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Physiology Cardio > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Atrial fibrillation

A

Most common arrhythmia

Risk increase with age, hypertension, CHF, and previous afib

Dilated atrium is more likely to afib

Characteristics:

  • narrow ORS
  • no clear P waves
  • irregularly irregular rhythm, R-R peaks are not the same length consistently
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2
Q

3rd degree AVN conduction block

A

Complete uncoupling of atrial and ventricular rhythms

P-P interval is shorter than the R-R interval

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3
Q

Premature ventricular complex

A

Irregular rhythm

No P waves

No measurable PR interval

Wide QRS complex with large amplitude

INVERTED T-WAVE - meaning that the ventricular repolarization follows in same direction as ventricular depolarization, rather the opposite like its supposed to

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4
Q

Ventricular tachycardia (monomorphic)

A

Wide QRS

Fast rate (100-250bpm)

No p wave

No measurable PR interval

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5
Q

Ventricular tachycardia (polymorphic, Torsade de Pointes)

A

Irregularly irregular rhythym

Fast rate (200-250bpm)

No p wave

No measurable PR interval

Wide QRS

Appearance of neighboring complexes differ

Can be drug induced

(Looks like a bunch of squiggle lines with the amplitude close to a QRS complex)

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6
Q

Sinus tachycardia

A

P-wave is present

Just has a fast heart rate (>100)

Everything else is normal

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7
Q

Ventricular fibrillation

A

Irregularly irregular

No measurable p wave, PR interval, or QRS

Squiggle lines with amplitude of a P-wave

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8
Q

Atrial flutter

A

Flutter waves look like P-waves but at very high rates in between QRS complexes

See several flutter waves —> QRS —> more flutter —> QRS …

More common in neonates

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9
Q

There are P-waves…but not every P-wave corresponds to a QRS complex

What are the possible arrhymthmias?

A

(Is the PR interval changing?)

YES = 2nd degree AV block (Mobitz Type 1)

NO = 2nd degree AV block (Mobitz Type 2)

P-waves and R waves are completely out of sync = 3rd degree AV block = uncoupled atrial and ventricular rhythym

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10
Q

There is a P-wave AND every P-wave corresponds to a QRS

Possible arryhthymias?

A

Is the heart rate normal?

YES = possible 1st degree AV block (if abnormally long PR interval)

NO = (Is it too fast or too slow?)
—> too fast = sinus tachy
—> too slow = sinus brady

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11
Q

No P-waves

Normal QRS complex

What arrhythmia(s)?

A

Atrial flutter (if several successive flutter waves between QRS complexes)

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12
Q

No p-waves

Wids QRS complex

Possible arrhythmias?

A

Is the T-wave inverted?

YES (but can’t see it) = monomorphic ventricular tachycardia

YES = premature ventricular complex (PVC)

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13
Q

No p-waves

Narrow QRS

Possible arrhythmias?

A

Is the wave pattern irregularly irregular?

YES = afib

NO = possibly paroxysmal supraventricular tachycardia (PVST) = pwaves maby be absent or inverted from AVN retrograde conduction

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14
Q

No p-waves

Twisting QRS complex

Possible arrhythmias

A

Multifocal ventricular tachycardia

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15
Q

No p-waves or QRS

Possible arrhythmias?

A

Are there undulations?

NO = asystole

YES = ventricular fibrillation (undulation baseline with no consistent pattern of waves or complexes)

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16
Q

The two main mechanisms of arrhythmias?

A
  1. Issue with conductance

2. Impulse formation issue (automaticity)

17
Q

The 3 types of conductance problems

A
  1. Membrane depolarization
  2. Reentry
  3. Conduction block

All three can lead to one another or occur at the same time

18
Q

The 3 types of automaticity issues

A
  1. Early after depolarizations (EADs)
  2. Ectopic automaticity
  3. Delayed after-depolarizations (DADs)

These are not linked like the conduction issues

19
Q

Conductance problem: membrane depolarization from myocardial ischemia

A

Lack of O2 and glucose —> fall in ATP…effects the tissue in 3 ways

  1. Fall in intracellular pH
    - due to switch to anaerobic glycolysis and build up of lactic acid
    - inhibits gap junctions between myocytes —> slows down conduction
  2. ATP-mediated K+ channels are no longer inhibited
    - normally blocked by ATP intracellularly
    - increase in K permeability
    - will lead to huge outflux of K+
    - E-k will now be closer to zero (less-negative)…therefore so will the resting membrane potential
  3. Na/K ATPase pump no longer functional
    - without ATP, the Na/K pump will not be able to reestablish the normal concentration

**all of the these changes will lead to HYPERKALEMIA —> RMP now more depolarized

—> inactivates more Na cahnnels, leading to slower or blocked conduction

20
Q

Effect of hyperkalemia to AP conduction

A

Slows them down

RMP will be more depolarized, since E-k will become less-negative

When this happens, more Na channels are inactivated…thus slowing down conduction

21
Q

Conductance problem: Re-entry

A

Reentry involves a repetitive circular pattern of excitation…requires the 3 following things to occur

  1. Presence of more than one parallel conduction pathway…
    —> meaning the excitation can flow along more than one route…if one route is blocked, excitation flowing down the others can come back around to flow along the original route in reverse direction
  2. One pathway must have a unidirectional conduction block
    —> one of the routes through which the excitation can flow is blocked in one direction…excitation from the other routes can come back around and flow in a retrograde direction along the blocked route
  3. Conduction time around the circuit must be longer than the ERP of any cells within the circuit…
    —> usually means the conduction is abnormally slow
    —> the cells must be able to be activate when teh excitation comes around, or the circuit will be stoped when teh signal reaches cells in their refractory period

Re-entry can be a result of conduction disturbances (myocardial ischemia) or dispersion of refreatoriness

22
Q

What is the normal mechanism of conduction when re-entry is not happening?

A

In normal sinus rhythm..

SAN —> AVN —> daughter branches —> muscles —> spread everywhere it can —> until runs into other routes of the signal —> stopped by other cells in ERPs —> one contraction takes place

23
Q

What events would lead to re-entry?

A
  1. An unidirectional block can occure from an atherosclerotic plaque in a coronary artery
    - blood flow will stop in the subendocardial region of the heart
    - closer to the endocardial surface, will be somewhat ischemic - slows conduction

The other branch of conduction can go through the partially ischemic zones in a salutatory manner and summate, slowly conducting back up into the normal tissue, and forming a reentrant circuit

24
Q

What disease states does reentry occur

A

Dilated cardiomyopathy

Myocardial infarction

Acute atrial dilation with heart failure

Exposure to ion channel blockers that produce unequal effects in different cells

25
Q

Arrhythmias caused by re-entry

A
  1. premature ventricular contrations (or atrial)
  2. Sustained atrial or ventricular tachycardia - caused by a sustained reentrant circuit
  3. Afib or vent-fib = can be the result of many reentrant circuits, causing loss of synchronization of stimulation
  4. Atrial flutter = one large reentrant loop around the right atrium, moving clockwise or counter-clock wise
26
Q

Conductance problem: conductance block

Types?

A
  1. His bundle conduction block
  2. R or L bundle block
  3. AV conduction block
27
Q

His bundle block

A

Atrial-ventricular uncoupling —> results in bradycardia if distal purkinje fibers starts to pace the ventricle

Can lead to asystole

28
Q

Right or left bundle block

A

Asynchronization —> loss of synced contraction leading to reduction of CO

29
Q

AV conduction block (all types)

A
  1. 1st degree = prolonged PR interval, with a QRS complex after it like normal
  2. 2nd degree
    - Mobitz Type 1 = progressive lengthening of the PR interval until the QRS complex drops out…repeat this (like EDM music)
    - Type 2 = PR interval is fixed and there is a periodic drop out of QRS without preceding changes to PR
  3. 3rd degree = no AV impulse conduction, p-waves are totally out of sync with QRS, p-waves are cycling at a different cycle length than the QRS
30
Q

Automaticity problem: ectopic pacemaker

A

If cardiac arrhythmias develop as a result of increased automaticity in a site outside the SAN (or decreased)…

An ectopic pacemaker can establish an abnormal heart rate or rhythm

= enhanced depolarization of phase 4 outside the SAN

31
Q

What can cause ectopic pacemakers

A
  1. Hypokalemia…can result of diuretics taken for congestive heart failure
    —> leads to decreased K+ conductance in purkinje fibers
    —> leads to a steeper slope of phase 4 depolarization
    (Does not affect SAN, because purkinjes are way more sensitive to K+)
  2. Localized sensitivity to catecholamines after ischemia
    —> MIs can lead to a disruption in sympathetic innervation or an area of the endcardium —> increased sensitivity as a result of denervation —> cells increase expression of beta1-receptors and/or decrease in catecholamine reuptake —> sympathetic stimulation enhanced
  3. Myocardial stretch —> stretched due to abnormal wall motion —> activates stretch-activated channels —> increases automaticity
32
Q

Automaticity problem: EADs

A

Phase 3 event

Slowed repolarization rate leads to extra depolarizations before the repolarization finishes

Can be caused by:
- drugs that block repolarization currents
—> K channel blockers, quinidine, sotalol, ibutilide, erthyromycin
- congenital ion channel mutations

Worsened by brady, hypokalemia, and low Mg

33
Q

Automaticity problem: DADs

A

phase 4 event

Extra AP develops

Ca2+ released by the SER spontaneously —> excess Ca influx —> Na/Ca exchange will occur during diastole —> Na/Ca depolarizing current produced —> extra beats can occur

Involves intracellular Ca2+ overload
- due to drug digoxin, catecholamine excess, or cardiomyopathy

Worsened by tachycadia

Physiology Cardio (11 decks)

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