LECTURE 26 11/04/22 (LECTURE 14 SLIDES: CARDIAC ARRHYTHMIAS/ ECG INTERPRETATIONS)

Question 1

What are causes of cardiac arrhythmias?

Answer 1

-Abnormal rhythmicity of pacemaker ( HR outside of 72 bpm)
-Action potential generated in wrong place.
-Abnormal pathways of transmission in the heart (ie: right main bundle branch block)
-Blocks at different points in transmission of cardiac impulse.
-Shift of pacemaker from SA node.

Question 2

For physiology, what is considered tachycardia?
For physiology, what is considered bradycardia?

Clinically, what is considered to be tachycardia?
Clinically, what is defined to be bradycardia?

Answer 2

Above 72 bpm
Below 72 bpm (09:00)

HR greater than 100 bpm (11:50)
HR less than 60 bpm (15:33)

Question 3

Causes of tachycardia?

Answer 3

1. Increase body temperature (MH, heat strokes)
2. Sympathetic stimulation (loss of blood/ reflex stimulation).
3. Toxic conditions of the heart (nicotine)

Question 4

What causes bradycardia?

Answer 4

1. Athletes who have large stroke volume (Lance Armstrong)
2. Can be caused by vagal stimulation (parsympathetic NS: ACh)
3. Neural reflex to drugs (reflex response to phenylephrine). (18:50)

Question 5

How does vagal stimulation decrease HR (2)?

Answer 5

1. Increase potassium permeability, reducing membrane potential, lengthening phase 4 to decrease HR.
2. Inhibition of adenyl cyclase, reduction of cAMP quantity, closing HCN channels. (19:40)

Question 6

What kind of receptors does Acetylcholine bind to in the heart? What part of the heart are these receptors in?

What does it do to heart rate?

Answer 6

Muscarinic Receptors on the SA and AV node.

K+ efflux was cause hyperpolarization of the membrane and decrease HR.
(Pharm/A&P Test Recall)

Question 7

What type of receptor does phenylephrine work on? Is it an agonist or antagonist?

What happens to blood pressure and HR?

Answer 7

Pure alpha-1 receptor agonist drug.

This will cause vasoconstriction of the periphery. There will be an increase in MAP.

Baroreceptors in aortic arch and carotid bifurcation will see an increase in MAP will result in reflex inhibition to the nodal tissues via vagal stimulation resulting in reflex bradycardia. (21:33)

Question 8

Term used in lecture which means coming and going to describe arrhythmias. How many syllables are in this term?

Answer 8

4, syllables in Paroxysmal (22:40)

Dr. Schmidt repeated this definition a couple times through the last couple lectures, might be a good fill in the blank question. Know how spell it

Question 9

1. What is another name for Supraventricular Tachycardia?
2. Where is the HR originating from?
3. What are symptoms you might experience if the tachycardia is really bad?
4. After what wave do we have filling?
5. How does SVT affect this?
6. What may may happen to the P and T wave?

Answer 9

1. Paroxysmal Atrial Tachycardia (23:30)
2. Somewhere in the atria, most likely the SA node, normal pathways are used
3. Sx: disoriented, dizziness, syncope, low CO (due to decrease T-P interval)
4. T-wave
5. Decrease filling time, decrease SV
6. There may be overlap of the P and T waves

Question 10

What is used to treat SVT?

Answer 10

Vagal reflex
Beta Blockers (slow phase 4, close HCN channels)
CCB (slow transmission of AP)
*Digoxin (block Na+/K+ pump, slow repolarization, decrease HR) (28:50)

*not the best choice.

Question 11

What places on the heart can generate its own action potential?

Answer 11

1. SA node
2. AV node
3. Purkinje Fibers

(30:39)

Question 12

What wave is absent in a complete Sinoatrial Block?

What will take over automaticity?

Whats the new HR?

Answer 12

P-wave (30:00)

AV node

40-60 bpm

Question 13

When the AV node takes over as the pacemaker of the heart, why is there a downward deflection of the P-wave?

Answer 13

AV nodal tissue can generate action potentials heading in two directions. Part of the AP moves into the ventricles and the other AP moves towards the atria which can reverse the order of depolarization resulting in a downward deflection.

(33:00)

Question 14

What condition will slow/block impulses through the AV node and AV bundles (of His)?

What can cause this (5)?

Answer 14

Atrioventricular Block

1. Ischemia of the AV node or AV bundle fibers (coronary ischemia)
2. Compression of A-V bundle (penetration portion of the AV bundle, d/t calcification or scar tissue)
3. AV node/ AV bundle inflammation
4. Excessive Vagal Stimulation (excess left-sided vagal stim and VX Reflex EYEBALLS)
5. Excessive Digitalis

(34:10)

Question 15

What type of medication is given to slow down scar tissue deposition after recovering from an MI?

Why?

Answer 15

ACE Inhibitors

ACE Inhibitors are growth factor inhibitors, which can prevent the unnecessary deposition of scar tissues?

(37:30)

Question 16

What vagus nerve innervates the AV node?

What vagus nerve innervates the SA node?

Describe how the vagus nerve innervation work in both SA and AV node?

Answer 16

Left Vagus Nerve - AV node

Right Vagus Nerve - SA node

Parasympathetic Nervous System can cause the vagus nerve to release ACh onto the muscarinic receptors located on either the SA or AV node which will cause K+ efflux.

Mechanical compression of the vagus nerve during a procedure or massage can cause them to fire as well.

(39:00)

Question 17

What is a normal PR-interval?

What PR-interval will be considered a 1st degree Incomplete Heart Block?

What is considered the PR interval on the EKG?

Answer 17

Normal PR Interval: 0.16 seconds

1st degree heart block PR Interval: >0.20 seconds

Initiation of the action potential in the SA node (P-wave) until it hits the ventricle and generates the QRS complex.

(42:00)

Question 18

How long is this PR interval?
Is it considered a 1st degree block?

Answer 18

PR Interval: 0.28 seconds
Yes, 1st degree block

Question 19

What block has progressive lengthening of PR intervals that results in a dropped QRS complex?

What block has a longed and fixed PR interval and has a ratio of beats to dropped beats.

Answer 19

2nd Degree Incomplete Heart Block: Mobitz Type I or Wenckebach periodicity. (45:40)

2nd Degree Incomplete Heart BlocK: Mobitz Type II (49:00)

Question 20

What is the range of PR Interval variability for 2nd Degree Heart Block?

What is going on with the conductions going through the AV node?

Answer 20

PR Interval: 0.25 to 0.45 seconds

Some impulses pass through the AV node, some do not resulting in dropped beats. (49:00)

Question 21

Which 2nd Degree Heart block is less tolerated? Interventions?

Answer 21

Mobitz Type II is more serious, less tolerated.
Mobitz Type II should be paced if possible. (51:30)

Motbitz Type I is more tolerated, less likely to fall into a lethal arrhythmia.

Question 22

What arrhythmia results in total AV Nodal Block or Bundle of His block?

What is relationship between the QRS complex and P waves?

Why is the ventricular escape between 15-40 bpm?

What is causing the elevated atrial rate in this block?

Answer 22

3rd Degree Complete Heart Block

Complete dissociation of QRS from P-waves

Since the AV node is not allowing any action potential through, action potential is generated by Purkinje fibers.

The decrease HR from the Purkinje fibers will result in a feedback from the body telling the heart there is not a normal SV or cardiac output. This will result in an increase sympathetic stimulation, resulting in an increase in atrial rate. (54:00)

Question 23

What causes atrial flutter?

What is the atrial rate of A-flutter?

Do all these rates pass through the AV node?

What is the distinct characteristics of the a-flutter waves?

Answer 23

A-flutter is caused by circular reentry pathways in the atria. If there is sick or dead tissue in the atria it will be more prone to re-entry. A stretched out atria can also result in a circular re-entry.

Atrial rate can be from 200 up to 300 bpm.

Not all the atrial rates pass into the ventricles, because the AV node will filter them out. Ventricular heart rate will be around the 100s.

Sawtooth pattern, elevated p-wave, and somewhat elevated QRS complex. (62:00)

Question 24

What percentage does the atria contribute to overall stroke volume under resting conditions in a healthy individual?

Answer 24

5% (79:00)

**Atrial contributions makes more of an impact when we are exercising, sick, or under anesthesia. (25%)

Question 25

What makes atrial fibrillation different from atrial flutter?

Answer 25

Unlike Atrial Flutter, Atrial Fibrillation are: 1. Not coordinated 2. Have irregular electrical activity 3. Have multiple ectopic pacemakers and circus movements (current is all over the place), where as A-flutter usually has one ectopic foci (87:00)

Question 26

What can contribute to ectopic pacemakers firing? Why don't we see defined P-waves in atrial fibrillation? What does increased turbulence in the walls of the atria produce?

Answer 26

Sick and ischemic tissues will cause rogue action potentials to be generated. (82:00) No coordinated movement in electricity to cause a synchronized depolarization of the atria. Blood clots (85:44)

Question 27

What are causes of Atrial Fibrillation?

Answer 27

1. Stretched out atria caused by bad valves between the atria and ventricles (stenotic valve or regurgitated valve). 2. Ischemic atrial tissues 3. Sick atrial tissues (84:00)

Question 28

How does a regurgitated AV valve cause hypertrophy in the atria?

Answer 28

A regurgitated AV valve does not close all the way, during ventricular contraction. Blood can be moved backwards into the atria, stretching the chamber out. (85:00)

Question 29

What is Stokes-Adams Syndrome: Fainting/Syncope?

Answer 29

This syndrome occurs d/t delay in the ventricular escape when the AV node is blocked. The slope to threshold for a Purkinje Fiber action potential is very flat (phase 4) which results in a delay of anywhere from 5 to 30 seconds before a ventricular depolarization. People can pass out if there are no contractions for 10-15 seconds b/c no blood is going to the brain and decrease BP. After the first beat, subsequent beats won't take as long. 15-40 bpm. (93:00)

Question 30

What OR procedures usually correlates with higher increases of Stokes-Adams Syndrome? Describe this process and what is this reflexed called?

Answer 30

Procedures where there is significant pressure placed on the eyes. When this happens the pressure on the eyes is picked up by the branch of the 5th cranial nerve (trigeminal nerve). Triggering a VX Reflex (Five and DIme Reflex). The efferent side of the output will be the Vagus Nerve ( 10th cranial nerve). This will result in a complete AV node block and you're waiting around for the first beat to occur after the initiation of the heart block. (100:00)

Question 31

What is another name of Incomplete Intraventricular Block? What makes up the alternating QRS pattern? Describe the abnormal QRS complex?

Answer 31

Electrical Alternans (102:30) Normal depolarization from the AV node and an ectopic depolarization from the muscles in the ventricles. QRS complexes is wider d/t depolarization moving from the muscle to the other side of the heart, QRS is >0.12 seconds. The abnormal QRS complex is very large d/t a huge depolarization heading in the same direction.

Question 32

What are causes of Premature Ventricular Contractions?

Answer 32

Caffeine Nicotine Stress Lack of Sleep Having to memorize a "short list" of formulas and numbers for this test..... (113:00)

Question 33

What causes the prolonged QRS complex in PVCs? What causes the high voltage QRS complex PVCs? What is the characteristic of the T-wave in a PVCs?

Answer 33

Ventricular muscle conduction is slower than Purkinje Fibers One ventricle depolarizes before the other, no current cancels out in the QRS complex T-wave is negative after a PVC (113:30)

Question 34

What can cause the depolarization in Premature Atrial Conductions? What are risk factors for PACs?

Answer 34

Ectopic tissues in the atria can fire action potentials early. Risk Factors: Ischemia, Irritation, or Calcified Plaques

Question 35

How can you tell if the ectopic pacemaker in a PAC is originating near a SA node or AV node?

Answer 35

If the PAC is originating near the SA node, there will be a positive P-wave. If the PAC is originating near the AV node, there will be an inverted/ negative P-wave. This is d/t the electrical signal going through the atria after it originates at the AV node and going through the bundle of His. (117:35)

Question 36

What is the radial pulse deficit in PACs?

Answer 36

Early depolarizations will result in less filling time and lower stroke volume. This will result in less pulse pressure in the radial artery. (118:30)

Question 37

Where is the origination of a premature contraction of the AV Node/Bundle Source? What is usually obscured?

Answer 37

Premature contraction is originating in the A-V node or in the A-V bundle. We will just say, middle of the AV junction. P-wave obscured by the QRS complex. (120:00)