SM 135a - Bradycardia Flashcards
How can you distinguish 2nd degree AV block type I and type II?
- 2nd degree type I
- Delay gets progressively longer
- Dropped beats
- 2nd degree type II
- Fixed delay
- More dropped beats than type I
What is more dangerous: a heart block at the AV node or a heart block at the His-Purkinje system?
A block at the His-Purkinje system is more dangerous; It indicates a significant structural abnormality
(2nd degree type II and 3rd degree AV blocks occur at the level of the His-Purkinje system)
List 4 major causes of disorders of impulse initiation (intrinsic SA node dysfunction)
Sinus bradycardia
Chronotropic incopetence
Tachy-brady syndrome
Sinus arrest
What are some possible symptoms of bradycardia?
Syncope
Presyncope (dizziness)
Poor exercise tolerance/fatigue
Congestive heart failure
No symptoms (possible presentation)
Describe the ECG manifestations of 1st degree heart block
1st degree heart block = AV block
- Beats are not dropped, but there is a delay between AV and ventriclular depolarization
- PR interval >200 ms
As heart rate increases, the dominant pacemaker within the SA node shifts ____________
As heart rate increases, the dominant pacemaker within the SA node shifts cranially
What is chronotropic incompetence?
Inadequate cardiac response to exercise
Maximum HR <80% of predicted max HR with exercise (220 - age)
On an ECG you see progressive shortening of the PP interval until one sinus pause is an exact multiple of the base PP interval
What is causing this?
2nd degree Type II AV block
Describe the ECG manifestations of sinus bradycardia
- Normal P-wave axis
- Every P-wave is followed by a QRS complex
- HR <60 BPM
What causes 1st degree AV block?
AV block = 1st degree heart block
May be caused by…
- Increased parasympathetic (vagal) tone
- AV node scarring
Describe the ECG manifestations of bradycardia-tachycardia syndrome
Alternating blocks of atrial bradycardia and tachycardia
What are the two major causes of intrinsic SA node dysfunction?
Disorders of impulse initiation (phase 4 depolarization)
Failure of conduction out of the SA node (Heart block)
Define bradycardia
Resting HR <50 BPM
How does catecholamine stimulation affect the rate of phase 4 depolarization in pacemaker cells?
Catecholamine stimulation increases the rate of phase 4 depolarization
-> increases rate of upstroke -> increaes heart rate
(Ex: Exercise)
How is intrinsic SA node dysfunction treated?
Pacemaker
Which heart blocks can be classified as “AV delay”
1st degree AV block
2nd degree type I AV block
What causes high-grade (3rd degree) AV block?
aka Complete Heart Block
- Occurs at the level of the His-Purkinje system
- There is no conduction from the atria to the ventricles
- QRS complexes come from subsidary or “escape” pacemakers
- Junctional (40-60 BPM) engages His-Purkinje
- Ventricular (20-40 BPM) spreads through gap junctions, causing a wider QRS complex
- QRS complexes come from subsidary or “escape” pacemakers
Define SA node dysfunction
Resting HR <40 BPM
OR
Pauses of >3 seconds between QRS complexes
Note: resting HR <40 may be normal in sleeping athletes
List 5 major causes of extrinsic SA node dysfunction
Medications
Electrolyte abnormalities
Severe hypotension
Severe hypoxemia
Hypothyroidism
A patient with high-grade AV block has normal-width QRS complexes on an ECG.
What is responsible for these QRS complexes?
What would you expect this patient’s heart rate to be?
A junctional escape rhythm is responsible for these QRS complexes. Depolarization engages the His-Purkinje system. This is fast, causing a normalQRS complex
You would expect heart rate to be 40-60 BPM
Describe the ECG manifestations of SA exit block
- Normal P-wave axis
- Progressive shortening of the PP interval until…
- One P-wave fails to conduct(2nd degree Type I block)
- The sinus pause is an exact multiple of the base PP interval (2nd degree Type II block)
In a complete heart block, there is no conduction from the atria to the ventricles.
Where do QRS complexes come from?
In complete heart block, QRS complexes come from subsidary or “escape” pacemakers
- Junctional escape rhythm
- 40-60 BPM
- Engages His-Purkinje
- Normal width of QRS complex
- Ventricular escape rhythm
- 20-40 BPM
- Spreads through gap junctions
- Wider QRS complex due to slow conduction
How does vagal stimulation affect the rate of phase 4 depolarization in pacemaker cells?
Vagal stimulation slows the rate of phase 4 depolarizaiton
-> decreases rate of upstroke -> decreases HR
List 4 major causes of heart block (failure to conduct signals out of the SA node)
Age-associated fibrosis
COronary arteriosclerosis
Fibrosis related to hypertension or diabetes
Any cardiovascular disease
A patient with high-grade AV block has wide QRS complexes on an ECG.
What is responsible for these QRS complexes?
What would you expect this patient’s heart rate to be?
A ventricular escape rhythm is responsible for these QRS complexes. Depolarization spreads through gap junctions. This is slower, causing a wider QRS complex
You would expect heart rate to be 20-40 BPM, due to slower conduction
Which AV blocks require implantation a pacemaker?
Why?
2nd degree type II and 3rd degree
These blocks occur at the level of the His-Purkinje system
On an ECG you see progressive shortening of the PP interval until one P-wave fails to conduct
What is causing this?
2nd degree Type I AV block
Describe the ECG manifestations of sinus arrest
- Normal P-wave axis
- Every P-wave followed by a QRS complex
- Pauses of >3 seconds without atrial activity (No p-waves)
What medications might cause extrinsic SA node dysfunction?
Beta blockers
Ca2+ channel blockers
Digoxin
Anti-arrhythmic drugs
How is extrinsic SA node dysfunction treated?
Remove the source
(ex: discontinue medication, fix electrolyte abormality, treat hypotension, hypoxemia, hypothyroidism)
