Cardiac Arrhythmias Flashcards

1
Q

What are the 3 requirements for re-entry of excitation?

A

1) Conduction loop geometry
2) Slow or delayed conduction
3) Unidirectional conduction block

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2
Q

How might an increase in vagal nerve activity affect EKG recordings?

A

Vagus n. has direct effects on SA, AV, and atrial nodal tissues only. Thus, it may inhibit SA node pacemaker activity, thereby slowing HR, or it may slow AV node conduction and lengthen P-R interval.

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3
Q

What are 3 major mechanisms by which dysrhythmias occur?

A

1) Altered automaticity (enhanced or depressed pacemaker activity)
2) Reentry of excitation
3) Triggered activity

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4
Q

Cardiac arrhythmias result from disturbances in _____ or ______ or both.

A

impulse formation; impulse conduction

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5
Q

What are the definitions of tachycardia and bradycardia in terms of heart rate?

A
  • tachy: greater than 100 bpm

- brady: less than 60 bpm

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6
Q

Alterations in pacemaker rate that are mediated through changes in pacemaker mechanisms that normally exist in pacemaker cells.

A

altered automaticity

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7
Q

What are some possible causes of tachy-dysrhythmias?

A
  • NE
  • stimulants (amphetamines)
  • stretching (ventricular aneurysm)
  • electrolytes (hypokalemia)
  • sick sinus syndrome, fever, and hypothyroidism
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8
Q

What are some possible causes of brady-dysrhythmias?

A
  • drugs (anti-arrhythmics, beta blockers, calcium antagonists, digitalis, barbiturates, anesthetics)
  • ischemia or infarct
  • sick sinus syndrome
  • aging (fibrosis)
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9
Q

True or false: re-entry of excitation can occur anywhere in the heart

A

true!

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10
Q

What are possible causes of re-entry of excitation?

A
  • ischemia
  • infarction
  • congenital bypass tracts (ex: WPW syndrome)
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11
Q

Where can triggered activity occur?

A

in atrial or ventricular tissues

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12
Q

Delayed After-Depolarization (DAD) is due to _______.

A

abnormally elevated intracellular [Ca2+]

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13
Q

DADs are clinically documented with dysrhythmias resulting from ______.

A

digitalis toxicity

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14
Q

What are the two types of triggered activity that we discussed in class?

A
  • Delayed After-Depolarization (DAD)

- Early After-Depolarization (EAD)

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15
Q

Are delayed after-depolarizations worse at high or low heart rates?

A

they’re worse at higher heart rates (more opportunities for Ca2+ to build up and cause one)

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16
Q

Are early after-depolarizations worse at high or low heart rates?

A

low heart rates, as slow HR lengthens AP (and EADs are related to prolongation of AP duration)

17
Q

During which phase do DADs occur vs. EADs?

A

DADs- phase 4 (complete repolarization)

EADs- phase 2 or 3 (peak of AP and slow repolarization)

18
Q

What are some of the anti-arrhythmic therapies we discussed?

A
  • drugs (Na+ channel blockers, K+ channel blockers, Ca2+ channel blockers, beta blockers)
  • radio-frequency ablation (abnormal tissue “zapped” using heat)
  • DC cardioversion (abnormal rhythm converted to normal rhythm using electricity)
  • implantable cardio-verter defibrillator (ICD)
19
Q

What is essentially happening with brady-dysrhythmias?

A

the heart beats so slowly that other pacemakers become more relevant