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CDM 2 Exam 1 > Lecture 7 - Arrhythmias 1 > Flashcards

Lecture 7 - Arrhythmias 1 Flashcards

1
Q

Sinoatrial (SA) or Sinus Node

A

dominant center of automaticity (dominant pacemaker) which initiates cardiac electronic impulse

generate sinus rhythm

paces heart at resting Tate of 60-100 bpm

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2
Q

Intranodal pathways

A

3 pathways going into right atrium

Bachmann’s bundle will connect right to left atrium

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3
Q

Atrioventricular (AV) node

A

known as junction box, delays SA node signal

area of specialized tissue that conducts normal electrical impulse from atria to the ventricles

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4
Q

Bundle of His

A

Transmits electrical impulses form the AV node to the point of the apex of the fascicular branches (bundles of specialized muscle fibers)

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5
Q

Bundle of His + AV Node =

A

AV Junction

between the Atria and ventricles lies a fibrous AV ring that will not permit electrical stimulation - hole in this can cause arrhythmia

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6
Q

K+ conc is….

A

higher inside cell

has greater effect on membrane potential because its more permeable

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7
Q

Na+ conc is….

A

higher outside cell

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8
Q

Nodal tissue action potential…..

A

slow, Ca2+ dependent

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9
Q

Rhythmic tissue action potential…..

A

Fast, Na+ dependent

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10
Q

5 phase of action potential of ventricular system

A

Phase 0 = Rapid depolarization, Na rushes in

Overshoot potential = results in brief initial repolarization or phase 1

Phase 1 = Partial repolarization, related to K+ efflux

Phase 2 = Plateau phase, increased influx of Ca2+, low efflux of K+

Phase 3 = Rapid depolarization, large K+ efflux, reduction of Ca2+/Na+ influx

Phase 4 = Resting membrane potential (-80/90)

Threshold potenital = juncture of phase 4-0, where rapid Na+ influx is initiated

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11
Q

Properties of Electrical Conduction System

A 
Excitability
Conductivity 
Contractility
Automaticity
Lusitropy
Autonomic nervous system control
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12
Q

Excitability

A

ability of cardiac tissue to respond to adequate stimuli by generating an action potential followed by a mechanical contraction

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13
Q

Bathmotropy

A

The influencing of the excitability of cardiac muscle

can be + or -

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14
Q

Factors affecting Excitability

A

RMP lvl
Threshold lvl
Behavior of Na+ channel
Refractory periods

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15
Q

Absolute refractory period

A

interval of AP during which no stimulus, regardless of its strength, can induce another impulse

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16
Q

Relative refractory period

A

interval of AP during which an impulse of significant magnitude may be elicited

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17
Q

Supranormal Period

A

Period at end of the action potential were an impulse can be generated by weaker than normal stimuli

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18
Q

Conductivity

A

Property of the cardiac muscle that allows the impulse to travel along tissue

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19
Q

Dromotropy

A

The influencing of the conductivity of cardiac muscle

inc conduct = +
dec conduct = -

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20
Q

Contractility

A

capacity of shortening in reaction to an appropriate membrane depolarization

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21
Q

Inotropy

A

The influencing of contractility

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22
Q

Automaticity

A

Ability of cardiac muscle to spontaneously depolarize in a regular constant manner

normally started by SA node

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23
Q

Chronotropy

A

Influencing of automaticity

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24
Q

Overdrive suppression basic idea

A

every tissue in heart has an inherent pacemaker

if SA node stops, another tissue will control HR

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25
P wave
Represents atrial depolarization
26
PR interval
atrial depolarization plus the normal AV nodal delay
27
QRS complex represents
Represents ventricular depolarization atrial repolarization is occurring simultaneously and the atrial T wave is hidden by the QRS complex
28
ST segment
occurs after ventricular depolarization has ended and before repolarization has begun tme for ECG silence initial part is termed the J point
29
T wave
represents ventricular repolarization
30
Prolonged QTc interval can lead to...
Ventricular arrhythmia that can lead to sudden cardiac death ** occurs at > 0.5 sec = 500msec ***
31
2 main mechanism of Arrhythmias
- Abnormal impulse generation | - Abnormal impulse propagation
32
Alterations in Sinus node automaticity
inc SA automaticity = sympatheitc dec SA automaticity = parasympathetic
33
Spontaneous Automaticity
Generated in latent pacemakers which generate electrical impulses at a rate that exceeds that of the SA nodes
34
Ectopic Focus
Some stimulus that stimulates cardiac cells and cranks them up, passing SA node rate
35
What influences spontaneous Automaticity?
increased slope of phase 4 depolarization that causes a heightened automaticity of tissues and competition with the SA node for dominance of cardiac rhythm
36
Causes of increased slope in phase 4 depolarization
``` Autonomic control = catecholamines Digoxin Metabolic Ischemia (leading cause) Hypokalemia Hypercalcemia Fiber stretch ```
37
Two types of Triggered Automaticity
Two types - Early after-depolarization - Delayed after-depolarization
38
Early after-depolarization = EAD
transient membrane depolarization that occurs during repolarization (phase 3) maybe precipitated by hypokalemia, antiarrhythmics, or slow stimulation rates ** implicated as cause of Torsades de pointes **
39
Cause of Torsades de pointess
EAD
40
Delayed after-depolarization = DAD
transient membrane depolarization that occurs after repolarization but prior to phase 4 of action potential maybe precipitated by digoxin** toxicity or excess catecholamine release
41
Most common influence of automaticity
Altered impulse conduction
42
Conduction block
occurs when a propagating impulse passes a region of the heart that is unexcitable
43
Reentry
concept that involves indefinite propagation of the cardiac impulse and continued activation of previously refractory tissue
44
3 requirements for reentry
1. 2 pathways for impulse conduction 2. area of unidirectional block in 1 of the pathways 3. slow conduction in other pathway
45
3 things that affect reentry
1. Timing (conduction velocity) 2. Refractorines (abs refract period) 3. Changes in autonomic control
46
Most common bypass pathway/tract
Bundle of Kent Shorter PR interval and wide QRS complex
47
Common causes of Arrhythmias
1. Normal physiology 2. Cardiac disorders (biggest category) 3. Pulmonary disorders 4. Disturbances of the autonomic system 5. Electrolyte Abnormalities 6. Medications
48
two most common classifications for Arrhythmias
Origin & Rate
49
Supraventricular Arrhythmias
Originate above bundle of His characterized by abnormal P waves but normal QRS and QTc intervals
50
Ventricular Arrhythmias
Originate below the bundle of His characterized by abnormal QRS and QTc interval but normal P waves ** Most serious arrhythmias ** V-fib = incompatible with life
51
Nodal and Junctional Arrhythmias
originate in AV nodal or junctional area typically as a result of less rate of impulse formation from SA node
52
Heart block
characterized by a disruption of impulses through the AV node 1st, 2nd, 3rd degree block
53
Bradyarrhythmias are
<60 bpm Sinus Bradycardia Heart block 1st-3rd degree
54
Tachyarrhythmias are
> 100bpm all the ones that aren't < 60bpm
55
Wenckebach
2nd degree AV block type I Biggest cause = inferior wall MI
56
Wolff-Parkinson-White Syndrome
Preexcitation syndrome AV conduction occurs through the bypass tract known as "the bundle of Kent", resulting in earlier activation "pre excitation" of the ventricles than if the impulse had traveled through the AV node
57
A-fib in WPW is deadly because it may go into....
V-fib
58
WPW treatment
1. slow conduction through the accessory pathway, NOT the AV node (usually req ablation or cardioversion) 2. if AV node is blocked unopposed in pts with WPW, rate of transmission through accessory pathway is increased potentially leading to V-fib
59
Which drugs do you avoid in WPW
1. Beta-blockers 2. non-DHP CCBs 3. digoxin they block AV node, can lead to deadly arrhythmia
60
Ventricular Tachycardia
V-tach Most common in HA, leads to V-fib and death
61
Torsades de Pointes
Twisting of the points Proceeded by QT prolongation QTc interval is usually > 500 msec
62
Torsades de Pointes causes (drugs)
1. Antiarrhythmics (Class IA,IC, III - amiodarone OK) 2. Typical antipsychotic (Haloperidol) 3. Atypical antipsychotics (ziprasidone) 4. Azole antifungals 5. Macrolide antibiotics 6. Methadone 7. Quinolones (moxifloxacin) 8. TCA 9. Chloroquine 10. Pentamidine 11. Ranolazine
63
Clinical Manifestations of Arrhythmias
1. Asymptomatic 2. Palpitations = heart pounding 3. SOB 4. Fatigue 5. Lightheadedness 6. Anxiety 7. Chest pain 8. Fainting
64
Complications of Arrythmias
1. Tachycardia-induced cardiomyopathy and HF 2. Valvular Heart disease 3. Cardioembolic embolism 4. cardiac arrest n death

CDM 2 Exam 1 (12 decks)

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