In non-pacemaker cells (i.e. ventricular cells), this is produced predominantly by the activation of  Na +  channels , which increases the membrane conductance (flow) of Na +  (g Na ). These channels are activated when an action potential arrives from a neighbouring cell, through  gap junctions . When this happens, the voltage within the cell increases slightly. If this increased voltage reaches the  threshold potential  (approximately −70 mV) it causes the Na +  channels to open. This produces a larger influx of sodium into the cell, rapidly increasing the voltage further to around +50 mV, [ 6 ]  i.e. towards the Na +  equilibrium potential. However, if the initial stimulus is not strong enough, and the threshold potential is not reached, the rapid sodium channels will not be activated and an action potential will not be produced; this is known as the  all-or-none law . [ 17 ] [ 18 ]  The influx of  calcium ions  (Ca 2+ ) through  L-type calcium channels  also constitutes a minor part of the depolarisation effect. [ 19 ]  The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change of the cardiac action potential and is known as dV/dt max .


In pacemaker cells (e.g.  sinoatrial node cells ), however, the increase in membrane voltage is mainly due to activation of L-type calcium channels. These channels are also activated by an increase in voltage, however this time it is either due to the  pacemaker potential  (phase 4) or an oncoming action potential. The L-type calcium channels are activated more slowly than the sodium channels, therefore, the depolarization slope in the pacemaker action potential waveform is less steep than that in the non-pacemaker action potential waveform. [ 11 ] [ 20 ]


This phase begins with the rapid inactivation of the Na +  channels by the inner gate (inactivation gate), reducing the movement of sodium into the cell. At the same time potassium channels (called I to1 ) open and close rapidly, allowing for a brief flow of potassium ions out of the cell, making the membrane potential slightly more negative. This is referred to as a 'notch' on the action potential waveform. [ 11 ]


There is no obvious phase 1 present in pacemaker cells.


This phase is also known as the "plateau" phase due to the  membrane potential  remaining almost constant, as the membrane slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase  delayed rectifier potassium channels  (I ks ) allow potassium to leave the cell while L-type calcium channels (activated by the influx of sodium during phase 0) allow the movement of calcium ions into the cell. These calcium ions bind to and open more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. These calcium ions are responsible for the contraction of the heart.


Calcium also activates chloride channels called I to2 , which allow Cl −  to enter the cell. Increased calcium concentration in the cell also increases activity of the sodium-calcium exchangers, while increased sodium concentration (from the depolarisation of phase 0) increases activity of the sodium-potassium pumps. The movement of all these ions results in the membrane potential remaining relatively constant, with K +  outflux, Cl −  influx as well as Na + /K +  pumps contributing to repolarisation and Ca 2+  influx as well as Na + /Ca 2+  exchangers contributing to depolarisation. [ 21 ] [ 11 ]  This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia).


There is no plateau phase present in pacemaker action potentials.


During phase 3 (the "rapid repolarization" phase) of the action potential, the L-type  Ca 2+  channels  close, while the  slow delayed rectifier  (I Ks )  K +  channels  remain open as more potassium leak channels open. This ensures a net outward positive current, corresponding to negative change in  membrane potential , thus allowing more types of K +  channels to open. These are primarily the  rapid delayed rectifier  K +  channels (I Kr ) and the  inwardly rectifying  K +  current, I K1 .
This net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize. The delayed rectifier K +  channels close when the membrane potential is restored to about -85 to -90 mV, while I K1  remains conducting throughout phase 4, which helps to set the resting membrane potential [ 22 ]


Ionic pumps as discussed above, like the  sodium-calcium exchanger  and the  sodium-potassium pump  restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost, the contraction stops and the heart muscles relax.


In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca 2+  and the opening of the rapid delayed rectifier potassium channels (I Kr ). [ 23 ]


Cardiac cells have two  refractory periods , the first from the beginning of phase 0 until part way through phase 3; this is known as the absolute refractory period during which it is impossible for the cell to produce another action potential. This is immediately followed, until the end of phase 3, by a relative refractory period, during which a stronger-than-usual stimulus is required to produce another action potential. [ 24 ] [ 25 ]


These two refractory periods are caused by changes in the states of  sodium  and  potassium channels . The rapid  depolarization  of the cell, during phase 0, causes the membrane potential to approach sodium's  equilibrium potential  (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state. During this state the channels cannot be opened regardless of the strength of the excitatory stimulus—this gives rise to the absolute refractory period. The relative refractory period is due to the leaking of potassium ions, which makes the membrane potential more negative (i.e. it is hyperpolarised), this resets the sodium channels; opening the inactivation gate, but still leaving the channel closed. Because some of the voltage-gated sodium ion channels have recovered and the voltage-gated potassium ion channels remain open, it is possible to initiate another action potential if the stimulus is stronger than a stimulus which can fire an action potential when the membrane is at rest. [ 26 ]


Gap junctions  allow the action potential to be transferred from one cell to the next (they are said to  electrically couple  neighbouring  cardiac cells ). They are made from the  connexin family  of proteins, that form a pore through which ions (including Na + , Ca 2+  and K + ) can pass. As potassium is highest within the cell, it is mainly potassium that passes through. This increased potassium in the neighbour cell causes the membrane potential to increase slightly, activating the sodium channels and initiating an action potential in this cell. (A brief chemical gradient driven efflux of Na+ through the  connexon  at peak depolarization causes the conduction of cell to cell depolarization, not potassium.) [ 27 ]  These connections allow for the rapid conduction of the action potential throughout the heart and are responsible for allowing all of the cells in the atria to contract together as well as all of the cells in the ventricles. [ 28 ]  Uncoordinated contraction of heart muscles is the basis for arrhythmia and heart failure. [ 29 ]


Ion channels are proteins that change shape in response to different stimuli to either allow or prevent the movement of specific ions across a membrane. They are said to be selectively permeable. Stimuli, which can either come from outside the cell or from within the cell, can include the binding of a specific  molecule  to a receptor on the channel (also known as  ligand-gated ion channels ) or a change in membrane potential around the channel, detected by a sensor (also known as  voltage-gated ion channels ) and can act to open or close the channel. The pore formed by an ion channel is aqueous (water-filled) and allows the ion to rapidly travel across the membrane. [ 33 ]  Ion channels can be selective for specific ions, so there are  Na + ,  K + ,  Ca 2+ , and  Cl −  specific channels. They can also be specific for a certain charge of ions (i.e. positive or negative). [ 34 ]


Each channel is coded by a set of DNA instructions that tell the cell how to make it. These instructions are known as a  gene . Figure 3 shows the important ion channels involved in the cardiac action potential, the current (ions) that flows through the channels, their main protein subunits (building blocks of the channel), some of their controlling genes that code for their structure, and the phases that are active during the cardiac action potential. Some of the most important ion channels involved in the cardiac action potential are described briefly below.


Hyperpolarization-activated cyclic nucleotide-gated channels (HCN channels)  are located mainly in pacemaker cells, these channels become active at very negative membrane potentials and allow for the passage of both Na +  and K +  into the cell (which is a movement known as a funny current, I f ). These poorly selective, cation (positively charged ions) channels conduct more current as the membrane potential becomes more negative (hyperpolarised). The activity of these channels in the SAN cells causes the membrane potential to depolarise slowly and so they are thought to be responsible for the pacemaker potential. Sympathetic nerves directly affect these channels, resulting in an increased heart rate (see below). [ 35 ] [ 14 ]


These  sodium channels  are voltage-dependent, opening rapidly due to depolarization of the membrane, which usually occurs from neighboring cells, through gap junctions. They allow for a rapid flow of sodium into the cell, depolarizing the membrane completely and initiating an action potential. As the membrane potential increases, these channels then close and lock (become inactive). Due to the rapid influx sodium ions (steep phase 0 in action potential waveform) activation and inactivation of these channels happens almost at exactly the same time. During the inactivation state, Na +  cannot pass through (absolute refractory period). However they begin to recover from inactivation as the membrane potential becomes more negative (relative refractory period).


The two main types of potassium channels in cardiac cells are inward rectifiers and voltage-gated potassium channels. [ citation needed ]


Inwardly rectifying potassium channels  (K ir)  favour the flow of K +  into the cell. This influx of potassium, however, is larger when the membrane potential is more negative than the  equilibrium potential  for K +  (~-90 mV). As the membrane potential becomes more positive (i.e. during cell stimulation from a neighbouring cell), the flow of potassium into the cell via the K ir  decreases. Therefore, K ir  is responsible for maintaining the resting membrane potential and initiating the depolarization phase. However, as the membrane potential continues to become more positive, the channel begins to allow the passage of K +   out  of the cell. This outward flow of potassium ions at the more positive membrane potentials means that the K ir  can also aid the final stages of repolarisation. [ 36 ] [ 37 ]


The  voltage-gated potassium channels  (K v ) are activated by depolarization. The currents produced by these channels include the transient out potassium current  I to1 . This current has two components. Both components activate rapidly, but  I to,fast  inactivates more rapidly than  I to, slow . These currents contribute to the early repolarization phase (phase 1) of the action potential. [ citation needed ]


Another form of voltage-gated potassium channels are the delayed rectifier potassium channels. These channels carry potassium currents which are responsible for the plateau phase of the action potential, and are named based on the speed at which they activate: slowly activating  I Ks , rapidly activating  I Kr  and ultra-rapidly activating  I Kur . [ 38 ]


There are two  voltage-gated calcium channels  within cardiac muscle:  L-type calcium channels  ('L' for Long-lasting) and  T-type calcium channels  ('T' for Transient, i.e. short). L-type channels are more common and are most densely populated within the  T-tubule  membrane of ventricular cells, whereas the T-type channels are found mainly within  atrial  and  pacemaker cells , but still to a lesser degree than L-type channels. [ citation needed ]


These channels respond to voltage changes across the membrane differently: L-type channels are activated by more positive membrane potentials, take longer to open and remain open longer than T-type channels. This means that the T-type channels contribute more to depolarization (phase 0) whereas L-type channels contribute to the plateau (phase 2). [ 39 ]


In the  heart's conduction system  electrical activity that originates from the  sinoatrial node  (SAN) is propagated via the  His - Purkinje  network, the fastest conduction pathway within the heart. The electrical signal travels from the sinoatrial node, which stimulates the  atria  to contract, to the  atrioventricular node (AVN) , which slows down conduction of the action potential from the atria to the  ventricles . This delay allows the ventricles to fully fill with blood before contraction. The signal then passes down through a bundle of fibres called the  bundle of His , located between the ventricles, and then to the  Purkinje fibers  at the bottom (apex) of the heart, causing ventricular contraction. [ citation needed ]


In addition to the SAN, the AVN and Purkinje fibres also have pacemaker activity and can therefore spontaneously generate an action potential. However, these cells usually do not depolarize spontaneously, simply because action potential production in the SAN is faster. This means that before the AVN or Purkinje fibres reach the threshold potential for an action potential, they are depolarized by the oncoming impulse from the SAN [ 40 ]  This is called "overdrive suppression". [ 41 ]  Pacemaker activity of these cells is vital, as it means that if the SAN were to fail, then the heart could continue to beat, albeit at a lower rate (AVN= 40-60 beats per minute,
Purkinje fibres = 20-40 beats per minute). These pacemakers will keep a patient alive until the emergency team arrives. [ citation needed ]


An example of premature ventricular contraction is the classic  athletic heart syndrome . Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to  atrioventricular block , where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death. [ 42 ]


The speed of action potential production in pacemaker cells is affected, but not controlled by the  autonomic nervous system .


The  sympathetic nervous system  (nerves dominant during the body's  fight-or-flight response ) increase heart rate (positive  chronotropy ), by decreasing the time to produce an action potential in the SAN. Nerves from the  spinal cord  release a molecule called  noradrenaline , which binds to and activates receptors on the pacemaker cell membrane called  β1 adrenoceptors . This activates a protein, called a G s -protein (s for stimulatory). Activation of this G-protein leads to increased levels of  cAMP  in the cell (via the  cAMP pathway ). cAMP binds to the HCN channels (see above), increasing the funny current and therefore increasing the rate of depolarization, during the pacemaker potential. The increased cAMP also increases the opening time of L -type calcium channels, increasing the Ca 2+  current through the channel, speeding up phase 0. [ 43 ]


The  parasympathetic nervous system  ( nerves  dominant while the body is resting and digesting) decreases heart rate (negative  chronotropy ), by increasing the time taken to produce an action potential in the SAN. A nerve called the  vagus nerve , that begins in the brain and travels to the sinoatrial node, releases a  molecule  called  acetylcholine (ACh)  which binds to a receptor located on the outside of the pacemaker cell, called an  M2 muscarinic receptor . This activates a  G i -protein  (I for inhibitory), which is made up of 3 subunits (α, β and γ) which, when activated, separate from the receptor. The β and γ subunits activate a special set of potassium channels, increasing potassium flow out of the cell and decreasing membrane potential, meaning that the pacemaker cells take longer to reach their threshold value. [ 44 ]  The G i -protein also inhibits the cAMP pathway therefore reducing the sympathetic effects caused by the spinal nerves. [ 45 ]


Antiarrhythmic drugs  are used to regulate  heart rhythms  that are too fast. Other drugs used to influence the cardiac action potential include  sodium channel blockers ,  beta blockers ,  potassium channel blockers , and  calcium channel blockers .


The  cardiac conduction system  ( CCS , also called the  electrical  conduction system of the heart ) [ 1 ]  transmits the  signals  generated by the  sinoatrial node  – the  heart 's  pacemaker , to cause the  heart muscle  to  contract , and pump blood through the body's  circulatory system . The  pacemaking  signal travels through the  right atrium  to the  atrioventricular node , along the  bundle of His , and through the  bundle branches  to  Purkinje fibers  in the  walls of the ventricles . The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles. [ 2 ]


The conduction system consists of specialized  heart muscle cells , situated within the  myocardium . [ 3 ]  There is a  skeleton of fibrous tissue  that surrounds the conduction system which can be seen on an  ECG . Dysfunction of the conduction system can cause  irregular heart rhythms  including rhythms that are  too fast  or  too slow .


Electrical signals arising in the  SA node  (located in the right  atrium ) stimulate the atria to contract. Then the signals travel to the  atrioventricular node  (AV node), which is located in the  interatrial septum . After a  short delay that gives the ventricles time to fill with blood,  the electrical signal diverges and is conducted through the left and right  bundle branches  of  His  to the respective  Purkinje fibers  for each side of the heart, as well as to the  endocardium  at the apex of the heart, then finally to the ventricular epicardium; causing the ventricles to  contract. [ 2 ]  These signals are generated rhythmically, which results in the coordinated rhythmic contraction and relaxation of the heart.


On the microscopic level, the wave of  depolarization  propagates to adjacent cells via  gap junctions  located on the  intercalated disc . The heart is a  functional syncytium  as opposed to a skeletal muscle  syncytium . In a functional syncytium, electrical impulses propagate freely between cells in every direction, so that the myocardium functions as a single contractile unit. This property allows rapid, synchronous depolarization of the myocardium. While advantageous under normal circumstances, this property can be detrimental, as it has potential to allow the propagation of incorrect electrical signals. These gap junctions can close to isolate damaged or dying tissue, as in a  myocardial infarction  (heart attack).


Embryologic evidence of generation of the cardiac conduction system illuminates the respective roles of this specialized set of cells. Innervation of the heart begins with a brain only centered  parasympathetic   cholinergic  first order. It is then followed by rapid growth of a second order  sympathetic   adrenergic  system arising from the formation of the  thoracic   spinal ganglia . The third order of electrical influence of the heart is derived from the  vagus nerve  as the other peripheral organs form. [ 4 ]


Cardiac muscle has some similarities to neurons and skeletal muscle, as well as important unique properties. Like a neuron, a given myocardial cell has a negative  membrane potential  when at rest. Stimulation above a threshold value induces the opening of  voltage-gated ion channels  and a flood of  cations  into the cell. The positively charged ions entering the cell cause the  depolarization  characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of  voltage-gated calcium channels   and release of Ca 2+  from the  t-tubules . This influx of calcium causes  calcium-induced calcium release  from the  sarcoplasmic reticulum , and free Ca 2+  causes  muscle contraction . After a delay,  potassium channels  reopen, and the resulting flow of K +  out of the cell causes  repolarization  to the resting state. [ 5 ] [ 6 ]


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's pacemaker activity.


In order to maximize efficiency of contractions and  cardiac output , the conduction system of the heart has:


An  electrocardiogram  is a recording of the electrical activity of the heart.


Under normal conditions, electrical activity is spontaneously generated by the  SA node , the cardiac pacemaker.  This electrical impulse is propagated throughout the right  atrium , and through  Bachmann's bundle  to the left  atrium , stimulating the  myocardium  of the atria to contract.  The conduction of the electrical impulses throughout the atria is seen on the  ECG  as the  P wave . [ 5 ] [ 7 ]


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 .


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, and part of atrial repolarization can be represented by the PR segment.


The distal portion of the AV node is known as the  bundle of His . [ 8 ]  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 papillary muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-tensioning of the chordae tendinae, increasing the resistance to flow through the mitral valve during left ventricular contraction. [ 5 ]  This mechanism works in the same manner as pre-tensioning of car seatbelts.


The two bundle branches taper out to produce numerous  Purkinje fibers , which stimulate individual groups of myocardial cells to contract. [ 5 ]


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


Atrial repolarization occurs and is masked during the  QRS complex   by ventricular depolarization on the ECG.


The last event of the cycle is the repolarization of the  ventricles . It is the restoring of the resting state. In the ECG, repolarization includes the J point, ST segment, and T and U waves. [ 9 ]
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 60–100 bpm is known as a normal  sinus rhythm . If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known as  sinus bradycardia . If SA nodal impulses occur at a rate exceeding 100 bpm, the consequent rapid heart rate is  sinus tachycardia . These conditions are not necessarily bad symptoms, however. Trained athletes, for example, usually show heart rates slower than 60 bpm when not exercising. If the SA node fails to initialize, the AV junction can take over as the main pacemaker of the heart. The AV junction consists of the AV node, the bundle of His, and the surrounding area; it has a regular rate of 40 to 60 bpm. These "junctional" rhythms are characterized by a missing or inverted P wave. If both the SA node and the AV junction fail to initialize the electrical impulse, the ventricles can fire the electrical impulses themselves at a rate of 20 to 40 bpm and will have a QRS complex of greater than 120 ms. This is necessary for the heart to be in good function.


An  arrhythmia  is an abnormal rhythm or speed of rhythm of the heartbeat. A slow  heart rate  of 60 or less beats per minute is defined as  bradycardia . A fast heart rate of more than 100 beats per minute is defined as  tachycardia .
An arrhythmia is defined as one that is not  physiological  such as the lowered heart rate that a trained athlete may naturally have developed; the resting heart rates may be less than 60 bpm.


When an arrhythmia cannot be treated by  medication  (or other standard  cardioversion  measures), an  artificial pacemaker  may be  implanted  to control the conduction system.


Cardiac monitoring  generally refers to continuous or intermittent  monitoring  of  heart  activity to assess a patient's condition relative to their  cardiac rhythm . Cardiac monitoring is usually carried out using  electrocardiography , which is a  noninvasive  process that records the heart's electrical activity and displays it in an electrocardiogram. [ 1 ]  It is different from  hemodynamic  monitoring, which monitors the  pressure  and  flow  of blood within the  cardiovascular system . The two may be performed simultaneously on  critical  heart patients. Cardiac monitoring for ambulatory patients (those well enough to walk around) is known as ambulatory electrocardiography and uses a small, wearable device, such as a  Holter monitor ,  wireless ambulatory ECG , or an  implantable loop recorder . Data from a cardiac monitor can be transmitted to a distant monitoring station in a process known as  telemetry  or  biotelemetry .


Cardiac monitoring in an  emergency department  setting focuses primarily on the monitoring of  arrhythmia ,  myocardial infarction , and  QT interval  monitoring. [ 2 ]  It is categorized into one of three classes using a rating system developed by the American College of Cardiology Emergency Cardiac Care Committee:


Class I: Cardiac monitoring is indicated in all or most patients.


Class II: Cardiac monitoring may be beneficial, but it is not essential.


Class III: Cardiac monitoring is not indicated because the patient's serious event risk is low. Monitoring will not have therapeutic benefit. [ 3 ]


In the setting of out-of-hospital  acute medical care , ambulance services and other  emergency medical services  providers utilize heart monitors to assess the patient's cardiac rhythm. Providers licensed or certified at the  Paramedic  level are qualified to interpret ECGs. Information obtained from ECGs can then be used to direct the patient's treatment at a care facility, particularly in catheterization labs. [ 4 ]


In the  emergency department , cardiac monitoring is a part of the monitoring of  vital signs  in  emergency medicine , and generally includes  electrocardiography . [ 2 ]


Some digital patient monitors, especially those used by EMS services, often incorporate a defibrillator into the patient monitor itself. These monitor/defibrillators usually have the normal capabilities of an ICU monitor, but have manual (and usually semi-automatic AED) defibrillation capabilities. This is particularly good for EMS services, who need a compact, easy to use monitor and defibrillator, as well as for patient transport.  Most monitor defibrillators also have transcutaneous pacing capability via large AED like adhesive pads (which often can be used for monitoring, defibrillation and pacing) that are applied to the patient in an anterior-posterior configuration. The monitor defibrillator units often have specialized monitoring parameters such as waveform capnography, invasive BP, and, in some monitors, Masimo Rainbow SET pulse oximetry, which can also monitor  carbon monoxide  and  methemoglobin  levels. Most modern monitors also allow for transmission of an ECG sample to an emergency department for interpretation; this process may be used to speed up patient care in certain situations, such as bypassing the ED and proceeding to a  cath lab .


Examples of monitor defibrillators are the Lifepak 12, 15 and 20 made by Physio Control, the Philips Heartstart MRx, and the E, R, and X Series by ZOLL Medical.


There are two broad classifications for cardiac event monitors: manual (or dumb) and automatic. Automatic ECG event monitors have the ability to monitor the patient's ECG and make recordings of abnormal events without requiring patient intervention. Manual ECG event recorders require the patient to be symptomatic and to activate the device to record an event; this makes these devices useless whilst, for example, the patient is sleeping. A third classification, the  implantable loop recorder , provides both automatic and manual abilities.


An example of automatic monitoring is the transtelephonic cardiac event monitor. This monitor contacts ECG technicians, via telephone, on a regular basis, transmitting  ECG  rhythms for ongoing monitoring. The transtelephonic cardiac event monitor can normally store approximately five "cardiac events" usually lasting 30–60 seconds.


Monitoring of the  heart rate  can be performed as part of  electrocardiography , but it can also be measured conveniently with specific  heart rate monitors . Such heart rate monitors are largely used by performers of various types of  physical exercise .


A generic cardiac monitor has the following functions:


There are many different types of cardiac monitors. In personal use, the  Holter monitor  is an external monitor which uses wires with patches that attach to the skin to continuously measure and record heart activity for 1–2 days. [ 5 ]  An Event Recorder can be worn on the body for up to 30 days. [ 6 ]  A Mobile Cardiac Telemetry unit is a wearable monitor that detects, records, and transmits heart rhythms for up to 30 days. For long term use, an  Insertable Cardiac Monitor  is placed under the skin and automatically detects and records abnormal heart rhythms for up to 5 years. [ 7 ]


Monitoring the fetal heart rate is becoming increasingly prevalent in the standard care of antepartum pregnant patients. [ 8 ]  As of 2002, 85% of pregnancies in the United States were monitored using electronic fetal monitoring. Electronic fetal monitoring generally uses Doppler ultrasound technology to provide real-time feedback on the fetus's cardiac activity during both gestation and labor, [ 9 ]  however other technologies such as analyzing the voltage generated by the contracting uterine muscle measured at the skin surface or recording both the fetal ECG and mother's ECG and filtering out the mother's ECG are emerging. [ 10 ]


The new wearable heart rate monitors indirectly measure the heart rate with reflectance photoplethysmography. The monitor illuminates the skin tissue with light emitting diode (LED) and detects the intensity of light reflected with the photodetector. [ 11 ]  Wearable optical heart rate monitors are less reliable than electrode-based heart rate monitors. The accuracy of the wearable optical heart rate monitors varies with the type of exercise. Skin tone and motion artifacts contributes to this error. [ 11 ] [ 12 ]


Cardiac muscle  (also called  heart muscle  or  myocardium ) is one of three types of  vertebrate   muscle tissues , the others being  skeletal muscle  and  smooth muscle . It is an involuntary,  striated muscle  that constitutes the main tissue of the  wall of the heart . The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall (the  pericardium ) and the inner layer (the  endocardium ), with blood supplied via the  coronary circulation .  It is composed of individual cardiac muscle cells joined by  intercalated discs , and encased by  collagen fibers  and other substances that form the  extracellular matrix .


Cardiac muscle  contracts  in a similar manner to  skeletal muscle , although with some important differences.  Electrical stimulation in the form of a  cardiac action potential   triggers the release of calcium from the cell's internal calcium store, the  sarcoplasmic reticulum .  The rise in calcium causes the cell's  myofilaments  to slide past each other in a process called  excitation-contraction coupling .
Diseases of the heart muscle known as  cardiomyopathies  are of major importance.  These include  ischemic  conditions caused by a restricted blood supply to the muscle such as  angina , and  myocardial infarction .


Cardiac muscle tissue or myocardium forms the bulk of the heart. The heart wall is a three-layered structure with a thick layer of myocardium sandwiched between the inner  endocardium  and the outer  epicardium  (also known as the visceral pericardium). The inner endocardium lines the cardiac chambers, covers the  cardiac valves , and joins with the  endothelium  that lines the blood vessels that connect to the heart. On the outer aspect of the myocardium is the  epicardium  which forms part of the  pericardial sac  that surrounds, protects, and lubricates the heart. [ 1 ]


Within the myocardium, there are several sheets of cardiac muscle cells or cardiomyocytes.  The sheets of muscle that wrap around the left ventricle closest to the endocardium are oriented perpendicularly to those closest to the epicardium.  When these sheets contract in a coordinated manner they allow the ventricle to squeeze in several directions simultaneously – longitudinally (becoming shorter from apex to base), radially (becoming narrower from side to side), and with a twisting motion (similar to wringing out a damp cloth) to squeeze the maximum possible amount of blood out of the heart with each heartbeat. [ 2 ]


Contracting heart muscle uses a lot of energy, and therefore requires a constant flow of blood to provide  oxygen  and nutrients.   Blood  is brought to the myocardium by the  coronary arteries .  These originate from the  aortic root  and lie on the outer or epicardial surface of the heart.  Blood is then drained away by the  coronary veins  into the  right atrium . [ 1 ]


Cardiac muscle cells  (also called  cardiomyocytes ) are the contractile  myocytes  of the cardiac muscle. The cells are surrounded by an  extracellular matrix  produced by supporting  fibroblast  cells. Specialised modified cardiomyocytes known as  pacemaker cells , set the rhythm of the heart contractions. The pacemaker cells are only weakly contractile without sarcomeres, and are connected to neighboring contractile cells via  gap junctions . [ 3 ]  They are located in the  sinoatrial node  (the primary pacemaker) positioned on the wall of the  right atrium , near the entrance of the  superior vena cava . [ 4 ]  Other pacemaker cells are found in the atrioventricular node (secondary pacemaker).


Pacemaker cells carry the impulses that are responsible for the beating of the heart.  They are distributed throughout the heart and are responsible for several functions.  First, they are responsible for being able to  spontaneously generate  and send out  electrical impulses .  They also must be able to receive and respond to electrical impulses from the brain.  Lastly, they must be able to transfer electrical impulses from cell to cell. [ 5 ]  Pacemaker cells in the sinoatrial node, and atrioventricular node are smaller and conduct at a relatively slow rate between the cells. Specialized conductive cells in the  bundle of His , and the  Purkinje fibers  are larger in diameter and conduct signals at a fast rate. [ 6 ]


The Purkinje fibers rapidly conduct electrical signals;  coronary arteries  to bring nutrients to the muscle cells, and  veins  and a  capillary  network to take away waste products. [ 7 ]


Cardiac muscle cells are the contracting cells that allow the heart to pump.  Each cardiomyocyte needs to contract in coordination with its neighboring cells - known as a  functional syncytium  - working to efficiently pump blood from the heart, and if this coordination breaks down then – despite individual cells contracting – the heart may not pump at all, such as may occur during  abnormal heart rhythms  such as  ventricular fibrillation . [ 8 ]


Viewed through a microscope, cardiac muscle cells are roughly rectangular, measuring 100–150μm by 30–40μm. [ 9 ]  Individual cardiac muscle cells are joined at their ends by  intercalated discs  to form long fibers.  Each cell contains  myofibrils , specialized protein contractile fibers of  actin  and  myosin  that slide past each other.  These are organized into  sarcomeres , the fundamental contractile units of muscle cells.  The regular organization of myofibrils into sarcomeres gives cardiac muscle cells a striped or  striated  appearance when looked at through a microscope, similar to skeletal muscle. These striations are caused by lighter  I bands  composed mainly of actin, and darker  A bands  composed mainly of myosin. [ 7 ]


Cardiomyocytes contain  T-tubules , pouches of  cell membrane  that run from the cell surface to the cell's interior which help to improve the efficiency of contraction.  The majority of these cells contain only one  nucleus  (some may have two central nuclei), unlike skeletal muscle cells which contain  many nuclei . Cardiac muscle cells contain many  mitochondria  which provide the energy needed for the cell in the form of  adenosine triphosphate  (ATP), making them highly resistant to fatigue. [ 9 ] [ 7 ]


T-tubules  are microscopic tubes that run from the cell surface to deep within the cell.  They are continuous with the cell membrane, are composed of the same  phospholipid bilayer , and are open at the cell surface to the  extracellular fluid  that surrounds the cell. T-tubules in cardiac muscle are bigger and wider than those in  skeletal muscle , but fewer in number. [ 9 ]  In the centre of the cell they join, running into and along the cell as a transverse-axial network.  Inside the cell they lie close to the cell's internal calcium store, the  sarcoplasmic reticulum .  Here, a single tubule pairs with part of the sarcoplasmic reticulum called a terminal cisterna in a combination known as a  diad . [ 10 ]


The functions of T-tubules include rapidly transmitting electrical impulses known as  action potentials  from the cell surface to the cell's core, and helping to regulate the concentration of calcium within the cell in a process known as  excitation-contraction coupling . [ 9 ]  They are also involved in mechano-electric feedback, [ 11 ]  as evident from cell contraction induced T-tubular content exchange (advection-assisted diffusion), [ 12 ]  which was confirmed by confocal and 3D electron tomography observations. [ 13 ]


The  cardiac syncytium  is a network of cardiomyocytes connected by  intercalated discs  that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium. There is an  atrial syncytium  and a  ventricular syncytium  that are connected by cardiac connection fibres. [ 14 ]  Electrical resistance through intercalated discs is very low, thus allowing free diffusion of ions. The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncytium obeys the  all or none law . [ 15 ]


Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical  syncytium  (in contrast to the skeletal muscle, which becomes a multicellular syncytium during  embryonic development ). The discs are responsible mainly for force transmission during muscle contraction.  Intercalated discs consist of three different types of cell-cell junctions: the actin filament anchoring  fascia adherens junctions , the intermediate filament anchoring  desmosomes , and  gap junctions . [ 16 ]  They allow action potentials to spread between cardiac cells by permitting the passage of ions between cells, producing depolarization of the heart muscle. The three types of junction act together as a single  area composita . [ 16 ] [ 17 ] [ 18 ] [ 19 ]


Under  light microscopy , intercalated discs appear as thin, typically dark-staining lines dividing adjacent cardiac muscle cells. The intercalated discs run perpendicular to the direction of muscle fibers. Under electron microscopy, an intercalated disc's path appears more complex. At low magnification, this may appear as a convoluted electron dense structure overlying the location of the obscured Z-line. At high magnification, the intercalated disc's path appears even more convoluted, with both longitudinal and transverse areas appearing in longitudinal section. [ 20 ]


Cardiac fibroblasts are vital supporting cells within cardiac muscle.  They are unable to provide forceful contractions like  cardiomyocytes , but instead are largely responsible for creating and maintaining the extracellular matrix which surrounds the cardiomyocytes. [ 7 ]   Fibroblasts play a crucial role in responding to injury, such as a  myocardial infarction .  Following injury, fibroblasts can become activated and turn into  myofibroblasts  – cells which exhibit behaviour somewhere between a fibroblast (generating extracellular matrix) and a  smooth muscle cell  (ability to contract).  In this capacity, fibroblasts can repair an injury by creating collagen while gently contracting to pull the edges of the injured area together. [ 21 ]


Fibroblasts are smaller but more numerous than cardiomyocytes, and several fibroblasts can be attached to a cardiomyocyte at once.  When attached to a cardiomyocyte they can influence the electrical currents passing across the muscle cell's surface membrane, and in the context are referred to as being electrically coupled, [ 22 ]  as originally shown in vitro in the 1960s, [ 23 ]  and ultimately confirmed in native cardiac tissue with the help of optogenetic techniques. [ 24 ]  Other potential roles for fibroblasts include electrical insulation of the  cardiac conduction system , and the ability to transform into other cell types including cardiomyocytes  and  adipocytes . [ 21 ]


The  extracellular matrix  (ECM) surrounds the cardiomyocyte and fibroblasts.  The ECM is composed of proteins including  collagen  and  elastin  along with  polysaccharides  (sugar chains) known as  glycosaminoglycans . [ 7 ]  Together, these substances give support and strength to the muscle cells, create elasticity in cardiac muscle, and keep the muscle cells hydrated by binding water molecules.


The matrix in immediate contact with the muscle cells is referred to as the  basement membrane , mainly composed of  type IV collagen  and  laminin .  Cardiomyocytes are linked to the basement membrane via specialised  glycoproteins  called  integrins . [ 25 ]


Humans are born with a set number of heart muscle cells, or cardiomyocytes, which increase in size as the heart grows larger during childhood development. Evidence suggests that cardiomyocytes are slowly turned over during aging, but less than 50% of the cardiomyocytes present at birth are replaced during a normal life span. [ 26 ]  The growth of individual cardiomyocytes not only occurs during normal heart development, it also occurs in response to extensive exercise ( athletic heart syndrome ), heart disease, or heart muscle injury such as after a myocardial infarction. A healthy adult cardiomyocyte has a cylindrical shape that is approximately 100μm long and 10–25μm in diameter.  Cardiomyocyte hypertrophy occurs through sarcomerogenesis, the creation of new sarcomere units in the cell.  During heart volume overload, cardiomyocytes grow through eccentric hypertrophy. [ 27 ]  The cardiomyocytes extend lengthwise but have the same diameter, resulting in ventricular dilation.  During heart pressure overload, cardiomyocytes grow through concentric hypertrophy. [ 27 ]  The cardiomyocytes grow larger in diameter but have the same length, resulting in heart wall thickening.


The physiology of cardiac muscle shares many similarities with that of  skeletal muscle .  The primary function of both muscle types is to contract, and in both cases, a contraction begins with a characteristic flow of  ions  across the  cell membrane  known as an  action potential .  The  cardiac action potential  subsequently triggers muscle contraction by increasing the concentration of  calcium  within the cytosol.


The  cardiac cycle  is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called  diastole , following a period of robust contraction and pumping of blood, dubbed  systole . After emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. A normally performing heart must be fully expanded before it can efficiently pump again.


The rest phase is considered polarized. The  resting potential  during this phase of the beat separates the ions such as sodium, potassium, and calcium. Myocardial cells possess the property of automaticity or spontaneous  depolarization . This is the direct result of a membrane which allows sodium ions to slowly enter the cell until the threshold is reached for depolarization. Calcium ions follow and extend the depolarization even further. Once calcium stops moving inward, potassium ions move out slowly to produce repolarization. The very slow repolarization of the CMC membrane is responsible for the long refractory period. [ 28 ] [ 29 ]


However, the mechanism by which calcium concentrations within the cytosol rise differ between skeletal and cardiac muscle.  In cardiac muscle, the action potential comprises an inward flow of both sodium and calcium ions.  The flow of sodium ions is rapid but very short-lived, while the flow of calcium is sustained and gives the plateau phase characteristic of cardiac muscle action potentials.  The comparatively small flow of calcium through the  L-type calcium channels  triggers a much larger release of calcium from the sarcoplasmic reticulum in a phenomenon known as   calcium-induced calcium release .  In contrast, in skeletal muscle, minimal calcium flows into the cell during action potential and instead the sarcoplasmic reticulum in these cells is directly coupled to the surface membrane.  This difference can be illustrated by the observation that cardiac muscle fibers require calcium to be present in the solution surrounding the cell to contract, while skeletal muscle fibers will contract without extracellular calcium.


During contraction of a cardiac muscle cell, the long protein  myofilaments  oriented along the length of the cell slide over each other in what is known as the  sliding filament theory .  There are two kinds of myofilaments, thick filaments composed of the protein  myosin , and thin filaments composed of the proteins  actin ,  troponin  and  tropomyosin .  As the thick and thin filaments slide past each other the cell becomes shorter and fatter.  In a mechanism known as  cross-bridge cycling , calcium ions bind to the protein troponin, which along with tropomyosin then uncover key binding sites on actin.  Myosin, in the thick filament, can then bind to actin, pulling the thick filaments along the thin filaments.  When the concentration of calcium within the cell falls, troponin and tropomyosin once again cover the binding sites on actin, causing the cell to relax.


It was commonly believed that cardiac muscle cells could not be regenerated. However, this was contradicted by a report published in 2009. [ 30 ]  Olaf Bergmann and his colleagues at the  Karolinska Institute  in  Stockholm  tested samples of heart muscle from people born before 1955 who had very little cardiac muscle around their heart, many showing with disabilities from this abnormality.  By using DNA samples from many hearts, the researchers estimated that a 4-year-old renews about 20% of heart muscle cells per year, and about 69% of the heart muscle cells of a 50-year-old were generated after they were born. [ 30 ]


One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal aging process. [ 31 ]


In the 2000s, the discovery of adult endogenous cardiac stem cells was reported, and studies were published that claimed that various stem cell lineages, including  bone marrow stem cells  were able to differentiate into cardiomyocytes, and could be used to treat  heart failure . [ 32 ] [ 33 ]
However, other teams were unable to replicate these findings, and many of the original studies were later  retracted  for scientific fraud. [ 34 ] [ 35 ]


Cardiac muscle forms both the atria and the ventricles of the heart.  Although this muscle tissue is very similar between cardiac chambers, some differences exist.  The myocardium found in the ventricles is thick to allow forceful contractions, while the myocardium in the atria is much thinner. The individual myocytes that make up the myocardium also differ between cardiac chambers.  Ventricular cardiomyocytes are longer and wider, with a denser  T-tubule  network.  Although the fundamental mechanisms of calcium handling are similar between ventricular and atrial cardiomyocytes, the calcium transient is smaller and decays more rapidly in atrial myocytes, with a corresponding increase in  calcium buffering  capacity. [ 36 ]  The complement of ion channels differs between chambers, leading to longer action potential durations and effective refractory periods in the ventricles. Certain ion currents such as  I K(UR)  are highly specific to atrial cardiomyocytes, making them a potential target for treatments for  atrial fibrillation . [ 37 ]


Diseases affecting cardiac muscle, known as  cardiomyopathies , are the leading cause of death in  developed countries . [ 38 ]  The most common condition is  coronary artery disease , in which the  blood supply to the heart is reduced . The  coronary arteries  become narrowed by  the formation of atherosclerotic plaques . [ 39 ]  If these narrowings become severe enough to partially restrict blood flow, the syndrome of  angina  pectoris may occur. [ 39 ]  This typically causes chest pain during exertion that is relieved by rest. If a coronary artery suddenly becomes very narrowed or completely blocked, interrupting or severely reducing blood flow through the vessel, a  myocardial infarction  or heart attack occurs. [ 40 ]  If the blockage is not relieved promptly by  medication ,  percutaneous coronary intervention , or  surgery , then a heart muscle region may become permanently scarred and damaged. [ 41 ]  Specific cardiomyopathies include: increased  left ventricular mass  ( hypertrophic cardiomyopathy ), [ 42 ]  abnormally large ( dilated cardiomyopathy ), [ 43 ]  or abnormally stiff ( restrictive cardiomyopathy ). [ 44 ]  Some of these conditions are caused by genetic mutations and can be inherited. [ 45 ]


Heart muscle can also become damaged despite a normal blood supply. The heart muscle may become inflamed in a condition called  myocarditis , [ 46 ]  most commonly caused by a viral infection [ 47 ]  but sometimes caused by the body's own  immune system . [ 48 ]  Heart muscle can also be damaged by drugs such as alcohol, long standing high blood pressure or  hypertension , or persistent abnormal  heart racing . [ 49 ]
Many of these conditions, if severe enough, can damage the heart so much that the pumping function of the heart is reduced. If the heart is no longer able to pump enough blood to meet the body's needs, this is described as  heart failure . [ 49 ]


Significant damage to cardiac muscle cells is referred to as  myocytolysis  which is considered a type of cellular  necrosis  defined as either coagulative or colliquative. [ 50 ] [ 51 ]


The  cardiac pacemaker  is the  heart 's natural rhythm generator. It employs pacemaker  cells  that produce electrical impulses, known as  cardiac action potentials , which control the rate of contraction of the  cardiac muscle , that is, the  heart rate . In most humans, these cells are concentrated in the  sinoatrial (SA) node , the primary pacemaker, which regulates the heart’s  sinus rhythm .


Sometimes a secondary pacemaker sets the pace, if the SA node is damaged or if the  electrical conduction system of the heart  has problems.  Cardiac arrhythmias  can cause  heart block , in which the contractions lose their rhythm. In humans, and sometimes 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  sinoatrial node  (SA node) is the primary pacemaker of the heart. It is a region of cardiac muscle on the wall of the upper  right atrium  near to the  superior vena cava  entrance. The cells that make up the SA node are specialized  cardiomyocytes  known as  pacemaker cells  that can spontaneously generate  cardiac action potentials . These signals are propagated through the heart's  electrical conduction system . [ 1 ] [ 2 ]  Only one percent of the heart muscle cells are conductive, the rest of the cardiomyocytes are  contractile .


The pacemaker cells are connected to neighboring contractile cells via  gap junctions , which enable them to locally depolarize adjacent cells. Gap junctions allow the passage of positive cations from the depolarization of the pacemaker cell to adjacent contractile cells. This starts the depolarization and eventual action potential in contractile cells. Having cardiomyocytes connected via gap junctions allow all contractile cells of the heart to act in a coordinated fashion and contract as a unit. All the while being in sync with the pacemaker cells; this is the property that allows the pacemaker cells to control contraction in all other cardiomyocytes.


Cells in the SA node spontaneously  depolarize , ultimately resulting in contraction, approximately 100 times per minute. This native rate is constantly modified by the activity of  sympathetic  and  parasympathetic  nerve fibers via the  autonomic nervous system , so that the average resting  heart rate  in adult humans is about 70 beats per minute.


Impulses from the sinus node reach the  atrioventricular node  which acts as the secondary pacemaker. 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 bundle branches , and the  Purkinje fibers , will also produce a spontaneous action potential at a rate of 30–40 beats per minute, so if the SA and AV node both fail to function, these cells can become pacemakers. These cells will be initiating action potentials and contraction at a much lower rate than the primary or secondary pacemaker cells.


The SA node controls the rate of contraction for the entire heart muscle because its cells have the quickest rate of spontaneous depolarization, thus they initiate action potentials the quickest. The action potential generated by the SA node passes down the  electrical conduction system of the heart , and depolarizes the other potential pacemaker cells (AV node) to initiate action potentials before these other cells have had a chance to generate their own spontaneous action potential, thus they contract and propagate electrical impulses to the pace set by the cells of the SA node. This is the normal conduction of electrical activity in the heart.


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 as phases one and two are absent, leaving only phases zero, three, and four.


The key to the rhythmic firing of pacemaker cells is that, unlike  neurons , these cardiomyocytes will slowly depolarize by themselves and do not need any outside innervation from the autonomic nervous system to fire action potentials.


In all other cells, the  resting potential  (-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. However, in pacemaker cells, this potassium permeability (efflux) decreases as time goes on, causing a slow depolarization. In addition, there is a slow, continuous inward flow of  sodium , called the "funny" or  pacemaker current . These two relative ion concentration changes slowly depolarize (make more positive) the inside membrane potential (voltage) of the cell, giving these cells their pacemaker potential. When the membrane potential gets depolarized to about -40mV it has reached threshold (cells enter phase 0), allowing an action potential to be generated.


Though much faster than the depolarization of phase 4, 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). Calcium enters the cell via voltage-sensitive calcium channels that open when the threshold is reached. This calcium influx produces the rising phase of the action potential, which results in the reversal of membrane potential to a peak of about +10mV. It is important to note that intracellular calcium causes muscular contraction in contractile cells, and is the effector ion. In heart pacemaker cells, phase 0 depends on the activation of  L-type calcium channels  instead of the activation of voltage-gated fast sodium channels, which are responsible for initiating action potentials in contractile (non-pacemaker) cells. For this reason, the pacemaker action potential rising phase slope is more gradual than that of the contractile cell (image 2).


The reversal of membrane potential triggers the opening of potassium leak channels, resulting in the rapid loss of potassium ions from the inside of the cell, causing repolarization (V m  gets more negative). The calcium channels are also inactivated soon after they open. In addition, as sodium channels become inactivated, sodium permeability into the cell is decreased. These ion concentration changes slowly repolarize the cell to resting membrane potential (-60mV). Another important note at this phase is that ionic pumps restore ion concentrations to pre-action potential status. The  sodium-calcium exchanger  ionic pump works to pump calcium out of the  intracellular space , thus effectively relaxing the cell. The  sodium/potassium pump  restores ion concentrations of sodium and potassium ions by pumping sodium out of the cell and pumping (exchanging) potassium into the cell. Restoring these ion concentrations is vital because it enables the cell to reset itself and enables it to repeat the process of spontaneous depolarization leading to activation of an action potential.


If the SA node does not function, or the impulse generated in the  SA node is blocked  before it travels down the electrical conduction system, a group of cells further down the heart will become its pacemaker. [ 3 ]  This center is typically represented by cells inside the  atrioventricular node  (AV node), which is an area between the  atria  and  ventricles , within the  atrial septum .  If the AV node also fails,  Purkinje fibers  are occasionally capable of acting as the default or "escape" pacemaker.


An  ectopic pacemaker  also known as an ectopic focus or ectopic foci, is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart. It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat. If chronic this can result in  arhythmias  such as  tachycardia ,  bradycardia , or  ventricular fibrillation . An  artificial pacemaker  may be used to counter this.


An artificial cardiac pacemaker (or artificial pacemaker, so as not to be confused with the natural cardiac pacemaker) or just pacemaker is an  implanted medical device  that generates electrical impulses delivered by electrodes to the chambers of the heart either the upper atria, or lower ventricles to cause the targeted chambers to contract and pump blood. By doing so, the artificial pacemaker takes over from the primary SA node pacemaker to regulate the function of the heart's electrical conduction system.


Cardiac Pacemakers, Inc.  ( CPI ),  doing business as   Guidant Cardiac Rhythm Management , manufactured implantable cardiac rhythm management devices, such as  pacemakers  and  defibrillators . It sold microprocessor-controlled insulin pumps and equipment to regulate heart rhythm. It developed therapies to treat irregular heartbeat. The company was founded in 1971 and is based in  Saint Paul, Minnesota , and is presently a subsidiary of  Boston Scientific . [ 1 ]


CPI was founded in February 1972 in  Saint Paul, Minnesota . The first $50,000 capitalization for CPI was raised from a phone booth on the  Minneapolis  skyway system. [ 2 ]  They began designing and testing their implantable cardiac pacemaker powered with a new longer-life lithium battery in 1971. The first heart patient to receive a CPI pacemaker emerged from surgery in June 1973. Within two years, the upstart company that challenged Medtronic had sold approximately 8,500 pacemakers. [ 3 ]


Medtronic  at the time had 65% of the artificial pacemaker market. CPI was the first spin-off from Medtronic. It competition using the world's first lithium-powered pacemaker. Medtronic's market share plummeted to 35%. [ 4 ] [ 5 ]


Founding partners  Anthony Adducci ,  Manny Villafaña , Jim Baustert, and Art Schwalm, were former Medtronic employees. Lawsuits ensued, all of which were settled out of court. [ 6 ]


The company sold 8,500 pacemakers, increasing sales from zero in 1972 to over $47 million.


In early 1978, CPI was concerned about a friendly takeover attempt. Despite impressive sales, the company's stock price had fluctuated wildly the year before, dropping from $33 to $11 per share. Some speculated that the stock was being sold short, while others attributed the price to the natural volatility of high-tech stock. As a one-product company, CPI was susceptible to changing market conditions, and its founders knew they needed to diversify. They considered two options: acquiring other medical device companies or being acquired themselves. They chose the latter.


Several companies expressed interest in acquiring CPI, including  3M , American Hospital Supply,  Pfizer , and  Johnson & Johnson . However,  Eli Lilly and Company , one of the premier pharmaceutical companies in the United States, was the most enthusiastic suitor. "Lilly had the research expertise, highly compatible interests, and similar values," Anthony Adducci recalls. "At CPI, we haven't been able to dedicate the dollars and time necessary to develop new products beyond our staple lithium-powered pacemaker. Lilly was a $2 billion company. We knew they had tremendous resources, especially in research and development." [ 6 ]  Additionally, Eli Lilly and CPI were already interested in developing  insulin  pumps, and Lilly was working with cardiovascular drugs, a natural link to CPI's heart pacemaker business.


Before the final negotiations in late 1978, there were numerous flights between Minneapolis and  Indianapolis  for CPI principals and representatives of  Piper, Jaffray & Hopwood's  corporate finance department. Lilly, a pharmaceutical giant, and CPI, the upstart pacemaker company, sat down at a bargaining table at a motel in suburban  Bloomington, Minnesota . CPI's negotiation team included Anthony Adducci, Art Schwalm, Tom King, and Hunt Greene.


In December 1978, the company was acquired by Eli Lilly and Company for $127 million. [ 7 ]


CPI designed and manufactured the world's first pacemaker with a lithium anode and a  lithium-iodide  electrolyte solid-state battery. The pacemaker structure is enclosed in a hermetically sealed metallic enclosure, allowing electrode leads to pass in a sealed relationship. The surface of the casing is polished metal, with a zone through which the external electrode leads pass. [ 8 ]


The Lithium-iodide or lithium anode cells revolutionized the medical industry by increasing the pacemaker life from 1 year up to 11 years. It became the standard for pacemaker designs.


Cardiac resynchronisation therapy  ( CRT  or  CRT-P ) is the insertion of  electrodes  in the left and right  ventricles  of the heart, as well as on occasion the right  atrium , to treat  heart failure  by coordinating the function of the left and right ventricles via a  pacemaker , a small device inserted into the anterior chest wall. [ 1 ]


CRT is indicated in patients with a low  ejection fraction  (typically <35%) indicating  heart failure , where electrical activity has been compromised, with prolonged  QRS  duration to >120  ms . [ 2 ]


The insertion of electrodes into the ventricles is done under  local anesthetic , with access to the ventricles most commonly via the  subclavian vein , although access may be conferred from the  axillary  or  cephalic veins . Right ventricular access is direct, while left ventricular access is conferred via the  coronary sinus  (CS).


CRT defibrillators ( CRT-D ) also incorporate the additional function of an  implantable cardioverter-defibrillator  (ICD), to quickly terminate an abnormally fast, life-threatening heart rhythm. CRT and CRT-D have become increasingly important therapeutic options for patients with moderate and severe heart failure. [ 3 ]  CRT with pacemaker only is often termed "CRT-P" to help distinguish it from CRT with defibrillator (CRT-D).


The key indication for CRT is  left bundle branch block  (LBBB) of the heart, a cardiac abnormality leading to delayed left ventricular contraction. LBBB causes a  QRS  prolongation of ≥120  ms  on the  electrocardiogram , contributing to poor left ventricular coordination and reduced systolic function, thereby reduced ejection fraction (<35%). This reduction in ejection fraction is considered heart failure. [ 2 ]


Heart failure patients are generally considered if in  New York Heart Association  (NYHA) class II or III heart failure. Current  National Institute for Health and Care Excellence  (NICE) guidelines state that CRT-D device placement is inappropriate for class IV heart failure, but placement of CRT-P devices may be appropriate in certain circumstances. [ 4 ] [ 5 ] [ 6 ]


CRT requires the placement of an electrical device for biventricular pacing, along with placement of (at least) two pacing leads, to facilitate stable left ventricular and right ventricular pacing. For all elements, the first stage of the process is local anaesthetic followed by incision to allow for approach from the appropriate vein. From here, the leads and device can be inserted. [ 1 ]


A  venipuncture   is made, and a guide wire inserted into the vein, where it is guided, with use of  real time X-ray imaging , through to the right ventricle. The guide wire is then used to assist in the placement of the electrode lead, which travels through the venous system into the right ventricle where the electrode is embedded. [ 1 ]


This is generally performed subsequent to RV lead placement, with the RV lead providing a backup in case of accidental damage to the  electric fibers of the heart , causing an  asystolic event . As with the RV lead, a guide wire is first inserted, allowing for the insertion of a  multi-delivery catheter . The catheter is subsequently maneuvered to the opening of the coronary sinus in the right atrium. From here a  contrast media  is injected, allowing the surgical team to obtain a coronary sinus  phlebogram  to direct the placement of the lead into the most suitable  coronary vein . [ 1 ]


Once the phlebogram has been obtained, the multi-delivery catheter is used to guide in the lead, from the chosen vein of entry, into the right atrium, through the coronary sinus and into the relevant cardiac vein. [ 1 ]


Left ventricular lead placement is the most complicated and potentially hazardous element of the operation, due to the significant variability of coronary venous structure. Alterations in heart structure, fatty deposits, valves and natural variations all cause additional complications in the process of cannulation. [ 1 ]  However, this risk can be reduced using AI-based [ 8 ]  preoperative visualization of LV venous anatomy using computer tomography (CT) imaging.


The device is inserted in a subcutaneous pocket created by the surgeon, the choice of left or right side of the chest wall is determined mainly by the patient's preference or location of preexisting device. The device, similar to that of a traditional  pacemaker , is generally no larger than a pocket watch and has inserts for the electrode leads. [ 1 ]


Several studies have also shown that CRT can decrease mortality, reverse  left ventricular remodeling , and improve quality of life, walking distance, and peak oxygen uptake ( VO 2  max ). [ 9 ]  A 2013 study showed that CRT improved the left ventricular ejection fraction (LVEF) by an average of 10.6% 12 months after placement. [ 10 ]


Key complications include: [ 2 ]


Several research papers [ 12 ] [ 13 ]  have proposed software platforms for planning and guiding the implantation of CRT devices. This research proposes using pre-operative images to characterize tissue and left ventricle activation to identify potential target regions for deploying the CRT leads.


Cardiac rhythmicity  is the spontaneous  depolarization  and  repolarization  event that occurs in a repetitive and stable manner within the cardiac muscle. Rhythmicity is often abnormal or lost in cases of cardiac dysfunction or  cardiac failure . It is the ability of the heart to maintain a relatively stable relation between its  systole  and  diastole . Not increasing one on the expense of the other. However, external factors may lead to the disruption of the heart's rhythmicity.


The  cardiac transient outward potassium current  (referred to as  I to1  or  I to [ 1 ]   ) is one of the  ion currents  across the cell membrane of  heart muscle cells . It is the main contributing current during the  repolarizing   phase 1 of the cardiac action potential . It is a result of the movement of positively charged  potassium  (K + ) ions from the  intracellular  to the  extracellular space . I to1  is complemented with I to2  resulting from Cl −  ions to form the transient outward current I to .


I to1  is rapidly activated and deactivated. [ 2 ]  It is activated after the fast increase of the membrane potential following the  phase 0 of the cardiac action potential . Once activated, (K + ) ions from inside the cells flow to the extracellular space. This outward flow of positively charged ions constitutes the I to1  and causes the  transmembrane voltage  to decrease. This decrease of the transmembrane potential is known as  repolarization . I to1  is then quickly deactivated, stopping the repolarization and ending the  phase 1  of the action potential.


I to1  is  Ca 2+ -independent [ 3 ]  and has been clearly demonstrated in myocytes from different cardiac regions and species. [ 3 ]  There are two kinetic variants of cardiac I to1 : fast I to1 , called I to1,f , and slow Ito, called I to1,s . The channel responsible for I to1,f  is formed by assembly of  Kv4.2  (KCND2) subunits,  Kv4.3  (KCND3) subunits or a combination of the two, while the channel responsible for I to1,s  is composed of  Kv1.4  (KCNA4) subunits. [ 2 ]  In addition, several regulatory subunits and pathways modulating the level and biophysical properties of cardiac I to  have been identified. [ 2 ]


I to1  affects the opening of Ca 2+  channels during Phase 2 of the Action Potential. As a result, changes in I to1  modulate changes in the action potential duration. [ 2 ]


Clinical cardiac electrophysiology  (also referred to as  cardiac electrophysiology  or simply  EP ), is a branch of the medical specialty of  cardiology   concerned with the study and treatment of  rhythm disorders  of the  heart . [ 1 ]  Cardiologists with expertise in this area are usually referred to as electrophysiologists.  Electrophysiologists are trained in the mechanism, function, and performance of the electrical activities of the  heart .  Electrophysiologists work closely with other cardiologists and cardiac surgeons to assist or guide therapy for heart rhythm disturbances ( arrhythmias ). They are trained to perform interventional and surgical procedures to treat cardiac arrhythmia.


The training required to become an electrophysiologist is lengthy and requires eight years after medical school (in the U.S.), entailing three years of  internal medicine   residency , three years of clinical  cardiology   fellowship , and two years of clinical cardiac electrophysiology. This is necessary due to the significant complexity of patients that electrophysiologists usually treat, the constant advances in methods and equipment used in their daily practice, making the field of electrophysiology one of the most demanding subspecialties of modern medicine.


An electrophysiology study is any of a number of invasive (intracardiac) and non-invasive recording of spontaneous electrical activity, as well as of cardiac responses to  programmed electrical stimulation . These studies are performed to assess  arrhythmias , elucidate symptoms, evaluate abnormal  electrocardiograms , assess risk of developing arrhythmias in the future, and design treatment.


In addition to diagnostic testing of the electrical properties of the heart, electrophysiologists are trained in therapeutic and surgical methods to treat many of the rhythm disturbances of the heart.  Therapeutic modalities employed in this field include  antiarrhythmic drug  therapy and surgical implantation of  pacemakers  and  implantable cardioverter-defibrillators .


Common rhythms dealt with include  atrial fibrillation ,  ventricular tachycardia , and the  supraventricular tachycardias . Abnormal rhythms have multiple ways they can be treated and choosing is often individualized based on symptoms and patient preference.


Electrophysiologists will commonly employ the following diagnostic tests and may be performed or interpreted exclusively by the electrophysiologist. Other tests such as  cardiac stress testing  may be included in an evaluation but are not exclusive to electrophysiology.


Initial administration and monitoring of the effect of drugs for treatment of heart rhythm disorders. Electrophysiologists are often involved when severe or life-threatening  arrhythmias  are being treated, or when multiple drugs must be used to treat an arrhythmia.
 Antiarrhythmic agents  such as  flecainide ,  dofetilide , and  amiodarone  are commonly used to try to control rhythms.


Ablation therapy is a catheter based ablation of lesions in the heart (with radiofrequency energy, cryotherapy (destructive freezing), microwave, or ultrasound energy) to cure or control arrhythmias (see  radiofrequency ablation ). Ablation is usually performed during the same procedure as the electrophysiology study during which arrhythmias are attempted to be induced as well as elucidating the mechanism of the arrhythmia for which ablation therapy is sought.


Implantation of devices include


Additionally, there are, at times, indications to remove these devices and extraction (ie, removal) of these devices can also be performed by electrophysiologists.


Once implanted, long-term clinical follow up and reprogramming of implanted devices also falls to the electrophysiologist.


Concealed conduction  is tissue stimulation without direct effect, but leading to a change in conduction characteristics. [ 1 ]  The term "concealed" is in reference to that the conduction is not observable by electrocardiogram.


A common example would be an  interpolated PVC  (a type of  premature ventricular contraction ) during  normal sinus rhythm ; the PVC does not cause an atrial contraction, because the retrograde impulse from the PVC does not completely penetrate the AV node. However, this AV node stimulation can cause a delay in subsequent AV conduction by modifying the AV node's subsequent conduction characteristics. Hence, the P-R interval after the PVC is longer than the baseline P-R interval. [ citation needed ]


Concealed conduction can be seen in  cardiac aberrancy  when a bundle branch temporarily blocks due to being refractory, and conduction from the other bundle branch conceals into the blocked branch retrograde thus perpetuation the bundle branch block morphology in subsequent beats. For example, if a  Premature atrial contraction  reaches the right bundle branch while refractory the PAC will conduct with RBBB morphology. As this PAC conducts down the left bundle, it will depolarize the septum then proceed retrograde up the right bundle. Eventually, this will reach refractory conduction tissue and stop. The subsequent beat — if early enough — will find the right bundle still refractory and the process will repeat yielding a continued RBBB morphology.


Another variation on this concept is seen in  atrial flutter . As a result of the rapid atrial rate, some of the atrial activity fails to get through the AV node in an antegrade direction but can alter the rate at which a subsequent atrial impulse is conducted. In this circumstance, an alteration in the F-wave to QRS relationship is seen. [ citation needed ]


Ross Cowie  (born 13 February 1960) is a charity-worker and former  shinty  player and manager,  from  Portree ,  Isle of Skye ,  Scotland .  He is affectionately known as  The Colonel .


Throughout his career, Cowie was involved with  Skye Camanachd  and was most notably manager when they won the   Camanachd Cup  in 1990 [ 1 ]  He was also captain of the Skye second team that had won the Sutherland Cup in 1988.


In all he has been manager of Skye Camanachd 3 times, covering an aggregate of 8 years.  [1]  His father, Willie played for Skye Camanachd also, as well as  Lovat Shinty Club .  His uncle Dave Cowie played for Aberdeen FC in 1939.


Because of a serious heart condition,  cardiomyopathy , Cowie retired from involvement in the playing side of the sport but retained a position as  president  of Skye Camanachd.
In December 2010, Cowie made a dramatic return to top-level shinty with his re-appointment as assistant manager of Skye.  He assisted manager Aonghas MacDonald and was supported by his two star players from the 1990 victory, his brother Willie and  Albert Smith Medal  winner, Willie MacRae. [2]


He spoke to the press in January 2010 about the need for his club to improve performances at all levels, but in particular at second team level. [3]  He became the Skye Camanachd "Director of Shinty" in late 2012.


Cowie stepped down from the Skye Camanachd committee in December 2018.  [4]  along with fellow club stalwart, Donnie Martin. [5]


Cowie was also an important player and coach for the now defunct Portree United FC, a football club which shared many players in common with Skye Camanachd.


After a cardiac arrest in December 2006, which saw him die for several minutes, he became involved in fundraising and raising awareness of cardiac conditions throughout the Highlands of Scotland thorough his charity,  Lucky2BHere . [6]   Lucky2BHere  focuses on making acute care available in remote areas of the Highlands. [7]  Lucky2BHere


The trustees of Lucky2BHere are Professor Steve Leslie, Angus MacDonald, Phil Cunningham and Malcolm Jones.


By 2019, Lucky2BHere had raised over £1,000,000 and had distributed over 600 defibrillators. These defibrillators had been instrumental in saving several lives.  [8]


Through 2021, and the aftermath of the  Christian Eriksen  incident at  Euro 2020 , Cowie made a call for the Scottish Government to have emergency life support training in every school in Scotland.  [9]


In 2022, Cowie talked about  Inverness  BID securing 5 new defibs for Inverness City Centre and Lucky2BHere is the biggest purchaser of defibs in Scotland and Northern Ireland. [10]


In May 2024, Cowie was recognised with a  Point of Light Award  and was recognised with an  early day motion  in the  UK Parliament . [11]


Defibrillation  is a treatment for life-threatening  cardiac arrhythmias , specifically  ventricular fibrillation  (V-Fib) and  non-perfusing ventricular tachycardia  (V-Tach). [ 1 ] [ 2 ]  A defibrillator delivers a dose of  electric current  (often called a  counter-shock ) to the  heart . Although not fully understood, this process  depolarizes  a large amount of the  heart muscle , ending the arrhythmia. Subsequently, the body's  natural pacemaker  in the  sinoatrial node  of the heart is able to re-establish normal  sinus rhythm . [ 3 ]  A heart which is in  asystole  (flatline) cannot be restarted by a defibrillator; it would be treated only by  cardiopulmonary resuscitation  (CPR) and medication, and then by cardioversion or defibrillation if it converts into a shockable rhythm.


In contrast to defibrillation, synchronized electrical  cardioversion  is an electrical shock delivered in synchrony to the  cardiac cycle . [ 4 ]  Although the person may still be  critically ill , cardioversion normally aims to end poorly perfusing  cardiac arrhythmias , such as  supraventricular tachycardia . [ 1 ] [ 2 ]


Defibrillators can be external, transvenous, or  implanted  ( implantable cardioverter-defibrillator ), depending on the type of device used or needed. [ 5 ]  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 no training. [ 2 ]


Defibrillation is often an important step in  cardiopulmonary resuscitation  (CPR). [ 6 ] [ 7 ]  CPR is an algorithm-based intervention aimed to restore cardiac and pulmonary function. [ 6 ]  Defibrillation is indicated only in certain types of  cardiac dysrhythmias , specifically  ventricular fibrillation  (VF) and  pulseless ventricular tachycardia . [ 1 ] [ 2 ]  If the heart has completely stopped, as in  asystole  or  pulseless electrical activity (PEA) , defibrillation is not indicated. Defibrillation is also not indicated if the patient is conscious or has a pulse. Improperly given electrical shocks can cause dangerous dysrhythmias, such as ventricular fibrillation. [ 1 ]


A defibrillation device that is often available outside of medical centers is the automated external defibrillator (AED), [ 8 ]  a portable machine that can be used with no previous training. That is possible because the machine produces pre-recorded voice instructions that guide the user. The device automatically checks the patient's condition and applies the correct electric shocks. There also exist written instructions that explain the procedure step-by-step. [ 9 ]


Survival rates for out-of-hospital  cardiac arrests  in North America are poor, often less than 10%. [ 10 ]  Outcome for in-hospital cardiac arrests are higher at 20%. [ 10 ]  Within the group of people presenting with cardiac arrest, the specific cardiac rhythm can significantly impact survival rates. Compared to people presenting with a non-shockable rhythm (such as asystole or PEA), people with a shockable rhythm (such as VF or pulseless ventricular tachycardia) have improved survival rates, ranging between 21 and 50%. [ 6 ] [ 11 ] [ 12 ]


Manual external defibrillators require the expertise of a healthcare professional. [ 13 ] [ 14 ]  They are used in conjunction with an  electrocardiogram , which can be separate or built-in. A healthcare provider first diagnoses the cardiac rhythm and then manually determine the voltage and timing for the electrical shock. These units are primarily 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.  [ citation needed ]  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.  [ citation needed ]


An internal defibrillator is often used to defibrillate the heart during or after cardiac surgery such as a  heart bypass . The electrodes consist of round metal plates that come in direct contact with the myocardium. Manual internal defibrillators deliver the shock through paddles placed directly on the heart. [ 1 ]  They are mostly used in the  operating room  and, in rare circumstances, in the emergency room during an  open heart procedure .


Automated external defibrillators (AEDs) are designed for use by untrained or briefly trained laypersons. [ 15 ] [ 16 ] [ 17 ]  AEDs contain technology for analysis of heart rhythms. As a result, it does not require a trained health provider to determine whether or not a rhythm is shockable. By making these units publicly available, AEDs have improved outcomes for sudden out-of-hospital cardiac arrests. [ 15 ] [ 16 ]


Trained health professionals have more limited use for AEDs than manual external defibrillators. [ 18 ]  Recent studies show that AEDs does not improve outcome in patients with in-hospital cardiac arrests. [ 18 ] [ 19 ]  AEDs have set voltages and does not allow the operator to vary voltage according to need. AEDs may also delay delivery of effective CPR. For diagnosis of rhythm, AEDs often require the stopping of chest compressions and rescue breathing. For these reasons, certain bodies, such as the European Resuscitation Council, recommend using manual external defibrillators over AEDs if manual external defibrillators are readily available. [ 19 ]


As early defibrillation can significantly improve VF outcomes, AEDs have become publicly available in many easily accessible areas. [ 18 ] [ 19 ]  AEDs have been incorporated into the algorithm for  basic life support  (BLS). Many  first responders , such as firefighters, police officers, and security guards, are equipped with them.


AEDs can be fully automatic or semi-automatic. [ 20 ]  A semi-automatic 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. Some types of AEDs come with advanced features, such as a manual override or an  ECG  display.


Implantable cardioverter-defibrillators , also known as automatic internal cardiac defibrillator (AICD), 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.


A  wearable cardioverter defibrillator  is a portable external defibrillator that can be worn by at-risk patients. [ 21 ]  The unit monitors the patient 24 hours a day and can automatically deliver a biphasic shock if VF or VT is detected. This device is mainly indicated in patients who are not immediate candidates for ICDs. [ 22 ]


The connection between the defibrillator and the patient consists of a pair of electrodes, each provided with  electrically 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 the person's skin after defibrillation. 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.


The most well-known type of electrode (widely depicted in films and television) is the traditional metal "hard" paddle with an insulated (usually plastic) handle. This type must be held in place on the patient's skin with approximately 25 lbs (11.3 kg) 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 reusable, 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 manual external units.


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.


Special pads are used for children under the age of 8 or those under 55 lbs. (22 kg). [ 23 ]


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 (anterior-lateral position) 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.


Researchers have created a software modeling system capable of mapping an individual's  chest  and determining the best position for an external or internal cardiac defibrillator. [ 24 ]


Defibrillation halts chaotic cardiac activity by forcibly depolarizing heart cells, disrupting re-entrant circuits, and allowing for the heart's natural pacemaker to take over. [ 25 ] [ 26 ]


Cardiac cells require a strong electrical stimulus to raise their transmembrane potential to the activation threshold. [ 25 ] [ 26 ]  Only a small amount of electrical current enters the cell due to high membrane impedance. [ 25 ] The intracellular voltage of the cell remains uniform, while the extracellular voltage rapidly increases or decreases depending on proximity to the electrodes. [ 25 ] This creates a voltage gradient that alters the transmembrane potential of cells, potentially resetting irregular electrical activity to restore normal cardiac rhythm. [ 25 ] [ 26 ]


Irregular rhythms often result from re-entrant circuits, where electrical impulses circle within the heart tissue due to areas of slow conduction or unidirectional block. [ 27 ]  The widespread depolarization from the shock interrupts these circuits, stopping the erratic propagation of electrical signals. [ 25 ] [ 26 ] [ 27 ]


After the cells depolarize, they enter a refractory period, during which they cannot be re-excited. [ 28 ] [ 29 ]  This allows the heart's natural pacemaker, the sinoatrial node, to resume control of the rhythm. During this period, ion pumps actively restore the normal distribution of ions, re-establishing the resting membrane potential. [ 28 ] [ 29 ]


Defibrillators were first demonstrated in 1899 by  Jean-Louis Prévost  and Frédéric Batelli, two  physiologists  from the  University of Geneva , Switzerland. They discovered that small electrical shocks could induce ventricular fibrillation in dogs, and that larger charges would reverse the condition. [ 30 ] [ 31 ]


In 1933, Dr. Albert Hyman, heart specialist at the Beth Davis Hospital of New York City and C. Henry Hyman, an electrical engineer, looking for an alternative to injecting powerful drugs directly into the heart, came up with an invention that used an electrical shock in place of drug injection. This invention was called the  Hyman Otor  where a hollow needle is used to pass an insulated wire to the heart area to deliver the electrical shock.  The hollow steel needle acted as one end of the circuit and the tip of the insulated wire the other end.  Whether the  Hyman Otor  was a success is unknown. [ 32 ]


The external defibrillator, as it is known today, was invented by electrical engineer  William Kouwenhoven  in 1930. Kouwenhoven studied the relationship between electric shocks and their effects on the human heart when he was a student at Johns Hopkins University School of Engineering. His studies helped him invent a device to externally jump start the heart. He invented the defibrillator and tested it on a dog, like Prévost and Batelli. The first use on a human was in 1947 by  Claude Beck , [ 33 ]  professor of surgery at  Case Western Reserve University .


Beck's theory was that ventricular fibrillation often occurred in hearts that were fundamentally healthy, in his terms "Hearts that are too good to die", and that there must be a way of saving them.  Beck first used the technique successfully on a 14-year-old boy who was having his  breastbone  separated from his  ribs  because of a congenital growth disorder, causing breathing problems. The boy's chest was surgically opened, and manual cardiac massage was undertaken for 45 minutes until the arrival of the defibrillator.  Beck used internal paddles on either side of the heart, along with  procainamide , an  antiarrhythmic  drug, and achieved return of a perfusing cardiac rhythm. [ citation needed ]