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Mechanisms of Cardiac Arrhythmias PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Mechanisms of cardiac arrhythmias" by Prof. Ján Hanácek.

This medical PowerPoint presentation talks about the mechanisms of cardiac arrhythmias.

Cardiac arrhythmias refer to any abnormality in the hearts rhythm, which can be caused by various mechanisms. Here are some of the mechanisms of cardiac arrhythmias:
Abnormal Automaticity: In some cases, certain cells within the heart muscle can generate electrical impulses independently of the normal pacemaker cells. These abnormal impulses can disrupt the normal rhythm of the heart, leading to arrhythmias.
Re-entry: This mechanism occurs when an electrical impulse circles back around to re-stimulate a part of the heart that has already been activated. If this re-stimulation occurs rapidly enough, it can lead to a sustained arrhythmia.
Triggered activity: This mechanism involves the spontaneous generation of electrical impulses within the heart muscle cells after the normal electrical activity has ended. These impulses can cause arrhythmias if they occur at an inappropriate time during the cardiac cycle.
Electrolyte imbalances: Abnormal levels of electrolytes such as potassium, calcium, and magnesium can affect the hearts electrical activity, leading to arrhythmias.
Ischemia: Insufficient blood flow to the heart muscle can cause arrhythmias by disrupting the normal electrical activity of the heart.
Structural abnormalities: Certain structural abnormalities of the heart, such as heart failure, valve disease, or congenital heart defects, can alter the hearts electrical activity and lead to arrhythmias.
Drugs and toxins: Certain medications and toxins can affect the hearts electrical activity, leading to arrhythmias.

These are just a few of the many mechanisms that can cause cardiac arrhythmias. The underlying cause of a specific arrhythmia can vary depending on the individual, and may require specialized medical attention to diagnose and treat.

Tags : Mechanisms of cardiac arrhythmias, hearts rhythm, cardiology

Published on : Mar 17, 2023 | Views : 1915 | Downloads : 3

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Mechanisms of cardiac arrhythmias Prof. Ján Hanáček
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Three main mechanisms of cardiac dysrhythmias Altered normal automaticity or abnormal automaticity 2) Triggered electrical activity a) early afterdepolarization b) delayed afterdepolarization 3) Reentry a) anatomic reentry b) functional reentry
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Altered normal automaticity (from SA node) supression = sinus bradycardia enhancement = sinus tachycardia
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Abnormal automaticity It is creation of electrical impulses by non-pacemaker cells of myocardium because thay acquire automaticity and spontaneously depolarize (eg in myocardial ischemia) Main mechanism: driving the maximal diastolic potential towards the threshold potential
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Triggered activity Impuls for myocardium depolarization is caused by afterdepolarization Afterdepolarization = cell membrane potential oscilations that occur during or immediately following a preceding action potential (trigger) When afterdepolarization potential reaches the threshold potential of cells a new action potential is generated
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Early afterdepolarization (EADs) - The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs – increased input of Ca2+) or during the late repolarization (phase 3 EADs -decreased of K+ output). Agents and Manipulations That May Lead to Early Afterdepolarizations.
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Delayed afterdepolarization A DAD is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4). These oscillations are caused by a variety of conditions that raise the diastolic intracellular Ca2+ concentration. Conditions: Toxic concentration of digitalis (inhibition of the Na/K pump, which promotes the release of Ca2+ from the sarcoplasmic reticulum), catecholamines (can cause DADs by causing intracellular Ca2+ overload via an increase in ICa-L and theNa+-Ca2+ exchange current), Ischemia-induced DADs Prolonged AP
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Reentry activity/mechanism During normal electrical activity, the cardiac cycle begins in the SA node and continues to propagate until the entire heart is activated. This impulse dies out when all fibers have been depolarized and are completely refractory. However, if a group of isolated fibers is not activated during the initial wave of depolarization, they can recover excitability in time to be depolarized before the impulse dies out. They may then serve as a link to reexcite areas that were previously depolarized but have already recovered from the initial depolarization. Such a process is commonly denoted as reentry, reentrant excitation, circus movement, reciprocal or echo beats, or reciprocating tachycardia (RT), referring to a repetitive propagation of the wave of activation, returning to its site of origin to reactivate that site.
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Prerequisites for reentry include: A substrate: the presence of joined myocardial tissue with different electrophysiological properties, conduction, and refractoriness. An area of block (anatomical, functional, or both): an area of inexcitable tissue around which the wavefront can circulate. A unidirectional conduction block. A path of slowed conduction that allows sufficient delay in the conduction of the circulating wavefront to enable the recovery of the refractory tissue proximal to the site of unidirectional block. A critical tissue mass to sustain the circulating reentrant wavefronts. An initiating trigger.
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Atrial fibrilation
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Atrial escape beats
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Junctional escape beats
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Ventricular escape beats