LECTURE 27 11/07/22 (LECTURE 14 SLIDES: CARDIAC ARRHYTHMIAS/ ECG INTERPRETATIONS)

Question 1

In Premature Contractions of the AV Nodal and Bundle Source, where is the source of the depolarization for the following:

Early P-wave and inverted

Late P-wave and inverted

Answer 1

High AV junction source for Early Inverted P-wave

Low AV Junction source for Late Inverted P-wave

**Inverted P-wave is d/t backwards travel through the atria; AV junction source. (20:00)

Question 2

Usually, V-fib is preceded by some type of ____________.

Answer 2

Ventricular Tachycardia (21:40)

Question 3

Where are the QRS originating in V-Tach?

Describe the QRS complex in V-tach?

How does this affect filling and left coronary perfusion?

Answer 3

Ventricles.

High Voltage, prolonged QRS.

Shortens fill time and shortens coronary perfusion which can lead to ischemia in the left ventricle. (22:00)

Question 4

During what phase of the heart do we have coronary perfusion in the left side of the heart?

Answer 4

During ventricular diastole, there is filling in ventricles and augmented coronary perfusion (23:40).

Question 5

What happens when Fast Na+ and L-Type Ca2+ are irritated in the ventricular myocytes?

How does this affect repolarization?

Answer 5

These ion channels can open on their own during phase 3 of repolarization resulting in an Early After Depolarization (EAD), rouge action potential. (28:00)

Prolongs repolarization and results in very inefficient pumping and inefficient electrical coordination. (45:50)

Question 6

How does the EKG interpret an EAD?

Answer 6

EKG will think it is a long QT interval.

Question 7

QT interval should be less than ________% of an R-R interval.

How long is a perfect R-R interval

QT intervals longer than _______ seconds would be considered a long QT interval.

Answer 7

Less than 40%.

0.83 seconds

0.42 seconds (greater than 50% of an R-R interval is considered a long QT interval.)

(30:16)

Question 8

What can prolong phase 3 in ventricular myocyte repolarization and increase the chance of an EAD.

Answer 8

Non-specific K+ channel blockers can block the K-IR and Delayed K+ channels to prolong phase 3.

The longer we sit in phase 3, the more of a chance we fire an action potential that is not going to be helpful (EAD). (32:00)

Question 9

What happens if you fire multiple EAD’s during phase 3?

Answer 9

You can go from long QT to Torsades de Pointes. (33:00)

Question 10

What does Torsades de Pointes translate to?

What do you give to calm this arrhythmia?

Answer 10

“Twisting of the Corners” (33:00)

Magnesium will slow Ca2+ entry so the heart can try to escape the arrhythmia (35:30).

Question 11

How does minor hyperkalemia affect HR?

How does minor hypokalemia affect HR?

Answer 11

Minor increase in ECF K+ decrease permeability of K+ efflux d/t change in the concentration gradient. The increase in K+ in the ICF, increases the cells Vrm which puts the cell closer to threshold resulting in a shorter phase 4. This will result in an increase HR.

Minor hypokalemia will result in increase efflux of K+, makes Vrm more negative, longer phase 4 slope, increase time to threshold, decrease HR.

(Recall from Exam 3) (36:50)

Question 12

What channels in the ventricular myocytes will be affected by hypokalemia?

How will this affect phase 3 and potential for EAD.

Answer 12

Low ECF K+ will tend to close the K-IR and the Delayed K+ channel. The cell will have a hard time trying to reset because fewer K+ are leaving the cell.

This will increase the length of phase 3, increasing the chance of a rogue Fast Na+ channel or L-type Ca2+ to depolarize during phase 3 resulting in an EAD.

EAD will cause a lengthening of the QT interval, leading to Torsades de Pointes and V-fib. (42:00)

Question 13

What can taking an excess amount of anti-histamine result in?

Answer 13

Anti-histamine will block muscarinic receptors on the heart which will decrease K+ permeability that can lead to a prolonged phase 3 resulting in an EAD. (44:00)

Question 14

List per lecture things that can cause EAD?

Answer 14

1. Antihistamines (blockin muscarinic receptors)
2. Hypokalemia (blocking KIR and K+ delayed Channels)
3. Irritated Fast Na+/ L-type Ca2+ channels.
4. Decrease Mg2+
5. Beta agonist drugs (Increase cAMP, increase PKA, increase Ca2+ sensitization). (59:00)

Question 15

What is a depolarization that happens after phase 3, but still considered a premature depolarization.

What is this usually a result of?

Answer 15

Delayed after depolarization (DAD) (45:00)

Vrm is higher than it should be will result in a DAD.

Question 16

What is going on in the ventricles in ventricular fibrillation?

Intervention for ventricular fibrillation.

Answer 16

There are multiple ectopic pacemakers firing and no coordination in the ventricles.

Defibrillation (47:00)

Question 17

What causes peaked t-waves.

Answer 17

Early to mid hyperkalemia , will result in an increase in potassium permeability by opening more delayed rectifying K+ channels. The T-wave will repolarize at a faster rate and an increase in amplitude (50:38).

Question 18

What does increase hyperkalemia do to Vrm?

How does the heart compensate this?

Answer 18

Increase in hyperkalemia will initially lower the permeability of K+ which will increase Vrm.

The heart will compensate by opening up more delayed K+ rectifying channels to increase K+ permeability. (52:14)

Question 19

What happens in the ventricular myocytes in late/extreme hyperkalemia?

Answer 19

At a certain point there are only so many potassium channel the cell can open to increase permeability of the ion. When hyperkalemia is extreme, there will be an increase in our Vrm and repolarization does not go down as far.

Eventually, we will have trouble resetting our Fast Na+ channels. Speed of conduction in the ventricular myocyte depends on the speed of which Na+ is coming in. If these Na+ channels are not reset, then the speed will depend on the L-type Ca2+ channels (slow conduction).

If K+ continues to increase, the Ca2+ channels won’t be able to reset. Game over at this point. No action potential, complete infarction. GG. (57:20)

Question 20

What does the Class I anti-arrhythmic drugs target?
What does this do to conduction?

Example of Class I drug.

Answer 20

Fast sodium channel blockers, that limit the speed of influx of Na+ during phase 0. This will slow down the conduction of the action potentials.

Caine derivatives, Lidocaine (74:00)

Question 21

What does the Class II anti-arrhythmic drugs target?
How does this slow down conduction?

What happens to the SERCA pump with Class II drugs?

What happens to the Calcium Channels?

Answer 21

Beta blockers will slow conduction down at the nodal tissues by reducing the activity of the HCN mediated channels. Decrease Na+ influx will lengthen phase 4, decreasing HR.

SERCA is slowed down, because phospholanbam is no longer being inhibited because there is no PKA.

Lowers phosphorylation in L-type Ca2+ channels d/t lack of PKA.

(76:00)

Question 22

What does the Class III anti-arrhythmic drugs target?

Example of a potassium channel blocker?

What drug can be classified in all four anti-arrhythmic category?

Answer 22

Potassium Channel Antagonist.

4-aminopyridine/ tetraethylammonium (TEA)

Amiodarone

(79:30)

Question 23

What does the Class IV anti-arrhythmic drugs target?

Effects of Class IV drugs?

Answer 23

Calcium Channels.

CCB slows down conduction in the nodal tissue (AV node). Reduce contractile force d/t decrease amount of Ca2+ influx. (80:00)

Question 24

What is the top side effect of digoxin?

Answer 24

Bradycardia, d/t increase time for the heart to reset itself because the Na+/K+ pump is slowed down. (83:00).

Question 25

What NT is adenosine similar to? What receptor does adenosine work on and effects of the receptor? Any special considerations when using adenosine?

Answer 25

Acetylcholine (84:00) A1-receptors. When adenosine binds to the A1 receptor, they can slow the heart down and reset by VASTLY increasing K+ conductance. Adenosine has really short half-life, so make sure you are close to the heart when you use it. (86:30)

Question 26

What does Inotropic mean? What does Chronotropic mean? What does Dromotropic mean? What does Lusitropy mean? What type of drug is an example of all four of these?

Answer 26

Something that increases contractile force of the heart or sensitivity to calcium. Something that increases the speed of the heart rate Refers to conduction speed in the heart. Refers to resetting speed of the heart (something to speed up the SERCA pump) Beta agonist drugs have all these qualities! (88:00)

Question 27

How can general anesthesia cause arrhythmias? How can local anesthetics cause arrhythmias? How can Vagal Stimulation cause arrhythmias? How can Intubation cause arrhythmias?

Answer 27

General anesthesia Increase sensitivity to arrhythmias, d/t reduction of reuptake of NE. (90:00) Unintentional spread of local anesthetic (lidocaine) into circulation can induce an arrhythmia by impairing phase 0. (91:00) Vagal stimulation like the Five and Dime reflex can cause a Heart Block. Heart does not respond well to foreign object being stuck in the trachea. Plenty of sensors in the larynx will trigger the nervous system to respond. (92:30)

Question 28

How can central lines cause arrhythmias? How can physical contact with the heart cause arrhythmias?

Answer 28

Cardiovascular system will respond to catheters placed in large veins. Heart doesn't respond well to physical touch, can respond in abnormal EKG.

Question 29

How can ventilation cause arrhythmias?

Answer 29

Ventilation can influence electrolytes. There are a lot of plasma proteins in our blood. The plasma proteins are made up of water soluble amino acids with a net negative charge that attract protons (H+). Protons (H+) are breathed out through CO2 removal. This frees up space on the plasma protein to bind to Ca2+. Reducing ECF of Ca2. This can affect the CICR in ventricular myocytes. (97:00)

Question 30

How does body temperature cause arrhythmias?

Answer 30

Increased or decreased body temperature will correlate with HR.

Question 31

How does Cessation of long term Beta Blockers cause arrhythmias? How does the body keep our potassium level in check during physical activity? How does a beta blocker affect this system?

Answer 31

When the body is use to having a beta blocker on board. Over time, the body will desensitize itself to the effects of that antagonist. Body develops resistance to the beta blocker, by putting out more beta receptors. By removing the beta blocker, the person will be over reactive to anything that sets up the sympathetic nervous system. (101:00) Most cells in the body has some sort of Beta catecholamine receptors located on them. When our activity levels increase, our adrenal glands are activated and released Epi and NE. These catecholamines will activate intracellular processes that keep our ECF potassium levels in check, by controlling the cycling of the Na+/K+ ATPase. Increase activity will speed up Na+/K+ ATPase to put K+ back into the cell. Using a beta blocker will inhibit this beta-receptor mediated process that might lead to increase K+ in the blood. (108:00)

Question 32

How can current or past myocardial infarction affect the heart? How can having a stretched heart muscle can cause arrhythmia?

Answer 32

MI usually results in scar tissues being formed. Scar tissue can prevent an area in the heart from ever seeing a depolarization. (109:00) A stretched heart muscle will take longer for depolarization to go from source to depolarization. The enhance time for depolarization increases the chances of having an arrhythmia.

Question 33

How does a healthy heart respond to increased stretch in the atria? What are the two forms of this process? How much of an increase in HR can each form generate?

Answer 33

When the atria is stretch this will induce stretched mediated Na+ and Ca2+ leak channels that will increase the rate depolarization in phase 4 of nodal action potential resulting in an increase in HR. 1. Direct Atria Stretched (DAS) - this is built in to the atria. This can increase HR by 10-15% 2. The Bainbridge Reflex is mediated through sensors from the NS that feedback onto the nodal tissue through reduction in vagal tone when there is increase stretched in the atria. Reduction in vagal tone will increase HR. The reflex can increase HR by 50%. 50-65% Increase in HR together.

Question 34

How does insulin affect the ATPase pump?

Answer 34

The insulin receptor is tethered to the Na+/K+ ATPase pump, if you give someone an insulin dose it will speed up the cycling rate of the Na+/K+ Pump and remove K+ from the ECF. (118:00)