- specific disorders
- specific disorders
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/17 21:43:54」(JST)[Wiki en表示]
ECG of a heart in normal sinus rhythm.
Electrocardiography (ECG or EKG from Greek: kardia, meaning heart) is the process of recording the electrical activity of the heart over a period of time using electrodes placed on a patient's body. These electrodes detect the tiny electrical changes on the skin that arise from the heart muscle depolarizing during each heartbeat.
In a conventional 12 lead ECG, ten electrodes are placed on the patient's limbs and on the surface of the chest. The overall magnitude of the heart's electrical potential is then measured from twelve different angles ("leads") and is recorded over a period of time (usually 10 seconds). In this way, the overall magnitude and direction of the heart's electrical depolarization is captured at each moment throughout the cardiac cycle. The graph of voltage versus time produced by this noninvasive medical procedure is referred to as an electrocardiogram (abbreviated ECG or EKG).
During each heartbeat, a healthy heart will have an orderly progression of depolarization that starts with pacemaker cells in the sinoatrial node, spreads out through the atrium, passes through the atrioventricular node down into the Bundle of His and into the Purkinje fibers spreading down and to the left throughout the ventricles. This orderly pattern of depolarization gives rise to the characteristic ECG tracing. To the trained clinician, an ECG conveys a large amount of information about the structure of the heart and the function of its electrical conduction system. Among other things, an ECG can be used to measure the rate and rhythm of heartbeats, the size and position of the heart chambers, the presence of any damage to the heart's muscle cells or conduction system, the effects of cardiac drugs, and the function of implanted pacemakers.
- 1 History
- 2 The electrodes and leads
- 2.1 Limb leads
- 2.2 Augmented limb leads
- 2.3 Precordial leads
- 2.4 Specialized leads
- 2.5 Lead locations on an EKG report
- 2.6 Contiguity of leads
- 3 Interpretation of the ECG
- 3.1 Rate and rhythm
- 3.2 Axis
- 3.3 Amplitudes and intervals
- 3.4 Ischemia and infarction
- 3.5 Artifacts
- 4 Medical indications for electrocardiography
- 5 See also
- 6 References
- 7 External links
The etymology of the word is derived from the Greek electro, because it is related to electrical activity, kardio, Greek for heart, and graph, a Greek root meaning "to write".
Alexander Muirhead is reported to have attached wires to a feverish patient's wrist to obtain a record of the patient's heartbeat in 1872 at St Bartholomew's Hospital. Another early pioneer was Augustus Waller, of St Mary's Hospital in London. His electrocardiograph machine consisted of a Lippmann capillary electrometer fixed to a projector. The trace from the heartbeat was projected onto a photographic plate that was itself fixed to a toy train. This allowed a heartbeat to be recorded in real time.
An initial breakthrough came when Willem Einthoven, working in Leiden, the Netherlands, used the string galvanometer he invented in 1901. This device was much more sensitive than both the capillary electrometer Waller used and the string galvanometer that had been invented separately in 1897 by the French engineer Clément Ader. Einthoven assigned the letters P, Q, R, S, and T to the various deflections, and described the electrocardiographic features of a number of cardiovascular disorders. In 1924, he was awarded the Nobel Prize in Medicine for his discovery.
Though the basic principles of that era are still in use today, many advances in electrocardiography have been made over the years. Instrumentation has evolved from a cumbersome laboratory apparatus to compact electronic systems that often include computerized interpretation of the electrocardiogram.
The electrodes and leads
Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel, embedded in the middle of a self-adhesive pad. The names and correct locations for each electrode are as follows:
|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, lateral calf muscle.|
|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 midaxillary line.|
The term "lead" in electrocardiography refers to the 12 different vectors along which the heart's depolarization is measured and recorded. There are a total of six limb leads and augmented limb leads arranged like spokes of a wheel in the coronal plane (vertical) and six precordial leads that lie on the perpendicular transverse plane (horizontal). In medical settings, the term leads is also sometimes used to refer to the ten electrodes themselves, although this is not technically a correct usage of the term.
Each of these leads represents the electrical potential difference between two points. For each lead, the positive pole is one of the ten electrodes. In bipolar leads, the negative pole is a different one of the electrodes, while in unipolar leads, the negative pole is a composite pole known as Wilson's central terminal. Wilson's central terminal VW is produced by averaging the measurements from the electrodes RA, LA, and LL to give an average potential across the body:
In a 12-lead ECG, all leads except the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).
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
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 Wilson's central terminal as their 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.
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.
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. Posterior leads 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.
An esophogeal lead can be inserted to a part of the tract 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.
Lead locations on an EKG report
A standard 12-lead ECG report 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-V6).
Contiguity of leads
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.
|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.
Interpretation of the ECG
A typical ECG tracing is a repeating cycle of three electrical entities: a P wave (atrial depolarization), a QRS complex (ventricular depolarization) and a T wave (ventricular repolarization). The EKG is traditionally interpreted methodically in order to not miss any important findings.
Rate and rhythm
A heart rate slower than 60 beats per minute is said to be bradycardic and a rate faster than 100 beats/minute is said to be tachycardic. There are different types of rhythms that can cause the heart rate to be to fast or to slow. Many athletes can have a normal resting heart rate of less than 60 beats a minute. The key indicator of whether this is a problem is if the person is actually having any kind of symptoms. One of the primary rhythms that can cause the heart rate to be slow and symptomatic is known as heart block. There are many different types of heart block but the most common heart block is AV Block's. There are also many different types of rhythms that can cause the heart rate to be fast. The most common one is probably sinus tachycardia. This means the depolarization is still starting in the normal pacemaker of the heart called the Sino-Atrial node or SA node. When the heart rhythm is no longer initiated in the SA node but is also initiating in various atrial foci then the the heart rate can become irregular and can develop into atrial fibrillation or atrial flutter. Atrial fibrillation can become unstable when the heart rate is above 100. The risk of this rhythm being to fast is that the heart is not beating efficiently and the blood that is pooling in the atria of the heart can begin to clot putting the person at a high risk for stroke or heart attack. This is the reason many of people with atrial fibrillation or A-fib have to take blood thinners for the rest of their life. Other fast rhythms include Supra ventricular Tachycardia (SVT), Ventricular Fibrillation, and Ventricular Tachycardia. The heart rate can be approximated quickly by dividing 300 by the number of large boxes between two consecutive QRS complexes on the EKG paper.
The physiologic rhythm of the heart is normal sinus rhythm, wherein the sinoatrial node initiates the cardiac cycle. In normal sinus rhythm a p-wave precedes every QRS complex and the rhythm is generally regular. If this is not the case, the patient may have a cardiac arrhythmia.
The heart's electrical axis is the general direction of the ventricular depolarization wavefront (or mean electrical vector) in the sagittal plane (the plane of the limb leads and augmented limb leads). The QRS axis can be determined by looking for the limb lead or augmented limb lead with the greatest positive amplitude of its R wave. A lead can only detect changes in voltage that are aligned with that lead; therefore the lead that is best aligned with the axis of ventricular depolarization will have the tallest positive QRS complex.
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.
|Normal||−30° to 90°||Normal|
|Left axis deviation||−30° to −90°||May indicate left ventricular hypertrophy, left anterior fascicular block, or an old inferior q-wave myocardial infarction|
|Right axis deviation||+90° to +180°||May indicate right ventricular hypertrophy, left posterior fascicular block, or an old lateral q-wave myocardial infarction|
|Indeterminate axis||+180° to −90°||Rarely seen; considered an 'electrical no-man's land'|
A normal axis can be quickly identified if the QRS complexes in leads I and aVF are both upright. Lead I is positioned at 0° and lead aVF is positioned at 90°. If the QRS is upright in both, its vector of depolarization must be somewhere between these two angles, and is therefore normal axis.
To make it easy to remember, if lead I is negative and lead II is positive so they are facing each other and if we imagine they are hands (we shake hands with the right hand so this is right axis deviation), Alansari Sign.
Amplitudes and intervals
All of the waves on an EKG 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.
For ease of measuring the amplitudes and intervals, an EKG is printed on graph paper at a standard scale: each 1 mm (one small box on the standard EKG paper) represents 40 milliseconds of time on the x-axis, and 0.1 millivolts on the y-axis.
|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 TCA 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, LVH, 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||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 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.||If the U wave is very prominent, suspect hypokalemia, hypercalcemia or hyperthyroidism.|
Ischemia and infarction
Ischemia or non-ST elevation myocardial infarctions may manifest as ST depression or inversion of T waves.
ST elevation myocardial infarctions 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 ST-elevation myocardial infarction based on the location of ST elevation. The LAD 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 RCA usually supplies the inferior aspect of the heart, and therefore causes ST elevations in inferior leads (II, III and aVF).
An EKG tracing is affected by patient motion. Some rhythmic motions (such as shivering or tremors) can create the illusion of cardiac dysrhythmia.
Medical indications for electrocardiography
Indications for performing electrocardiography include:
- Suspected myocardial infarction
- Suspected pulmonary embolism
- A third heart sound, fourth heart sound, a cardiac murmur or other findings to suggest structural heart disease
- Perceived cardiac dysrhythmias
- Syncope or collapse
- Monitoring the effects of a cardiac medication
- Assessing severity of electrolyte abnormalities, such as hyperkalemia
The United States Preventive Services Task Force does not recommend electrocardiography for routine screening procedure in patients without symptoms and those at low risk for coronary heart disease. This is because an ECG may falsely indicate the existence of a problem, leading to misdiagnosis, the recommendation of invasive procedures, or 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.
Continuous ECG monitoring is used to monitor critically ill patients, patients undergoing general anesthesia, and patients who have an infrequently occurring cardiac dysrhythmia that would be unlikely be seen on a conventional ten second ECG.
- Electrical conduction system of the heart
- Heart rate monitor
- Is also known as Electrocardiovascular Gaugometer
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|Wikimedia Commons has media related to ECG.|
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- Electrocardiography (ECG or EKG  from Greek: kardia, meaning heart ) is the recording of the electrical activity of the heart. Traditionally this is in the form of a transthoracic (across the thorax or chest) interpretation of the electrical ...
- Electrocardiography Definition Electrocardiography is a commonly used, noninvasive procedure for recording electrical changes in the heart. The record, which is called an electrocardiogram (ECG or EKG), shows the series of waves ...
|拡張検索||「ambulatory electrocardiography」「unipolar lead electrocardiography」|
- 心臓は拍動のたびに電気を発生し、これを心起電力(cardiac electromotive force)と呼ぶ。
- 縦軸：10mm = 1mV
- 横軸： 5mm = 0.2s
- 標準肢誘導(I,II,III) + 単極肢誘導(aVR, aVF, aVL) + 胸部誘導(V1, V2, V3, V4, V5, V6) = 12誘導
- P波：心房の電気的興奮。：0.12-0.20s (3-5mm)
- QRS複合：心室の電気的興奮：0.06-0.15s ：正常; 0.06-0.08s (1.5-2mm), 不完全脚ブロック; 0.08-0.12s (2-3mm), 完全脚ブロック ≧0.12s (≧3mm)
- I,IIにおいてP, QRS, Tが全て正 → 100G096
- 1. 心臓内の興奮伝導の障害
- ex. 房室ブロック
- 2. 不整脈：脈拍のリズムと心拍数の異常
- 3. 冠循環の異常
- ex. 心筋梗塞
- 4. 心室肥大
- 5. 血漿中の電解質濃度の異常
- 電気軸：右軸偏位 → 左軸偏位 胎児循環では右心系が主に体循環に関わっていたが、成人で見られる循環では左心系が関わる。生後一ヶ月らいまでは+120～130°程度の右軸偏位
- 心膜炎 心外膜炎：90%の患者に異常が見られる。aVR, V1を除いたST上昇。いくつかの電極でPR部の低下(PR segment depression)
- 肥大型心筋症：ST-T変化(ストレイン型の陰性T波は、上に凸のST低下を伴い、非対称性陰性T波)。Sv1, Rv5の増大。QRS時間の延長。
- ブルガダ症候群：右側胸部誘導(V1-V2(V3))のST上昇(coved型あるいはsaddle back型) 。完全あるいは不完全右脚ブロック様QRS波形(つまり、V1-V3でJ波が見られる)。
- WPW症候群：Δ波。PQ短縮、QRS延長。V1に特徴的変化「A型: 高いR波。左室自由壁」「B型: rS型。右側」「C型: Qr/QS。中隔」