Lecture 8 - Cardiac Pacemaker Mechanisms Flashcards
What is the primary pacemaker with the fastest inherent beating rate?
SA node!
What are the latent/ectopic (subsidiary) pacemakers? When do they come into play?
Atrial and Ventricular
- come into play when SA Node malfunctions
How are pacemakers arranged in the heart?
ANATOMICALLY
What is the hierarchy of anatomical pacemakers and what is it based on?
Based on INHERENT BEATING RATE (fastest is first)
- Sa Node
- Latent Atrial Pacemakers
- AV Node/ Bundle of His
- Bundle Branches
- Purkinje FIbers
The SA node pacemaker is primarily based on what?
DIASTOLIC DEPOLARIZATION (Phase 4 of Slow Calcium channels)
What are the 4 mechanisms that underlie SA node pacemaker activity?
- T- type Calcium current
- Hyperpolarization activated inward current (If channel of Na into cell)
- Deactivation of K+ current (IK)
- Inward Na/Ca exchange current activated by intracellular Calcium release
Diastolic depolarization occurs primarily in what two areas?
- SA Node
2. Purkinje fibers
What is the most vital to Purkinje fibers in order to achieve diastolic depolarization?
- If current (funny)
- Deactivation of K+ current (decrease in outward K current means membrane potential becomes more positive & can achieve depolarization)
Diastolic depolarization corresponds to which phase of the slow response Ca release?
Phase 4
What activates the If current?
HYPER POLARIZATION of the cell
What is the function of If channels?
inward Na current, hyper polarization
- controls the SA rate –> thus the CARDIAC RATE
Pacemaker cells upstroke is reliant on what? This is different from non-pacemaker cells how?
- dépendant on CALCIUM
- non-pacemaker cells are only dependent on Na
How does parasympathetic (vagal) and sympathetic stimulation change the diastolic depolarization graph?
- Vagal = decrease slope, - slow HR
2. Sympathetic = increase slope - increase HR
A decrease in K permeability is necessary to achieve Diastolic Depolarization. Why?
decrease in potassium conductance means less( + ) charge leaving the cell
- more positive charge in cell and hyperpolarization activated inward Na channels (If) both contribute to diastolic depolarization
- deactivating K makes Na influx more affective in depolarizing diastolic voltage by decreasing outward positive current
= cell DEPOLARIZES when at threshold
What are the 4 mechanisms responsible for changes in heart rate? (pacemaker cell changes)
- Change in the slope of DIASTOLIC depolarization
- Change in MAX diastolic potential
- CHange in threshold
- Pacemaker shifts - changes in pacemaker site can cause abrupt changes in HR buck of the HIERARCHY of pacemaker activities
How would decreasing and increasing max diastolic potential affect the Heart Rate?
- Decrease max diastolic potential = increase firing = increase HR
- Increase max diastolic potential = decrease firing = decrease HR
How would decreasing and increasing Diastolic threshold potential affect the firing frequency (heart rate)?
- Decreasing = increase firing rate
2. Increase Diastolic threshold = decrease firing rate
Define the following:
When Pacemaker is stimulated (driven) at a frequency HIGHER than its intrinsic frequency,
STOPPING the stimulation results in a temporary SUPPRESSION OF PACEMAKER activity
OVERDRIVE SUPPRESSION
- SA node normally “overdrives” all subsidiary (ectopic0 pacemakers in the heart
- thus suppresses ectopic pacemaker activity
What are the 3 mentioned clinical applications of OVERDRIVE SUPPRESSION?
- SA nodal or AV nodal Block (2nd or 3rd degree block)
2nd = not all P followed by QRS (2:1) 3rd = complete AV nodal block = no consistent P-R interval
- Stopping artificial pacemakers
- Sick sinus syndrome
How do sympathetics & parasympathetics affect AV nodal conduction?
sympathetics INCREASE AV NODAL conduction
- parasympathetics DECREASE conduction
Why does stopping artificial pacemakers bring Cardiac Output to ZERO?
latent pacemakers not at the same speed as SA Node (SA node suppresses electrical activity of other pacemakers)
- thus need to bring pacemaker to rate of latent pacemakers (which are slower than SA node)
How does VAGAL stimulation affect the pacemakers? Norepinephrine? (sympathetic)
- INHIBITS PACEMAKERS within the SA node, atria, and AV nodal regions
- STIMULATE all cardiac pacemakers
How does Vagal stimulation (ACETYLCHOLINE) affect the following:
- K+ permeability
- Adenylate Cyclase activity (cAMP synthesis)
- Slope of diastolic depolarization and maximum diastolic potential?
- INCREASES
- AC activity decreases (less cAMP –> less CA released )
- slope DECREASES and maximum diastolic potential HYPERPOLARIZED (more negative)–> need greater stimulus to reach threshold
- If (Na+) channels only activated at certain (-) value BUT this value has become even MORE negative than threshold
What is Sinus Arrhythmia?
Normal variability in pacemaker cycle length (heart rate) caused primarily by respiratory changes in PARASYMPATHETIC (vagal) nerve activity to SA NODE!!
How does ACETYLCHOLINE affect L-Type Ca2+ current and If current?
INHIBITS L-type Calcium current and If current by inhibiting cAMP synthesis
How is Sinus Arrhythmia in aerobically trained individuals compared to more sedentary individuals?
Sinus Arrhythmia is more pronounced (have lower resting heart rate)
How does Inspiration and Expiration change the cycle length (heart rate)? How is it affected by the parasympathetic activity?
- Inspiration = decreased cycle length (increased HR)
- inhibit parasympathetic nerve activity - Expiration = increased cycle length (decrease HR)
- stimulate parasympathetic nerve activity
How does NE (sympathetic stimulation) affect slow inward L-Type Calcium current? Does it increase or decrease cAMP synthesis?
INCREASE slow inward L-type Ca2+ current and If
- by increasing cAMP synthesis
Does NE increase or decrease the slope of diastolic depolarization?
Increases the slope of Diastolic Depolarization
How does SA node decrease the cycle length upon inspiration and expiration?
VAGAL MODULATION
- inspire = inhibit vagal stimulation
- expire = stimulate vagus
What does SINUS TACHYCARDIA resemble?
looks like SUPRAVENTRICULAR TACHYCARDIA
- appears this way when we exercise
In sinus Bradycardia, what increases on an EKG
- long Q-T interval
= long diastole
What does inotropic mean??
Affecting the contractility of muscular tissue
Is there an RMP in pacemaker cells?
NO!!
- pacemaker cell are never at rest so they do not have a resting membrane potential
What is Sick Sinus Syndrome?
Sick sinus syndrome (SSS), also called sinus node dysfunction (SND),
is an umbrella term for a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the SINUS node, the heart’s primary pacemaker
How does hypokalemia affect HR? It exerts this affect by changing the slope of what? (does it also increase or decrease the slope)
- Latent pacemakers HAVE anomalous rectification: thus during low K extracellularly, this decreases the permeability of K across the membrane and prevents K from leaving the cell
- this allows for the action potential to reach threshold sooner (since it has a more positive threshold) & depolarize QUICKLY
resulting in a quicker AP and an increased SLOPE of diastolic depolarization
LATENT PACEMAKERS overcome the overdrive suppression of the SA node, thus causing a quicker HR due to faster conduction times
(always a transient increase in K+)
What are 3 reasons a slurred QRS can occur?
- Hyperkalemia
- Ischemia
- ventricular Tachycardia
What is a reason for a notched QRS?
Right or Left Bundle Branch block
