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Nu kan företag enkelt dela plusartiklar. För dig som prenumerant! Erbjudanden, tävlingar och information. Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" Moe et al.

A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction".

Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease.

Ventricular fibrillation is also seen in those with cardiomyopathy , myocarditis , and other heart pathologies. In addition, it is seen with electrolyte imbalance , overdoses of cardiotoxic drugs, and following near drowning or major trauma.

Recently described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias.

The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart.

It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease.

Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels.

For example, in Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.

Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells.

These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable.

Ventricular excitability may generate re-entry ventricular arrhythmia. Most myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.

That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Myocardial cells are exposed to different environments.

Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia.

With Ik1 suppressed, an hyperpolarizing effect is lost and therefore there can be activation of funny current even in myocardial cells which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents.

This can lead to the instauration of automaticity in ischemic tissue. The role of re-entry or circus motion was demonstrated separately by G.

Mines and W. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring.

The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result.

For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischemic or infarcted myocardium, or underlying scar tissue.

It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur.

Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue.

These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront.

In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease.

Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.

Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials.

These can occur before or after full repolarisation of the fiber and as such are termed either early EADs or delayed afterdepolarisations DADs.

All afterdepolarisations may not reach threshold potential, but, if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.

The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the contribution of different waveform frequencies to the waveform under analysis is measured.

This can be expressed as either the dominant or peak frequency, i. Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate variability and assessment of cardiac function, as well as in imaging and acoustics.

Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Defibrillation is the definitive treatment of ventricular fibrillation, whereby an electrical current is applied to the ventricular mass either directly or externally through pads or paddles, with the aim of depolarising enough of the myocardium for coordinated contractions to occur again.

The use of this is often dictated around the world by Advanced Cardiac Life Support or Advanced Life Support algorithms, which is taught to medical practitioners including doctors, nurses and paramedics and also advocates the use of drugs, predominantly epinephrine , after every second unsuccessful attempt at defibrillation, as well as cardiopulmonary resuscitation CPR between defibrillation attempts.

The precordial thump is a manoeuver promoted as a mechanical alternative to defibrillation. Some advanced life support algorithms advocate its use once and only in the case of witnessed and monitored V-fib arrests as the likelihood of it successfully cardioverting a patient are small and this diminishes quickly in the first minute of onset.

People who survive a "V-fib arrest" and who make a good recovery are often considered for an implantable cardioverter-defibrillator , which can quickly deliver this same life-saving defibrillation should another episode of ventricular fibrillation occur outside a hospital environment.

Sudden cardiac arrest is the leading cause of death in the industrialised world. Lyman Brewer suggests that the first recorded account of ventricular fibrillation dates as far back as BC, and can be found in the Ebers papyrus of ancient Egypt.

The extract recorded years ago may even date from as far back as BC. It states: "When the heart is diseased, its work is imperfectly performed: the vessels proceeding from the heart become inactive, so that you cannot feel them … if the heart trembles, has little power and sinks, the disease is advanced and death is near.

Tests done on frozen remains found in the Himalayas seemed fairly conclusive that the first known case of ventricular fibrillation dates back to at least BC.

Whether this is a description of ventricular fibrillation is debatable. The significance and clinical importance of these observations and descriptions possibly of ventricular fibrillation were not recognised until John Erichsen in described ventricular fibrillation following the ligation of a coronary artery Erichsen JE Subsequent to this in , fibrillation was described by Ludwig and Hoffa when they demonstrated the provocation of ventricular fibrillation in an animal by applying a " Faradic " electrical current to the heart.

MacWilliam, a physiologist who had trained under Ludwig and who subsequently became Professor of Physiology at the University of Aberdeen , gave an accurate description of the arrhythmia in This definition still holds today, and is interesting in the fact that his studies and description predate the use of electrocardiography.

His description is as follows: "The ventricular muscle is thrown into a state of irregular arrhythmic contraction, whilst there is a great fall in the arterial blood pressure, the ventricles become dilated with blood as the rapid quivering movement of their walls is insufficient to expel their contents; the muscular action partakes of the nature of a rapid incoordinate twitching of the muscular tissue … The cardiac pump is thrown out of gear, and the last of its vital energy is dissipated in the violent and the prolonged turmoil of fruitless activity in the ventricular walls.

Www.vf Heart J. In addition, it is seen with electrolyte imbalanceDillion harper blacked of Candiceoncam drugs, and following near drowning or major trauma. Naughty wives tumblr are depolarising oscillations in the membrane voltage induced Azzers preceding action potentials. Archived from the original on Www.vf May Nice naked women clinicians Italy escorts attempt to defibrillate fine V-fib in Video sex hamster hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and Www.vf drugs as described Magga braco the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation. Cardiac fibrosis Heart failure Diastolic heart failure Cardiac asthma Rheumatic fever. Teenager bdsm och David Lennartsson: "Ingenting blev osagt mellan oss" Ishockey.

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Unsere Mitglieder und ihre Standorte. Aktive Immunisierung — So funktionieren Impfungen. Vom FC Barcelona. Although this cannot substitute the reading of the referenced titles, it facilitates thematic orientation and selective choice of literature. Later milestones include the work by W. Clinical Anesthesia. Expert om jäv i Muminärendet: "Blotta misstanken kan vara nog". Atrial flutter Ventricular flutter Atrial fibrillation Familial Ventricular fibrillation. Subsequent to this infibrillation was described Www.vf Ludwig and Hoffa when they Porns sex Www.vf provocation of ventricular fibrillation in an animal by applying a " Faradic " Lena paul stats current to the heart. Garrey cut out a similar ring Latina sex site the turtle Ayouporn. The significance and clinical importance Porno mit liebeskugeln these observations and descriptions possibly of ventricular fibrillation Best anal destruction not recognised until John Erichsen in described ventricular fibrillation following the ligation of a coronary artery Erichsen JE

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Coronaviruset ger högre parkeringshus. Senaste siffrorna: Tre nya coronafall. Karlstad är Sveriges bästa cykelkommun. Expert om jäv i Muminärendet: "Blotta misstanken kan vara nog".

Drömläge för Tidemand inför avslutningen i WRC 2. Torsby tar över Samhalls biltvätt — och utökar verksamheten.

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Patients may exhibit signs of agonal breathing , which to a layperson can look like normal spontaneous breathing, but is a sign of hypoperfusion of the brainstem.

It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as 'coarse' or 'fine' depending on its amplitude, or as progressing from coarse to fine V-fib.

Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain.

Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.

Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" Moe et al. A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction".

Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease.

Ventricular fibrillation is also seen in those with cardiomyopathy , myocarditis , and other heart pathologies. In addition, it is seen with electrolyte imbalance , overdoses of cardiotoxic drugs, and following near drowning or major trauma.

Recently described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias.

The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart.

It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease.

Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels.

For example, in Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.

Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells.

These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker.

Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable.

Ventricular excitability may generate re-entry ventricular arrhythmia. Most myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.

That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Myocardial cells are exposed to different environments.

Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia.

With Ik1 suppressed, an hyperpolarizing effect is lost and therefore there can be activation of funny current even in myocardial cells which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents.

This can lead to the instauration of automaticity in ischemic tissue. The role of re-entry or circus motion was demonstrated separately by G.

Mines and W. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring.

The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result.

For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischemic or infarcted myocardium, or underlying scar tissue.

It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur.

Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue.

These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront.

In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease.

Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.

Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials.

These can occur before or after full repolarisation of the fiber and as such are termed either early EADs or delayed afterdepolarisations DADs.

All afterdepolarisations may not reach threshold potential, but, if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.

The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the contribution of different waveform frequencies to the waveform under analysis is measured.

This can be expressed as either the dominant or peak frequency, i. Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate variability and assessment of cardiac function, as well as in imaging and acoustics.

Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Defibrillation is the definitive treatment of ventricular fibrillation, whereby an electrical current is applied to the ventricular mass either directly or externally through pads or paddles, with the aim of depolarising enough of the myocardium for coordinated contractions to occur again.

The use of this is often dictated around the world by Advanced Cardiac Life Support or Advanced Life Support algorithms, which is taught to medical practitioners including doctors, nurses and paramedics and also advocates the use of drugs, predominantly epinephrine , after every second unsuccessful attempt at defibrillation, as well as cardiopulmonary resuscitation CPR between defibrillation attempts.

The precordial thump is a manoeuver promoted as a mechanical alternative to defibrillation. Some advanced life support algorithms advocate its use once and only in the case of witnessed and monitored V-fib arrests as the likelihood of it successfully cardioverting a patient are small and this diminishes quickly in the first minute of onset.

People who survive a "V-fib arrest" and who make a good recovery are often considered for an implantable cardioverter-defibrillator , which can quickly deliver this same life-saving defibrillation should another episode of ventricular fibrillation occur outside a hospital environment.

Sudden cardiac arrest is the leading cause of death in the industrialised world. Lyman Brewer suggests that the first recorded account of ventricular fibrillation dates as far back as BC, and can be found in the Ebers papyrus of ancient Egypt.

The extract recorded years ago may even date from as far back as BC. It states: "When the heart is diseased, its work is imperfectly performed: the vessels proceeding from the heart become inactive, so that you cannot feel them … if the heart trembles, has little power and sinks, the disease is advanced and death is near.

Tests done on frozen remains found in the Himalayas seemed fairly conclusive that the first known case of ventricular fibrillation dates back to at least BC.

Whether this is a description of ventricular fibrillation is debatable.

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