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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
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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

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3
Q

What defines tachycardia?

A

Heart rate GREATER than 100 beats/min

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4
Q

What defines bradycardia?

A

Heart rate less than 60 beats per minute

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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
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6
Q

Dysthrythmias primarily result from alterations in what?

A
  1. Impulse FORMATION
  2. Impulse CONDUCTION (from SA)
  3. or BOTH
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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!

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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
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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
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10
Q

How do amphetamines cause TACHY-dysrthymias?

A

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

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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

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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
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13
Q

Does potassium affect the SA node?

A

NO

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14
Q

Fever and hyperthyroidism will increase or decrease HR?

A

INCREASE HR

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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)
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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
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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)
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18
Q

How do barbiturates and anesthetics affect the heart?

A

Slow it down

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19
Q

What is sick sinus syndrome?

A

Rapid heart rate mixed with slow HR

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20
Q

What are EKG manifestations of BRADY-dysrhythmia?

A

Sinus Bradycardia

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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
What are EKG manifestations of Re-Entry of Excitation?
1. Premature Atrial or Ventricular Beats 2. Atrial or Ventricular Tachycardia 3. Supraventricular Tachycardia 4. Atrial Flutter 5. Atrial or Ventricular Fibrillation
26
What is the only cause of Atrial Fibrillation?
Re-entry of Excitation
27
What is atrial flutter?
Rapid rate, so few impulses get through to the ventricle (filtered by AV node)
28
What can WPW result in?
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
What is fibrillation?
Chaotic re-entry and tissue is completely asynchronous
30
Where can triggered activity occur?
Atrial or Ventricular TIssue
31
What is responsible for the automaticity of cardiac Pacemaker cells?
``` Diastolic Depolarization (Phase 4) - SLOW depolarization of the membrane potential that is responsible for the AUTOMATICITY of cardiac pacemaker cells ```
32
the following are 2 possible causes of what? 1. Elevated INTRACELLULAR CALCIUM 2. Digitalis toxicity (causing dysrhythmia)
Delayed After Depolarization
33
Define a Delayed after depolarization
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
Define a Early after depolarization. What is often the cause?
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
The following are possible causes of DAD or EAD? 1. Digitalis Toxicity 2. Elavated Catecholamines (NE) 3. Rapid Heart Rate 4. all in combo
DAD!!!
36
How would a DAD look on a EKG?
1. Premature Atrial (PAC) or Ventricular Contractions (PVC) | 2. Atrial or Ventricular TACHYCARDIA
37
When you increase HR, does DAD activity increase or decrease?
INCREASE - TRIGGERED AP = as a premature beat or tachycardia
38
What is the mechanism behind DAD's?
1. Increase in intracellular Ca taken up by SR 2. SR overloaded with Ca, AP can trigger release of Ca AFTER AP has ended 2. Activates Na/Ca exchanged 3. 3Na in for 1 Ca out generates net inward current of Na 4. More positive RMP can lead to DAD (depolarization occurring in Phase 4) 5. if threshold reached = AP is generated make SINGLE or Multiple beats = PVC/PAC, or tachycardia
39
What are EAD's often related to? (3)
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
The following are possible causes of EAD or DAD? 1. ACIDOSIS 2. Hypokalemia 3. Quinidine (class 1 anti-arrhythmic drug) 4. SLOW HEART RATE
EAD
41
What are possible EKG manifestations of EAD's?
1. PAC or PVC (like in DAD) 2. Atrial or Ventricular Tachycardia (torsades de pointes) - looks like M
42
If K+ conduction is blocked, is an AP lengthened or shortened?
LENGTHENED
43
Acidosis as caused by Ischemia, prolongs or decreases the AP?
PROLONGS
44
Which are most similar to R on T, EAD or DAD?
EAD - spontaneous beat on relative refractory period of previous beat - hitting relative refractory period can cause a VF
45
The following can lead to what? 1. Altered Automaticity 2. Re-Entry of Excitation 3. Triggered Activity
DYS-RHYTHMIA!!
46
What are some anti-arrhythmic therapies?
1. Drugs (Na/K, Ca blockers, Beta-blockers 2. DC Cardioversion 3. Implantable Cardio-verter-Defibrillator (ICD)
47
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
-DC Cardioversion
48
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.
Implantable Cardioverter-Defribrillator (ICD)
49
Where is the ICD implanted?
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
What is the average P-R interval?
0.12-0.20 (120-200ms)
51
What are the average values for the following: 1. P-R Interval 2. QRS Complex 3. Q-T interval 4. Tachycardia 5. Bradycardia
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)

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