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I don't really know how to phrase the question, but to put it as clearly as I can, I don't get why it is the P wave "flattens down" when the atria have completely depolarized. I get that the charge is uniform across the atria, but the ventricles are still polarized (and therefore of a different charge compared to the now completely depolarized atria), wouldn't this create a difference in charge and therefore a voltage to produce a current? I think this GIF can help explain my question better:
At frame 12:
I don't understand why there's no current flow and no deflection on the ECG leads despite the charge difference. Rather, why does the GIF deal with the current and charge difference in the atria and ventricles separately? I thought this all might be because of the fibrous cardiac skeleton, which acts as an electrical insulator, but that doesn't make complete sense either; sure it prevent current flow within the heart, but it wouldn't influence current flow outside of it, right?
I'd suggest reading the rest of the Wikipedia article on EKG rather than focusing on the particular cartoon you are using right now, because that cartoon does not depict the dipoles that are measured.
The key interpretation that you are missing is that the signals measured are not voltage differences between intracellular compartments of the heart (like between the atria and ventricles, or between the depolarized and polarized part of one compartment), but a moving dipole created during polarization changes.
As the atria depolarize, there is a wave of negative extracellular charge as positive ions enter cells, creating a dipole: there is more negative charge at the most recently depolarized point than ahead of the wave where cells haven't yet depolarized. This is the signal you measure. If you were to pause this process at any moment, those extracellular charges are free to move and the potential dissipates quickly.
There is too much conductivity in the extracellular space for the dipole to be maintained without the rapid polarization changes that occur when ion channels open. You can think of this as a high-pass filter; the amplitude of the dipole measured would approach zero as the speed is reduced regardless of static differences in intracellular voltage measured against some reference.
This is what happens during the brief "pause" between atrial and ventricular contraction: there is still a dipole, but it is much smaller as it travels through the AV node than in the muscle and would only be measurable from local electrodes. You begin to see the signal again once the ventricles contract.
http://umdberg.pbworks.com/f/Hobbie-EKG-1.pdf may also be useful.
ST-segment resolution (STR) represents the simplest clinical evidence of effective myocardial reperfusion and lack of STR is suggestive of the occurrence of no reflow (NR)  . In clinical practice, STR can be assessed by either continuous monitoring or static ECG recordings. Schröder et al. suggested that a STR <50% or <70% should be considered as indicative of NR. However, approximately one-third of patients with myocardial blush grade (MBG) 2–3 and TIMI flow grade 3 (which has represented for many years the gold standard definition for NR) do not exhibit STR  . Conversely, a consistent proportion of patients with angiographic evidence of NR show STR. Thus, STR is an immediate, but not very accurate method to evaluate NR.
Despite these limitations, however, many reports have shown that a rapid and significant resolution of ST-segment elevation during and after the treatment of ST-segment elevation acute myocardial infarction (STEMI) is associated with a better prognosis [4,5] .
Specific grades of STR at specific times allow a good stratification of the risk of major adverse cardiovascular events (MACE). Continuous ECG-recording has a better accuracy since it discriminates the dynamics of the ST-segment between the recordings. For example, recurrent ST-elevations during thrombolysis predict subsequent re-occlusion  and eventually worse clinical outcome  .
However, even small fluctuations of the ST-segment during the first 4 hours of observation have a negative impact on clinical outcome [8,9] .
Assessing pacemaker function
The base rate is the lowest heart rate allowed by the pacemaker intrinsic cardiac activity below the base rate will trigger pacing. The base rate is usually set to 60 beats/min. The base rate is virtually always >50 beats/min, meaning that any heart rate below 50 beats/min is most likely not paced. An intrinsic heart rate faster than the base rate should inhibit the pacemaker.
The appearance of the P-wave depends on where the atrial lead is fixed. Typically, the atrial lead is fixed next to the right atrial appendage, or atrial ceiling, which yields P-waves similar to those seen during normal sinus rhythm (i.e, positive P-wave in lead II). If the atrial lead is placed distally in the atrium, activation may proceed in the opposite direction, which results in negative (retrograde) P-waves in lead II.
QRS morphology also depends on where the pacing stimulus is delivered. Typically, the lead tip is fixed apically in the right ventricle activation starts in the right ventricle and spreads slowly to the left ventricle. As mentioned above, this is similar to the situation in left bundle branch block (LBBB), which explains why paced QRS complexes are similar to the QRS morphology during LBBB.
Stimulation in other regions of the ventricle may result in a different QRS morphology. If the lead tip is fixed in the septum, the impulse may actually enter the conduction system (His-Purkinje network), which results in rapid impulse transmission and thus shorter QRS duration (as compared with apical pacing).
Because ventricular pacing results in abnormal depolarization, repolarization will also be abnormal, resulting in discordant ST-T segments (i.e the QRS complex and T-wave display opposite directions).
Below follows ECG tracings demonstrating these aspects.
Figure 2. Atrial pacing with normal conduction to the ventricles via the AV system. The ventricles are depolarized via the His-Purkinje network, resulting in normal QRS duration. Figure 3. Spontaneous atrial activity is sensed by the atrial lead and triggers ventricular stimulations. The QRS complex is wide due to ventricular depolarization proceeding outside the conduction system. Figure 4. Pacing in the right atrium and the right ventricle. Figure 5. Atrial fibrillation and third-degree AV block, with ventricular pacing. Figure 6. Missing, or delayed, sinus impulse invokes atrial pacing. Figure 7. AV block (blocked P-wave), invoking ventricular pacing.
The overall goal of performing an ECG is to obtain information about the electrical function of the heart. Medical uses for this information are varied and often need to be combined with knowledge of the structure of the heart and physical examination signs to be interpreted. Some indications for performing an ECG include the following: [ citation needed ]
- Chest pain or suspected myocardial infarction (heart attack), such as ST elevated myocardial infarction (STEMI)  or non-ST elevated myocardial infarction (NSTEMI) 
- Symptoms such as shortness of breath, murmurs, fainting, seizures, funny turns, or arrhythmias including new onset palpitations or monitoring of known cardiac arrhythmias
- Medication monitoring (e.g., drug-induced QT prolongation, Digoxin toxicity) and management of overdose (e.g., tricyclic overdose) , such as hyperkalemia monitoring in which any form of anesthesia is involved (e.g., monitored anesthesia care, general anesthesia). This includes preoperative assessment and intraoperative and postoperative monitoring. (CTA) and magnetic resonance angiography (MRA) of the heart (ECG is used to "gate" the scanning so that the anatomical position of the heart is steady) , in which a catheter is inserted through the femoral vein and can have several electrodes along its length to record the direction of electrical activity from within the heart.
ECGs can be recorded as short intermittent tracings or continuous ECG monitoring. Continuous monitoring is used for critically ill patients, patients undergoing general anesthesia,  and patients who have an infrequently occurring cardiac arrhythmia that would unlikely be seen on a conventional ten-second ECG. Continuous monitoring can be conducted by using Holter monitors, internal and external defibrillators and pacemakers, and/or biotelemetry.
Evidence does not support the use of ECGs among those without symptoms or at low risk of cardiovascular disease as an effort for prevention.    This is because an ECG may falsely indicate the existence of a problem, leading to misdiagnosis, the recommendation of invasive procedures, and overtreatment. However, persons employed in certain critical occupations, such as aircraft pilots,  may be required to have an ECG as part of their routine health evaluations. Hypertrophic cardiomyopathy screening may also be considered in adolescents as part of a sports physical out of concern for sudden cardiac death. [ citation needed ]
Electrocardiograms are recorded by machines that consist of a set of electrodes connected to a central unit.  Early ECG machines were constructed with analog electronics, where the signal drove a motor to print out the signal onto paper. Today, electrocardiographs use analog-to-digital converters to convert the electrical activity of the heart to a digital signal. Many ECG machines are now portable and commonly include a screen, keyboard, and printer on a small wheeled cart. Recent advancements in electrocardiography include developing even smaller devices for inclusion in fitness trackers and smart watches.  These smaller devices often rely on only two electrodes to deliver a single lead I.  Portable six-lead devices are also available.
Recording an ECG is a safe and painless procedure.  The machines are powered by mains power but they are designed with several safety features including an earthed (ground) lead. Other features include:
- protection: any ECG used in healthcare may be attached to a person who requires defibrillation and the ECG needs to protect itself from this source of energy. is similar to defibrillation discharge and requires voltage protection up to 18,000 volts.
- Additionally, circuitry called the right leg driver can be used to reduce common-mode interference (typically the 50 or 60 Hz mains power).
- ECG voltages measured across the body are very small. This low voltage necessitates a low noise circuit, instrumentation amplifiers, and electromagnetic shielding.
- Simultaneous lead recordings: earlier designs recorded each lead sequentially, but current models record multiple leads simultaneously.
Most modern ECG machines include automated interpretation algorithms. This analysis calculates features such as the PR interval, QT interval, corrected QT (QTc) interval, PR axis, QRS axis, rhythm and more. The results from these automated algorithms are considered "preliminary" until verified and/or modified by expert interpretation. Despite recent advances, computer misinterpretation remains a significant problem and can result in clinical mismanagement. 
Electrodes are the actual conductive pads attached to the body surface.  Any pair of electrodes can measure the electrical potential difference between the two corresponding locations of attachment. Such a pair forms a lead. However, "leads" can also be formed between a physical electrode and a virtual electrode, known as Wilson's central terminal (WCT), whose potential is defined as the average potential measured by three limb electrodes that are attached to the right arm, the left arm, and the left foot, respectively. [ citation needed ]
Commonly, 10 electrodes attached to the body are used to form 12 ECG leads, with each lead measuring a specific electrical potential difference (as listed in the table below). 
Leads are broken down into three types: limb augmented limb and precordial or chest. The 12-lead ECG has a total of three limb leads and three augmented limb leads arranged like spokes of a wheel in the coronal plane (vertical), and six precordial leads or chest leads that lie on the perpendicular transverse plane (horizontal). 
In medical settings, the term leads is also sometimes used to refer to the electrodes themselves, although this is technically incorrect. [ citation needed ]
The 10 electrodes in a 12-lead ECG are listed below. 
|Electrode name||Electrode placement|
|RA||On the right arm, avoiding thick muscle.|
|LA||In the same location where RA was placed, but on the left arm.|
|RL||On the right leg, lower end of inner aspect of calf muscle. (Avoid bony prominences)|
|LL||In the same location where RL was placed, but on the left leg.|
|V1||In the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum (breastbone)|
|V2||In the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum.|
|V3||Between leads V2 and V4.|
|V4||In the fifth intercostal space (between ribs 5 and 6) in the mid-clavicular line.|
|V5||Horizontally even with V4, in the left anterior axillary line.|
|V6||Horizontally even with V4 and V5 in the mid-axillary line.|
Two types of electrodes in common use are a flat paper-thin sticker and a self-adhesive circular pad. The former are typically used in a single ECG recording while the latter are for continuous recordings as they stick longer. Each electrode consists of an electrically conductive electrolyte gel and a silver/silver chloride conductor.  The gel typically contains potassium chloride – sometimes silver chloride as well – to permit electron conduction from the skin to the wire and to the electrocardiogram. [ citation needed ]
The common virtual electrode, known as Wilson's central terminal (VW), is produced by averaging the measurements from the electrodes RA, LA, and LL to give an average potential of the body:
In a 12-lead ECG, all leads except the limb leads are assumed to be unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6). The measurement of a voltage requires two contacts and so, electrically, the unipolar leads are measured from the common lead (negative) and the unipolar lead (positive). This averaging for the common lead and the abstract unipolar lead concept makes for a more challenging understanding and is complicated by sloppy usage of "lead" and "electrode". In fact, instead of being a constant reference, VW has a value that fluctuates throughout the heart cycle. It also does not truly represent the center-of-heart potential due to the body parts the signals travel through. 
Limb leads Edit
Leads I, II and III are called the limb leads. The electrodes that form these signals are located on the limbs – one on each arm and one on the left leg.    The limb leads form the points of what is known as Einthoven's triangle. 
- Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode:
- Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode:
- Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode:
Augmented limb leads Edit
Leads aVR, aVL, and aVF are the augmented limb leads. They are derived from the same three electrodes as leads I, II, and III, but they use Goldberger's central terminal as their negative pole. Goldberger's central terminal is a combination of inputs from two limb electrodes, with a different combination for each augmented lead. It is referred to immediately below as "the negative pole".
- Lead augmented vector right (aVR) has the positive electrode on the right arm. The negative pole is a combination of the left arm electrode and the left leg electrode:
- Lead augmented vector left (aVL) has the positive electrode on the left arm. The negative pole is a combination of the right arm electrode and the left leg electrode:
- Lead augmented vector foot (aVF) has the positive electrode on the left leg. The negative pole is a combination of the right arm electrode and the left arm electrode:
Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane. [ citation needed ]
Older versions of the nodes (VR, VL, VF) use Wilson's central terminal as the negative pole, but the amplitude is too small for the thick lines of old ECG machines. The Goldberger terminals scale up (augments) the Wilson results by 50%, at the cost of sacrificing physical correctness by not having the same negative pole for all three. 
Precordial leads Edit
The precordial leads lie in the transverse (horizontal) plane, perpendicular to the other six leads. The six precordial electrodes act as the positive poles for the six corresponding precordial leads: (V1, V2, V3, V4, V5, and V6). Wilson's central terminal is used as the negative pole. Recently, unipolar precordial leads have been used to create bipolar precordial leads that explore the right to left axis in the horizontal plane. 
Specialized leads Edit
Additional electrodes may rarely be placed to generate other leads for specific diagnostic purposes. Right-sided precordial leads may be used to better study pathology of the right ventricle or for dextrocardia (and are denoted with an R (e.g., V5R). Posterior leads (V7 to V9) may be used to demonstrate the presence of a posterior myocardial infarction. A Lewis lead (requiring an electrode at the right sternal border in the second intercostal space) can be used to study pathological rhythms arising in the right atrium. [ citation needed ]
An esophogeal lead can be inserted to a part of the esophagus where the distance to the posterior wall of the left atrium is only approximately 5–6 mm (remaining constant in people of different age and weight).  An esophageal lead avails for a more accurate differentiation between certain cardiac arrhythmias, particularly atrial flutter, AV nodal reentrant tachycardia and orthodromic atrioventricular reentrant tachycardia.  It can also evaluate the risk in people with Wolff-Parkinson-White syndrome, as well as terminate supraventricular tachycardia caused by re-entry. 
An intracardiac electrogram (ICEG) is essentially an ECG with some added intracardiac leads (that is, inside the heart). The standard ECG leads (external leads) are I, II, III, aVL, V1, and V6. Two to four intracardiac leads are added via cardiac catheterization. The word "electrogram" (EGM) without further specification usually means an intracardiac electrogram. [ citation needed ]
Lead locations on an ECG report Edit
A standard 12-lead ECG report (an electrocardiograph) shows a 2.5 second tracing of each of the twelve leads. The tracings are most commonly arranged in a grid of four columns and three rows. The first column is the limb leads (I, II, and III), the second column is the augmented limb leads (aVR, aVL, and aVF), and the last two columns are the precordial leads (V1 to V6). Additionally, a rhythm strip may be included as a fourth or fifth row. [ citation needed ]
The timing across the page is continuous and not tracings of the 12 leads for the same time period. In other words, if the output were traced by needles on paper, each row would switch which leads as the paper is pulled under the needle. For example, the top row would first trace lead I, then switch to lead aVR, then switch to V1, and then switch to V4, and so none of these four tracings of the leads are from the same time period as they are traced in sequence through time. [ citation needed ]
Contiguity of leads Edit
Each of the 12 ECG leads records the electrical activity of the heart from a different angle, and therefore align with different anatomical areas of the heart. Two leads that look at neighboring anatomical areas are said to be contiguous. [ citation needed ]
|Inferior leads||Leads II, III and aVF||Look at electrical activity from the vantage point of the inferior surface (diaphragmatic surface of heart)|
|Lateral leads||I, aVL, V5 and V6||Look at the electrical activity from the vantage point of the lateral wall of left ventricle|
|Septal leads||V1 and V2||Look at electrical activity from the vantage point of the septal surface of the heart (interventricular septum)|
|Anterior leads||V3 and V4||Look at electrical activity from the vantage point of the anterior wall of the right and left ventricles (Sternocostal surface of heart)|
In addition, any two precordial leads next to one another are considered to be contiguous. For example, though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another.
The study of the conduction system of the heart is called cardiac electrophysiology (EP). An EP study is performed via a right-sided cardiac catheterization: a wire with an electrode at its tip is inserted into the right heart chambers from a peripheral vein, and placed in various positions in close proximity to the conduction system so that the electrical activity of that system can be recorded. [ citation needed ]
Interpretation of the ECG is fundamentally about understanding the electrical conduction system of the heart. Normal conduction starts and propagates in a predictable pattern, and deviation from this pattern can be a normal variation or be pathological. An ECG does not equate with mechanical pumping activity of the heart, for example, pulseless electrical activity produces an ECG that should pump blood but no pulses are felt (and constitutes a medical emergency and CPR should be performed). Ventricular fibrillation produces an ECG but is too dysfunctional to produce a life-sustaining cardiac output. Certain rhythms are known to have good cardiac output and some are known to have bad cardiac output. Ultimately, an echocardiogram or other anatomical imaging modality is useful in assessing the mechanical function of the heart. [ citation needed ]
Like all medical tests, what constitutes "normal" is based on population studies. The heartrate range of between 60 and 100 beats per minute (bpm) is considered normal since data shows this to be the usual resting heart rate. [ citation needed ]
Interpretation of the ECG is ultimately that of pattern recognition. In order to understand the patterns found, it is helpful to understand the theory of what ECGs represent. The theory is rooted in electromagnetics and boils down to the four following points:
- depolarization of the heart towards the positive electrode produces a positive deflection
- depolarization of the heart away from the positive electrode produces a negative deflection
- repolarization of the heart towards the positive electrode produces a negative deflection
- repolarization of the heart away from the positive electrode produces a positive deflection
Thus, the overall direction of depolarization and repolarization produces positive or negative deflection on each lead's trace. For example, depolarizing from right to left would produce a positive deflection in lead I because the two vectors point in the same direction. In contrast, that same depolarization would produce minimal deflection in V1 and V2 because the vectors are perpendicular, and this phenomenon is called isoelectric.
Normal rhythm produces four entities – a P wave, a QRS complex, a T wave, and a U wave – that each have a fairly unique pattern.
- The P wave represents atrial depolarization.
- The QRS complex represents ventricular depolarization.
- The T wave represents ventricular repolarization.
- The U wave represents papillary muscle repolarization.
Changes in the structure of the heart and its surroundings (including blood composition) change the patterns of these four entities.
The U wave is not typically seen and its absence is generally ignored. Atrial repolarisation is typically hidden in the much more prominent QRS complex and normally cannot be seen without additional, specialised electrodes.
Background grid Edit
ECGs are normally printed on a grid. The horizontal axis represents time and the vertical axis represents voltage. The standard values on this grid are shown in the adjacent image:
- A small box is 1 mm × 1 mm and represents 0.1 mV × 0.04 seconds.
- A large box is 5 mm × 5 mm and represents 0.5 mV × 0.20 seconds.
The "large" box is represented by a heavier line weight than the small boxes.
Not all aspects of an ECG rely on precise recordings or having a known scaling of amplitude or time. For example, determining if the tracing is a sinus rhythm only requires feature recognition and matching, and not measurement of amplitudes or times (i.e., the scale of the grids are irrelevant). An example to the contrary, the voltage requirements of left ventricular hypertrophy require knowing the grid scale.
Rate and rhythm Edit
In a normal heart, the heart rate is the rate in which the sinoatrial node depolarizes since it is the source of depolarization of the heart. Heart rate, like other vital signs such as blood pressure and respiratory rate, change with age. In adults, a normal heart rate is between 60 and 100 bpm (normocardic), whereas it is higher in children. A heart rate below normal is called "bradycardia" (<60 in adults) and above normal is called "tachycardia" (>100 in adults). A complication of this is when the atria and ventricles are not in synchrony and the "heart rate" must be specified as atrial or ventricular (e.g., the ventricular rate in ventricular fibrillation is 300–600 bpm, whereas the atrial rate can be normal [60–100] or faster [100–150]). [ citation needed ]
In normal resting hearts, the physiologic rhythm of the heart is normal sinus rhythm (NSR). Normal sinus rhythm produces the prototypical pattern of P wave, QRS complex, and T wave. Generally, deviation from normal sinus rhythm is considered a cardiac arrhythmia. Thus, the first question in interpreting an ECG is whether or not there is a sinus rhythm. A criterion for sinus rhythm is that P waves and QRS complexes appear 1-to-1, thus implying that the P wave causes the QRS complex. [ citation needed ]
Once sinus rhythm is established, or not, the second question is the rate. For a sinus rhythm, this is either the rate of P waves or QRS complexes since they are 1-to-1. If the rate is too fast, then it is sinus tachycardia, and if it is too slow, then it is sinus bradycardia.
If it is not a sinus rhythm, then determining the rhythm is necessary before proceeding with further interpretation. Some arrhythmias with characteristic findings:
- Absent P waves with "irregularly irregular" QRS complexes is the hallmark of atrial fibrillation.
- A "saw tooth" pattern with QRS complexes is the hallmark of atrial flutter.
- A sine wave pattern is the hallmark of ventricular flutter.
- Absent P waves with wide QRS complexes and a fast heart rate is ventricular tachycardia.
Determination of rate and rhythm is necessary in order to make sense of further interpretation.
The heart has several axes, but the most common by far is the axis of the QRS complex (references to "the axis" imply the QRS axis). Each axis can be computationally determined to result in a number representing degrees of deviation from zero, or it can be categorized into a few types. [ citation needed ]
The QRS axis is the general direction of the ventricular depolarization wavefront (or mean electrical vector) in the frontal plane. It is often sufficient to classify the axis as one of three types: normal, left deviated, or right deviated. Population data shows that a normal QRS axis is from −30° to 105°, with 0° being along lead I and positive being inferior and negative being superior (best understood graphically as the hexaxial reference system).  Beyond +105° is right axis deviation and beyond −30° is left axis deviation (the third quadrant of −90° to −180° is very rare and is an indeterminate axis). A shortcut for determining if the QRS axis is normal is if the QRS complex is mostly positive in lead I and lead II (or lead I and aVF if +90° is the upper limit of normal). [ citation needed ]
The normal QRS axis is generally down and to the left, following the anatomical orientation of the heart within the chest. An abnormal axis suggests a change in the physical shape and orientation of the heart or a defect in its conduction system that causes the ventricles to depolarize in an abnormal way. [ citation needed ]
|Normal||−30° to 105°||Normal|
|Left axis deviation||−30° to −90°||May indicate left ventricular hypertrophy, left anterior fascicular block, or an old inferior STEMI|
|Right axis deviation||+105° to +180°||May indicate right ventricular hypertrophy, left posterior fascicular block, or an old lateral STEMI|
|Indeterminate axis||+180° to −90°||Rarely seen considered an 'electrical no-man's land'|
The extent of a normal axis can be +90° or 105° depending on the source.
Amplitudes and intervals Edit
All of the waves on an ECG tracing and the intervals between them have a predictable time duration, a range of acceptable amplitudes (voltages), and a typical morphology. Any deviation from the normal tracing is potentially pathological and therefore of clinical significance. [ citation needed ]
For ease of measuring the amplitudes and intervals, an ECG is printed on graph paper at a standard scale: each 1 mm (one small box on the standard ECG paper) represents 40 milliseconds of time on the x-axis, and 0.1 millivolts on the y-axis. [ citation needed ]
|P wave||The P wave represents depolarization of the atria. Atrial depolarization spreads from the SA node towards the AV node, and from the right atrium to the left atrium.||The P wave is typically upright in most leads except for aVR an unusual P wave axis (inverted in other leads) can indicate an ectopic atrial pacemaker. If the P wave is of unusually long duration, it may represent atrial enlargement. Typically a large right atrium gives a tall, peaked P wave while a large left atrium gives a two-humped bifid P wave.||<80 ms|
|PR interval||The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. This interval reflects the time the electrical impulse takes to travel from the sinus node through the AV node.||A PR interval shorter than 120 ms suggests that the electrical impulse is bypassing the AV node, as in Wolf-Parkinson-White syndrome. A PR interval consistently longer than 200 ms diagnoses first degree atrioventricular block. The PR segment (the portion of the tracing after the P wave and before the QRS complex) is typically completely flat, but may be depressed in pericarditis.||120 to 200 ms|
|QRS complex||The QRS complex represents the rapid depolarization of the right and left ventricles. The ventricles have a large muscle mass compared to the atria, so the QRS complex usually has a much larger amplitude than the P wave.||If the QRS complex is wide (longer than 120 ms) it suggests disruption of the heart's conduction system, such as in LBBB, RBBB, or ventricular rhythms such as ventricular tachycardia. Metabolic issues such as severe hyperkalemia, or tricyclic antidepressant overdose can also widen the QRS complex. An unusually tall QRS complex may represent left ventricular hypertrophy while a very low-amplitude QRS complex may represent a pericardial effusion or infiltrative myocardial disease.||80 to 100 ms|
|J-point||The J-point is the point at which the QRS complex finishes and the ST segment begins.||The J-point may be elevated as a normal variant. The appearance of a separate J wave or Osborn wave at the J-point is pathognomonic of hypothermia or hypercalcemia. |
|ST segment||The ST segment connects the QRS complex and the T wave it represents the period when the ventricles are depolarized.||It is usually isoelectric, but may be depressed or elevated with myocardial infarction or ischemia. ST depression can also be caused by LVH or digoxin. ST elevation can also be caused by pericarditis, Brugada syndrome, or can be a normal variant (J-point elevation).|
|T wave||The T wave represents the repolarization of the ventricles. It is generally upright in all leads except aVR and lead V1.||Inverted T waves can be a sign of myocardial ischemia, left ventricular hypertrophy, high intracranial pressure, or metabolic abnormalities. Peaked T waves can be a sign of hyperkalemia or very early myocardial infarction.||160 ms|
|Corrected QT interval (QTc)||The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Acceptable ranges vary with heart rate, so it must be corrected to the QTc by dividing by the square root of the RR interval.||A prolonged QTc interval is a risk factor for ventricular tachyarrhythmias and sudden death. Long QT can arise as a genetic syndrome, or as a side effect of certain medications. An unusually short QTc can be seen in severe hypercalcemia.||<440 ms|
|U wave||The U wave is hypothesized to be caused by the repolarization of the interventricular septum. It normally has a low amplitude, and even more often is completely absent.||A very prominent U wave can be a sign of hypokalemia, hypercalcemia or hyperthyroidism. |
Limb leads and electrical conduction through the heart Edit
The animation shown to the right illustrates how the path of electrical conduction gives rise to the ECG waves in the limb leads. Recall that a positive current (as created by depolarization of cardiac cells) traveling towards the positive electrode and away from the negative electrode creates a positive deflection on the ECG. Likewise, a positive current traveling away from the positive electrode and towards the negative electrode creates a negative deflection on the ECG.   The red arrow represents the overall direction of travel of the depolarization. The magnitude of the red arrow is proportional to the amount of tissue being depolarized at that instance. The red arrow is simultaneously shown on the axis of each of the 3 limb leads. Both the direction and the magnitude of the red arrow's projection onto the axis of each limb lead is shown with blue arrows. Then, the direction and magnitude of the blue arrows are what theoretically determine the deflections on the ECG. For example, as a blue arrow on the axis for Lead I moves from the negative electrode, to the right, towards the positive electrode, the ECG line rises, creating an upward wave. As the blue arrow on the axis for Lead I moves to the left, a downward wave is created. The greater the magnitude of the blue arrow, the greater the deflection on the ECG for that particular limb lead. [ citation needed ]
Frames 1–3 depict the depolarization being generated in and spreading through the Sinoatrial node. The SA node is too small for its depolarization to be detected on most ECGs. Frames 4–10 depict the depolarization traveling through the atria, towards the Atrioventricular node. During frame 7, the depolarization is traveling through the largest amount of tissue in the atria, which creates the highest point in the P wave. Frames 11–12 depict the depolarization traveling through the AV node. Like the SA node, the AV node is too small for the depolarization of its tissue to be detected on most ECGs. This creates the flat PR segment. 
Frame 13 depicts an interesting phenomenon in an over-simplified fashion. It depicts the depolarization as it starts to travel down the interventricular septum, through the Bundle of His and Bundle branches. After the Bundle of His, the conduction system splits into the left bundle branch and the right bundle branch. Both branches conduct action potentials at about 1 m/s. Interestingly, however, the action potential starts traveling down the left bundle branch about 5 milliseconds before it starts traveling down the right bundle branch, as depicted by frame 13. This causes the depolarization of the interventricular septum tissue to spread from left to right, as depicted by the red arrow in frame 14. In some cases, this gives rise to a negative deflection after the PR interval, creating a Q wave such as the one seen in lead I in the animation to the right. Depending on the mean electrical axis of the heart, this phenomenon can result in a Q wave in lead II as well.  
Following depolarization of the interventricular septum, the depolarization travels towards the apex of the heart. This is depicted by frames 15–17 and results in a positive deflection on all three limb leads, which creates the R wave. Frames 18–21 then depict the depolarization as it travels throughout both ventricles from the apex of the heart, following the action potential in the Purkinje fibers. This phenomenon creates a negative deflection in all three limb leads, forming the S wave on the ECG. Repolarization of the atria occurs at the same time as the generation of the QRS complex, but it is not detected by the ECG since the tissue mass of the ventricles is so much larger than that of the atria. Ventricular contraction occurs between ventricular depolarization and repolarization. During this time, there is no movement of charge, so no deflection is created on the ECG. This results in the flat ST segment after the S wave.
Frames 24–28 in the animation depict repolarization of the ventricles. The epicardium is the first layer of the ventricles to repolarize, followed by the myocardium. The endocardium is the last layer to repolarize. The plateau phase of depolarization has been shown to last longer in endocardial cells than in epicardial cells. This causes repolarization to start from the apex of the heart and move upwards. Since repolarization is the spread of negative current as membrane potentials decrease back down to the resting membrane potential, the red arrow in the animation is pointing in the direction opposite of the repolarization. This therefore creates a positive deflection in the ECG, and creates the T wave. 
Ischemia and infarction Edit
Ischemia or non-ST elevation myocardial infarctions (non-STEMIs) may manifest as ST depression or inversion of T waves. It may also affect the high frequency band of the QRS.
ST elevation myocardial infarctions (STEMIs) have different characteristic ECG findings based on the amount of time elapsed since the MI first occurred. The earliest sign is hyperacute T waves, peaked T waves due to local hyperkalemia in ischemic myocardium. This then progresses over a period of minutes to elevations of the ST segment by at least 1 mm. Over a period of hours, a pathologic Q wave may appear and the T wave will invert. Over a period of days the ST elevation will resolve. Pathologic Q waves generally will remain permanently. 
The coronary artery that has been occluded can be identified in an STEMI based on the location of ST elevation. The left anterior descending (LAD) artery supplies the anterior wall of the heart, and therefore causes ST elevations in anterior leads (V1 and V2). The LCx supplies the lateral aspect of the heart and therefore causes ST elevations in lateral leads (I, aVL and V6). The right coronary artery (RCA) usually supplies the inferior aspect of the heart, and therefore causes ST elevations in inferior leads (II, III and aVF). [ citation needed ]
An ECG tracing is affected by patient motion. Some rhythmic motions (such as shivering or tremors) can create the illusion of cardiac arrhythmia.  Artifacts are distorted signals caused by a secondary internal or external sources, such as muscle movement or interference from an electrical device.  
Distortion poses significant challenges to healthcare providers,  who employ various techniques  and strategies to safely recognize  these false signals. [ medical citation needed ] Accurately separating the ECG artifact from the true ECG signal can have a significant impact on patient outcomes and legal liabilities.  [ unreliable medical source? ]
Improper lead placement (for example, reversing two of the limb leads) has been estimated to occur in 0.4% to 4% of all ECG recordings,  and has resulted in improper diagnosis and treatment including unnecessary use of thrombolytic therapy.  
Numerous diagnoses and findings can be made based upon electrocardiography, and many are discussed above. Overall, the diagnoses are made based on the patterns. For example, an "irregularly irregular" QRS complex without P waves is the hallmark of atrial fibrillation however, other findings can be present as well, such as a bundle branch block that alters the shape of the QRS complexes. ECGs can be interpreted in isolation but should be applied – like all diagnostic tests – in the context of the patient. For example, an observation of peaked T waves is not sufficient to diagnose hyperkalemia such a diagnosis should be verified by measuring the blood potassium level. Conversely, a discovery of hyperkalemia should be followed by an ECG for manifestations such as peaked T waves, widened QRS complexes, and loss of P waves. The following is an organized list of possible ECG-based diagnoses. [ citation needed ]
Electrocardiogram (ECG or EKG)
The electrocardiogram (ECG or EKG) is a noninvasive test that is used to reflect underlying heart conditions by measuring the electrical activity of the heart. By positioning leads (electrical sensing devices) on the body in standardized locations, health care professionals can learn information about many heart conditions by looking for characteristic patterns on the EKG.
What does an ECG (EKG) measure? What heart problems can it diagnose?
The EKG measures:
- The underlying rate and rhythm mechanism of the heart
- The orientation of the heart (how it is placed) in the chest cavity
- Evidence of increased thickness (hypertrophy) of the heart muscle
- Evidence of damage to the various parts of the heart muscle
- Evidence of acutely impaired blood flow to the heart muscle
- Patterns of abnormal electric activity that may predispose the patient to abnormal cardiac rhythm disturbances
Electrocardiograms can diagnose:
- Abnormally fast or irregular heart rhythms
- Abnormally slow heart rhythms
- Abnormal conduction of cardiac impulses, which may suggest underlying cardiac or metabolic disorders
- Evidence of the occurrence of a prior heart attack (myocardial infarction)
- Evidence of an evolving, acute heart attack
- Evidence of an acute impairment to blood flow to the heart during an episode of a threatened heart attack (unstable angina)
- Adverse effects on the heart from various heart diseases or systemic diseases (such as high blood pressure, thyroid conditions, etc.)
- Adverse effects on the heart from certain lung conditions (such as emphysema, pulmonary embolus [blood clots to lung])
- Certain congenital heart abnormalities
- Evidence of abnormal blood electrolytes (potassium, calcium, magnesium)
- Evidence of inflammation of the heart or its lining (myocarditis, pericarditis)
What Does an EKG Test For?
What Are Heart Disease Types?
Heart disease refers to various types of conditions that can affect heart function. These types include:
- Coronary artery (atherosclerotic) heart disease that affects the arteries to the heart
- Valvular heart disease that affects how the valves function to regulate blood flow in and out of the heart
- Cardiomyopathy that affects how the heart muscle squeezes
- Heart rhythm disturbances (arrhythmias) that affect the electrical conduction
- Heart infections where the heart has structural problems that develop before birth
How do I prepare for an ECC (EKG)?
EKG leads are attached to the body while the patient lies flat on a bed or table. Leads are attached to each extremity (four total) and to six pre-defined positions on the front of the chest. A small amount of gel is applied to the skin, which allows the electrical impulses of the heart to be more easily transmitted to the EKG leads. The leads are attached by small suction cups, Velcro straps, or by small adhesive patches attached loosely to the skin. The test takes about five minutes and is painless. In some instances, men may require the shaving of a small amount of chest hair to obtain optimal contact between the leads and the skin.
Why is it done?
An ECG gives two major kinds of information. First, by measuring time intervals on the ECG, a doctor can determine how long the electrical wave takes to pass through the heart. Finding out how long a wave takes to travel from one part of the heart to the next shows if the electrical activity is normal or slow, fast or irregular. Second, by measuring the amount of electrical activity passing through the heart muscle, a cardiologist may be able to find out if parts of the heart are too large or are overworked.
Abstract—To clarify the source of electrocardiographic ST depression associated with ischemia, a sheep model of subendocardial ischemia was developed in which simultaneous epicardial and endocardial ST potentials were mapped, and a computer model using the bidomain technique was developed to explain the results. To produce ischemia in different territories of the myocardium in the same animal, the left anterior descending coronary artery and left circumflex coronary artery were partially constricted in sequence. Results from 36 sheep and the computer simulation are reported. The distributions of epicardial potentials from either ischemic source were very similar (r=0.77±0.14, P<0.0001), with both showing ST depression on the free wall of the left ventricle and no association between the ST depression and the ischemic region. However, endocardial potentials showed that ST elevation was directly associated with the region of reduced blood flow. Insulating the heart from the surrounding tissue with plastic increased the magnitude of epicardial ST potentials, which was consistent with an intramyocardial source. Increasing the percent stenosis of a coronary artery increased epicardial ST depression at the lateral boundary and resulted in ST elevation starting from the ischemic center as ischemia became transmural. Computer simulation using the bidomain model reproduced the epicardial ST patterns and suggested that the ST depression was generated at the lateral boundary between ischemic and normal territories. ST depression on the epicardium reflected the position of this lateral boundary. The boundaries of ischemic territories are shared, and only those appearing on the free wall contribute to external ST potential fields. These effects explain why body surface ST depression does not localize cardiac ischemia in humans.
Electrocardiographic ST-segment depression has long been recognized as a sign of ischemia, 1 2 but the explanations of the responsible mechanisms have been controversial. 3 4 5 6 Much of the current opinion regarding the genesis of ST-segment depression is derived from interpretations based on certain theoretical considerations 7 8 and indirect evidence from animal experiments. 1 2 Ischemic muscle generates intracellular currents, which effectively cause TQ depression and ST elevation over the ischemic area 9 10 and which conventional electrocardiography with AC-coupled amplifiers reflects as ST elevation. ST-segment depression recorded at the epicardium has been considered to be secondary to an injury current in the underlying subendocardium. 11 12 13 14
In conventional stress testing, as myocardial demand exceeds the ability of the narrowed coronary arterial bed to increase blood flow, the ischemic threshold is exceeded, and reversible ST-segment depression is produced. However, the location of this ST depression does not enable us to localize the ischemic region. 15 16 17 18 19 The difficulty in localizing myocardial ischemia from ST depression cannot be explained by the classic theories, 7 8 20 21 which all suggest that ST depression should provide the means for localizing ischemia. Studies 22 of computer-derived epicardial maps in patients with inferior infarction and patients having ST depression without infarction have hypothesized that ST depression on the ECG originates from current flow from a region of endocardial ischemia and progresses back to the outside of the heart through the great vessels and atria. To test this hypothesis, we measured the epicardial and endocardial potential distributions in the in vivo sheep heart after generating regional subendocardial ischemia, which was confirmed by fluorescent microspheres. A computer bidomain model was developed to explain the experimental results.
Materials and Methods
A total of 36 Polworth/Comeback cross sheep (30 to 45 kg) of both sexes were used in this study. Table 1 shows the groups of animals subjected to different experimental procedures.
In group 1 (control, n=5), the epicardial ST potential fields were recorded before and during pacing at a rate of 120, 140, 160, 180, 220, and 240 bpm, and the RMBF was measured before and during pacing at the set rate of 180 bpm.
Group 2: Partial Occlusion of Either LCX or LAD in Different Animals With Interventions
In group 2, either the LAD or the LCX was partial occluded (LAD occlusion, n=3 LCX occlusion, n=14). The epicardial ST potential distributions were recorded before and after 2, 5, 10, 15, and 20 minutes of ischemia. The endocardial electrograms were simultaneously recorded by a quadripolar electrode catheter. The following tests were performed to investigate the nature of the ischemic source after the production of subendocardial ischemia:
(1) Insulating the Heart From Surrounding Tissues (n=8).
A thin plastic bag was placed onto the heart, covering the right and left ventricles and portions of both atria, to insulate the heart from the surrounding tissues during ischemia. The epicardial ST potential changes were recorded. The insulator was quickly removed, and the potentials were again recorded and compared with those during insulation. The time difference between the two recordings was ≈10 seconds.
(2) Transforming Subendocardial Ischemia to Full-Thickness Ischemia (n=5).
The percent stenosis of a coronary artery was increased by fully inflating the hydraulic occluder at 10 to 15 minutes of partial coronary occlusion to transform the subendocardial ischemia to full-thickness ischemia. In 2 animals, the potential changes were recorded before and 2, 30, 60, 90, and 120 seconds after the transition. In another 3 animals, the potential changes during the transition were recorded continuously for a period of 30 seconds (n=2) and 50 seconds (n=1).
Group 3: Alternate LAD and LCX Partial Occlusion in the Same Animal
In group 3 (n=6), posterior subendocardial ischemia and anterior subendocardial ischemia were produced in the same animal by alternate partial occlusion of the LAD and the LCX plus pacing. Each partial occlusion lasted for 20 minutes, followed by 30 minutes of rest before the next partial occlusion (the flow and pressure returned to the control level after 30 minutes of rest). The epicardial potential maps were constructed, and the epicardial potential distributions between these two types of ischemia were compared.
Group 4: Epicardial and Endocardial Potential Mapping in Relation to RMBF
In group 4 (n=8), the subendocardial ischemia production was similar to that in group 3 ie, there was alternate LAD and LCX occlusion in the same animal. Both the epicardial and the endocardial ST potentials were then recorded and compared. The RMBF was measured before and during ischemia, and the flow maps were constructed.
Anesthesia was induced intravenously with sodium pentobarbital (30 mg/kg) and then maintained at 3 to 8 mg/kg per hour throughout the experiment. The animals were artificially ventilated at a rate of 18 to 20 breaths/min with room air. The animals were heparinized before instrumentation. A left thoracotomy was performed in the fourth intercostal space, and the heart was suspended in a pericardial cradle. The left ventricular pressure was measured by a 7F side-hole catheter introduced into the left ventricular cavity retrogradely from a femoral artery approach. The LCX and the LAD were each isolated proximally near their origin for the electromagnetic flow transducer (NARCO, Carolina Medical Inc) for blood flow measurement and, again, 10 to 20 mm distally for the hydraulic occluder (In Vivo Metric) for inducing arterial stenosis. Another cannula (PE-90) was inserted through the left atrial appendage into the left atrium for microsphere injection. Two pacing wires were sutured to the left atrial appendage for left atrial pacing.
The subendocardial ischemic sheep model, combining pacing with partial occlusion of an artery, was previously validated in our laboratory by fluorescent microspheres. 23 In brief, stenosis was achieved by inflating the hydraulic occluder, causing a reduction in flow to ∼50% of the control level, and then the left atrium was paced by a stimulator (SRI, Scientific and Research Instruments Ltd). The pacing started with a rate of 120 bpm and increased gradually by 10 bpm every 2 minutes until it reached 180 bpm.
Perfusion Beds and RMBF Measurement
RMBF was measured before ischemia and at 20 minutes of ischemia by using fluorescent microspheres (Molecular Probes, Inc) as previously described. 23 The fluorescent microsphere suspension was mixed with 10 mL of warm blood, and the mixture was administered over 10 seconds via the implanted left atrial cannula. The cannula was then flushed with 10 mL of saline. The reference flow was established using an in-line electromagnetic flow transducer. After completion of the experiment, 10 mL of 0.1% methylene blue dye (Sigma) was injected into the LAD, and 10 mL of normal saline was simultaneously injected into the LCX to delineate the nonischemic and the ischemic areas, depending on which coronary artery was stenosed. These data were used to support the measurement of regional myocardial blood flow as displayed in Figures 2 and 5 . The ischemic boundary was expected to be well defined in the absence of functionally significant collateral blood vessels. 24 The left ventricle was divided into three to five circumferential rings from the base to the apex. The circumferential rings were then cut into sections of epicardial arc (length, 12 mm per piece). Sections of the myocardium were divided into endocardial, middle, and epicardial thirds. The anatomic location of each myocardial piece was recorded on the tracing of the left ventricle wall and related to the positions of the electrodes, so that potential and flow mapping could be made (see below). The dimensions of each piece were roughly 12×10×3 mm 3 . The LCX- and the LAD-supplied areas were cut into 30 pieces on average. The average weight of each piece was 1.1 g (0.5 to 1.5 g). Each sample was placed into a screw-cap polystyrene tube to which 2 mL of 4 mol/L KOH was added, and the tube was placed in a 37°C water bath for 12 hours. After digestion, 3 mL of ethyl acetate was added, and the tube was vortexed for 1 minute and then centrifuged for 2 minutes at 2500 rpm. The upper layer of solvent was transferred to a quartz cuvette, where fluorescence intensity was read at the appropriate wavelengths by a Perkin-Elmer 650-10S fluorescence spectrophotometer (Hitachi Ltd).
RMBF in each sample was expressed both in absolute terms (as milliliters per minute per gram of myocardium) and in relative terms (as a percentage of the control flow obtained before ischemia). The endo/epi flow ratio was obtained by dividing the flow to the endocardial third by the flow to the epicardial third. After the flow for each sample was calculated, maps of the left ventricular blood flow were constructed from both the absolute flow and the relative flow. The flow maps were combined with the endocardial contour potential maps.
Epicardial and Endocardial Potential Recording
The epicardial potentials were recorded using an epicardial sock containing 64 electrodes (Cardiovascular Research and Training Institute, University of Utah, Salt Lake City). Each electrode was constructed of fine silver wire mounted in a nylon sock. The arrangement of the 64 electrodes provided extensive coverage of the epicardial surface of the left and right ventricles (Figure 1 ). Endocardial electrograms were recorded using a home-made 40-electrode basket mapping apparatus. The apparatus was oval-shaped and constructed with spring steel wire (diameter, 0.25 mm) as the skeleton and polyethylene tube (outer diameter, 1.27 mm) as the outer covering, on which 40 silver electrodes were mounted. The steel skeleton consisted of eight arms. Each arm was insulated with a polyethylene tube and mounted with five unipolar silver electrodes (0.15×4 mm). To avoid injury current, the electrodes were mounted on the inside of the cage in such a manner that they were not in direct contact with the endocardium. The eight arms were at equal distance and were connected to each other at both ends, so that when the apparatus was expanded, a uniform distribution of electrodes resulted. Two arms were marked with different colors for orientation. The apparatus was 50 mm long and 32 mm across when fully opened. Placement of the apparatus was accomplished by using thin-wall tubing (inserter) with an outer diameter of 8 mm via the apex. The closed apparatus was placed inside the inserter, and a left apical ventriculotomy of ≈10 mm was performed. The inserter was introduced into the apex, and the apparatus was placed into the left ventricle while the inserter was withdrawn. The apparatus was secured by a purse-string suture around the point of insertion. The time for positioning the apparatus was a matter of seconds. Once inside the left ventricle, the apparatus deploys, placing the eight arms into position, with each maintaining constant contact with the endocardium. The electrodes were not in direct contact with the endocardium, but they detected the potential changes from the nearest endocardium. At the end of each experiment, the sheep was killed, and the heart was opened to verify the positions of the electrodes. The electrode positions corresponded to the tissue samples subsequently taken for measurement of RMBF, so that the ST-segment changes after coronary artery occlusion could be correlated with the blood flow of each sample. From the postmortem examination, the distance between the electrodes and the endocardium ranged from 1.3 to 3.0 mm.
Initial experiments comparing the noncontact electrodes with contact electrodes showed barely detectable differences in QRS amplitude between the two but no ST-segment shifts in the noncontact electrodes. From the computed intracavity potential fields, one would expect the only significant change over 3 mm to occur at the boundary where a powerful dipole exists. The apparatus enabled the authors to record the signal from a working heart and to map the whole endocardial surface at one time, although at a moderate spatial resolution. The apparatus removes the difficulties of conventional methods and makes it possible to record the potential while ischemia has been induced with the heart in situ.
Hemodynamic measurements of LV pressure and heart rate in our experiments confirmed that the insertion of the 40-pole intracavity electrodes into the left ventricle did not cause significant hemodynamic deterioration (Table 2 ). The electrodes did not provoke arrhythmias or injury currents, and they remained in their positions throughout the experiments. The quality of all unipolar electrical signals remained satisfactory.
The potentials were sampled simultaneously at 1000 samples per second per channel by a 128-channel data acquisition system directly onto computer memory through an S11W (Engineering Design Team, Inc) interface to a portable computer based on Sbus (BriteLite RDI Computer Corp). 25 All data were recorded with 12 bits and a bandwidth of 0.1 to 500 Hz. Individual gains could be set for each channel, but for these experiments the gain was the same for all channels. All the potentials were recorded in reference to the left leg. An instant display of the sampled ECG signals enabled a check on the quality of the data. During data acquisition, the opening in the chest wall was covered by moisturized warm saline pads not touching the myocardium. To avoid the interference of injury currents, we obtained recordings at least 20 minutes after setting up, when the ST-T shifts had disappeared almost completely.
Construction of Isopotential Maps and Map Display
At the termination of each experiment, the sheep was killed, and the heart carefully removed from the chest cavity. After marking the epicardial electrode position with mapping pins, the heart was opened, and the endocardial electrode positions were verified and marked. The electrode positions corresponded to the tissue samples subsequently taken for measurement of RMBF, so that the ST-segment changes after the coronary artery occlusion could be correlated with the blood flow of each sample. By making an incision from the posterior edge to the apex, the ventricles could be opened flat (for endocardial mapping, the incision was made from the middle of the septum). The electrode positions, the epicardial vascular patterns, and the outlines of the ventricles were traced on transparent plastic and transferred to paper, where the coordinates of the whole picture were measured and reconstructed using our own mapping program and the S-Plus statistical package. The picture was then combined with the ST potential contour map to give either an epicardial or an endocardial potential map as illustrated in Figure 1 . For each sheep, detailed epicardial maps were built from both the left and right ventricular potentials. In 8 sheep, detailed endocardial maps were constructed from the endocardial potentials of the left ventricle recorded at 20 minutes of ischemia. The endocardial potential maps were then combined with the flow maps constructed from the simultaneously measured RMBF.
The electrograms were plotted, and their quality was evaluated. Missing or poor electrograms were discarded, with between 3% and 10% (average, 6%) being discarded as bad leads. These bad leads were picked out and replaced by interpolation from the surrounding leads. The onset of the QRS complex was chosen manually from plots, and potentials during a 10-millisecond portion of the PR segment were averaged for use as a zero-potential reference level. The ST-segment maps were each constructed from data averaged over a 20-millisecond interval centered on a point 80 milliseconds after the QRS onset (the QRS interval of the sheep is shorter than that in the humans, ≈40 milliseconds). The ST-segment potential distributions were displayed as isopotential contour maps in the format shown in Figure 1 . Isopotential contours were drawn at 1- to 2-mV intervals using linear interpolation. All maps displayed are difference maps computed by subtracting the control (preischemic) values from the ischemic values for each map site.
Data Analysis and Statistics
Left ventricular pressure, left atrial pressure, and coronary flows were recorded on a multichannel recorder (Grass Instrument Co) they were also recorded by a Macintosh II computer via an analog-to-digital converter (NB-DMA-8 and NI-488 for Mac-SN 3643 and Labview software, National Instruments Corp) at a sampling rate of 100 Hz. All data points were averaged over at least 40 cardiac cycles and were processed by a SUN workstation (SUN Microsystems, Inc).
Results were expressed as mean±SD. Hemodynamic data were analyzed by two-tailed Student paired t test with the 0.05 level of probability considered as being significant. The correlation coefficient (r) was used to analyze the similarity between two potential distributions. In all correlations, the recorded signals were used without interpolation, and it was assumed that the electrode arrays had not shifted throughout the procedure. Epicardial and endocardial arrays were tested separately. The resulting correlation coefficient is between −1 and 1, with the correlation coefficient approaching 1 if the data sets are identically shaped and a zero correlation coefficient if there is no association between the two data sets. This technique has been used previously for analyzing body surface map data. 26
Endocardial and epicardial potentials were simulated in a bidomain model of an isolated heart. The ischemic region was constructed from the measurements of RMBF during observed subendocardial ischemia. 23
Bidomain Model and the Source
The myocardium was represented by the bidomain model, in which intracellular and extracellular volumes occupy the same space and were separated everywhere by the membrane. According to previous studies, 21 27 the intracellular potential (Φi) and the extracellular potential (Φe) are governed by the following equations:
The ST segment corresponds to the plateau phase of the action potential. In the normal ECG, the ST segment remains isoelectric because of the zero source (no spatial gradient). When ischemia occurs, the transmembrane potential of injury cells changes, producing nonzero source in the injury boundary, which, in turn, gives rise to ST-segment shifts.
According to the divergence theorem, if there is no current flowing out of the heart (body) surface, the net source in the volume must be zero. In case of subendocardial ischemia, the positive source takes less space than does the negative source, so the positive source must be stronger than the negative one. If the myocardium is assumed to be isotropic, the source is a dipole layer type, but one with different strengths for negative and positive sources.
From Equation 2 , one can see that intracellular conductivity, ςi affects the source directly, and the myocardial bulk conductivity, ς, affects the potential field as the property of a part of the volume conductor. The intracellular conductivity, ςi, used in this model was 0.175 S/m the myocardial bulk conductivity, ς, was 0.244 S/m 28 and blood conductivity was 0.67 S/m. 29
We simulated only the true ST-segment shift for which the reduction of transmembrane potentials during plateau phase is responsible. According to our experimental measurements of the RMBF, we assumed that the epicardial layer of the “ischemic” region is normal tissue, the middle layer is transition zone, and the endocardial layer is the ischemic zone. Since the transmembrane potential (during plateau phase) in early transmural ischemia is reduced to −40 mV while the normal cells remain at −10 mV, 9 30 in our model in which ischemia was less severe, we assumed that the transmembrane potential during the plateau phase was −30 mV for ischemic cells and −10 mV for normal cells and that the potential changed linearly from −30 to −10 mV for myocardial cells in the transition zone.
It is currently accepted that there is a sharp interface (1 to 2 mm) 31 between ischemic and nonischemic regions in the lateral boundary, whereas there is a gradual ischemic change in the transmural boundary. 32 We ignored the difference between the transmural boundary and lateral boundary for the convenience of mathematical calculation. The boundary transitional zone was assumed to be 2 mm in both transmural and lateral boundaries in the simulations.
In this study, the geometry of the heart of a normal 58-year-old woman was constructed from a magnetic resonance imaging scan. It includes the atria, the ventricles, the myocardium, part of the inferior and superior vena cava, the pulmonary artery, and the aorta. Subendocardial ischemia from two different arterial territories was simulated. According to our RMBF measurement, for either the LAD or the LCX occlusion, almost half of the left ventricle was involved. Since the ischemic region incorporated only the endocardial area supplied by the involved artery, the ischemic boundaries included the transmural boundary (parallel to the epicardium) and the lateral boundaries (perpendicular to the epicardium). The lateral boundaries were in the central septum on one side, and the left free wall was on the other. Both ischemic regions share the same lateral ischemic boundaries.
A numerical method, the finite-element method, was used to solve Equation 2 . Eight-node brick elements were used to mesh the heart, which was divided into 60 661 elements (2×2×2 mm 3 ). The source was calculated from the width of the boundary, the given conductivity, and transmembrane potentials as discussed above. The source values were assigned to the corresponding elements. To be able to obtain a unique solution of Equation 2 , an inner node was assigned to a given potential. To simulate the Wilson terminal, the mean potential on the epicardium served as a reference potential to present ECG data.
RMBF and Hemodynamic Response
The flow and the hemodynamic responses to pacing and ischemia are shown in Tables 2 and 3 . Pacing alone to the rate of 180 bpm had no significant effect on the left ventricular pressures and the mean left atrial pressure but increased the anterograde coronary flow (Table 2 ). The RMBF to each third of the myocardium was also increased during pacing (Table 3 ). The increase to the epicardial third was slightly higher than that to the endocardial third, but the endo/epi flow ratio reduction was not significant (P>0.05).
Stenosis with tachycardia caused a marked decrease in flow to the endocardial third of the ischemic area (from 1.19±0.28 to 0.64±0.22 mL · min −1 · g −1 , P<0.001 averaging of the LAD and the LCX occlusion values), whereas flow to the epicardial third had a less significant change (from 0.99±0.22 to 0.80±0.19 mL · min −1 · g −1 , P<0.05) (Table 3 ). The endo/epi flow ratios (Table 3 ) in the ischemic area decreased from 1.23±0.21 to 0.80±0.17 (P<0.001) at 20 minutes of ischemia. The ratio in the nonischemic region was unchanged (from 1.23±0.17 to 1.12±0.25, P=NS). The ischemia was accompanied by a marginal increase in the left ventricular end-diastolic pressure and a decrease in the left ventricular systolic pressure (both P=0.01, Table 2 ). In the nonischemic area, there was also a mild decrease in the RMBF in all the animals, but the change was not significant (Table 3 ).
Figure 2 displays the spatial flow distributions across the left ventricular wall before and during LAD occlusion. It was plotted with the RMBF data of one experiment from group 4. Before ischemia (control), there were marked variations of RMBF from piece to piece within a layer and from layer to layer across the ventricular wall. Generally speaking, flow to the inner layer was higher than flow to the outer layer. During ischemia, flow to the ischemic regions decreased, with the maximum reduction in the inner layer and the minimum reduction in the outer layer. This disproportionate flow reduction produced a gradual flow transition from the endocardium to the epicardium.
Epicardial Potential Distributions
During pacing alone, the magnitude of ST potentials and their spatial features did not change until a pacing rate of 240 bpm was reached. When the pacing rate reached 240 bpm, minor ST depression (with a peak magnitude of −4 mV) occurred over the anterior region and the apex in 3 of the 5 sheep. In the rest of the sheep, ST potential did not change even when the heart was paced to 240 bpm.
From group 2, in which either the LAD or the LCX was partial occluded in different animals, we recorded general ST depression with maximum change in the anterolateral wall of the left ventricle, and the potential distribution was similar in various subendocardial ischemic locations. When alternate LAD and LCX partial occlusions were tested in the same animal (group 3), we obtained even more similar ST potential patterns during ischemia. Representative maps of epicardial ST potential distributions from three typical experiments are displayed in Figure 3 . The epicardial ST potential change in each individual electrode position during the LAD occlusion was compared with that during the LCX occlusion. When such potential changes from the 64 electrode positions in each of 6 sheep of group 3 were tested, we obtained a correlation coefficient of 0.77±0.14 on average (ranging from 0.66 to 0.97, all P<0.0001). The correlations for each animal are shown in Table 4 .
Endocardial Potential Distributions
The simultaneous epicardial and endocardial ST potential changes induced by ischemia are displayed in Figure 4 . From the epicardium, general ST depression was recorded. The potential changes were independent of the partial occluded artery. From the endocardium, localized ST elevations were registered, and the ST elevations corresponded to the partial occluded artery.
Epicardial and Endocardial Potential Distributions in Relation to RMBF
Figure 5 displays the spatial relationship between endocardial RMBF and ST potential changes during ischemia. Figure 5A was constructed by combining the epicardial potential contour map with the endocardial RMBF image map. Figure 5B was constructed by combining the endocardial potential contour map with the endocardial RMBF image map. As demonstrated by these maps, the most negative epicardial ST depression did not coincide with the lowest flow region (Figure 5A ) however, the positive endocardial ST potential was related to the low flow region (Figure 5B ). Figure 5B also shows that the endocardial flow reduction in the ischemic region was relatively uniform from the ischemic center to the boundary (compared with the transmural flow distribution in Figure 2 ), producing a sharp lateral interface between ischemic and normal regions. The peak endocardial and epicardial ST potentials, based on the average of the peak three values, were of similar order, with endocardial control potentials being 1.2±0.83 mV and endocardial ischemic potentials being 6.8±2.56 mV (LCX), and 8.07±3.01 mV (LAD). Epicardial potentials were 1.71±0.85 mV (control), 7.57±2.69 mV (LCX ischemia), and 8.29±3.27 mV (LAD ischemia).
Potential Changes by Insulation
The magnitude of the epicardial ST depression was increased by insulation (from 9±2 to 12±4 mV), but the distribution patterns were not changed (Figure 6A ). Routine ECG limb leads showed a significant decrease in the magnitude of QRS complex and T wave (Figure 6B ). The effects of insulation in three animals are illustrated in Figure 6A , and surface ECGs from one animal are shown in Figure 6B . The values from all experiments are shown in Table 5 .
Transition of Subendocardial Ischemia to Transmural Ischemia
To transform subendocardial ischemia into full-thickness ischemia, the percent stenosis of a coronary artery was increased by fully inflating the hydraulic occluder at 10 to 15 minutes of subendocardial ischemia in 5 sheep of group 2, and the instant potential changes were recorded. From 50 seconds of continuous recording, it was found that ST depression increased gradually as ischemia progressed, until ST elevation ensued at 30 to 35 seconds (Figure 7 ). The increase of the ST depression occurred at the lateral boundary in either the LCX or the LAD occlusion, whereas the ST elevation started from the posterior wall of the heart in LCX occlusion (Figure 7 ) and the anterior wall in LAD occlusion. The ST changes were not captured in the 30-second recording because the recording period was not long enough.
The simulated results are displayed in Figure 8 , where either the LAD or the LCX ischemia shows a similar pattern on the epicardium, with ST depression mainly occurring on the lateral boundary. On the cross section of the heart, endocardial ST elevation appears over the ischemic region, whereas epicardial ST depression occurs on the lateral boundary, ie, the left free wall for either the LCX or the LAD ischemia.
Epicardial ST Depression Does Not Predict Ischemic Region
A major finding of the present study is that ischemic ST depression on the epicardium can not predict the location of an ischemic region. As shown in Figure 3 , the distributions of epicardial ST depression are independent of the responsible ischemic location. Either LAD or LCX ischemia gave a similar epicardial ST distribution pattern, although the absolute values of the potentials varied. The bidomain model produced similar results when applied to the same regions of ischemia (Figure 8 ). Although epicardial ST depression is generated by subendocardial ischemia, the position of the ST change does not localize the responsible myocardium. Unlike body surface recording, epicardial potential recordings are free of the intervening structures, such as lungs, bone, and skeletal muscle, and therefore directly relate to the underlying myocardium. If epicardial ST depression cannot distinguish an ischemic region, neither will the body surface ST depression. These results explain the difficulty in localizing ischemia from body surface ST depression. 15 16 17 18 19 However, they are not consistent with classic ECG theories, 7 8 20 all of which suggest that ST depression should enable us to localize ischemia.
The Origin of Ischemic ST Depression
In transmural ischemia, epicardial ST elevation occurs when injury currents flow between the ischemic regions and the normal myocardium. 9 10 The region of ST elevation is closely related to the region of ischemia. 9 At a cellular level, two major mechanisms are considered to underlie ST-segment displacement: (1) a localized shortening of action potential duration and diminishing of the amplitude of the action potential and (2) a localized decrease in resting membrane potential. The former generates current only during the ST segment. The latter generates a steady injury current that is interrupted during the ST segment when all the cells are depolarized. The injury current produces a TQ-segment shift that cannot be directly detected on the ECG because the amplifiers are AC-coupled however, the interruption of the injury current during the ST segment produces an apparent ST shift, which is equal and opposite the TQ-segment shift on the AC-coupled ECG.
With ST depression, there is no satisfactory explanation of the cardiac electrophysiological changes. Early work 1 2 33 in isolated hearts suggested that the ST-segment response to myocardial injury was elevation and that the ST-segment depression recorded at the epicardium was the reciprocal of ST elevation in the underlying subendocardium. This amplified the dipole theory, which was developed by Wilson and coworkers in 1930s. 20 33 The dipole model considered the active myocardial event as a single dipole source that contained both the maximum and the minimum potentials. Accordingly, an injured region of the myocardium acts in systole as the positive pole of a layer of dipoles situated on its boundary with normal myocardium, whereas the latter acts as the negative pole. In the event of subendocardial ischemia, the ventricular surface and the precordium over the ischemic region faces the negative pole of the dipole the cavity faces the positive pole. Thus, the electrodes over the ischemia should record depressed ST segments, and the cavity should yield elevated ST segments. 2 34 35 However, this theory does not explain either the clinical difficulty in localizing ischemia by ST depression or our results. The limitations of the single dipole model have been demonstrated 36 37 38 and discussed 39 40 41 42 extensively.
Prinzmetal and coworkers 5 6 proposed that ST depression was a primary effect of abnormal membrane polarization rather than a reciprocal effect of ST elevation. From their canine model, Prinzmetal and his coworkers 4 5 6 recorded relative ST-segment depression (true TQ-segment elevation) from the epicardium of “mild” ischemic areas produced by severe hemorrhagic hypotension. The TQ-segment elevation coincided with the increase in membrane resting potential. Injection of a high concentration of sodium or a low concentration of potassium solutions produced the same results. Prinzmetal and coworkers 5 6 then, alternatively, suggested that mild subepicardial ischemia may generate ST depression independent of subendocardial damage. However, there are two major concerns in their experiment: (1) The model they used was not a real subendocardial ischemia produced by vessel stenosis, and regional myocardial blood flow was not measured in those experiments thus, the “mild” ischemia could not be validated. (2) The reference electrode used for intracellular potential recording was placed in a small pool of Ringer’s solution in the region of the exposed femoral vein 6 43 instead of on the epicardial surface of the recording cell. The intracellular electrogram would be affected by extrinsic cardiac potentials using this long-distance reference electrode. 44 No other workers have recorded ST depression at a cellular level from ischemia. The simultaneous epicardial and endocardial electrogram recordings from our experiments (Figures 4 and 5 ) were also inconsistent with their point of view. Furthermore, the RMBF measurement in the present study (Figure 2 ) revealed that epicardial ST depression occurs when blood flow to the deeper myocardial layers decreases. The ECG reflects the potential difference between two electrodes or points on the body surface a region of ST depression implies that there is a region of potential that is more negative than the reference electrode. Our endocardial recording of the ST elevation in the ischemic region (Figures 4 and 5 ) and computer simulation of subendocardial ischemia (Figure 8 ) along with Kleber’s work 9 on intracellular recording have suggested that the source of the ischemic ECG is related to the endocardium. In the present study, the minimum potential was independent of the lowest flow region (Figure 5A ), whereas the maximum potential was related to the low flow region (Figure 5B ), suggesting that the ischemic source relates to the endocardial ST change but not the epicardial ST change. This finding can not be interpreted by the solid angle theory.
The solid angle theory, a concept developed from a mathematical formula and applied to interpret ECGs by Wilson et al 20 in 1933, was expanded to ECG theory by Holland and Arnsdorf. 39 The theory, by taking into account the geometry of the ischemic boundaries, the degree of transmembrane or action potential duration differences, and alterations in intracellular and extracellular conductivities, has provided a geometrical ischemic heart model that quantitatively links changes in ST shifts to the distribution of transmembrane potential changes in the ischemic region. In this model, the ventricle is represented by a sphere of specified thickness, and a region of ischemia is represented by the intersection of the sphere with a cone, the apex of which lies at the center of the sphere. The ischemic boundary is defined as the annular shell that interfaces the cone and the sphere. The ischemic source is assumed to have a uniform potential gradient at the injury boundary. According to this model, the magnitude of ST depression (Φ) recorded at a surface electrode over the ischemic region is as follows:
Theoretically, the solid angle model is a solution of Equation 2 in the particular case when the double layer is in an infinite, homogeneous, and isotropic conducting medium and the exploring point is far from the source. To be able to use the approximation that a potential gradient is proportional to the source strength for a dipole layer–type source, these conditions must be met. Unfortunately, they are hardly met in reality eg, the source is surrounded by a bounded inhomogeneous medium, and the exploring point is very close to the source, especially when the point is on the epicardium. In a finite inhomogeneous volume conductor, the potential distribution around the source is greatly affected by its surrounding medium and is unlikely to have a uniform potential gradient at the injury boundary.
A bidomain model, which was developed by Miller and Geselowitz in 1978, 45 46 has provided a good simulation of the body surface ECG for the normal heart and infarction. In this digital computer model, the ventricles of a human heart were represented in detail and were taken to be located in a torso with realistic surface boundaries. 45 Ischemia and infarction were simulated by altering the shape of transmembrane action potentials assigned to the injured regions of the heart model. 46 A simulation in which action potentials with decreased resting potentials were assigned to anterior subendocardial region has resulted in body surface ST depression in leads V2 to V5 and leads I and aVL. Unfortunately, ST depression was not fully evaluated in this model because neither the endocardial nor epicardial potential was simulated. In addition, the anisotropy and inhomogeneity of the body as a volume conductor were ignored in this model. 45 46
On the basis of their studies using body surface mapping and an inverse transformation 22 47 48 in 219 patients with acute inferior infarction and 93 patients with ST depression and no infarction, Kilpatrick et al 22 postulated that ST depression on ECG originates from current flowing from an endocardial ischemic region to the outside of the heart through the great vessels and atria. This hypothesis explained the difficulty in localizing ischemia from body surface ST depression, but to be a valid explanation, the current paths from the heart would need to be demonstrated. In the present study, the paths have been interrupted by insulating the heart from the return current, resulting in an increase in the magnitude of ST depression when the epicardial surface was insulated, which is inconsistent with the hypothesis. Insulation increased the magnitude of epicardial ST depression by 2 to 8 mV (P<0.05) without altering the distribution patterns (Figure 6A ), whereas the magnitudes of the QRS complex and T wave in the routine ECG limb leads showed a significant decrease (Figure 6B ). Since the present study was carried out in an open-chest preparation with the anterior wall of the left ventricle not in contact with the thorax, insulating the heart would change the amount of the lateral and posterior wall of the left ventricle and the right ventricle in contact with the surrounding tissues. Being nearly fully encircled by the plastic bag, the ventricles were well insulated. The increase in ST depression strongly implies that the source of the ST depression is intramyocardial and does not involve external current paths.
A recent study has demonstrated that the amplitude of the epicardial QRS potentials from both intact and isolated hearts was markedly higher when the heart was surrounded by an insulating medium but that the QRS potential distribution patterns were less affected by the insulating medium. 49 The introduction of the insulating material has the effect of reducing the net flow of current from the heart into the surrounding medium. Because of this effect, the magnitudes of the epicardial ST potential increased (Figure 6A ), whereas the magnitudes of the limb QRS potentials decreased (Figure 6B ). The excitation of the heart can be detected by the ECG primarily because of the existence of the potential difference between the activated cells and the resting cells during the propagation of the action potential in the ventricles. The similar increase in the magnitude of the epicardial ST potentials might represent the same behavior, suggesting that the current source is intramural. This contention was further tested by the transition of subendocardial ischemia to transmural ischemia.
From the transition of subendocardial ischemia to full-thickness ischemia, it was found that epicardial ST depression increased gradually over the boundary region as ischemia progressed and ST elevation ensued over the ischemic region as ischemia became transmural (Figure 7 ). The increase of ST depression before the occurrence of ST elevation was also observed in a study with a perfused canine heart by Guyton et al 50 in 1977. The electrical transition from ST depression to ST elevation was consistent with the contention that the current path is in the myocardium.
In the normal ECG, the ST segment remains isoelectric because there are no great potential differences occurring in the myocardium during this period. In transmural ischemia, epicardial ST elevation occurs when injury currents flow at the boundary between the ischemic regions and the normal myocardium because of the potential difference between these two regions. 9 10 Since the myocardial cells in subendocardial ischemia undergo changes qualitatively similar to those in transmural ischemia, 51 it is likely that the injury currents in subendocardial ischemia also originate from the ischemic boundary. Since subendocardial ischemia involves only the inner layer of the ventricular wall, the boundary between the ischemic region and the normal myocardium should include the transmural boundary parallel to the endocardium and the lateral boundary perpendicular to the endocardium. However, the flow distribution during subendocardial ischemia demonstrated that transmurally there was a gradual flow transition from the endocardium to the epicardium (Figure 2 ) but that at the lateral boundary, flow changed sharply from the ischemic zone to the nonischemic zone, producing a sharp lateral interface between ischemic and normal regions (Figure 5B ). Studies on transmural ischemia also found a sharp lateral interface between ischemic and normal cells with severely ischemic tissue lying adjacent to normal well-perfused tissue. 31 52 53 In ischemic pig hearts, transmembrane action potential recordings using floating microelectrodes also demonstrated a sharp and distinct transition from electrophysiologically abnormal to normal cells. 54 As shown in Equation 2 , the injury current is directly associated with the spatial gradient of the transmembrane potentials. A greater potential gradient exists at the lateral boundary, which in turn produces a stronger current. Under such circumstances, the greater epicardial potential change should appear at the lateral boundary regions with less change in the ischemic center, where the transmural boundary is located and less injury current occurs. Accordingly, in the present study, the maximum epicardial potential change should be at the lateral wall and middle septum, where the LAD and the LCX share their borders, and this explains the experimental results. The transition of subendocardial ischemia to full-thickness ischemia showed that as ischemia progressed, ST depression increased gradually until ischemia became transmural and ST elevation ensued in the ischemic center (Figure 7 ). The increased ST depression occurred at the lateral border, whereas the ST elevation started at the ischemic center. ST elevation gradually progressed toward the ischemic border. These results support the postulate that the major source of electrical current in subendocardial ischemia is located at the lateral boundary of the ischemia. This postulate was verified by our computer simulation, which showed clearly that the current source was at the lateral boundary (Figure 8 ).
Our computer simulation, in which a bidomain model was used to represent the myocardium, took many factors into account. Those included the four chambers of the heart, parts of the big vessels, and the blood inside the heart. A distinguishing feature of our model was that we used volume current density for the source and a real injury boundary with both lateral and transmural boundaries. From our model, we obtained epicardial ST depression over the lateral region in either the LAD or the LCX partial occlusion and endocardial ST elevation over the ischemic region (Figure 8 ). These results correlated well with those from the experiments (Figures 3 and 6 ). We believe that the major source of epicardial ST depression is the lateral boundary of the ischemia in the free wall of the left ventricle. The boundary parallel to the endocardium has high currents normal to the boundary that are localized to a narrow region 3 to 4 mm in maximum dimension and that result in no observable field at the epicardium. At the endocardial side of the left lateral boundary, the injury current flows from the ischemic region to the normal region through the highly conductive intracavity blood. We observed a resulting depression of epicardial ST potential over the boundary. Since the LAD and the LCX share their boundary at the lateral wall, ST potentials showed a similar distribution pattern of lateral ST depression (Figures 3 and 8 ). The source at the lateral boundary in the septum is not seen on the epicardium because it is surrounded by the highly conductive blood of the right ventricle. These explanations are derived from the cross-sectional potential contours from Figure 8 .
The simulation data we presented here are from the model in which anisotropy was not taken into account (because of the computer package limitation). In a similar but simpler simulation, 55 we included the anisotropy in both the source and the volume conductor, and we found that both the endocardial ST elevation and the epicardial ST depression were increased three times compared with the isotropy solution and that ST depression spread over the left free wall, with the most negative depression appearing on the lateral boundary, a pattern of ST distribution that was more close to the experimental results.
The cardiac ischemic source–surface potential relationship, which is fundamental in electrocardiography, is recognized to be complex. Source orientation and strength, volume-conductor characteristics of the body, and source location are all factors in the relationship. This multiplicity of factors makes it difficult to rigidly prove and quantitatively define the roles for each. Despite this, findings in the present study strongly suggest that epicardial potential patterns are not substantially affected by the cardiac locations of responsible subendocardial ischemia and that the ECG changes are generated by the lateral boundary on the free wall, where the LAD and the LCX share their borders.
Evaluation of Experimental Method
The present study was based on the previously validated subendocardial ischemic sheep model produced by a combination of partial arterial stenosis coupled with left atrial pacing. 23 The presence of the subendocardial ischemia was evidenced by the reduction in the endo/epi flow ratio in the ischemic area (Table 3 ). In the absence of a stenosis, the myocardial blood flow increased with a pacing rate of 180 bpm (Table 3 ). This was primarily due to a decrease in the coronary vascular resistance, 56 57 which maintains uniform net transmural perfusion even if a marked reduction in diastolic perfusion time or higher heart rates are achieved. 58 59 In the presence of a coronary artery obstruction, pacing to a rate of 180 bpm caused a decrease in the subendocardial flow, with a less significant change in the subepicardial perfusion and thus a reduction in the endo/epi flow ratio in the ischemic area (Table 3 ). 60 61 The susceptibility of the subendocardium to ischemia is due to its limited reserve for vasodilation, the extrinsic compression from the higher wall stress to which it is subjected, and the resultant high metabolic demands 62 in this region. Atrial pacing was associated with a decrease in diastolic perfusion time, an increase in oxygen demand, 63 and an increase in stenosis resistance. 64 Therefore, partial coronary occlusion plus the added atrial pacing would produce a degree of subendocardial ischemia similar to that reported during the exercise, as indicated by the elevation of the ST segment in the endocardial recording and depression of the ST segment in the epicardial recording.
Sheep have few native coronary collateral anastomoses 24 and are similar to humans, and the anatomy of the coronary arterial circulation is remarkably consistent. Thus, in sheep, the ischemic size is determined primarily by the size of the occluded vascular bed because of the lack of collateral connection. 65 These coronary anatomic features in sheep permit predictable and reproducible myocardial ischemia with small standard deviations. The present study provides an alternative model for ischemic research.
The advantage of seeing an epicardial distribution is that the electrogram changes directly reflect the source. In the present study, we used the epicardial distribution during the ST segment to test the hypothesis of ST depression. The methods in the present study differed in certain aspects from those used by others. To avoid variables introduced by the isolated heart, the study was carried out with the heart in situ. The epicardial ST potentials were recorded from 64 electrodes spread over the whole surface of the heart. The endocardial ST was recorded by a 40-pole basket electrode. Previous studies have been performed in the isolated heart in which the epicardial ST changes after physical or chemical injury were only recorded in the injured region. 1 2 33 For those in the in situ heart, ST depression was either not produced, 8 66 or the epicardial and the endocardial potential changes during subendocardial ischemia were not investigated. 60 61
The first limitation occurs in the experimental work. Attempts at intramural recordings were not successful because of injury currents thus, the definite current flow path was unable to be confirmed. The second limitation was in the computer simulation, in that the torso was not included in our model therefore, the influence of the body as a volume conductor was not evaluated. However, according to the experimental results of insulation (Figure 6A ) and one other study in this area, 49 the torso would change (decrease) the magnitudes of only the ST shifts but not the distribution patterns.
The clinical significance of our results is that data are provided for further study of ST depression. Many workers have shown that although body surface ST elevation was highly related to the region of ischemia, body surface ST depression was poorly related, if at all. 15 16 17 18 19 Our results explain this poor localization of ischemia by ST depression in humans and suggest that the source might be at the lateral boundary of endocardial ischemia. The present data support the following conclusions: (1) Epicardial potential patterns are not substantially affected by the cardiac location of the responsible subendocardial ischemia. (2) ST depression is not due to the endocardial current flow back on to the cardiac surface and is not fully explained by the current models of the ST depression. (3) Ischemic ST depression originates from the injury current, which flows at the lateral boundary of subendocardial ischemia.
Selected Abbreviations and Acronyms
|LAD||=||left anterior descending coronary artery|
|LCX||=||left circumflex coronary artery|
|RMBF||=||regional myocardial blood flow|
Figure 1. Schematic drawings illustrating the potential recording system, the map construction, and display. The left diagram represents the electrode matrix on the surface of the heart. The distances between electrodes were between 5 and 10 mm. The right diagrams depict the unwrapped epicardial surface of the left ventricle and right ventricle (A) and the unwrapped endocardial surface of the left ventricle (B). All contour maps were constructed from potentials measured during the ST segment. The thick solid lines reflect the position of the coronary arteries, with the occluded arteries indicated by bars across the coronary. The thin solid and dotted lines indicate ST elevation and ST depression, respectively. The numbers inside maps indicate values of voltages in millivolts. LV indicates left ventricle OM, obtuse marginal branch PDA, posterior descending coronary artery and RV, right ventricle.
Figure 2. Spatial flow distributions in the left ventricular myocardium of a sheep before and during partial LAD occlusion. Intensities represent the quantity of RMBFs (mL · g −1 · min −1 ). Each circle represents a ring of left ventricle ≈1 cm thick. In each 45° arc, there are three slices from endocardium to epicardium. The four arcs above represent the myocardium of the LCX bed the four arcs below represent the myocardium of the LAD bed. For each ring, the septum is on the left, the free wall is on the right, the posterior wall is above, and the anterior wall is below.
Figure 3. Epicardial potential distributions after 10 minutes of ischemia in different territories (from the three different sheep). The format of the contour maps is described in the Figure 1 legend. The contour interval is 2 mV. Each row represents a different sheep with partial LAD occlusion on the left and partial LCX occlusion on the right.
Figure 4. Simultaneous records of epicardial (upper) and endocardial (lower) potential distributions at 2 minutes of LCX (left) and LAD (right) occlusions (isopotential difference maps from the same sheep). The format of the contour maps is described in the Figure 1 legend. The colors are scaled from blue (ST depression) to red (ST elevation).
Figure 5. Endocardial flow decrease related to epicardial potential change (A) and endocardial potential change (B) at 20 minutes of ischemia. The potential changes are represented by contour lines. The format of the contour maps is described in the Figure 1 legend. The flow decrease (percentage of control) is represented by shade. Intensities represent the quantity of flow.
Figure 6. A, Epicardial potential distributions with and without insulation. During insulation, the magnitude of ST depression was increased, but the pattern of ST distribution remained unchanged (isopotential difference maps at 20 minutes of partial LCX occlusion). Results from three sheep are shown with the contour interval being 2 mV. B, Routine analog body surface ECG recordings with and without insulation. During insulation, the magnitudes of QRS and T waves were significantly reduced. The ECGs were recorded at a speed of 25 mm/s a calibration of 10 mm=1 mV. The format of the contour maps is described in the Figure 1 legend.
Figure 7. Sequential epicardial potential distributions during the transition of subendocardial to full-thickness ischemia in the LCX occlusion (contour interval=4 mV). The format of the contour maps is described in the Figure 1 legend.
Figure 8. Top, Epicardial potential distributions from the three-dimensional modeling. ST depression occurs at the lateral region in both the LAD and LCX ischemia. Bottom, Cross-sectional slices through the three-dimensional model showing isopotential distributions. The major source of ST depression is the lateral boundary between the ischemic and normal region. The format of the contour maps is described in the Figure 1 legend. LV indicates left ventricle RV, right ventricle.
Table 1. Animal Groups and Treatments
Table 2. Hemodynamic Responses to Pacing, Endocardial Electrodes, and Ischemia
Control 1 indicates before ischemia without endocardial electrodes control 2, before ischemia with endocardial electrodes LVSP, left ventricular systolic pressure LVDP, left ventricular diastolic pressure LAP, mean left atrial pressure and LCX flow, flow to left circumflex coronary artery by EM flow probe. Values are mean±SD.
Table 3. RMBF During Pacing and Ischemia
Endo indicates endocardium Mid, middle Epi, epicardium Trans, transmural and Ratio, endocardial/epicardial flow ratio. Values are mean±SD.
2 P<0.001 vs control (pacing, n=5 ischemia, n=16).
Table 4. Correlation Coefficient of Epicardial Potentials Between LAD and LCX Ischemia
Table 5. Maximal ST Depression in Ischemia With and Without Insulation
Chapter 4 - Machine learning in biomedical signal processing with ECG applications
The research in the field of ECG signal analysis and classification is an active research topic. ECG signal analysis plays an essential role in detecting cardiovascular diseases (e.g., occlusion of coronary arteries, heart enlargement, conduction defects, rhythm, and ionic effects). Cardiologists are trained on how to interpret ECG signals for identifying arrhythmias. For example, ECG beats are examined by determining distinctive morphological and interval-based features. However, manual analysis is time-consuming, requires expert training, and is prone to error.
Automated ECG signal analysis technology has become widely available thanks to the advances in machine learning and biomedical signal processing. ECG analysis is noninvasive and has shown impact in various applications including medicine, emotion recognition, biometric identification, and sports wearable technology. This chapter is concerned with automated electrocardiogram (ECG) analysis for the diagnosis of cardiovascular diseases. The main aim of this chapter is to help the biomedical engineer to build a machine learning model to perform automatic classification of ECG beats. I will start with an overview of clinical ECG, ECG views, heartbeat types, and arrhythmias. Then a simple model for ECG heartbeat classification is illustrated, showing the various stages from data selection, preprocessing, feature generation, and training a machine learning model.
NSCC 7150 Module 2/3
The direction of flow is from R to L and downwards toward the positive electrode.
Arrow is directed away from the positive electrode, therefore we get a negative or downward deflection on the ECG strip.
this causes a large positive, upright, deflection on the monitor
The Sequence method: Memorization of 300,150,100,75,60,50.
Large Squares method. quick and fairly accurate.. count number of large squares between 2 consecutive R waves (or p waves), and divide into 300
A slight variation is acceptable and rhythm is essentially regular, variation should be within 0.16 seconds.
Variation over 0.16 seconds is considered irregular.
Should be consistent throughout the strip
Normal range is 0.12-0.20 seconds.
If the wave of electrical activity proceeds in a normal, orderly fashion from the junction, through the remainder of conduction system and over the R and L ventricles, then we will see a normal QRS complex.
ST segment depression may reflect myocardial ischemia
ST segment elevation may reflect myocardial injury.
Life-threatening dysrrhythmias can be associated with lengthening of the QT intervals.
consider site of impulse formation
1. what implications does this rhythm have for CO? (Ventricle rate too slow, potential for decrease in CO d/t slow ventricle hr)
(Ventricle rate too fast, leads to decreased ventricular filling time, decreased coronary artery perfusion, increased myocardial demand, all of which lead to decrease in CO)
(Is there a P wave? without one there is the potential loss of atrial kick and therefore a decrease in preload which therefore leads to decrease in CO)
(Are there any ST changes? potential for ischemia/injury to myocardium and potential for decrease in contractility which leads to decrease in CO)
interventions will be mainly determined on what implications the rhythm has for the patient.
Rate too slow - intervention will be to speed it up with drugs or pacemaker
Rate too fast - intervention will be to slow it down with drugs or electrical conversion (cardioversion/defibrillation)
No P wave - potential intervention to chemically/electronically convert rhythm.
|Phase||EKG||Heart sounds||Semilunar valves||Atrioventricular valves|
|B||Ventricular systole - Isovolumetric/isovolumic contraction||QRS||S1 ("lub")||closed||closed|
|C1||Ventricular systole - Ejection 1||-||open||closed|
|C2||Ventricular systole - Ejection 2||T||open||closed|
|D||Ventricular diastole - Isovolumetric/isovolumic relaxation||-||S2 ("dub")||closed||closed|
|E1||Ventricular diastole - Ventricular filling 1||-||S3*||closed||open|
|E2||Ventricular diastole - Ventricular filling 2||-||closed||open|
Note that during isovolumetric/isovolumic contraction and relaxation, all the heart valves are closed. At no time are all the heart valves open [ citation needed ] .