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6902 test 2 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

T or F - all tissue can produce AP to depolarize the heart

A

True

The SA node has the highest intrinsic rate so it suppresses the others by keeping them in refractory. Then it depolarizes the fastest so it’s ready to go again.

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2
Q

Increased automaticity

A

caused by afterdepolarizations - the membrane potential oscillates during or after repolarization and if another stimulus hits in this relative refractory period, premature AP leading to beats occur. Repeated, becomes sustained arrhythmia

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3
Q

Early After Depolarizations

A

more commonly occur in Purkinje fibers. They are enhanced by slow heart rate and are treated by speeding up the heart rate.

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4
Q

Delayed afterdepolarizations

A

come from increased intracellular calcium (catecholamines, digitalis, HF) and are enhanced by fast heart rates, so are treated by slowing the heart rate.

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5
Q

Premature beats and tachyarrhythmias originate from

A

re-entry mechanisms

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6
Q

Re-entry mechanisms

A

comes from an impulse being delayed in one region and re-exciting adjacent tissue that has had time to repolarize.

Atrial depolarization is conducted ia the AVN and an accessory pathway. Pre-excitation occurs bc there was no AVN so the impulse conduced faster

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7
Q

When scar tissue forms (think re entry)

A

it can create an alternative pathway for electrical impulses to double back

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8
Q

Function re-entry

A

Occurs when repolarization is delay - usually from ischemia

Multiple wave fronts of depolarization are formed and they eventually collide. Where collisions occur, some “whirlpools” of depolarizations occur that are called rotors.

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9
Q

Tachydysrhythmias

A

Have a HR >100

Those coming from the AV node or higher are narrow complex and are supraventricular

Those coming from the ventricular are wide complex

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10
Q

Cardiac conduction system cells

A

gap junctions

Allows AP to spread to muscle to cause contraction

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11
Q

RMP

A

-80 to -90 mV
established by Na/K ATP-ase

After reaching threshold, cell depolarizes to 20-30 mV

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12
Q

SA node

A

Typically generates impulses and is the PM

Has dense sympathetic and parasympathetic nerve endings

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13
Q

SA node is perfused by

A

RCA in most ppl. Left circumflex in some

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14
Q

Bundle of HIS

A

Diverges into RBBB and LBBB

LBBB into fascicles

Then into Purkinje fibers

Both BB receive blood form LAD. LAD also receives from posterior descending

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15
Q

1st degree AVB

A

Block of AV node

avoid increasing vagal tone.

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16
Q

2 degree AVB - Type 1

A

can be associated with drugs (antiarrhythmics)

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17
Q

2 degree AVB - Type 2

A

More severe, usually ischemia, high chance of becoming complete HB

Atropine unlikely to help, isoproterenol can help. Pacing can help

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18
Q

RBB

A

can be benign

RBBB with LAHB common bc both get blood from LAD

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19
Q

LBBB

A

due to dual vascularity. Usually indicates more severe disease.

Pulmonary Artery Catheters contraindicated in pts with LBBB bc of HB risk

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20
Q

3rd degree AVB

A

complete heart block
can cause syncope, CHF, SOB
Isoproterenol to treat, pacers

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21
Q

Sinus arrhythmia

A

normal irregular R-R rhythm with a sinus origin.

Occurs due to the Bainbridge reflex

22
Q

Bainbridge reflex

A

occurs when the intrathoracic pressure increases, so does the HR (with inspiration). Opposite, the HR slows as intrathoracic pressure lowers

23
Q

Supraventricular Tachycardia

A

caused by SA node stimulation through sympathetic stim or parasympathetic suppression

Diastole is shorted relative to systole, which decreases time for CA blood flow

Most common SVT in the OR

Treated by addressing the specific cause:
-light anesthesia
vagolytic drugs
hypovolemia
hypoxia
hypercarbia
HG
ischemia
fever
infection
24
Q

Premature Atrial Complexes

A

a beat comes from some ectopic focus in the atria. Usually a pause following the PAC until the next sinus beat. usually benign

symptoms: Chest fluttering
causes: stress, caffeine, ETOH, nicotine

25
Q

Paroxysmal SVT

A

HR 160-220 that begins and ends spontaneously

26
Q

AVN re-entry tachycardia

A

occurs from a re-entry circuit or increased automaticity of secondary pathways

ight-headedness, dizziness, fatigue, chest pain, dyspnea, syncope

Orthodromic or Antidromic

ACLS algorithm. Adenosine first line for stable.
Cardioversion for unstable pts

27
Q

Orthodromic AVNRT

A

QRS is narrow
more common
treatment is vagal maneuvers

28
Q

Antidromic AVNRT

A

wide QRS

29
Q

WPW

A

syndrome associated with re-entry type tachycardias

pre-excitation mechanism (delta wave) and tachycardia

The delta wave occurs as a form of conduction block with a slow depolarization front. The resulting PR interval is short and slurs in to the QRS. Most have a PAC that triggers the re-entry.

Most pts have AVNRT

Drugs that slow AVN increase accessory conduction and are BAD. CCB will potentiate the accessory pathway and can lead to VF

treatment is with procainamide 10 mg/kg slowly or cardioversion

30
Q

Multifocal atrial tachycardia

A

originates from various ectopic PM

P waves have 3 or more morphologies and have variable PR intervals

Most common in pts with lung disease

treatment is to improve oxygenation

31
Q

AF

A

most common sustained arrhythmia

fatigue, weakness, palpitations, hypotension, syncope, angina, SOB

32
Q

If new onset AF occurs before surgery

A

surgery should be postponed until rate is controlled or conversion to NSR

33
Q

If AF occurs in surgery and is hemodynamically unstable

A

cardioversion to treat

34
Q

If AF occurs in surgery and is stable

A

managed with BB, CCB, digoxin

35
Q

Chronic AF

A

anticoagulated by CHAAD score
low score get aspiring
high scores (3-4) get warfarin

36
Q

A flutter

A

organized atrial rates of 250-350 and sawtooth p waves
cardioversion
amiodarone or CCB

37
Q

SVTs as a rhythm?

A

not a rhythm - figure out what the underlying rhythm is

38
Q

PVCs

A

unifocal or multifocal

patterned - bigeminy or trigeminy

danger occurs from R on T phenomena

PVCs produce less volume ejection than a sinus beat.

Occur at rest and disappear with exercise

39
Q

Under anesthesia - 6 or more PVCs per minute increases the risk of

A

developing life threatening arrhythmias

Have defib ready

BB are the most useful drug to suppress ventricular ectopy

40
Q

VT/Monomorphic VT

A

occurs when 4 or more consecutive PVCs occur with a rate > 120

Can be paroxysmal

Cardioversion with sustained and hemodynamic changes

41
Q

Vfib

A

incompatible with life bc no stroke volume
AICD implantation
immediate vfib - highest survival within 3-5 minutes

42
Q

Prolonged QT

A

when QTC is longer than 460 ms

isoflurane, sevo, ondansetron, hypokalemia, hyperventilation

Correct lytes, discontinue drugs that are causing it

Treatment can be pacing

Torsade’s is the major concern

AICD

43
Q

Sinus brady

A 
HR < 60
oculocardiac stim (afferent V, efferent X), celiac plexus stimulation, laryngoscopy, abdominal insufflation, nausea, pain, BB, opioids, succ, hypothermia SA node disease

Treat the cause

Doses of atropine < 0.5 mg can worsen due to preferential presynaptic M2 inhibition

44
Q

If BB or CCB overdose causing bradycardia

A

glucagon 3-5 mg 1 3-5 minutes for max of 10 mg

45
Q

SB and neuraxial blockade

A

unopposed parasympathetic activation remains after sympathetic blockade of the cardiac accelerator fibers of T1-T4.

Treatment is aggressive with pacing and fluids, stopping opioids, addressing hypercarbia

atropine, epi, dopamine are options

46
Q

Junctional brady rhythms

A

HR 40-60
causes AV dyssynchrony, loss of atrial kick

fatigue, weakness, angina, CHF, hypotension

associate with myocardial inflammation and ischemia

not uncommon during GA with halogenated anesthetics

atropine

47
Q

Monophasic defib

A

dose of 360J

48
Q

Biphasic dib

A

doses of 120-200 but 200 J is where to start

49
Q

Maze proceudre

A

Afib surgery
create several incisions in specified pattern around the atria to create scar tissue that blocks re-entry circuits that cause afib

most commonly done if Afib exists with concurrent valve replacement/repairs

requires CPB and will involve ligation of left atrial appendage

50
Q

CHADS VASC

A

high scores correlate to higher risk of thrombus formation - LV, HF, HTN, 65, DM, prior CVA, vascular disease, female

Low risk need no anticoag

6902 test 2 (8 decks)

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