Tachyarrhythmias Flashcards
1
Q
What is a normal heart rate range?
What qualifies as tachycardia?
What qualifies as bradycardia?
A
Normal: 60-100 bpm
Tachycardia: greater than 100 bpm
Bradycardia: less than 60 bpm
2
Q
What are the inherent pacing rates of automaticiy for the following foci?
SA node
Atria
AV node/junction
Ventricle
A
- SA node rate
- 60-100 bpm
- Atria automaticity rate
- 60-80 bpm
- AV node/junction rate
- 40-60 bpm
- Ventricular rate
- 20-40 bpm
3
Q
What are the steps to evaluating a normal EKG?
A
- Rate
- find QRS that aligns with dark line on ECG, then cound “300, 150, 100, 70…”
- Look to see if there are P waves in front of QRS
- are they upright?
- How far are they from the QRS
- Are there T waves?
- how far are they from the Q?
- are they upright?
- Look to see if rhythm looks regular
- Check out the axises
4
Q
What are the characteristics that define tachyarrhythmias?
A
- Identified by location where foci originate
- sinus node (SA) vs atrial ventricular (AV) node
- supraentricular vs ventricular
- most are propagated through reentry pathways
5
Q
What is the difference between anatomical and functional reentry circuits?
A
- Anatomic
- by-pass tracts (accessory pathways)
- pathways you have been born with and are not necessarily present in everyone
- they can bypass the normal conduction pathway & create a circle pathway on their own
- Functional
- microcircuits in areas of the heart
- w/ Afib, there is a lot of small foci throughout the atria & the form their own circular pathway
6
Q
What is the dominant mechanism for supraentricular tachycardis & ventricular tachycardia?
What does it require?
A
Reentry
Requires bifurcating pathways of different velocities adn refractory periods
OR
accessory pathway
7
Q
Describe what is happening in this image
A
- A
- Normal conduction pathway
- A: long, fast pathway
- refractory to come up to normal is slower
- B: short, shlow pathway
- going back to normal is faster
- the impulses that split at the top will meet down at the distal common pathway to continue its course
- sometimes it can go back up retrograde
- when the retrograde pathway meets the slow pathway, they usually cancel each other out & you don’t have any problems
- B
- if there is a block in the fast pathway that interrupted the course
- the slow pathway made it to the bottom first and was able to go up through the faster pathway & get back up before it was fully refractory, starting the reentry circuit
8
Q
Supraventricular tachycardia is what type of tachycardia?
How common is it?
How are they classified?
What is the most common site of origin?
A
- narrow complex tachycardia
- most common of in all age groups
- classification depends on
- site of origin, nature of arrhythmia or mechanism
- Origin (most commonly above bundle of His):
- SA node, atrium, AV node and proimal bundle of His
- automaticity, triggered or reentrant mechanism
- some wide complex tachycardias can be supraventricular
- Origin (most commonly above bundle of His):
- site of origin, nature of arrhythmia or mechanism
9
Q
What are the type of supraventricular tachycardia?
A
- sinus tachycardia
- AV node reentrant tachycardia (AVNRT)
- AV reentrant tachycardia (AVRT)
- SA nodal reentrant tachycardia (SANRT)
- junctional tachycardia
- atrial fibrillation
- atrial flutter
- multifocal atrial tachycardia (MAT)
10
Q
What are the risk factors for supraventricular tachycardia?
A
- Sympathomimetic use
- caffein overdos, alcohol us, tocabo use
- beta adrenergic medications used in asthma or COPD
- Illicit drugs such as methamphetamines and cocaine
- ADHD medications
- other medications or supplements that can increase heart rate
- OTC cold medications containing phenylephrine or pesudophedrine
- Fat burners or pre-work out supplements
- phentermine for weight loss
- digoxin toxicity
- Underlying medical conditions
- hyperthyroidism, catecholamine producing tumors, previous MI
- Stress, emotional upheaval or tiredness less commonly
- congenital or acquired reentrant pathway, icreased automaticity
11
Q
What is the clinical presentation of supraventricular tachycardia?
What is the first thing you need to differentiate?
A
- Need to differentiate stable from unstable
- may be asymptomatic & incidental finding on ECG or exam
- most commonly atrial fibrillation
- Sudden onset of palpitations is most common complaint
- shortness of breath (mild to severe)
- chest pain
- dizziness
- syncope
- diaphoresis
- acute heart failure
12
Q
What is the initial workup for a patient presenting with supraventricular tachycardia?
A
ECG
13
Q
Identify the differential diagnosis for each of the provided scenarios
A
- Narrow
- Regular
- Sinus tachycardia
- physiologic sinus tachycardia
- inappropriate sinus tachycardia
- AVNRT
- AVRT
- Focal AT
- Atrial flutter
- Junctional tachycardia
- SANRT
- rarely ventricular tachycardia
- Sinus tachycardia
- Irregular
- AF
- Multifocal AT (or sinus tachycardia with frequent atrial ectopy(
- Focal AT with variable AV block
- Atrial flutter with variable AV block
- Regular
- Wide
- Regular
- Monomorphic VT
- Any SVT with aberrant conduction, ventricular pacing, preexcitation, certain antiarrhythmic medications, or significant electrolyte abnormalities
- antidromic ARVT with antegrade AV conduction via accessory pathway (WPW syndrome)
- Irregular
- AF, atrial flutter, or focal AT with aberrant conduction
- AF, atrial flutter or focal AT with antegrade conduction via accessory pathway (WPW syndrome)
- Polymorphic VT (including torsade de pointes)
- Ventricular fibrillation
- Antidromic AVRT due to nodoventricular/nodofascicular accessory pathway with variable VA conduction
- Regular
14
Q
What is the next work up step following the EKG?
If there are no abnormalities?
If there are?
What labs are you ordering?
A
- If no abnormalities / symptoms are intermittent can proceed to further work-up outpatient
- If abnormality found on EKG
- abnormal rhythm shoudl be treated & further work-up postponed until patient is stable
- Labs
- electrolytes
- thyroid functin
- anemia if suspect substance abuse (CBC)
- urine drug screen
15
Q
Describe the appropriate cardiac monitors to precribe for out-patient work up
A
- Cardiac Monitors
-
Holter monitor
- continuous ECG monitors
- Not patient activated
- but patients should write down when they have symptoms
- Short duration of use (24-48hrs up to 2 weeks)
- for use of daily or every other day symptoms
- Event monitors
- patient activation recording
- if symptom happens at night, you may miss a recording
- longer duration of monitoring sometimes up to 1 month
- patient activation recording
- Mobile Cardiac Telemetry
- Both patient activation and set parameter auto-trigger (HR, length of a pause, etc.)
- Can be used for longer monitoring (30+ days)
- Loop Recorder
- implanted under the skin (usually over the heart)
- can be work 2-3 years
-
Holter monitor
16
Q
Describe the possible out-patient work up procedures that can be used in addition to cardiac monitoring
A
- Echocardiogram
- rule out any structureal abnormalities and assess myocardial wall function/ejection fraction
- Exercise Testing to induce exertional arrhythmias or underlying CAD
- Electrophysical Study (EPS)
- invasive, multipolar electrode catheter based study of area suspected to contain the reentry pathway to evaluate for or induce arrhythmia at time of study
- complications: myocardial perforation with cardiac tamponade, pseudoaneurysms at arterial access site adn provocation of nonclinical arrhythmias
- invasive, multipolar electrode catheter based study of area suspected to contain the reentry pathway to evaluate for or induce arrhythmia at time of study
- Direct cardiac mapping
- potentials recorded directly from the heart are spatially depicted as functin of time in an integrated manner
17
Q
What is the treatment for active, current supraventricular tachycardia?
A
- In stable patients, you can do a vagal maneuver, carotid massage or cold water/ice on face
- in older people must ensure no carotid artery disease prior to carotid massage
- Adenosine can also be used if initial maneuvers are unsuccessful (into large vein)
- 6mg x1 and may repeat at 12 mg x2
- If adenosine does not work can use IV beta-blockers or non-dihydropyridine CCB (verapamil, diltiazem)
- Class III or Clas IC drugs can be used as alternatives
- Caution in WPW as can precipitate VF (choose procainamide or amiodarone)
- If continued arrhythmia or patient become unstable, immediate direct current cardioversion with sedation required
18
Q
What is the treatment for chronic intermittent supreventricular tachycardias?
A
- Chronic pharmacological suppression in mild, less frequent cases “pill in the pocket”
- oral beta-blockers, non-dihydropyridine calcium channel blockers, class IC antiarrhythmic drug flecainide typically used
- Cryoablation or radiofrequence catheter ablation in recurrent, severe cases is definitive treatment
19
Q
Describe the characteristics of Sinus Tachycardia
Rate?
ECG findings?
Causes?
Clinical presentation?
Treatment?
A
- Rate: 100-180 bpm
- P-wave before every QRS with stable PR interval
- Causes vary but include
- excessive caffein use
- Illicit drug use
- Normal resonse to exercise
- pulmonary emboli
- hyperthyroidism
- stress/andiety disorders
- pheochromocytoma
- sepsis
- Presentation
- gradual onset & termination
- In patients with underlying coronary artery disease (CAD) can precipitate chest pain
- Treatment
- typically aimed at cessation of of offending agends or target underlying disease
- beta-blockers or nondihydropyridine calcium channel blockers may be used to decrease heart rate
- Ivabradine has been usefulin patients with inappropriate or refractory sinus tachycardia
20
Q
Describe the characteristics of Premature Atrial Complexes
Origination?
How common are they?
ECG?
Causes?
Clinical Presentation?
Treatment?
A
- Origination
- originate froma ny area of the atrium
- Frequency
- most common cause of irregular pulse & palpitations
- common in normal hearts & increase with age
- ECG
- P-wave is typically different from teh p-wave of the dominating rhythm indicating different focus or origin
- P-R interval can often exceed 120 ms
- non-conducted PACs can often be buried in the T-wave if occurrign late int eh cardiac cycle
- P-wave is typically different from teh p-wave of the dominating rhythm indicating different focus or origin
- Cause - may situations
- infection
- inflammation
- MI
- anxiety
- excessive caffeine
- illicit drugs
- Clinical features
- can precipitate the occurrence of SVT
- Treatment
- do not generally require therapy except in symptomatic persons, then beta blocker or calcium channel blocker can be attempted
21
Q
Describe the characteristics of Atrial Flutter
Rate?
How common are they?
Origination?
ECG?
Causes?
A
- Rate
- 250-350 bpm
- Frequency
- less common than atrial fibrillation
- Origination
- Reentrant tachycardia in the right atrium
- use 2 similar circuits clockwise (upright waves) or counterclockwise (inverted waves) around the tricuspid annulus
- rates and flutter pattern consistent and predictable
- Reentrant tachycardia in the right atrium
- ECG
- Regulat “saw-tooth” flutter waves without isoelectric wave between flutter waves
- seen best in II, III, aVF, or V1
- Atrial conduction to ventricular conduction
- Regulat “saw-tooth” flutter waves without isoelectric wave between flutter waves
- Causes
- reentry without significant heart disease
- septal defects
- pulmonary emboli
- mitral or tricuspid stenosis and regurgitation
- heart failure
- scaring from previous ablations
- aging
- toxic & metabolic derangements
- thyrotoxicosis, alcoholism, pericarditis
22
Q
What are things to be aware of during an physical exam on a patient with atrial flutter?
A
- anxious patient
- may be hypotensive
- rapid flutter waves in the jugular venous pulse
- palpable pulse is typically regular
- EKG consistent with regularly regular sawtooth flutter waves
23
Q
Treatment/Management for Atrial Flutter?
A
- Carotid massage or adenosine can slow rate but rarely terminates
- Acute therapy: rate vs. rhythm
- early restoration of sinus rhythm preferred
- IV beta or calcium channel blockers, amiodarone, digoxin
- if pharmacological agents not tolerated, direct cardioversion
- If rhythm initiated by acute event (sepsis, surgery, etc) treatment for up to 1 month
- Therapy for transient, chronic episodes
- long term oral beta-blocker, calcium channel blocker, amiodarone, flecainide, sotalol
- similar to treatment for trial fibrillation
- requires anticoagulation
- definitive treatment is catheter ablation
24
Q
Describe the characteristics of Atrial Fibrillation
Clinical Presentation?
ECG?
Causes?
Treatment?
A
- Clinical Presentation
- chaotic atrial rhythm relted to continuous, variable activation of the atria
- recurrent, paroxysmal, perisistent or permanent
- ECG
- irregularly irregular QRS comlplexes on ECT with no distinct P-waves
- rates are variable & can fluctuate widely
- Cause
- higher risk with age & other chronic conditions
- can be heriditary
- Treatment
- similar to atrial flutter
- anticoagulation based on risk for stroke
- CHADS2
- CHA2DS2-VASc
25
Describe the ECG characteristics of Focal Atrial Tachycardias (FAT)
* ECG
* irregularly irregular rath WITH visible P-waves
* Atrial rates of 150-200 bpm
* P-wave contour typically differrent from that of sinus P-wave
* those AT with foci near SA node may resenble sinus P-wave
* there are isoelectric intervals between P-waves (unlike A-flutter)
* positive or biphasic P-wave in V1=left atrial focus
* negative P-wave in V1 = right atrial focus
* can occur in short, recurrent bursts with spontaneous termination
26
Describe the clinical presentation fo FAT.
What is the managment?
* _Clinical Presentation/Exam_
* Often occur in patients with CAD, HF, corpulmonale, digitalis toxicity
* Symptoms correlate to underying cause
* chest pain
* shortness of breath
* palpitations
* presyncope
* stimulants can provoke episodes
* Physical exam findings:
* variable rhythm on auscultation
* cariable intensity of S1 on auscultation
* variable systolic blood pressure
* Patient may anxious only or exhibit signs of heart failure
* _Management_
* carotid masage and adenosine typically do not terminate arrhythmia but can slow AV conduction and ventricular rate
* If digoxin toxicity, replace K if low and reverse digoxin with DIGIfab
* Beta-blockers or calcium channel blockers to slow ventricular rate initially
* Class IA, IC, or III drugs as add ons
* Catheter ablation generally effective
27
Describe the characteristics of Multifocal Atrial Tachycardia (MAT)
ECG?
Clinical presentation?
Treatment?
* ECG
* Marked variation in P-wave morphology
* Very irregular P-P intervals and variable P-R intervals
* Atrial rates between 100-130 bpm
* Most P-waves are conducted o the ventricles
* Clinical presentation
* occurs in teh elderly with COPD & CHF
* May transition to AF
* seen more frequently when theophyline was used for severe COPD
* Treatment
* directed at underlying disease
* antiarrhythmic drugs often ineffective at slowing the rate
* beta blockers should be avoided in patients with bronchospasm pulmonary disease but can be effective if tolerated
* calcium channel blockers (verapimil) and amiodarone are useful
* ablation may be effective in some cases
28
Describe the characteristics of Atrioventricular Nodal Reentry Tachycardia (AVNRT)
ECG?
Origincation
Clinical presentation including symptoms?
Treatment?
* ECG
* HR between 150-280 bpm
* P-waves buried in QRS complex but when visible are positive & narrow appearing
* Origination
* reetry circuit located within the right atrium or AV node
* Clinical presentation
* most common form of reentry SVT
* often triggered by PAC and PVC less commonly (1/3)
* paroxysmal, more common in women (~75%)
* categorized as slow-fast (90%- top ECG) or fast-slow (~10%- bottom ECG) depending on which reentry pathway is activated
* Symptoms
* sudden onset, rapid regular palpitations
* may have sudden fall in BP with presyncope or syncope
* may have chest pain and shortness of breath
* Treatment
* vagal maneuvers, carotid massage
* adenosine, beta-blockers, calcium channel blockers if nonresponsive to adenosine
* class III (amiodarone) or class IC agents can be used
* catheter ablation definitive treatment
29
Describe the characteristics of Atrioventricular Reentry Tachycardia (AVRT)
Origination?
ECG?
Clnical presentation?
Treatment?
* Origination
* Accessory pathway that connects the atrium or AV node to the ventricle outside the normal AV nodal His-Purkinje conduction system
* Accessory pathway can conduct anterograde (antidromic) and retrograde pathway (orthodromic)
* retrograde or orthodromic pathway is the most common
* ECG
* RP- interval is often short, rate is 200-300 bpm and regular
* antidromic will have wide QRS due to abnormal ventricle depolarization from accessory pathway
* Clinical Presentation
* symptoms when activated are palpitations, dizziness, presyncope/syncope, chest pain
* physical exam
* unvarying, regular ventricular rhythm, with constant intensity of the first heart sound and blood pressure
* jugular vein may show larger A wave
* Treatment
* similar to AVNRT except with antidromic reentry pathway, consider class IC and III antiarrhythmics
* DC cardiovert is unstable or refractory to medications
* ablation definitive therapy
30
What is Wolfe-Parkinson White Syndrome?
Origination?
How common is it?
Clinical features?
Treatment?
* Origination
* Congenital accessory pathway: bundle of Kent
* as the pathwy goes through the ventricle & bypasses the AV node it excites the ventricle first (delta wave)
* Common
* Prevalence 1:1000
* Clinical features
* sudden onset & termination
* symptoms similar to AVNRT
* Treatment
* acute episode caution using adenosine, beta-blockers or Ca-channel blockers
* can cause decompensation
* chronic suppression with class IA, IC or III agents
* medication side effects
* ablation curative 95%
31
What ECG features would you see on an asymptomatic atient with WPW?
What are the other general characteristics of WPW on ECG?
* Asymptomatic
* delta waves on ECG
* WPW Pattern (type A- top image; and B- bottom image)
* A: large R wave in V1
* B: deep S wave in V1
* have good prognosis & rarely need treatment
* Characteristics of WPW on ECG
* PR interval less than 120 miliseconds durign sinus rhythm
* QRS complex duration exceeding 120 miliseconds with a slurred, slowly rising onset of the QRS in some leads (delta wave) and usually a normal terminal QRS portion
* ST-T wave discordant changes
* Ventricular rates of 150-250 bpm with regular rhythm
32
What is the major risk associated with WPW?
Treament?
Prevention?
* Risk
* High risk or progression to ventricular fibrillation
* must avoid adenosine, beta-blockers, digoxin or non-dihydropyridien calcium-channel blockers
* Treatment
* Unstable requires immediate cardioversion
* Can use procainamide IV to terminate arrhythmias
* Prevention
* Waiting for ablation can use oral class IC or III antiarrhythmic drugs
* IC: flecainide, propafenone
* Class III: amiodarone
* ablative therapy is curative
33
What are ventricular arrhythmias?
Origination?
Types?
* Wide complex tachycardias
* Origination
* do not depend on SA node, AV node or atrium
* similar physiologic mechanism as SVT
* reentrant most common
* Types
* monomorphic ventricular tachyardia (including ventricular flutter)
* polymorphic ventricular tachycardia (Torsade de Pointes)
* Ventricular fibrillation
34
What constitututes a Pre-ventricular contraction (PVC)?
Clinical Presentation?
ECG features?
* less than 4 consecutive extrasystole contractions originating from the ventricle
* Clinical presentation
* frequently found in excessive sympathomimetic (caffeine/tobacco) agent use
* may feel like heart sipped a beat
* do not require work up
* frequent PVVs seen on monitory or ECG in persons with structural heart disease can be concerning
* ECG
* wide QRS complex
* Treatment
* cessation of offendign agents
35
What constitutues ventricular tachycardis (VT)?
Clinical features/origination?
Types?
* 4 or more consecutive beats that origiinate from the ventricle
* Clincal features
* rate must be at least 100 beats per minute
* trigger by similar mechanism as other tachyarrythmias
* **reentry**, enhanced automaticity or triggered activity
* reentry typically around area of prior MI scar
* Types
* nonsustained VT (NSVT)
* lasts _less than 30 seconds_
* does not require intervention due to hemodynamic instability
* otherwise is called sustained VT
* monomorphic VT
* sometimes includes ventricular flutter
* polymorphic VT
* torsades de pointes
36
What are the risk factors for ventricular tachycardia?
* Acue MI
* chronic ischemic heart disease
* structural cardiad disease
* dilated cariomyopathy, reduced ejection fraction HF, hypertrophic cardiomyopathy (HCOM), inherited arrhythmogenic cardiomyopathy, chagas heart disease
* inherited channelopathhies
* long QT syndrome (LQTS)- defibrilator at young age
* brugada syndrome
* electrolyte abnormalities
* magnesium, calcium, potassium
* Infiltrative disease
* sarcoidosis, amyloidosis
* congenital heart disease
* HOCM
* drugs that prolong the QT interval
* certain antibiotics, antiarrhythmics, antipsychotics and antidepressants
37
The following ECG is an example of what type of syndrome?
Long QT syndrome
can be inherited or acquired from long-term use of drugs known to cause Long QT-syndrome
38
The following ECGs are an example of what type of syndrome?
Brugada Syndrome
inherited disease
Type 1 is most common- sometimes mistaken for a heart attack
39
What are the symptoms of ventricular arrhythmisa & what should you be looking for onteh physical exam?
* Symptoms
* shortness of breath
* chest pain
* palpitations
* syncope or presyncope
* malaise
* exertional symptoms
* sudden cardiac arrest
* Physical exam
* often non specific findings
* tachycardia typically greater than 100 bpm
* marked fluctuations in blood pressure
* difficulty differentiating heart sounds due to rate of tachycardia but may vary in intensity
* cannon "A" waves
40
The provided ECG show what cardaic condition?
regular appearing rhythm, wide complex
41
Describe the characteristics of monomorphic ventriculat tachycardia (MMVT)
Origination?
ECG?
Clnical presentation?
* Origination
* usually originate from the saem area of the ventricle
* Clinical features
* beats appear to be identical
* ventricular flutter may be included
* rates a greater than 300 beats per minute
* ECG
* SVT may appear as wide complex tachycardia in some cases
* with aberrancy in bundle branch blocks
* accessory pathway such as WPW syndrome
* can use Brugada slgorithm to determine origin of wide complex tachycardias
42
What is the treatment for monomorphic VT?
* Acute MMVT treatment per ACLS protocol
* After acute treatment
* treat underlying cause
* electrolyte replacement, cardiac cath if MI
* echocardiogram to assess underlying structural disease
* may consider cardiac MRI if suspect infiltrative cause
* holter monitor
* stress test if suspect is underlying CAD but without acute MI
* electrophysiological studies with possible ablation
* suppression with oral antiarrhythmics
* beta-blocker, amiodarine, sotalol
* consider ICD in those high risk patients
43
Describe the characterisitcs of Polymorphic VT (Torsadees de Pointe)
* ECG
* undulatign baseline with varying QRS complexes
* like a ribbon being twisted
* unstable rhythm, often progresses to Vfib
* Clinical Presentation
* associated with electrolyte imbalance, specifically hypomagnesium
* patient may be responsive or unresponsive
* Symptoms
* extreme palpatations
* chest pain
* shortness of breath
* dizziness
* syncope
* confusion
* hypotension
44
What is treatment for polymorphic VT?
* Magnesium
* Unstable PVT WITH a pulse, follow ACLS protocol
* If no pulse, go straight to pulseless ACLS resuscitation protocol
45
The provided ECG is an example of what cardiac condition?
polymorphic VT into ventricular fibrillation
46
The provided ECG is an example of what cardiac condition?
Ventricular Fibrillation
47
What is ventricular fibrillation & what is the treatment?
* Erratic irregular rhythm with no meaninful cardiac output
* Requires immediate CPR & initiaion of ACLS resuscitation protocol
* Start CPR
* shock
* epinephrine
* Causes vary but often fatal
