of the heart muscles. Due to ventricular fibrillation, there is an irregular or rapid heart rhythm. Fig. Ventricular fibrillation Fig. Normal heart beat

Slide 3: Ventricular fibrillation can be converted into a more efficient rhythm by applying a high energy shock to the heart. This sudden surge across the heart causes all muscle fibres to contract simultaneously. The instrument for administering the shock is called a

DEFIBRILLATOR. Possibly , the fibres may then respond to normal physiological pacemaking pulses. NEED FOR A DEFIBRILLATOR

TYPES OF DEFIBRILLATORS : 4 TYPES OF DEFIBRILLATORS Internal External

TYPES OF DEFIBRILLATORS : TYPES OF DEFIBRILLATORS Internal defibrillator Electrodes placed directly to the heart Eg.-Pacemaker External defibrillator Electrodes placed directly on the heart Eg.-AED

THE POWER OF DEFIBRILLATION : 6 THE POWER OF DEFIBRILLATION Higher voltages are required for external defibrillation than for internal defibrillation. A corrective shock of 750-800 volts is applied within a tenth of a second . That is the same voltage as 500-533 no of AA batteries!

Slide 7: DEFIBRILLATOR ELECTRODES Types of Defibrillator electrodes:- Spoon shaped electrode Applied directly to the heart. Paddle type electrode Applied against the chest wall Pad type electrode Applied directly on chest wall

Slide 8: DEFIBRILLATOR ELECTRODES

Slide 9: Fig.- Pad electrode DEFIBRILLATOR ELECTRODES

Slide 10: PRINCIPLE OF DEFIBRILLATION Energy storage capacitor is charged at relatively slow rate from AC line. Energy stored in capacitor is then delivered at a relatively rapid rate to chest of the patient. Simple arrangement involve the discharge of capacitor energy through the patient’s own resistance.

Slide 11: PRINCIPLE OF DEFIBRILLATION

Slide 12: PRINCIPLE OF DEFIBRILLATION The discharge resistance which the patient represents as purely ohmic resistance of 50 to 100Ω approximately for a typical electrode size of 80cm2. This particular waveform Fig 13.9(b) is called ‘ Lown’ waveform. The pulse width of this waveform is generally 10 ms.

Classes of discharge waveform : Classes of discharge waveform Monophasic pulse or waveform Bi-phasic pulse or waveform

Slide 14: Classes of discharge waveform There are two general classes of waveforms: mono-phasic waveform Energy delivered in one direction through the patient’s heart Biphasic waveform Energy delivered in both direction throuth the patient’s heart

Slide 15: Classes of discharge waveform Fig:- Generation of bi-phasic waveform

Slide 16: Classes of discharge waveform The biphasic waveform is preferred over monophasic waveform to defibrillate .why????? A monophasic type, give a high-energy shock, up to 360 to 400 joules due to which increased cardiac injury and in burns the chest around the shock pad sites. A biphasic type, give two sequential lower-energy shocks of 120 - 200 joules, with each shock moving in an opposite polarity between the pads.

Slide 17: AUTOMATIC EXTERNAL DEFIBRILLATOR

Slide 18: AEDs require self-adhesive electrodes instead of hand held paddles. AED is a type of external defibrillation process. AUTOMATIC EXTERNAL DEFIBRILLATOR AED is a portable electronic device that automatically diagnoses the ventricular fibrillation in a patient. Automatic refers to the ability to autonomously analyse the patient's condition. The AED uses voice prompts, lights and text messages to tell the rescuer what steps have to take next.

Slide 19: ELECTRODE PLACEMENT OF AED Anterior electrode pad Apex electrode pad Fig. anterior –apex scheme of electrode placement

Slide 20: WORKING OF AED turned on or opened AED. AED will instruct the user to:- Connect the electrodes (pads) to the patient. Avoid touching the patient to avoid false readings by the unit. The AED examine the electrical output from the heart and determine the patient is in a shockable rhythm or not.

Slide 21: When charged, the device instructs the user to ensure no one is touching the victim and then to press a red button to deliver the shock. when device determined that shock is warranted, it will charge its internal capacitor in preparation to deliver the shock. WORKING OF AED Many AED units have an 'event memory' which store the ECG of the patient along with details of the time the unit was activated and the number and strength of any shocks delivered.

Slide 22: PRECAUTIONS IN DEFIBRILLATION PROCESS The paddles used in the procedure should not be placed:- on a woman's breasts over an internal pacemaker patients. Before the paddle is used, a gel must be applied to the patient's skin

Defibrillation : Defibrillation Mechanism Current depolarizes myocardium Induces asystole temporarily Allows one pacemaker to regain control

Defibrillation : Defibrillation Factors to consider Duration of VF The longer VF lasts, the harder it is to cure The quicker the better Shock early-Shock often Likelihood of resuscitation decreases 7-10% with each passing minute

Defibrillation : Defibrillation Factors to consider Myocardial environment/condition Hypoxia, acidosis, hypothermia, electrolyte imbalance, drug toxicity impede conversion Do NOT delay shock trying to correct problems

Defibrillation : Defibrillation Factors to consider Heart size/body weight Pedi requirement lower than adult 2 J/kg initial shock 4 J/kg repeat shocks Direct size/energy relationship in adults unknown 200 to 360 J

Defibrillation : Defibrillation Previous countershock Repeated shocks lower resistance Give three initial shocks in 30-45 sec One quickly after another with little time between

Defibrillation : Defibrillation Factors to consider Paddle size Adults (large paddles) 10-13 cm diameter Pediatric (small paddles usually < 1 yr) Children 8 cm Infants 4.5 cm

Defibrillation : Defibrillation Use largest size that completely contacts chest without paddles touching Small paddles: concentrate current, burn heart Large paddles: reduce current density

Defibrillation : Defibrillation Paddle placement One to right of sternum below clavicle; Other to left of left nipple in anterior axillary line Reversing paddles marked “apex--sternum” does NOT affect defibrillation AP placement can be used to defib small children with adult paddles

Defibrillation : Defibrillation Paddle-skin interface Cream, paste, saline pads, gelled pads Decreases resistance to current flow Avoid smearing or running: “bridges” charge NEVER use alcohol!!!

Defibrillation : Defibrillation Paddle contact pressure Firm pressure of 25 pounds Deflates lungs; Shortens current path Do not lean on paddles; They slip

Cardioversion : Cardioversion Definitions Cardioversion Use of electrical shock to interrupt tachycardia Used in Non-Arrest patients only Only VF/VT (pulseless) can be defibrillated

Cardioversion : Cardioversion Definitions Synchronized cardioversion Timing of shock to avoid peak of T-wave Prevents VF caused by delivering shock during vulnerable period

Cardioversion : Cardioversion Indications Tachyarrhythmias which: Cause or worsen hemodynamic compromise Cause or worsen ischemic heart disease Are resistant to drug therapy

Cardioversion : Cardioversion Procedure Oxygen, ECG monitor, IV Patient must be on leads to cardiovert Sedate with Valium or Versed Do NOT make patient unresponsive

Cardioversion : Cardioversion Procedure Activate synchronizer Observe marking of complexes May need to unsynchronize if: Random synching occurs Double-synching occurs

Cardioversion : Cardioversion Procedure Charge to desired energy setting Depress buttons; Hold until discharge occurs If VF occurs, unsynchronize before defibrillating

Cardioversion : Cardioversion If a patient is in VF, why might the defibrillator not discharge if the synchronizer is on

Defibrillation is a common treatment for life-threatening cardiac arrhythmias, ventricular fibrillation, and pulseless ventricular tachycardia. Defibrillation consists of delivering a therapeutic dose of electrical energy to the affected heart with a device called a defibrillator. This depolarizes a critical mass of the heart muscle, terminates the arrhythmia, and allows normal sinus rhythm to be reestablished by the body's natural pacemaker, in the sinoatrial node of the heart. Defibrillators can be external, transvenous, or implanted, depending on the type of device used or needed. Some external units, known as automated external defibrillators (AEDs), automate the diagnosis of treatable rhythms, meaning that lay responders or bystanders are able to use them successfully with little, or in some cases no training at all

Manual external defibrillator

External defibrillator / monitor

The units are used in conjunction with (or more often have inbuilt) electrocardiogram readers, which the healthcare provider uses to diagnose a cardiac condition (most often fibrillation or tachycardia although there are some other rhythms which can be treated by different shocks).

Manual external defibrillator monitor

The healthcare provider will then decide what charge (in joules) to use, based on proven guidelines and experience, and will deliver the shock through paddles or pads on the patient's chest. As they require detailed medical knowledge, these units are generally only found in hospitals and on some ambulances. For instance, every NHSambulance in the United Kingdom is equipped with a manual defibrillator for use by the attending paramedics and technicians. In the United States, many advanced EMTs and all paramedics are trained to recognize lethal arrhythmias and deliver appropriate electrical therapy with a manual defibrillator when appropriate.

[edit]Manual internal defibrillator

These are the direct descendants of the work of Beck and Lown. They are virtually identical to the external version, except that the charge is delivered through internal paddles in direct contact with the heart. These are almost exclusively found in operating theatres, where the chest is likely to be open, or can be opened quickly by a surgeon.

Automated external defibrillator (AED)

Main article: Automated external defibrillator

An AED at a railway station in Japan. The AED box has information on how to use it in

Japanese, English, Chinese and Korean, and station staff are trained to use it.

These simple-to-use units are based on computer technology which is designed to analyze the heart rhythm itself, and then advise the user whether a shock is required. They are designed to be used by lay persons, who require little training to operate them correctly. They are usually limited in their interventions to delivering high joule shocks for VF (ventricular fibrillation) and VT (ventricular tachycardia) rhythms, making them generally of limited use to health professionals, who could diagnose and treat a wider range of problems with a manual or semi-automatic unit.

The automatic units also take time (generally 10–20 seconds) to diagnose the rhythm, where a professional could diagnose and treat the condition far more quickly with a manual unit.[8] These time intervals for analysis, which require stopping chest compressions, have been shown in a number of studies to have a significant negative effect on shock success.[9] This effect led to the recent change in the AHA defibrillation guideline (calling for two minutes of CPR after each shock without analyzing the cardiac rhythm) and some bodies recommend that AEDs should not be used when manual defibrillators and trained operators are available.[8]

Automated external defibrillators are generally either held by trained personnel who will attend incidents, or are public access units which can be found in places including corporate and government offices, shopping centres, airports, restaurants, casinos, hotels, sports stadiums, schools and universities, community centers, fitness centers and health clubs.

An automated external defibrillator, open and ready for pads to be attached

The locating of a public access AED should take in to account where large groups of people gather, and the risk category associated with these people, to ascertain whether the risk of a sudden cardiac arrest incident is high. For example, a center for teenage children is a particularly low risk category (as children very rarely enter heart rhythms such as VF (Ventricular Fibrillation) or VT (Ventricular Tachycardia), being generally young and fit, and the most common causes of pediatric cardiac arrest are respiratory arrest and trauma - where the heart is more likely to enter asystole or PEA, (where an AED is of no use). On the other hand, a large office building with a high ratio of males over 50 is a very high risk environment.[dubious – discuss]

Automated-external-defibrillator

In many areas, emergency services vehicles are likely to carry AEDs. EMT-Basics in most areas are not trained in manual defibrillation, and often carry an AED instead. Some ambulances carry an AED in addition to a manual unit. In addition, some police or fire service vehicles carry an AED for first responder use. Some areas have dedicated community first responders, who are volunteers tasked with keeping an AED and taking it to any victims in their area. It is also increasingly common to find AEDs on transport such as commercial airlines and cruise ships. The presence of an AED can be a particularly decisive

factor in cardiac patient survival in these scenarios, as professional medical assistance may be hours away.

There are 2 types of AEDs: Fully Automated and Semi Automated. Most AEDs are semi automated. A semi automated AED automatically diagnoses heart rhythms and determines if a shock is necessary. If a shock is advised, the user must then push a button to administer the shock. A fully automated AED automatically diagnoses the heart rhythm and advises the user to stand back while the shock is automatically given. Also, some types of AEDs come with advanced features, such as a manual override or an ECG display.

In order to make them highly visible, public access AEDs often are brightly coloured, and are mounted in protective cases near the entrance of a building. When these protective cases are opened, and the defibrillator removed, some will sound a buzzer to alert nearby staff to their removal but do not necessarily summon emergency services. All trained AED operators should also know to phone for an ambulance when sending for or using an AED, as the patient will be unconscious, which always requires ambulance attendance.

[edit]Implantable cardioverter-defibrillator (ICD)

Main article: Implantable cardioverter-defibrillator

Also known as automatic internal cardiac defibrillator (AICD). These devices are implants, similar to pacemakers (and many can also perform the pacemaking function). They constantly monitor the patient's heart rhythm, and automatically administer shocks for various life threatening arrhythmias, according to the device's programming. Many modern devices can distinguish between ventricular fibrillation, ventricular tachycardia, and more benign arrhythmias like supraventricular tachycardia and atrial fibrillation. Some devices may attempt overdrive pacing prior to synchronised cardioversion. When the life threatening arrhythmia is ventricular fibrillation, the device is programmed to proceed immediately to an unsynchronized shock.

There are cases where the patient's ICD may fire constantly or inappropriately. This is considered a medical emergency, as it depletes the device's battery life, causes significant discomfort and anxiety to the patient, and in some cases may actually trigger life threatening arrhythmias. Some emergency medical services personnel are now equipped with a ring magnet to place over the device, which effectively disables the shock function of the device while still allowing the pacemaker to function (if the device is so equipped). If the device is shocking frequently, but appropriately, EMS personnel may administer sedation.

[edit]Wearable cardiac defibrillator

A development of the AICD is a portable external defibrillator that is worn like a vest.[10] The unit monitors the patient 24 hours a day and will automatically deliver a biphasic shock if needed. This device is mainly indicated in patients awaiting an implantable defibrillator. Currently[when?] only one company manufactures these and they are of limited availability.

Interface with the patient

The connection between the defibrillator and the patient consists of a pair of electrodes, each provided with electricity conductive gel in order to ensure a good connection and to minimize electrical resistance, also called chest impedance (despite the DC discharge)

which would burn the patient. Gel may be either wet (similar in consistency to surgical lubricant) or solid (similar to gummi candy. Solid-gel is more convenient, because there is no need to clean the used gel off of patient's skin after defibrilation (the solid gel is easily lifted off of the patient). However, the use of solid-gel presents a higher risk of burns during defibrillation, since wet-gel electrodes more evenly conduct electricity into the body. Paddle electrodes, which were the first type developed, come without gel, and must have the gel applied in a separate step. Self-adhesive electrodes come prefitted with gel. There is a general division of opinion over which type of electrode is superior in hospital settings; the American Heart Association favors neither, and all modern manual defibrillators used in hospitals allow for swift switching between self-adhesive pads and traditional paddles. Each type of electrode has its merits and demerits, as discussed below.

[edit]Paddle electrodes

The most well-known type of electrode (widely depicted in films and television) is the traditional metal paddle with an insulated (usually plastic) handle. This type must be held in place on the patient's skin with approximately 25 lbs of force while a shock or a series of shocks is delivered. Paddles offer a few advantages over self-adhesive pads. Many hospitals in the United States continue the use of paddles, with disposable gel pads attached in most cases, due to the inherent speed with which these electrodes can be placed and used. This is critical during cardiac arrest, as each second of nonperfusion means tissue loss. Modern paddles allow for monitoring (electrocardiography), though in hospital situations, separate monitoring leads are often already in place.

Paddles are reuseable, being cleaned after use and stored for the next patient. Gel is therefore not preapplied, and must be added before these paddles are used on the patient. Paddles are generally only found on the manual external units. Paddles require approximately 25 lbs of force to be applied while the shock is delivered.

[edit]Self-adhesive electrodes

Newer types of resuscitation electrodes are designed as an adhesive pad, which includes either solid or wet gel. These are peeled off their backing and applied to the patient's chest when deemed necessary, much the same as any other sticker. The electrodes are then connected to a defibrillator, much as the paddles would be. If defibrillation is required, the machine is charged, and the shock is delivered, without any need to apply any additional gel or to retrieve and place any paddles. Most adhesive electrodes are designed to be used not only for defibrillation, but also for transcutaneous pacing and synchronized electrical cardioversion. These adhesive pads are found on most automated and semi-automated units and are replacing paddles entirely in non-hospital settings. In hospital, for cases where cardiac arrest is likely to occur (but has not yet), self-adhesive pads may be placed prophylactically.

Pads also offer an advantage to the untrained user, and to medics working in the sub-optimal conditions of the field. Pads do not require extra leads to be attached for monitoring, and they do not require any force to be applied as the shock is delivered. Thus, adhesive electrodes 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 be up to several feet away. (The risk of electrical shock to others remains unchanged, as does that of shock due to operator misuse.) Self-adhesive electrodes are single-use only. They may be used for multiple shocks in a single course of treatment, but are replaced if (or in case) the patient recovers then reenters cardiac arrest.

[edit]Placement

Resuscitation electrodes are placed according to one of two schemes. The anterior-posterior scheme 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.

Description

Defibrillation - is the treatment for immediately life-threatening arrhythmias with which the patient does not have a pulse, i.e.ventricular fibrillation (VF) or pulseless ventricular tachycardia(VT).

Cardioversion - is any process that aims to convert an arrhythmia back to sinus rhythm. Electrical cardioversion is used when the patient has a pulse but is either unstable, or chemical cardioversion has failed or is unlikely to

be successful. These scenarios may be associated with chest pain, pulmonary oedema, syncope or hypotension. It is also used in less urgent cases, e.g. atrial fibrillation (AF) to try to revert the rhythm back to sinus. This article only deals with electrical cardioversion.

The aim in both is to deliver electrical energy to the heart to stun the heart

momentarily and thus allow a normal sinus rhythm to kick in via the heart's

normal electricity centre, i.e. the sinoatrial node.

This article will discuss the following

1. Defibrillation2. Implantable cardiac defibrillators (ICDs)3. Cardioversion

Defibrillation

At the end of the 18th century two physiologists, Prévost and Batelli, performed

shock experiments on the hearts of dogs. They applied electrical shocks and

discovered that small shocks put the dogs' hearts in to VF and this was

successfully reversed with a larger shock. It was first used in humans by Claude

Beck, a cardiothoracic surgeon - on a 14 year-old boy undergoing cardiothoracic

surgery forcongenital heart disease. Electrodes were placed across the open

heart. Closed chest defibrillation was not discovered until the 1950s in Russia.

But it was not until 1959 that Bernard Lown designed the modern-day

monophasic defibrillator. This is based on the charging of capacitors and then

delivering of a shock by paddles over a few milliseconds. In the 1980s the

biphasic waveform was discovered. This provided a shock at lower levels of

energy which were just as efficacious as monophasic shocks.

Also see separate article Adult Cardiopulmonary Arrest, dealing with adult

advanced life support1Differences between monophasic and biphasic systems

In monophasic systems, the current travels only in one direction - from one paddle to the other.

In biphasic systems, the current travels towards the positive paddle and then reverses and goes back; this occurs several times.2

Biphasic shocks deliver one cycle every 10 milliseconds. They are associated with fewer burns and less myocardial damage. With monophasic shocks, the rate of first shock success in cardiac arrests

due to a shockable rhythm is only 60%, whereas with biphasic shocks, this increases to 90%.2

However, this efficacy of biphasic defibrillators over monophasic defibrillators has not been consistently reported. The Transthoracic Incremental Monophasic Versus Biphasic Defibrillation by Emergency Responders (TIMBER) trial failed to detect any differences in survival using

either system. Also the same study failed to find any differences between the defibrillators in terminating VF.3

Types of defibrillators

1. Automated external defibrillators (AEDs)4 These are useful, as their use does not require special medical training They are found in public places, e.g. offices, airports, train stations,

shopping centres They analyse the heart rhythm and then charge and deliver a shock if

appropriate However, they cannot be overridden manually and can take 10-20

seconds to determine arrhythmias2. Semi-automated AEDs

These are similar to AEDs but can be overridden and usually have an ECG display

They tend to be used by paramedics They also have the ability to pace

3. Standard defibrillators with monitor - may be monophasic or biphasic4. Transvenous or implanted

Paddles versus adhesive patches

Paddles were originally used but their use is being superseded by adhesive patches

Adhesive patches are placed most commonly anterio-apically - anterior patch goes under the right clavicle and the apical patch is placed at the apex

Adhesive electrodes are better, as they stick to the chest wall, so there is no mess with gels

Paddles require at least 25 lbs of pressure, which is not needed with adhesive electrodes

Adhesive electrodes also allow good ECG trace without interference They are also safer, as no operator required - although, before discharging a

shock, it is important to ensure everyone is clear of the patientEnergy levels for defibrillation (usually written on machine)

Monophasic - the cardiopulmonary resuscitation (CPR) algorithm recommends single shocks started at and repeated at 360 J1

Biphasic - the CPR algorithm recommends shocks initially of 150-200 J and subsequent shocks of 150-360 J1

The Biphasic Trial in 2007 compared lower fixed (150, 150, 150 J) and gradually

increasing energy (200, 300, 360 J) shocks for out-of-hospital cardiac

arrests.5 Escalating energy shocks were associated with more frequent

conversion and termination of VF as opposed to low-level fixed shocks. This

applied to patients who remained in VF after the first shock.Implantable cardiac defibrillators

ICDs were discovered in the 1970s, although research had been going on for

almost a decade prior to this.

ICDs can

Sense atrial and ventricular signals Detect and thus classify sensed signals Provide therapy to terminate VF/VT Pace and/or perform cardiac resynchronisation

They continuously monitor the patient's heart rhythm and then deliver a shock if

there is an abnormal rhythm, usually VF or VT. They monitor and record the

heart rhythm throughout an arrhythmia.

Sudden cardiac death (SCD) occurs in patients with cardiac conditions, including

QT prolongation and left ventricular dysfunction. Mortality from SCD is highest in

New York Heart Association (NYHA) class II onwards, i.e. those with well-

compensated heart failure are at risk.6ICDs should be considered for the following groups6,7

Secondary prevention Survived a cardiac arrest due to either VF/VT Spontaneous sustained VT causing syncope or haemodynamic compromise Sustained VT and who have an associated reduction inejection fraction - left

ventricular ejection fraction (LVEF) of less than 35%Primary prevention

Previous myocardial infarction (more than four weeks) and either:o Left ventricular dysfunction with an LVEF of less than 35% and non-sustained

VT on Holter or on electrophysiological testing.o OR, left ventricular dysfunction with an LVEF of less than 30% and QRS

duration of equal to or more than 120 milliseconds. Familial cardiac conditions with a high risk of SCD including long QT

syndrome, hypertrophic cardiomyopathy, Brugada's syndrome or arrhythmogenic right ventricular dysplasia(ARVD), or have undergone surgical repair of congenital heart disease

Primary prevention of SCD

The antiarrhythmics versus ICD (AVID) trial reported that survival was greater for

patients inserted with an ICD after VF, VT with syncope or sustained VT with a

low ejection fraction, compared with drug treatments (mostly amiodarone).This

trial along with two other randomised trials - the Canadian Implantable

Defibrillator Study (CIDS) and the Cardiac Arrest Study Hamburg (CASH) -

revealed an overall 15-23% reduction in mortality in patients with an

ICD.6 Similar conclusions have been reached in trials looking at the benefits of

ICD in ischaemic cardiomyopathy (with an ejection fraction <35%).6Problems with ICDs

Firing continuously and inappropriately - occurs in up to 25% of patients.8 This is a medical emergency, as it may lead to another life-threatening

arrhythmia. The battery may also run out and shocks usually cause a lot of discomfort to patients.

Patients who receive more than one shock or are unwell need to be evaluated as for ischaemic heart disease, as they may have had an ischaemic event or ongoing arrhythmias. Placing a magnet over the ICD

causes it to stop functioning - only advisable in a hospital setting with cardiac monitoring.

Other problems can occur during the placement of an ICD, e.g. pneumothorax, infection and cardiac tamponade.

Practical issues surrounding ICDs

They are usually placed in the left infraclavicular region and are palpable (rarely they are located in the abdomen or right infraclavicular regions)

Patients are followed up every 1-6 months which includes interrogation and testing of the ICD device

ICDs treat arrhythmias but do not prevent them from occurringCost-effectiveness

There has been much concern that ICD therapy is not cost-effective. Each unit

costs tens of thousands of pounds. Further work in this area is currently

underway.

Cardioversion

Uses

Decompensated rapid AF with a rapid ventricular response, e.g. hypotensive patient, not responding to medical therapy9

VT with a pulse Supraventricular tachycardias including AF; not acutely urgent10

In cardioversion the shock has to be properly timed, so that it does not occur

during the vulnerable period, i.e. during the T wave. If this occurs then VT can be

triggered.

Atrial fibrillation

Cardioversion is used for rhythm control Not all cardioversion is successful and, at one year, 50% redevelop AF11 Medical treatments and cardioversion are of similar efficacy (unless

permanent AF) Cardioversion of AF is associated with increased risk ofthromboembolic

disease (TED); thus, anticoagulation is required for at least three weeks before and at least four weeks afterwards11

Some centres use transoesophageal echocardiogram during the procedure in order to look for thrombus, although a few patients still develop TED despite negative results12

Sotalol or amiodarone can be given for at least four weeks prior to cardioversion in patients who have had a previous failure to cardiovert or early recurrence of AF11

Others advocate the use of medications such as sotalol and amiodarone to maintain sinus rhythm after cardioversion13

How to cardiovert

Cardioversions are performed under general anaesthesia or sedation

The majority of cardioversions are elective procedures; however, some are performed when patients are acutely unwell with tachycardia, e.g. chest pain, breathlessness

Turn on the machine and attach adhesive electrodes (efficacy may be better with anterior-posterior electrodes)14

Choose the energy level Get a clearly visible trace on the monitor, e.g. using lead II Hit the 'synch' button - usually a blip or dot appears on the monitor, marking

each QRS complex Higher starting energy is associated with better success and fewer shocks14 Monophasic - begin with 300 - 360 J for AF and lower for atrial tachycardia or

VT (and escalate if necessary; up to 300 J)14 Biphasic - begin with 200 J14 Charge Ensure all is clear around the bed Discharge or shock - there may be a 1 to 2-second delay as the machine

ensures synchronisation Check rhythm after the shock - if sinus rhythm then stop; if not, then you

may need to deliver another shock at higher energy levels Look for burns afterwards and obtain a 12-lead ECG

PACEMAKER

The contraction of heart (cardiac) muscle in all animals with hearts is initiated by chemical impulses. The rate at which these impulses fire controls the heart rate. The cells that create these rhythmical impulses are called pacemaker cells, and they directly control theheart rate.

In humans, and occasionally in other animals, a mechanical device called an artificial pacemaker (or simply "pacemaker") may be used after damage to the body's intrinsic conduction system to produce these impulses synthetically.

The pacemaker is located in the wall of the right atrium.[1]

Primary (SA node)

One percent of the Cardiomyocytes in the myocardium possess the ability to generate electrical impulses (or action potentials).A specialized portion of the heart, called the sinoatrial node, is responsible for atrial propagation of this potential.

The sinoatrial node (SA node) is a group of cells positioned on the wall of the right atrium, near the entrance of the superior vena cava. These cells are modified cardiomyocyte. They possess rudimentary contractile filaments, but contract relatively weakly.

Cells in the SA node spontaneously depolarize, resulting in contraction, approximately 100 times per minute. This native rate is constantly modified by the activity of sympathetic and parasympatheticnerve fibers, so that the average resting cardiac rate in adult humans is about 70 beats per minute. Because the sinoatrial node is responsible for the rest of the heart's electrical activity, it is sometimes called the primary pacemaker.

[edit]Secondary (AV junction & Bundle of His)

If the SA node does not function, a group of cells further down the heart will become the heart's pacemaker, this is known as an ectopic pacemaker. These cells form the atrioventricular node (AV node), which is an area between the left atria and the right ventricles, within the atrial septum.

The cells of the AV node normally discharge at about 40-60 beats per minute, and are called the secondary pacemaker.

Further down the electrical conducting system of the heart is the Bundle of His. The left and right branches of this bundle, and the Purkinje fibres, will also produce a spontaneous action potential at a rate of 30-40 beats per minute, if the SA and AV node both do not function. The reason the SA node controls the whole heart is that its action potentials are released most often to the heart's muscle cells; this will produce contraction. The action potential generated by the SA node passes down the cardiac conduction system, and arrives before the other cells have had a chance to generate their own spontaneous action potential. This is the normal conduction of electrical activity in the heart.

[edit]Generation of action potentials

There are three main stages in the generation of an action potential in a pacemaker cell. Since the stages are analogous to contraction of cardiac muscle cells, they have the same naming system. This can lead to some confusion. There is no phase one or two, just phases zero, three and four.

[edit]Phase 4 - Pacemaker potential

The key to the rhythmic firing of pacemaker cells is that, unlike muscle and neurons, these cells will slowly depolarize by themselves.

As in all other cells, the resting potential of a pacemaker cell (-60mV to -70mV) is caused by a continuous outflow or "leak" of potassium ions through ion channel proteins in the membrane that surrounds the cells. The difference is that this potassium permeability decreases as time goes on, partly causing the slow depolarization. As well as this, there is a slow inward flow of sodium, called the funny current, as well as an inward flow of calcium. This all serves to make the cell more positive.

This relatively slow depolarization continues until the threshold potential is reached. Threshold is between -40mV and -50mV. When threshold is reached, the cells enter phase 0.

Phase 0 - Upstroke

Though much faster than the depolarization caused by the funny current and decrease in potassium permeability above, the upstroke in a pacemaker cell is slow compared to that in an axon.

The SA and AV node do not have fast sodium channels like neurons, and the depolarization is mainly caused by a slow influx of calcium ions. (The funny current also increases). The calcium is let into the cell by voltage-sensitive calcium channels that open when the threshold is reached.

[edit]Phase 3 - Repolarization

The calcium channels are rapidly inactivated, soon after they open. Sodium permeability is also decreased. Potassium permeability is increased, and the efflux of potassium (loss of positive ions) slowly repolarises the cell.

Electrical conduction system of the heart

The normal intrinsic electrical conduction of the heart allows electrical propagation to be transmitted from the Sinoatrial Node through both atria and forward to the Atrioventricular Node. Normal/baseline physiology allows further propagation from the AV node to the ventricle or Purkinje Fibers and respective bundle branches and subdivisions/fascicles. Both the SA and AV nodes stimulate the Myocardium. Time ordered stimulation of the myocardium allows efficient contraction of all four chambers of the heart, thereby allowing selective blood perfusion through both the lungs and systemic circulation.

Electrochemical mechanism

Main article: Cardiac action potential

Cardiac neurons innervating the myocardium bear limited similarities to those of skeletal muscle as well as other important differences. Cardiac neurons are uniquely subject to influence by the sympathetic and parasympathetic influence of the autonomic nervous system unlike skeletal muscle.

Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening ofvoltage-gated ion channels with inducted flow of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. After depolarization, there's a brief repolarization that takes place with the eflux of potassium through fast acting potassium channels. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels - meanwhile potassium channels have closed - and are followed by a titrated release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, slow acting Potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state.

Note that there are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most importantly the spontaneous depolarizations necessary for the SA node pacemaker activity.

[edit]Conduction pathway

Action potentials arising in the SA node (and propagating to the left atrium via Bachmann's bundle) cause the atria to contract. In parallel, action potentials travel to the AV node via internodal pathways. After a delay, the stimulus is conducted through the bundle of His to the bundle branches and then to the purkinje fibers and the endocardium at the apex of the heart, then finally to the ventricular myocardium. The pathway can be summarized as: SA node-> internodal pathway->transitional fibers->AV node->penetrating fibers->distal fibers->Bundle of his/AV bundle->right and left bundle branches->Purkinje fibers. The total time taken by the nerve impulse to travel from the SA node to the ventricular myocardium is 0.19 seconds. Microscopically, the wave of depolarization propagates to adjacent cells via gap junctions located on the intercalated disk. The heart is a functional syncytium (not to be confused with a true "syncytium" in which all the cells are fused together, sharing the same plasma membrane as in skeletal muscle). In a functional syncytium, electrical impulses

propagate freely between communicating cells via gap junctions, so that the myocardium functions as a single contractile unit. This property allows rapid, synchronous depolarization of the myocardium. While normally advantageous, this property can be detrimental as it potentially allows the propagation of incorrect electrical signals (e.g., via an ectopic pacemaker). Gap junctions can close, e.g., after a cardiac ischemic event such asmyocardial infarction, thus isolating damaged or dying tissue in the myocardium, which then no longer participate in synchronous myocardial contractility.

Depolarization and the ECG

Schematic diagram of normal sinus rhythm for a human heart as seen on ECG

See also: Electrocardiogram

[edit]SA node: P wave

Under normal conditions, electrical activity is spontaneously generated by the SA node, the physiological pacemaker. This electrical impulse is propagated throughout the right atrium, and through Bachmann's bundle to the left atrium, stimulating the myocardium of both atria to contract. The conduction of the electrical impulse throughout the left and right atria is seen on the ECG as the P wave.

As the electrical activity is spreading throughout the atria, it travels via specialized pathways, known as internodal tracts, from the SA node to the AV node.

[edit]AV node/Bundles: PR interval

The AV node functions as a critical delay in the conduction system. Without this delay, the atria and ventricles would contract at the same time, and blood wouldn't flow effectively from the atria to the ventricles. The delay in the AV node forms much of the PR segment on the ECG. Part of atrial repolarization can be represented by the PR segme

The distal portion of the AV node is known as the bundle of His. The bundle of His splits into two branches in the interventricular septum, the left bundle branch and the right bundle branch. The left bundle branch activates the left ventricle, while the right bundle branch activates the right ventricle. The left bundle branch is short, splitting into the left anterior fascicle and the left posterior fascicle. The left posterior fascicle is relatively short and broad, with dual blood supply, making it particularly resistant to ischemic damage. The left posterior fascicle transmits impulses to the papillary muscles, leading to mitral valve closure. As the left posterior fascicle is shorter and broader than the right, impulses reach the erection muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-ejaculating of the chordae tendinae, increasing the resistance to flow through the mitral valve during left ventricular contraction.

[edit]Purkinje fibers/ventricular myocardium: QRS complex

The two bundle branches taper out to produce numerous purkinje fibers, which stimulate individual groups of myocardial cells to contract.

The spread of electrical activity (depolarization) through the ventricular myocardium produces the QRS complex on the ECG.

[edit]Ventricular repolarization: T wave

The last event of the cycle is the repolarization of the ventricles. The transthoracically measured PQRS portion of an electrocardiogram is chiefly influenced by the sympathetic nervous system. The T (and occasionally U) waves are chiefly influenced by the parasympathetic nervous system guided by integrated brainstem control from the vagus nerve and the thoracic spinal accessory ganglia.

An impulse (action potential) that originates from the SA node at a relative rate of 60 - 100bpm is known as normal sinus rhythm. If SA nodal impulses occur at a rate less than

60bpm, the heart rhythm is known as bradycardiac sinus. If it occurs with a rate greater than 100bpm, it is called tachycardiac sinus.

ARTIFICAL PACEMAKER

A pacemaker (or artificial pacemaker, so as not to be confused with the heart's natural pacemaker) is a medical device that uses electrical impulses, delivered by electrodes contacting the heart muscles, to regulate the beating of the heart. The primary purpose of a pacemaker is to maintain an adequateheart rate, either because of the heart's native pacemaker is not fast enough, or there is a block in the heart's electrical conduction system. Modern pacemakers are externally programmable and allow the cardiologist to select the optimum pacing modes for individual patients. Some combine a pacemaker and defibrillator in a single implantable device. Others have multiple electrodes stimulating differing positions within the heart to improve synchronisation of thelower chambers (ventricles) of the heart.

Methods of pacing

An ECG in a person with an atrial pacemaker. Note the circle around one of the sharp

electrical spike in the position where one would expect the P wave.

[edit]Percussive pacing

Percussive pacing, also known as transthoracic mechanical pacing, is the use of the closed fist, usually on the left lower edge of the sternum over the right ventricle in the vena cava, striking from a distance of 20 – 30 cm to induce a ventricular beat (the British Journal of Anesthesia suggests this must be done to raise the ventricular pressure to 10 - 15mmHg to induce electrical activity). This is an old procedure used only as a life saving means until an electrical pacemaker is brought to the patient.[16]

[edit]Transcutaneous pacing

Main article: Transcutaneous pacing

Transcutaneous pacing (TCP), also called external pacing, is recommended for the initial stabilization of hemodynamically significant bradycardias of all types. The procedure is performed by placing two pacing pads on the patient's chest, either in the anterior/lateral position or the anterior/posterior position. The rescuer selects the pacing rate, and gradually increases the pacing current (measured in mA) until electrical capture (characterized by a wide QRS complex with a tall, broad T wave on the ECG) is achieved, with a corresponding pulse. Pacing artifact on the ECG and severe muscle twitching may make this determination difficult. External pacing should not be relied upon for an extended period of time. It is an

emergency procedure that acts as a bridge until transvenous pacing or other therapies can be applied.

[edit]Epicardial pacing (temporary)

Main article: Epicardial

ECG rhythm strip of a threshold determination in a patient with a temporary (epicardial)

ventricular pacemaker. The epicardial pacemaker leads were placed after the patient

collapsed during aortic valve surgery. In the first half of the tracing, pacemaker stimuli at 60

beats per minute result in a wide QRS complex with a right bundle branch block pattern.

Progressively weaker pacing stimuli are administered, which results in asystole in the

second half of the tracing. At the end of the tracing, distortion results from muscle

contractions due to a (short) hypoxic seizure. Because decreased pacemaker stimuli do not

result in a ventricular escape rhythm, the patient can be said to be pacemaker-dependent

and needs a definitive pacemaker.

Temporary epicardial pacing is used during open heart surgery should the surgical procedure create atrio ventricular block. The electrodes are placed in contact with the outer wall of the ventricle (epicardium) to maintain satisfactory cardiac output until a temporary transvenous electrode has been inserted.

[edit]Transvenous pacing (temporary)

Main article: Transvenous pacing

Transvenous pacing, when used for temporary pacing, is an alternative to transcutaneous pacing. A pacemaker wire is placed into a vein, under sterile conditions, and then passed into either the right atrium or right ventricle. The pacing wire is then connected to an external pacemaker outside the body. Transvenous pacing is often used as a bridge to permanent pacemaker placement. It can be kept in place until a permanent pacemaker is implanted or until there is no longer a need for a pacemaker and then it is removed.

Permanent pacing

Permanent pacing with an implantable pacemaker involves transvenous placement of one or more pacing electrodes within a chamber, or chambers, of the heart. The procedure is performed by incision of a suitable vein into which the electrode lead is inserted and passed along the vein, through the valve of the heart, until positioned in the chamber. The procedure is facilitated by fluoroscopy which enables the physician to view the passage of the electrode lead. After satisfactory lodgement of the electrode is confirmed, the opposite end of the electrode lead is connected to the pacemaker generator.

There are three basic types of permanent pacemakers, classified according to the number of chambers involved and their basic operating mechanism:[17]

Single-chamber pacemaker. In this type, only one pacing lead is placed into a chamber of the heart, either the atrium or the ventricle.[17]

Dual-chamber pacemaker. Here, wires are placed in two chambers of the heart. One lead paces the atrium and one paces the ventricle. This type more closely resembles the natural pacing of the heart by assisting the heart in coordinating the function between the atria and ventricles.[17]

Rate-responsive pacemaker. This pacemaker has sensors that detect changes in the patient's physical activity and automatically adjust the pacing rate to fulfill the body's metabolic needs.[17]

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.

Considerations

[edit]Insertion

A pacemaker is typically inserted into the patient through a simple surgery using either local anesthetic or a general anesthetic. The patient may be given a drug for relaxation before the surgery as well. An antibiotic is typically administered to prevent infection.[26] In most cases the pacemaker is inserted in the left shoulder area where an incision is made below the collar bone creating a small pocket where the pacemaker is actually housed in the patient's body. The lead or leads (the number of leads varies depending on the type of pacemaker) are fed into the heart through a large vein using a fluoroscope to monitor the progress of lead insertion. The Right Ventricular lead would be positioned away from the apex (tip) of the right ventricle and up on the inter ventricular septum, below the outflow tract, to prevent deterioration of the strength of the heart. The actual surgery may take about 30 to 90 minutes.

Following surgery the patient should exercise reasonable care about the wound as it heals. There is a followup session during which the pacemaker is checked using a "programmer" that can communicate with the device and allows a health care professional to evaluate the system's integrity and determine the settings such as pacing voltage output. The patient should have the strength of their heart analyzed frequently with echocardiography, every 1 or 2 years, to make sure the that placement of the right ventricular lead has not led to weakening of the left ventricle.

The patient may want to consider some basic preparation before the surgery. The most basic preparation is that people who have body hair on the chest may want to remove the hair by clipping just prior to surgery or using a depilatory agent (preoperative shaving has been on the decline as it can cause skin breakage and increase infection risk of any surgical procedure) as the surgery will involve bandages and monitoring equipment to be afixed to the body.

Since a pacemaker uses batteries, the device itself will need replacement as the batteries lose power. Device replacement is usually a simpler procedure than the original insertion as it does not normally require leads to be implanted. The typical replacement requires a surgery in which an incision is made to remove the existing device, the leads are removed from the existing device, the leads are attached to the new device, and the new device is inserted into the patient's body replacing the previous device.

[edit]Pacemaker patient identification card

International pacemaker patient identification cards carry information such as patient data (among others, symptom primary, ECG, aetiology), pacemaker center (doctor, hospital),IPG[disambiguation needed ] (rate, mode, date of implantation, manufacturer, type) and lead.[27][28]

[edit]Living with a pacemaker

[edit]Periodic pacemaker checkups

Two types of remote monitoring devices used by pacemaker patients

Once the pacemaker is implanted, it is periodically checked to ensure the device is operational and performing appropriately. Depending on the frequency set by the following physician, the device can be checked as often as is necessary. Routine pacemaker checks are typically done in-office every six (6) months, though will vary depending upon patient/device status and remote monitoring availability.

At the time of in-office follow-up, the device will be interrogated to perform diagnostic testing. These tests include:

Sensing: the ability of the device to "see" intrinsic cardiac activity (Atrial and ventricular depolarization).

Impedance: A test to measure lead integrity. Large and/or sudden increases in impedance can be indicative of a lead fracture while large and/or sudden decreases in impedance can signify a breach in lead insulation.

Threshold: this test confirms the minimum amount of energy (Both volts and pulse width) required to reliably depolarize (capture) the chamber being tested. Determining the threshold allows the Allied Professional, Representative, or Physician to program an output that recognizes an appropriate safety margin while optimizing device longevity.

As modern pacemakers are "on-demand", meaning that they only pace when necessary, device longevity is affected by how much it is utilized. Other factors affecting device longevity include programmed output and algorithms (features) causing a higher level of current drain from the battery.

An additional aspect of the in-office check is to examine any events that were stored since the last follow-up. These are typically stored based on specific criteria set by the physician and specific to the patient. Some devices have the availability to display intracardiac electrograms of the onset of the event as well as the event itself. This is especially helpful in diagnosing the cause or origin of the event and making any necessary programming changes.

[edit]Lifestyle considerations

A patient's lifestyle is usually not modified to any great degree after insertion of a pacemaker. There are a few activities that are unwise such as full contact sports and activities that involve intense magnetic fields.

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 the harness should fall across the pacemaker insertion site.

Any kind of an activity that involves intense magnetic fields should be avoided. This includes activities such as arc welding possibly, with certain types of equipment,[29] or maintaining heavy equipment that may generate intense magnetic fields (such as a magnetic resonance imaging machine).

However, in February 2011 the FDA approved a new pacemaker device called the Revo MRI SureScan which is the first to be proven safe for MRI use. There are several limitations to its use including certain patients qualifications, body parts, and scan settings.

A 2008 U.S. study has found[30] that the magnets in some headphones included with portable music players, when placed within an inch of pacemakers, may cause interference.

Some medical procedures may require the use of antibiotics to be administered before the procedure. The patient should inform all medical personnel that they have a pacemaker. Some standard medical procedures such as the use of magnetic resonance imaging may be ruled out by the patient having a pacemaker.

In addition, according to the American Heart Association, some home devices have a remote potential to cause interference by occasionally inhibiting a single beat. Cellphones available in the United States (less than 3 watts) do not seem to damage pulse generators or affect how the pacemaker works.[31]

[edit]Turning off the pacemaker

According to a consensus statement by the Heart Rhythm Society, it is legal and ethical to honor requests by patients, or by those with legal authority to make decisions for patients, to deactivate implanted cardiac devices. Lawyers say that the legal situation is similar to removing a feeding tube. A patient has a right to refuse or discontinue treatment, including a pacemaker that keeps him or her alive. Physicians have a right to refuse to turn it off, but they should refer the patient to a physician who will.[32] Some patients believe that hopeless, debilitating conditions like strokes, in combination with dementia, can cause so much suffering to themselves and their families that they would prefer not to prolong their lives with supportive measures, such as cardiac devices.[33]

[edit]Privacy and security

Security and privacy concerns have been raised with pacemakers that allow wireless communication. Unauthorized third parties may be able to read patient records contained in the pacemaker, or reprogram the devices, as has been demonstrated by a team of

researchers.[34] The demonstration worked at short range; they did not attempt to develop a long range antenna. The proof of concept exploit helps demonstrate the need for better security and patient alerting measures in remotely accessible medical implants.[34]

[edit]Complications

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.[35] Treatment of PMT typically involves reprogramming the pacemaker.[

Pacemaker syndrome is a disease that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony, regardless of the pacing mode, after the pacemaker plantation.[1][2] It is an iatrogenic disease—an adverse effect resulting from medical treatment—that is often underdiagnosed.[1][3] In general, the symptoms of the syndrome are a combination of decreased cardiac output, loss of atrial contribution to ventricularfilling, loss of total peripheral resistance response, and nonphysiologic pressure waves.[2][4][5]

Individuals with a low heart rate prior to pacemaker implantation are more at risk of developing pacemaker syndrome. Normally the first chamber of the heart (atrium) contracts as the second chamber (ventricle) is relaxed, allowing the ventricle to fill before it contracts and pumps blood out of the heart. When the timing between the two chambers goes out of synchronization, less blood is delivered on each beat. Patients who develop pacemaker syndrome may require adjustment of the pacemaker timing, or another lead fitted to regulate the timing of the chambers separately.

Signs and symptoms

No specific set of criteria has been developed for diagnosis of pacemaker syndrome. Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline. In the lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.[5][6][7]

Symptoms commonly documented in patients history, classified according to etiology:[2][8][5][6][9]

Neurological - Dizziness, near syncope, and confusion.

Heart failure - Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema.

Hypotension - Seizure, mental status change, diaphoresis, and signs of orthostasis and shock.

Low cardiac output - Fatigue, weakness, dyspnea on exertion, lethargy, and lightheadedness.

Hemodynamic - Pulsation in the neck and abdomen, choking sensation, jaw pain, right upper quadrant (RUQ) pain, chest colds, and headache.

Heart rate related - Palpitations associated with arrhythmias

In particular, the examiner should look for the following in the physical examination, as these are frequent findings at the time of admission:[2][5][8][6]

Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.

Pulse amplitude may vary, and blood pressure may fluctuate.

Look for neck vein distension[disambiguation needed ] and cannon waves in the neck veins.

Lungs may exhibit crackles.

Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.

Liver may be pulsatile, and the RUQ may be tender[disambiguation needed

] to palpation. Ascites may be present in severe cases.

The lower extremities may be edematous.

Neurologic examination may reveal confusion, dizziness, or altered mental status.

Prevention

At the time of pacemaker implantation, AV synchrony should be optimized to prevent the occurrence of pacemaker syndrome. Where patients with optimized AV synchrony have shown great results ofimplantation and very low incidence of pacemaker syndrome than those with suboptimal AV synchronization.[1][4][5]

[edit]Treatment

[edit]Diet

Diet alone cannot treat pacemaker syndrome, but an appropriate diet to the patient, in addition to the other treatment regimens mentioned, can improve the patient's symptoms. Several cases mentioned below:

For patients with heart failure, low-salt diet is indicated.[15]

For patients with autonomic insufficiency, a high-salt diet may be appropriate.[15]

For patients with dehydration, oral fluid rehydration is needed.[15]

[edit]Medication

No specific drugs are used to treat pacemaker syndrome directly because treatment consists of upgrading or reprogramming the pacemaker.[15]

[edit]Medical Care

For some patients who are ventricularly paced, usually the addition of an atrial lead and optimizing the AV synchrony usually resolves symptoms.[1][4][8][10]

In patients with other pacing modes, other than ventricular pacing, symptoms usually resolve after adjusting and reprogramming of pacemaker parameters, such as tuning the AV delay, changing the postventricular atrial refractory period[disambiguation needed ], the sensing level, and pacing threshold voltage. The optimal values of these parameters for each individual differ. So, achieving theoptimal values is by experimenting with successive reprogramming and measurement of relevant parameters, such as blood pressure, cardiac output, and total peripheral resistance, as well as observations of symptomatology.[1][4][8][10]

In rare instances, using hysteresis to help maintain AV synchrony can help alleviate symptoms in ventricularly inhibited paced (VVI) patients providing they have intact sinus node function. Hysteresis reduces the amount of time spent in pacing mode, which can relieve symptoms, particularly when the pacing mode is generating AV dyssynchrony.[4]

[10]

If symptoms persist after all these treatment modalities, replacing the pacemaker itself is sometimes beneficial and can alleviate symptoms.[1][4][8]

Medical care includes supportive treatment, in case any of the following complications happen, medical team should be ready. Possible complications include heart failure, hypotension,tachycardia, tachypnea, and oxygenation deficit.[1][8][6]

Complications

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.[7]

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