Arrhythmias Flashcards
T or F - all tissue can produce AP to depolarize the heart
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.
Increased automaticity
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
Early After Depolarizations
more commonly occur in Purkinje fibers. They are enhanced by slow heart rate and are treated by speeding up the heart rate.
Delayed afterdepolarizations
come from increased intracellular calcium (catecholamines, digitalis, HF) and are enhanced by fast heart rates, so are treated by slowing the heart rate.
Premature beats and tachyarrhythmias originate from
re-entry mechanisms
Re-entry mechanisms
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
When scar tissue forms (think re entry)
it can create an alternative pathway for electrical impulses to double back
Function re-entry
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.
Tachydysrhythmias
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
Cardiac conduction system cells
gap junctions
Allows AP to spread to muscle to cause contraction
RMP
-80 to -90 mV
established by Na/K ATP-ase
After reaching threshold, cell depolarizes to 20-30 mV
SA node
Typically generates impulses and is the PM
Has dense sympathetic and parasympathetic nerve endings
SA node is perfused by
RCA in most ppl. Left circumflex in some
Bundle of HIS
Diverges into RBBB and LBBB
LBBB into fascicles
Then into Purkinje fibers
Both BB receive blood form LAD. LAD also receives from posterior descending
1st degree AVB
Block of AV node
avoid increasing vagal tone.
2 degree AVB - Type 1
can be associated with drugs (antiarrhythmics)
2 degree AVB - Type 2
More severe, usually ischemia, high chance of becoming complete HB
Atropine unlikely to help, isoproterenol can help. Pacing can help
RBB
can be benign
RBBB with LAHB common bc both get blood from LAD
LBBB
due to dual vascularity. Usually indicates more severe disease.
Pulmonary Artery Catheters contraindicated in pts with LBBB bc of HB risk
3rd degree AVB
complete heart block
can cause syncope, CHF, SOB
Isoproterenol to treat, pacers
Sinus arrhythmia
normal irregular R-R rhythm with a sinus origin.
Occurs due to the Bainbridge reflex
Bainbridge reflex
occurs when the intrathoracic pressure increases, so does the HR (with inspiration). Opposite, the HR slows as intrathoracic pressure lowers
Supraventricular Tachycardia
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
Premature Atrial Complexes
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
Paroxysmal SVT
HR 160-220 that begins and ends spontaneously
AVN re-entry tachycardia
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
Orthodromic AVNRT
QRS is narrow
more common
treatment is vagal maneuvers
Antidromic AVNRT
wide QRS
WPW
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
Multifocal atrial tachycardia
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
AF
most common sustained arrhythmia
fatigue, weakness, palpitations, hypotension, syncope, angina, SOB
If new onset AF occurs before surgery
surgery should be postponed until rate is controlled or conversion to NSR
If AF occurs in surgery and is hemodynamically unstable
cardioversion to treat
If AF occurs in surgery and is stable
managed with BB, CCB, digoxin
Chronic AF
anticoagulated by CHAAD score
low score get aspiring
high scores (3-4) get warfarin
A flutter
organized atrial rates of 250-350 and sawtooth p waves
cardioversion
amiodarone or CCB
SVTs as a rhythm?
not a rhythm - figure out what the underlying rhythm is
PVCs
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
Under anesthesia - 6 or more PVCs per minute increases the risk of
developing life threatening arrhythmias
Have defib ready
BB are the most useful drug to suppress ventricular ectopy
VT/Monomorphic VT
occurs when 4 or more consecutive PVCs occur with a rate > 120
Can be paroxysmal
Cardioversion with sustained and hemodynamic changes
Vfib
incompatible with life bc no stroke volume
AICD implantation
immediate vfib - highest survival within 3-5 minutes
Prolonged QT
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
Sinus brady
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
If BB or CCB overdose causing bradycardia
glucagon 3-5 mg 1 3-5 minutes for max of 10 mg
SB and neuraxial blockade
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
Junctional brady rhythms
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
Monophasic defib
dose of 360J
Biphasic dib
doses of 120-200 but 200 J is where to start
Maze proceudre
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
CHADS VASC
high scores correlate to higher risk of thrombus formation - LV, HF, HTN, 65, DM, prior CVA, vascular disease, female
Low risk need no anticoag
