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
Q

P wave

A

Represents atrial depolarization

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26
Q

PR interval

A

atrial depolarization plus the normal AV nodal delay

27
Q

QRS complex represents

A

Represents ventricular depolarization

atrial repolarization is occurring simultaneously and the atrial T wave is hidden by the QRS complex

28
Q

ST segment

A

occurs after ventricular depolarization has ended and before repolarization has begun

tme for ECG silence

initial part is termed the J point

29
Q

T wave

A

represents ventricular repolarization

30
Q

Prolonged QTc interval can lead to…

A

Ventricular arrhythmia that can lead to sudden cardiac death

** occurs at > 0.5 sec = 500msec ***

31
Q

2 main mechanism of Arrhythmias

A
  • Abnormal impulse generation

- Abnormal impulse propagation

32
Q

Alterations in Sinus node automaticity

A

inc SA automaticity = sympatheitc

dec SA automaticity = parasympathetic

33
Q

Spontaneous Automaticity

A

Generated in latent pacemakers which generate electrical impulses at a rate that exceeds that of the SA nodes

34
Q

Ectopic Focus

A

Some stimulus that stimulates cardiac cells and cranks them up, passing SA node rate

35
Q

What influences spontaneous Automaticity?

A

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
Q

Causes of increased slope in phase 4 depolarization

A
Autonomic control = catecholamines
Digoxin
Metabolic
Ischemia (leading cause)
Hypokalemia
Hypercalcemia
Fiber stretch
37
Q

Two types of Triggered Automaticity

A

Two types

  • Early after-depolarization
  • Delayed after-depolarization
38
Q

Early after-depolarization = EAD

A

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
Q

Cause of Torsades de pointess

A

EAD

40
Q

Delayed after-depolarization = DAD

A

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
Q

Most common influence of automaticity

A

Altered impulse conduction

42
Q

Conduction block

A

occurs when a propagating impulse passes a region of the heart that is unexcitable

43
Q

Reentry

A

concept that involves indefinite propagation of the cardiac impulse and continued activation of previously refractory tissue

44
Q

3 requirements for reentry

A
  1. 2 pathways for impulse conduction
  2. area of unidirectional block in 1 of the pathways
  3. slow conduction in other pathway
45
Q

3 things that affect reentry

A
  1. Timing (conduction velocity)
  2. Refractorines (abs refract period)
  3. Changes in autonomic control
46
Q

Most common bypass pathway/tract

A

Bundle of Kent

Shorter PR interval and wide QRS complex

47
Q

Common causes of Arrhythmias

A
  1. Normal physiology
  2. Cardiac disorders (biggest category)
  3. Pulmonary disorders
  4. Disturbances of the autonomic system
  5. Electrolyte Abnormalities
  6. Medications
48
Q

two most common classifications for Arrhythmias

A

Origin & Rate

49
Q

Supraventricular Arrhythmias

A

Originate above bundle of His

characterized by abnormal P waves but normal QRS and QTc intervals

50
Q

Ventricular Arrhythmias

A

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
Q

Nodal and Junctional Arrhythmias

A

originate in AV nodal or junctional area typically as a result of less rate of impulse formation from SA node

52
Q

Heart block

A

characterized by a disruption of impulses through the AV node

1st, 2nd, 3rd degree block

53
Q

Bradyarrhythmias are

A

<60 bpm

Sinus Bradycardia
Heart block 1st-3rd degree

54
Q

Tachyarrhythmias are

A

> 100bpm

all the ones that aren’t < 60bpm

55
Q

Wenckebach

A

2nd degree AV block type I

Biggest cause = inferior wall MI

56
Q

Wolff-Parkinson-White Syndrome

A

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
Q

A-fib in WPW is deadly because it may go into….

A

V-fib

58
Q

WPW treatment

A
  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
Q

Which drugs do you avoid in WPW

A
  1. Beta-blockers
  2. non-DHP CCBs
  3. digoxin

they block AV node, can lead to deadly arrhythmia

60
Q

Ventricular Tachycardia

A

V-tach

Most common in HA, leads to V-fib and death

61
Q

Torsades de Pointes

A

Twisting of the points

Proceeded by QT prolongation
QTc interval is usually > 500 msec

62
Q

Torsades de Pointes causes (drugs)

A
  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
Q

Clinical Manifestations of Arrhythmias

A
  1. Asymptomatic
  2. Palpitations = heart pounding
  3. SOB
  4. Fatigue
  5. Lightheadedness
  6. Anxiety
  7. Chest pain
  8. Fainting
64
Q

Complications of Arrythmias

A
  1. Tachycardia-induced cardiomyopathy and HF
  2. Valvular Heart disease
  3. Cardioembolic embolism
  4. cardiac arrest n death