Bradyarrythmias Flashcards

1
Q

Why is the sinoatrial node the natural pacemaker of the heart?

A

Sino-atrial node has most # slow Na+ channels, fastest spontaneous rate = natural pacemaker

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2
Q

What antagonizes phase 4 current?

A

Na+/K+ ATPase pump always tries to keep cell voltage –ve = antagonizes Phase 4 depolarization from slow Na+ current

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3
Q

Where does the overdrive suppression occur and why?

A

a higher pacemaker forces a latent pacemaker to fire faster than its native rate

- ->  excess Na+ enters cell 
- -> ‘revs up’ Na+/K+ ATPase 
- -> slows Phase 4 even more

= OVERDRIVE suppression of latent pacemakers

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4
Q

What increases firing rate of SA node?

A

sympathetic nervous input (‘fight or flight’)
Catecholamines in blood (adrenaline)
–> opens more Phase 4 channels, ↑ slope.
–> Also the threshold is lowered

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5
Q

What decreases the SA node rate?

A

para-sympathetic nervous input (‘relax & rest’ system)
e.g. vagal maneuvers
closes more Phase 4 channels, decreased slope
–> increased threshold voltage
More negative at beginning of diastole

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6
Q

What are drugs that decrease SA node rate?

A

Drugs that decrease Sino-Atrial = decrease Heart Rate
beta-blockers
Cholinergics
some Ca++ channel blockers

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7
Q

What are drugs that increase SA node rate?

A

Drugs that increase Sino-Atrial = increase Heart Rate
Catecholamines (especially -agonists)
Anti-cholinergics (e.g. Atropine)
?theobromides (e.g. caffeine excess)

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8
Q

What is sinus brachycardia?

A

by definition, Sinus rhythm < 60 beats */ min

Clinically, don’t worry about bradycardia unless <50 for most patients

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9
Q

What causes bradycardia?

A

high para-sympathetic / vagal tone:

  • physiological (e.g. fit athlete  slow resting HR)
  • central nervous system autonomic imbalance
  • nausea or other reflexes (e.g. carotid body massage)
  • drugs (see previous list)
  • age-related degeneration of SA node = Sick Sinus Syndrome
  • damage to SA node (e.g. at time of surgery, or infarct)
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10
Q

What is sick sinus syndrome?

A

common age-related degeneration of SA node, usually related to fibrosis

inappropriate sinus bradycardia, and / or inability to appropriately raise HR (e.g. exercise)

often associated with sudden tachycardias arising from chaotic atrial rhythms  ‘tachy – brady syndrome’

can be episodic, unpredictably cause too slow HR  patient (nearly) faints (often post-tachy)

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11
Q

Why might fast non-sinus atrial rhythms occur more in sick sinus patients (tachy-brady syndrome)?

A

If sinus node fails –> other latent atrial pacemakers activated, and if several activated at nearly same time –> chaotic atrial rhythms –> tachycardia

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12
Q

Why might the sinus take several seconds to start firing after such a tachycardia  patient faints?

A

Sinus node already ‘sluggish’ and is overdrive suppressed by preceding tachycardia

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13
Q

What are escape rhythms?

A

if sinus node stops firing / fires too slowly, other latent pacemakers can take over = escape rhythms

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14
Q

Which types of AV node blocks actually cause bradycardia?

A

only 2nd and 3rd cause actual bradycardia

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15
Q

What is a first degree AV node block?

A

1st degree = 1° = every P wave conducts, but >200ms delay between start P & QRS

–> >200ms, >5mm delay from start PQRS

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16
Q

What is a secondary degree AV node block?

A

2nd degree = 2° = only a proportion of P waves conducted by AV node (2 types)

17
Q

What is a third degree AV node block?

A

3rd degree = 3 ° = NO P waves conducted –> need escape rhythm @ or below AVN

18
Q

What makes up the PR internal?

A

Time from atrial activation to ventricular activation. 0.120 sec (3 small boxes) to 0.200 sec (5 small boxes):

  • Conduction time from SA node to AV node
  • AV node conduction time
  • Conduction time from AV node to first ventricular activation.
19
Q

What causes a prolonged PR interval?

A
Increased vagal tone
AV node ischemia
B-blockers and some calcium channel blockers
--> Depress conduction through AV node
Chronic degenerative changes (fibrosis)
Infarct
20
Q

What are the two types of secondary AV node blocks?

A

Mobitz I = ‘Wenckebach

Mobitz II:

21
Q

What is Mobitz II?

A

no preceding PR prolongation, sudden blocked P (ie. the P doesn’t lead to QRS complex)
often, fixed ratio of P’s conduct: 2:1, 3:1, 4:1 etc.
–> 2:1 means 2 p-waves for every 1 QRS

22
Q

What is Mobitz I = ‘Wenckebach?

A

P-waves conduct with progressive increase in PR

  • -> finally, AV blocks = non-conducted P, no QRS
  • -> After the non conducted P wave the next P-wave conducts with most normal PR
  • -> cycle repeats (eg. 2:1, 3:2, 4:3, 5:4 … P: QRS)
23
Q

What is the hallmark of Wenckenbach?

A

Grouped beating

24
Q

T or F: Wenckenbach is unhealthy

A
F:
Benign and seen in:
Trained athletes
Children
Sleeping
Vagal tone
Temporarily seen in ischemia to AV node
25
Q

What causes Wenckebach?

A

can be sign of high vagal /parasympathetic tone (e.g. athletes)
can be consequence of myocardial infarct

26
Q

When is Wenckebach concerning?

A

generally doesn’t cause major problems, unless already slow P-wave rate, or if 2:1 conduction

27
Q

What is treatment for Wenckebach?

A

generally responds to anti-cholinergic drug

28
Q

T or F: Mobitz II is more than dangerous than I

A

T:

more dangerous than Mobitz I, especially if high P:QRS ratios, easily –> complete 3° AV block

29
Q

What usually causes Mobitz II?

A

Usually due to conduction disturbance below the AV node

often seen with infarcts or age-related degeneration of the His-Purkinje system.

30
Q

What is treatment of Mobitz II?

A

Treatment is usually required with a pacemaker

31
Q

What is a tertiary AV node block?

A
  • totally dissociated P-waves / QRS’s, therefore no relationship between atrium and ventricle
  • regular P-P and R-R, but no relation
  • need escape rhythm beneath AV node
  • can cause fainting or even death
  • age-related degeneration, or infarcts
32
Q

How is a pacemaker wired?

A

wire threaded into vein  R.atrium  R.Ventricle

33
Q

What is indicated for a pacemaker?

A

if major bradycardia, no easily reversible cause, need electronic pacemaker