Lecture 5: ARRHYTHMIAS Pathophys. Flashcards

1
Q

Learning Obj: Describe the Normal Conduction of the heart

A
  • The conduction of the heart normally begins at the SA node, located in the right atria
  • The SA-node initializes depolarization of atrial muscle cells
    -The AV-Node, located between the atria and ventricles, is activated and, after a delay, initiates the conduction impulse through the ventricles
  • The Purkinje Fibers carry the signal through the septum to the apex and the rest of the ventricular mass
    .
    NOTE: all conduction begins at the SA node (on top of right atrium. the electrical energy comes out of SA and will hit atrial myocyte which will general impulse thru atrial. the impulse will then come to AV node and will hesitate for a second and then will go to purkinjie system and will contract ventricle! We can measure this conduction thru electrocardiogram (ECG)!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Learning Obj: Define P, QRS, T waves

A

this is an ECG (how we can measure these electrical impulse):
-P wave: atrial depolarization (contraction)
-QRS: ventricular depolarization (contraction)
- T waves: ventricular repolarization (cells going back to baseline/ relaxation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Learning Obj: What is the normal range of PR, QRT, and QT intervals? And what do they represent?

A

PR interval : measuring how long impulse gets thru the AV node. (drugs will effect conduction thru the AV node! it will slow the impulses thru AV node. We do not wanna give too much drug cuz that will cause NO impulses to go thru! and one way we can measure this to make sure it does not happen is by measuring PR intervals! and if PR interval gets too long we have to back down on the drugs!
.
QT interval: As the QT interval prolongs, this can cause ventricular arrhythmias! antiarrhythmic drugs not only treat arrhythmia but it can cause arrythmia!! So you need to have the right amount! too much can cause arrhythmia! We can measure the QT interval to make sure it doesn’t get too long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PR Interval: Define

A
  • A time interval that represent AV-node conduction (time impulse travels through the AV-node)
  • Drugs are often used to slow impulses through the AV node.
  • Drugs and disease states may increase time interval or action potential conduction that may lead to blockage of the impulse.
  • Need to monitor PR interval with certain drugs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

LC: QT and QTc interval: Define

A

What happen to the QT interval is that as your heartrate slows, it prolongs! so we must correct for heart rate. You do not need to know that formula but just know what QTC means! (QT/ squared RR) . RR is is time between 2 QRS complex. YOU NEED TO MONITOR DRUGS THAT PROLONG QT INTERVALS TO PREVENT PROARRHYTHMIC EVENTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Action Potential: general

A

Action Potential (usually generated from SA node) –> Electrical Impulses –> Heart Beat –> ECG
.
P - QRS - T (then repeat. this is normal!). In normal conditions the intervals are pretty consistent and the same. in irregular, you may be missing waves and/or the intervals are inconsistent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Action potential: graph and phases- explain what happens

A

Cells are usually at resting membrane level as value become more positive as we have more current coming into the cell (Na and Ca) that comes into cell and raises membrane pot to threshold pot! Contraction happens when it reaches threshold pot! it reaches here and Na channel rapidly open! and we get a flood of Na coming into cell further raising/ more positive! This generate electricity and contractility of cells! Then you go into phase 2 which is the plateau phase then phase 3 and phase 4 (more info to come)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phase 0: talk more about it

A
  • Na+ Dependent : Atrium, Ventricles (this is where Na comes in)
  • Ca++ Dependent: SA and AV node
    .
    NEED TO KNOW (and how it relates to antiarrhythmic therapy – Calcium channel blocking drugs, sodium channel blocking drugs). So will a Ca blocker work in the atrium or ventricle? NO! and vice versa!
    .
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Impulse Generation “Leak”

A
  • During Phase 4, a gradual slope (caused by background K+ and Na+ currents) in the potential leads to activation of voltage-gated sodium
    channels –THRESHOLD POTENTIAL and Phase 0!!! – electrical energy and start of one heart beat.
  • Altering the characteristics of this slope or the sensitivity of sodium channels can alter cardiac pacing (i.e, heart rate)
    .
    In phase 4 we get a leaky membrane and a lot of different cations are coming in the cell, thus raising the resting membrane potential so that’s why we see a slope! when it reaches the threshold we get a heart beat and it starts all over again!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Slope of Phase 4

A
  • Increase slope, increase automaticity (heart rate)
  • Sympathetic activity (by getting scares, working out, etc, increase in epi and noreepi!) increases slope of phase 4 and thus HR.
  • Cholinergic activity (acetylcholine- we can increase it by breathing in slow!) decreases slope of phase 4 and thus slowing/ lower HR
  • Some antiarrhythmic drugs can change slope of phase 4 and change heart rate
    .
    As we change the slope we can change the heart rate!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Impulse Generation/ how many BPM
.
Question 1: Which one has the highest Phase 4 slope (between SA, AV, or ventricle)?
Question 2: If the SA node does not generate an electrical impulse what would be the heart rate?

A
  • SA node – 60 to 100 beats/minute (most leaky ion currents thus SA node is the primary pacemaker cell in the heart)
  • AV node – 30 to 50 beats/minute
  • Ventricles - < 30 beats/minute
    .
    Question 1: Which one has the highest Phase 4 slope? SA Node! It fires first! Let’s say SA node does not fire..what would happen (Question 2)? no heart rate.. BUT we have AV node! so our heart rate would be 30-50 BPM (via AV node! AV will still fire but not much as SA) …but if AV node fail or AV node block? SA fire but it stops at AV cuz there’s a block…so the ventricles will take over and fire ..although it is v slow (less than 30 BPM) so you’re alive but barely lols. It’s good to have these back up firing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe how the rate of the pacemaker cells may be affected
by changes with the action potential

A

Altering the pacemaking cells (altering heart rate)
.
How we can alter heart rate 4 ways:
-We can decrease or increase slope of phase 4
-We can decrease or increase max. diastolic potential (to increase the max diastolic pot we make it more negative so it makes it harder to reach threshold/ action potential.
-We can increase the threshold potential (take longer to reach it)
-we can increase actional pot duration - will take longer to depolarized and stuff .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Effective or Absolute Refractory Period

A

When the cell contrast there is a pd of time which is called effective refractory pd. (ERP) in which no matter what you do to it…it will NOT contrast! the impulse come but if cell is in effective refractory pd. the impulse will get terminated/ it stops… this is important in arrythmia as you may want to prolong the ERP so that the impulse stops and SA node takes over
.
Relative Refractory Period? We wont really worry about that…just look at picture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Q: What would a MOA be for an antiarrhythmic drug to decrease automaticity (heart rate)?

A

Decrease slope of phase 4!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Q: What would a MOA be for an antiarrhythmic drug to decrease or slow down impulses.

A

We can prolong action pot or decrease slope of phase 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ARRHYTHMIAS and where they can occur/ what they are called based on the location it occur

A

anywhere in the heart! They can occur! SVT is a general classification basically meaning “anything above the ventricles.

17
Q

LO: List the names of fast arrhythmias and slow arrhythmias

A

Fast Arrhythmias:
– Sinus Tachycardia (SA node)
– Atrial Tachycardia
– Atrial fibrillation/flutter
– AV- nodal re-entry tachycardia
– Wolff- Parkinson White Syndrome (WPW)
– Ventricular Tachycardia
– Ventricular Fibrillation
.
Slow Arrhythmias:
– Sinus Bradycardia (SA node)
– AV-nodal block: 1st, 2nd, 3rd degree block
– Asystole

18
Q

Heart Rates in beats per minute in abnormal situations

A
19
Q

LO: What are the 2 main etiologies and subheadings for developing
arrhythmias

A

1.) Metabolic abnormalities
– Ectopic conduction/Early afterdepolarizations
– Ischemic tissue (cells will lyse and release of electrolytes and when that is next to normal cell…that can cause reentry circuits/ electrolyte abnormality like low K+ and high K+ can cause arrythmia!!! / messes up the environment for other health cells!)
– Genetic abnormalities (QT-prolongation)
– Electrolyte Abnormalities
– Drug Toxicity (eg. spironolactone, lisinopril, diuretics, etc)
.
2.) Structural abnormalities
– Scarring/fibrotic areas of no conduction
– Hypertrophy and cardiomyopathy (when heart gets larger it messes up the conduction!)
– Accessory pathways/block/congenital malformations
.
NOTE: two ways arrythmia patient die: heart failure and sudden cardiac death arrythmia

20
Q

LO: What are the 2 main mechanisms and subheadings for developing
arrhythmias? Arrhythmia Formation – 2 Main Mechanisms
(GENERAL)

A

Two Major Mechanisms:
.
1.) Disorder of impulse generations
- Abnormal automaticity
- Triggered activity, early or delayed afterdepolarizations (EAD or DAD)
.
2.) Abnormal impulse conduction
- Block
- Reentry

21
Q

1.) ARRHYTHMIA FORMATION – DISORDER OF IMPULSE GENERATION (in depth/ the different ways there are disorder of impulse generation)

A
  • Disorder of Impulse Generation – Abnormal Automaticity: Think about the slope of phase 4! If we change the slope of phase 4 we can increase or decrease heart rate.
    .
  • Disorder of Impulse Generation: After Depolarizations
  • Early AD – altered openings of CA++ or Na++ channels. Also K+ channels
  • Delayed AD - elevated cystolic Ca++ concentrations
    NOTE: in certain conditions, we get generation due to excessive leaky current that us outside of phase 4!this happen during repolarization that allow us to reach actional potential and allow us to fire too early! So before the signal comes from SA node.. the cell fire early and causes a contraction before SA node signal even gets there (pic)!!
    .
    Why do EAD’s and DAD’s only occur in the late Phases of the action potential? b/c of effective refectory period! cell that are depolarized cannot fire again so that’s why it does not occur until later after depolarization
22
Q

SUMMARY ARRHYTHMIA FORMATION – DISORDER OF IMPULSE GENERATION

A
23
Q

2.) ARRYTHMIA FORMATION - ABNORMAL IMPULSE CONDUCTION (Block vs Reentry)

A

1.) Abnormal Impulse Generation - Block
- Area of tissue that does not conduct electrical impulse (action
potential)
- Most important areas – SA node, AV node, or His-purkinje system
(i.e., bundle branch)
NOTE: if there is a block we cannot conduct. Look at picture. There is no association between P wave and QRS!
.
2.)Abnormal Impulse Generation - Reentry (PIC)
EXAMPLE: AV-Node Reentry Arrhythmia
- AV-node has embedded a slow and fast pathway
- Often, a premature beat can set up a AV-nodal reentry arrhythmia or damage area altering speed of conduction. Common arrhythmia
NOTE: There are area of heart where we have bifurcation.. but when different impulses meet each other = they cancel! one way block (uni) signal can go back up!

24
Q

QUESTIONS:
1.) How would you terminate a reentry arrhythmia?
2.) Describe two mechanisms to slow down a fast heart rate that originates in the SA node

A

1.) To terminate need to increase refractoriness (two way block) or slow conduction (abnormal impulse hit refractory tissue)
.
2.) decrease phase 4 slope, increase max diastolic pot, increase threshold, and increase action pot duration