W6 Arrhythmias (See Study Guide) Flashcards
Week 6 study guide
Make sure you know these
How do pacemaker APs and cardiac muscle APs differ?
Driven by?
Which channels?
RMP?
No. Of phases?
SA: 60-100 bpm (primary pacemaker)
AV: 40-60 bpm
Below: 20-40bpm
pacemaker
—funny current
—Na+ channels
—unstable RMP -60 - -55
—3 phases
cardiac
—ventricle muscle cells
—NO funny Na+ channels
—RMP -90mV
—4 phases
—NO automaticity
—need stimulus
No static resting voltage of -90 mV
They have gradual depolarization of phase 4 of the action potential caused by current through slow Na channels which drives the cell to an action potential threshold of ~ -40 mV
Upstroke of the AP is caused by slow inward Ca movement
Repolarization occurs by K efflux (to -60 mV)
Automatic cells — rates of firing for:
SA node
AV node & bundle of his
Purkinje
How do APs spread?
—SA node is the dominant pacemaker cell: 60 - 100 bpm
—AV nodal area and Bundle of His: 40 - 60 bpm
—Purkinje Fibers: 30 - 40 bpm
**Myocardial cells have gap junctions where action potentials spread
What regulates the SA node automaticity?
—SA node automaticity is regulated by the autonomic nervous system
—Sympathetic stimulation stimulates the SA node and heart rate increases
—Parasympathetic activity, the vagus nerve, controls the heart rate at rest and therefore reduces the heart rate
Tachyarrhythmias
What is the HR?
What are the THREE reasons they occur?
Explain them briefly (each have their own card)
-
Abnormal automaticity
—latent pacemaker cell develops intrinsic rate that is faster than the SA node — it is outpacing the SA node, not b/c SA node failed
—catecholamine surge / hypoxia / Ischemia / electrolyte imbalance / drug toxicities
—ectopic beat if singular and ectopic rhythm is persists
—different looking P wave : there will be a P wave but it won’t look like the SA node P wave
—“that patient had a lot of ectopy” = there are a lot of ectopic beats -
Triggered activity
—additional AP triggers an additional DEpolarisation during REpolarisation -
Re-entrant
—electrical impulse circulates repeatedly around a re entry path and depolarises that cardiac tissue
—triggered by a PAC.
A) bidirectional flow reentrant circuit as seen in AV node reentrant tachycardia (AVNRT)
B) accessory path reentrant circuit: Wolff-Parkinson White Syndrome
Tachyarrhythmias: triggered activity
What are the 2 types
What can triggered beats cause?
early after depolarisations:
—occur before repolarisation has finished (partial blockade of Ik)
—prolong the action potential
—hence QT interval on EKG predisposes someone to early afterdepolarisation 🔑 (takeaway)
delayed after depolarisations:
—occur after membrane potential has returned to normal (from raised intracellular Ca2+ such as 🔑 digitalis toxicity)
—fairly uncommon
triggered beats can cause torsades de pointes
Difference between an escape beat and an escape rhythm
If the SA node is suppressed or fails to fire, a latent (backup) pacemaker takes over to control the next heartbeat. This is called an ESCAPE BEAT.
If the backup pacemaker cell persists, this is an ESCAPE RHYTHM.
We know this one is a ventricular rhythm b/c there is not a P wave
What does the top image depict?
What about the bottom image?
Top image
—prolonged QT
—eyeball R-R, T wave should fall under that halfway mark
—cautious about what medications you give that patient
Bottom image
—premature ventricular complex on the T wave
— “R on R wave phenomenon”
—leads to Vfib
—when a PVC lands on a T wave, it happens in clinical practice
—this happens when you blindly cardiovert someone, you have to sync first before you shock someone
Tachyarrhythmias: re-entrant
What is this?
What are the two types?
An electric impulse circulates repeatedly around a reentry path and therefore recurrently depolarizes that region of cardiac tissue
-
AV node reentrant tachycardia (AVNRT):
—Bidirectional flow reentrant circuit
—impulses goes round and meet at AV before going down, sometimes one will go faster than the other, go round one half of circle, the other slower one finally reaches (PAC) but doesn’t go down the bundle of His, instead keeps looping round and round the atria
—need to PAC to come in and go down the slow pathway, reaches the AV node but ventricle isn’t ready to depolarise but it can go back up the fast pathway
—fast pathways take longer to repolarise
—slow pathways repolarise quicker
47 minute audio. Slide 22 -
Wolff-Parkinson White Syndrome
—refers to the presence of a congenital accessory pathway (AP) and episodes of tachyarrhythmias. The term is often used interchangeablely with pre-excitation syndrome
—PR interval < 120ms
—Delta wave: slurring slow rise of initial portion of the QRS
—QRS prolongation > 110ms
—Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major component of the QRS complex)
Treatment: bradyarrhythmias (2 meds)
Discuss the pharm and pacemaker options
Pharmacologic Therapy
—modifies autonomic input
—Anticholinergic Drugs reduce the vagal effect and increase heart rate (atropine: works for AV node and up but not as successful for junctional/ventricle)
—Beta-1 Receptor Agonists (Isoproterenol) mimic catecholamines and increase heart rate
Electronic Pacemakers
—apply electrical stimulation to the heart to initiate depolarizations at a desired rate and therefore assume control of the rhythm
—Temporary: external pads or indwelling transvenous pacemaker (not very reliable, match w/ pulse)
—Permanent: sense activity and pace when needed. The bullet looking one is the “micra”. Often pacemaker leads get staph infections on them, layered with endothelial tissue, have to take it out, treat them and put it back in. The Micra just slides into the RV
Treatment: tachyarrhythmias
4
Cardioversion & defibrillation
Pharm therapies
Vagotonic maneuvers
Catheter ablation
-
Cardioversion and Defibrillation
—terminate the arrhythmia.
—depolarize the bulk of the myocardium
—interrupt reentrant circuits
—establish electrical homogeneity ➡️ SA node to take over.
Cardioversion:
—synchronizing the electrical discharge to the QRS complex. Don’t want R on T phenomenon
—good for: flutter, AVNRT, AVRT (elective treatment, sedated).
—Check for a clot w/ TEE for flutter/afib, or anticoag for 3w before procedure so it doesn’t cause a stroke.
Defibrillation:
—terminates ventricular fibrillation but is asynchronous as there is no organized ventricular activity
Implantable Cardioverter Defibrillators
—monitor for abnormal activity and can appropriately shock if necessary to terminate a ventricular arrhythmia. Usually less energy as internal.
Pharmacologic Therapy
—aims to alter the underlying mechanism: automaticity, reentrant circuit, or triggered activity
Vagotonic Maneuvers
—focus on increasing transmission of impulses through the AV node, which is sensitive to vagal stimulation, to slow conduction and terminate reentrant rhythms.
—carotid massage and bearing down.
Catheter Ablation
—burn responsible myocardium/tissue/circuit by radiofrequency to permanently fix the disturbance.
—99% success rate
What is sinus arrhythmia?
Beat to beat variation in the P to P interval producing an irregular rate, or R-R
—Sinus arrhythmia is a normal, physiological phenomenon commonly seen in young, healthy people
—Heart rate varies due to reflex changes in vagal tone during the respiratory cycle
—Inspiration increases the heart rate by decreasing vagal tone
—Expiration restores the vagal tone and decreases the heart rate
Sinus bradycardia
Firing of the SA node < 60 bpm
—At rest, sleep , or in a highly trained athlete with elevated vagal tone = normal and benign finding
Pathologic disease results from
—Intrinsic SA node disease → aging or diseases affecting the atrium such as ischemia and cardiomyopathy
—Extrinsic SA node disease → suppress SA node activity and include drugs (beta blockers) and metabolic causes (hypothyroidism, hypothermia, OSA)
—Usually asymptomatic however can cause dizziness or syncope and require treatment (CO = HR x SV)
—can give atropine
—B1 agonist
Junctional escape beats/ rhythms
Escape beats and rhythms
—cells in the AV Node/Junctional and His-Purkinje system are capable of automaticity
—can take over for the SA node if the SA node is impaired or there is a conduction block of the impulse from the SA node.
Junctional (AV) Escape Beats or Rhythms
note: junction means AV
—⭐️normal, narrow QRS complex with a rate of 40-60 bpm.
—⭐️ NO P waves b/c impulse originates below the atria.
—Can see retrograde P waves as the impulse travels from the AV node backwards to the atrium to depolarize it.
—P waves follow the QRS complex and are inverted indicating activation of the atrium from an inferior direction (before the T wave).
in the image attached, no P wave, narrow QRS, slow, regular = junctional
Ventricular escape beats and rhythms
Characterised by what on EKG?
Rates?
—characterized by wide QRS complexes
—slower rates of 30-40 bpm because outside the normal conduction system, have to go cell by cell via gap junctions.
—the complexes are wide as the ventricles are not depolarized from the normal rapid and simultaneous conduction over the right and left bundle branches but rather from a more distal point in the conducting system.
—Ventricular myocardium or purkinje fibers
—If originates in the left bundle, it produces a RIGHT BUNDLE BRANCH block/pattern because the impulse depolarizes the LV first then spreads more slowly to the RV
—If originates in the right bundle, it produces a LEFT BUNDLE BRANCH block/pattern as the impulse depolarizes the RV first then spreads to the LV
Distinguish between RBBB and LBBB
RBBB
RR’ in V2
Slurred S wave in V6
LBBB
Scooped Rs in V5/V6
Why do escape rhythms happen?
What might a patient feel?
Causes?
—protective backup rhythms that maintain HR and CO when the sinus node or normal AV conduction fails.
—dizzy or have syncope associated with hypotension
Causes can be:
—Intrinsic including aging, calcified conduction system, ischemia, and cardiomyopathies
—Extrinsic including medications that suppress conduction or metabolic (hypoxic, hypothermia, hypoglycemia, OSA)
Escape rhythms — treatment 5
—Remove aggravating factors or treat underlying cause
—If at the AV node or higher, can give atropine (anticholinergic)
—B-Adrenergic agent like Isoproterenol
—Temporary pacing
—If the condition can not be corrected, placement of a permanent pacemak
First degree AV block
3 EKG characteristics
—Prolongation of the normal delay between the atrial and ventricular depolarization
— = PR prolongation (> 0.2 seconds/5 little boxes).
—1:1 relationship between P and QRS complexes remains.
The impairment is caused by:
—Transient reversible causes such as heightened vagal tone, AV nodal ischemia, drugs that suppress the AV node (BB, CCB< digoxin, antiarrhythmics)
—Structural defects resulting from a myocardial infarction or chronic degenerative disease of conduction
Generally a benign, asymptomatic condition
Second degree AV block
Mobitz 1 (Wenckeback)
=INTERMITTENT failure of AV conduction
—resulting in some P waves not followed by a QRS complex.
Two kinds:
Mobitz I and Mobitz II
Mobitz I (Wenckebach) block:
—PR interval gradually increases with each beat until an impulse is completely blocked such that a QRS does not follow a p wave for a single beat.
—Results from impaired conduction in the AV node
—Typically benign and and seen in children, trained athletes, and people with high vagal tone (sleep apnea).
—No treatment is necessary.
summary
—The P to P interval remains relatively constant
—The greatest increase in the PR interval duration is typically between the 1st and 2nd beats of the cycle
—The R to R interval progressively shortens with each beat of the cycle
The pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3, or 5:4
Second degree AV Block
Mobitz II
EKG characteristic
Associated with?
Possible etiologies ?
Treatment?
—sudden intermittent loss of AV conduction WITHOUT preceding gradual lengthening of the PR interval.
—It may persist for two or more beats indicating high grade AV block.
—Usually caused by conduction block beyond the AV node (bundle of his or Purkinje system) and is associated with a BBB
—severe structural disease such as an infarction, idiopathic fibrosis or calcification, autoimmune or infiltrative disease, inflammatory conditions from infection (rheumatic fever, lyme, myocarditis), post cardiac surgery, drugs (BB, CCB)
—Can progress to third degree block without warning therefore
—treatment is with a pacemaker
second image
—2:1 AV block w/ evidence Mobitz I in past telemetry
—if no evidence of Mobitz I in past, probably Mobitz II
—need long strip
—p wave, QRS, T wave, P wave and then nothing
Summary
—The PR interval in the conducted beats remains constant
—The p waves “march through” at a constant rate
—The RR interval surrounding the dropped beat is an exact multiple of the preceding RR interval (double the preceding RR interval for a single dropped beat, triple for 2 dropped beats, etc)
Third degree heart block
—P and QRS is dissociated
—atria and ventricles beat independently
—P waves march out at a rate higher and unrelated rate to QRS complexes
—need pacemaker
—may progress to ventricular standstill and sudden death
Note these are all bradyarrhythmias
Note these are all tachyarrhythmias
Wide QRS: Ventricular
Narrow QRS: supraventricular
If it’s irregular : Afib (no distinct p waves)
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What is this?
—SA node discharge > 100 bpm
—normal P waves and QRS complexes
Results from:
—increased sympathetic activity and is an APPROPRIATE physiologic response to exercise or pathologic conditions.
Treatment
—🔺treat the underlying cause including: hyperthyroidism, fever/sepsis, hypoxia, anemia, pain, and hypovolemia.
Note the difference between atrial flutter and atrial fibrillation
Flutter
—These can form thrombi/clots
—🔺Stroke risk🔺
—150 bpm could be flutter, that would be running at 300 bpm in the atria.
—remember the atria circuit rate does not translate down to the ventricles because of the refractory AV node.
Afib
—originates around the pulmonary veins, often.
—Tx can involve ablating around the pulmonary veins
What is atrial flutter?
What is the rate for a 2:1 block
3:1 blocks?
Symptoms ?
EKG characteristics?
Caused by counterclockwise reentry circuit in the right atrium. (Can also have circuits in the left atrium(.
The atrial rate is 180-350 bpm however the AV node is refractory to most impulses to slow the ventricular rate. Typically this is a fraction of the atrial rate.
Example if the atrial rate is 300 bpm:
2:1 block = 150 bpm
3:1 block = 100 bpm
Symptoms
—dizziness, palpitations, or dyspnea.
EKG/Telemetry:
—Typically a regular rhythm
—Typically a narrow complex QRS
—Has a 🔺SAW TOOTH🔺 pattern due to the atrium depolarizing throughout the cycle
Usually occurs in people with preexisting heart disease. May be paroxysmal (occurs on and off), persistent (lasing days to weeks), or permanent.
Difficulty seeing flutter w/ 2:1 AV conduction
Giving adenosine shows the flutter waves well but stopping the QRS, lasts 6 seconds, patient feels awful but you can see 2:1 conduction
Atrial flutter EKG pattern?
SAW TOOTH
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What is this?
Atrial flutter
4:1 block
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What is this rhythm?
Atrial flutter with 3:1 block
saw tooth pattern
Atrial flutter
Medical management?
Hypotension🚨 vs normotensive [know]
🚨if HYPOTENSIVE and in rapid atrial flutter, immediate cardioversion 🚨
If normotensive:
Rate control with
—AV nodal blocking agents: BB, CCB, digoxin
Rhythm Control
—Anti-arrhythmics (class IA, IC, III) 💊amiodarone = superior to all others! Remember this med
—Cardioversion (rule out clot with TEE prior to shock)
—Ablation
—Burst pacing (if have a pacemaker)
—Need to discuss anticoagulation given the elevated risk of thrombus and STROKE
What is Afib?
What is the rate?
What disease processes responsible?
What do you see on EKG?
What is the Tx?
Chaotic, irregular rhythm with an atrial rate so fast (350 - 600 bpm) p waves are not discernible on the EKG.
Most commonly seen in disease processes that enlarge the atrium including:
—hypertension
—valvular disease
—sleep apnea
—heart failure
—CAD
EKG:
—Irregular, irregular with NO p waves and a variable ventricular rate
Treatment is the same as atrial flutter but ablation less successful (80%).
Other options:
—MAZE procedure where multiple incisions in both atria prevent the formation of reentry circuits
—AV node ablation is utilized when rhythm control and rate control fails. Induces heart block therefore a pacemaker is required.
Studies
AFFIRM TRIAL: in patients with nonvalvular atrial fibrillation, there is no survival benefit between rate and rhythm control
CHADS-VASc score: clinical prediction tool for estimating the risk of stroke. The score is used to determine whether or not anticoagulation or antiplatelet therapy is required.
Patho
—Many of the impulses encounter a refractory AV node and therefore only some will depolarize the ventricles giving the characteristic “irregular, irregular” rhythm.
—The mechanism involves multiple, wandering reentrant circuits within the atria with ENLARGED ATRIA increasing the potential for it to occur.
—Rapid rates can decrease cardiac output (decrease LV filling) and increase the risk of stroke due to the formation of thrombi from blood stasis.
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Which rhythm is this?
AFIB
No P waves
Variable ventricular rate
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What rhythm is this?
What could you treat it with?
AFIB
No P waves
Variable ventricular rate
Rate control them!
What is an aberrant conduction?
What do you see on EKG?
Ventricular conduction disturbance where an impulse is blocked due to the ventricular system not being repolarized in time to accept the impulse.
Results in a wide QRS of either a LBBB or RBBB appearance.
This is afib with an aberrant beat
—then a wide QRS complex, sometimes called PVCs but it’s an aberrantly conducted rhythm
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What rhythm is this?
Afib with aberrant beat
Watchman
—patients can’t be on anticoagulants, high fall risk, older, bleeding etc
—watchman device: occlude the left atrium appendage percutaneously, via femoral artery, b/c this is where thrombi typically form
—it will endothelialise over. Could still develop a clot but it won’t get out.
Paroxysmal Supraventricular Tachycardia (SVT)
QRS characteristics?
Setting of?
Clinical features?
Which 2 mechanisms?
—sudden onset and termination of a narrow complex tachycardia
—atrial rates between 140 - 250 bpm.
—setting of exertion, high stress states, stimulants, alcohol, and hyperthyroidism.
Clinical features
—Sudden onset of rapid palpitations with anxiety and shortness of breath.
—Can cause dizziness form a drop in blood pressure. If the patient has underlying CAD, can cause angina
—Typically well tolerated and rarely life threatening
—rarely includes syncope
two mechanisms
-
Reentrant Tachycardia (AVNRT):
—Dual pathway AV node with a slow and fast pathway. —Usually stimulated by a premature atrial contraction encountering a refractory fast pathway and going down the slow pathway.
—Once down the slow pathway, the fast pathway is repolarized and accepts the impulse propagating it backwards to the atrium and creating a reentrant circuit.
—regular narrow complex QRS tachycardia
—p waves may not be apparent because retrograde atrial depolarisation occurs simultaneously with ventricular depolarisation -
Atrioventricular Reentrant Tachycardia (AVRT):
—Has an accessory pathway that connects the atrial and ventricular tissue separately from the normal conduction system.
—During sinus rhythm, activation of the ventricle through the accessory pathway causes a characteristic SHORT PR INTERVAL (ventricular stimulation is earlier than through the AV node) and a WIDE QRS with a DELTA WAVE (ventricular activation is slower than through the purkinje fibers)
During the tachyarrhythmia -> regular, narrow complex tachycardia with retrograde p waves if conduction goes down the AV node first and then back up the accessory pathway.
If the impulse goes down the accessory pathway first, the QRS is wide and difficult to distinguish from Ventricular Tachycardia.
Premature Atrial Contraction / Ectopic Beat
—beat comes in early
—different P wave morphology
—pause after PAC because the AV node was refractory and not ready for the SA node’s impulse
⭐️Blocked PAC
Aberrant conduction
Blocked PACs
—Sometimes PAC comes in too early and AV node not ready
—P waves w/ NO QRS
—P wave will look different than SA node P wave
—you would give this patient a BB, even though the patient has a HR in the 40s. BB will stop the PACs
Aberrant conduction
—conducts through the AV node BUT hits parts of the conduction pathway that are refractory or damaged.
—might just go down one bundle branch and then SLOWLY go round the other side via gap junctions
— = wide QRS
—aberrant on the first arrow, not on the second arrow, it went through, you can tell because the QRS is like the rest, not wide, it conducted
—notice the T wave on the first arrow is probably burying a P wave because it’s pointier.
[SKILSS OSCE]
What is this?
Ectopic rhythm
Pacemaker pacing
—steps in if the natural conduction fails
—you‘ll see a P wave after the spike (atrial pacing)
—ventricle is sensing = it didn’t need to pace the ventricle
—when spike is before the QRS, the pacemaker has paced for the ventricles.
—if a spike is before the P wave and QRS, it’s pacing the atria and ventricles
—wide QRS
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What is this?
AVNRT
Little tiny p-wave RIGHT after the QRS
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What is this?
AVNRT
Narrow complex QRS
Hard to see p waves or inverted
AVRT
What three things are you looking for on EKG?
—delta wave (WPW)
—orthodromic: goes through AV node, then back up : retrograde p waves. 95% of case
—antidromic: goes through AP first then back up the AV node: retrograde p waves. Wide QRS
WPW Treatment
—Preferred agents: Class IA and IC antiarrhythmics — sodium channel blockers which SLOW accessory pathway conduction (procainamide) OR class III antiarrhythmic (Ibutilide) that prolong refractoriness in the accessory pathway and terminates the arrhythmia
—Pharmacologic treatment is more CAUTIOUS than AVNRT
—AV nodal blocking agents (BB, CCB, digoxin) block conduction through the AV node but are LESS EFFECTIVE at the accessory pathway
—They can SHORTEN the refractory period of the accessory pathway and SPEED conduction and increase ventricular rates, especially during atrial flutter/fibrillation
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What is this?
Which med to treat?
[know]
WPW
Memorise
Treatment: procainamide
Tachycardia
Accessory pathway, or bundle of Kent
Patch of conducive tissue
Bypassing AV node
Allows impulses to arrive soon
Pre-excitement
Shortened PR interval
Ventricular depolarisation happens slower, hence slurring, delta wave
WPW > develops into tachycardia, and is AVRT, can be orthodromic or antidromic
Watch video on slide 88
SVT: AVNRT/AVRT
Treatment:
—Increase vagal tone by Valsalva or carotid massage
—AVNRT: IV Adenosine which affects the AV node and aborts the abnormal rhythm (AVNRT), v. Bradycardia, dizzy, nauseous, short half life, temporary. Hopefully circuit breaks and SA node takes over and reboot the heart. Can slow flutter down so you can see the saw tooth pattern. So it can be diagnostic
—AVRT, WPW: procainamide
—IV AV nodal blockers including BB, CCB, and digoxin to break the rhythm
—Prophylactic therapy with oral AV nodal blockers
—Ablation is curative but has a small risk of pacemaker dependency.
Atrial tachycardia
—Typically results from increased automaticity of an ectopic atrial site
—Usually paroxysmal and of short duration. If prolonged, can cause palpitations, anxiety, shortness of breath, dizziness, or angina (if have underlying CAD).
EKG:
—Looks like sinus tachycardia but the P WAVE MORPHOLOGY IS DIFFERENT indicating depolarization of the atrium from an abnormal site.
—Typically caused by elevated sympathetic tone
—Treatment: Same as SVT with BB, CCB, digoxin, or anti-arrhythmics. Can also perform an ablation of the abnormal foci. Vagal maneuvers typically do not work.
[know]
Narrow QRS tachycardia treatment
3
Is pretty much always:
BB
CCB
OR Digoxin
Give a little first and see
Even if you don’t know the rhythm, always these three meds!
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What is this?
Atrial tachycardia
Narrow complex QRS
P wave hidden in T wave
But looks different than first 2
Single foci
When they break, there’s a little pause and sinus resumes
Multifocal Atrial Tachycardia
Rhythm
Morphology
Rate
EKG shows:
—Irregular rhythm
—Multiple P waves (at least three different morphologies)
—Rate > 100 bpm
—Caused by abnormal automaticity in several foci of the atrium
—MOST OFTEN OCCURS IN PULMONARY DISEASE and states of HYPOXIA.
Treatment is aimed at the underlying disease process but can use CCB and digoxin.
Avoid BB if severe COPD.
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What is this?
MAT
Remember MAT >100
Wandering < 100 (think about wandering around being slower)
What is tachy-Brady syndrome?
—Combination of slow and fast dysrhythmias secondary to to atrial fibrosis that impairs the SA NODE and predisposes (usually) to ATRIAL FIBRILLATION or FLUTTER.
—During the tachyarrhythmia, overdrive suppression of the SA node occurs
—Tachycardia then terminates followed by period of profound sinus bradycardia
Treatment: combo of antiarrhythmic drug to suppress the tachyarrhythmia PLUS a permanent pacemaker to prevent bradycardia
What are the ventricular arrhythmias
—Ventricular Premature Beats
—Ventricular Tachycardia
—Ventricular Fibrillation
—Torsades de Pointes
Wide complex QRS are much more dangerous than supraventricular tachycardias often leading to cardiac arrest and death.
Questions:
Wide or narrow?
Hypotension?
Premature Ventricular Contraction
—Occurs when a ventricular foci fires an action potential
—Appears as a wide QRS beat (impulse travels from the ectopic foci through the ventricles via slow cell to cell connections rather than the purkinje system). The ectopic beat is NOT associated with a preceding p wave.
—Can be asymptomatic and benign to concerning in patients with underlying structural heart disease, CAD, or Heart Failure
—Usually no treatment is necessary. If symptomatic with palpitations, can order a BB. If have underlying heart disease, could indicate a worsening prognosis
—QRS is wide (> 120 msec) with an abnormal morphology
—Premature -> occur before the next provided impulse
—Discordant ST segment and T wave changes
—Termed bigeminy if every other beat is a PVC.
—Termed trigeminy if have 2 normal beats followed by a PVC (pattern)
—Consecutive PVC’s are couplets if 2 in a row; triplets if 3 in a row
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What is this?
Trigeminy
PVC
Ventricular Tachycardia
—More than three consecutive PVCs is defined as ventricular tachycardia.
—Further divided by time.
—If it persists for > 30 seconds, it is termed SUSTAINED VT. —Self terminating runs < 30 seconds are termed NONSUSTAINED VT.
—Can be MONOMORPHIC (most common) where every QRS complex appears the same and is a regular rate.
—Can be POLYMORPHIC where the QRS complexes continually change in shape and the rate varies from beat to beat (includes torsades)
Ventricular tachycardia
Mechanisms
Mechanisms:
1. Enhanced automaticity
2. Enhanced trigger activity
3. Re-entry
Causes of VT usually indicate a structural abnormality to the heart that promotes a reentrant circuit including a myocardial scar from a prior heart attack, cardiomyopathy, LV dysfunction, channelopathies (Brugada syndrome, Long QT Syndrome). and ongoing ischemia.
Electrolyte abnormalities, certain drugs, and hypothermia can prolong the QT and predispose to VT
Ventricular Tachycardia
Clinical presentation
Clinical presentation: depends on the RATE of the tachycardia, DURATION, and underlying CONDITION of the heart.
Sustained VT at a rapid ventricular rate typically causes
—low cardiac output
—hypotension
—syncope,
—pulmonary edema.
—it can progress to CARDIAC ARREST and death.
If sustained VT is relatively slow (< 130 bpm) it may be tolerated and only cause palpitations.
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What is this
Ventricular tachycardia
Ventricular tachycardia
Management
Acute?
If hemodynamically stable? Which two drugs?
ACUTE treatment is ELECTRICAL CARDIOVERSION.
—If hemodynamically stable:
—can try antiarrhythmic drugs (amiodarone, lidocaine, or procainamide).
—Sustained VT can cause low cardiac output, hemodynamic instability, and progress to ventricular fibrillation and death.
—Once stable and in a NSR, evaluate for underlying causes such a ischemia, LV dysfunction, electrolytes, drug toxicities).
—Consider ICD Placement
Is this an SVT w/ abberancy or VT?
—🔺VT until proven otherwise
—VT is VERY wide, SVT is not AS wide
—in VT, there is AV dissociation, ventricle is just firing off impulses
—in SVT, impulse is still doing from atria, there should still be a P wave in there somewhere
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What is this?
Torsades
Torsades de Pointes
Triggered in patients with?
“Twisting of the points” is a form of polymorphic VT that presents with varying amplitudes of the QRS as if they were twisting around a baseline.
—Results from early afterdepolarizations (triggered activity)
—in patients that have a PROLONGED QT INTERVAL (longer action potential)
Causes include:
—drugs that block potassium currents (anti-arrhythmics)
—electrolyte disturbances (HYPO-kalemia/magnesiumia)
—persistent bradycardia
—hypothermia
—channelopathies (long QT syndrome)
Torsades de Pointes
Symptoms
Treatment
Can be self limiting and asymptomatic to more sustained with symptoms of dizziness and syncope. It can degenerate into ventricular fibrillation.
Treatment:
—If hemodynamically unstable, cardiovert
—IV Magnesium (decreases Ca influx which decreases early afterdepolarizations)
—Treat the underlying cause
—Preventive strategy is to shorten the QT by increasing the heart rate (Isoproterenol, pacemaker)
—Consider an ICD
Ventricular Fibrillation
Treatment
Disorganized, rapid stimulation of the ventricles with NO COORDINATED CONTRACTIONS.
Life threatening arrhythmia with cessation of cardiac output and death if not reversed.
Occurs typically in patients with significant structural heart disease including MI
EKG:
—Chaotic, irregular appearance without discrete QRS waveforms
Treatment:
—Only effective treatment is prompt electrical defibrillation.
—Once in a stable rhythm, treat underlying or culprit causes.
—IV antiarrhythmics to prevent further occurrences.
—Patients will need an ICD if no reversible cause.
[SKILLS OSCE]
What is this
How do you treat ?
Vfib — defibrillate
Pass out
Low blood pressure
Cardiac arrest
Ventricles not squeezing any blood out
Code blue
Brugada Syndrome
What is it?
What is the typical EKG pattern?
How do you unmask this pattern?
—Autosomal dominant mutation in a sodium channel gene
—can cause life threatening POLYMORPHIC VT or VF in young, otherwise healthy people
(someone died young in the family)
CLUE: specific EKG pattern in
—V1-3 of a prominent ST elevation.
—Pattern may persist or be intermittent.
—If intermittent, can be unmasked by administering sodium channel blocking antiarrhythmic drugs
ICD often required to prevent SUDDEN DEATH
Congenital long QT syndrome
Prolonged ventricular REPOLARIZATION which can lead to polymorphic VT (torsades)
Mutations can occur in multiple genes and prolong the action potential duration
—ENHANCE the depolarizing Na ion channel current
—IMPAIR the repolarizing K current
The degree of QT prolongation is a predictor of arrhythmic risk
Can be ASYMPTOMATIC and only be discovered by an abnormal EKG Or sudden death in family
~450 is normal
Female 460
Male 440
Above 500 is concerning
Inherited Arrhythmia Disorders
Others present with syncope, torsades, or sudden death
LQT1 and LGT2 mutations cause ventricular arrhythmias more with exercise and emotional stress while LQT3 occur during rest or sleep
Other triggers include: HYPOkalemia, HYPOmagnesemia, HYPOcalcemia, and drugs that prolong the AT (including many antiarrhythmics)
BETA BLOCKERS REDUCE the risk of arrhythmias even though they do not shorten the QT interval
High risk patients will get an ICD
