Ventricular Rhythms Flashcards
when do fast ventricular rhythms occur?
when an irritable focus/multiple foci in the ventricles take over the pacing of the heart from intrinsic pacemaker sites
when do slow ventricular rhythms occur?
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
where do PVCs originate from?
an irritable focus within the ventricles that fired prematurely, resulting in an ectopic or abnormal beat
what are the types of PVCs?
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
what are PVCs?
premature or early beats; are events within an underlying rhythm
are there P waves in a PVC?
there is no P wave preceding the QRS because the impulse originates in the ventricle; atria are not depolarized
what does the QRS complex look like in a PVC?
wide and bizarre, >0.12 sec as electrical impulse travels through ventricular muscle tissue, resulting in a longer depolarization
are ST segment and T waves normal in PVCs?
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
ventricular bigeminy
When every second beat is a PVC
ventricular trigeminy
When every third beat is a PVC
ventricular quadrigeminy
When every fourth beat is a PVC
couplet
two PVCs occurring together
triplet
three PVCs occurring together
run or salvo
more than three PVCs occurring together
what BP reading is typical with a PVC?
a lower BP because the PVC is ectopic and does not produce well-perfused heartbeats
characteristics of PVC in NSR
- rate
- rhythm
- P wave
- PRI
- QRS complex
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
conduction problem for PVC
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
causes of PVC
Hypoxia, stress, electrolyte imbalances, digoxin toxicity, MI, CHF
implications to O2 supply and demand for PVC
- 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
intervention for PVCs
- if pt not symptomatic, monitor
- if pt is symptomatic, determine and treat the cause
- check lytes
ventricular tachycardia
- 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
how does depolarization work in v-tach?
atria usually continue to be depolarized but independent of the ventricles
can you see P waves in v tach?
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)
what do QRS complexes look like in v tach?
wide and bizarre because depolarization is longer
how can you measure the width of VT when J point is not always visible?
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
O2 supply and demand implications for VTach
- 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
characteristics of VTach
- rate
- rhythm
- P Wave
- PRI
- QRS complex
- conduction problem
- 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
causes of Vtach
heart disease (ischemic or valvular) = biggest culprit. hypoxemia, dig tox, lyte imbalances, acid base disturbances
interventions for VTach
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
ventricular fibrillation
- 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
O2 supply and demand implications for vfib
there is no organized depolarization of the ventricles and therefore no CO. It is an emergency situation.
characteristics of vfib
unable to determine rate, rhythm is chaotic, no p wave/PRI/QRS. site of impulse formation is ventricular tissue.
causes of vfib
MI = main cause.
dig tox, lyte imbalances, and acid base imbalances
intervention for vfib
no pulse - call a code, begin CPR, insert IV, provide O2, intubate. early defibrillation. anticipate drugs such as epinephrine.
which tachycardias are narrow complex tachys (<0.10sec)?
- RST
- atrial tachycardia
- uncontrolled a-flutter
- uncontrolled afib
- junctional tachycardia
which tachycardia is a wide complex tachycardia (>0.12sec)?
ventricular tachycardia
why do impulses arising from above ventricles depolarize faster?
travel the normal pathway of conduction after they leave atrial tissue and use bundle branches
summary of using ACLS algorithm
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.
what drugs are commonly used in vtach?
adenosine, amiodarone
what drugs are commonly used in narrow QRS tachys?
adenosine, amiodarone, calcium channel blockers, beta blockers
ventricular escape rhythm
- 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
what is the intrinsic rate of VER?
20-40bpm
what are the QRS complexes like in VER?
wide and bizarre
what are ST segments like in VER?
they are always abnormal but it is a result of abnormal depolarization and may not be clinically significant
O2 supply and demand implications of VER
- slow ventricular rate = decreased CO
- loss of atrial kick due to non-depolarization of atria = decreased preload and decreased CO
characteristics of VER
- rate
- rhythm
- P wave
- PRI
- QRS complex
- conduction problem
- 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
cause of VER
- occurs when a higher pacemaker site has failed
- body’s last resort to maintain some CO
- MI, dig toxicity, electrolyte and acid base imbalances
intervention for VER
- assess pt (ABCs)
- atropine and external pacemaker
accelerated idioventricular rhythm - what is it and characteristics?
when the intrinsic rate of VER is increased above 40 bpm; usually rate is 40-100bpm. has same characteristics as VER
