Cardiac Arrhythmias Flashcards

1
Q

What is a cardiac arrhythmia?

A

Disturbance in normal heart rate or rhythm (PQRST sequence) of the heartbeat

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2
Q

What is considered a normal sinus rhythm?

A
  • SA node working correctly and setting the correct heart rate and activation sequence order
  • Heart rate is between 60 and 100 bpm
  • 5 squares is one second on an ECG, each square is 0.2 seconds
  • If peak of QRS go exactly at the 1 second interval, sinus rhythm is 60 bpm
  • To evaluate whether the patient is in normal sinus rhythm must look at time of the P wave and Q to T wave and width of QRS and other lovely stuff
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3
Q

What is sinus bradychardia?

A

Rate is less than 60/min, can be completely physiologic (normal, not pathologic) and is seen when one is asleep or indicating good physical health (very active)

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4
Q

What is sinus tachycardia?

A

Rate is over 100/min, can be completely physiologic (not pathologic) and is seen when people exercise

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5
Q

What is sinus arrythmia?

A
  • Physiologic
  • On inspiration, rate goes up and on expiration, rate goes down (normal in healthy young people)
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6
Q

What is a 2:1 atrioventricular block? What is it caused by?

A

We see 2 P waves for 1 QRS, only 1/2 P waves is followed by a QRS complex, so every other AP from the atria does not make it to the ventricles. Since there is a P wave, SA node is working fine, but the block can be at the AV node, at the His bundle or even at the bundle branches.

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7
Q

Why is 2:1 atrioventricular block problematic?

A

If it is in the AV node, the 2:1 can turn into a 3:1 and then continue to increase until resulting in a complete atrioventricular block (serious for its own reasons, will see soon).

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8
Q

What is the treatment for 2:1 atrioventricular block?

A

Electronic pacemaker

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9
Q

What is a complete atrioventricular block? What does it look like on the ECG?

A

Happens overtime often a result of 2:1 atrioventricular block and it means that the ventricles simply never get depolarized, so they do not contract anymore. On the ECG, we will only see a P wave and the subsequent atrial repolarization waves which are usually not visible because of the QRS complex masking them. They may be seen on one of the 12 clinical ECG leads, but if they are not seen at all anywhere, it is usually not cause for concern. In a paper, it was seen that a patient had a transient complete AV block, so the ventricles would stop beating but then they started beating again.

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10
Q

Why is complete atrioventricular block so serious?

A

If ventricles do not beat, no cardiac output, no organ perfusion, very often results in death.

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11
Q

What is the treatment for complete AV block?

A

Electronic pacemaker

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12
Q

How does an electronic pacemaker work?

A

Picks up ECG and when an irregularity is detected will sends a current, electrical wave to the ventricle to make sure they beat

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13
Q

What to look for in an ECG to detect arrhythmia?

A

We first look for QRS complex and then the P wave.

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14
Q

What is a complete AV block with subsidiary pacemaker? and what does the ECG look like?

A
  • The AP are not making their way from the atria to the ventricles, however the ventricles are still beating just with a different rhythm indicating a 2nd pacemaker at play, a subsidiary pacemaker somewhere in the heart that takes over when there is a block but in some patients there is no subsidiary pacemaker or it just never gets activated resulting in a complete AV block
  • On an ECG there are P waves and QRS waves, but the duration between a P wave and a QRS wave is variable, may even happen at the same time. They both have particular rhythms, they are just very different from one another indicating that the two rhythms are controlled by two different pacemakers
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15
Q

What is premature ventricular contraction? what is it caused by? What does it look like on an ECG?

A
  • The ventricle beats before it repolarizes often due to an action potential caused by another pacemaker, a focus or an area in the ventricle (could be ventricular muscle or purkinje fibers). It is also referred to as an ectopic beat because the pacemaker in the wrong place is dictating ventricle contraction (wrong pacemaker).
  • In the ECG the QRS wave will happen even before the T wave ends and the shape of this premature QRS and the following T wave will be very different as well. Can tell the premature beat is ventricular because it is the QRS that comes earlier.
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16
Q

What is a holter recorder?

A

An instrument that people can have on them for a while to record ECGs and keeps these recording for 24 hours, 48 hours even a whole week sometimes. Kind of like a take home ECG

17
Q

What is a common consequence of premature ventricular contraction? How does it look on an ECG? Explain

A
  • Ventricular tachycardia, especially if many consecutive PVCs can induce V-tach
  • QRSTs are all merged, so much chaose, the heart is beating extremely fast (hence tachycardia, fast cardia)
  • People can faint during a tachycardic episode since ventricles do not get filled up and stroke volume falls to 0, cardiac output falls to 0, bp to 0, organs not perfused
  • Can degenerate into V-fib (fatal if nothing done) but if it does not degenerate, and person returns to normal sinus rhythm (no sudden V-fib or cardiac arrest), not fatal, just quite annoying, I mean you keep fainting
18
Q

V-tach can degenerate into which fatal cardiac arrhytmia? What does it look like on an ECG?

A
  • Ventricular fibrillation (V-fib) fatal if nothing done, can also go directly into V-fib from a PVC
  • very irregular, low amplitude activity from ventricles
19
Q

How may V-fib be detected in a hospital setting?

A
  • ECG or through the arterial pulse measured on a finger
  • If suddenly no arterial pulse, can be V-fib since no bp, no perfusion to organs, cannot be felt at finger
20
Q

What is the treatment for V-fib? How does it work?

A
  • Defibrillation with an AED often (automated external defibrillator)
  • When the AED detects V-fib (automatically, recording ECG) will deliver an automatic shock to restore normal sinus rhythm
21
Q

What is a direct way to map cardiac electrical activity?

A
  • Epicardial sock array
  • Mesh with about 64 electrodes at different points on the heart each attached to a wire, all 64 wires connect to a computer, simultaneous recording of signal at 64 electrodes at all times
  • Computer can construct activation wavefront direction at any point in time with all 64 electrode recordings
  • Electrodes arranged in lines pointing away from apex radially
22
Q

What is reentrant ventricular tachycardia?

A
  • Starts somewhere and reenters at starting point to keep going around instead of dying out
  • Chronic and does not generally degenerate into Vfib, faints each time V-tach
23
Q

How can reentrant ventricular tachycardia be treated?

A
  • Anti arrhythmic drugs, if those don’t work can perform surgery if surgery is indicated
24
Q

How to map reentrant ventricular tachycardia to determine cause and see whether surgery is indicated?

A
  • Using the epicardial sock array and inducing V-tach to map it with a succession of stimuli to replicate the effect of PVC which can generally induce V-tach
25
Q

When they mapped the V-tach of a specific patient what did they find? What caused it? How can it be fixed?

A
  • Activation wavefront starts at an arbitrary point 0 and moves counterclockwise around an obstacle
  • Took 200 ms for the AP to go around completely and reach the starting point, 200 ms is often the length of the refractory period, so the AP can “reenter” at re-excitable cardiac muscle and go around again
  • heart is beating faster => tachycardia
  • This is known as circus movement reentry (reentry from circle movement around an obstacle)
  • Caused by anatomical obstacle, scar tissue from previous heart attack (myocardial infarction => cardiac muscle dies and becomes fibrous and becomes obstacle for AP to keep going around)
  • Fixed by removal of scar tissue
26
Q

How can reentrant ventricular tachycardia pose a fatal risk?

A
  • Heart was not made to beat this fast, slowly the refractory period increases and inhomogeneously, so an AP may reach one tired part of the heart and stall there but the AP can breakup from 1 wave into multiple wavelets (so chaotic) can lead to fibrillation (DEATH)
27
Q

What was one discovery of our king George Ralph Mines?

A
  • Basically circus movement reentry
  • took the free wall of the ventricles and cut a whole in the middle (obstacle like the scar tissue) (refractory period is inhomogeneous so can be different at different points)
  • So the depolarization starts at one point, the rest of the free wall is resting, as the AP moves around the cells behind are in the refractory period being repolarized then more and more cells are depolarized and the back cells are more and more repolarized (stil refractory period)
    HOWEVER if the AP is spreading slow enough or the ring is long enough, when the AP reaches the starting point again, the cells are excitable once again and the AP can reactivate and go for another circle
28
Q

What is atrial fibrillation? How does it look like on the ECG? What is the treatment?

A
  • Just like in a ventricle, an atrium can go into fibrillation following a PAC (premature atrial contraction) caused by an ectopic beat, the second pacemaker is often not in the atrial muscle but in the atrial cells near the 4 pulmonary veins
  • Often multiple wavelets circulating in the atria
  • There are multiple P waves instead of nice regular P waves, these are known as fibrillatory waves/chaotic activity in atria caused by a PAC, the PAC itself will be smaller than a PVC on the ECG since atrial muscle area is smaller than the ventricular muscle area
  • Treatment is Pulmonary vein isolation
29
Q

What is pulmonary vein isolation?

A
  • Put smt hot or cold on muscle near the pulmonary veins (different techniques possible but in this one go around 4 veins) and kill those muscle cells so they are replaced by fibrous tissue so if ectopic AP from vein area cannot reach atrial muscle (though travels through sleeve of valve and tries to reach atrium)
30
Q

Why is the refractory period longer in heart muscle than in skeletal muscle?

A

Prolonged plateau phase of the action potential