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  • Atrial Fibrillation
    Atrial fibrillation (AF or A-fib) is the most common cardiac arrhythmia (irregular heart beat). It may cause no symptoms, but it is often associated with palpitations, fainting, chest pain, or congestive heart failure. However, in some people atrial fibrillation is caused by otherwise idiopathic or benign conditions.

    AF increases the risk of stroke; the degree of stroke risk can be up to seven times that of the average population, depending on the presence of additional risk factors (such as high blood pressure). It may be identified clinically when taking a pulse, and the presence of AF can be confirmed with an electrocardiogram (ECG or EKG) which demonstrates the absence of P waves together with an irregular ventricular rate.

    In AF, the normal regular electrical impulses generated by the sinoarial node are overwhelmed by disorganized electrical impulses usually originating in the roots of the pulmonary veins, leading to irregular conduction of impulses to the ventricles which generate the heartbeat. AF may occur in episodes lasting from minutes to days ("paroxysmal"), or be permanent in nature. A number of medical conditions increase the risk of AF, particularly mitral stenosis (narrowing of the mitral valve of the heart).


    Atrial fibrillation may be treated with medications to either slow the heart rate to a normal range ("rate control") or revert the heart rhythm back to normal ("rhythm control"). Synchronized electrical cardioversion can be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may be used to prevent recurrence of AF in certain individuals. People with AF often take anticoagulants such as warfarin to protect them from stroke, depending on the calculated risk. The prevalence of AF in a population increases with age, with 8% of people over 80 having AF. Chronic AF leads to a small increase in the risk of death.


    Reference: https://en.wikipedia.org/wiki/Atrial_Fibrillation

    Post by: Harvey Chen , 帕金森氏症的抗病心路歷程


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  • Atrial Fibrillation, Coarse

    Descriptions: Rapid irregular atrial signal with no real P-waves. Irregular ventricular rate.

    Normal Sinus Rhythm


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  • Atrial Fibrillation, Fine

    Descriptions: Rapid irregular atrial signal with no real P-waves. Irregular ventricular rate.

    Normal Sinus Rhythm


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  • Atrial Flutter

    Descriptions: Large regular P-waves (sinus rate of 250~350BPM). Ventricular response varies.

    Normal Sinus Rhythm

    Atrial flutter (AFL) is an
    abnormal heart rhythm that occurs in the atria of the heart.[1] When it first occurs, it is usually associated with a fast heart rate or tachycardia (beats over 100 per minute),[2] and falls into the category of supra-ventricular tachycardias. While this rhythm occurs most often in individuals with cardiovascular disease (e.g. hypertension, coronary artery disease, and cardiomyopathy) and diabetes, it may occur spontaneously in people with otherwise normal hearts. It is typically not a stable rhythm, and frequently degenerates into atrial fibrillation (AF). However, it does rarely persist for months to years.

    Signs and symptoms

    While atrial flutter can sometimes go unnoticed, its onset is often marked by characteristic sensations of regular palpitations. Such sensations usually last until the episode resolves, or until the heart rate is controlled.

    Atrial flutter is usually well tolerated initially (a high heart rate is for most people just a normal response to exercise), however, people with other underlying heart disease or poor exercise tolerance may rapidly develop symptoms, which can include shortness of breath, chest pains, lightheadedness or dizziness, nausea and, in some patients, nervousness and feelings of impending doom.

    Prolonged fast flutter may lead to decompensation with loss of normal heart function (heart failure). This may manifest as effort intolerance (exertional breathlessness), nocturnal breathlessness, or swelling of the legs or abdomen.

    Atrial flutter is recognized on an electrocardiogram by presence of characteristic flutter waves at a regular rate of 240 to 440 beats per minute. Individual flutter waves may be symmetrical, resembling p-waves, or may be asymmetrical with a "sawtooth" shape, rising gradually and falling abruptly or vice versa. If atrial flutter is suspected clinically but is not clearly evident on ECG, acquiring a Lewis lead ECG may be helpful in revealing flutter waves.

    Pathophysiology

    Atrial flutter is caused by a reentrant rhythm in either the right or left atrium. Typically initiated by a premature electrical impulse arising in the atria, atrial flutter is propagated due to differences in refractory periods of atrial tissue. This creates electrical activity that moves in a localized self-perpetuating loop. For each cycle around the loop, there results an electric impulse that propagates through the atria.

    The impact and symptoms of atrial flutter depend on the heart rate of the patient. Heart rate is a measure of the ventricular rather than atrial activity. Impulses from the atria are conducted to the ventricles through the atrio-ventricular node. Due primarily to its longer refractory period, the AV node exerts a protective effect on heart rate by blocking atrial impulses in excess of about 180 beats/minute, for the example of a resting heart rate. (This block is dependent on the age of the patient, and can be calculated roughly by subtracting patient age from 220). If the flutter rate is 300/minute only half of these impulses will be conducted, giving a ventricular rate of 150/minute, or a 2:1 heart block. The addition of rate-controlling drugs or conduction system disease can increase this block substantially (see image below).

    Reference: https://en.wikipedia.org/wiki/Atrial_flutter

    Post by: Harvey Chen , 帕金森氏症的抗病心路歷程


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  • First-degree atrioventricular heart block
    First-degree AV block, or PR prolongation, is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds[1].

    In first-degree AV block, the impulse conducting from atria to ventricles through the AV node is delayed and travels slower than normal. It has a prevalence in the normal (young adult) population of 0.65-1.1% and the incidence is 0.13 per 1000 persons.

    Causes

    The most common causes of first-degree heart block are an AV nodal disease, enhanced vagal tone (for example in athletes), myocarditis, acute myocardial infarction (especially acute inferior MI), electrolyte disturbances and medication. The drugs that most commonly cause first-degree heart block are those that increase the refractory time of the AV node, thereby slowing AV conduction. These include calcium channel blockers, beta-blockers, cardiac glycosides, and anything that increases cholinergic activity such as cholinesterase inhibitors. Digitalis is a sodium/potassium ATPase inhibitor and also prolongs AV conduction.

    Diagnosis

    In normal individuals, the AV node slows the conduction of electrical impulse through the heart. This is manifest on a surface ECG as the PR interval. The normal PR interval is from 120 ms to 200 ms in length. This is measured from the initial deflection of the P wave to the beginning of the QRS complex.

    In first-degree heart block, the diseased AV node conducts the electrical activity more slowly. This is seen as a PR interval greater than 200 ms in length on the surface ECG. It is usually an incidental finding on a routine ECG.


    First-degree heart block does not require any particular investigations except for electrolyte and drug screens, especially if an overdose is suspected.

    Treatment

    The management includes identifying and correcting electrolyte imbalances and withholding any offending medications. This condition does not require admission unless there is an associated myocardial infarction. Even though it usually does not progress to higher forms of heart block, it may require outpatient follow-up and monitoring of the ECG, especially if there is a comorbid bundle branch block. If there is a need for treatment of an unrelated condition, care should be taken not to introduce any medication that may slow AV conduction. If this is not feasible, clinicians should be very cautious when introducing any drug that may slow conduction; and regular monitoring of the ECG is indicated.

    Prognosis

    Isolated first-degree heart block has no direct clinical consequences. There are no symptoms or signs associated with it. It was originally thought of as having a benign prognosis. In the Framingham Heart Study, however, the presence of a prolonged PR interval or first degree AV block doubled the risk of developing atrial fibrillation (irregular heart beat), tripled the risk of requiring an artificial pacemaker, and was associated with a small increase in mortality. This risk was proportional to the degree of PR prolongation[2].

    A subset of individuals with the triad of first-degree heart block, right bundle branch block, and either left anterior fascicular block or left posterior fascicular block (known as trifascicular block) may be at an increased risk of progression to complete heart block.

    Reference: https://en.wikipedia.org/wiki/First-degree_atrioventricular_block

    Post by: Harvey Chen , 帕金森氏症的抗病心路歷程









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  • Irregular ECG(2)

    Descriptions: ST depression, reverse T wave.

    Normal Sinus Rhythm

    ST depression refers to a finding on an electrocardiogram

    Measurement

    ST segment depression may be determined by measuring the vertical distance between the patient's trace and the isoelectric line at a location 2[3]-3 millimeters from the QRS complex.

    It is significant if it is more than 1 mm in V5-V6, or 1.5 mm in AVF or III.


    In a cardiac stress test, an ST depression of at least 1 mm after adenosine administration indicates a reversible ischaemia, while an exercise stress test requires an ST depression of at least 2 mm to significantly indicate reversible ischaemia.

    Physiology
     
    For non-transmural ischemia, the pathophysiological cause of ST depression is a slightly elevated resting potential in myocardial cells, but with the ST segment less affected, as it represents a depolarized state. Still, the resting potential is the reference line in ECG, making it display an apparent ST depression rather than an elevation of the other segments.

    Causes
     
    It is often a sign of myocardial ischemia, of which coronary insufficiency is a major cause. Other ischemic heart diseases causing ST depression include:

    Subendocardial ischemia[5] or even infarction[3]. 
    Non Q-wave myocardial infarction[5]
    Reciprocal changes in acute Q-wave myocardial infarction (e.g., ST depression in leads I & aVL with acute inferior myocardial infarction)[5]

    Depressed but upsloping ST segment generally rules out ischemia as a cause.

    Also, it can be a normal variant or artifacts, such as:

    Pseudo-ST-depression, which is a wandering baseline due to poor skin contact of the electrode[5]
    Physiologic J-junctional depression with sinus tachycardia[5]
    Hyperventilation[5]
     

    Other, non-ischemic, causes include:

    Side effect of digoxin[3][5]
    Hypokalemia[3][5]
    Right or left ventricular hypertrophy[5]
    Intraventricular conduction abnormalities (e.g., right or left bundle branch block, WPW, etc.)[5]
    Hypothermia[3]
    Tachycardia[3]
    Reciprocal ST elevation[3]
    Mitral valve prolapse[5]
    CNS disease[5]
     
    Reference: https://en.wikipedia.org/wiki/ST_depression


    Post by: Harvey Chen , 帕金森氏症的抗病心路歷程


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  • Left Bundle Branch Block (LBBB)

    Descriptions: Wide QRS, and wide S wave, caused by partial or complete blockage of signal along the right branch below the bundle of HIS.

    Normal Sinus Rhythm

    Left bundle branch block (LBBB) is a cardiac conduction abnormality seen on the
    electrocardiogram (ECG).[1] In this condition, activation of the left ventricle is delayed, which causes the left ventricle to contract later than the right ventricle.

    ECG diagnosis

    LBBB

    Electrocardiogram showing left bundle branch block and irregular rhythm due to supraventricular extrasystoles.

    LBBB

    A left bundle branch block
    The criteria to diagnose a left bundle branch block on the electrocardiogram:

    The heart rhythm must be supraventricular in origin
    The QRS duration must be ≥ 120 ms[2]
    There should be a QS or rS complex in lead V1
    There should be a RsR' wave in lead V6.
     

    The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.

    Left bundle branch block
    Classification and external resources

    ECG characteristics of a typical LBBB showing wide QRS complexes with abnormal morphology in leads V1 and V6.
    ICD-10 I44.4 - I44.7
    DiseasesDB 7352
    eMedicine ped/2501

    Causes

    Among the causes of LBBB are:

     

    Aortic stenosis
    Dilated cardiomyopathy
    Acute myocardial infarction
    Extensive coronary artery disease
    Primary disease of the cardiac electrical conduction system
    Long standing hypertension leading to aortic root dilatation and subsequent aortic regurgitation

    Treatment

    Patients with LBBB require complete cardiac evaluation, and those with LBBB and syncope or near-syncope may require a pacemaker.
    Some patients with LBBB, a markedly prolonged QRS (usually > 150 ms), and systolic heart failure may benefit from a biventricular pacemaker, which allows for better synchrony of heart contractions

     


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