Arrhythmia Review

60-80 bpm

40-60 bpm

20-40 bpm

0.16-0.2

0.06-0.1

• Bazzetts formula
• QT / square root of the RR interval

F, it should be LESS than half

Positive

• + LA
• - RA

• + LL
• - RA

• + LL
• - LA

hypovolemia, fever, exercise, SNS stimulation, hyperthyroidism

• -normal variation due to alterations in ANS tone
• -associated with the respiratory cycle
• -HR increases with inspiration and decreases with expiration
• -common in kids and young adults
• -when seen in geri its it may be a precursor to sick sinus syndrome

• -sinus node does not conduct or initiate an impulse
• -due to an automaticity or conduction issue
• -causes: increased vagal tone, infarction, drugs (BB or CCB)

-an impulse that originates near the AVJ

Non-compensatory

The QRS before the premature beat to the QRS after equals 2 R-R intervals

The QRS before the premature beat to the QRS after equals less than 2 R-R intervals

The premature depolarization of the atria by the PAC results in subsequent premature depolarization of the SA node which causes it to reset itself earlier than expected

The SA node is not depolarized by the premature beat and thus is not reset and so the underlying rhythm appears at the expected time after the pause

Yes

If it occurs very early then the impulse reaches the bundle branches before repolarization is complete.  The R bundle is slower to repolarize than the L bundle, so they are depolarized sequentially and the QRS is wide and measures >0.12 seconds.

PAC usually has a non-compensatory pause

• The ectopic atrial focus occurs so early that the AV node is still refractory and so the impulse is not conducted to the ventricles.
• Get a P wave with no QRS.

nicotine, stress, caffeine, ETOH

• -ectopic PM in the atria produces a rapid regular atrial rhythm
• -rate 150-250 bpm
• -occurs in bursts (hence paroxysmal)
• -may not be able to differentiate between T and P waves
• -QRS complex is narrow

• -same as PACs
• -also due to COPD and digoxin toxicity

• -decreased CO as ventricular filling is impaired
• -possible palpitations
• -increased myocardial O2 consumption

cardioversion

• -sedation
• -vagal maneuvers
• -adenosine
• -dig, BB, CCB (pt with normal cardiac function)
• -ablation

• -P has different morphologies due to different foci
• -HR is usually normal but can be slow or irregular

increased vagal stimulation of the SA node, this slows the rate of SA node depolarization and gives an opportunity for ectopic PM to kick in

• No, it's common in young healthy pts and athletes, especially with sleep.
• No treatment required.

• -wandering atrial PM with a rate > 100 bpm
• -seen with severe COPD- the associated PH puts strain on the RV and RA

• -vagal maneuvers
• -adenosine
• -BB, CCB, amio
• -NOT cardioversion

• -ectopic PM in atria with rate of 250-350 bpm
• -sawtooth P waves are called F waves
• -about half of the atrial impulses are conducted to the ventricles, usually in even ratios (2:1, 4:1)
• -regular or irregular

• -dilt or other CCB or BB
• -IV heparin and r/o atrial clot with TEE
• -then cardioversion within 24 hours followed by 4 weeks of anti-coagulation

• -dilt, amio, or dig
• -cardioversion

• -If abnormal rhythm is less than 48 hours in duration, then CV can be performed without initial anti-coagulation
• -If abnormal rhythm duration is > 48 hours, then need to anti-coagulate for 3 weeks, then CV can be performed, pt must con't anti-coags for 4 weeks after

• -blocks K+ channels and prolongs depolarization
• -increases duration of AP
• -increases duration of refractory period
• -decreases excitability

decreases rate of spontaneous phase 4 depolarization

inhibits the slow Ca++ channels

• -atria fire at a faster rate > 350-400 bpm
• -atria just quiver
• -no P waves, called small F (fib) waves
• -irregular

rate < 100 bpm

AF

• self-limiting:
• -excess ETOH (holiday heart)
• -stress
• -drugs
• chronic:
• -valvular disease (especially MV)
• -HTN, CAD, PE, hyperthyroid, common after cardiac surgery

same as Aflutter: rate control, rhythm conversion, anti-coagulation

T

• -prototypical pre-excitation syndrome
• -due to a congenital malformation where strands of conducting myocardial tissue form between the atria and ventricles and form an accessory pathway called "bundle of kent"

• -QRS is distorted by a delta wave (slurred upstroke)
• -short PR interval because conduction going thru accessory pathway is faster than thru AV node
• -rate 60-100 bpm

• -pts with WPW have no greater incidence of AF 
• -risk of RVR due to accessory pathway

• std treatment: rate control, anti-coag, rhythm conversion
• -CV and amio are recommended
• -pts with normal heart can also get flecainide or procainamide
• -adenosine, BB, and CCB are CLASS 3 (harmful) in pts with WPW

• upper- atrial nodal, has PM cells
• middle- nodal
• lower- nodal His, has PM cells

• -takes on role of secondary PM
• -inherent rate of 40-60 bpm 
• -rhythm originating here is a junctional rhythm (rate 40-60 bpm)

• -With the AV node as the heart's PM, the depolarization spreads backward (to the atria)  and forward (to the ventricles)
• -P wave inverted due to retrograde conduciton
• -P wave in QRS if atria and vent are depolarized simultaneously
• -P wave after QRS if vent are depolarized before ventricles

• -like a PAC
• -an early ectopic beat from the AVJ
• -followed by non-compensatory pause usually
• -P wave can be in QRS or after or inverted
• -short PR interval of <0.1 sec
• -normal P wave and QRS
• -treat underlying cause

• -dig toxicity
• -enhanced automaticity in the AVJ
• -CAD
• -HF
• -valve disease

• -rate 60-100 bpm
• -originates in AVJ
• -only difference between accel junctional and junctional is the rate

• -treat underlying cause
• -treat low CO if present

• -rate 100-180 bpm
• -same P wave variances as in junctional rhythm

dig toxicity and ACS

• -treat cause
• -if cause unknown then vagal stim or adenosine
• -preserved heart function: amio, BB, CCB
• -impaired heart function: just amio
• -NO CV!! (class 3)

No, they require treatment of the underlying problem.  They may be responsive to BB and CCB.  

• -sinus impulse is normally conducted to the AV node but then is delayed longer than usual before being conducted to the ventricles
• -PR > 0.2 secs
• -PR interval is constant
• -rhythm is regular

• -drugs
• -hyperkalemia
• -acute rheumatic fever
• -myocarditis
• -MI (especially inferior)
• -degeneration of conduction pathways from age
• -idiopathic
• -increased vagal tone

No, it's asymptomatic and requires no treatment, however it may progress to more serious types of AVB.  Causes should be looked for.

• -failure of some sinus impulses to be transmitted to the ventricles
• -each successive impulse has more difficulty passing thru the AV node until finally an impulse is not conducted
• -PR interval widens, eventually a P wave appears that is not followed by a QRS
• -irregular ventricular rhythm
• -"group beating"

In Mobitz I the P-P intervals will remain constant

With a non-conducted P wave the P wave will occur early and will have a different morphology

Often asymptomatic unless rate becomes very slow.  If there is HD compromise due to bradycardia then atropine may help to improve conduction, TC pacing, catecholamines may also be used (dopamine).  

• -failure of some sinus impulses to be transmitted to the ventricles
• -there's more than 1 P wave before each QRS, finally 1 is conducted to the ventricles
• -PR interval is constant
• -conduction ratio can vary (2:1, 3:1)
• -QRS width can vary

• It depends on where the conduction disturbance is.  
• -QRS is narrow if the disturbance is in the bundle of His
• -QRS is wide if the disturbance is in the bundle branches

• -anterior MI
• -degeneration of the conduction system due to age
• -acute myocarditis
• -NOT a result of increased vagal tone or dig toxicity

Mobitz II, as the conduction disturbance is lower in the conduction system, making it easier for it to progress to complete heart block or ventricular standstill with little or no warning

• -TV or TC pacing  
• -atropine should be used cautiously
• -dopamine or epi may be indicated if significant hypotension develops 
• -possible permanent pacer

It will increase firing of the SA node but will not improve conduction thru the AV node.  It may cause paradoxical slowing of the ventricular rate

• -AV dissociation
• -no conduction btw atria and ventricles
• -atria paced at usual rate of 60-100 bpm
• -ventricles paced by AVJ escape PM at 40-60 bpm or by the ventricles themselves at 30-40 bpm 
• -PR interval varies
• -QRS width depends on location of anatomic block

temporary or reversible usually has narrow QRS and is due to: inferior MI, ischemic heart disease, increased vagal tone, drugs (dig, BB, CCB, amio), hyperkalemia, acute rheumatic fever, myocarditus

chronic CHB usually has wide QRS and is due to: acute AMI, degeneration of the conduction system (in the elderly); NOT due to increased vagal tone or drug toxicity

stokes-adams

• -elderly may be asymptomatic
• -syncope (decreased CO due to slow rate and loss of atrial kick)
• -chest pain
• -hypotension

• -TC pacer while awaiting TV wire
• -permanent pacer
• -atropine may work in narrow complex CHB but not in a wide complex 
• -dopa or epi for significant hypotension

• -ventricles are not depolarized simultaneously due to obstruction in LBB, RBB, or bundle of His
• -QRS > 0.12 sec

Yes, but you need a 12 lead EKG to differentiate between L and R BBB

• -heart disease (CAD, HTN, cardiomyopathy, acute anteroseptal MI)
• -congenital
• -chronic degeneration
• -may be rate related
• -may be temporary or permanent

• -usually due to heart disease (similar causes as with RBBB)
• -can be temporary or permanent

• -A BBB alone does not require treatment.  
• -Pacing may be indicated if it develops 2/2 an MI

• -premature ectopic impulse originating in the ventricle
• -unlike a PJC it doesn't travel thru normal conduction pathways but rather thru the ventricle muscles and hence they are depolarized sequentially causing a wide QRS
• -QRS differs in appearance from normal QRS

Yes, so measuring from the QRS prior to the PVC to the QRS after the PVC = the sum of 2 R-R intervals of the underlying rhythm.  This is b/c the SA node is not depolarized by the PVC and so the normal rhythm resumes on time.  

PVC sandwiched inbetween 2 regularly occurring SR beats without disturbing the regularity of the underlying rhythm.  A compensatory pause does NOT occur.  

PVC occurs during vulnerable period of ventricular repolarization, so on or near the peak of the T wave.  Stimulation of the ventricles at this time can precipitate VT or VF.  

They get more common as we age.  

• -enhanced automaticity
• -ETOH, caffeine, nicotine
• -cardiomyopathy
• -electrolyte imbalances (decreased K and Mg)
• -ischemia or infarction
• -increased catecholamines

treat the underlying cause

• PVC that occurs late 
• -occur due to increased vagal tone on the SA node not due to increased automaticity
• -protective mechanism after a pause in the normal rhythm
• -no treatment needed

• -originates in an ectopic focus in the ventricle
• -wide QRS
• -no atrial activity
• -rate 140-250 bpm
• -monomorphic or polymorphic 

Yes, but the P waves are hidden in the QRS

• any of the following:
• 1) amio bolus and infusion
• 2) lido bolus and infusion
• 3) procainamide infusion

if unresponsive to drugs CV starting at 100 J and increasing with subsequent attempts

hypotension, bradycardia, prolonged QT

slurred speech, bradycardia, muscle twitching, seizure, altered LOC

hypotension and prolonged QT

• -a form of VT where the ventricular rate is so fast that the QRS has a sawtooth appearance
• -there's no CO so hemodynamics become compromised quickly

• -a form of polymorphic VT
• -direction of QRS complex rotates
• -"twisting of the points"
• -ventricular rate is faster than in monomorphic VT so HD instability occurs quickly

• -prolonged QT due to 5HT-3 blockers, phenathiazines, quinidine, tricyclics, procainamide, amio)
• -electrolyte disturbances (decreased K, Mg, or Ca)
• -bradycardia
• -liquid protein diet

• -meds used to treat monomorphic VT can cause torsades
• -treat underlying causes
• -Mg
• -overdrive pacing
• -CV but torsades will likely recur if precipitating factors are not corrected
• -isopril (pharm overdrive pacing)
• -lido or phenytoin in select cases

• -ventricles just quiver
• -haphazard depolarization of the ventricles
• -no P or QRS

• coarse- large waves
• fine- small waves

Coarse.  Fine VF is the most common cause of sudden cardiac death in pts after an acute MI

• CPR
• defib at 200J- 300J- 360J
• vasopressin
• amio
• lido (indeterminate class)

• -AKA asystole
• -absence of all electrical activity in the ventricles
• -may get just P waves (due to advanced AV block preceding)

acidosis, hypoxia, hyperkalemia, hypothermia, drug OD

• -treat underlying cause
• -CPR
• -epi, TC pacing, and atropine may be tried

• -SA or AV node dysfunction
• -chronic bifascicular block
• -post MI
• -arrhythmia avoidance
• -hypersensitive carotid sinus syndrome

• -VT or VF
• -low EF (<35%)
• -cardiomyopathy
• -long QT

• -Lithium battery generates an impulse, goes from the battery to the wires and leads, stimulates the endocardial cells, and creates a wave a depolarization in myocardium.
• -Circuitry senses spontaneous electrical activity in the heart.

• 1st letter- chamber paced
• 2nd- chamber sensed
• 3rd- response of the pacer to sensed signal (inhibit, trigger, or dual)
• 4th- adaptive abilities (can vary with metabolic needs)
• 5th- anti-tachycardia capabilities

The ventricles are not depolarized simultaneously.  Usually the RV is depolarized before the LV.  

• pacer fires at same time as normal electrical impulse, both impulses reach ventricle at
• same time and a fusion beat is the result, thus QRS has characteristics of paced and
• native beat

• -heart does not respond to pacer stimulus
• -see a pacer spike with no P wave or QRS

• -tip of electrode is not in contact with endocardium 
• -tip is in an area of infarct 
• -inadequate electrical current

minimum amt of current required to stimulate the heart

• -pacer does not sense native beats
• -EKG shows a pacer spike that occurs earlier than it should 

• -tip of electrode not in contact with endocardium
• -sensitivity set too low
• -PM in asynchronous mode meaning sensing is turned off

• -unipolar caudery
• -RF ablation
• -MRI
• -lithotripsy
• -radiation therapy

CV implantable electronic device

• -operative team and CIED team collaborate to determine best plan of action for the pt
• -we need to tell the CEID team about the procedure type and anatomic location, type of cautery to be used, where we'd likely place the bovie pad, and exact location where the surgeon will be using the mono polar unit

Monopolar as the current flows thru the pt's body to a bovie pad.

Bipolar causes no electromagnetic interference unless it's placed directly on the device

• -device inhibition
• -reset of pulse generation

• -maintain a distance btw current path of bovie and
• pulse generator of > 6 inches
• -place bovie below umbilicus
• -minimize length of use of cautery to 5
• sec or less