Bradyarrhythmias Flashcards
What is a bradyarrythmia?
How are they categorized & what are the types?
HR less than 60 bpm
- Categorized based on level of disturbance
- SA node
- AV node
- His-Purkinje system
- Types of bradyarrhythmias
- sinus bradycardia
- sinoatrial node dysfuntion & blocks
- atrioventricular blocks
- 1st, 2nd Mobitz I and II, 3rd degree
Describe the clinical presentation of a bradyarrhythmia
- range from asymptomatic to critical
- sometimes dependent on bradyarrhythmia
- sinus bradycardia often asymptomatic, complete heart block symptomatic
- Most common presentation is
- fatigue
- shortness of breath
- dizziness
- Severe symptoms
- syncope
- chest pain
- heart failure
- sudden cardiac arrest
- Exam findings are often vague and vary with severity of symptoms
- HR is slow, pulses may be weak
- level of consciousness may be impaired in severe cases
- ECT imperative as first order of testing
What are the work-up steps for a patient presenting with a bradycardia?
- ECG to assess rate and rhythm
- stop any offendign agents
- beta-blockers, nondihydropyridine calcium channel blockers, digoxin
- Check Thyroid stimulating hormone (TSH)– low
- Transthoracic echocardiography
- assess structural integrity of myocardium & valves
- assess synchrony of ventricular wall contractions
- are the atria & ventricles talking to each other?
- Outpatient holter monitor, event monitory or loop recorder
- some rhythms may take months to capture
- exercise stress test - heart should respond appropriately by increasing
- help evaluate if patient needs to be evaluated for a pacemaker
- EPS study
- how the electrical activity of the heart is working in that patient
The treatment of bradycardia depends on what factor?
if they are stable or unstable
What is the treatment workup for an unstable patient with bradyarrhytmia with & without evidence of a MI?
- Unstable without evidence of myocardial infarction
- atropine & dopamine
- transplanted hearts will not respond to atropine due to vagus nerve denervation
- in ineffective, temporary transcutaneus pacing should be initiated
- atropine & dopamine
- Unstable with evidenc of myocardial infarction on EKG
- urgent catheterization
- inferior MI can cause intermittent heart blocks due to stunning of the SA node
- often resolves after a few days post-cardiac catheterization or permanent if there is damage to the conduction system
- urgent catheterization
- Any symptomatic bradycardia should be evaluated for temporary or permanent pacemaker placement
Fill out the blanks on the provided flow chart
What is sinus bradycardia?
Clinical Presentation?
Cause?
Treatment?
- HR less than 60 bpm with normal PR interval
- Clinical presentation
- responds appropriately to exercise if physiologic
- seen in young, healthy individuals and athletes, awake or asleep
- can be pathologic in persons w/ underlying diseases with vague symptoms
- dizziness, fatigue, dyspnea with exertion, chest pain, heart failure
- Cause
- can be caused by medications that slow the HR
- beta-blockers incuding topical, non-dihydropyridine calcium channel blockers, amiodarone
- can be caused by medications that slow the HR
- Treatment
- if asymptomatic, no treatment necessary, Monitory for symptoms
- If on medicatoins that slow HR, consider decreasing if HR gets below 50 bpm
- screen for OSA (sleep apnea) in obese who have night time bradycardia & pauses
What is Sinoatrial (SA) Node Dysfunction?
Clinical patterns on ECG?
Treatment?
- Inability of the SA node to generate a HR that meets the physiologic demands of the individual
- often called sick sinus syndrome if symptomatic
- Incidence increases witha ge and accounts for 1/2 of pacemaker implantation
- clinical patterns on ECG
- persistent or episodic sinus bradycardia that does not increase with exercise
- sinus pauses greater than 3 seconds in duratin
- combination of both is common
- in symptomatic patients, pacemaker is definitive treatment
What is Tachycardia-Bradycardia (Tachy-Brady) Syndrome?
In what situations does it most commonly occur?
How is it treated?
- Inappropriate alternation beween atrial arrthmias with concamitant sinus node dysfunction
- typically atrial fibrillation is the atrial arrhythmia
- often with long pauses or sinus arrest after termination of AF
- Often induced by treatment of AF
- high doses of bet or calcium channel blockers induce secondary SA node dysfunction
- Treatment with pacemaker placement
What are Sinoatrial Exit Blocks?
What are the 3 different types & how would they present on an ECG?
Why is there not complete asystole?
Cause?
Treatment?
- Failure of SA node depolarization to reach the atria
- Transient are often asymptomatic or cause syncope (b/c long pause/moment of asystole, so they could lost blood flow to the brain)
- 3 different types
- 1st degree: not seen on ECG
- 2nd degree: intermittent absent P-waves
- 3rd degree: complete abscence of P-waves on ECG with sinus arrest
- Junctional escape beats prevent complete asystole
- arise from the AV junction/bundle of His between 40-60 bpm
- Cause:
- excessive vagal stimulatin, acute myocarditis, MI or atrial fibrosis (anything that scars the pathway between the SA & AV nodes)
- Drugs: quinidine, procainamide, flecainide, digitalis
- Treatment
- same for sinus bradycardia with pacemaker placement in higher blocks
What are AV Conduction Disturbances?
Where can it occur?
What are the 3 different categories?
Causes?
- Slowed or complete block of conduction of the atrial impulse to the ventricle
- can occur at the AV node, His bundle or bundle branches
- prolonged PR interval greater than 200ms in most cases when impulse conducted
- Categoreis
- 1st degree: conduction time prolonged but all impulses conducted
- 2nd degree:
- Mobitz Type I: progressive lengthening of conduction time (PR interval) until an impulse is not conducted (QRS)
- Mobitz Type II: repetitive sudden block of conduction of an impulse. No prior measurable lengthening of time
- 3rd degree: no impulses conducted
- Both 1st & 2nd degree can be seen in normal, healthy childen & healthy athletic adults
- Causes
- inceased vagal tone
- druge side effets: dignoxin toxicity, beta and calcium channel blockers
- Acute MI (especially inferior MI)
- Congenital
- Infections: syphilis, lyme disease, mononucleosis
- Sarcoidosis, amyloidosis
- Aging and degenrative disease
What class of drug is Digoxin?
What is it used for?
Class V antiarrhythmic
used in atrial fibrillation & systolic congestive heart failure with reduced EF
shortens atrial & ventriculat refractory periods
increases vagal affects at hte AV node
What are the typical ECG changes that are seen with digoxin use?
- Downsloping ST depression
- “salvador dali moustache” sign
- Flattened, inverted or biphasic T waves
- Shortened QT interval
** does not indicate toxicity
What are the symptoms of Digoxin Tocity?
What ECG changes can you expect to accompany Digoxin toxcity?
- Symptoms
- Gastrointestinal
- Nausea, vomiting, anorexia, diarrhea
- Visual
- blurred vision, yellow/green discoloration of vision, halos
- Cardiovascular
- palpitations, syncope, dyspnea
- Neurological
- confusion, dizziness, delirium, fatigue
- Electrolyte imbalances particularly hyperkalemia
- Gastrointestinal
- ECG features
- can cause many different dysrhythmias
- 2 classic arrhythmias
- SVT due to increased automaticity
- Slow ventricular response due to decreased AV conduction
- Other arrhythmias with digoxin toxicity
- frequent PVC
- sinus bradycardia
- slow atrial fibrillation
- any type o AV block
- ventricular tachycardia
What things can induce digoxin toxicity?
Treatment?
- higher doses of medication
- bolus a patient to get the medication in their system & decrease to a maintance dose (if not done properly, medication can build up in their system)
- Renal clearance
- at certain decline of kidney function, the medicine may not be cleared
-
Treatment: digifab
- binds to digoxin & removes it from the system
What are the characteristics of a 1st degree AV block?
ECG findings?
Treatment?
- ECG
- PR interval > 0.20s
- every impulse conducted
- a P with every QRS
- Treatment
- does not need immediate treatment
- stop or reduce dose of offending agents
- very low progression to complete heart block
What are the characteristics of a 2nd degree AV block - Mobitz I?
ECG findings?
It is commonly seen in what scenarios?
Treatment?
- ECG
- gradual prolongation fo impulse (PR-interval) until the impulse drops off
- there is a QRS associated with every P unitl the dropped impuse
- QRS is typically notmal (unless BBB present) indicatign location at the AV node above this His bundle
- often seen in inferior MI and is transient and does not require pacemaker
- Treatment
- stop or reduce offending agent
- monitoring for symptoms in healthy patients without underlying heart conditions
- often not symptomatic & no treatment warranted unless concurrent bundle branch block in the elderly with underlying heart disease
- can progress to complete heart block
- treatment similar to mobitz 2
What are the characteristics of a 2nd degree AV block - Mobitz 2?
ECG findings?
It is commonly seen in what scenarios?
What additional concerns can this cause?
- ECG
- repetitive sudden block of conduction of an impulse
- 2:1, 3:1, 4:1, pattern
- P is not always associated with QRS, but P waves in regular pattern
- QRS slightly wider indicating block in His-Purkinje
- Associated more with anterior MI and often is not transient wiht high rate of mortality
- Additional Concerns
- high rate of progression to complete block
- may manifest in Adam-Stroke syndrome
- periodic fainting spell due to heart block that results in loss of spontaneous circulation adn inadequate cerebral perfusion
How do you differentiate atrial flutter from 2nd degree Mobits II AV block?
a flutter never go down to an isoelectric line
How do you differentiate Mobits II AV block from complete heart block?
Mobitz: regular, consistent P wave with no QRS
Complete heart block: P waves are everywhere
What are the characteristics of a 3rd degree (complete) AV block?
ECG characteristics?
Origination?
- No atrial activity is conducted to the ventricles
- atrial & ventricles are controlled yb independent pacemakers (complete AV dissociation)
- ECG
- P-waves are not in regular pattern, sporadic
- origination
- atrial pacemaker can be sinus or ectopic
- ventricular focus typicaly right below the block
- closer to HIS bundle are most stable with faster rates than further in the ventricle
- ventricular rte is often below 40 bpm
What are the guidelines for prescribing a temporary pacemaker?
-
symptomatic sinus bradycardia, 1st degree AV block or Mobitz II 2nd degree AV block
- with HR (<50) and SBP <80 unresponsive to drugs
- Mobitz II 2nd degree AV block
- 3rd degree AV block
- bilateral BBB (regardless or age)
- alternating BBB
- RBBB with LPFB
- RBBB or LBBB
- with first degree AV block
- Asystole
** BBB = branch bundle block
Describe the most common pacing combos utilized in pacemakers
- VVI mode:
- basic single-chamber ventricular mode
- (ie. atrial fibrillation w/ high AV block)
- AAI mode:
- the correspondign single-chamber atrial pacing mode
- (ie. SA node dysfunction with intact AV node conduction)
-
DDD mode is the dual chamber atrial and ventricular pacing mode
- ability to “track” intrinsic atrial activity so that a ventricular beat follows each P wave in order to maintain AV synchrony
- Atriventricular pacing preferred to avoid asynchrony and pacemaker syndrome
Describe the characteristics of the ECG that indicate it is from a ventricular paced pacemaker?
How could it be mistaken?
spike before the QRS, indicating there is an electrical charge stimulating the ventricles to contract
sometimes easy to miss if you think the spike is an R wave, but if you look below you can see the spike
What are the possible pacemaker complications?
- Sensing malfunction
- Battery depletion
- Lead fracture or Lead failure
- Pacemaker Syndrome
- due to asynchronous atria & ventricles
- Fatigue, dizziness, syncope
- Will see neck pulsations (cannon a-waves)
- indicative of atrial contraction against a closed tricuspid valve
- Preventable by dual chamber pacemaker
- avoid VVI
