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
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
Q
Describe the ECG characteristics of Focal Atrial Tachycardias (FAT)
A
- 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
27
Q
Describe the characteristics of Multifocal Atrial Tachycardia (MAT)
ECG?
Clinical presentation?
Treatment?
A
- 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
Q
Describe the characteristics of Atrioventricular Nodal Reentry Tachycardia (AVNRT)
ECG?
Origincation
Clinical presentation including symptoms?
Treatment?
A
- 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
Q
Describe the characteristics of Atrioventricular Reentry Tachycardia (AVRT)
Origination?
ECG?
Clnical presentation?
Treatment?
A
- 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
Q
What is Wolfe-Parkinson White Syndrome?
Origination?
How common is it?
Clinical features?
Treatment?
A
- 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)
- Congenital accessory pathway: bundle of Kent
- 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%
- acute episode caution using adenosine, beta-blockers or Ca-channel blockers
31
Q
What ECG features would you see on an asymptomatic atient with WPW?
What are the other general characteristics of WPW on ECG?
A
- 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
Q
What is the major risk associated with WPW?
Treament?
Prevention?
A
- Risk
- High risk or progression to ventricular fibrillation
- must avoid adenosine, beta-blockers, digoxin or non-dihydropyridien calcium-channel blockers
- High risk or progression to ventricular fibrillation
- 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
- Waiting for ablation can use oral class IC or III antiarrhythmic drugs
- ablative therapy is curative
34
Q
What constitututes a Pre-ventricular contraction (PVC)?
Clinical Presentation?
ECG features?
A
- 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
37
Q
The following ECG is an example of what type of syndrome?
A
Long QT syndrome
can be inherited or acquired from long-term use of drugs known to cause Long QT-syndrome
38
Q
The following ECGs are an example of what type of syndrome?
A
Brugada Syndrome
inherited disease
Type 1 is most common- sometimes mistaken for a heart attack
40
Q
The provided ECG show what cardaic condition?
A
regular appearing rhythm, wide complex
42
Q
What is the treatment for monomorphic VT?
A
- 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
- treat underlying cause
43
Q
Describe the characterisitcs of Polymorphic VT (Torsadees de Pointe)
A
- 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
45
Q
The provided ECG is an example of what cardiac condition?
A
polymorphic VT into ventricular fibrillation
46
Q
The provided ECG is an example of what cardiac condition?
A
Ventricular Fibrillation
