Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FHB Exam 1 - Cardiovascular Physiology > Lecture 9 - Cardiac Electrophysiology > Flashcards

Lecture 9 - Cardiac Electrophysiology Flashcards

1
Q

Name 3 general mechanisms of cardiac dysrhythmias.

A
  1. Altered AUtomaticity
  2. Re-Entry of Excitation
  3. Triggered Activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is altered automaticity?

A

Changes in pacemaker rate that are mediated through changes in pacemaker MECHANISMS that exist in pacemaker cells

(SA or latent pacemakers/purkinje fibers)

THUS ACTION POTENTIALS ARE FORMED INNAPROPRIATELY

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

What defines tachycardia?

A

Heart rate GREATER than 100 beats/min

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

What defines bradycardia?

A

Heart rate less than 60 beats per minute

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

What are the 5 possible causes of TACHY-dysrhythmias?

A
  1. NE (sympathetic NS)
  2. Stimulants - amphetamines
  3. ISCHEMIA (lack of blood flow)
  4. STRETCHING (ventricular aneurisms)
  5. Sick sinus syndrome, fever, hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dysthrythmias primarily result from alterations in what?

A
  1. Impulse FORMATION
  2. Impulse CONDUCTION (from SA)
  3. or BOTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AUTOMATICITY is an issue with impulse formation or conduction in atrial or ventricular muscle. True or False?

A

FALSE

- no normal automatic mechanisms
if channels are only in SA and purkinje!

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

How is a premature beat seen and felt?

A

it is an extra beat, but when you take a pulse you feel a PAUSE

  • premature beat does not generate enough tension in the heart - feel thumping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does a phosphodiesterase inhibitor do?

A

Inhibits breakdown of cAMP (2nd messenger in sympathetic nerve stimulation)

  • INCREASE HR & SYMPATHETIC RESPONSE since cAMP not broken down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do amphetamines cause TACHY-dysrthymias?

A

Block the degradation of NE and enhance the affects of NE = fatal arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an aneurism?

A

Weakening of the wall of heart or artery = causes a bulge –> pressure pushes and can rupture causing you to bleed OUT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Does hypokalemia lead to tachy-dysrhythmia or bradydysrhythmia?

A
  1. Because of anomalies rectification, low K+ values do not significantly change the RMP
  2. Lengthen the AP = prolonged Q-T syndrome
  3. Enhance latent pacemaker activity (ventricles stimulated abnormally) –> POTASSIUM NEVER AFFECTS SA node
  4. Enhance diastolic depolarization
  5. Fire premature beats = TACHYCARDIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Does potassium affect the SA node?

A

NO

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

Fever and hyperthyroidism will increase or decrease HR?

A

INCREASE HR

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

What are 5 EKG manifestations of TACHY-Dysrhythmia?

A
  1. Sinus Tachycardia (sitting still not during exercise–> normal C.O.)
  2. Premature Atrial Contraction (PAC)
  3. Premature Ventricular Contraction (PVC)
  4. Atrial or Ventricular Tachycardia (AT, VT)
  5. Supraventricular Tachycardia (SVT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are 5 possible causes of BRADY - Dysrhythmias?

A
  1. Drugs (anti-arrhythmatics, beta-blockers, Ca antagonists, DIGITALIS)
  2. Barbiturates,anesthetics
  3. Ischemia/infarct
  4. Sick Sinus Syndrome
  5. AGING - fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does digitalis affect the heart?

A

Slows down SINUS rate by enhancing Vagal stimulation

  • increase strength of VENTRICULAR contraction (benefit)
  • slows down the heart = USES LESS OXYGEN (need to manage oxygen consumption of the heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do barbiturates and anesthetics affect the heart?

A

Slow it down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is sick sinus syndrome?

A

Rapid heart rate mixed with slow HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are EKG manifestations of BRADY-dysrhythmia?

A

Sinus Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the most common type of dysrhythmia?

A

Re-entry of Excitation

22
Q

What are 3 requirements for Re-Entry of excitation?

A
  1. Geometry for a conduction loop
  2. Slow or delayed conduction
  3. UNIDIRECTIONAL CONDUCTION BLOCk
23
Q

What are the 3 possible causes of Re-Entry of Excitation?

A
  1. Ischemia
  2. Infarct
  3. Congenital Bypass tracts (Wolf-Parkinson-White = WPW)
24
Q

What determines the speed of conduction? How does ischemia change this?

A
  1. RMP

2. Ischemia causes early depolarization, lose Na channels = SLOW AP

25
Q

What are EKG manifestations of Re-Entry of Excitation?

A
  1. Premature Atrial or Ventricular Beats
  2. Atrial or Ventricular Tachycardia
  3. Supraventricular Tachycardia
  4. Atrial Flutter
  5. Atrial or Ventricular Fibrillation
26
Q

What is the only cause of Atrial Fibrillation?

A

Re-entry of Excitation

27
Q

What is atrial flutter?

A

Rapid rate, so few impulses get through to the ventricle (filtered by AV node)

28
Q

What can WPW result in?

A
  1. due to RE-ENTRY OF EXCITATION
    - impulse travels up again through bypass tract connecting Right Atrium & Right Ventricle
    - stimulates Right atrium again
    = SUPRAVENTRICULAR TACHYCARDIA
29
Q

What is fibrillation?

A

Chaotic re-entry and tissue is completely asynchronous

30
Q

Where can triggered activity occur?

A

Atrial or Ventricular TIssue

31
Q

What is responsible for the automaticity of cardiac Pacemaker cells?

A 
Diastolic Depolarization (Phase 4)
- SLOW depolarization of the membrane potential that is responsible for the AUTOMATICITY of cardiac pacemaker cells
32
Q

the following are 2 possible causes of what?

  1. Elevated INTRACELLULAR CALCIUM
  2. Digitalis toxicity (causing dysrhythmia)
A

Delayed After Depolarization

33
Q

Define a Delayed after depolarization

A

depolarization of the membrane following an Action potential due to intracellular Calcium increase or DIGITALIS toxicity (increases Ca)

= increase contraction of the heart
- occur during increased heart rate
-

34
Q

Define a Early after depolarization. What is often the cause?

A

Depolarization of membrane during either
1. plateau of phase 2
or
2. phase 3 repolarization

  • when AP prolonged (prolonged Q-T syndrome) and HR is SLOW
  • AP prolonged = increase in CA channels that have recovered from inactivation even b4 cell fully depolarizes = trigger an AP
  • SLOPE CONSTANTLY INCREASING (but not diastolic depolarization)
35
Q

The following are possible causes of DAD or EAD?

  1. Digitalis Toxicity
  2. Elavated Catecholamines (NE)
  3. Rapid Heart Rate
  4. all in combo
A

DAD!!!

36
Q

How would a DAD look on a EKG?

A
  1. Premature Atrial (PAC) or Ventricular Contractions (PVC)

2. Atrial or Ventricular TACHYCARDIA

37
Q

When you increase HR, does DAD activity increase or decrease?

A

INCREASE

  • TRIGGERED AP = as a premature beat or tachycardia
38
Q

What is the mechanism behind DAD’s?

A
  1. Increase in intracellular Ca taken up by SR
  2. SR overloaded with Ca, AP can trigger release of Ca AFTER AP has ended
  3. Activates Na/Ca exchanged
  4. 3Na in for 1 Ca out generates net inward current of Na
  5. More positive RMP can lead to DAD (depolarization occurring in Phase 4)
  6. if threshold reached = AP is generated

make SINGLE or Multiple beats

= PVC/PAC, or tachycardia

39
Q

What are EAD’s often related to? (3)

A
  1. Prolonged AP
  2. Re-activation of slow inward Ca+ current
  3. May contribute to Prolonged Q-T syndrome by extending AP
  • SLOWER HR = Ca channels can recover from inactivation even before cell fully depolarizes = can trigger AP
40
Q

The following are possible causes of EAD or DAD?

  1. ACIDOSIS
  2. Hypokalemia
  3. Quinidine (class 1 anti-arrhythmic drug)
  4. SLOW HEART RATE
A

EAD

41
Q

What are possible EKG manifestations of EAD’s?

A
  1. PAC or PVC (like in DAD)
  2. Atrial or Ventricular Tachycardia (torsades de pointes)
  • looks like M
42
Q

If K+ conduction is blocked, is an AP lengthened or shortened?

A

LENGTHENED

43
Q

Acidosis as caused by Ischemia, prolongs or decreases the AP?

A

PROLONGS

44
Q

Which are most similar to R on T, EAD or DAD?

A

EAD

  • spontaneous beat on relative refractory period of previous beat
  • hitting relative refractory period can cause a VF
45
Q

The following can lead to what?

  1. Altered Automaticity
  2. Re-Entry of Excitation
  3. Triggered Activity
A

DYS-RHYTHMIA!!

46
Q

What are some anti-arrhythmic therapies?

A
  1. Drugs (Na/K, Ca blockers, Beta-blockers
  2. DC Cardioversion
  3. Implantable Cardio-verter-Defibrillator (ICD)
47
Q

The following is a description of what therapy? (DC Cardioversion or ICD)

  • large current sent through heart, depolarizes all cells to plateau so they all synchronize & depolarize together
  • SA node retakes activity
A

-DC Cardioversion

48
Q

The following is a description of ICD or DC Cardioversion?

Large electrode is placed on the heart and senses the electrical activity. Sends shocks when the heart is not in synchronous activity.

A

Implantable Cardioverter-Defribrillator (ICD)

49
Q

Where is the ICD implanted?

A

Through left subclavian vein through SVC into the RIGHT atrium (lead is placed there) and the defirbrillation coil is placed in Right ventricle (electrode)

  • HR is sensed in RA
50
Q

What is the average P-R interval?

A

0.12-0.20 (120-200ms)

51
Q

What are the average values for the following:

  1. P-R Interval
  2. QRS Complex
  3. Q-T interval
  4. Tachycardia
  5. Bradycardia
A
  1. 0.12-0.2 seconds (120-200msec)
  2. 0.07 to 0.10 sec (70-100 msec)
  3. 0.25 - 0.43 (250-430 msec)
  4. HR > 100 beats/min
    - cycle length SHORTER than 0.6 sec (600 msec)
  5. HR<60 beats/min
    - cycle length LONGER than 1.0 second (1000 sec)

FHB Exam 1 - Cardiovascular Physiology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions