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EKG > Dubin's week 2: pgs 93-190 > Flashcards

Dubin's week 2: pgs 93-190 Flashcards

1
Q

Arrythmia / dysrythmia

A

without rhythm

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2
Q

SA node dischrages regular pacing at ____ bpm that depolarize the ____

A

60 - 100bpm and depolarize the atria

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3
Q

Warnings of rhythm disturbance

A
  1. breaks in continuity / pause
  2. premature beats
  3. sudden / dramatic rate change
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4
Q

Sinus Arrythmia

A

ANS causes barely detectable changes relating to phases of respiration
-NOT pathological + functions in humans at all times
-normal variations in SA node pacing

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5
Q

Sympathetic stimulation of the SA node in relation to Sinus Arrythmia

A

results in a slight increase in HR due to inspiration activation of sympathetic NS

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6
Q

Parasympathetic stimulation of SA node in relation to Sinus Arrythmia

A

results in a slight decrease in HR due to expiration activation of parasympathetic NS

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7
Q

Specialized internodal tracts of atrial conduction system

A

Right atrium: anterior, middle, posterior
Left atrium: Bachmann’s bundle

originate in SA node and distribute depolarization to each atria

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8
Q

Depolarization of atrial myocardium results in a ____ wave

A

P wave

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9
Q

When the depolarization stimulus reaches the AV node, the stimulus slows, producing a ____ on EKG

A

pause / horizontal baseline between P wave and QRS complex
(blood from atria is passing to ventricles)

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10
Q

Ventricular depolarization produces a ____ complex

A

QRS complex

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11
Q

“Concealed” conduction of Purkinje fibers

A

depolarization passing through Purkinje fibers is too weak to record on EKG

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12
Q

Purkinje fibers role in depolarization

A

rapidly conduct depolarization away from AV node to endocardial surface of ventricles

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13
Q

Ventricular contraction on EKG

A

persists through both phases of repolarization to the end of the T wave
(begins + ends during QT interval)

initiated by ventricular depolarization

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14
Q

Overdrive suppression

A

allows the automaticity center with the fastest rate to be the dominant pacemaker without competition

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15
Q

Irregular rhythms are caused by

A

multiple active automaticity sites and lack a constant duration between paced cycles

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16
Q

Entrance block / Parasystole

A

resistance to overdrive suppression
-any incoming depolarization is blocked and the automaticity focus cannot be overdrive suppressed (parasytolic)

typically in pts with hypoxia or structural pathology

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17
Q

Wandering Pacemaker

Rhythm

A

irregular rhythm produced by pacemaker activity wandering from SA node to nearby atrial foci
-cycle length variation
-P’ wave shape varies
-overall rate within the normal range
-atrial rate less than 100
-irregular ventricular rhythm
-acceleration into tachycardia = Multifocal Atrial Tachycardia

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18
Q

P’ wave

A

represents atrial depolarization by an automaticity focus opposed to normal sinus paced P wave

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19
Q

Multifocal Atrial Tachycardia

(MAT)

Rhythm

A

irregular rhythm of patients with COPD with HR over 100 bpm
-P’ shape varies (3+ atrial foci involved)
-shows early signs of parasystole (entrance block)
-sometimes associated with digitalis toxicity (heart disease pts)
-tachycardic form of Wandering Pacemaker

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20
Q

Atrial Fibrillation

Rhythm

A

continuous rapid firing of multiple atrial automaticity foci
-occasional random atrial depolarization reaches AV node (produces irregular QRS rhythm)
-suffering from entrance block
-no P waves
-continuous chaotic spikes
-irregular ventricular rhythm

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21
Q

Escape Rhythm

Rhythm

A

automaticity focus escapes overdrive suppression to pace at its inherent rate
-atrial, junctional, or ventricular
-SA node pacing ceases entirely

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22
Q

Escape Beat

Rhythm

A

automaticity focus transiently escapes overdrive suppression to emit one beat
-atrial, junctional or ventricular
-pause in pacing is brief (one cycle missed)
-emit single beat before returning to normal sinus rhythm

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23
Q

Sinus Arrest

Rhythm

A

diseased SA node ceases pacing completely
-automaticity foci will backup pacemaking
-atrial focus will quickly escape overdrive suppression to become dominant pacemaker (Atrial escape rhythm)

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24
Q

Atrial Escape Rhythm

A

originiates in atrial automaticity foci by escaping overdrive suppression to become dominant pacemaker at 60-80 bpm
-P’ waves are not identical to P waves produced by SA node

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25
Q

Junctional Escape Rhythm

“idiojunctional rhythm”

A

AV junctional automaticity focus assumes dominant pacemaking ability (40-60 bpm) when all regular pacing stimuli from above fail
-OR there is a conduction block in proximal end of AV node
-usually mainly conducts to ventricles
-series of lone QRS complexes
-slow conduction from AV node may delay ventricular depolarization

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26
Q

Junctional Escape Rhythm causing retrograde atrial depolarization

A

mainly conducts to ventricles due to location but may unexpectedly depolarize the atria from below
-inverted P’ waves with upright QRS
-atrial and ventricular depolarization proceed in opposite directions
-slow conduction from AV node may delay retrograde atrial depolarization
-3 recognition patterns:
1. inverted P’ immediately before each QRS
2. inverted P’ after each QRS
3. inverted P’ buried within each QRS

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27
Q

Ventricular Escape Rhythm

“idioventricular rhythm”

A

ventricular automaticity foci is not stimulated from above so it escapes overdrive suppression to become a ventricular pacemaker at 20-40 bpm
-may cause Stokes-Adams Syndrome
-results from:
1. complete conduction block below AV node but high within ventricular conduction system results in no stimulation of ventricular foci from atrial depolarizations
2. downward displacement of pacemaker = total failure of SA node and all automaticity foci above ventricles (rare)

accelerate above inherent range = accelerated idioventricular rhythm

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28
Q

Stokes-Adams Syndrome

Ventricular Escape Rhythm

A

slow ventricular foci as the dominant pacemaker significantly reduces blood flow to the brain to the point of syncope
-must maintain airway

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29
Q

With transient sinus block, unhealthy SA node misses a pacing stimulus (one cycle), producing a pause. Atrial automaticity foci will escape overdirve suppression to emit an ____

A

escape beat

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30
Q

Atrial Escape Beat

A

transient sinus block of one pacemaking stimulus (SA node misses one cycle) and atrial automaticity foci escape overdrive suppression to emit an atrial escape beat
-emit single stimulus
-pause followed by P’ wave differing from P waves
-SA node quickly resumes pacing and atrial automaticity ofci is overdrive suppressed again

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31
Q

Junctional Escape Beat

A

AV node will emit a single beat when SA node misses one pacing cycle and the atrial automaticity foci also fail to respond
-normal QRS complex results
-SA node re-assumes pacemkaing ability
-may produce retrograde atrial depolarization that records as inverted P’ wave before or after QRS

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32
Q

Ventricular Escape Beat

A

SA node fails and ventricular automaticity foci are not stimulated from above foci so it escapes overdrive suppression to emit one beat
-produces an enormous QRS complex
-can act in the event of parasympathetic stimulation (SA, atrial and AV junctional foci cannot)
-SA node will assume pacemaking responsibility again

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33
Q

Premature Beat

A

irritable focus spontaneously fires a single stimulus
-atrial, junctional or ventricular
-evidence of depolarization earlier than expected in the rhythm
-mimc serious conditions (conduction block)
-ventricular automaticity foci become irrtiable when they sense low O2

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34
Q

Atrial and Junctional foci become irritable due to:

Premature Beats

A

-adrenaline (epinephrine) released by adrenals
-increased sympathetic stimulation or decreased/blockage of parasympathetic effects
-caffeine, amphetamines, cocaine + other B1 receptor stimulants
-excess digitalis, toxins, occasionally ethanol
-hyperthyroidism (direct stim. + oversensitive heart to adrenergic stimulation)
-stretch
-low O2 to some extent

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35
Q

Premature Atrial Beat (PAB)

A

originates suddenly in an irritable atrial automaticity focus
-produces P’ wave earlier than expected
-tall T wave
-each PAB depolarizes the SA node (pacemaking resets to start next stimulus one cycle length from premature beat or P’ wave)
-pacing rate of SA node before and after PAB remains the same

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36
Q

Premature Atrial Beat with aberrant ventricular conduction

A

PAB is conducted to the ventricles and they are depolarized earlier than usual
-one of the bundle branches is not completely repolarized + is temporarily refractory to stimuli / depolarization
-depolarization of one ventricle is immediate while the other is delayed
-non-simultaneous depolarization of ventricles = slightly widened QRS for premature cycle only
-normal ventricular conduction resumes with normal cycle

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37
Q

Non-conducted Premature Atrial Beat

A

AV node is completely unreceptive to premature atrial depolarization because it reaches the AV node prematurely (still in refractory period of repolarization)
-does not depolarize the ventricles
-does depolarize the SA node to reset pacemaking
-premature P’ wave with no ventricular response (no QRS complex = harmless span of empty baseline)

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38
Q

Atrial Bigeminy

Premature Atrial Beat

A

irritable atrial focus repeatedly couples a PAB to the end of each normal cycle

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39
Q

Atrial Trigeminy

Premature Atrial Beat

A

irritable atrial focus prematurely fires after two normal cycles and the couplet repeats continuously

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40
Q

Premature Junctional Beat (PJB)

A

irritable junctional automaticity focus fires premature stimulus conducted to + depolarizes ventricles (sometimes atria too in retrograde fashion)
-one ventricle depolarizes on time while the other is delayed = premature slightly widened QRS complex (typical PJB with aberrant ventricular conduction)

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41
Q

Premature Junctional Beat with Retrograde Atrial Depolarization

A

conducts to ventricles due to location but unexpectedly depolarizes atria from bottom up
-atria and ventricles depoalrize in opposite directions
-P’ inverted in leads with upright QRS
-sometimes P’ comes after QRS or is absent
-SA node pacing is reset in PJB with atrial depolarization (empty baseline between couplets)

42
Q

AV Junctional Bigeminy

Premature Junctional Beat

A

PJB after each normal SA node generated cycle
-inverted P’ wave

43
Q

AV Junctional Trigeminy

Premature Junctional Beat

A

PJB is coupled with 2 consecutive normal cycles in a repeating series of couplets
-inverted P’ wave

44
Q

Ventricular focus can be made irritable by:

Premature Beats

A
  1. low O2: airway obstruction, drowning/near suffocation, air with poor O2 content, minimal blood oxygenation in lungs (P.E. or pneumo), reduced C.O. (hypovolemic/cardiogenic shock), poor coronary blood supply (insufficiency or infarction)
  2. low K+: reduced serum potassium (hypokalemia)
  3. pathology: MVP, stretch, myocarditis
  4. QT prolonging medications
  5. to a lesser extent - B1 adrenergic stimulants

*cocaine causes coronary spasm = hypoxia + irritable ventricular foci

45
Q

Premature Ventricular Contraction (PVCs)

A

irritable ventricular automaticity foci producing giant ventricular complex on EKG
-prematurely stimulated ventricles are not completely filled so it is weaker than normal
-one area of ventricular wall depolarizes before the rest of ventricle and slowly moves to other ventricle
-only depolarizes the ventricles NOT SA node (SA node still discharges on schedule)
-occur early in the cycle
-enormous amplitude and depth of QRS
-opposite direction / polarity of the pt’s normal QRS
-compensatory pause after large QRS as ventricles finish repolarizing
-most likely due to hypoxia

46
Q

Unifocal PVCs

A

originate in the same irritable ventricular focus
-each PVC is identical
-frequent unifocal PVCs = poor oxygenation of single focus due to diminished blood supply

47
Q

How many PVcs per minute is considered pathological?

A

6 or more PVCs / min

48
Q

Ventricular Bigeminy

PVCs

A

PVC coupled to a normal cycle and the pattern continues wuth every cycle in succession

49
Q

Ventricular Trigeminy

PVCs

A

repetitive pattern of PVC coupling with every 2 normal cycles

50
Q

Ventricular Parasystole

A

ventricular automaticity focus suffering from entrance block but is NOT irritable
-not vulnerable to overdrive suppression
-paces at inherent rate
-results in dual rhythm of pacing from SA node and ventricular focus
-interval between normal cycle and large QRS complex is not always consistent

51
Q

Ventricular Tachycardia (VT)

PVCs

A

a run or 3 or more PVCs in rapid succession from a very irritable ventricular focus
-typically due to even further reduced oxygenation
-lasting longer than 30 seconds = sustained VT

52
Q

Multifocal PVCs

A

multiple, very irritable (hypoxic) ventricular foci PVCs caused by severe cardiac hypoxia
-requires immediate intervention
-can develop into V-Fib

53
Q

PVCs originating in the same ventricular focus all appear the ____

A

same

54
Q

Mitral Valve Prolapse (MVP)

(Barlow Syndrome)

PVCs

A

floppy mitral valve bulging into left atrium during systole that pull on chordae in LV; traction localizes stretch and ischemia and irritates ventricular foci
-causes PVCs including runs of V-Tach and multifocal PVCs
-benign condition
-1.5% of males
-6-17% of females - slender body, chest deformity, dizzy spells, anxiety prone, first symptoms after age 20
-mid-systolic click and decrescendo murmur

Dr. JB Barlow in 1968

55
Q

R on T phenomenon

PVCs

A

PVC falls on a T wave in situations of hypoxia or low serum potassium during “vulnerable period”
-may result in dangerous arrythmias
-PVCs usually occur after T wave of normal cycle
-warning sign for patient who suffered from dangerous arrythmia

56
Q

Tachy-arrhythmias

A

rapid rhythms originating in very irritable automaticity foci
-sometimes more than one active focus is generating pacing stimuli simultaneously
-easily recognized by rate alone
-specific diagnosis requires location determination

57
Q

Paroxysmal Tachycardia

A

irritable automaticity focus suddenly paces rapidly
-atrial, junctional or ventricular
-150 to 250 bpm
-single premature stimulus from another focus can provoke an irritable focus into paroxysmal tachycardia
-also caused by stimulants or hypoxia
-R to R cycle for rate will fall between 250 and 150 on black lines

58
Q

Sinus tachycardia

A

does not originate in an automaticity focus and is not pathological
-gradual response to excitement or exercise

59
Q

Paroxysmal Atrial Tachycardia (PAT)

A

sudden rapid firing of irritable atrial automaticity focus
-150-250 bpm
-overdrive supresses SA node and all other automaticity foci
-P’ waves present
-normal appearing P’-QRS-T cycles
-also may be set off by premature stimulus from other focus

60
Q

Paroxysmal Atrial Tachycardia (PAT) with AV Block

A

more than one P’ wave (commonly 2 P’ waves) spike after every QRS response
-digitalis excess/toxicity and/or low serum potassium
-only every 2nd stimulus conducts to ventricles (digitalis inhibits AV node)
-rapid rate spiked P’ waves
-2:1 ratio of P’:QRS

61
Q

Paroxysmal Junctional Tachycardia (PJT)

A

sudden rapid pacing of irritable AV junctional automaticity focus
-induced by stimulants or well timed premature beat from another focus
-150 - 200 bpm
-LBB depolarizes before RBB (reverse in some patients) = aberrant ventricular conduction producing widened QRS
-may also depolarize the atria from below in retrograde fashion:
1. inverted P’ immediately before upright QRS
2. inverted P’ after each upright QRS
3. inverted P’ buried within QRS (hard to detect)

62
Q

Paroxysmal Junctional Tachycardia with AV Nodal Re-entry (AVNRT)

“circus re-entry”

A

continuous re-circuit develops (includes AV node and lower atria) + rapidly paces atria and ventricles
-gives off depolarization stimulus to atria and ventricles with each pass in circuit
-each pacing stimulus records from origin near coronary sinus (loaded with automaticity foci)
-catheter ablation can eliminate AVNRT

63
Q

Supraventricular tachycardia (SVT)

A

very irritable automaticity foci produce both paroxysmal atrial tachycardia (PAT) + paroxysmal junctional tachycardia (PJT)
-all atrial and junctional foci (above ventricles)
-P’ waves run into preceding T waves (indistinguishable)
-QRS should be 0.14 sec or less in duration
-caused by adrenergic stimulants or premature beat from another focus
-SVT with aberrant conduction or pre-existing bundle branch block can produce widened QRS that mimics VT (CAUTION)
-never give same medications as SVT to a patient with VT

64
Q

Paroxysmal Ventricular Tachycardia (PVT / VT)

A

very irritable ventricular automaticity focus suddenly pacing 150-250 bpm
-enormous, consecutive PVC like complexes (hide P wave)
-SA node still paces atria (AV dissociation)
-occasional atrial depolarization catches AV node in receptive state and conducts to ventricles
-presence of capture or fusion beats confirms diagnosis (not present in SVT)
-QRS usually greater than 0.14 seconds and very wide
-signifies ischemia (coronary insufficiency) or other causes of cardiac hypoxia
-common in elderly
-never give same medications as SVT to a patient with VT

65
Q

Capture Beat

Paroxysmal Ventricular Tachycardia

A

occasional atrial depolarization catches AV node in receptive state and conducts to ventricles
-producing normal QRS in the midst of ventricular tachycardia

66
Q

Fusion Beat

Paroxysmal Ventricular Tachycardia

A

atrial depolarization finds a receptove AV node but ventricular depolarization does not fully proceed as it meets with depolarization coming from ventricular focus
-blending of normal QRS with PVC

67
Q

Torsades de Pointes

A

rapid ventricular rhythm caused by low K+, medications that block K+ channels or congential abnormalities (Long QT syndrome) all which lengthen QT segment
-variable 250-350 bpm
-ventricular complexes point upwards then point downwards in repeating continuum (amplitude increases then decreases - spindle shaped)
-typically brief + self terminating
-no effective ventricular pumping
-Dr. F Dessertenne (1966) - caused by two competitive foci in different ventricular areas pacing at the same rate
-unreseolved = deadly arrythmia

68
Q

Atrial Flutter

A

originates in atrial automaticity focus with rapid succession of identical back to back atrial depolarization waves
-250-350bpm
-suggestive of re-entry origin
-baseline appears to vanish between flutter waves (“saw tooth” baseline”)
-rapid QRS rate (2:1 ratio of flutter waves to QRS)
-cannot drive the ventricles at the same successive rate (1/2 atrial depolarizations reach ventricles)
-diagnose by vagal maneuvers (increase AV refractoriness = fewer flutter waves to conduct to ventricles that are easier to identify on EKG)
-47% developed A-Flutter post-op from “Maze” surgical procedure; creates channels in atria for continuous pathway from SA node to AV node

69
Q

Ventricular Flutter

A

produced by singular ventricular automaticity focus diring at 250-350 bpm
-smooth sine waves of similar amplitude
-ventricles hardly have enough time to fill bc they contract too fast
-no effective C.O. + coronary arteries do not receive enough blood
-rapid deterioration into deadly arrythmia (V-Fib)
-rarely self-resolves

70
Q

Fibrillation

A

erratic rhythm caused by continuous, rapid discharges from numerous automaticity foci in either atria or ventricles
-350-450 bpm (not true but hypothetical)
-A-Fib or V-Fib
-parasystolic (entrance block - cannot be overdrive suppressed)
-uncoordinated rhythm with indistinct waves
-fibrillating chambers do not effectively pump

71
Q

Atrial Fibrillation

A

many irritable parasystolic atrial foci firing at rapid rates
-350-450 bpm
-initiated by parasystolic foci in pulmonary vein of left atrium
-wavy baseline with no identifiable P or P’ waves
-irregular ventricular response [QRS] either fast or slow (foci near AV node conduct to ventricles)
-small portion of atria is depolarized by any one discharge from atrial focus

72
Q

Ventricular Fibrillation

A

rapid discharges from many irritable parasystolic ventricular automaticity foci
-erratic rapid twitching of ventricles = no mechanical pumping
-350-450 bpm
-lack of any identifiable waves / no predictable pattern
-type of cardiac arrest
-requires immediate defibrillation

“bag of worms”

73
Q

Cardiac Standstill

Cardiac Arrest

A

SA node + escape mechanisms of automaticity foci are unable to assume pacing responsibility
-asystole
-no detectable cardiac activity
-rare

74
Q

Pulseless Electrical Activity (PEA)

Cardiac Arrest

A

a dying heart produces weak signs of electrical activity but the heart cannot respond mechanically
-no detectable pulse

75
Q

Implantable Cardioverter Defibrillator (ICD)

A

implanted under the chest skin of patients likely to develop V-Fib and deliver a defibrillating shock
-can also detect other arrythmias + treat with timed electrical stimuli
-can pace if bradycardia ensues

76
Q

Wolff-Parkinson-White Syndrome (WPW)

A

abnormal accessory AV conduction pathway (bundle of Kent) can “short circuit” the usual delay of ventricular conduction in AV node
-prematurely depolarizes (pre-excites) a portion of ventricles
-delta wave represents depolarization of an area of ventricular pre-excitation
-delta wave illusion = shortened PR interval + lengthened QRS
-can have paroxysmal tachycardia by 3 ways:
1. rapid conduction - SVT conducted 1:1 producing high ventricular rates
2. kent bundles containing automaticity foci
3. re-entry - ventricular depolarization may restimulate atria in retrograde fashionvia accessory pathway

77
Q

Lown-Ganong-Levine (LGL) Syndrome

A

AV node is bypassed by an extension of anterior internodal tract (“James” bundle) which conducts atrial depolarizations directly to HIS bundle without delay
-lack of AV node filtering of supraventricular rhythms
-poses serious problems with rapid atrial rhythms
-transmit atrial rates directly 1:1 to HIS bundle = drive ventricles at rapid rate
-no significant PR interval delay
-P waves adjacent to QRS

78
Q

Heart Blocks

A

prevent the conduction of depolarization
-occur in SA node, AV node or ventricular conduction system

79
Q

Sinus Block

A

unhealthy SA node may temporarily fail to pace for at least one cycle
-missed cycle has no P wave
-pause may produce an escape beat
-SA node will resume pacing at the same rate prior to the block
-P wave before and after will be identical (both originate in SA node)

80
Q

Sinus Sick Syndrome (SSS)

Blocks

A

wastebasket of arrythmias caused by SA node dysfunction associated with unresponsive supraventricular automaticity foci (no escape mechanism)
-characterized by sinus bradycardia without normal escape mechanisms
-may present as recurrent episodes of sinus block or sinus arrest
-elderly patients with heart disease
-young conditioned athletes also exhibit signs of SSS (pseudo)
-pts may develop intermittent SVT, A-Flutter or A-Fib with bradycardia (Bradycardia-Tachycardia Syndrome)

81
Q

Bradycardia-Tachycardia Syndrome

Sinus Sick Syndrome

A

pts with SSS may develop intermittent SVT, A-Flutter or A-Fib with bradycardia

82
Q

AV Blocks

A

prolongs or eliminate conduction from atria to ventricles
-minor: lengthen the brief pause between atrial depolarization and ventricular depolarization
-most completely block all or some supraventricular impulses from reaching ventricles
-1st, 2nd or 3rd degree

83
Q

1st Degree AV Block

A

prolongs AV node conduction
-PR interval greater than one large square (0.2 sec) is consistent in every cycle
-P-QRS-T sequence is normal in every cycle

84
Q

2nd Degree AV Blocks

A

allow some atrial depolarizations (P waves) to conduct to the ventricles (QRS response) while some atrial depolarizations are blocked (lone P waves without QRS)
-Wenckebach: occur in AV node
-Mobitz: occur below AV node

85
Q

Wenckebach 2nd Degree AV Block

A

block of AV node producing a series of cycles with progressive blocking of AV node conduction until final P wave is totally blocked
-no QRS response or normal
-PR interval gradually lengthens in successive cycles (first cycle can be fairly normal)
-last P wave of the series fails to conduct to ventricles and is totally blocked (dropped QRS)
-series repeats
-consistent P:QRS ratio (3:2, 4:3, 5:4, etc)
-2 to 8 or more cycles
-sometimes caused by parasympathetic excess (inhibits AV node)

86
Q

Mobitz 2nd Degree AV Block

A

block of Purkinje fibers (below AV node) producing series of cycles consisting of one normal P-QRS-T cycle preceded by paced P waves that fail to conduct through AV node
-widened QRS response (bundle branch block pattern)
-PR interval is normal
-consistent P wave to QRS ratio (3:1, 4:1, 5:1, etc)
-slow ventricular rates can lead to syncope
-every cycle missing QRS has regular P wave (never premature P’ wave)

87
Q

Diagnosing Wenckebach vs Mobitz 2nd Degree AV Block

A

vagal maneuvers that inhibit AV node
-AV node supplied with parasympathetic innervation
-maneuver
-Wenckebach: maneuver will increases number of cycles/series to 3:2 or 4:3
-Mobitz: block will be eliminated or produce 1:1 AV conduction (no effect)

88
Q

A prolonged PR interval can alert you to the existence of

A

1st degree, 2nd degree or 3rd degree AV block

89
Q

EKG with P waves lacking a QRS response can expose:

A

2nd and 3rd degree AV blocks

90
Q

AV Block EKG Checks

A

-PR Interval:
1. increased consistently in 1st degree AV block
2. increased in each series of cycles in Wenckebach
3. variable in 3rd degree AV block
4. decreased in WPW + LGL syndrome

-P without QRS response:
1. Wenckebach and Mobitz 2nd degree AV blocks
2. 3rd degree AV block (independent atrial and ventricular rates)

91
Q

Complete 3rd Degree AV Block

A

total block of atrial depolarizations/conduction to the ventricles
-automaticity focus below the complete block paces ventricles at inherent rate (depends on location of block)
-upper AV node: junctional focus escapes to pace ventricles
-below AV node: ventricular focus escapes to pace ventricles
-atria remain independently paced by SA node
-usually normal P wave and slow QRS
-AV dissociation

92
Q

Complete 3rd Degree AV Block with Junctional Focus

“idiojunctional rhythm”

A

upper AV node junctional focus no longer overdrive suppressed and escapes to pace ventricles
-sinus paced P waves and narrow/normal QRS complex
-sometimes wide QRS if depolarization is delayed
-ventricular rate ranges from 40-60 bpm

93
Q

Complete 3rd Degree Block with Ventricular Focus

A

below AV junction; ventricular focus escapes overdrive suppression to pace ventricles at its slow inherent rate
-20-40 bpm
-cerebral blood flow is compromised and will result in syncope (Stokes-Adams Syndrome)
-AV dissociation (separate atrial P wave)
-large wide PVC-like complexes (supposed to be QRS)
-continuous maintenance of airway
-will eventually need a pacemaker
-“downward displacement of pacemaker” - absence of atrial activity with bradycardia
-hyperkalemia can produce aystole + mimic

94
Q

Bundle Branch Block (BBB)

A

caused by block of conduction in R or L bundle branch that delays depolarization to the ventricle it supplies
-blocked branch ventricle depolarizes later than unblocked
-widened QRS with 2 peaks increases in duration to 3 small squares (0.12 sec or greater) - 2 peaks labeled R + R’
-R’ represents delayed depolarization of blocked ventricle
-may imitate ventricular tachycardia

95
Q

Left Bundle Branch Block (LBBB)

A

left ventricular depolarization is delayed
-seen in V5 + V6
-sometimes looks like a flattened peak with 2 tiny points

96
Q

Right Bundle Branch Block (RBBB)

A

right ventricular depolarization is delayed
-seen in V1 + V2

97
Q

Rate dependent Bundle Branch Block

A

produces tachycardia with wide QRS that imitates ventricular tachycardia
-one bundle branch conducts before the other

98
Q

Incomplete Bundle Branch Block

A

R,R’ peaks in a normal QRS

99
Q

Intermittent Mobitz (2nd degree AV block)

A

RBBB/LBBB (wide QRS pattern) + intermittent RBBB/LBBB (records as AV block - P waves without QRS)

permament bundle branch block on one side, intermittent other side

100
Q

Hemiblock

A

block of 1/2 fasicles (subdivisions) of LBB

EKG (4 decks)

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