Cardiac EP Flashcards
What is conduction pathway of the heart?
SA>AV>Bundle HIS> mainstem bundle branch> anterosuperior bundle> posterioinferior bundle> purkinje fibers > right bundle branch
Which parts of conduction pathway represent pacemaker activity?
SA Node and AV node
What factors affect conduction speed of the heart?
membrane excitability (funny sodium channels), size of tissue, CT around heart, and the connexins of gap junctions
What allows for functional syncytium?
desmosomes and gap junctions
Phase 4 in pacemakers
Rest stage pacemakers are unstable, decreased in K+ channel opening, increased Ca transient channels
Phase 0 in pacemakers
open L type calcium channels
Phase 1 in pacemakers
There is no repolarization
Phase 2 in pacemakers
there is no plateu
Phase 3 in pacemakers
L type Ca channels close and K+channels slowly open
Ectopic focus
when purkinje fibers takes over heart activity
Phase 4 in contractile cells
Stable (-90); leaky channels still open
Phase 0 in contractile cells
Funny sodium channels open (fast voltage gated)
Phase 1 in contractile cells
inactivation of Na+ channels and K+ voltage gate channels open
Phase 2 in contractile cells
L type Ca channels open and voltage gated K+ close
Phase 3 contractile cells
L type Ca channels close and leaky K+ channels open
What are 3 effects of Ach on M2 receptors on heart?
- decrease funny sodium channel activation to reduce steepness of phase 4
- Increase potassium conductance to maximize diastolic potential (lets heart fill)
- Decrease transient Ca channels activity reducing phase 4
What are 2 effects of B1 receptors on heart?
- Increases activity funny sodium channels increasing steepness of phase 4
- increase of transient Ca activity which increases steepness of phase 4 and makes threshold more negative
What are 2 adrenergic receptors of the heart?
B1 and B2 which are both Gs coupled which increase AC activity
What is the cholinergic receptor on the heart?
M2 which is Gi and decreases AC activty
period during which the cell membrane cannot be reexcited by an external stimulus, regardless of the level of external voltage applied
Absolute Refractory Period
Period during which only a local response can be produced by a larger than normal depolarizing stimulus. During this period, a propagated AP cannot be generated
Effective Refractory Period
It starts at the end of the ERP. Period during which a propagated AP can be generated with a depolarizing stimulus that is larger than normal
Relative Refractory Period
Short interval during which the cell is more excitable than normal, so a weaker than usual depolarizing stimulus can initiate a propagated AP
Supernormal Period
the period from the onset of the AP to the end of the supernormal period.
Full Recovery Time
How is excitation and contraction coupled?
Calcium does the membrane depolarization and the contraction via entry through L type Ca channels then tha CICR from SR
record obtained from the body surface that registers the differences in electrical potential generated by the heart
ECG (EKG)
P wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
PR interval
time from the beginning of the P wave to the beginning of the QRS complex
ST segment
time from the end of ventricular depolarization to the beginning of the T wave
where are lead attachments
Mean Electrical Axis
Average of all the instantaneous mean electrical vectors during depolarization of the ventricles
Right axis deviation
lead 1 is negative and aVF (lead 3) is positive
left axis deviation
positive lead 1 and negative aVf
What can’t you see on ECG?
SA node, AV node, bundle his, bundle branches, and purkinje network
How do you calculate HR?
300/# of big boxes between two R waves
Rapid heart rate of >100 beats per minute
P waves of successive beats are closer together
Tachycardia
Slow heart rate of <60 beats per minute
P waves of successive beats are farther apart
Bradycardia
3 causes of arrhythmia
Conduction Blocks (aka Heart Blocks), Premature depolarizations, Fibrillations
Conduction to ventricles is slightly delayed, Prolonged P-R interval, No treatment necessary,
May occur in those with some structural heart disease
First Degree Block
Conduction to ventricles is intermittently blocked
Ratios from ECG = 3:1 or 2:1 (2Ps:1QRS), Block is above or below Bundle of His, some patients require artificial pacemaker
Second Degree Block
No impulses from atria reach the ventricles,
No relationship between P waves and QRS,
Bradycardia, Ventricle pumping is severely compromised, Artificial pacemaker required
Third Degree Block
What causes PAC and PVC
enhanced automaticity due to ectopic foci or extra systoles
When Cardiac muscle undergoes irregular contraction that is ineffectual in propelling blood
Re-entry with multiple irregular loop circuits
Fibrillation
Atrial Fibrillation
Since atria don’t significantly help with ventricular filling…
Compatible with life and full activity; may be seen in those with chronic heart disease
No P waves; treat w/ β-blockers to drop HR and re-establish sinus rhythm
Ventricular fibrillation
Twitching of ventricular muscles >not pumping blood >loss of consciousness within seconds death unless immediate intervention (defibrillator)
What is function of defibrillator?
Applies a strong electrical current that will force the entire myocardium into a brief refractory state
Depolarizes the entire heart at once (stops the heart!) This forced refractory state gives the SA node the chance to take over as boss again and establish sinus rhythm
