Dubin's week 2: pgs 93-190 Flashcards

Question

Junctional Escape Rhythm | "idiojunctional rhythm"

Answer 1

**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

Answer 2

**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

Answer 3

**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

Answer 4

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

Answer 5

escape beat

Answer 6

**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

Answer 7

**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

Answer 8

**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

Answer 9

**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

Answer 10

-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

Answer 11

**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

Answer 12

**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

Answer 13

**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)

Answer 14

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

Answer 15

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

Answer 16

**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)

Answer 17

**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)

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

**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

Answer 22

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

Answer 23

6 or more PVCs / min

Answer 24

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

Answer 25

repetitive pattern of PVC coupling with every 2 normal cycles

Answer 26

**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

Answer 27

**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

Answer 28

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

Answer 29

**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

Answer 30

**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

Answer 31

**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

Answer 32

**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

Answer 33

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

Answer 34

**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

Answer 35

**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

Answer 36

**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)

Answer 37

**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

Answer 38

**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

Answer 39

**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

Answer 40

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

Answer 41

**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

Answer 42

**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

Answer 43

**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

Answer 44

**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

Answer 45

**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

Answer 46

**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

Answer 47

**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"

Answer 48

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

Answer 49

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

Answer 50

**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

Answer 51

**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

Answer 52

**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

Answer 53

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

Answer 54

**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)

Answer 55

**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)

Answer 56

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

Answer 57

**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

Answer 58

**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

Answer 59

**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

Answer 60

**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)

Answer 61

**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)

Answer 62

**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)

Answer 63

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

Answer 64

2nd and 3rd degree AV blocks

Answer 65

-**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)

Answer 66

**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

Answer 67

**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

Answer 68

**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

Answer 69

**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

Answer 70

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

Answer 71

**right ventricular depolarization is delayed** -seen in V1 + V2

Answer 72

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

Answer 73

R,R' peaks in a normal QRS

Answer 74

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

Answer 75

block of 1/2 fasicles (subdivisions) of LBB

Dubin's week 2: pgs 93-190 Flashcards

(100 cards)