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Cardiac Dysrhythmias > Background > Flashcards

Flashcards in Background Deck (43):

What is an arrhythmia?

Disturbance in the electrical activity of the heart


Why is the timing of the cardiac cycle important?

Cardiac timing is important in order for the heart to work efficiently. Atrial contraction happens before ventricle contraction in order to allow the ventricle time to fill while in diastoli. If arrhythmia in the atria, vetricle won't get enough time to fill = will have to work much harder to reach desired CO = increased HR. Ventricular fibirilation = alterations in timing = fatal.


what is the body's way of naturally preventing arrhythmias?

The refractory period


What channels are inactivated while the heart is refractory?

Na+ channels


What needs to happen in order to move na+ channels from inactive to closed?

They need to be exposed to a -ve charge


The effective refractory period is the period where the sodium channels are completely inactive, what is the RELATIVE refractory period?

When the membrane has started to become more -ve (under 0 but not yet at -80mv). At this point there is a slight probability that if a big enough stimulus comes along, the channel might open and generate a second AP in the cell.


What are the two things that happen in the cells during arrhythmia?

An AP is generated outside the SA node and the dysfunction is passed on to the neighbouring cell.


What do we call a normal wave of AP?

Sinus rhythm


What would happen if there was dysfunction - one lazy cell takes longer to re polarise but does so within the refractory period?

Normal sinus rhythm = Neighbouring cells would be inactive during the dysfunction so it is not transmitted = second AP is not generated in neighbouring cells


What would haven if there was a dysfunction that lead to one very lazy cell that stays depolarized for longer than the refractory period?

After the refractory period, the neighbouring cells are all repolarized so the lazy cell will cause a second AP and depolarize the neighbouring cells causing an extra beat = TACHYCARDIA


AP moves through a circular length of tissue at a certain speed. Normally, if it moves quickly enough, it will return to the top of the circuit while the cells are still in the refractory period so the AP is stopped. What would cause a self-sustaining circuit i.e. by the time reacheed the top of the circuit cells would be re-polarized = continuous AP?

1.) Longer pathway length (hypertrophied hearts)
2.) Slower conduction around circuit (ischaemia)


What is fibrillation?

A self-sustaining arrhythmia = heart beat is out of the control of the SA node - sets up a localised area of contraction that is not in co ordination = no ejection


What is the theory on CRITICAL MASS?

The idea that you need a certain amount of tissue in order to achieve a self-sustaining circuit = can't stimulate fibrillation in mice = not enough tissue mass


Is atrial fibrillation (self-sustaining circuit in atria) survivable? Explain why

Yes. The AV node can generate its own action potential = the dysfunction in the atria is isolated and the ventricles will still contract just at a slower rate = IDIOPATHIC VENTRICULAR RATE


How would an ECG look during atrial fibrillation?

the p wave woud be missing but would still see QRS


What is the name of the condition where the atria and ventricles can communicate without the AV node?

Wolff-parkinson-white syndrome
*atrial fibrillation would be fatal here*


What would the ECG of someone with wolff-parkinson-white syndrome look like?

They would have a shorter P-Q interval


Is ventricular fibrillation survivable? Expain why

No, ventricular co ordination is essential for ejection.


What would happen during the initiation of VF and what would the patient experience?

The conduction through the ventricle starts to become impaired = uneven ECG -patient is still conscious but experiences palpitations


What would happen when the initiation transitions into full on fibrillation?

Completely un-cordinated ECG. patient BP would plummet, no ejection, brain turns everything off would fall unconscious, sudden cardiac death


How are cardiac arrhythmias classified?

According to the site of origin and the effect it has on heart rate


What is sinus badycardia?

A normal decrease in HR. AP is still generated in the SA node. Is due to fluctuation in the autonomic tone. Can be caused by exhaling, hypothermia, b-blockers, antiarrhythmics


What is sinus tachycardia?

A normal increase in HR. AP is still generated in the SA node. Is due to fluctuation in the autonomic tone. Can be caused by inhaling, fever, hyperthyroidism, infection, dehydration, decongestant, caffeine,exercise


What is an ectopic pacemaker?

When another part of the heart other than the SA node can generate the fastest AP = it takes over as the pacemaker.


Name a drug that might cause an AP to be generated elsewhere? What happens?

Dobutamine - causes overactivation of the funny current = increased rate of depolarisation during phase 4 = SYMPATHETIC overstimulation. The funny current can generate an AP quicker than the AV node. Causes an increased heart rate. We have lost control of HR - it is no longer controlled by the PNS or ANS.


If the ectopic foci was in the ventricle what kind of dysrhythmia would this cause?

Ventricular tachycardia
(ectopic foci = the area that has taken over from SA)


Issues with what ion pump causes Delayed after depolarisations (DADs)?

Na+/Ca2+ exchanger


What is the role of the Na+/Ca2+ exchanger?

After contraction, the exchanges pumps 1 ca2+ in exchange for 3 sodiums in order for the myocardium to relax. Three positive charges come in and one leaves meaning that there is a slight positive net charge. The efflux of K+ from the Na/K ATPase pump normally overrides this.


What happens if the Na+/Ca2+ exchanger becomes overactive?

The positive infflux will overdide the negetivity caused by K+ and the membrane will become positive enough to reach threshold and trigger a second AP = an extra beat before the next expected normal AP.


Name two causes of DADs and how they work

1.) Ischamemia = cut off blood supply = not much ATP supply (O2 needed to generate ATP) . ATP is needed to pump the Ca 2+ out of the cell through the pump on the SR so we get a Ca2+ overload in the cell. This stiumlates the Na+/Ca2+ exchanger so we get a massive influx in Na+ = positive charge = threshold reached early
2.) Digitalis - blocks the Na/K ATPase pump so we get an increase in intracellular Ca2+. This reduces the activity of the Na+/Ca2+ exchanges so we get an increase in intracellular Ca2+.In the heart, increased intracellular calcium causes more calcium to be released by the sarcoplasmic reticulum, thereby making more calcium available to bind to troponin-C, which increases contractility = increased heart rate


If DAD happened in the ventricle what would it be called?

Ventricular tachycardia


What is the other name for early afterdepolarisations?

Long QT syndrome


What happens in long QT syndrome?

You have one lazy cell that fails to repolarize before the end of the refractory period so its neighbouring cells are depolarized straight away = a second AP IS GENERATED BEFORE REACHING -80MV = EXTRA BEAT.
Unlike DAD where one is generated fully and then a second just a little earlier than expected, in EAD the voltage doesn't return to resting membrane potential before a second is generated.


what would an EAD in the atria be called?

Super ventricular tachycardia


Why do we worry about tachycardia?

The ventricle isn't allowed enough time to be filled = ejection is not efficient.


Why is it called long QT syndrome?

Q-T = from ventricle depolarisation to repolarisation. In long q-t there is a delay in repolarisation = heart stays depolarized for longer.


What ion efflux is involved in repolarisation? What does this indicate about long QT syndrome?

K+. This indicates that the k+ channel subunit is involved.


What can lead to problems with the K+ channel?

1.) Drugs - k+ channel binds to lots of drugs = can be a major problem in DD
2.) Polymorphism in genes - can predispose people to problems with drugs = channel is affected more by drugs
3.) Inherited mutations in the k+ channel genes


What is re-entry?

Is essentially a sustained circuit = circus movement of cardiac AP


What causes re-entry?

Damaged tissue - it slows AP conduction down = increases pathway length. If damage is severe, the cells will be out of the refractory period and ready to depolarize again = continued AP


What is 1st degree AV block?

Slowing down of conduction through the AV node = ventricle will take longer to contract = longer p-q interval


What is 2nd degree AV block?

Atrial depolarisation that sometimes doesn't lead to ventricular depolarisation = missed beats = SUPERVENTRICULAR BRADCARDIA
*missed beat on ECG - would see P wave but QRS woud not follow until next contraction


What is 3rd degree block?

Complete breakdown in conduction between the atria and the ventricles = AV doesn't work. In this case the ventricle would be driven by ectopic foci = ventricular escape - HR is driven by funny current. Much slower than normal HR = BRADYCHARDIA
*loss of co ordination between p + QRS on ECG