What Causes Atrial Flutter?

The 2-3 minor peaks in between the large ventricle beats
are a signature of atrial flutter.

Atrial Flutter has many causes. It is when a rogue section of the atrial wall that starts sending out its own electrical signals; generally much faster than the SA or AV nodes.

Atrial flutter has several supposed causes, but the following list seems pretty random to me:
ischemia (decreases blood flow to the heart),
high blood pressure,
heart disease, bad heart valves, disfunction of the sinus node, hypertropy (enlarged heart), overactive thyroid, blood clots in the lungs, other lung diseases, alcohol, and stimulants from cocaine to caffeine.

Despite the huge number of potential causes, one third of atrial flutter cases have no assigned cause.

This site discusses magnesium deficiency as a reason for atrial flutter. Essentially Magnesium clogs the ion channels and regulates the intake of Calcium.

Cardizem and Diltiazem

An obviously
photoshopped picture
of a bottle of
Cardizem

Cardizem (Diliazem)

Caridzem (diltiazem) is a calcuim blocker, and it has a nice description on Wikipedia.  These block calcuim channels in the cardiac cell walls. Calcium channels ordinarily open when there is low potential in the cell wall, and then close when potential is higher. Blocking the calcuim channel will keep the cell wall at lower potential, and it will send fewer and less powerful signals to adjacent cells.

L-TYPE CA2+CHANNELS are multisubunit, transmembrane proteins controlling Ca2+ influx into cells and play a pivotal role in the physiological regulation of the cardiac, vascular, endocrine and central nervous system. Alterations in the density or function of L-type Ca2+ channels have been implicated in a variety of diseases, including atrial fibrillation (1 , 2) , ventricular hypertrophy (3) , and heart failure (4) . In the heart, the L-type Ca2+ channel is composed of the pore-forming α1C subunit (Cav1.2a) and the auxiliary subunits α2δ and β2 (reviewed in ref 5 ). A crucial signaling pathway that regulates the heart beat is the sympathetic stimulation of Ca2+ channel activity, which increases the amplitude of the Ca2+ inward current (ICaL), leads to a leftward shift in current-voltage relationship and a slowing of channel inactivation (reviewed in ref 6 ). These effects are believed to result from PKA-mediated phosphorylation of the channel subunits α1C (7 , 8) and β2 (9 , 10) or still undefined associated proteins (11) . In a previous attempt to define the molecular details of Ca2+ channel phosphorylation in response to the sympathetic agonist, isoprenaline, we identified ahnak, a 700 kDa PKA substrate (5643 aa) as Ca2+ channel-associated protein (12) .





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