Human heart in ventricular fibrillation.

Ventricular fibrillation is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. It is the most commonly identified arrhythmia in cardiac arrest patients.

While there is some activity, the lay person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography.

Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole (“flatline”). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain-dead, due to the effects of cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.

Causes of ventricular fibrillation are:

  • Abnormal automaticity: In the healthy myocardium, the rhythm of contraction is regulated by sinoatrial node,that acts like a pacemaker and generates the normal sinus rhythm. Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously, separated from the sinoatrial node. The product of a hypoxic myocardium can be hyperirritable myocardial cells and 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. It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.
  • Re-entry: The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. 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 ischaemic or infarcted myocardium, or underlying scar tissue.

Miguel Valderrabano

Alcohol may ease the nerves that cause atrial fibrillation

About 1 in 12 Americans over age 80 has atrial fibrillation, a kind of heart arrhythmia. Surgeons and cardiologists have come a long way, honestly, in treating the disorder, which weakens heart flow and significantly increases the chances of ischemia, as well as blood clot-caused strokes. Doctors have even figured out how to fix atrial fibrillation (also called a fib or a-fib) intravenously, via catheter.

The typical treatment now is to burn areas cardiac nerve clusters that are known to be part of the electrical cascade that causes a-fib. Sounds sort of dangerous, but it was the big breakthrough about 10 years ago.

Problem, though, is that this does not seem to be a permanent solution for a lot of people. The nerves somehow repair, or else nearby pathways are recruited for mayhem… and the a-fib returns.

A new technique involves doing all that burning stuff, but ALSO injecting 98% ethanol into a nerve cluster near one of the major cardiopulmonary veins. Electrophysiological measurements at the site (what CAN’T they do through catherers these days?) shows this might be a more permanent solution for a-fib patients.

More here.

Heart arrhythmias detected in deep-diving marine mammals

A new study of dolphins and seals shows that despite their remarkable adaptations to aquatic life, exercising while holding their breath remains a physiological challenge for marine mammals. The study, published January 15 in Nature Communications, found a surprisingly high frequency of heart arrhythmias in bottlenose dolphins and Weddell seals during the deepest dives.

The normal dive response in marine mammals has long been understood to involve a marked reduction in heart rate (called bradycardia) and other physiological changes to conserve limited oxygen reserves while the air-breathing animals are underwater. How marine mammals cope with the exertion needed to pursue prey at depth has been unclear, however, since the normal physiological response to exercise is an increase in heart rate (called tachycardia). The new study shows that these conflicting signals to the heart can lead to cardiac arrhythmias, said lead author Terrie Williams, a professor of ecology and evolutionary biology at UC Santa Cruz.

“This study changes our understanding of bradycardia in marine mammals,” Williams said. “The heart is receiving conflicting signals when the animals exercise intensely at depth, which often happens when they are starting their ascent. We’re not seeing lethal arrhythmias, but it is putting the heart in an unsteady state that could make it vulnerable to problems.”

Terrie M. Williams, Lee A. Fuiman, Traci Kendall, Patrick Berry, Beau Richter, Shawn R. Noren, Nicole Thometz, Michael J. Shattock, Edward Farrell, Andy M. Stamper, Randall W. Davis. Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals. Nature Communications, 2015; 6: 6055 DOI: 10.1038/ncomms7055

This is an image of a Weddell seal in Antarctica. Researchers studied the heart rates of seals during deep dives beneath the Antarctic sea ice. Credit: Peter Rejcek, NSF

Left panel shows the eye of a hurricane. Right panel shows the striking similarity of the rotor or localized source of an arrhythmia in a patient with atrial fibrillation. Ablation targeted at these rotors or “eyes of the storm” successfully terminated and eliminated atrial fibrillation in the CONFRIM trial. Photo credit: UCSD/UCLA.

New Technology Improves Heart Rhythm Treatment
CONFIRM study results point to a doubling of success in treating heart rhythm disorder

Researchers  from UC San Diego, the University of California Los Angeles and Indiana University report having found, for the first time, that atrial fibrillation  or irregular heart rhythms is caused by small electrical sources within the heart, in the form of electrical spinning tops (“rotors”) or focal beats.  Importantly, they found a way of detecting these key sources, then precisely targeting them for therapy that can shut them down in minutes with long lasting results.
The team, which included cardiologists, physicists and bioengineers, report the findings in the July issue of the Journal of the American College of Cardiology as the CONFIRM trial (Conventional Ablation for Atrial Fibrillation
With or Without Focal Impulse and Rotor Modulation). 

Currently, many patients treated for atrial fibrillation with standard therapies will experience a recurrence due to the difficulty of finding the source of the arrhythmia.  The new findings will help cardiologists better target and treat arrhythmias.

The CONFIRM study examined 107 patients with atrial fibrillation referred for a non-surgical catheter ablation procedure.  During this procedure, doctors thread a wire with a metal-tipped catheter inside the body, from a vein in the groin, to apply heat to the area of the heart that is producing the arrhythmia to stop it. 

In one group of patients, the team used the new technique to help perform precise burns, called Focal Impulse and Rotor Modulation (FIRM) that were aimed directly at the fundamental source of the arrhythmia – tiny electrical disturbances in the heart called rotors or focal sources that look like mini tornadoes or spinning tops. 

Remarkably, this new procedure shut down atrial fibrillation or very significantly slowed it in 86 percent of patients in an average of only 2.5 minutes. 

More here

A little Valentine’s reminder to be vigilant with your pups around chocolate! Vets say it’s one of the most common causes of dog poisoning. Remember, the darker the chocolate (Including baker’s chocolate), the more dangerous the chocolate.

“Chocolate toxicosis may result in potentially life-threatening cardiac arrhythmias"—Merck Veterinary Manual

"A chocolate chip cookie can cause problems for a little dog, and a bag of chocolate chips can spell trouble for a big one.”
—pets webMD

Via Red and Howling

The most lovable soul - my parents seven month old puppy passed away suddenly this morning due to a cardiac arrhythmia and coagulation abnormalities. She lived the happiest seven months in the most amazing home. Happy thoughts needed today for the whole family.

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Some people who can walk need parking permits

I’m almost seven months pregnant, I have asthma, and just found out I have cardiac arrhythmia. My heart rate gets out of hand spontaneously and also when I’m exerting too much force to the point where I can pass out. I can’t take medication to keep it under control because of my pregnancy.

I’ve been wanting to get permission for handicap parking even if its just temporary while I’m in college because I have to walk very far and it’s triggering my palpitations and I’ve recently started feeling my legs start to give out so I have to sit down or stop halfway on stairs and stuff and then continue.

The only thing holding me back is that even if my doctor signs for it I’ll feel guilty for getting one and that I’ll look bad or selfish or lazy. Should I go ahead and get the permission for handicap parking or should I save those spaces for other people who probably need it more?

realsocialskills said:

I think you should get a permit. 

Parking permits exist to make it possible for people to go where they need to go, when a disability or medical condition makes it impossible or unsafe to park in the regular spots.

A lot of people have permits because it is not safe for them to walk across a parking lot, or because they can’t safely walk those distances. It’s an accepted legitimate category. If you’re at serious risk of passing out, falling, or being unable to continue walking in a parking lot, that’s a major safety issue. Being unable to get out of the way of cars is not safe. It’s not safe for you, and it’s not safe for the drivers either.

If/when you get a permit, it’s good to be mindful of which spots you are parking in. Not all handicapped parking spots are the same. Some are pretty much the same as regular parking spots, except closer to the door. Others are designed for people who use a wheelchair lift to get out of their van. Those spots have extra space marked off with lines for the lift. If there are other spaces available that you can use, you shouldn’t park in the van spaces. 

tl;dr Accessible parking permits are for people who need them, not just people who fit a particular image of what disability looks like. If your condition means that you need a parking permit in order to be able to go places safely, it’s ok to try to get one.


23. ME/cfs and cardiac arrhythmias - Prof. F.C. Visser, cardiologist (by WetenschapvMEcvsVer)

he broke my heart — so gross to think about someone literally doing this

it warms my heart — yeah and this seems medically problematic?

my heart skipped a beat — and that is your classic cardiac arrhythmia

be still my beating heart — great idea if you want to die

it tugs my heartstrings — ugh do hearts have strings? imma barf

my heart bleeds — that will affect your other organs i’m sure of it

eat your heart out — what? that has got to be illegal

my heart is in my mouth — i mean, go to the doctor immediately

wearing my heart on my sleeve — oh my god oh dear god what is happening call the police

Green Bay Packers DE Reggie White tackles Tennessee Oilers RB Eddie George at Lambeau Field on Dec. 20, 1998 in Green Bay, Wis. “The Minister of Defense" Reggie White, a 13-time Pro Bowl defensive end and one of the best in NFL history, died ten years ago today at the age of 43 after suffering from cardiac arrhythmia. (John Biever/SI)

GALLERY: Rare SI Photos of Reggie White

Did Cardiac Arrhythmia Influence Beethoven’s Music?

Could it be that, when Ludwig van Beethoven composed some of the greatest masterpieces of all time, he was quite literally following his heart? The striking rhythms found in some of Beethoven’s most famous works may have been inspired by his own heartbeat, says a team of researchers from the Univ. of Michigan and Univ. of Washington that includes a cardiologist, medical historian and musicologist.

Authors of an essay that appears in Perspectives in Biology and Medicine analyzed several of Beethoven’s compositions for clues of a heart condition some have speculated he had. The rhythms of certain parts of renowned works, researchers say, may in fact reflect the irregular rhythms of Beethoven’s own heart caused by cardiac arrhythmia.

Why does Digoxin toxicity result in increased automaticity?

Hey everyone!

Digitalis and other cardiac glycosides are known to cause an AV nodal delay.

Then why does too much Digoxin result in some arrhythmias that are due to increased automaticity?

Brady arrhythmias are explainable. But why tachy arrhythmias?

You see, cardiac glycosides reversibly inhibit the sodium-potassium-ATPase, causing an increase in intracellular sodium and a decrease in intracellular potassium. The increase in intracellular sodium prevents the sodium-calcium antiporter from expelling calcium from the myocyte, which increases intracellular calcium. The net increase in intracellular calcium augments inotropy.

Excessive intracellular calcium may cause delayed after-depolarizations, which may in turn lead to premature contractions and trigger arrhythmias. Cardiac glycosides shorten repolarization of the atria and ventricles, decreasing the refractory period of the myocardium, thereby increasing automaticity and the risk for arrhythmias.

That’s all!


A couple years ago I passed out on Matt Smith and went into cardiac arrhythmias from chronic illnesses during a photo-op and he helped hold me up for the photo, carried me to a chair(and I’m no skinny woman, I’m hefty), and stayed with me until I got better despite the waiting fans. It was one of the kindest things that anyone who doesn’t know me has ever done for me.