Cardiac Electric Stimulators Theoretical Analysis Biology Essay

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The purpose of this assignment is to analyse theoretically and physically the subject of Cardiac Electric Stimulators available nowadays.

This assignment has been divided in to 3 parts.

The first part describes the electrical system of the heart and its functioning and the most common heart problems affecting the human being with a brief explanation of what's the Electric Cardiogram (ECG) and what it represents.

The second part concentrates on what's the meaning of the term Cardiac Electric Stimulators were we conclude that we can state that the common ground of all this type of instruments its that they all work by generating electrical impulses to the heart's muscle cells, and the most important stimulators nowadays: the Defibrillator and the Pacemaker, where we concentrate on explaining the basic physical function of each component and the role is has controlling or restarting the heart beat.

The third and final part of this assignment explores the impact that Cardiac Electric Stimulators have on enhancing and extending life expectation and the limitations of this type of instruments and the limitations it has with its surrounding.

Contents

Abstract i

1. HEART FUNCTIONING 2

1.1Cardiac Cells And Its Electrical Event 2

1.2Electrical events in a heart beat and their connection to the Electrocardiogram (ECG or EKG) 4

2. HEART DISEASES AND DISORDERS 6

3. ARTIFICIAL STIMULATORS 9

3.1 Let's talk now of pacemakers 9

3.2 With respect to ICDs 13

3.3 The CRT 14

3.4 External defibrillators 15

3.4.1 Automated External Defibrillator 15

3.5.2 Manual External Defibrillator 15

4. CARDIAC ELECTRIC STIMULATORS LIMITATIONS 17

5. FUTURE OF CARDIAC ELECTRIC STIMULATORS 19

6. REFERENCES 20

1. HEART FUNCTIONING

Cardiac Cells And Its Electrical Event

The heart of one adult human beats approximately once a second for his whole life and it can't rest.

The performance of the heart must adjust rapidly in order to meet the needs the body has, in order to his work effectively the heart requires a special and unique type of muscle, this special muscle is called the cardiac muscle and it has a unique structure and a type of contraction.

When observed under the microscope, cardiac muscle consists of interlacing bundles of cardiac myocytes (muscle cells). The resembles between skeletal muscle and cardiac muscle do not come has as surprise, they are both striated with narrow dark and light bands due to the parallel arrangement the actin and myosin filaments that extend from end to end of each myocyte, but when it comes to shape we can see that the cardiac myocytes are more narrower and shorter.

One difference we can also see microscopically of this type of muscle structure is the increase of the number of mitochondria's in it, they are responsible for all the energy the muscle has to produce to create contraction, we can also see that it presents only one nucleus in each cell.

A unique feature of cardiac muscle is the presence of irregularly-spaced dark bands between each myocytes, this is known as intercalated discs, it can be seen in areas where the membranes of adjacent myocytes come extremely close together.

The intercalated discs have two important functions:

To keep the myocytes together when the heart contracts;

To allow an electrical connection between the cells.

The electrical connection between the intercalated discs is made via special junctions (gap junctions) between adjoining myocytes, this junctions contain pores that allow small ions to pass creating an electrical current allowing them to be referred as a continuous cellular material (syncytium).

"Cardiac myocytes can contract when the voltage across the membrane is reduced to a value that allows the initiation of an action potential. In most parts of the heart this is caused by an action potential in an adjacent myocyte being transmitted through the gap junctions. The action potential starts with a very rapid reduction in voltage toward zero, which is due to sodium ions entering the myocyte. This phase of the action potential is also seen in skeletal muscle and nerves. In cardiac muscle, however, the membrane potential then remains close to zero for about 0.3 sec - the plateau phase, which is largely due to entry of calcium ions. It is this entry of calcium that leads to contraction. At the end of the plateau phase the membrane potential returns to resting levels. The plateau means that cardiac muscle action potentials last much longer than those in skeletal muscle or nerves, where calcium does not enter the cell and there is therefore no plateau phase.

When an action potential is initiated in one myocyte, it causes an electrical current to pass through gap junctions in the intercalated discs to its neighbours. This current initiates action potentials in these cells, which in turn stimulate their neighbours. As a result, a wave of activation, and therefore contraction, passes through the heart. This process allows synchronization of contraction throughout the heart, and is vital for proper function. When it is disrupted, as in some types of heart disease, the myocytes may lose synchronization.

The amount of calcium entering the myocyte during an action potential is not enough to cause contraction. However, its entry causes more calcium to be released from stores in the sarcoplasmic reticulum, a membranous structure within the myocyte. This is known as calcium-induced calcium release. The amount of calcium released depends on the amount that enters during the action potential. This is increased by adrenaline and the autonomic nervous system. At the end of the beat, calcium is rapidly taken back into the sarcoplasmic reticulum, causing relaxation. Excess calcium - the amount that entered during the action potential - is expelled from the myocyte during the interval between beats by pumps in the membrane. If the heart rate increases there is less time to remove this calcium. As a result there is more calcium in the myocyte for the next beat, and so the force developed increases. This staircase effect allows the heart to expel blood more rapidly when the heart rate is increased.

Some areas of the heart contain myocytes that have special functions:

The Sino-Atrial node (SA node) also known as the pacemaker region in the right atrium, where we can find modified myocytes responsible for generating action potentials automatically, initiating the heartbeat;

The Atrio-Ventricular node (AV node) is a non-conducting band separating the atrias and ventricules. This node consists of small myocytes that do conduct, but delay the impulse from the pacemaker, thus allowing the atria to contract before the ventricles. From here the impulse is distributed rapidly around the ventricles via bundles of specialized large myocytes called Purkinje fibres;

Note that although nervous activity is not required for the heart to beat, the autonomic nervous system can modulate the activity of the pacemaker and therefore enhance the heart rate."1

Figure 1 - Electrical System of the Heart

Electrical events in a heart beat and their connection to the Electrocardiogram (ECG or EKG)

The electrocardiogram (ECG or EKG) is today used worldwide as a relatively simple way of diagnosing heart conditions, it consists of a recording of the small electric waves being generated during heart activity.

The start of each beat of the heart begins with an electrical signal from the SA node, located in the heart's right atrium, then when the heart's right atrium is full with blood, the electrical signal spreads across the cells of the heart's right and left atria, this signal then leads to the contraction of the atria that pumps blood through the open valves, from the atria into both ventricles, this contraction is marked as the P wave on the ECG.

The signal then arrives at the AV node which is near the ventricles, here it suffers a slowdown, this slowing allows the heart's right and left ventricles to fill with blood, this interval is represented by the start of the line segment between the P and Q wave.

After the filling the signal is released and proceeds next to the bundle of His located in the heart's ventricles, from here the signal fibers is divided into left and right bundle branches that run through the heart's septum, this step is represented by the Q wave.

The signal now leaves both bundle branches through the Purkinje fibers that connect directly to the cells in the walls of the heart's ventricles, the signal then spreads quickly across the heart's ventricles causing both ventricles to suffer a contraction. The contraction of both ventricles aren't simultaneous, the left ventricle contracts an instant before the right one pushing the blood through the pulmonary valve to the lungs and the contraction of the heart's right ventricle pushes blood through the aortic valve to the rest of the body, this contractions are represented as the R wave and the S wave respectively.

After this the step the walls of the heart's ventricles relax, this is represented by the T wave.

Any defects of this conduction system may lead to a disordered heartbeat.

Figure 2 - ECG

2. HEART DISEASES AND DISORDERS

Millions of people experience irregular heartbeats at some point in their lives. Most of these episodes, called arrhythmia, are harmless and happen when the natural pacemaker of the heart fails to generate or conduct a proper electrical signal. Sometimes, rhythm disturbances can be serious or even fatal. This Abnormal heart rhythms leave to the heartbeat may be too slow or too fast. It may remain steady or become chaotic.

Arrhythmias cause symptoms such as palpitations or dizziness and can cause the heart to pump less effectively.

Cardiac arrhythmias sometimes are classified according to their origin as either ventricular arrhythmias (occurs in ventricles) or supraventricular arrhythmias (occurs in atria).

This disorders also can be classified according to their effect on the heart rate:

Bradycardia: characterized by a heart rate of less than 60 beats per minute.

Tachycardia: characterized by a heart rate of more than 100 beats per minute.

Some common types of cardiac arrhythmias include:

Sinus node dysfunction

This usually causes a slow heart rate (bradycardia), with a heart rate of 50 beats per minute or less.

Atrial fibrillation (AF)

AF occurs when the electrical impulses in the atria become disorganised, overriding the heart's normal rate and rhythm.

Supraventricular tachycardia (SVT)

Most SVTs are caused by the occurrence of an extra electrical pathway in the heart, between the atria and the ventricles. This allows electrical impulses to 'short-circuit' and re-enter the atria. The impulses end up travelling around the heart in a circle.

SVT can make your heart beat very quickly; up to 160 beats per minute.

Ventricular tachycardia (VT)

In VT, the electrical impulses fire too quickly from the ventricles, causing blood to be pumped out quicker than normal. The ventricles may not have enough time to fill up properly with blood.

Ventricular fibrillation (VF)

In VF, electrical impulses start firing from multiple sites in the ventricles, very rapidly and in an irregular rhythm. This makes the heart quiver and unable to beat properly. If prompt treatment isn't given, you may have a cardiac arrest, which can be fatal.

Heart block

If you have heart block, it means there is a problem affecting how the electrical impulses are transmitted through your heart. Heart block can occur in the atrioventricular node or in the muscle fibres that lead into the ventricles.

Treatment may include medications, a pacemaker (Figure 3) or an implantable defibrillator (Figure 4).

Figure 3: Implantable Pacemaker in Heart

Figure 4: Implated Cardioverter Defibrillator

The treatment of a cardiac arrhythmia depends on its cause:

Sinus node dysfunction: In people with frequent, severe symptoms, the usual treatment is a permanent pacemaker.

Supraventricular tachyarrhythmias: The specific treatment depends on the cause of the arrhythmia. In some people, massaging the carotid sinus in the neck will stop the problem. Other people need medications such as beta-blockers, calcium channel blockers, digoxin (Lanoxin)and amiodarone (Cordarone). Some patients respond only to a procedure called radiofrequency catheter ablation, which destroys an area of tissue in the A-V node to prevent excess electrical impulses from being passed from the atria to the ventricles.

Atrial fibrillation: Atrial fibrillation resulting from an overactive thyroid can be treated with medications or surgery. Fibrillation resulting from rheumatic heart disease may be treated by replacing damaged heart valves. Medications, such as beta-blockers (for example atenolol and metoprolol), digoxin, amiodarone, diltiazem (Cardizem, Tiazac), or verapamil (Calan, Isoptin, Verelan), can be used to slow the heart rate. Drugs such as amiodarone can be used to reduce the chances that the atrial fibrillation will return. Other treatment options include radiofrequency catheter ablation, or electrical cardioversion, a procedure that delivers a timed electrical shock to the heart to restore normal heart rhythm.

A-V block First-degree: A-V block typically does not require any treatment. People with second-degree A-V block may be monitored with frequent EKGs, especially if they do not have any symptoms and have a heart rate that is adequate for their daily activities. Some patients with second-degree heart block may require permanent pacemakers. Third-degree A-V block is almost always treated with a permanent pacemaker.

VT Non-sustained: VT may not need to be treated if there is no structural damage to the heart. Sustained VT always needs treatment, either with intravenous medication or emergency electrical shock (defibrillation), which can restore the heart's normal rhythm.

Ventricular fibrillation: This is treated with defibrillation, giving the heart a measured electrical shock to restore normal rhythm. The electrical shock can be delivered on the skin over the heart in an emergency situation. People who have survived ventricular fibrillation and those at high risk are potential candidates for an automatic implantable cardioverter defibrillator. The device is similar to a pacemaker, with wires attached to the heart that connect an energy source placed under the skin.

3. ARTIFICIAL STIMULATORS

The cardiac stimulators can be classified as internal and external. In the internal we have the pacemakers, the implantable cardioverter-defibrillators (ICD) and the cardiac resynchronization therapy (CRT).

All are used to treat arrhythmias.

3.1 Let's talk now of pacemakers

A pacemaker is a small device, which it's put under the skin, just beneath the collarbone. Are usually used in patients who show signs of bradycardia.

The pacemaker continuously monitors the hearth and when it detects a heart rhythm very slow (below 60 beats per second) will stimulate the heart so that it returns to its normal rhythm. This stimulus will be sent in the form of an electrical signal; however the patient does not feel.

The pacemaker is an electrical system with two parts containing a pulse generator and one or two leads.

The pulse generator is coated with a metallic shell, and inside it has an electrical circuit to monitor the heart and regulate the function of the pacemaker, as well as a battery power source to the device.

The leads are insulated wires that are connected to the wall of right atria, right ventricle or both. Leads both receive information from the heart (sensing) as it sends electric shocks (packing).

There are three types of pacemakers:

Single chamber pacemakers, in this type of pacemaker is used only one lead, which is connected or on the right atria or on the right ventricle. When connects the lead to the atria is when the heart's natural pacemaker (sinus node) does not work properly, i.e. when the node sends signals that are very slow or irregulars. To use this method it is necessary that the rest of the heart is functioning properly.

When the lead is connected to the ventricle is when the flow of electricity is slowed or blocked in the region of the atrioventricular node (AV) and the natural impulses of the atria cannot reach the ventricle. This cause the heart rate decreases, then the pacemaker causes the heart to beat at a steady rate.

Dual chamber pacemakers, in this type of pacemaker are used two leads, one connect to the right atria and the other to the right ventricle. This type mimics closely the normal heart beat, because it can make a sequential beat from atria to ventricle, maximizing the ability of the heart it to pump blood out of him. To have to leads allows the pulse generator continuously regulate the heart's electrical activity.

This type of pacemaker is the most used actually.

Rate responsive pacemakers, during the 24-hour heart rate fluctuate depending on the activity performed. During sleep, cardiac activity decreases, but under stress or physical activity that increases. There are individuals who are unable to increase their heart activity due to physical activity and, and they were the main recipients of such pacemakers. These pacemakers have incorporated into the pulse generator special sensors that can sense increases in activity by the increase in body movements and/or increased breathing rate. Then these sensors will automatically adjust the heart rate depending on the needs of the body.

3.2 With respect to ICDs

As the pacemaker, ICD is a small device that is placed under the skin. This device is intended to prevent sudden death from cardiac arrest. These devices are used in people who show signs of tachycardia. The functioning of these is very similar to the pacemakers, sending electrical shocks to terminate the abnormal rhythm and restore normal.

http://www.chrsonline.ca/images/icd3.jpg

As regards the composition they have one or more leads and a defibrillator unit. The unit defibrillator is a small titanium box that inside have a microchip, a capacitor and a battery.

The leads conduct electrical signals between the heart and the unit defibrillator.

The microchip monitors the heart and instructs the capacitor to provide electric shocks during a tachycardia and determines the strength of the shocks.

Currently there are programmable ICDs, in which the physician has the possibility to determine the heart rate that enables the defibrillator. He can also determine the strength of the shocks and the number of shock per tachycardia.

The ICD continuously monitors the heart, if it detects any abnormality, will provide low-energy pulses to the heart to restore normal rhythm. If that pulses do not have enough power to reset the rhythm, the ICD automatically readjusts to the pulses to a high-energy pulses. That capacity of ICD can vary the energy of the pulses is one of the principal differences between pacemakers and ICDs, because pacemakers only use pulses of low-energy.

The high energy pulses last only a split second, but can be painful.

3.3 The CRT

There are patients with heart failure caused by dilated cardiomyopathy that needs a device that connects to the two ventricles to pump blood out of the heart. Mode of operation is very similar to the pacemaker.

The big difference between of a pacemaker and a CRT is that with a pacemaker only one ventricle is being paced while with the CRT the two ventricles are being paced.

https://www.clevelandclinic.org/heartcenter/images/guide/disease/electric_/bivpm.jpg

3.4 External defibrillators

3.4.1 Automated External Defibrillator

Figure 1 - http://www.aedsystems.net/images/defibgif.gifThese 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 limited for use by 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. 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. 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. 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.

3.5.2 Manual External Defibrillator

Figure 2- http://www.dremed.com/catalog/images/zoll_pd-2000_lg.jpgThe 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). 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 NHS ambulance 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.

4. CARDIAC ELECTRIC STIMULATORS LIMITATIONS

These type of devices are highly reliable and there have been tremendous advancements and improvements in the last years but there are still some limitations, for example: since they are electrical devices it needs a constant supply of energy to work and it is vulnerable to electromagnetic interference, known as EMI.

The most limitations about this instruments are focused on Pacemakers, the batteries used on these instruments are lithium type batteries that wears out slowly lasting from 5 to 10 years on the average of 7, but still they wear out because the device longevity depends upon two factors:

How much energy is required to pace the heart;

The way the system was programmed to work.

If the device doesn't have energy it won't do its purpose so it has to be replaced has many times has necessary since for most people this device will be needed for the rest of their life.

Sometimes the device has to be removed because of an infection in this case the need for a new device is reassessed since it is better to life with the problem if it is not to serious rather than undergo the significant risk of getting a new device after as infection.

Note that if the patient is a children the case gets a little more complicated because has a children grow up it has to endure multiple surgeries in order to replace the device because of the new needs.

Most day-to-day routines the patient will not be aware of the limitations of the device although they are present, for example when passing though a metal detector it may sound the alarm because has said the device if metal but for cases like this every patient has a ICD identification card which allow everyone to know that you have a pulse generator. The ICD card also contains some information about the device itself and personal data that may come in handy in any medical emergency.

In an overall view the limitations are minimal except when facing an electromagnetic inference (EMI), this is in the opinion of most professional the main and only limitation of cardiac electric stimulators.

EMI can be caused by some short of electrical appliances and this is the real problem nowadays with this sort of devices because has the technology evolves more and more our need for electrical devices advance, a EMI is a electromagnetic energy that adversely affects the performance of electrical/electromagnetic equipment by creating undesirable response or complete operational failure. The interference sources may be external or internal to electronic equipment and they may propagate by radiation or conduction.

Most home appliances will not produce any amount of EMI if they are working in good working order, so they are safe to use, this includes appliances like toasters, microwave ovens, blenders, televisions, VCRs, and so on. The same thing happens in most office equipment and most medical equipment, the device will work properly in cases like when enduring chest and dental x-rays, diagnosis ultrasound, CT scan, mammography and fluoroscopy.

When facing a EMI source the patient can in most cases just walk away from the source or turn the device off, on most cases the patient might feel some lightheadedness and/or palpitations while and after being near an EMI source.

There are some medical procedures that cannot be done by someone carrying a pulse generator like electrosurgery, external defibrillation, radiation therapy, Magnetic resonance imaging (MRI), basically all procedures that require the use of the emission of any source of electronic impulse would be unwise.

Most devices are now relatively immune to EMI sources, this happens because their circuit is hermetically sealed in a cocoon, which is composed of titanium or stainless steel and often prevents additional isolation, there is also the fact that it is now being used a bipolar leads on most devices giving an additional protection to EMI interference but this is not 100% certain.

There have been some relative doubt about the interference the use of mobile phones and multi-media player may have in cardiac electric stimulators, but still there is no actual prove that they influence the correct functioning of this sort of devices, but there are studies on the way, for example on St. Jude Medical some limited data suggests that while the device was being evaluated in the hospital or clinic, use of one of these electronic "gadgets" within 12 inches of the implanted device or the programmer wand, could disrupt the communication that is maintained between the programmer and the pacemaker. Thought there is no data that carrying and using any type of this "gadgets" affect the device.

Another limitation of the devices available is that in some cases the heart muscle is so damaged that prevents the propagation of the electrical signal around the organ, this results in a slightly out of phase beating with therefore translates in a reduce to the blood pumping.

Now turning to defibrillators limitations we can say that they almost don't exist although there is still the main problem has any electric stimulator have when facing a EMI interference and that a pacemaker patient can not suffer a defibrillation because the combination of the pacemaker and the defibrillator electric shock might cause irreversible damage to the patient and most likely it may cause his death.

5. FUTURE OF CARDIAC ELECTRIC STIMULATORS

Although in the past years the Cardiac Electric Stimulators have suffered an enormous development, there is still a long way to go to have something resemble to perfection.

There are two main approaches one can have about the future of the subject of pacemaker improvements, one is the development and perfection of the devices available on the market today focusing on the problems the current instruments have, mainly the EMI interference. The other one needs a more creativity point of view, it consists in the use of muscular precursor cells (myoblast) to create an electrical tissue that can then be linked to the atrias and ventricles, correcting effectively the hearts pacing, but this is still under tight development but has recently come to clinical tests, with rats has subjects and it has shown promising results. In case of success it will be able to solve most limitations and implantations problems, because it will be like "getting a new hearth".

In any case if the pacemaker suffer any evolution we can say that the defibrillator will accompany any development. Not a long time ago we thought that the future of the defibrillator would be the possibility of them being fully automatic something we have now achieved and with a good perfection rate if we can call it that. The future of the defibrillator will focus mainly on 3 subjects, reducing its size, perfection of its capability of being fully automatic and try to come up with an even more success rate.

The future is said to be what we make of it on the present, has the years go bye we can look back and see the development our society is suffering and now it is said to be the time for health-electronic development so we might say the future in still unfolding before our own eyes so every future we might draw today can be seen has a past tomorrow.

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