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NSCC 7150 > Ventricular Rhythms > Flashcards

Ventricular Rhythms Flashcards

1
Q

when do fast ventricular rhythms occur?

A

when an irritable focus/multiple foci in the ventricles take over the pacing of the heart from intrinsic pacemaker sites

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2
Q

when do slow ventricular rhythms occur?

A

when the SA node or AV junction pacemaker sites fail, or their impulses are completely blocked from entering the ventricles, prompting the pacemaker site in the Purkinje fibres to assume the pacemaker role

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3
Q

where do PVCs originate from?

A

an irritable focus within the ventricles that fired prematurely, resulting in an ectopic or abnormal beat

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4
Q

what are the types of PVCs?

A

1) unifocal: aka monomorphic PVCs, look like each other as they arise from the same irritable focus

2) multifocal PVCs: aka polymorphic PVCs, look different from each other as they originate from different irritable foci; more ominous, indicate ventricular irritability

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5
Q

what are PVCs?

A

premature or early beats; are events within an underlying rhythm

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6
Q

are there P waves in a PVC?

A

there is no P wave preceding the QRS because the impulse originates in the ventricle; atria are not depolarized

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7
Q

what does the QRS complex look like in a PVC?

A

wide and bizarre, >0.12 sec as electrical impulse travels through ventricular muscle tissue, resulting in a longer depolarization

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8
Q

are ST segment and T waves normal in PVCs?

A

no; ST segments are often elevated or depressed in PVCs, but result from abnormal depolarization/repolarization as opposed to issues with poor coronary artery O2 supply

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9
Q

ventricular bigeminy

A

When every second beat is a PVC

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10
Q

ventricular trigeminy

A

When every third beat is a PVC

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11
Q

ventricular quadrigeminy

A

When every fourth beat is a PVC

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12
Q

couplet

A

two PVCs occurring together

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13
Q

triplet

A

three PVCs occurring together

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14
Q

run or salvo

A

more than three PVCs occurring together

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15
Q

what BP reading is typical with a PVC?

A

a lower BP because the PVC is ectopic and does not produce well-perfused heartbeats

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16
Q

characteristics of PVC in NSR
- rate
- rhythm
- P wave
- PRI
- QRS complex

A

Rate: usually normal but may depend on underlying rhythm

Rhythm: usually regular but PVC may make it look irregular

P Wave: positive, upright, one P before each QRS except for PVCs

PRI: 0.12-0.20 sec, absent for the PVCs

QRS Complex: 0.10 sec or less in underlying rhythm, appears wide and bizarre for the PVCs

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17
Q

conduction problem for PVC

A

site of impulse formation is the SA node and the ventricle tissue. Occasional PVCs are not a problem. More frequent PVCs can be a precursor for ventricular tachycardia becoming a significant problem

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18
Q

causes of PVC

A

Hypoxia, stress, electrolyte imbalances, digoxin toxicity, MI, CHF

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19
Q

implications to O2 supply and demand for PVC

A
  • if frequent, CO is affected and patients may show signs such as hypotension, SOB, chest pain, and decrease in LOC
  • frequent PVCs may be precursors to lethal arrhythmias such as ventricular tachycardia or ventricular fibrillation
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20
Q

intervention for PVCs

A
  • if pt not symptomatic, monitor
  • if pt is symptomatic, determine and treat the cause
  • check lytes
21
Q

ventricular tachycardia

A
  • 3 or more ventricular ectopics in a row resulting from a rapid discharge of an abnormal ventricular focus or foci
  • rate is > 100/min and < 250/min
  • rhythm is often very regular but can be slightly irregular
22
Q

how does depolarization work in v-tach?

A

atria usually continue to be depolarized but independent of the ventricles

23
Q

can you see P waves in v tach?

A

typically no because they are buried in the bizarre-looking QRS complexes; even if visible, there is no relationship between them and the QRS complexes (are dissociated from ventricular activity)

24
Q

what do QRS complexes look like in v tach?

A

wide and bizarre because depolarization is longer

25
Q

how can you measure the width of VT when J point is not always visible?

A

look for a slight change in direction as the R wave transitions to the S wave when examining the QRS complex. This is where you would measure the QRS width

26
Q

O2 supply and demand implications for VTach

A
  • increased HR = increased myocardial/O2 demand
  • decreased VFT = decreased preload + stroke volume = decreased CO
  • decreased CPT = decreased contractility
  • decrease or loss of atrial kick d/t dissociation or desynch between atria and ventricles
27
Q

characteristics of VTach
- rate
- rhythm
- P Wave
- PRI
- QRS complex
- conduction problem

A
  • rate: 100-250bpm but can be higher
  • rhythm: usually regular
  • P wave: difficult to identify, if present is hidden by QRS
  • PRI: n/a if no P wave
  • QRS complex: >0.12sec, wide and bizarre
  • Conduction problem: site of impulse formation is ventricular tissue
28
Q

causes of Vtach

A

heart disease (ischemic or valvular) = biggest culprit. hypoxemia, dig tox, lyte imbalances, acid base disturbances

29
Q

interventions for VTach

A

1) check if pt has a pulse or no pulse
2) if pulse = is there hemodynamic compromise? if yes, cardiovert.
3) if no pulse = call code, CPR, early defibrillation
3) refer to ACLS guideline

30
Q

ventricular fibrillation

A
  • lethal arrhythmia
  • heart’s electrical activity is chaotic, irregular, and disorganized
  • ventricles quiver rather than contracting in an organized manner, and therefore there is no effective cardiac output and no pulse
31
Q

O2 supply and demand implications for vfib

A

there is no organized depolarization of the ventricles and therefore no CO. It is an emergency situation.

32
Q

characteristics of vfib

A

unable to determine rate, rhythm is chaotic, no p wave/PRI/QRS. site of impulse formation is ventricular tissue.

33
Q

causes of vfib

A

MI = main cause.
dig tox, lyte imbalances, and acid base imbalances

34
Q

intervention for vfib

A

no pulse - call a code, begin CPR, insert IV, provide O2, intubate. early defibrillation. anticipate drugs such as epinephrine.

35
Q

which tachycardias are narrow complex tachys (<0.10sec)?

A
  • RST
  • atrial tachycardia
  • uncontrolled a-flutter
  • uncontrolled afib
  • junctional tachycardia
36
Q

which tachycardia is a wide complex tachycardia (>0.12sec)?

A

ventricular tachycardia

37
Q

why do impulses arising from above ventricles depolarize faster?

A

travel the normal pathway of conduction after they leave atrial tissue and use bundle branches

38
Q

summary of using ACLS algorithm

A

1) pulse or no pulse?
2a) pulse = hemodynamic compromise? then cardiovert
2b) pulse = stable? use drugs to convert/slow down rhythm. if doesn’t work or unstable again, cardiovert
3) no pulse? call a code.

39
Q

what drugs are commonly used in vtach?

A

adenosine, amiodarone

40
Q

what drugs are commonly used in narrow QRS tachys?

A

adenosine, amiodarone, calcium channel blockers, beta blockers

41
Q

ventricular escape rhythm

A
  • aka idioventricular rhythm
  • occurs when the SA node and AV junction fail as pacemaker sites and the Purkinje fibres take over
  • last line of defense that prevents the heart from extreme slowing or going asystolic
42
Q

what is the intrinsic rate of VER?

A

20-40bpm

43
Q

what are the QRS complexes like in VER?

A

wide and bizarre

44
Q

what are ST segments like in VER?

A

they are always abnormal but it is a result of abnormal depolarization and may not be clinically significant

45
Q

O2 supply and demand implications of VER

A
  • slow ventricular rate = decreased CO
  • loss of atrial kick due to non-depolarization of atria = decreased preload and decreased CO
46
Q

characteristics of VER
- rate
- rhythm
- P wave
- PRI
- QRS complex
- conduction problem

A
  • rate: 20-40bpm
  • rhythm: regular
  • P wave: n/a
  • PRI: n/a
  • QRS complex: >0.12 sec, wide and bizarre
  • conduction problem: site of impulse formation is ventricular tissue
47
Q

cause of VER

A
  • occurs when a higher pacemaker site has failed
  • body’s last resort to maintain some CO
  • MI, dig toxicity, electrolyte and acid base imbalances
48
Q

intervention for VER

A
  • assess pt (ABCs)
  • atropine and external pacemaker
49
Q

accelerated idioventricular rhythm - what is it and characteristics?

A

when the intrinsic rate of VER is increased above 40 bpm; usually rate is 40-100bpm. has same characteristics as VER

NSCC 7150 (10 decks)

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