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(A brief chemical gradient driven efflux of Na+ through the connexon at peak depolarization causes the conduction of cell to cell depolarization, not potassium.) [27] These connections allow for the rapid conduction of the action potential throughout the heart and are responsible for allowing all of the cells in the atria to contract together ...
The most obvious abnormal finding will be abnormal P waves. One of three options can occur: [12] 1. There are no P waves. This is because of either failure of retrograde flow to the atria or the P wave is hidden in the QRS. If the P wave is hidden that implies the atria depolarize at the same time as the ventricles. 2.
Delayed afterdepolarizations (DADs) begin during phase 4, after repolarization is completed but before another action potential would normally occur via the normal conduction systems of the heart. They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity.
The depolarization front is carried through the atria along semi-specialized conduction pathways including Bachmann's bundle resulting in uniform shaped waves. Depolarization originating elsewhere in the atria (atrial ectopics) result in P waves with a different morphology from normal.
These cells produce an electrical impulse known as a cardiac action potential that travels through the electrical conduction system of the heart, causing it to contract. In a healthy heart, the SA node continuously produces action potentials, setting the rhythm of the heart (sinus rhythm), and so is known as the heart's natural pacemaker.
Pre-excitation is caused by an abnormal electrical connection or accessory pathway between or within the cardiac chambers. Pre-excitation may not cause any symptoms but may lead to palpitations caused by abnormal heart rhythms. It is usually diagnosed using an electrocardiogram, but may only be found during an electrophysiological study. [2]
The plateau lasts on the order of 100 ms. At the time that calcium channels are getting activated, channels that mediate the transient outward potassium current open as well. This outward potassium current causes a small dip in membrane potential shortly after depolarization. This current is observed in human and dog action potentials, but not ...
This is the property of the AV node that prevents rapid conduction to the ventricle in cases of rapid atrial rhythms, such as atrial fibrillation or atrial flutter. The AV node's normal intrinsic firing rate without stimulation (such as that from the SA node) is 40–60 times/minute. [ 13 ]