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كورس The ECG course رسم القلب {ج1.}

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The ECG course
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Arrhythmias:
- supraventricular
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AV Conduction
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Myocardial Infarction
QRS axis and voltage
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Page information This page was last edited on 3 March 200


===========================

Introduction


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«/ Basics»
 

Author(s) J.S.S.G. de Jong, MD
Moderator J.S.S.G. de Jong, MD
Supervisor

some notes about authorship




A short ECG registration of normal heart rhythm (sinus rhythm)

The aim of this course is to enable the student to understand and recognize normal ECGs and interpret abnormalities. The course is divided into two different sections. First the basics will be presented. This is followed by the interpretation of the normal ECG according to the 7+2 step plan:
7+2 step plan

Step 1: Rhythm
Step 2: Rate
Step 3: Conduction (PQ,QRS,QT)
Step 4: Heart axis
Step 5: P wave morphology
Step 6: QRS morphology
Step 7: ST morphology
Step 7+1: Compare the current ECG with a previous one
Step 7+2: Conclusion


Note: It is important to realize that not all these steps may be applicable when you encounter ECG abnormalities. If, for example, the rhythm is not sinus in the first step, the algorithm to analyze arrhythmias should be followed. If a Left Bundle Branch Block is present in step 3, ST morphology will be strongly influenced by this defect.

Finally the real world is presented through practice ECGs.

After you have finished the course you are invited to come back to read more about abnormal ECGs in the ECG textbook.
ECG textbook

Normal Tracing
A Concise History of the ECG
Technical Problems
Sinus Rhythms Sinus Tachycardia
Sinus Bradycardia
Arrhythmias: Supraventricular
Junctional
Ventricular
Genetic
Ectopic Beats
AV Conduction
Intraventricular Conduction
Myocardial Infarction
Chamber Hypertrophy
Repolarization
Clinical Disorders
Electrolyte Disorders
Pacemaker
ECGs in Athletes
ECGs in Children
Accuracy of Computer Interpretation Also read our Frequently Asked Questions section.
=====

Basics

Jump to navigation Jump to search

«Introduction Step 1: Rhythm»
 
Author(s) I.A.C. van der Bilt, MD
Moderator I.A.C. van der Bilt, MD
Supervisor

some notes about authorship

Contents 1 How do I begin to read an ECG?
2 What does the ECG register?
3 The ECG represents the sum of the action potentials of millions of cardiomyocytes
4 The electric discharge of the heart
5 The different ECG waves
6 The history of the ECG
7 The ECG electrodes 7.1 The Extremity Leads
7.2 The Chest Leads
8 ECG variants
9 Color coding of the ECG leads
10 Special Leads
11 Ladder diagram
12 Technical Problems
13 References
How do I begin to read an ECG?




A short ECG registration of normal heart rhythm (sinus rhythm)


An example of a normal ECG. Click on the Image for an enlargement

Click on the ECG to see an enlargement. Where do you start when interpreting an ECG? On the top left are the patient's information, name, sex and date of birth
At the right of that are below each other the Frequency, the conduction times (PQ,QRS,QT/QTc), and the heart axis (P-top axis, QRS axis and T-top axis)
Farther to the right is the interpretation of the ECG written (this may be missing in a 'fresh' ECG, but later the interpretation of the cardiologist or computer will be added)
Down left is the 'paper speed' (25 mm/s on the horizontal axis), the sensitivity (10mm/mV) and the filter's frequency (40Hz, filters noise from eg. lights).
There is a calibration. At the beginning of every lead is a vertical block that shows with what amplitude a 1 mV signal is drawn. So the height and depth of these signals are a measurement for the voltage. If this is not set at 10 mm, there is something wrong with the machine setting.
Finally we have the ECG leads themselves.These will be discussed below.

Note that the layout is different for each machine, but most machines will show the information above somewhere.

What does the ECG register? The electrocardiogramAn electrocardiogram (ECG or EKG) is a register of the heart's electrical activity.

Just like skeletal muscles, heart muscles are electrically stimulated to contract. This stimulation is also called activation or excitation. Cardiac muscles are electrically charged at rest. The inside of the cell is negatively charged relative to the outside (resting potential). If the cardiac muscle cells are electrically stimulated, they depolarize (the resting potential changes from negative to positive) and contract. The electrical activity of a single cell can be registered as the action potential. As the electrical impulse spreads through the heart, the electrical field changes continually in size and direction. The ECG is a graph of these electrical cardiac signals.
The ECG represents the sum of the action potentials of millions of cardiomyocytes




Ion currents of the cardiomyocytes


The heart consists of approximately 300 billion cells


In rest the heart cells are negatively charged. Through the depolarization by surrounding cells they become positively charged and they contract.
<youtube>j9w1qylp4TY</youtube>
This movie shows the contraction of a single (rabbit) heart cell. The glass electrode measures the electrical current in the heart cell (with thepatch-clamp method). The electrical signal is written in blue and shows the action potential. Courtesy of Arie Verkerk and Antoni van Ginneken, AMC, Amsterdam, The Netherlands.



The individual action potentials of the individual cardiomyocytes are averaged. The final result, which is shown on the ECG, is actually the average of billions of microscopic electrical signals.

During the depolarization, sodium ions stream into the cell. Subsequently, the calcium ions stream into the cell. These calcium ions cause the actual muscular contraction.

Finally the potassium ions stream out of the cell. During repolarization the ion concentration returns to its precontraction state. On the ECG, an action potential wave coming toward the electrode is shown as a positive (upwards) signal. Here the ECG electrode is represented as an eye.

The electric discharge of the heart


The conduction system of the heart



The sinoatrial node (SA node) contains the fastest physiological pacemaker cells of the heart; therefore, they determine the heart rate. First the atria depolarize and contract. After that the ventricles depolarize and contract. The electrical signal between the atria and the ventricles goes from the sinus node via the atria to the AV-node (atrioventricular transition) to the His bundle and subsequently to the right and left bundle branches, which end in a dense network of Purkinje fibers. The depolarization of the heart results in an electrical force which has a direction and magnitude; an electrical vector. This vector changes every millisecond of the depolarization. In the animation vectors for atrial depolarization, ventricular depolarization and ventricular repolarization are shown.

The different ECG waves


The origin of the different waves on the ECG




The QRS complex is formed by the sum of the electric avtivity of the inner (endocardial) and the outer (epicardial) cardiomyocytes


Example of the different QRS configurations

The P wave is the result of the atrial depolarization. This depolarization starts in the SA (sinoatrial) node. The signal produced by pacemaker cells in the SA node is conducted to the right and left atria. Normal atrial repolarization is not visible on the ECG (but can be visible during atrial infarction and pericarditis).

The QRS complex is the average of the depolarization waves of the inner (endocardial) and outer (epicardial) cardiomyocytes. As the endocardial cardiomyocytes depolarize slightly earlier than the outer layers, a typical QRS pattern occurs (figure).

The T wave represents the repolarization of the ventricles. There is no cardiac muscle activity during the T wave.

One heart beat consists of an atrial depolarization --> atrial contraction --> p-wave, ventricular depolarization --> ventricular contraction --> ORS-complex and the resting phase (including the repolarization during the T-wave) between two heart beats.

Have a look at this [animation of the heart cycle]

The origin of the U wave is unknown. This wave possibly results from "afterdepolarizations" of the ventricles.

The letters "Q", "R" and "S" are used to describe the QRS complex
Q: the first negative deflection after the p-wave. If the first deflection is not negative, the Q is absent.
R: the positive deflection
S: the negative deflection after the R-wave
Small print letters (q, r, s) are used to describe deflections of small amplitude. For example: qRS = small q, tall R, deep S.
R`: is used to describe a second R-wave (as in a right bundle branch block)

See figure for some examples of this.



The history of the ECG

A concise history of the ECG is presented in a different chapter.

The ECG electrodes




The limb leads


The chest leads

Electrical activity going through the heart can be measured by external (skin)electrodes. The electrocardiogram (ECG) registers these activities from electrodes which have been attached onto different places on the body. In total, twelve leads are calculated using ten electrodes.

The ten electrodes are: The four extremity electrodes: LA - left arm
RA - right arm
N - neutral, on the right leg (= electrical earth, or point zero, to which the electrical current is measured)
F - foot, on the left leg

It makes no difference whether the electrodes are attached proximal or distal on the extremities. However, it is best to be uniform in this. (eg. do not attach an electrode on the left shoulder and one on the right wrist). The six chest electrodes: V1 - placed in the 4th intercostal space, right of the sternum
V2 - placed in the 4th intercostal space, left of the sternum
V3 - placed between V2 and V4
V4 - placed 5th intercostal space in the nipple line. Official recommendations are to place V4 under the breast in women.[1]
V5 - placed between V4 and V6
V6 - placed in the midaxillary line on the same height as V4 (horizontal line from V4, so not necessarily in the 5th intercostal space)




With the use of these 10 electrodes, 12 leads can be derived. There are 6 extremity leads and 6 precordial leads.
The Extremity Leads



The extremity leads are: I from the right to the left arm
II from the right arm to the left leg
III from the left arm to the left leg

An easy rule to remember: lead I + lead III = lead II This is done with the use of the height or depth, independent of the wave (QRS, P of T). Example: if in lead I, the QrS complex is 3 mm in height and in lead III 9mm, the height of the QRS-complex in lead II is 12mm.

Other extremity leads are: AVL points to the left arm
AVR points to the right arm
AVF points to the feet

The capital A stands for "augmented" and V for "voltage".

(aVR + aVL + aVF = 0)

The Chest Leads

The precordial, or chest leads, (V1,V2,V3,V4,V5 and V6) 'observe' the depolarization wave in the frontal plane.

Example: V1 is close to the right ventricle and the right atrium. Signals in these areas of the heart have the largest signal in this lead. V6 is the closest to the lateral wall of the left ventricle.
ECG variants

Besides the standard 12 lead ECG a couple of variants are in use: The 3 channel ECG uses 3 or 4 ECG electrodes. Red is on the right, yellow on the left arm, green on the left leg ('sun shines on the grass') and black on the right leg. These basic leads yield enough information for rhythm-monitoring. For determination of ST elevation, these basic leads are inadequate as there is no lead that gives (ST) information about the anterior wall. ST changes registered during 3-4 channel ECG monitoring should prompt acquisition of a 12 lead ECG.
The 5 channel ECG uses 4 extremitiy leads and 1 precordial lead. This improves ST segment accuracy, but is still inferior to a 12 lead ECG. [2][3]
In vector electrocardiography the movement of electrical acitivity of the P, QRS and T wave is described. Additional X,Y and Z leads are recorded. Vector electrocardiography is rarely used nowadays, but is sometimes useful in a research setting.
In body surface mapping several arrays are used to accurately map the cardiac electrical wavefront as it moves over de body surface. With this information the electrical acitivity of the heart can be calculated. This is sometimes used in a research setting.
Color coding of the ECG leads

Two systems for ECG lead color coding are used: the AHA (American Heart Association) system and the IEC (International Electrotechnical Commission) system:

AHA (American Heart Association) IEC (International Electrotechnical Commission)
Location Inscription Colour Inscription Colour
Right Arm RA White R Red
Left Arm LA Black L Yellow
Right Leg RL Green N Black
Left Leg LL Red F Green
Chest V1 Brown/Red C1 White/Red
Chest V2 Brown/Yellow C2 White/Yellow
Chest V3 Brown/Green C3 White/Green
Chest V4 Brown/Blue C4 White/Brown
Chest V5 Brown/Orange C5 White/Black
Chest V6 Brown/Purple C6 White/Violet

Special Leads




Leads V7,V8 and V9 can be helpful in the diagnosis of posterior myocardial infarction


Changed lead positions of leads V3 and V5 to increase the sensitiviy to 'catch' a Brugada pattern on the ECG.




A patient with atrial fibrillation with a 'Lewis Lead' positioning of the leads. Compared with the normal lead configuration, the atrial signal is enlarged. Although some parts have a 'sawtooth' appearance consistent with atrial flutter, the rhythm is atrial fibrillation as there is a changing pattern in the atrial activity.


The same patient with a normal lead configuration. The rhythm is atrial fibrillation. The atrial activity in lead V1 is organized probably due to a organisation of electrical activity after it enters the right atrial appendage, close to lead V1.

Throughout history extra lead positions have been tried. Most are rarely used in practice, but they can deliver very valuable diagnostic clues in specific cases. Leads to improve diagnosis in right ventricular en posterior infarction:

In case of an inferior wall infarct, extra leads may be used: 1. On a right-sided ECG, V1 and V2 remain on the same place. V3 to V6 are placed on the same place but mirrored on the chest. So V4 is in the middle of the right clavicle. The ECG should be marked as a Right-sided ECG. V4R (V4 but right sided) is a sensitive lead for diagnosing right ventricular infarctions. 2. Leads V7-V8-V9 can be used to diagnose a posterior infarct. After V6, leads are placed towards the back. See the chapter Ischemia for other ways of diagnosing posterior infarction.


Leads to improve detection of atrial rhythm: In wide complex tachycardia, good detection of atrial rhythm and atrio-ventricular dissociation can be very helpful in the diagnosis process. An esophagal ECG electrode placed close to the atria can be helpful. Another, less invasive, method is the Lewis Lead. This is recorded by changing the limb electrodes, placing the right arm electrode in the second intercostal space and the left arm electrode in the fourth intercostal space, both to the right of the sternum. Furthermore gain is increased to 20mm/mV and paper speed to 50mm/sec.[4]ß Lead positioning to enhance detection of Brugada syndrome



Ladder diagram


A ladder diagram is a diagram that shows the presumed origin of impulse formation and conduction in the heart. A = atrial, AV = AV node, V = ventricles

A ladder diagram is a diagram to explain arrhythmias. The figure shows a simple ladder diagram for normal sinus rhythm, followed by av-nodal extrasystole. The origin of impulse formation (sinus node for the first two beats and AV junction for the third beat) and the conduction in the heart are shown. 



Technical Problems

Also read the chapter about Technical Problems. That will help you recognize electrical disturbances and lead reversals.


References Kligfield P, Gettes LS, Bailey JJ, Childers R, Deal BJ, Hancock EW, van Herpen G, Kors JA, Macfarlane P, Mirvis DM, Pahlm O, Rautaharju P, Wagner GS, American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology, American College of Cardiology Foundation, Heart Rhythm Society, Josephson M, Mason JW, Okin P, Surawicz B, and Wellens H. Recommendations for the standardization and interpretation of the electrocardiogram: part I: The electrocardiogram and its technology: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the International Society for Computerized Electrocardiology. Circulation. 2007 Mar 13;115(10):1306-24. DOI:10.1161/CIRCULATIONAHA.106.180200 | PubMed ID:17322457 | HubMed [Kligfield]
Rodrigues de Holanda-Miranda W, Furtado FM, Luciano PM, and Pazin-Filho A. Lewis lead enhances atrial activity detection in wide QRS tachycardia. J Emerg Med. 2012 Aug;43(2):e97-9. DOI:10.1016/j.jemermed.2009.08.057 | PubMed ID:20022196 | HubMed [Lewis1]



Du Bois-Reymond, E. Untersuchungen über thierische Elektricität. Reimer, Berlin: 1848. [Dubois]



Hoffa M, Ludwig C. 1850. Einige neue versuche uber herzbewegung. Zeitschrift Rationelle Medizin, 9: 107-144 [Hoffa]



Waller AD. A demonstration on man of electromotive changes accompanying the heart's beat. J Physiol (London) 1887;8:229-234 [Waller]



Einthoven W. Le telecardiogramme. Arch Int de Physiol 1906;4:132-164 [Einthoven]



Einthoven W. Über die Form des menschlichen Electrocardiogramms. Pfügers Archiv maart 1895, pagina 101-123 [Einthoven2]



Marey EJ. Des variations electriques des muscles et du couer en particulier etudies au moyen de l'electrometre de M Lippman. Compres Rendus Hebdomadaires des Seances de l'Acadamie des sciences 1876;82:975-977 [Marey]
Márquez MF, Colín L, Guevara M, Iturralde P, and Hermosillo AG. Common electrocardiographic artifacts mimicking arrhythmias in ambulatory monitoring. Am Heart J. 2002 Aug;144(2):187-97. DOI:10.1067/mhj.2002.124047 | PubMed ID:12177632 | HubMed [Marquez]
Hurst JW. Naming of the waves in the ECG, with a brief account of their genesis. Circulation. 1998 Nov 3;98(18):1937-42. DOI:10.1161/01.cir.98.18.1937 | PubMed ID:9799216 | HubMed [Hurst] All Medline abstracts: PubMed | HubMed ======================

الثلاثاء، 25 يوليو 2023

جلطة القلب {Myocardial Infarction }



Myocardial Infarction
موقع المشاركة https://en.ecgpedia.org/index.php?title=Main_Page
 
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Contents 1 Risk assessment of Cardiovascular disease
2 Risk assessment of ischemia
3 Diagnosis of myocardial infarction
4 The location of the infarct
5 Development of the ECG during persistent ischemia
6 Subendendocardial Ischemia
7 References
8 External Links
Author(s) I.A.C. van der Bilt, MD
Moderator I.A.C. van der Bilt, MD
Supervisor

some notes about authorship

Ischemia occurs when part of the heart muscle, the myocardium, is deprived of oxygen and nutrients. Common causes of ischemia are: Narrowing or obstruction of a coronary artery.
A rapid arrhythmia, causing an imbalance in supply and demand for energy.
A short period of ischemia causes reversible effects: The heart cells will be able to recover. When the episode of ischemia lasts for a longer period of time, heart muscle cells die. This is called a heart attack or myocardial infarction. That is why it is critical to recognize ischemia on the ECG in an early stage.
Severe ischemia results in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment.
Signs and symptoms of myocardial ischemia: Crushing pain on the chest (angina pectoris), behind the sternum, often radiating to the lower jaw or the left arm
Fear of dying
Nausea
Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock
Rhythm disturbances (in particular, increasing prevalence of ventricular ectopia, ventricular tachycardia, AV block)

Risk assessment of Cardiovascular disease
Narrowing of the coronary artery, leading to a myocardial infarction, usually develops over several years. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or cerebrovascular accident, can be estimated using SCORE system which is developed by the European Society of cardiology (ESC). As shown in the figure, the most important risk factors for myocardial infarction are: Male sex
Smoking
Hypertension
Diabetes Mellitus
Hypercholesterolemia
Risk assessment of ischemia
An exercise test such as a bicycle or treadmill test, may be useful in detecting myocardial ischemia after exercise.[1] In such a test, continuous ECG monitoring is performed during exercise. The ST-segment, blood pressure and clinical status of the patient (i.e. chest complaints) are monitored during and after the test.
An exercise test is positive for myocardial ischemia when the following criteria are met: Horizontal or downsloping ST-depression of >1mm, 60 or 80ms after the J-point
ST elevation of > 1.0 mm

Diagnosis of myocardial infarction

ST elevation is measured at the junctional or J-point
The diagnosis of acute myocardial infarction is not only based on the ECG. A myocardial infarction is defined as:[2] Elevated blood levels of cardiac enzymes (CKMB or Troponin T) AND
One of the following criteria are met: The patient has typical complaints,
The ECG shows ST elevation or depression.
pathological Q waves develop on the ECG
A coronary intervention had been performed (such as stent placement)
So detection of elevated serum cardiac enzymes is more important than ECG changes. However, the cardiac enzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So, especially in the first few hours after the myocardial infarction, the ECG can be crucial.
ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and LBBB)are [3]: ST elevationNew ST elevation at the J-point in two contiguous leads with the cut-off points: ≥0.2 mV in men or ≥ 0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads.ST depression and T-wave changes.New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads; and/or T inversion ≥0.1 mVin two contiguous leads with prominent R-wave or R/S ratio ≥ 1
A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST segment depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction (sensitivity increase from 50% to 84%).[4]
Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but it is explained in these seperate chapters: MI diagnosis in left bundle branch block or paced rhytm
MI Diagnosis in RBBB

The location of the infarct



An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.



Overview of the separate ECG leads. The lead with ST segment elevation 'highlights' the infarct. An infarction of the inferior wall will result in ST segment elevation in leads II, III and AVF. A lateral wall infarct results in ST segment elevation in leads I and AVL. An Anterior wall infarct results in ST segment elevation in the precordial leads.



The coloured figure shows contiguous leads in matching colors



The ST segment elevation points at the infarct location. Inferior MI=ST segment elevation in red regions (lead II,III and AVF). Lateral MI = ST elevation in blue leads (lead I, AVL, V5-V6). Anterio MI: ST segment elevation in yellow region (V1-V4). Left main stenosis: ST elevation in gray area (AVR)



The coronary blockade can cause conduction block, on AV nodal, His or bundle branch level.
The heartmuscle itself is very limited in its capacity to extract oxygen in the blood that is being pumped. Only the inner layers (the endocardium) profit from this oxygenrich blood. The outer layers of the heart (the epicardium) are dependent on the coronary arteries for the supply of oxygen and nutrients. With aid of an ECG, the occluded coronary can be identified. This is valuable information for the clinician, because treatment and complications of for instance an anterior wall infarction is different than those of an inferior wall infarction. The anterior wall performs the main pump function, and decay of the function of this wall will lead to decrease of bloodpressure, increase of heartrate, shock and on a longer term: heart failure. An inferior wall infarction is often accompanied with a decrease in heartrate because of involvement of the sinusnode. Longterm effects of an inferior wall infarction are usually less severe than those of an anterior wall infarction.
The heart is supplied of oxygen and nutrients by the right and left coronary arteries. The left coronary artery (the Left Main or LM) divides itself in the left anterior descending artery (LAD) and the ramus circumflexus (RCX). The right coronary artery (RCA) connects to the ramus descendens posterior (RDP). With 20% of the normal population the RDP is supplied by the RCX. This called left dominance.
Below you can find several different types of myocardial infarcation. Click on the specific infarct location to see examples.

Help with the localisation of a myocardial infarct localisation ST elevation Reciprocal ST depression coronary artery
Anterior MI V1-V6 None LAD
Septal MI V1-V4, disappearance of septum Q in leads V5,V6 none LAD-septal branches
Lateral MI I, aVL, V5, V6 II,III, aVF LCX or MO
Inferior MI II, III, aVF I, aVL RCA (80%) or RCX (20%)
Posterior MI V7, V8, V9 high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view) RCX
Right Ventricle MI V1, V4R I, aVL RCA
Atrial MI PTa in I,V5,V6 PTa in I,II, or III RCA

The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On the CAG report, the place of the occlusion is often graded with a number (for example LAD(7)) using the classification of the American Heart Association.[5]

Development of the ECG during persistent ischemia

The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalisation with a persistent Q wave

A pathological Q wave

Wellens syndrome: symmetrical negative T wave in pre-cordial leads without R loss of R waves can regularly be observed in early anterior ischemia. Many patients with Wellens syndrome / sign turn out to have a critical proximal LAD stenosis[6].

Typical negative T waves post anterior myocardial infarction. This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated.[7][8][9]
The cardiomyocytes in the subendocardial layers are especcially vulnerable for a decreased perfusion. Subendocardial ischemia manifests as ST depression and is usually reversible. In a myocardial infarction transmural ischemia develops.
In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.
Wellens syndrome or sign (see image) can be an early ECG warning sign of critical anterior ischemia before the development of overt mocardial infarction.
Evolution of the ECG during a myocardial infarct Time from onset of symptoms ECG Changes in the heart
minutes hyperacute T waves (tall T waves), ST-elevation reversible ischemic damage
hours ST-elevation, with terminal negative T waves, negative T waves (these can last for days to months) onset of myocardial necrosis

days Pathologic Q Waves scar formation



Subendendocardial Ischemia

An example of subendocardial ischemia with diffuse ST depression
Subendocardial ischemia is ischemia that is not transmural. It is mostly caused by demand ischemia where energy supply to cardiomyocytes is insufficient for the work force, e.g. during extreme hypertension, aortic valve stenosis, extreme left ventricular hypertension, anemia, atrial fibrillation with rapid ventricular response. On the ECG often diffuse ST depression is present. Cardiac enzymes (CK-MB, Troponine) may or may not be elevated depending on the severity.

الاثنين، 24 يوليو 2023

قائمة الحوادث النووية والإشعاعية حسب عدد القتلى

 

قائمة الحوادث النووية والإشعاعية حسب عدد القتلى من ويكيبيديا، الموسوعة الحرة

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هناك العديد من الحوادث النووية والإشعاعية التي تؤدي إلي الوفاة، مثل حوادث محطات الطاقة النووية، وحوادث الغواصات النووية، وحوادث العلاج الإشعاعي.

قائمة الحوادث

الوفيات الحادثة التاريخ تفاصيل

متنازع عليها كارثة كيشتيم 29 سبتمبر 1957 عدد الوفيات غير معروف، وتتراوح التقديرات من 50 إلى أكثر من 8000

متنازع عليها كارثة تشيرنوبل 26 أبريل 1986

متنازع عليها حريق يندسكال 8 أكتوبر 1957

17 معهد الأورام الدولي في بنما أغسطس 2000 – مارس 2001 يتلقى المرضى جرعات مميتة من العلاج الكيمياوي للعلاج من سرطان البروستاتا وسرطان الرحم.

13 حادث العلاج الإشعاعي في كوستاريكا 1996 تلقى 114 مريضا جرعة زائدة من الإشعاع من مصدر الكوبالت 60 الذي كان يستخدم للعلاج الإشعاعي.

11 حادث العلاج الإشعاعي في سرقسطة، إسبانيا ديسمبر 1990 أصيب 27 مريضا من مرضى السرطان الذين يتلقون العلاج الإشعاعي.

10 الغواصة السوفيتية K-431 10 أغسطس 1985 تعرض 49 شخص للإشاعات النووية.

10 حادث العلاج الإشعاعي في كولومبوس 1974–1976 88 إصابات من مصدر الكوبالت 60.

9 الغواصة السوفيتية K-27 24 مايو 1968 تعرض 83 شخص للإصابة.

8 الغواصة السوفيتية K-19 4 يوليو 1961 أكثر من 30 شخص تعرضوا للإشعاع.

8 حادثة الإشعاع في المغرب 1984 مارس 1984

7 حادث العلاج الإشعاعي في هيوستن 1980

5 مصدر الإشعاع المفقود، باكو، أذربيجان، الاتحاد السوفيتي 5 أكتوبر 1982 13 إصابة.

4 حادثة غويانيا الإشعاعية 13 سبتمبر 1987 249 مصاب في حالة خطرة.

4 حادث الإشعاع مدينة مكسيكو عام 1962 1962

 

3 حادثة المفاعل الثابت منخفض الطاقة الأول في الجيش الأمريكي 1961

 

3 حادث سامون براكان الإشعاعي فبراير 2000 ثلاثة قتلى وعشرات من المصابين.

2 حادثة توكايمورا النووية 30 سبتمبر 1999

2 ميت حلفا، مصر مايو 2000 وفاة شخصين.

1 حادثة ميابوري، الهند أبريل 2010

1 دايجو فوكوريو مارو 1 مارس 1954

 

1 لويس سلوتن 21 مايو 1946

 

1 هاري دغليان 21 أغسطس 1945 في مختبر لوس ألاموس الوطني في نيو مكسيكو.

1 حادثة سيسيل كيلي 30 ديسمبر 1958 في مختبر لوس ألاموس الوطني في نيو مكسيكو.

1 وود ريفر جانكشن، رود آيلاند 1964 خطأ المشغل في منشأة نووية، توفي روبرت بيبودي 49 ساعة في وقت لاحق

1 مركز كونستويينتس الذري 23 سبتمبر 1983 عطل INES المستوى 4 في مفاعل RA2 في الأرجنتين، توفي المشغل أوزفالدو روجوليتش بعد أيام.

1 سان سلفادور، السلفادور 1989 وفاة واحدة بسبب انتهاك قواعد السلامة في 60Co تشعيع مرفق.

1 تاميكو، إستونيا 1994 وفاة واحدة من مصدر 137C.

1 ساروف، روسيا يونيو 1997 وفاة واحدة نتيجة انتهاك قواعد السلامة. 

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ملصق سلامة مصمم للمكاتب الهندسية التي تصور جوهر مفاعل SL-1 المذاب. مدينة بريبيات المهجورة مع مفاعل تشيرنوبيل.

من الأحداث ذات الوفيات المتنازع عليها

كارثة تشيرنوبيلتختلف تقديرات العدد الإجمالي للوفيات التي يحتمل أن تكون ناجمة عن كارثة تشيرنوبيل بشكل كبير: أكد تقرير الأمم المتحدة عن وجود 45 حالة وفاة مؤكدة، اعتبارا من عام 2008. ويشمل هذا العدد حالتين وفاة غير متعلقة بإشعاع يوم الحادث، و 28 حالة بسبب جرعات الإشعاع في الأشهر التالية مباشرة، 15 حالة وفاة بسبب سرطان الغدة الدرقية، 131 حالة من المحتمل أن يكون سببها هو تلوث اليود؛ وهو لا يشمل 19 شخصًا إضافيًا تم تشخيصهم في بداية الأمر بمتلازمة الإشعاع الحادة الذين توفوا أيضًا بحلول عام 2006، لكن لا يُعتقد أنهم ماتوا بسبب جرعات الإشعاع. في عام 2006، لمحت منظمة الصحة العالمية أن الوفيات الناجمة عن السرطان يمكن أن تصل إلى 4,000 شخص من بين أكثر من 600,000 شخص معرضين بشدة،

وهي مجموعة تضم عمال الطوارئ والمقيمين القريبين والمُجليين، ولكنها تستثني سكان المناطق المنخفضة التلوث.

في عام 2006، صدر تقرير، بتكليف من حزب الخضر وتحت رعاية مؤسسة ألتنر كومبيشر، توقع وفاة ما بين 30,000 إلي 60,000 حالة وفاة نتيجة السرطان في جميع انحاء العالم، فقامت تشيرنوبيل بافتراض نموذج خطي بلا عتبة لجرعات منخفضة للغاية. حيث صدر تقرير جرينبيس بتوقع 200,000 حالة وفاة أو أكثر. كما صدر أيضا تقرير روسي متنازع عليه، يفترض وجود 985,000 حالة وفاة مبكرة وقعت في جميع أنحاء العالم بين عامي 1986 و 2004 نتيجة للتلوث الإشعاعي من تشيرنوبيل.

كارثة كيشتيمتم تصنيف كارثة كيشتيم، التي وقعت في ماياك في روسيا في 29 سبتمبر 1957، على أنها المستوى السادس على المقياس الدولي للحوادث النووية، وهو ثالث أخطر حادثة بعد تشيرنوبيل وفوكوشيما. بسبب السرية الشديدة المحيطة بماياك، من الصعب تقدير عدد القتلى في كيشتيم. كتاب واحد يدعي أنه «في عام 1992، وجدت دراسة أجراها معهد الفيزياء الحيوية في وزارة الصحة السوفيتية السابقة في تشيليابينسك أن 8015 شخص لقوا حتفهم خلال ال 32 سنة السابقة نتيجة للحادث».علي عكس ذلك، فقد تم العثور علي 6,000 شهادة وفاة فقط لسكان ضفة النهر بين عامي 1950 و 1982 من جميع أسباب الوفاة، علي الرغم من أن الدراسة السوفيتية اعتبرت أن المنطقة كبيرة جغرافيا، لذلك فهي متأثرة بالأعمدة المحمولة جوا. التقديرات الأكثر شيوعا هي 200 حالة وفاة بسبب السرطان، لكن أصل العدد غير واضح. تشير الدراسات الوبائية الأكثر حداثة إلى أن يوجد حوالي من 49 إلى 55 حالة توفيت بسبب السرطان من بين سكان النهر ويمكن أيضا أن ترتبط بالتعرض للإشعاع. وسيشمل ذلك تأثيرات جميع الإطلاقات المشعة في النهر، والتي حدثت 98% منها قبل وقت طويل من حادث 1957، ولكنها لن تشمل آثار عمود الهواء المحمول جواً الذي تم نقله شمال شرق البلاد. أنتجت المنطقة الأقرب إلى الحادث 66 حالة تم تشخيصها من متلازمة الإشعاع المزمن، مما يوفر الجزء الأكبر من البيانات حول هذه الحالة.

حريق ويندسكالنتج عن حريق ويندسكال مالا يقل عن 33 حالة وفاة في ويندسكال والمملكة المتحدة (حسب تقديرات حكومة المملكة المتحدة). في 8 أكتوبر 1957، نتج عن حريق ويندسكال تلوث مزارع الألبان المحيطة، عندما اشتعل الوقود المعدني لليورانيوم داخل أكوام إنتاج البلوتونيوم.

كارثة فوكوشيماتطبيق Crystal Clear kdict.png هو مقال تفصيلي عن خسائر فوكوشيما دايتشي النووية. في تقرير عام 2013، ذكرت لجنة الأمم المتحدة العلمية المعنية بآثار الإشعاع الذري أن المخاطر الصحية العامة الناجمة عن كارثة فوكوشيما أقل بكثير من مخاطر تشيرنوبيل. لم تكن هناك آثار حتمية ملحوظة أو متوقعة. في حالات الحمل، لم تكن هناك زيادة متوقعة في حالات الإجهاض التلقائي أو الإجهاض أو الوفيات المحيطة بالولادة أو العيوب الخلقية أو الضعف الإدراكي. أخيرًا، لم تكن هناك زيادة ملحوظة متوقعة في مرض وراثي أو زيادات ملحوظة متعلقة بالإشعاع في أي سرطانات، مع استثناء محتمل لسرطان الغدة الدرقية. ومع ذلك، فإن ارتفاع معدلات الكشف عن العقيدات الدرقية والخراجات والسرطان قد يكون نتيجة لفحص مكثف. في ورقة بيضاء 2015، صرحت لجنة الأمم المتحدة العلمية المعنية بآثار الإشعاع الذري أن نتائجها من عام 2013 لا تزال صالحة وغير متأثرة إلى حد كبير بالمعلومات الجديدة، والمعلومات الجديدة تدعم ذلك أيضا، فإن الكشف عن ارتفاع الغدة الدرقية من المحتمل أن يكون بسبب فحص أكثر كثافة.لم يمت أي من العمال في موقع فوكوشيما دايتشي بسبب التسمم بالإشعاع الحاد، على الرغم من أن ستة عمال ماتوا لأسباب مختلفة، بما في ذلك أمراض القلب والأوعية الدموية، أثناء جهود الاحتواء أو العمل على تثبيت زلزال وتسونامي في الموقع.في المقابل، تشير مقالة رأي في صحيفة وول ستريت جورنال إلى دراسة يابانية لعام 2013، لخصت معدل الوفيات بسبب «إجهاد الإجلاء» من المنطقة المحيطة بفوكوشيما قد وصل إلى أكثر من 1600. ويشمل ذلك الوفيات الناجمة عن الانتحار وعدم القدرة على الوصول إلى الصحة الحرجة. الرعاية، ولكن ليس من الإشعاع، أو زيادة السرطان، أو أي نتيجة مباشرة أخرى للحادث النووي. ويذكر المؤلف أيضًا أن هذه الوفيات حدثت بين الأشخاص الذين تم إجلاؤهم من مناطق تشكل فيها الإشعاعات خطرًا ضئيلًا أو لا يشكل أي خطر على صحتهم، وهي مناطق قد يتعرضون فيها لمخاطر أقل من الكمية المعتادة التي يتلقاها السكان في فنلندا.هناك دعوي جماعية رفعها البحارة على المدمرة الأمريكية ريغان ضد شركة طوكيو إليكتريك باور (تيبكو) الذين يدعون أنهم يعانون من أمراض شديدة تسبب فيها الإشعاع. كانت سفينة يو إس إس ريجان جزءًا من عملية «توموداشي» لتوصيل الإمدادات الأساسية للمجتمعات التي دمرتها في أعقاب كارثة تسونامي في 11 مارس 2011. كانت الرياح تهب في البحر من حادث فوكوشيما. إذا كانت تهب غربًا بدلاً من الشرق، فلن يكون البحارة قد تأثروا.

انظر أيضًاالوفيات الناجمة عن كارثة تشيرنوبيل.

منتدى تشيرنوبيل.

فاسيلي إجناتنكو.

فاليري خودمتشوك.

ليونيد تلياتنيكوف

ألكسندر أكيموف

أناتولي راسكازوف