[转帖]心电及心电监护背景知识--英文

Electrocardiography

12 Lead ECG of a 26-year-old male.

Image showing patient with connected to the 10 electrodes necessary for a 12-lead ECG

Electrocardiography (ECG or EKG) is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes. ^[1] It is a noninvasive recording produced by an electrocardiographic device. The etymology of the word is derived from electro, because it is related to electrical activity, cardio, Greek for heart, graph, a Greek root meaning "to write".

Electrical impulses in the heart originate in the sinoatrial node and travel through the intrinsic conducting system to the heart muscle.The impulses stimulate the myocardial muscle fibres to contract and thus induce systole. The electrical waves can be measured at selectively placed electrodes (electrical contacts) on the skin. Electrodes on different sides of the heart measure the activity of different parts of the heart muscle. An ECG displays the voltage between pairs of these electrodes, and the muscle activity that they measure, from different directions, also understood as vectors. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle. It is the best way to measure and diagnose abnormal rhythms of the heart,^[2] particularly abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or abnormal rhythms caused by levels of dissolved salts (electrolytes), such as potassium, that are too high or low.^[3] In myocardial infarction (MI), the ECG can identify damaged heart muscle. But it can only identify damage to muscle in certain areas, so it can't rule out damage in other areas.^[4] The ECG cannot reliably measure the pumping ability of the heart; for which ultrasound-based (echocardiography) or nuclear medicine tests are used.

Contents 1 History 2 ECG graph paper 3 Filter selection 4 Leads 4.1 Placement of electrodes 4.2 Unipolar vs. bipolar leads 4.3 Limb leads 4.4 Augmented limb leads 4.5 Precordial leads 5 Waves and intervals 5.1 P wave 5.2 QRS complex 5.3 PR/PQ interval 5.4 ST segment 5.5 T wave 5.6 QT interval 5.7 U wave 6 Clinical lead groups 7 Axis 8 Electrocardiogram heterogeneity 8.1 Background 8.2 Research 8.3 Future applications 9 See also 10 References 11 Additional images 12 External links

 History

Alexander Birmick Muirhead is reported to have attached wires to a feverish patient's wrist to obtain a record of the patient's heartbeat while studying for his Doctor of Science (in electricity) in 1872 at St Bartholomew's Hospital.^[5] This activity was directly recorded and visualized using a Lippmann capillary electrometer by the British physiologist John Burdon Sanderson.^[6] The first to systematically approach the heart from an electrical point-of-view was Augustus Waller, working in St Mary's Hospital in Paddington, London.^[7] His electrocardiograph machine consisted of a Lippmann capillary electrometer fixed to a projector. The trace from the heartbeat was projected onto a photographic plate which was itself fixed to a toy train. This allowed a heartbeat to be recorded in real time. In 1911 he still saw little clinical application for his work.

An initial breakthrough came when Willem Einthoven, working in Leiden, The Netherlands, used the string galvanometer that he invented in 1903[3]. This device was much more sensitive than both the capillary electrometer that Waller used and the string galvanometer that had been invented separately in 1897 by the French engineer Clément Ader.^[8]

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.^[9]

Though the basic principles of that era are still in use today, there have been many advances in electrocardiography over the years. The instrumentation, for example, has evolved from a cumbersome laboratory apparatus to compact electronic systems that often include computerized interpretation of the electrocardiogram.^[10]

 ECG graph paper

One second of ECG graph paper

Timed interpretation of an ECG was once incumbent to a stylus and paper speed. Computational Analysis now allows considerable study of Heart Rate Variability. A typical electrocardiograph runs at a paper speed of 25 mm/s, although faster paper speeds are occasionally used. Each small block of ECG paper is 1 mm². At a paper speed of 25 mm/s, one small block of ECG paper translates into 0.04 s (or 40 ms). Five small blocks make up 1 large block, which translates into 0.20 s (or 200 ms). Hence, there are 5 large blocks per second. A diagnostic quality 12 lead ECG is calibrated at 10 mm/mV, so 1 mm translates into 0.1 mV. A calibration signal should be included with every record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is two large squares on ECG paper.

 Filter selection

Modern ECG monitors offer multiple filters for signal processing. The most common settings are monitor mode and diagnostic mode. In monitor mode, the low frequency filter (also called the high-pass filter because signals above the threshold are allowed to pass) is set at either 0.5 Hz or 1 Hz and the high frequency filter (also called the low-pass filter because signals below the threshold are allowed to pass) is set at 40 Hz. This limits artifact for routine cardiac rhythm monitoring. The high-pass filter helps reduce wandering baseline and the low-pass filter helps reduce 50 or 60 Hz power line noise (the power line network frequency differs between 50 and 60 Hz in different countries). In diagnostic mode, the high-pass filter is set at 0.05 Hz, which allows accurate ST segments to be recorded. The low-pass filter is set to 40, 100, or 150 Hz. Consequently, the monitor mode ECG display is more filtered than diagnostic mode, because its passband is narrower.^[11]

 Leads

Graphic showing the relationship between positive electrodes, depolarization wavefronts (or mean electrical vectors), and complexes displayed on the ECG.

In electrocardiography, the word, "lead" refers to the signals transmitted and received between two electrodes. These electrodes are attached to the patient's body, usually with very sticky circles of thick tape-like material (the electrode is embedded in the center of this circle).^[12]

ECG leads record the electrical signals of the heart from a particular combination of recording electrodes which are placed at specific points on the patient's body.

 Placement of electrodes

Ten electrodes are used for a 12-lead ECG. They are labeled and placed on the patient's body as follows:^[13], ^[14],

Proper placement of the limb electrodes, color coded as recommended by the American Health Association. Note that the limb electrodes can be far down on the limbs or close to the hips/shoulders, but they must be even (left vs. right). [2]

ELECTRODE LABEL (in the USA)	ELECTRODE PLACEMENT
RA	On the right arm, avoiding bony prominences (in the UK, it is taught that it is better to place on bony prominences!).
LA	In the same location that RA was placed, but on the left arm this time.
LL	On the left leg, avoiding bony prominences.
RL	In the same place that LL was positioned, but on the right leg.
V1	In the fourth intercostal space (between ribs 4 & 5) to the right of the sternum (breastbone).
V2	In the fourth intercostal space (between ribs 4 & 5) to the left of the sternum.
V3	Between leads V2 and V4.
V4	In the fifth intercostal space (between ribs 5 & 6) in the midclavicular line (the imaginary line that extends down from the midpoint of the clavicle (collarbone).
V5	Horizontally even with V4, but in the anterior axillary line. (The anterior axillary line is the imaginary line that runs down from the point midway between the middle of the clavicle and the lateral end of the clavicle; the lateral end of the collarbone is the end closer to the arm.)
V6	Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line is the imaginary line that extends down from the middle of the patient's armpit.)

 Unipolar vs. bipolar leads

There are two types of leads—unipolar and bipolar. Bipolar leads have one positive and one negative pole.^[15] In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads have only one true pole (the positive pole). The negative pole is a "composite" pole made up of signals from lots of other electrodes.^[16] In a 12-lead ECG, all leads besides the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).

 Limb leads

In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbs—one on each arm and one on the left leg.^[17], ^[18], ^[19] The limb leads form the points of what is known as Einthoven's triangle.[4]

• Lead I is the signal between the (negative) aVR electrode (on the right arm) and the (positive) aVL electrode (on the left arm). ^[20]
• Lead II is the signal between the (negative) aVR electrode (on the right arm) and the (positive) aVF electrode (on the left leg).
• Lead III is the signal between the (negative) aVL electrode (on the left arm) and the (positive) aVF electrode (on the left leg).

**Note that the aVL electrode functions as the positive end of the connection in lead I and the negative end of the connection in lead III. ^[21]

 Augmented limb leads

Leads aVR, aVL, and aVF are 'augmented limb leads'. They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of 'Wilson's central terminal', which is derived by adding leads I, II, and III together and plugging them into the negative terminal of the ECG machine. This zeroes out the negative electrode and allows the positive electrode to become the "exploring electrode" or a unipolar lead. This is possible because Einthoven's Law states that I + (-II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I - II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5, and V6.

• Lead aVR or "augmented vector right" has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm.
• Lead aVL or "augmented vector left" has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm.
• Lead aVF or "augmented vector foot" has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg.

The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. 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.

aVR = -(I + II)/2

aVL = I - II/2

aVF = II - I/2

 Precordial leads

The electrodes for the precordial leads (V1, V2, V3, V4, V5, and V6,) are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. Wilson's central terminal is used for the negative electrode, and these leads are considered to be unipolar (recall that Wilson's central terminal is the average of the three limb leads. This will approximate ground).The precordial leads view the heart's electrical activity in the so-called horizontal plane. The heart's electrical axis in the horizontal plane is referred to as the Z axis.

 Waves and intervals

Schematic representation of normal ECG

A typical ECG tracing of a normal heartbeat (or cardiac cycle) consists of a P wave, a QRS complex and a T wave.^[22] A small U wave is normally visible in 50 to 75% of ECGs. The baseline voltage of the electrocardiogram is known as the isoelectric line. Typically the isoelectric line is measured as the portion of the tracing following the T wave and preceding the next P wave. The four deflections were originally named ABCDE but renamed PQRST after correction for artifacts introduced by early amplifiers.^{[citation needed]}

 P wave

During normal atrial depolarization, the main electrical vector is directed from the SA node towards the AV node, and spreads from the right atrium to the left atrium. This turns into the P wave on the ECG, which is upright in II, III, and aVF (since the general electrical activity is going toward the positive electrode in those leads), and inverted in aVR (since it is going away from the positive electrode for that lead). A P wave must be upright in leads II and aVF and inverted in lead aVR to designate a cardiac rhythm as Sinus Rhythm.

• The relationship between P waves and QRS complexes helps distinguish various cardiac arrhythmias.
• The shape and duration of the P waves may indicate atrial enlargement.
• Absence of the P wave may indicate atrial fibrillation.
• A saw tooth formed P wave may indicate atrial flutter.

 QRS complex

Various QRS complexes with nomenclature.

See also: Electrical conduction system of the heart

The QRS complex is a recording of a single heartbeat on the ECG that corresponds to the depolarization of the right and left ventricles. Ventricles contain more muscle mass than the atria, therefore the QRS complex is considerably larger than the P wave. The His/Purkinje cardiac nerves coordinate the depolarization of both ventricles, the QRS complex is 0.08 to 0.12 sec (80 to 120 ms) in duration represented by three small squares or less, but any abnormality of conduction takes longer, and causes widened QRS complexes.

Not every QRS complex contains a Q wave, an R wave, and an S wave. By convention, any combination of these waves can be referred to as a QRS complex. However, correct interpretation of difficult ECGs requires exact labeling of the various waves. Some authors use lowercase and capital letters, depending on the relative size of each wave. For example, an Rs complex would be positively deflected, while a rS complex would be negatively deflected. If both complexes were labeled RS, it would be impossible to appreciate this distinction without viewing the actual ECG.

• The duration, amplitude, and morphology of the QRS complex is useful in diagnosing cardiac arrhythmias, conduction abnormalities, ventricular hypertrophy, myocardial infarction, electrolyte derangements, and other disease states.

• Q waves can be normal (physiological) or pathological. Pathological Q waves refer to Q waves that have a height of 25% or more than that of the partner R wave and/or have a width of greater than 0.04 seconds. Normal Q waves, when present, represent depolarization of the interventricular septum. For this reason, they are referred to as septal Q waves, and can be appreciated in the lateral leads I, aVL, V5 and V6.

• Q waves greater than 1/4 the height of the R wave, greater than 0.04 sec (40 ms) in duration, or in the right precordial leads are considered to be abnormal, and may represent myocardial infarction.

• "Buried" inside the QRS wave is the atrial repolarization wave, which resembles an inverse P wave. It is far smaller in magnitude than the QRS and is therefore obscured by it.

Animation of a normal ECG wave.

 PR/PQ interval

The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It is usually 120 to 200 ms long. On an ECG tracing, this corresponds to 3 to 5 small boxes. In case a Q wave was measured with a ECG the PR interval is also commonly named PQ interval instead.

• A PR interval of over 200 ms may indicate a first degree heart block.
• A short PR interval may indicate a pre-excitation syndrome via an accessory pathway that leads to early activation of the ventricles, such as seen in Wolff-Parkinson-White syndrome.
• A variable PR interval may indicate other types of heart block.
• PR segment depression may indicate atrial injury or pericarditis.
• Variable morphologies of P waves in a single ECG lead is suggestive of an ectopic pacemaker rhythm such as wandering pacemaker or multifocal atrial tachycardia

 ST segment

Main article: Myocardial infarction

The ST segment connects the QRS complex and the T wave and has a duration of 0.08 to 0.12 sec (80 to 120 ms). It starts at the J point (junction between the QRS complex and ST segment) and ends at the beginning of the T wave. However, since it is usually difficult to determine exactly where the ST segment ends and the T wave begins, the relationship between the RT segment and T wave should be examined together. The typical ST segment duration is usually around 0.08 sec (80 ms). It should be essentially level with the PR and TP segment.

• The normal ST segment has a slight upward concavity.
• Flat, downsloping, or depressed ST segments may indicate coronary ischemia.
• ST segment elevation may indicate myocardial infarction. An elevation of >1mm and longer than 80 milliseconds following the J-point. This measure has a false positive rate of 15-20% (which is slightly higher in women than men) and a false negative rate of 20-30%.^[23]

 T wave

The T wave represents the repolarization (or recovery) of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period (or vulnerable period).

In most leads, the T wave is positive. However, a negative T wave is normal in lead aVR. Lead V1 may have a positive, negative, or biphasic T wave. In addition, it is not uncommon to have an isolated negative T wave in lead III, aVL, or aVF.

• Inverted (or negative) T waves can be a sign of coronary ischemia, Wellens' syndrome, left ventricular hypertrophy, or CNS disorder.
• Tall or "tented" symmetrical T waves may indicate hyperkalemia. Flat T waves may indicate coronary ischemia or hypokalemia.
• The earliest electrocardiographic finding of acute myocardial infarction is sometimes the hyperacute T wave, which can be distinguished from hyperkalemia by the broad base and slight asymmetry.
• When a conduction abnormality (e.g., left bundle branch block, paced rhythm) is present, the T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance.

 QT interval

Main article: QT interval

The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Normal values for the QT interval are between 0.30 and 0.44 seconds.^{[citation needed]} The QT interval as well as the corrected QT interval are important in the diagnosis of long QT syndrome and short QT syndrome. Long QT intervals may also be induced by antiarrythmic agents that block potassium channels in the cardiac myocyte. The QT interval varies based on the heart rate, and various correction factors have been developed to correct the QT interval for the heart rate. The QT interval represents on an ECG the total time needed for the ventricles to depolarize and repolarize.

The most commonly used method for correcting the QT interval for rate is the one formulated by Bazett and published in 1920.^[24] Bazett's formula is , where QTc is the QT interval corrected for rate, and RR is the interval from the onset of one QRS complex to the onset of the next QRS complex, measured in seconds. However, this formula tends to be inaccurate, and over-corrects at high heart rates and under-corrects at low heart rates.

QTc may also be found via the following formula: QTc = QT + 1.75(Ventricular Rate - 60).

 U wave

An electrocardiogram of an 18-year-old man showing U waves, most evident in lead V3.

The U wave is not always seen. It is typically small, and, by definition, follows the T wave. U waves are thought to represent repolarization of the papillary muscles or Purkinje fibers.^[25] Prominent U waves are most often seen in hypokalemia, but may be present in hypercalcemia, thyrotoxicosis, or exposure to digitalis, epinephrine, and Class 1A and 3 antiarrhythmics, as well as in congenital long QT syndrome and in the setting of intracranial hemorrhage. An inverted U wave may represent myocardial ischemia or left ventricular volume overload.^[26]

 Clinical lead groups

Diagram showing the contiguous leads in the same color

Main article: Myocardial infarction

There are twelve leads in total, each recording the electrical activity of the heart from a different perspective, which also correlate to different anatomical areas of the heart for the purpose of identifying acute coronary ischemia or injury. Two leads that look at the same anatomical area of the heart are said to be contiguous (see color coded chart).

• The inferior leads (leads II, III and aVF) look at electrical activity from the vantage point of the inferior (or diaphragmatic) surface.
• The lateral leads (I, aVL, V₅ and V₆) look at the electrical activity from the vantage point of the lateral wall of left ventricle. The positive electrode for leads I and aVL should be located distally on the left arm and because of which, leads I and aVL are sometimes referred to as the high lateral leads. Because the positive electrodes for leads V5 and V6 are on the patient's chest, they are sometimes referred to as the low lateral leads.
• The septal leads, V₁ and V₂ look at electrical activity from the vantage point of the septal wall of the ventricles.
• The anterior leads, V₃ and V₄ look at electrical activity from the vantage point of the anterior surface of the heart.
• In addition, any two precordial leads that are next to one another are considered to be contiguous. For example, even though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another.
• Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the endocardial wall to the surface of the right atrium, from its perspective on the right shoulder.

 Axis

Diagram showing how the polarity of the QRS complex in leads I, II, and III can be used to estimate the heart's electrical axis in the frontal plane.

The heart's electrical axis refers to the general direction of the heart's depolarization wavefront (or mean electrical vector) in the frontal plane. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system, although -30^o to +90^o is considered to be normal.

Normal	-30o to 90o	Normal	Normal
Left axis deviation	-30o to -90o	May indicate left anterior fascicular block or Q waves from inferior MI.	Left axis deviation is considered normal in pregnant women and those with emphysema.
Right axis deviation	+90o to +180o	May indicate left posterior fascicular block, Q waves from high lateral MI, or a right ventricular strain pattern.	Right deviation is considered normal in children and is a standard effect of dextrocardia.
Extreme right axis deviation	+180o to -90o	Is rare, and considered an 'electrical no-man's land'.

In the setting of right bundle branch block, right or left axis deviation may indicate bifascicular block.

 Electrocardiogram heterogeneity

Electrocardiogram (ECG) heterogeneity is a measurement of the amount of variance between one ECG waveform and the next. This heterogeneity can be measured by placing multiple ECG electrodes on the chest and by then computing the variance in waveform morphology across the signals obtained from these electrodes. Recent research suggests that ECG heterogeneity often precedes dangerous cardiac arrhythmias.

 Background

There are over 350,000 cases of sudden cardiac death (SCD) in the United States each year, and over twenty percent of these cases involve people with no outward signs of serious heart disease. For decades, researchers have been attempting to come up with methods of identifying electrocardiogram (ECG) patterns that reliably precede dangerous arrhythmias. As these methods are found, devices are being created that monitor the heart in order to detect the onset of dangerous rhythms and to correct them before they cause death.

 Research

Research being conducted^[27] suggests that a crescendo in ECG heterogeneity, both in the R-wave and the T-wave, often signals the start of ventricular fibrillation. In patients with coronary artery disease, exercise increases T-wave heterogeneity, but this effect is not seen in normal patients. These results, when combined with other pieces of emerging evidence, suggest that R-wave and T-wave heterogeneity both have predictive value.

 Future applications

In the future, researchers hope to automate the process of heterogeneity detection and to augment the clinical evidence supporting the validity of ECG heterogeneity as a predictor of arrhythmia. Someday soon, implantable devices may be programmed to measure and track heterogeneity. These devices could potentially help ward off arrhythmias by stimulating nerves such as the vagus nerve, by delivering drugs such as beta-blockers, and if necessary, by defibrillating the heart.^[28]

 See also

• Advanced cardiac life support (ACLS)
• Angiogram
• HEART scan
• Ballistocardiograph
• Bundle branch block
• Cardiac cycle
• Echocardiogram
• Electrical conduction system of the heart
• Electrocardiogram technician
• Electroencephalography
• Electrogastrogram
• Electropalatograph
• Electroretinography
• Heart rate monitor
• Holter monitor
• Intrinsicoid deflection
• Magnetic field imaging
• Magnetocardiography
• Myocardial infarction
• Open ECG project
• Treacherous technician syndrome

 References

1. ^ ECG- simplified. Aswini Kumar M.D
2. ^ Braunwald E. (Editor), Heart Disease: A Textbook of Cardiovascular Medicine, Fifth Edition, p. 108, Philadelphia, W.B. Saunders Co., 1997. ISBN 0-7216-5666-8.
3. ^ "The clinical value of the ECG in noncardiac conditions." Chest 2004; 125(4): 1561-76. PMID 15078775
4. ^ "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." Circulation 2005; 112: IV-89 - IV-110.
5. ^ Ronald M. Birse, rev. Patricia E. Knowlden [1] Oxford Dictionary of National Biography 2004 (Subscription required) - (original source is his biography written by his wife - Elizabeth Muirhead. Alexander Muirhead 1848 - 1920. Oxford, Blackwell: privately printed 1926.)
6. ^ Burdon Sanderson J (1878). "Experimental results relating to the rhythmical and excitatory motions of the ventricle of the frog heart". Proc Roy Soc Lond 27: 410–14. doi:10.1098/rspl.1878.0068. 
7. ^ Waller AD (1887). "A demonstration on man of electromotive changes accompanying the heart's beat". J Physiol (Lond) 8: 229–34. 
8. ^ Einthoven W. Un nouveau galvanometre. Arch Neerl Sc Ex Nat 1901; 6:625
9. ^ Cooper J (1986). "Electrocardiography 100 years ago. Origins, pioneers, and contributors". N Engl J Med 315 (7): 461–4. PMID 3526152. 
10. ^ Mark, Jonathan B. (1998). Atlas of cardiovascular monitoring. New York: Churchill Livingstone. ISBN 0443088918. .
11. ^ Mark JB "Atlas of Cardiovascular Monitoring." p. 130. New York: Churchill Livingstone, 1998. ISBN 0-443-08891-8.
12. ^ See images of ECG electrodes here: https://www.superboverseas.com/show_product.asp?id=104 or here: https://images.google.com/images?q=ecg+electrode&oe=UTF-8&rls=org.mozilla:en-US:official&client=firefox-a&um=1&ie=UTF-8&sa=N&tab=wi&ei=IOEHSqCELp3ItgeY8_2HBw&oi=property_suggestions&resnum=0&ct=property-revision&cd=1)
13. ^ https://library.med.utah.edu/kw/ecg/ecg_outline/Lesson1/lead_dia.html
14. ^ https://www.welchallyn.com/documents/Cardiopulmonary/Electrocardiographs/PC-Based Exercise Stress ECG/poster_110807_pcexerecg.pdf
15. ^ https://academic.cuesta.edu/fjohnson/PowerPoint_PDF/12leadecg.pdf
16. ^ https://www.cvphysiology.com/Arrhythmias/A013.htm
17. ^ https://davidge2.umaryland.edu/~emig/ekgtu03.html
18. ^ https://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/limb_leads.php
19. ^ https://library.med.utah.edu/kw/ecg/ecg_outline/Lesson1/index.html#orientation
20. ^ https://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/bipolar_leads.php
21. ^ https://davidge2.umaryland.edu/~emig/ekgtu03.html
22. ^ Watch a movie by the National Heart Lung and Blood Institute explaining the connection between an ECG and the electricity in your heart at this site https://www.nhlbi.nih.gov/health/dci/Diseases/hhw/hhw_electrical.html
23. ^ Sabatine MS (2000). Pocket Medicine (Pocket Notebook). Lippincott Williams & Wilkins. ISBN 0-7817-1649-7. 
24. ^ Bazett HC (1920). "An analysis of the time-relations of electrocardiograms". Heart 7: 353–70. 
25. ^ Pérez Riera AR, Ferreira C, Filho CF, et al. (2008). "The enigmatic sixth wave of the electrocardiogram: the U wave". Cardiol J 15 (5): 408–21. PMID 18810715. https://www.cardiologyjournal.org/en/darmowy_pdf.phtml?indeks=86&indeks_art=1123. 
26. ^ Conrath C, Opthof T (2005). "The patient U wave". Cardiovasc Res 67 (2): 184–6. doi:10.1016/j.cardiores.2005.05.027. PMID 15979057. 
27. ^ In the lab of Richard L. Verrier of Harvard Medical School
28. ^ Verrier, Richard L. “Dynamic Tracking of ECG Heterogeneity to Estimate Risk of Life-threatening Arrhythmias.” CIMIT Forum. September 25, 2007.

 External links

• Explanation of what an ECG is, who needs one, what to expect during one, etc. Written by the National Heart Lung and Blood Institute (a division of the NIH) [5]
• Introduction to EKG's as written by a medical student and a cardiologist [6]
• ECG in 100 steps: Slideshow
• A teaching guide "designed for student nurses who know nothing at all about Cardiology" [7]
• ECGpedia: Course for interpretation of ECG
• ECG library
• Forum on cardiology discussions - Free registration
• 12-lead ECG library
• Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
• Minnesota ECG Code
• openECGproject - help develop an open ECG solution
• A guide to reading ECG's written by a college (not medical school) professor [8]
• Electrocardiogram (ECG) and intravascular Doppler ultrasound - combined to accurately guide and place vascular access devices

Medical monitor

 

Medical monitor as used in anesthesia

A medical monitor is an automated medical electronic device that measures a patient's vital signs and displays the data so obtained, which may or may not be transmitted on a monitoring network.

Monitors may be classified as

1. Handheld
2. Portable
3. Tabletop
4. Networkable / non-networkable
5. Mains powered or mains + battery powered

In critical care units of hospitals, it allows continuous monitoring of a patient, with medical staff being continuously informed of the changes in general condition of a patient.

Old patient monitors resembled oscilloscopes and computer monitors and use superficially similar technology. However, medical monitors have been safety engineered so that failures are either apparent or unimportant.^{[citation needed]}

Some monitors (for example ECG and EEG) have an electrical contact with the patient. There are strict limits on how much current and voltage can be applied, even if the unit fails or becomes wet.^{[citation needed]} They must typically withstand electrical defibrillation without damage.

In the past, medical monitors tended to be highly specialized. One monitor would track a patient's blood pressure, while another would measure pulse oximetry. Today the trend is toward multi-parameter monitors that can track many different vital signs at once.^{[citation needed]}

 See also

• Medical equipment
• Medical test
• BIS monitor
• Pulse oximeter

Cardiology

A diagram of a heart with an ECG indicator; diagrams like this are used in Cardiology.

Cardiology (from Greek καρδίᾱ, kardiā, "heart"; and -λογία, -logia) is a specialty dealing with disorders of the heart and blood vessels. The field includes diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians specializing in this field of medicine are called cardiologists. Cardiologists should not be confused with cardiac surgeons, cardiothoracic, and cardiovascular who are surgeons who perform cardiac surgery - operative procedures on the heart and great vessels.

The term cardiology is derived from the Greek word καρδιά (transliterated as kardia and meaning heart or inner self).

Contents   1 The Cardiac Muscle 1.1 Cardiac pacemaker (Electrical system of the heart) 1.2 Basic cardiac physiology 2 Disorders of the heart 3 Disorders of the coronary circulation 4 Sudden cardiac death (The abrupt reduction or cessation of blood flow to the myocardium, leading to death) 4.1 Treatment of sudden cardiac death 5 Disorders of the myocardium (muscle of the heart) 6 Disorders of the pericardium (outer lining of the heart) 7 Disorders of the heart valves 8 Disorders of the electrical system of the heart (Cardiac electrophysiology) 9 Inflammation and infection of the heart 10 Congenital heart disease 11 Diseases of blood vessels (Vascular diseases) 12 Procedures done for coronary artery disease 13 Devices used in cardiology 14 Diagnostic tests and procedures 15 Cardiac pharmaceutical agents 16 See also 17 External links

 The Cardiac Muscle

Main article: heart

 Cardiac pacemaker (Electrical system of the heart)

• Electrical conduction system of the heart
  • Action potential
    • Ventricular action potential
• Sinoatrial node
• Atrioventricular node
• Bundle of His
• Purkinje fibers
• Heart Attack (Myocardial Infarction)

 Basic cardiac physiology

• Systole
• Diastole
• Heart sounds
• Preload
• Afterload
• Kussmaul's sign

 Disorders of the heart

Main article: Heart Disease

 Disorders of the coronary circulation

• Atherosclerosis
• Restenosis
• Coronary heart disease (Ischaemic heart disease, Coronary artery disease)
• Acute coronary syndrome
  • Angina
  • Myocardial infarction (Heart attack)

 Sudden cardiac death (The abrupt reduction or cessation of blood flow to the myocardium, leading to death)

• Cardiac arrest

 Treatment of sudden cardiac death

• Cardiopulmonary resuscitation (CPR)

Anemia

 Disorders of the myocardium (muscle of the heart)

• Cardiomyopathy
  • Ischemic cardiomyopathy
  • Nonischemic cardiomyopathy
    • Amyloid cardiomyopathy
    • Hypertrophic cardiomyopathy (HCM)
      • Hypertrophic obstructive cardiomyopathy (HOCM) (Idiopathic hypertrophic subaortic stenosis (IHSS))
      • hypertrophic cardiomyopathy
    • Dilated cardiomyopathy
      • Alcoholic cardiomyopathy
      • Tachycardia induced cardiomyopathy
      • Takotsubo cardiomyopathy (Transient apical ballooning, stress-induced cardiomyopathy)
    • Arrhythmogenic right ventricular dysplasia (Arrhythmogenic right ventricular cardiomyopathy)
    • Restrictive cardiomyopathy
• Congestive heart failure
  • Cor pulmonale
• Ventricular hypertrophy
  • Left ventricular hypertrophy
  • Right ventricular hypertrophy
• Primary tumors of the heart
  • Myxoma
• Myocardial rupture

 Disorders of the pericardium (outer lining of the heart)

• Pericarditis
• Pericardial tamponade
• Constrictive pericarditis

 Disorders of the heart valves

• Aortic valve disorders
  • Aortic insufficiency
  • Aortic stenosis
  • Aortic valve replacement
  • Aortic valve repair
  • Aortic valvuloplasty
• Mitral valve disorders
  • Mitral valve prolapse
  • Mitral regurgitation
  • Mitral stenosis
  • Mitral valve replacement
  • Mitral valve repair
  • Mitral valvuloplasty
• Pulmonary valve disorders
  • Congenital pulmonic stenosis
• Tricuspid valve disorders

 Disorders of the electrical system of the heart (Cardiac electrophysiology)

• Tachycardia
• Cardiac arrhythmias
  • Supraventricular tachycardia (Fast rhythms that originate above the ventricles)
    • Atrial fibrillation
    • Atrial flutter
    • Atrial tachycardia
    • Sick sinus syndrome
      • AV nodal reentrant tachycardia (AVNRT)
      • AV reentrant tachycardia (AVRT)
  • Bigemin
  • Premature ventricular contraction
  • Ventricular tachycardia
    • Torsades de pointes
  • Ventricular fibrillation
  • Bundle branch block
    • Left bundle branch block
    • Right bundle branch block
  • Heart block
    • First degree AV block
    • Second degree AV block
    • Bifascicular block
    • Trifascicular block
    • Third degree AV block
      • Lev's disease
• Specific diseases of the electrical system of the heart
  • Brugada syndrome
  • Long QT syndrome
    • Andersen-Tawil syndrome
    • Romano-Ward syndrome
    • Jervell and Lange-Nielsen syndrome
  • Short QT syndrome
  • Wolff-Parkinson-White syndrome (WPW syndrome)

 Inflammation and infection of the heart

• Endocarditis
  • Rheumatic heart disease
• Myocarditis
• Pericarditis

 Congenital heart disease

• Atrial septal defect
• Ventricular septal defect
• Patent ductus arteriosus
• Bicuspid aortic valve
• Tetralogy of Fallot
• Transposition of the great vessels (TGV)
• Hypoplastic left heart syndrome
• Truncus Arteriosus

 Diseases of blood vessels (Vascular diseases)

• Vasculitis
• Atherosclerosis
• Aneurysm
• Varicose veins
• Economy class syndrome
• Diseases of the aorta
  • Coarctation of the aorta
  • Aortic dissection
  • Aortic aneurysm
• Diseases of the carotid arteries
  • Carotid artery disease
  • Carotid artery dissection

 Procedures done for coronary artery disease

• Percutaneous coronary intervention
  • Atherectomy
  • Angioplasty (PTCA)
  • Stenting
• Coronary artery bypass surgery (CABG)
• Enhanced external counterpulsation (EECP)

 Devices used in cardiology

• Stethoscope
• Devices used to maintain normal electrical rhythm
  • Pacemaker
  • Defibrillator
    • Automated external defibrillator
    • Implantable cardioverter-defibrillator
• Devices used to maintain blood pressure
  • Artificial heart
  • Heart-lung machine
  • Intra-aortic balloon pump
  • Ventricular assist device

 Diagnostic tests and procedures

• Blood tests
• Echocardiogram
• Cardiovascular Magnetic Resonance
• Cardiac stress test
• Auscultation (Listening with the Stethoscope)

Electrocardiogram (ECG or EKG)

• • QT interval
  • Osborn wave
• Ambulatory Holter monitor
• Electrophysiologic study
  • Programmed electrical stimulation
• Sphygmomanometer (Blood pressure cuff)
• Cardiac enzymes
• Coronary catheterization
  • Myocardial Fractional Flow Reserve (FFRmyo)
  • IVUS (IntraVascular UltraSound)

 Cardiac pharmaceutical agents

The followings are medications commonly prescribed in cardiology:

• Antiarrhythmic agents
  • Type I (sodium channel blockers)
    • Type Ia
      • Quinidine
    • Type Ib
      • Lidocaine
      • Phenytoin
    • Type Ic
      • Propafenone
  • Type II (beta blockers)
    • Metoprolol
  • Type III (potassium channel blockers)
    • Amiodarone
    • Dofetilide
    • Sotalol
  • Type IV (slow calcium channel blockers)
    • Diltiazem
    • Verapamil
  • Type V
    • Adenosine
    • Digoxin
• ACE inhibitors
  • Captopril
  • Enalapril
  • Perindopril
  • Ramipril
• Angiotensin II receptor antagonists
  • Candesartan
  • Eprosartan
  • Irbesartan
  • Losartan
  • Telmisartan
  • Valsartan
• Beta blocker
• Calcium channel blocker

 See also

• Interventional cardiology
• Clinical cardiac electrophysiology
• American Heart Association
• National Heart Foundation of Australia

 External links

• Cardiology News
• Cardiology Rounds
• European Society of Cardiology
• U.S. National Institute of Health (NIH) : Heart and Circulation
• American College of Cardiology
• Virtual Cardiac Centre - information from the field of Cardiology.
• Cardiovascular Physiology - basic concepts in cardiology.
• Preventive Cardiology
• A cardiac atlas using CMR images

Heart

The heart is a muscular organ in all vertebrates responsible for pumping blood through the blood vessels by repeated, rhythmic contractions, or a similar structure in annelids, mollusks, and arthropods. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδιά, kardia, for "heart."

The heart of a vertebrate is composed of cardiac muscle, an involuntary striated muscle tissue which is found only within this organ. The average human heart, beating at 72 beats per minute, will beat approximately 2.5 billion times during a lifetime (about 66 years). It weighs on average 250 g to 300 g in females and 300 g to 350 g in males.^[1]

Contents   1 Early development 2 Structure 3 Functioning 4 First aid 5 History of discoveries 6 Healthy heart 7 See also 8 References 9 External links

 Early development

Main article: Heart development

The mammalian heart is derived from embryonic mesoderm germ-layer cells that differentiate after gastrulation into mesothelium, endothelium, and myocardium. Mesothelial pericardium forms the inner lining of the heart. The outer lining of the heart, lymphatic and blood vessels develop from endothelium. Myocardium develops into heart muscle. ^[2]

From splachnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity and begin to fuse together and are completely fused at approximately 21 days.^[3]

At 21 days after conception, the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating.

The human embryonic heart begins beating around 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. It is unknown how blood in the human embryo circulates for the first 21 days in the absence of a functioning heart. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM).

The embryonic heart rate (EHR) then accelerates approximately 100 BPM during the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, an increase of 100 BPM in the first month.^[4] After 9.1 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 BPM) BPM at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is: Age in days = EHR(0.3)+6.

There is no difference in male and female heart rates before birth.^[5]

 Structure

The structure of the heart varies among the different branches of the animal kingdom. (See Circulatory system.) Cephalopods have two "gill hearts" and one "systemic heart". Fish have a two-chambered heart that pumps the blood to the gills and from there it goes on to the rest of the body. In amphibians and most reptiles, a double circulatory system is used, but the heart is not always completely separated into two pumps. Amphibians have a three-chambered heart.

Human heart removed from a 64-year-old male.

Surface anatomy of the human heart. The heart is demarcated by:
-A point 9 cm to the left of the midsternal line (apex of the heart)
-The seventh right sternocostal articulation
-The upper border of the third right costal cartilage 1 cm from the right sternal line
-The lower border of the second left costal cartilage 2.5 cm from the left lateral sternal line.^[6]

Birds and mammals show complete separation of the heart into two pumps, for a total of four heart chambers; it is thought that the four-chambered heart of birds evolved independently from that of mammals.

In the human body, the heart is usually situated in the middle of the thorax with the largest part of the heart slightly offset to the left (although sometimes it is on the right, see dextrocardia), underneath the sternum. The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is fed by the coronary circulation and enclosed by a sac known as the pericardium and is surrounded by the lungs. The pericardium comprises two parts: the fibrous pericardium, made of dense fibrous connective tissue; and a double membrane structure (parietal and visceral pericardium) containing a serous fluid to reduce friction during heart contractions. The heart is located in the mediastinum, the central sub-division of the thoracic cavity. The mediastinum also contains other structures, such as the esophagus and trachea, and is flanked on either side by the right and left pulmonary cavities, which house the lungs. ^[7]

The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. It is located posterior to the 5th intercostal space just medial of the left mid-clavicular line. In normal adults, the mass of the heart is 250-350 g (9-12 oz), or about twice the size of a clenched fist (it is about the size of a clenched fist in children), but extremely diseased hearts can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria and the two lower ventricles.

 Functioning

In mammals, the function of the right side of the heart (see right heart) is to collect de-oxygenated blood, in the right atrium, from the body (via superior and inferior vena cavae) and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through the passive process of diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body (via the aorta). On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.

Starting in the right atrium, the blood flows through the tricuspid valve to the right ventricle. Here it is pumped out the pulmonary semilunar valve and travels through the pulmonary artery to the lungs. From there, blood flows back through the pulmonary vein to the left atrium. It then travels through the mitral valve to the left ventricle, from where it is pumped through the aortic semilunar valve to the aorta. The aorta forks and the blood is divided between major arteries which supply the upper and lower body. The blood travels in the arteries to the smaller arterioles, then finally to the tiny capillaries which feed each cell. The (relatively) deoxygenated blood then travels to the venules, which coalesce into veins, then to the inferior and superior venae cavae and finally back to the right atrium where the process began.

The heart is effectively a syncytium, a meshwork of cardiac muscle cells interconnected by contiguous cytoplasmic bridges. This relates to electrical stimulation of one cell spreading to neighboring cells.

Some cardiac cells are self-excitable, contracting without any signal from the nervous system, even if removed from the heart and placed in culture. Each of these cells has its own intrinsic contraction rhythm. A region of the human heart called the sinoatrial node SA node, or pacemaker, sets the rate and timing at which all cardiac muscle cells contract. The SA node generates electrical impulses, much like those produced by nerve cells. Because cardiac muscle cells are electrically coupled by inter-calated disks between adjacent cells, impulses from the SA node spread rapidly through the walls of the artria, causing both artria to contract in unison. The impulses also pass to another region of specialized cardiac muscle tissue, a relay point called the atrioventricular (AV) node, located in the wall between the right artrium and the right ventricle. Here, the impulses are delayed for about 0.1s before spreading to the walls of the ventricle. The delay ensures that the artria empty completely before the ventricles contract. Specialized muscle fibers called Purkinje fibers then conduct the signals to the apex of the heart along and throughout the ventricular walls. The Purkinje fibres form conducting pathways called bundle branches. The impulses generated during the heart cycle produce electrical currents, which are conducted through body fluids to the skin, where they can be detected by electrodes and recorded as an electrocardiogram (ECG or EKG).^[8]

 First aid

Heart

Cardiac arrest is the sudden cessation of normal heart rhythm which can include a number of pathologies such as tachycardia, an extremely rapid heart beat which prevents the heart from effectively pumping blood, fibrillation which is an irregular and ineffective heart rhythm, and asystole which is the cessation of heart rhythm entirely. Without intervention, death can occur within minutes of cardiac arrest.

If a person is found in cardiac arrest, cardiopulmonary resuscitation (CPR) should be started and help called. A defibrillator, either manual or automated external defibrillator (AED), may be used by trained first responders to attempt to restore a normal heart rhythm. Note that only ventricular fibrillation and tachycardia are reversible using a defibrillator. Other irregular rhythms and asystole cannot be reversed using a defibrillator. If a normal rhythm cannot be restored, CPR should continue. In any case, the patient should be transported rapidly to a hospital where they can be treated in the Emergency Department and cardiac care unit.

A precordial thump (striking a person on the chest) should never be used by untrained personnel in an attempt to restart a heart. A precordial thump is only effective when it is done precisely and when timed by a cardiac monitoring electrocardiograph (EKG or ECG).

Cardiac Tamponade is a condition in which the fibrous sac surrounding the heart fills with excess fluid or blood, suppressing the heart's ability to beat properly. Tamponade is treated by pericardiocentesis, the gentle insertion of the needle of a syringe into the pericardial sac (avoiding the heart itself) on an angle, usually from just below the sternum, and gently withdrawing the tamponading fluids.

 History of discoveries

A heart with a gun shot wound

The valves of the heart were discovered by a physician of the Hippocratean school around the 4th century BC. However, their function was not properly understood then. Because blood pools in the veins after death, arteries look empty. Ancient anatomists assumed they were filled with air and that they were for transport of air.

Philosophers distinguished veins from arteries but thought that the pulse was a property of arteries themselves. Erasistratos observed that arteries that were cut during life bleed. He ascribed the fact to the phenomenon that air escaping from an artery is replaced with blood that entered by very small vessels between veins and arteries. Thus he apparently postulated capillaries but with reversed flow of blood.

The 2nd century AD, Greek physician Galenos (Galen) knew that blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions. Growth and energy were derived from venous blood created in the liver from chyle, while arterial blood gave vitality by containing pneuma (air) and originated in the heart. Blood flowed from both creating organs to all parts of the body where it was consumed and there was no return of blood to the heart or liver. The heart did not pump blood around, the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.

Galen believed that the arterial blood was created by venous blood passing from the left ventricle to the right by passing through 'pores' in the inter ventricular septum, air passed from the lungs via the pulmonary artery to the left side of the heart. As the arterial blood was created 'sooty' vapors were created and passed to the lungs also via the pulmonary artery to be exhaled.

The first major scientific understanding of the heart was put forth by the medieval Arab polymath Ibn Al-Nafis, regarded as the father of circulatory physiology.^[9] He was the first physician to correctly describe pulmonary circulation,^[10] the capillary^[11] and coronary circulations.^[12]

Prior to Ibn Al-Nafis, the theory that was widely accepted was that of Galen's, which was slightly improved upon by Avicenna. Ibn Al-Nafis rejected the Galen-Avicenna theory and corrected many wrong ideas that were put forth by it, and also adding his new found observations of pulse and circulation to the new theory.

Ibn Al-Nafis' major observations include (as surmised by Dr. Paul Ghalioungui):^[11]

1. "Denying the existence of any pores through the interventricular septum."

2. "The flow of blood from the right ventricle to the lungs where its lighter parts filter into the pulmonary vein to mix with air."

3. "The notion that blood, or spirit from the mixture of blood and air, passes from the lung to the left ventricle, and not in the opposite direction."

4. "The assertion that there are only two ventricles, not three as stated by Avicenna."

5. "The statement that the ventricle takes its nourishment from blood flowing in the vessels that run in its substance (i.e. the coronary vessels) and not, as Avicenna maintained, from blood deposited in the right ventricle."

6. "A premonition of the capillary circulation in his assertion that the pulmonary vein receives what comes out of the pulmonary artery, this being the reason for the existence of perceptible passages between the two."

Ibn Al-Nafis also corrected Galen-Avicenna assertion that heart has a bone structure through his own observations and wrote the following criticism on it:^[13]

"This is not true. There are absolutely no bones beneath the heart as it is positioned right in the middle of the chest cavity where there are no bones at all. Bones are only found at the chest periphery not where the heart is positioned."

 Healthy heart

Obesity, high blood pressure and high cholesterol can increase the risk of developing heart disease. However, fully half the amount of heart attacks occur in people with normal cholesterol levels. Heart disease is a major cause of death (and the number one cause of death in the Western World).

Of course one must also consider other factors such as lifestyle and overall health (mental and social as well as physical).^{[14][15][16][17]}

 See also

• Cardiac cycle
• Heart disease
• Human heart
• Electrocardiogram
• Electrical conduction system of the heart
• Physiology

 References

1. ^ Kumar, Abbas, Fausto: Robbins and Cotran Pathologic Basis of Disease, 7th Ed. p. 556
2. ^ Animal Tissues
3. ^ Main Frame Heart Development>
4. ^ OBGYN.net "Embryonic Heart Rates Compared in Assisted and Non-Assisted Pregnancies"
5. ^ Terry J. DuBose Sex, Heart Rate and Age
6. ^ Gray's Anatomy of the Human Body - 6. Surface Markings of the Thorax
7. ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey: Prentice Hall. ISBN 0-13-981176-1. OCLC 32308337. 
8. ^ Campbell, Reece-Biology, 7th Ed. p.873,874
9. ^ Chairman's Reflections (2004), "Traditional Medicine Among Gulf Arabs, Part II: Blood-letting", Heart Views 5 (2): 74-85 [80]
10. ^ S. A. Al-Dabbagh (1978). "Ibn Al-Nafis and the pulmonary circulation", The Lancet 1: 1148
11. ^ ^{a b} [1] Dr. Paul Ghalioungui (1982), "The West denies Ibn Al Nafis's contribution to the discovery of the circulation", Symposium on Ibn al-Nafis, Second International Conference on Islamic Medicine: Islamic Medical Organization, Kuwait (cf.) The West denies Ibn Al Nafis's contribution to the discovery of the circulation
12. ^ Husain F. Nagamia (2003), "Ibn al-Nafīs: A Biographical Sketch of the Discoverer of Pulmonary and Coronary Circulation", Journal of the International Society for the History of Islamic Medicine 1: 22–28.
13. ^ Dr. Sulaiman Oataya (1982), "Ibn ul Nafis has dissected the human body", Symposium on Ibn al-Nafis, Second International Conference on Islamic Medicine: Islamic Medical Organization, Kuwait (cf. Ibn ul-Nafis has Dissected the Human Body, Encyclopedia of Islamic World).
14. ^ "Eating for a healthy heart". MedicineWeb. https://www.medicineweb.com/nutrition-/eating-for-a-healthy-heart. Retrieved on 2009-03-31. 
15. ^ Division of Vital Statistics; Arialdi M. Miniño, M.P.H., Melonie P. Heron, Ph.D., Sherry L. Murphy, B.S., Kenneth D. Kochanek, M.A. (2007-08-21). "Deaths: Final data for 2004" (PDF). National Vital Statistics Reports (United States: Center for Disease Control) 55 (19): 7. https://www.cdc.gov/nchs/data/nvsr/nvsr55/nvsr55_19.pdf. Retrieved on 2007-12-30. 
16. ^ White House News. "American Heart Month, 2007". https://georgewbush-whitehouse.archives.gov/news/releases/2007/02/20070201-2.html. Retrieved on 2007-07-16. 
17. ^ National Statistics Press Release 25 May 2006

 External links

• Heart contraction and blood flow (animation)
• Heart Disease
• eMedicine: Surgical anatomy of the heart
• Interactive 3D heart This realistic heart can be rotated, and all its components can be studied from any angle.
• Heart Information

aVR = -(I + II)/2

aVL = I - II/2

aVF = II - I/2

这个公式值得保留 2通道出5道就是用的这个公式